Cardiovascular Review
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Transcript of Cardiovascular Review
![Page 1: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/1.jpg)
CARDIOVASCULAR
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ATHEROSCLEROSIS
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Atherosclerosis is the leading cause of
Morbidity and Mortality in Western Society
Most Common Factors:
Hypertension
Smoking
Hypercholesterolemia
Diabetes
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Risk Factors• Dyslipidemia: When in excess, LDL accumulates in subendothelial space and can start to
damage the intima, initiating and perpetuating development of atherosclerotic lesions. Treatments slow progression of atherosclerotic plaques.
• Smoking: Tobacco smoking could lead to atherosclerotic disease in several ways, including enhanced oxidative modification of LDL, decreased circulating HDL levels, endothelial dysfunction owing to tissue hypoxia and increased oxidant stress, increased platelet adhesiveness among others.
• Hypertension: Hypertension injures vascular endothelium and may increase the permeability of the vessel wall to lipoproteins. Antihypertensive results like lipid-reducing treatments, halting of atherosclerotic progression
• DM: High blood sugar may result in nonenzymatic glycosylation of lipoproteins (which enhances uptake of cholesterol by scavenger macrophages, as described earlier), or to a prothrombotic tendency and antifibrinolytic state that is often present. Diabetics frequently have impaired endothelial function, gauged by the reduced bioavailability of NO and increased leukocyte adhesion. Managing DM may halt progression
• Elevated CRP: Atherosclerosis is thought to arise from an inflammatory reaction; CRP is a marker of inflammation.
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ATHEROSCLEROSIS
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Atherosclerosis is an INTIMAL PROCESS
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Progression of Atherosclerosis
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What are the steps of Atherosclerosis?
• Endothelial Activation
• LDL, monocytes, endothelium
• Foam Cells
• Oxidized LDL, macrophages
• Fibrous Cap
• SMCs
• Calcification
• Ulceration
• Thrombosis
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Name the important molecules involved in
mediating atherosclerosis
• 1. Monocyte attaches to VCAM-1
• 2. MCP-1 is released to attract more monocytes
• 3. Macrophages release MPO to oxidize LDL
• 4. Scavenger receptor on macrophage allows LDL uptake
• 5. Lipid core releases PDGF to stimulate SMCs
• 6. SMCs release MMP, plaque is destabilized
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What are the important complications of
atherosclerosis?
• Occlusion of vessel
• Thrombus
• Ulceration and hemorrhage
• Atheroembolism
• Narrowing of lumen (stenosis)
• Weakening of wall (aneurysm)
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Atherosclerosis end results
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Name the Complications
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Dangers of Complicated Plaques
• Simple atheromas have a fibrous cap that conveys a great deal of
plaque stability. Thus with simple atheromas, patients may present
with arterial stenosis resulting in hypoperfusion but are unlikely to
present with thrombotic or embolic events.
• Complicated atheromas can have an ulcerated cap, which expose
procoagulants in plaque to circulation increasing chance of thrombus
at the site or lead to greater occlusion of vessel. Rupture of a plaque
in complicated atheromas can also lead to hemorrhage. Also
complicated atheromas can have calcifications, which can increase
the fragility of the plaque and thus likelihood of thrombotic events.
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Atheroembolism will show cholesterol
plaques
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Hyperlipidemia Drugs
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Mechanism Competitively inhibit HMG-CoA reductase:
(1) Decreases intracellular cholesterol induces SREBP
increases expression of LDL-R
(2) VLDL and IDL are cleared more rapidly due to cross-
recognition with hepatic LDL-R
(3) Hepatic VLDL production falls due to reduced cholesterol
availability reduced LDL and triglycerides
Modify platelets and endothelium (e.g., enhanced NO
synthesis)
Suppress inflammation
Effects Decreases LDL 18-55%
Decreases TG 7-30%
Increases HDL 5-15% (unclear mechanism)
Side Effects Myopathy (increased w/ niacin, fibrates), hepatotoxicity, drug
interactions (CYP3A4 inhibition: macrolides, azoles, HIV
protease inhibitors)
Statins
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Mechanism Inhibits NPC1L1 at brush border of epithelial cells in
small intestine reduced chylomicron production
less cholesterol delivered to liver compensatory
increase in hepatic LDL-R increased LDL clearance
Effects Decreases LDL 18%
Has additive effect w/ statins and fibrates on LDL
Side Effects Muscle weakness (slightly higher w/ statin),
transaminitis (slightly higher w/ statin)
Ezetimibe
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Mechanism (+)-charged amines bind (-)-charged bile acids and prevent
recycling in liver
hepatic cholesterol (FXR, CYP7A ) LDL-R
UNLIKE statins, new cholesterol production is stimulated (b/c
HMG-CoA reductase is not inhibited) VLDL production
serum TGs
Effects Decreases LDL 15-30%
Increases HDL 4%
No change/slight increase in TGs
Side Effects GI, drug interactions (fat-soluble drugs: esp warfarin, digoxin),
absorption of fat-soluble vitamins, pancreatitis, cholesterol
gallstones
*Not absorbed systemically, so no systemic side effects*
Bile Acid Resins
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Mechanism Decreases lipolysis in adipose tissue less FAs available for
TG synthesis in liver
Decreases VLDL synthesis, so less LDL
Increases HDL by decreasing hepatic removal of HDL
Effects Decreases LDL 5-25%
Increases HDL 15-30%
Decreases TGs 20-50%
Side Effects Cutaneous flushing (due to prostaglandins; take aspirin), GI
(nausea, PUD), hepatotoxicity, insulin resistance and
hyperglycemia (caution w/ diabetics), gout (raises serum uric
acid levels), myopathy (increases w/ statin)
Niacin (Vitamin B3)
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Mechanism Activate PPARα-RXR
(1) Enhanced oxidation of FAs in liver and muscle
decreased TG levels decreased VLDL
(2) Increased expression of LPL
(3) Increased rate of HDL-mediated reverse cholesterol
transport (due to apo AI transcription)
Effects Decreases LDL 5-20%
Increases HDL 10-20%
Decreases TGs 20-50%
*Larger decreases in TGs and increases in HDL than statins.
Side Effects GI (dyspepsia, abdominal pain, diarrhea), cholesterol
gallstones, myopathy (increased w/ liver and kidney
dysfunction; worse w/ statins), augment effects of oral
hypoglycemic drugs (avoid in diabetes)
Fibrates
Gemfibrozil inhibits glucuronidation of most statins, which can increase statin-
related side effects. Fenofibrate does not.
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Gemofibrizil vs. Fenofibrate
• Drugs that block CYP3A4 slow statin metabolism, increasing the risk
of side effects.
• Gemfibrozil inhibits the glucuronidation of statins and increases the
chances of side effects.
• Choose Fenofibrate in patients taking Statins.
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Mechanism Not well defined, ?agonist of PPARα,
?binds enzymes in TG synthesis but
cannot be utilized
Effects Variable effect on LDL
Increases HDL 9%
Decreases TGs 50%
Side
Effects
Minimal, may prolong bleeding time
(caution use w/ NSAIDs, ASA,
warfarin), caution w/ shellfish
hypersensitivity
Fish Oil (omega-3 FA)
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Major SE of Hyperlipidemia Tx
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4 Major Statin Treatment Groups
• Individuals with clinical atherosclerotic cardiovascular disease (ASCVD).• Tx recommendations:
• High-intensity statin if < 75 years old
• Moderate-intensity statin if > 75 years old (or < 75 y/o and not a candidate for high-intensity)
• Individuals with primary elevations of LDL-C >190 mg/dL.• Tx recommendation: High-intensity statin (or moderate if not a candidate)
• Individuals w/ diabetes aged 40-75 yrs with LDL-C 70-189 mg/dL and w/o clinical ASCVD.• Tx recommendation:
• Estimated 10-year risk of ASCVD < 7.5%: Moderate-intensity statin
• Estimated 10-year risk of ASCVD > 7.5%: High intensity statin
• Individuals w/o clinical ASCVD or diabetes with LDL-C 70-189 mg/dL and 10 year ASCVD risk > 7.5%.• Tx recommendation: Moderate or high intensity statin
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HDL… Good or Bad?
• HDL is an important player in Reverse Cholesterol Transport and
removes cholesterol from circulation. Also there is an inverse
correlation between HDL levels and CVD risk- high HDL = low CVD
risk
• Controversy: Two clinical trials aimed to increase HDL failed in phase
III due to adverse off target effects and lack of efficacy. Another
clinical trial using niacin that increases HDL showed no added benefit.
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Lifestyle Guidelines
• Consume a dietary pattern that emphasizes intake of vegetables, fruits, and whole grains; includes low-fat dairy products, poultry, fish, legumes, nontropical vegetable oils, and nuts; and limits intake of sweets, sugar-sweetened beverages, and red meats.
• Adapt this dietary pattern to appropriate calorie requirements, personal and cultural food preferences, and nutrition therapy for other medical conditions (including diabetes).
• Achieve this pattern by following plans such as the DASH dietary pattern, the US Department of Agriculture (USDA) Food Pattern, or the AHA Diet.
• Aim for a dietary pattern that achieves 5% to 6% of calories from saturated fat.
• Reduce percentage of calories from saturated fat.
• Reduce percentage of calories from trans fat.
• Engage in aerobic physical activity to reduce LDL-C and non–HDL-C: 3 to 4 sessions per week, lasting on average 40 minutes per session, and involving moderate- to vigorous- intensity physical activity.
•
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PCSK9
• PCSK9 is a protein that promotes the degradation of LDL receptors
and decreases the amount of LDL receptors on cell surface. Any
manipulation that will decrease the functionality or availability of
PCSK9 will result in increased LDL receptors on cell surface and thus
lower circulating LDL levels.
• Potential Future RNA interference drug
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CARDIOVASCULAR
HEMODYNAMICS
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Define mean arterial pressure (MAP) and
describe how changes in cardiac output
(CO), systemic vascular resistance (SVR),
and central venous pressure (CVP) affect
MAP.
• Mean arterial pressure (MAP) - the average arterial pressure during a single cardiac cycle.
• MAP=(CO x SVR) + CVP
• MAP = PDIAS + PPULSE/3
• MAP is not the arithmetic mean of PDIAS and PSYS since the heart spends twice as long in diastole than systole under resting conditions
• Increases in the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (SVR) will increase the mean arterial pressure.
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Compare the pressures, flows, and
resistances in the pulmonary circulation
with those in the systemic circulation.
• Pressure: Pulmonary < Systemic
• Flow: Pulmonary = Systemic
• Resistance: Pulmonary < Systemic
• Pulmonary v. Systemic- Pressures in the pulmonary circulation are
not as high as the pressures found in the systemic circulation. The
pressure in the pulmonary circulation is 25/10mmHg. The blood
volume output has to be equal on both sides of the heart so as to
ensure that there are no major blood volume changes between the
pulmonary and systemic circulations. Although is there is resistance
within the pulmonary circulation, it is less than the resistance found in
system circulation.
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Define central venous pressure (CVP)
and how this pressure relates to stroke
volume and cardiac output (CO).
• Central venous pressure (CVP) is the pressure found in the vena
cava near the right atrium.
• Same in same out.
• CVP is a measure of how much blood is going into the heart, which is
equal to how much blood is coming out of the heart. Blood flows from
peripheral venous pool (PVP) to central venous pool (CVP). The
difference in pressure between PVP and CVP is the driving force
pushing blood into the heart. By increasing the difference in pressure
between the two systems, you create a larger flow from PVP to CVP,
which results in more blood going into the right atrium GREATER
STROKE VOLUME AND CARDIAC OUTPUT
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Explain how each of the following affects
CVP: Blood volume, venous compliance,
gravity, respiration, and muscle
contraction.
• Blood volume: increased blood volume increased venous return increased CO
• Venous compliance: decrease in venous compliance increases central venous pressure.
• Gravity: Blood pools in LE momentary decrease in venous return/CO before compensatory mechanisms kick in
• Respiration: during inspiration, the intrapleural pressure decreases. This leads to a decrease in CVP, increase in pressure gradient, increase in venous return/CO
• Muscle Contraction: muscle contraction in the leg helps facilitate the movement of blood from the veins in the lower extremities. This mechanism works against gravity to help increase CVP and increase CO.
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Define the formula that relates blood flow
through an arteriole to (a) pressure
difference down the length of an arteriole
and (b) resistance to that flow.
• The formula that relates blood flow (F) through an arteriole to
pressure (P) down a length and resistance (R) is
• Q = ΔP/R
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Explain what key factors are responsible
for the pressure difference and resistance
to flow.• Resistance depends upon viscosity of blood (n), vessel length (l) and
vessel radius (r)
• R = (n*l)/ (r^4)
• Q = Delta P * (r ^4)/ (n*l)
• Flow is directly related to pressure difference and inversely related to
resistance
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Explain why the decrease in pressure
across arterioles is much greater than the
pressure drop across other vessel types.• Resistance is related to radius to the 4th power, vessel length and
viscosity of the blood.
• Resistance is strongly related to the diameter of the vessel lumen: the smaller the diameter of the vessel lumen, the greater the resistance. Taken as an individual vessel, the individual capillary would exhibit greater resistance than the individual arteriole, because the diameter of the typical capillary lumen is smaller, but, if one looks at the entire vascular system as a whole, much more of the resistance of the system is contributed by arterioles than by capillaries
• There are so many more capillaries and with many capillaries in parallel, that allows collectively a lot of blood flow whereas arterioles tend to be found individually and they also tend to be much longer than capillaries (which also increases resistance). Thus, In the larger system, arterioles are the greater contributor to resistance.
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Define the formula that relates resistance
to blood flow to (a) length of the arteriole,
(b) viscosity of blood, and (c) internal
radius of the arteriole.
• Resistance = (viscosity * length)/ (radius^4)
• The radius has the greatest effect (note it is to the fourth power), so
vasoconstriction and vasodilation greatly affect resistance.
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Explain which one of these factors has the
greatest influence on the resistance to
blood flow and what in turn are the
greatest influences on it.
• Radius has greatest effect on flow because it is to the fourth power
• Blood volume and vessel compliance, vasodilation/constriction, and
pathologic sclerosis may affect radius.
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Predict the relative changes in flow
through an arteriole caused by changes in
arteriole length, arteriolar radius, fluid
viscosity, and pressure difference.
• Using the equations Q = ΔP/R and Resistance = (viscosity *
length)/radius4
• Increase in length → more resistance → less flow
• Increase in radius → less resistance → more flow
• Increase in viscosity → more resistance → less flow
• Increase in pressure difference → more flow
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Differentiate between the pressures and
forces that influence the caliber of intra-
alveolar capillaries and those that
influence extra-alveolar resistance
vessels.• Intra-alveolar capillaries are very closely associated with alveoli, which expand
upon inhalation. This causes the capillaries to also stretch, thus decreasing their diameter. This results in a greater resistance.
• For capillaries, increased lung volume means greater resistance
• Extra-alveolar resistance vessels, on the other hand, are tethered to the pleural cavity. When the lung volume expands, the connective tissue attaching them to the pleural cavity pulls on their walls to expand their diameter
• For bigger vessels, decreased lung volume means greater resistance
• There is a sweet spot in the middle where the lung volume causes the resistance to be the least for both capillaries and the resistance vessels and this is the “working lung volume.”
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Explain the effects of gravity on
pulmonary blood flow.
• When standing up, CVP drops since venous blood pools in the legs.
This decreases venous return and cardiac output, also decreasing
pulmonary blood flow. Also when the person is standing up, the blood
flow is lowest at the apex of the lung and highest at the base.
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Describe how pulmonary blood flow
varies from the base of the lungs to the
apex.• Due to effects of gravity, the base of the lung receives more blood
than the apex. This leads to poor “V/Q” matching, since ventilation (V)
is not matched to blood flow (Q) at different areas of the lung.
• The V/Q ratio at the top of the lungs is high, while the V/Q ratio at the
base of the lungs is low.
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Describe the changes in pulmonary
vascular resistance when the pressures in
pulmonary arteries and pulmonary veins
increase.
• Q = ΔP/R;
• If pressure increases, resistance also increases proportionately in
order to keep the flow constant. However, pulmonary circulation has a
much lower resistance because the vessels have thinner walls, have
less smooth muscle, are more distensible and they can do
“recruitment”. Therefore, the pressure can remain low while
maintaining the same flow
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Describe the roles of recruitment and
distension in decreasing pulmonary
vascular resistance.
• The CO of the right and left sides of the heart are equal. Because
the pressures on the systemic side is so much greater than on the
pulmonary side, the pulmonary system must have much less
resistance. Pulmonary circulation is able to accomplish this lower
resistance with thinner vessel walls, less smooth muscle in the vessel
walls, greater distensibility, and recruitment of non-perfused vessels.
• Recruitment is adding new vessels in parallel circuit to lower the total
resistance, while distension is decreasing the resistance in each
vessel by expanding its diameter
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Use the Fick Principle to estimate
pulmonary blood flow.
• Assumption: in the steady state, the cardiac output of the L and R
ventricles are equal
• O2 consumption = Blood flow ( Arterial-venous O2 Difference)
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Explain the mechanism and significance
of hypoxic vasoconstriction.
• When PAO2 is normal (around 100 mmHg), O2 diffuses from the
alveoli into the nearby arteriolar smooth muscle cells, keeping the
arterioles relatively relaxed and dilated. When PAO2 decreases to
below 70 mmHg, the smooth muscle cells can recognize the reduced
amount of O2 coming in from the alveoli. This causes them to
contract, reducing the amount of pulmonary blood flow to that region
• Significance:
• This reduces pulmonary blood flow to poorly ventilated areas.
Pulmonary blood flow is directed away from poorly ventilated regions
of the lung and redirected to other, better oxygenated regions
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COAGULATION CASCADE
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PT- Extrinsic Pathway
PTT – Intrinsic Pathway (TENET)
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Summarize the mechanism for the
initiation of a blood clot and identify the
essential enzymes involved in this
mechanism.• Tissue Factor (TF) is usually in the subendothelial membrane on
smooth muscle and collagen. When tissue is injured, it is released,
activating the coagulation cascade. This activates the Extrinsic
Pathway by forming a complex with factor 7a.
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Predict the effect of vitamin K deficiency
on the coagulation system
• Factors II, VII, IX, and X require gamma carboxylation
from Vitamin K in order to bind Ca on the surface of a clot. Vitamin K is
absorbed in the intestine and metabolized in the liver. Therefore, people
with end-stage liver disease or people who are not adequately absorbing
Vit K in their intestines will see prolongation of the PT. We see a
prolongation of the PT because the Extrinsic Pathway is most affected.
• Vitamin K is also required for activation of anticoagulant proteins C and
S. These proteins are the first to drop in Vit K deficiency, so we often see
a transient pro-thrombotic state before the clotting factors drop.
• (This is especially important to remember with administration of heparin).
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Explain why a patient with end stage liver
disease may have abnormal coagulation
function.
• Vitamin K is metabolized in the liver. Therefore, people with end
stage liver disease are going to have a Vitamin K deficiency and won’t
be able to activate Factors II, VII, IX, and X.
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Describe the conversion of fibrinogen to
fibrin and the role of factor XIII in this
reaction.
• Thrombin (IIa) converts fibrinogen (I) into fibrin (Ia), which is
necessary to form a clot. Once fibrinogen gets converted into fibrin, it
creates fibrin bonds and forms a fibrin mesh with crosslinks. That
mesh gets activated and covalently bonds in the presence of factor
XIII (activated by thrombin). Factor XIII stabilizes the clot in normal
hemostasis. Factor XIII does not prolong PT or PTT.
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Outline the steps of fibrinolysis and
identify the inhibitors of fibrin degradation.
• Tissue plasminogen activator (t-PA) is released from damaged
vessels and cleaves plasminogen to the active enzyme plasmin.
• In the circulation, plasminogen activator inhibitors 1 and 2 rapidly
inactivate t-PA.
• However, t-PA binds to fibrin locally at the site of release, and
converts fibrin-bound plasminogen to plasmin. Plasmin splits both
fibrinogen and fibrin into degradation products (D-dimer), and if this
occurs at the site of a thrombus it produces lysis of the clot matrix.
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Diagram the formation of the D-dimer and
explain its utility in diagnosis of venous
thromboembolic disease.
• D-dimer: cross-linked regions of fibrin that have been degraded - “you
have a clot, you’ve broken it down, and now you have d-dimer in your
blood” - specific for fibrinolysis (however, not fibrinogenolysis) and
useful for excluding thrombosis
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Given values for various clotting factor
concentrations, be able to predict which
screening tests of coagulation will be
abnormal.
• PT (prothrombin time): tests function of common and extrinsic
pathway (factors I (Fibrinogen), II (Prothrombin) , V, VII, and X).
Defect in any of these factors => increased PT
• PTT (partial thromboblastin time): tests function of common and
intrinsic pathway (factors I, II, XII, XI, IX, VIII, X). Defect in any of
these factors => increased PTT
• Vitamin K deficiency => increase in both because factors II, VII, IX, X
require Vitamin K, so all pathways are affected).
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Explain how activated protein C and
antithrombin act as inhibitors of
coagulation.
• Thrombomodulin (TM), which is normally present on the endothelial
cells, binds thrombin.
• Protein C (a vitamin K dependent factor that is normally found in the
blood) binds to the Thrombin/TM complex, and becomes activated as
Activated Protein C.
• Protein S binds activated Protein C (APC), accelerating its activity.
• APC inhibits coagulation by inactivating Factors V and VIII.
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CV ELECTRICAL ACTIVITY
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Define the roles of (a) If Na+-channels, (b)
K+-channels, (c) voltage-gated Ca2+-
channels, and (d) K-Ach channels, in
pacemaker activity of SA cells.• a) If Na+-channels: Voltage and receptor gated. Contribute to phase 4 pacemaker funny
current (repolarized state to depolarized state) due to a slow inward movement of Na+. • Note: “diastolic depolarization” refers to pacemaker phase/phase 4 and it represents the non-
contracting time between heartbeats (diastole)
• b) K+ channels: outflux of K+ in phase 3 contributes to repolarization
• c) Voltage-gated Ca2+ channels: influx of Ca2+ during phase 0 contributes to depolarization
• d) K-ACh channels: ACh activated K+ channels are activated by ACh and adenosine and are G-protein coupled. They slow SA nodal firing upon VAGAL stimulus.
• 1. ACh is released from vagal nerve terminals (parasympathetic innervation of heart) near SA node
• 2. ACh binds to ACh activated K+ channels and K+ channels open
• 3. Resting potential approaches reversal potential for K+, about -90 mV
• 4. As a result, SA cells take longer to reach threshold for firing
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Describe the effects and mechanisms by
which NE and Ach affect the activity of
these ions channels and therefore HR.
• NE: causes positive chronotropy (increase in heart rate).
• Sympathetic activation of SA node increases slope of phase 4 and lowers threshold, increasing pacemaker frequency
• NE released by sympathetic adrenergic nerves binds to 𝛃1 adrenoreceptors (𝛃1AR above) coupled to a stimulatory Gs-protein which activates adenylyl cyclaseand increases cAMP
• This leads to an increase in funny current (If) and an earlier opening of Ca2+ channels, both of which increase rate of depolarization
• Ach: causes negative chronotropy (slowing of heart rate).
• Vagal nerve stimulation releases ACh at SA node which decreases slope of phase 4 by inhibiting funny currents, hyperpolarizing the cell, and increasing threshold voltage required to trigger phase 0.
• ACh binds to M2 receptors and decreases cAMP via inhibitory Gi protein
• ACh also activates K-ACh channels that hyperpolarizes the cell by increasing K+ conductance
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Define the roles of (a) fast Na+-channels,
(b) K+-channels, (c) voltage-gated Ca2+-
channels, and (d) Na+-Ca2+ exchanger,
in cardiac muscle contraction.
• a) Fast Na+ channels: voltage-gated, open during phase 0, results in rapid depolarization. The upstrokes of all the ventricular muscle cell APs corresponds to the QRS complex
• b) K+ channels: Two types; Transient outward type involved in phase 1 initial repolarization. Delayed rectifier type involved in phase 3 repolarization
• c) Voltage-gated Ca2+ channels: contribute to slow inward, long-lasting current, plateau phase 2
• d) Na+-Ca2+ exchanger: one mechanism to remove calcium from cells after it accumulates after action potentials. 3 Na+ ions in exchanged for 1 Ca2+ ion out.
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Membrane Potentials• Chemical or Concentration Gradient:
• created by concentration differences of ions
• Electrostatic gradient: • positive ions will move to negative charge and vice-versa
• Nernst Equation provides information about the membrane potential that is necessary to oppose the outward movement of a particular ion down its concentration gradient (the equilibrium potential of particular ion). • Ek=-61log[K+]inside/[K+]outside=-96 mV
• But the membrane potential is also dependent on the conductance. This is where the semi-permeable characteristic of plasma membranes becomes important. • Em=g'K(EK)+g'Ca(ECa)+g'Na(ENa)
• The equilibrium potential changes very little due to the relatively small changes in ion concentration. Thus the most important factor determining membrane potential is the differences in ion conductances.
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List the major ions involved in establishing
the cardiac membrane potential.
• Na+, K+, and Ca2+ are the major ions that dictate membrane potential.
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Define equilibrium potential and know its
normal value for K+ and Na+ ions.
• Equilibrium potential: the potential difference across the membrane
required to maintain the concentration gradient across the membrane.
• NOTE: Resting membrane potential for a cardiomyocyte is -90 mV
(quite close to the equilibrium potential for K+). This is due to the fact
that the membrane is much more permeable to K+ in a resting state.
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Sketch a typical action potential in a
pacemaker cell.
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Sketch a typical action potential in a
ventricular cell.
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Describe the ion channels that contribute
to each phase of the cardiac AP.
• Nodal: Ca+ inflow, K+ Outflow, If current
• AV node: Ca+ inflow, K+ Outflow, If current
• Ventricular muscle: Na+ inflow, K+ outflow, Ca2+ inflow, K+ outflow
• Purkinje cells: Na+ and Ca2+ inflow, K+ outflow, K+ outflow, If current
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Describe the role of ion channels in AP
generation and the effects of sympathetic
and parasympathetic nerves on AP
generation and HR.• Ion channels dictate the speed at which signals propagate through the heart. For
instance during phase 0 in nonpacemaker cells, the rate of depolarization depends on the number of activated fast sodium channels. The more sodium channels the more rapidly the cell depolarizes. The faster the cell depolarizes, the faster the adjoining cell will depolarize and thus the more quickly the signal will propagate through the tissue.
• Therefore conditions that decrease the availability of fast sodium channels (e.g., depolarization caused by cellular hypoxia), decreases the rate and magnitude of phase 0, thereby decreasing conduction velocity within the heart.
• Sympathetic NS act on 𝛃1-adrenoceptors with norepinephrine to increase conduction velocity and thus heart rate.
• Parasympathetic NS act on M2 receptors with acetylcholine to decrease conduction velocity and thus heart rate.
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SPECTRUM OF CAD
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Describe the spectrum of ischemic heart
disease and its societal effects.
• Ischemic heart disease is the leading cause of death in the world
among men and women (7 million per year).
• Coronary arteries cannot provide enough perfusion to keep up with
myocardial demand. This results over time due to atherosclerotic
narrowing of the arteries, along with superimposed degrees of plaque
changes, thrombosis, and vasospasm.
• CAD usually presents as an MI, Angina pectoris (most common),
Chronic IHD with heart failure, and sudden cardiac death.
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Compare Stable angina pectoris,
Unstable angina pectoris, Acute MI.
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What is the most common ECG finding
during episodes of stable and unstable
angina?
• ST Depression
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Define subendocardial versus transmural
infarction and be able to differentiate the
ECG segment changes
• Subendocardial infarction involves small areas in the subendocardial
wall of the left ventricle, ventricular septum, or papillary muscle ; ST
depression.
• Transmural infarction is associated with atherosclerosis in a major
coronary artery; the infarct extends through the thickness of the heart
muscle, resulting from nearly complete occlusions; ST elevation.
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Identify ST elevation and pathologic Q
waves and distinguish these findings
associated with the anterior, lateral, or
inferior walls.
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Coronary Atheromatous Plaque
• Plaque disruption is initiated by the release of substances from inflammatory cells within the fibrous cap. These weakened caps could then either rupture spontaneously or be due to a physical force such as in increase in intraluminal BP.
• Following plaque rupture, a thrombus forms due to the activation of platelets (subendothelial collagen), the coagulation cascade, and narrowing of the vascular lumen (vasoconstrictors).
• Dysfunctional endothelium no release of vasodilators such as NO, which would normally oppose the effects of the vasoconstrictors and reduce platelet aggregation.
• Destruction of myocytes in acute coronary syndromes quickly impairs ventricular contraction, which is seen as systolic dysfunction.
• Ischemia/infarction will also impair diastolic relaxation, which reduces left ventricular compliance and leads to elevated filling pressure.
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Identify the main difference between
stunned and hibernating myocardium.
• Stunned myocardium occurs when transient ischemia produces a
prolonged (days to weeks) yet reversible period of contractile
dysfunction. This may occur in UA (unstable angina) patients or
surrounding areas of infarction.
• Hibernating myocardium occurs when blood supply is chronically
reduced, resulting in chronic contractile dysfunction. It promptly
improves when adequate perfusion is restored.
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Diagnostic Tests for CAD
• ECG - look for ST segment elevation/depression and T wave changes
- easy but may not “catch” episodes in outpatients
• Stress test - provocative exercise or pharmacologic
• Nuclear imaging - Te99 or Th201 perfusion studies
• Coronary angiography
• CT
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Diabetics may be more likely to have
silent angina
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Describe the two main determinants of
coronary blood flow.
• The two main determinants of coronary blood flow are (diastolic)
pressure and resistance (governed most strongly by a r^4 term).
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Differentiate endothelial-dependent
vasodilation from endothelial-independent
vasodilation, and name one compound
that works through each mechanism.
• Endothelial-dependent vasodilation
• NO
• Prostacyclin
• In atherosclerotic vessels, the endothelium is dysfunctional and fewer of these vasodilating molecules are released.
• Endothelial-independent vasodilation
• Adenosine
• Lactate
• Acetate
• H+
• CO2
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Myocardial O2 Supply and Demand
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Name the primary mechanism by which
coronary blood flow is maintained in the
presence of moderate epicardial coronary
artery stenosis.
• Coronary arteries consist of both large, proximal epicardial segments
and smaller, distal resistance vessels (arterioles). Atherosclerosis and
narrowing almost always occur in the proximal vessels while the
arterioles usually stay free of flow-limiting plaques. Thus, blood flow is
maintained by the arterioles that can adjust their tone and dilate in
response to metabolic needs. However, if the artery narrowing
continues, the arterioles will eventually be unable to fully compensate.
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Correlate the coronary artery that is
occluded to the anatomic distribution of an
acute myocardial infarction.
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ComplicationsVentricular Wall Rupture: 3 to 7 days (associated with macrophages)
The anterolateral wall at the midventricular level is the most common site. Gross photo shows tan yellow, soft
infarct of 3-5 days duration with rupture of the ventricular wall. Due to excessive phagocytosis from infiltrating
macrophages. Often fatal due to cardiac tamponade.
Papillary muscle dysfunction: 2-7 days (associated with macrophages)
Rupture of a papillary muscle may occur following an MI causing mitral regurgitation. More frequently,
postinfarct mitral regurgitation results from ischemic dysfunction of a papillary muscle and underlying
myocardium and later from papillary muscle fibrosis and shortening, or from ventricular dilation.
Pericarditis: 2-3 days (associated with PMNs)
A fibrinous pericarditis usually develops following a transmural infarct is a result of PMN infiltration in reaction
to necrosis and myocardial inflammation.
Mural thrombus: Within 10 days
With any infarct, the combination of a local abnormality in contractility (causing stasis) and endocardial
damage (creating a thrombogenic surface) can foster mural thrombosis and potentially thromboembolism.
Ventricular Aneurysm:
True aneurysms of the ventricular wall are bounded by myocardium that has become scarred. Aneurysms of
the ventricular wall are a late complication (4-8 wks) of large transmural infarcts that experience early
expansion. The thin scar tissue wall of an aneurysm paradoxically bulges during systole. Complications of
ventricular aneurysms include mural thrombus, arrhythmias, and heart failure; rupture of the tough fibrotic wall
is rarely a concern.
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Describe the indications for coronary
revascularization, including the need for
coronary stenting
• For angina patients, coronary revascularization is pursued if:
• 1) Angina symptoms do not respond to anti-anginal therapy
• 2) Drug therapy results in unacceptable side effects
• 3) Patient is found to have high-risk coronary disease for which
revascularization is known to improve survival
• Persistent angina
• Significant stenosis in 1 or 2 coronary arteries
• Lower-risk patients with stenosis in all 3 CA
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Limitations of Stenting
• Restenosis:
• Neointimal proliferation (migration of smooth muscle cells + ECM production) can
occur over the stent, restenosing the vessel
• Solution: cover the stent with an anti-proliferative medication that prevents
neointimal proliferation. This decreases restenosis by 50%.
• Unfortunately, this also slows endothelialization of the stent, resulting in a greater
incidence of thrombosis if antiplatelet therapy is discontinued too early.
• Give Prasugrel or Clopidogrel for 12 months for drug eluting stents and 1-2 months
for bare metal stents
• Thrombosis
• Stent material is thrombogenic (promotes formation of clots)
• Solution: Antiplatelet drug therapy
• Give Prasugrel or Clopidogrel for 12 months for drug eluting stents and 1-2 months for
bare metal stents
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Coronary Bypass Surgery
• More effective long-term relief of angina than PCI
• Improved survival in patients with:• >50% left main stenosis
• 3 vessel CAD, especially if LV contractile function is impaired
• 2 vessel disease with >75% LAD stenosis
• Diabetes patients with multiple vessels involved
• More complete revascularization than PCI
• Internal Mammary Artery vs. Veins
• Veins are vulnerable to accelerated atherosclerosis (50% are occluded after 10 years) and lower 10 yr. patency rate (80%)
• Arteries are have higher 10 yr. patency rates (90%) and are more resistant to atherosclerosis.
• Specifically, the internal mammary artery appears to be fairly resistant to atherosclerosis
• Limitations: stenosis of the grafted vessel due to atherosclerosis, surgical risk v benefits, comparison of benefits of CABG with PCI
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CAD: PCI versus CABG
PCI
• Brief hospitalization
• Less expensive
• Minimally uncomfortable -
percutaneous
• Restenosis-9%
• Stent thrombosis
• Clopidogrel
CABG
• 5-7 days
• More expensive
• Painful
• Usually definitive
• Survival advantage
• 3VD + reduced LVEF
• Left main CAD
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Exercise Testing
• Positive if chest pain or ECG abnormalities are produced.
• Exercise test considered markedly positive* if:
• 1. Ischemic ECG changes develop in first 3 minutes or persist 5
minutes after exercise stops
• 2. Magnitude of ST segment depressions > 2 mm
• 3. Systolic blood pressure abnormally falls during exercise (due to
ischemia-induced impairment of contractile function)
• 4. High-grade ventricular arrhythmias develop
• 5. Patient cannot exercise for at least 2 minutes because of
cardiopulmonary limitations
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Coronary Angiography
• Coronary Angiography
• Most direct means of identifying coronary artery stenosis
• Atherosclerotic lesions visualized radiographically following injection
of radiopaque contrast material into artery
• Procedure generally safe, but small risk of complication due to
invasive nature
• Reserved for patients whose angina symptoms do not respond to
pharmacologic therapy, have an unstable presentation, or when
results of noninvasive testing are so abnormal that severe CAD
warranting revascularization is likely.
• “Gold Standard” for CAD diagnosis, however…
• Only provides anatomic information
• Clinical significance of lesions depends on pathophysiologic consequences
• Standard arteriography does not reveal composition of plaque or vulnerability to
rupture
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Coronary Blood Flow• In coronary arteries, most of blood flow to the myocardium occurs during diastole.
• During systole: contraction of myocardium compresses ventricular microvasculature
• Blood flow is reduced to the greatest extent within innermost regions of ventricular wall (subendocardium) where compressive forces are greatest
• More susceptible to injury in ischemic events, CAD, reduced aortic pressure
• Blood flow reaches peak in early diastole – where compressive forces removed
• Aortic pressure during diastole thus is most crucial for perfusing coronaries
• In left ventricle – mechanical forces affecting coronary flow are greatest• Due to the higher pressures associated
• Right ventricle and the two atria show some effects of contraction and relaxation of blood flow
• However, it’s much less apparent than the L ventricle
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Explain how arterio-venous O2 difference
and O2 extraction in the heart is unique
when compared with other body organs.
• Unlike most tissues, the heart cannot increase oxygen extraction on demand, because in its basal state it removes almost as much oxygen as possible from its blood supply.
• So any additional oxygen requirement must be met by an increase in blood flow.
• Autoregulation of coronary vascular resistance is most important mediator of this process
• Factors regulating coronary vascular resistance:
• Accumulation of local metabolites
• Endothelium-derived substances
• Neural innervation
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Describe what is meant by coronary
vascular reserve and the role of collateral
blood vessels.
• Coronary flow reserve is the maximum increase in blood flow through
the coronary arteries above normal resting volume.
• The CFR is reduced in coronary artery disease, i.e. there is reduced
vasodilator reserve
• When O2 delivery to heart limited by disease, collateral vessels arise
through angiogenesis
• Process stimulated by chronic stress (hypoxia, exercise training, etc.)
• Collateralization increases myocardial blood supply by increasing the
number of parallel vessels
• Reduces vascular resistance within myocardium
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List the four major coronary arteries and
identify the structures they supply.
• Left main coronary artery• Left anterior descending artery
• Circumflex Artery
• Right main coronary artery
• Left coronary artery supply• Left ventricle
• Left atrium
• Interventricular septum
• Right Coronary Artery supply• Right Atrium
• Right ventricle
• SA node
• AV node
• Interventricular septum
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CHRONIC CORONARY
SYNDROMES
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Identify the factors that regulate
myocardial oxygen consumption and
myocardial oxygen delivery.• The myocardium has one of the highest O2 extraction ratio of all body organs. In
a normal human being at rest the heart consumes 11 % of total body oxygen but receives only about 4 % of the cardiac output as coronary blood flow.
•
• Supply of oxygen depends upon:
• · Oxygen content of blood (systemic oxygenation and hemoglobin)
• · Coronary blood flow (perfusion pressure and coronary vascular resistance)
•
• Myocardial oxygen demand depends upon:
• · Wall stress
• · Heart rate
• · Contractility
•
• O2 demand is increased by ↑ HR, ↑ heart contractility, ↑ preload, ↑ afterload, ↑ ejection time.
• O2 supply is reduced by ↑ HR, ↑ preload, ↓ artery diameter (atherosclerosis).
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Stable Angina
• Angina is an imbalance between coronary blood flow and cardiac O2
consumption leading to ischemia
• Stable angina (classic angina, or angina of effort; most common
form):
• Ischemia is caused by stable coronary artery narrowing (atheromatous plaque)
• Predictable pain on exertion or psychological stress.
• Unchanged in severity, frequency, and duration over weeks to months
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Pharmacologic treatments for angina
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Diagram the neural pathway involved in
anginal pain.• The myocardium is innervated by chemosensitive sensory afferent that are
activated by products of hypoxia such as adenosine (a breakdown product of ATP), acidification (caused by anaerobiosis) and the release of autacoids such as serotonin and prostaglandins E.
• The peripheral axons of these sensory afferents travel within the sympathetic chain. Their cell bodies are located in dorsal root ganglia (DRGs) at thoracic level. The central process contact spinal interneurons located in the dorsal horn of the spinal cord which in turn activate spino-reticular and spinothalamic pathways. The spino-reticular pathway activate the vasomotor center and therefore increases sympathetic tone to the heart potentially causing further ischemic damage by increasing oxygen demand.
• Activation of the spinothalamic pathway causes anginal pain (except in people with silent angina). If pain occurs, this causes further increase in SNA via descending pathways through the medullary vasomotor center.
• Anginal pain is referred to the neck shoulder and arm region because nociceptive afferents that originate from these regions of the bodies and cardiac nociceptorsconverge on the same spino-thalamic neurons.
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Recall the mechanism whereby coronary
blood flow is coupled to myocardial
workload.• Increased contractility/HR increases ATP breakdown leading to
increased local concentration of adenosine, stimulating vasodilation
and increased coronary flow to meet the O2 demands with the
increased myocardial workload.
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Explain why pain, anxiety or exercise can
exacerbate cardiac ischemia.
• Pain, anxiety or exercise cause release of chemical mediators: NE, 5-HT that activate the sympathetic nervous system.
• (1) The increase in sympathetic activity (β1 receptors) and the decrease in parasympathetic activity produce an increase in HR.
• (2) The increase in sympathetic activity (β1 receptors) produces an increase in contractility and a resulting increase in SV.
• Together, the increases in heart rate and stroke volume produce an increase in cardiac output.
• This leads increased O2 demand will exacerbate cardiac ischemia.
• Furthermore, pts with cardiac ischemia often have narrowed coronary arteries (atherosclerosis) so they have dysfunctional endothelium (less vasodilatory/antithrombogenic properties) along with increased resistance so that it is hard for the heart to keep up enough of an O2 supply with the increased workload.
• Stimulation of alpha receptors by catecholemines released during stress, exercise and pain can lead to vasconstriction and without enough local metabolites like endothelial NO to offset that with vasodilatiion (dysfunctional endothelium) one could see less sympatholysis.
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Identify the main goals of therapy for
patients with stable angina.
• Decrease frequency of anginal attacks
• Prevent acute coronary syndromes
• Prolong survival
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MOA of nitroglycerin and isosorbide
mononitrate on vascular smooth muscle
and identify which blood vessels are
preferentially targeted by low doses• Nitroglycerine is converted to Nitric oxide which activates guanylate cyclase leading to
an increase in cGMP in smooth muscle. This leads to dephosphorylation of Myosin Light Chains which regulate the contractile state of smooth muscle and lead to vasodilation.
• Nitroglycerin has a fast onset (2-5 minutes) with sublingual administration and a short duration (30 min). Low dose – relaxation of great veins
• It is used for acute attacks of angina
• Isosorbide Mononitrate: Organic nitrate that causes vasodilation through enzymatic conversion of sulfhydryl groups to nitric oxide
• Slower onset, longer duration
• Used for chronic treatment
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Explain why nitroglycerin must be
administered sublingually while isosorbide
dinitrate or mononitrate is given orally.
• Rapid onset of action and are useful as prophylaxis
• Sublingual admin leads to fast absorption directly into the systemic circulation, thereby avoiding delay inherent to intestinal absorption
• First pass metabolism (degradation) by the liver → nitroglycerin cannot be taken orally because it would be entirely degraded by the liver
• Very lipid soluble compound that is well absorbed by the mucosa of the tongue and mouth
• Spray more stable → in this formulation it stays active for years while tablets take up moisture which degrades the nitroglycerine within a month
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Explain why NO donors and PDE5
inhibitors (e.g. sildenalfil) should not be
co-administered.• The combination of a PDE5 inhibitor (sildenafil (Viagra), etc) and
nitrates extreme hypotension
• If PDE5 is inhibited cGMP cannot be converted to GMP, so much
more cGMP is produced leading to extreme vasodilation
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Nitrate tolerance
• The main limitation to chronic nitrate therapy is the development of
drug tolerance
• Overcome this with:
• 1) a nitrate-free interval for a few hrs (8-12 hrs each day)
• 2) add drugs that reduce the requirement for nitrates (such as B-
blockers or Ca++ channel blockers)
• Mechanism theories include:
• 1) Sulfhydryl hypothesis depletion of SH groups need for
conversion to NO
• 2) Neurohormonal hypothesis reflex increase in vasoconstrictor
hormones (NE, tissue RAS, endothelin)
• 3) Free radical hypothesis free radicals destroy NO
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Explain the rationale for the potential
benefit of combining a beta-blocker with a
nitrate in treating stable angina.
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Statins
Mechanism Competitively inhibit HMG-CoA reductase:
(1) Decreases intracellular cholesterol induces SREBP
increases expression of LDL-R
(2) VLDL and IDL are cleared more rapidly due to cross-
recognition with hepatic LDL-R
(3) Hepatic VLDL production falls due to reduced cholesterol
availability reduced LDL and triglycerides
Modify platelets and endothelium (e.g., enhanced NO
synthesis)
Suppress inflammation
Effects Decreases LDL 18-55%
Decreases TG 7-30%
Increases HDL 5-15% (unclear mechanism)
Side Effects Myopathy (increased w/ niacin, fibrates), hepatotoxicity, drug
interactions (CYP3A4 inhibition: macrolides, azoles, HIV
protease inhibitors)
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Niacin
Mechanism Decreases lipolysis in adipose tissue less FAs available for
TG synthesis in liver
Decreases VLDL synthesis, so less LDL
Increases HDL by decreasing hepatic removal of HDL
Effects Decreases LDL 5-25%
Increases HDL 15-30%
Decreases TGs 20-50%
Side Effects Cutaneous flushing (due to prostaglandins; take aspirin), GI
(nausea, PUD), hepatotoxicity, insulin resistance and
hyperglycemia (caution w/ diabetics), gout (raises serum uric
acid levels), myopathy (increases w/ statin)
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Fibrates
Mechanism Activate PPARα-RXR
(1) Enhanced oxidation of FAs in liver and muscle
decreased TG levels decreased VLDL
(2) Increased expression of LPL
(3) Increased rate of HDL-mediated reverse cholesterol
transport (due to apo AI transcription)
Effects Decreases LDL 5-20%
Increases HDL 10-20%
Decreases TGs 20-50%
*Larger decreases in TGs and increases in HDL than statins.
Side Effects GI (dyspepsia, abdominal pain, diarrhea), cholesterol
gallstones, myopathy (increased w/ liver and kidney
dysfunction; worse w/ statins), augment effects of oral
hypoglycemic drugs (avoid in diabetes)
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List the major side effects of antianginal
medications, including which drugs when
combined have an increased risk of SEs• Nitrates: headache, lightheadedness, hypoTN, palpitations, nausea, dizziness, reflex sinus
tachycardia (BP decrease causes heart to compensate and beat faster).
• DO NOT ADMINISTER with PDE5 inhibitors.
• B-blockers: bronchospasm AVOID in pts with COPD, reduced HR contraindicated in pts with bradycardia, fatigue, sexual dysfunction, may worsen diabetic control and can mask tachycardia and other signs that indicate hypoglycemia *** Diabetic pts
• Calcium channel blockers: associated with an increased incidence of MI and mortality, Headache, flushing, decreased LV contraction (esp with Verapamil and Diltiazem) , pedal edema (esp with Nifedipine and Diltiazem), constipation (esp with Verapamil)
• Combining a B-blocker with a nondihydropyridine Ca++ channel blocker (Verapamil or Diltiazem): negative chronotropic (“changing HR”) effect that can cause excessive bradycardia, combined with a negative inotropic effect, could precipitate heart failure in pts with LV contractile dysfunction
• Ranolazine: dizziness, headache, constipation, nausea
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Describe the mechanism of Prinzmetal
(variant) angina• Prinzmetal’s (variant) angina is ischemia due to focal coronary artery
spasm.
• Mechanism: Patient has intense vasospasm. → Reduced coronary oxygen supply → Prinzmetal’s Angina.
• The cause of the vasospasm is unknown, but it is thought that it may be caused by increased sympathetic activity + endothelial dysfunction.
• Patient presentation: Typical anginal discomfort, usually at rest rather than upon exertion. The pain is often very severe.
• ECG findings: ST segment elevations during the intense vasospasm. ST segment elevation signifies injury.
• Good antianginal drugs for this type of angina: Verapamil & Diltiazem
• Beta Blockers are contraindicated as they may worsen the condition
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Describe the typical ECG findings during
an episode of stable angina.
• ST segment and T wave changes
• Transient horizontal or downsloping ST segment
depressions
• T wave flattening or inversions
• Occasionally ST segment elevations are seen,
suggesting more severe transmural myocardial
ischemia
• In contrast to an acute MI, ST deviations
caused by angina quickly normalize with
resolution of the patient’s symptoms.
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Describe the findings of a positive
exercise ECG treadmill stress test.
• The test is considered positive if the patient’s typical chest discomfort
is reproduced or if ECG abnormalities consistent with ischemia
develop (ex: >1 mm horizontal or downsloping ST segment
depressions)
• The test is considered markedly positive if one or more of the
following signs of ischemic heart disease occur:
• Ischemic ECG changes develop in the first 3 minutes of exercise OR persist 5
minutes after exercise has stopped
• The magnitude of ST segment depressions is >2 mm
• The systolic blood pressure abnormally falls during exercise (i.e. resulting from
ischemia induced impairment of contractile function)
• High grade ventricular arrhythmias develop
• The patient cannot exercise for at least 2 minutes because of cardiopulmonary
limitations
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Recall the effect of a 60% epicardial
coronary artery stenosis on resting
coronary blood flow versus its effect on
maximal coronary flow.
• This is pointing to the fact that if
an epicardial coronary artery is
stenosed to a level of 60%, this
will limit the maximum amount
of blood that can flow through a
coronary artery (and therefore
may lead to angina when you
are exercising or exerting
yourself), but it will have no
effect on the resting coronary
blood flow, which is much less.
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Explain why nuclear cardiac imaging and
echocardiography are sometimes
performed in conjunction with exercise
stress testing.
• Some patients have baseline ST segment abnormalities or T wave
abnormalities (particularly LVH with strain). For these patients, the
ECG findings provided by the exercise stress test aren’t very useful.
• Also, the exercise stress test can yield ambiguous results - this is
especially of concern when there is a high clinical suspicion of
ischemic heart disease.
• Exercise stress testing in conjunction with nuclear cardiac imaging or
echocardiography increases sensitivity and specificity.
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Explain the most common reasons that
percutaneous revascularization (PCI) is
offered to patients with stable angina.
• Many patients with stable angina can be managed with
pharmacologic therapy alone.
• PCI is offered to patients with stable angina if:
• The patient’s symptoms of angina do not respond adequately to
antianginal drug therapy
• Unacceptable side effects of medications occur
• The patient has high risk coronary disease for which
revascularization is known to improve survival
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Name one criterion by which patients are
selected for CABG instead of PCI.
• CABG is good for:
• >50% left main stenosis
• 3 vessel CAD, especially if LV contractile function is impaired
• 2 vessel disease with >75% LAD stenosis
• Diabetes patients with multiple vessels involved
• PCI is good for:
• Patients with persistent episodes of angina and significant stenoses in one to two
coronary arteries
• Some lower risk patients with three-vessel disease
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ACUTE CORONARY
SYNDROMES
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Describe the pathophysiologic events that
change a stable atherosclerotic plaque
into the unstable plaque of ACS
• Increasing size and protrusion of lipid core mechanical stress
focused on plaque border
• Local accumulation of foam cells and T lymphocytes releasing MMPs
increases degradation of ECM.
• Thin fibrous cap vulnerability to rupture
• Rupture of plaque exposure of procoagulants thrombosis
• Causes occlusion and infarction
• Endothelial dysfunction prevents release of endogenous vasodilators
(NO, prostacyclin) which also normally inhibit platelets, thus impairing
protective mechanisms against thrombosis.
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Compare and contrast the
pathophysiologic and clinical features of
unstable angina, non-STEMI and STEMI.
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Recognize the non-atherosclerotic causes
of an acute coronary syndrome.
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Describe the functional alterations
impairing contractility and compliance.
• Systolic dysfunction - destruction of functional myocardial cells
leading to impaired ventricular contraction
• Hypokinetic: a localized region of reduced contraction
• Akinetic - a segment that does not contract at all
• Dyskinetic - a segment that bulges outward during contraction of the remaining
functional portions of the ventricle
• Diastolic dysfunction - compromise of the left ventricle when
ischemia/infarction causes elevated ventricular filling pressures
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Define and distinguish the terms “stunned
myocardium”, “ischemic preconditioning”
and “infarct expansion”
• Stunned myocardium - prolonged but reversible period of contractile dysfunction after a period of transient ischemia. The tissue prolongs systolic dysfunction even after restoration of blood flow. Contractile force is regained days to weeks later. If the tissue is simply stunned rather than necrotic, its function will recover.
• Ischemic preconditioning - brief ischemic insults to a region of myocardium that make that region more resistant to subsequent episodes. Thus, patients who have an MI after recent anginal pain often have less morbidity and mortality than those with an “out-of-the-blue” MI. The conditioning may be triggered by substances released during ischemia like adenosine and bradykinin.
• Infarct expansion - in an early post-MI period, the affected ventricular segment enlarges without additional myocyte necrosis - occurs by thinning and dilatation of the necrotic zone from “slippage” between muscle fibers.
• The increase in ventricular size 1) augments wall stress, 2) impairs systolic contractile function, and 3) increases the likelihood of aneurysm formation
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Cellular Changes of Acute MI
• Occluded coronary vessel falling O2 levels switch from aerobic to anaerobic
metabolism lactic acid accumulation lowered pH (Metabolic Acidosis)
• The decrease in high-energy phosphates like ATP interfere with Na+/K+ ATPase
elevation in intracellular Na+ and extracellular K+
• Rising intracellular Na+ cellular edema
• Membrane leakage and rising extracellular K+ altered transmembrane
electrical potentials and predisposition to arrhythmias
• Intracellular Ca2+ accumulation activates degradative lipases and proteases and
contributes to final pathway of cell destruction.
• Metabolic changes decrease function within 2 minutes of an occlusive thrombosis.
• Without intervention, irreversible cell injury ensues within 20 minutes
• Proteolytic enzymes leak across membrane and damage myocardium
• Release of macromolecules into circulation (Troponin @ 4 hours)
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Compare and contrast the use and time
course of troponin and CPK-MB in
diagnosis an acute MI• Troponins
• The specific troponins used for the diagnosis of MI are cTnI and cTnT, because these are the cardiac forms of troponin I and are also structurally unique, and thus easier to assay.
• These markers tend to increase 3-4 hours after onset of discomfort, peak between 18-36 hrs and may be present for up to 2 weeks.
• CPK-MB
• Isoenzyme of creatine kinase that exists in the heart - CPK-MB.
• The measurement for CPK-MB is calculated by the ratio of CPK-MB: total CPK. • Values of >2.5% usually indicative of cardiac injury
• Levels of CPK-MB rises between 3-8 hrs following infarction, peaks at 24 hrs and goes back to normal after 48-72 hrs.
• This makes it a useful indicator for REINFARCTS.
• Neither of these markers are good for early diagnosis of MI, since they take a few hours to peak. In early situations, ECG and history are most important.
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Do not use Fibrinolytic treatment
regimens for NSTEMI
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Name at least two fibrinolytic agents and
explain the benefits, limitations and major
risks of thrombolytic therapy.• Alteplase, tPA
• Reteplase, rPA
• Tenecteplase - TNK-tPA
• Very effective in lysing the intracoronary thrombi found in STEMI.Patients who receive FT quickly (within 2 hours of onset of symptoms) have half the rate of mortality of STEMI pts who get it after 6 hrs
• Fibrinolytic therapy does not benefit patients suffering from UA or NSTEMI.
• Bleeding is the most common complication of fibrinolytic therapy, patients who require effective fibrin clotting are contraindicated for this therapy. That includes post-op patients, those with a bleeding disorder or recent stroke.
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Define the term “primary percutaneous
coronary intervention” and explain the
benefits, limitations and major risks• Angioplasty + stenting of the vessel
• Medications given during PCI: Aspirin, Heparin, IV GP IIb/IIIa receptor antagonist• *may substitute Direct Thrombin Inhibitor (e.g. Bivalirudin) for Heparin + GP IIb/IIIa antagonist combo
• If receiving a stent → Oral Thienopyridines (e.g. Clopidogrel) given to reduce risk of ischemic complications & stent thrombosis
• Clopidogrel or Prasugrel given for >12 months after stent placed
• Benefits:
• Treat patients with contraindications to Fibrinolytic therapy or unlikely to do well with fibrinolysis (e.g. late presentation to hospital - more than 3 hrs with symptoms, in cardiogenic shock)
• Treat patients initially treated with fibrinolytic therapy without adequate response (e.g. ST segment elevations)
• In comparison to Fibrinolytic Therapy:
• Greater survival & Lower rates of reinfarction and bleeding
• Preferred method IF performed by experienced operator within 90 mins of arriving
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TIMI Risk Score
• Patients with “most concerning clinical features” →
identified by risk assessment algorithms (higher scores: ≥
3)TI
• Age > 65 years old
• ≥ 3 Risk factors for coronary artery disease
• Known Coronary Stenosis of ≥ 50% by prior angiography
• ST segment deviations on ECG at presentation
• ≥ 2 anginal episodes in prior 24 hrs
• Use of Aspirin in 7 days prior
• Elevated serum troponin or CK-MB
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Identify the most important predictor of
post-MI outcome, and describe how to
risk-stratify a patient after acutely treating
their myocardial infarction.• Most important predictor of post-MI outcome - LV Dysfunction
• Identify patients at high risk for complications:• Exercise treadmill testing
• Attention to underlying cardiac factors
• Smoking
• Hypertension
• Diabetes
• LV ejection fraction of less than or equal to 30% after MI high risk of sudden cardiac death• Prophylactic placement of implantable cardioverter-defibrillator recommended
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Ejection Fraction of <30% after MI is high
risk for sudden cardiac death and
suggests prophylactic placement of ICD.
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INTRO TO EKG
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Know the electrode placements and
polarities for a 12‐lead electrocardiogram
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Frontal Plane Electrodes
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Standard values for EKG print out
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Correlate tracing to electrical state of heart
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Systematic Approach
• Rate
• Rhythm
• Axis
• Intervals
• Hypertrophy
• Ischemia
• Special Changes
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RATE
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A rate of 60-100 is normal <60 is
bradycardia and >100 is tachycardia
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Method 1 for Determining Rate
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Method 2 for Determining Rate
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Method 3 for Determining Rate
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RHYTHM
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Criteria for Normal Rhythm
• A P wave morphology P wave (atrial contraction) precedes every
QRS complex
• A QRS complex follows every P wave
• The rhythm is regular, but varies slightly during respirations
• The rate ranges between 60 and 100 beats per minute
• The P waves maximum height at 2.5 mm in II and/or III
• The P wave is positive in I and II, and biphasic in V1
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Is there a QRS after every P?
• NO
• If rate < 100:
• a) 2 block type I ("Wenkebach," gradually lengthening PR until one
beat is dropped)
• b) 2 block type II (dropped beat without change in PR), or
• c) 3 AV block (no correlation between P and QRS)
• If rate >100:
• atrial or nodal tachycardia (SVT) or atrial flutter, both with block.
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Is there a P before every QRS?
• NO• a) if a single slow beat: escape beat
• atrial if different P
• nodal if no P
• ventricular if QRS>0.12
• b) if a slow rhythm: escape rhythm
• nodal if no P at rate 50-60
• ventricular if QRS>0.12 & rate <40
• c) if a single fast beat: premature beat
• PAC if different P
• PJC if no P
• PVC if QRS>0.12
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Tachycardic
• a) if wide (>0.12) and rate >120 then ventricular tachycardia until
proven otherwise
• b) if narrow and regular then atrial (with preceding P) or AV nodal (no
P) tachycardia
• c) if irregularly irregular then either
• 1) atrial fibrillation (no P waves and coarse baseline)
• 2) multifocal atrial tachycardia (MAT, three different P wave morphologies).
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AXIS
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Define mean electrical vector (axis) of the
heart and give the normal range.
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Determine the mean electrical axis from
knowledge of the magnitude of the QRS
complex in the standard limb leads.
• Inspect limb leads and
determine QRS that is most
isoelectric, the mean axis is
perpendicular to that lead
• Inspect the lead that is
perpendicular to the
isoelectric complex, if the
QRS is primarily upward,
then the mean axis points
towards the (+) pole of the
lead.
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Quadrant Approach
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INTERVALS
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Intervals
• PR
• Measure of the health of the AV node and bundle of His
• Normal: < 0.2 s (1 big box)
• Pathology: Prolonged interval: AV blocks 1,2,3
• QRS
• Measure of the health of the His-Purkinje system
• Normal: < 0.12 s (3 small boxes)
• Pathology: Conduction delay: LBBB,RBBB, fascicular blocks
• QT
• Measure of repolarization
• Normal: < 0.45 s
• Pathology: Long QT syndrome, electrolyte imbalance, ischemia
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First Degree AV Block
• Prolonged PQ Interval >.2s
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Second Degree AV Block- Wenkebach
• In second degree AV block type I, the PQ interval prolongs from beat
to beat up until the drop-out of one QRS complex. The characteristics
of a Wenkebach block:
• QRS complexes cluster
• The PQ interval prolongs every consecutive beat
• The PQ interval that follows upon a dropped beat is the shortest.
• The amount of block decreases during exercise
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Second Degree AV Block – Mobitz II
• In second degree AV block type II, beats are dropped irregularly
without PQ interval prolongation.
• As the drop out of beats is irregular, no clustering of QRS complexes can be seen
as in second degree block type I.
• Second degree AV block type II marks the starting of trouble and is a class I
pacemaker indication
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Third Degree AV Block
• Third degree AV block is synonymous to total block: absence of
atrioventricular conduction. The P-waves and QRS complexes have
no temporal relationship: AV dissociation. The ventricular rhythm can
be nodal, idioventricular or absent.
• During third degree AV block the blood supply to the brain can insufficient, leading to
loss of consciousness. Adams Stokes attacks attacks are attacks of syncope or pre-
syncope in the setting of third degree AV block.
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QRS Interval
• Measure QRS interval, if > 0.12 then Look at V1 for LBBB and RBBB
• Left bundle branch block (downgoing)
• Right bundle branch block with (bunny ears and upgoing)
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LBBB
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RBBB
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LAFB
• Left Axis Deviation
• qR in the lateral leads
• rS in the inferior leads
• Mild QRS widening
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LPFB
• Right Axis Deviation
• rS in lateral leads
• qR in inferior leads
• Mild or no QRS widening
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QT Interval
• Bazett’s Formula
• QTc = [QT Interval] / √[R-R interval]
• Important due to R on T risks
• Acquired
• Medications
• Electrolyte abnormalities
• Ischemia
• Hypothermia
• Genetic
• Sodium Channel abnormalities
• Potassium Channel abnormalities
• High risk for ventricular fibrillation
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Brugada Syndrome
• ST elevation ≥2 mm and a coved type ST segment followed by a
negative T wave. This morphology must be present in >1 right
precordial lead (V1-V3).
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Wolff Parkinson White
• Short PR interval with delta wave
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Digoxin Intoxication
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HYPERTROPHY
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Differentiate left atrial enlargement from
right atrial enlargement on an ECG
• Right Atrial Enlargement
• Lead II – P wave > 2.5 mm
• Lead V1 – Biphasic p wave with upright deflection larger
• Left Atrial Enlargement
• Lead II – The P wave is broader
• P mitrale
• Lead V1 – Biphasic p wave with terminal component larger
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Atrial Enlargement
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Right Atrial Enlargement
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Left Atrial Enlargement
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LEADS II AND V1 ARE MOST PARALLEL
TO ATRIAL DEPOLARIZATION BEST
AREA TO VIEW P WAVE
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ECG of ventricular hypertrophy
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Left Ventricular
Hypertrophy
• R in V5 or V6 + S in V1 >35 mm
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Look for ST depression STRAIN
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Right Ventricular
Hypertrophy
• QRS duration < 120ms
• Right heart axis (> 110 degrees)
• Dominant R wave in V1
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INFARCTION
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Infarction
• Ischemia: inverted T waves or ST depression
• Injury: ST elevation
• Necrosis: Pathologic Q waves
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Myocardial Ischemia
• ST depression and T-wave changes.
• New horizontal or down-sloping ST depression >0.05 mV in two contiguous leads;
and/or T inversion ≥0.1 mV in two contiguous leads with prominent R-wave or R/S
ratio ≥ 1
• ST elevation
• New ST elevation at the J-point in two contiguous leads with the cut-off points: ≥0.2
mV in men or ≥ 0.15 mV in women in leads V2–V3 and/or ≥ 0.1 mV in other leads.
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Myocardial Infarction
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Myocardial Necrosis
• Pathologic Q waves – irreversible injury
• Localize based upon which arteries are involved
• Any Q wave > 1 small box in duration and more than 1/3 the height of
the R wave in 2 contiguous leads.
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Predict which coronary artery is affected in
a patient experiencing an acute
myocardial infarction.
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Anterior Hemiblock
• LAD occlusion
• Normal or slightly widened QRS
• Q1S3
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The only upside down QRS complex
allowed is in AVR. Do not assess Q waves
in AVR.
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ST segment depression in NSTEMI is
nonlocalizing to specific arteries
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Be careful about diagnosing an infarct in
the presence of LBBB.
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THE CARDIAC CYCLE
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Outline the phases of the cardiac cycle
and describe which phases demarcate
systole and diastole.
• There are 7 phases in the cardiac cycle.
• Systole: phases 2-4
• ventricular contraction and ejection
• Diastole: phases 5-7 and 1
• ventricular relaxation and filling
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The Cardiac Cycle
• 1. During diastole the mitral valve is open so LA and LV have equal
pressure
• 2. Late diastole, LA contraction causes small rise in pressure (a wave)
• 3. Systolic contraction, LV pressure rises and MV closes when LV
exceeds LA pressure (S1)
• 4. When LV pressure exceeds aortic pressure, AV valve opens (silent)
• 5. Ventricle relaxes, pressure drops below aorta, AV closes (S2)
• 6. LV pressure falls below and MV opens (silent)
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Atrial Waveform
• a wave: Increase due to atrial contraction.
• x descent: Fall in atrial pressure due to end of atrial contraction.
• c wave: Increase due to bulging of AV valves back into atrial
chambers.
• x’ descent: Fall in atrial pressure after ‘c wave’ due to rapid ventricular
ejection.
• v wave: Peak due to continuing venous return just prior to AV valves
opening.
• y descent: Rapid fall in atrial pressure after ‘v wave’ due to opening of
AV valves.
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Systole occurs approximately between
the S1 and S2 heart sounds
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Derive the stroke volume and left
ventricular ejection fraction from the left
ventricular end-systolic and end-diastolic
volumes.
• SV= LVEDV-LVESV
• EF = SV/LVEDV
• Normal ≥ 55%
• The left ventricular ejection fraction is the percentage of blood that
leaves the left ventricle with each contraction.
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Diagram the timing of the s1, s2, s3, and
s4 heart sounds to the left ventricular
pressure curves and identify the
mechanical events that cause each
sound.• S1 = Mitral valve closes
• S2 = Aortic valve closes
• S3 = Mitral valve opens. This can be normal in children and pregnant women but is pathological in adults. Systolic defect associated with ventricular dilation.
• S4 = Pathological. Blood is being forced against a stiff ventricle. Ex: Left ventricular hypertrophy. Diastolic defect.
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Describe the relative contribution of
passive and active left ventricular filling
and the effects of heart rate and
sympathetic activation on this ratio.• Active ventricular filling is associated with atrial contraction, while passive ventricular
filling depends on venous return and occurs before atrial contraction.
• At Rest: Active filling accounts for approximately 10% of total left ventricular filling.
• At High Heart Rates (Exercise): Active filling accounts for up to 40% of left ventricular filling. This increased contribution results from two factors:
• Increased heart rate leads to shortened periods of diastolic filling → Reduced amount of blood entering the ventricle during passive filling.
• Sympathetic nerve activation increases the force of atrial contraction → Increased amount of blood entering the ventricle during active filling.
• This phenomenon is known as “atrial kick”
• Clinical Aside: In atrial fibrillation, atrial contraction does not contribute to ventricular filling. This leads to inadequate filling that is exacerbated during physical activity.
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State the mean right and left atrial
pressures and peak and mean right and
left ventricular pressures
• Mean Right Atrial Pressure: 4 mmHg (average)
• Mean Right Ventricular Pressure: 25 mmHg (systolic) and 4 mmHg
(diastolic)
• Mean Left Atrial Pressure: 8 mmHg (average)
• Mean Left Ventricular Pressure: 120 mmHg (systolic) and 8 mmHg
(diastolic)
• The left heart has higher average pressures because the left ventricle
must eject blood into the entire systemic circulation. The right heart
has lower average pressures because it is responsible for ejecting
blood only to the lungs.
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Dicrotic Notch in Pressure Tracing
• A very brief and transient increase in aortic pressure that corresponds
with closure of the aortic valve at the conclusion of systole.
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Define cardiac output and cardiac index
and describe their relationship
• Cardiac Output: CO = SV X HR
• Cardiac Index (CI) = CO / BSA
• Cardiac index is a variation of cardiac output that normalizes for the
size of the individual.
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Describe the relationship between SV and
HR and their relative influence on cardiac
output.• CO = HR X SV is the basic relationship. However, since changes in
heart rate can affect stroke volume, changes in heart rate do not
correspond to an exactly proportional change in cardiac output.
• Examples:
• As heart rate increases through pacemaker stimulation, ventricles
have less time to fill with blood during diastole. Less ventricular filling
corresponds with a decreased stroke volume.
• When heart rate increases by 2X due to pacemaker stimulation alone,
cardiac output increases less than 2X.
• When heart rate increases by 2X due to exercise, cardiac output
increases more than 2X.
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STEMI TBL
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Know the symptoms and signs acute
coronary syndrome
• Retrosternal pressure radiating to neck, jaw or left shoulder and arm
(C7-T4); more severe and lasts longer than previous anginal attacks
• Sympathetic response: Diaphoresis, tachycardia, cool, clammy skin
• Systolic dysfunction: dyspnea
• Ventricular noncompliance: S4 and S3 heart sounds
• Inflammation: Fever
• Serum Markers: Increased troponin and CK-MB
• ECG: ST depression or elevation, inverted T wave, Q wave
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ECG of Unstable Angina and NSTEMI
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ECG findings of an acute MI
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Localize the site of an infarction and know
the likely infarct related artery based on an
ECG.
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Ventricular Fibrillation and Tachycardia
• Rapid, disorganized electrical activity of the ventricles
• Most fatal before arrival at hospital
• If present 48 hours after MI, then typically reflects severe left
ventricular dysfunction and is associated with high mortality rates
• If it presents <48 after MI, prognosis is much better and often due to
transient electrical instability
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Atrial Fibrillation
• Result from atrial ischemia or atrial distension second to LV failure
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Sinus Tachycardia and Bradycardia
• Bradycardia: due to excessive vagal stimulation or SA nodal ischemia
in the setting of inferior wall MI
• Tachycardia: due to pain, anxiety, heart failure, drug administration or
intravascular volume depletion
• Can exacerbate ischemia
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Complete Heart Block
• May result from ischemia or necrosis of conduction tracts
• May develop transiently from increased vagal tone
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Explain the difference between ST
elevation MI (STEMI) and non STEMI and
discuss why a timely diagnosis is most
important for a STEMI.
• A STEMI involves the complete occlusion of one of the coronary arteries and leads to severe ischemia
• ST elevation localizes on ECG based on which artery is involved
• A timely diagnosis is extremely important for as irreversible damage to
myocytes begins to occur after about 20 minutes.
• Changes seen later in ECG such as inversion of the T wave and abnormal Q waves can also be avoided following successful treatment if MI is recognized.
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Fibrinolysis vs. primary PCI for treatment
of an acute MI.• NSTEMI: With a NSTEMI, fibronolysis is never used as patients do not benefit
from this therapy. The decision whether to proceed with PCI is based upon a patient’s TIMI score. An early invasive strategy is recommended in patients with higher scores (≥3). If an early invasive approach is adopted, the patient should undergo angiography within 24 hours.
• STEMI: In contrast to UA and NSTEMI, the culprit artery in STEMI is typically completely occluded, and therefore, the major focus of acute treatment is to achieve prompt reperfusion of the jeopardized myocardium using either fibrinolyticdrugs or percutaneous coronary mechanical revascularization.
• Primary PCI is usually the preferred reperfusion approach in acute STEMI, if the procedure can be performed by an experienced operator within 90 minutes of hospital presentation.
• In addition, primary PCI is preferred for patients who have contraindications to fibrinolytic therapy or are unlikely to do well with fibrinolysis, including those who present late (>3 hours from symptom onset to hospital arrival) or are in cardiogenic shock. Furthermore, “rescue” PCI is recommended for patients initially treated with fibrinolytic therapy who do not demonstrate an adequate response.
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Describe the rationale and the indication
for adjunctive therapies for the
management of the ACS• Focus of treatment for STEMI, UA and NSTEMI consists of anti-
ischemic medications to restore the balance between myocardial oxygen supply and demand and anti-thrombotic therapy aimed at preventing further growth, and facilitating resolution of the underlying occlusive coronary thrombus.
• Beta blocker: lower heart rate
• Propanolol
• Metoprolol, Atenolol, esmolol, acebutolol
• Aspirin/Clopidogrel: antiplatelet
• Aspirin
• Clopidogrel
• Prasugrel
• Ticagrelor
• ACE Inhibitors: reduces LV remodeling
• Statins: treats atherosclerosis
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Define "cardiogenic shock" and explain
the clinical manifestations of this
syndrome.• Cardiogenic shock is a condition of severely decreased cardiac
output and hypotension (systolic blood pressure < 90 mm Hg) with
inadequate perfusion of peripheral tissues that develops when
>40% of the LV mass has infarcted (after MI).
• Chest pain/pressure, tachypnea, tachycardia, weak pulse, skin that is
pale/blotchy/sweaty, lightheaded, disoriented, syncope, coma,
decreased urination.
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List the four types of "non-cardiogenic
shock" and be able to explain the
differences from cardiogenic shock.• 1. Hypovolemic shock accompanies significant hemorrhage, or fluid loss from severe burns,
chronic diarrhea, or prolonged vomiting. The direct consequence of hypovolemia is inadequate cardiac filling and reduced stroke volume reduced CO.
• 2. Anaphylactic shock is a result of an allergic reaction. This immediate hypersensitivity reaction is mediated by histamine, prostaglandins, leukotrienes, bradykinin that results in substantial arteriolar vasodilation, increases in microvascular permeability, and loss of peripheral venous tone. These combine to reduce both total peripheral resistance and cardiac output.
• 3. Septic shock is also caused by profound vasodilation but specifically from substances released into the circulating blood by infective agents
• 4. Neurogenic shock is produced by loss of vascular tone due to inhibition of the normal tonic activity of the sympathetic vasoconstrictor nerves and often occurs with deep general anesthesia or in reflex response to deep pain associated with traumatic injuries. It may also be accompanied by an increase in vagal activity, which significantly slows the cardiac beating rate. This type of shock is often referred to a vasovagal syncope.
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Explain the cardiovascular alterations
occurring in shock (both compensatory
and decompensatory).
• Compensatory: Increased sympathetic and decreased
parasympathetic response.
• Rapid, shallow breathing increase venous return
• Renin, vasopressin, epinephrine release increase vasoconstriction,
• Glycogenolysis fluid shift
• Decreased organ blood flow (particularly kidneys)
• Decompensatory : Reduced organ blood flow Drive to reduce
arterial pressure positive feedback cycle
• These decompensatory mechanisms are compounded by a reduction in
sympathetic drive and a change from vasoconstriction to vasodilation with
a further lowering of blood pressure. Can lead rapidly to death.
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Outline the initial management in the
treatment of cardiogenic shock.
• Early cardiac catheterization and revascularization can improve
prognosis prior to occurrence.
• Tx of shock:
• IV inotropic agents Dobutamine, Dopamine
• Increase contractile force
• Arterial vasodilators Hydralazine and Ca2+ Channel Blockers
• Once BP improves to reduce resistance to LV contraction
• Placement of intra-aortic balloon pump into aorta via femoral artery
• Percutaneous Left Ventricular Assist Device (LVAD)
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Main difference of cardiogenic shock vs.
noncardiogenic shock physiology is that
cardiogenic shock causes decreased CO
by DIRECTLY IMPACTING THE
CONTRACTILITY OF THE
MYOCARDIUM while the other forms of
shock indirectly impact CO.
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Describe how the susceptibility to
infarction varies between the myocardial
layers.
• Transmural infarcts
• Span the entire thickness of the myocardium
• Result from total, prolonged occlusion of an epicardial coronary artery
• Subendocardial infarcts
• Exclusively involve innermost layers of the myocardium (usually of the
left ventricle, ventricular septum, or papillary muscles)
• Subendocardium is MORE susceptible to ischemia because:
• It is the zone subjected to highest pressure from the ventricular chamber
• It has few collateral connections that supply it
• It is perfused by vessels that must pass through layers of contracting
myocardium
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Factors Determining Infarct Size
• The amount of tissue that infarcts relates to:
• The mass of myocardium perfused by the occluded vessel
• The magnitude and duration of impaired coronary blood flow
• The oxygen demand of the affected region
• The adequacy of collateral vessels that provide blood flow
• The degree of tissue response that modifies the ischemic process
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Arrhythmias
• Occur frequently during acute MI and are a major source of mortality
prior to hospital arrival
• Upon arrival, arrhythmia associated deaths are uncommon
• Due to anatomic interruption of blood flow to conduction structures
• Accumulation of toxic metabolic products
• Membrane leaks causing abnormal cellular ion concentrations
• Autonomic stimulation
• Administration of arrhythmogenic drugs
• Detection: EKG
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Ventricular arrhythmias within 48 hours
solely suggest unstable electrical currents,
but after 48 hours it is an indication for
ICD implantation
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Pericarditis
• Early in post-MI period: Days 1-3
• Cause: inflammation from necrosis/healing spreads from myocardium
to pericardium
• Detection:
• Sharp pleuritic pain
• Fever
• Pericardial Friction Rub
• Resolved with aspirin
• Incidence limited by acute reperfusion strategies post MI
• Anticoagulants contraindicated
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Mechanical Complications• LV Papillary Muscle Rupture:
• Detection: Loud holosystolic murmur due to severe acute mitral regurgitation may be fatal
• Partial rupture moderate regurgitation sxs of heart failure or pulmonary edema
• Posteromedial LV papillary muscle is more susceptible
• Ventricular Free Wall Rupture (rare/infrequent): occurs within 2 weeks following MI
• Necrotic myocardium free wall rupture hemorrhage into pericardial space rapid cardiac tamponade (restricts ventricular filling)
• Fatal
• Detection: Imaging studies surgical repair
• Ventricular Septal Rupture 3-7 days• Blood shunted from LV to RV congestive heart failure (JVD)
• Detection: Loud holosystolic murmur @ Left Sternal Border (transseptal flow)
• Use Doppler echocardiography to distinguish between acute mitral regurgitation (or O2 saturation in chambers)
• True Ventricular Aneurysm: Late complication (weeks to months after MI)• Weakened ventricular wall due to phagocytic clearance of necrotic tissue outward bulge
• Suspected with persistent ST segment elevations on ECG (weeks later) and/or bulge on CXR
• Detection: Confirmed by echocardiography
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Holosystolic Murmurs
• VSD
• Mitral Regurgitation
• Tricuspid Regurgitation
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Heart Failure
• Due to impaired LV contractility (systolic dysfunction) and myocardial
stiffness (diastolic dysfunction)
• Detection:
• Dyspnea
• Pulmonary Rales
• Third heart sound (S3)
• Rx: ACE inhibitors, Diuretics, Beta blockers,
• Beta Agonists
• Vasodilators
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Cardiogenic Shock
• When >40% of LV mass has infarcted
• Decreased Cardiac Output (CO)
• Hypotension: Systolic BP <90 mmHg
• Low BP decreased coronary perfusion increases ischemic
damage decreased stroke volume increased LV size
enhances myocardial oxygen demand
• Mortality >70%
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PRESSURE VOLUME
LOOPS
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Diagram a pressure-volume loop
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ESPVR and EDPVR
• The end-diastolic pressure-volume relationship is the passive filling
curve of the ventricle, the slope of which is the inverse of ventricular
compliance. (A completely stiff, non-compliant ventricle would have a
really steep slope.)
• The end-systolic pressure-volume relationship is the max pressure
that the ventricle can muster for a specific volume given a specific
inotropic state. The PV curves cannot “cross” this limit.
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Preload
• Preload is the initial stretching of cardiac myocytes prior to
contraction. EDV and EDP are used as estimates.
• Increasing venous return and ventricular preload leads to an increase in SV.
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Determinants• Factors directly proportional to preload
• Venous pressure - Increase in venous BP → more atrial filling → more ventricular filling
• Ventricular compliance - increased compliance, increased ventricular filling at given pressure
• Atrial inotropy - increase in atrial contraction by sympathetic activation can enhance ventricular filling
• Outflow resistance -Increase in outflow resistance impairs the ability of the RV to empty Increase in preload.
• Examples: Pulmonic valve stenosis, pulmonary hypertension, aortic valve stenosis, elevated aortic pressure
• Factors inversely proportional to preload
• Heart rate - Increased heart rate → Less time in diastole → less time for filling → lower preload.
• Inflow resistance - Elevated inflow resistance reduces the rate of ventricular filling and decreases ventricular preload
• Example: Tricuspid valve stenosis, mitral valve stenosis
• Ventricular inotropy - Reduced inotropy → higher end-systolic volume → blood “backs up” in ventricle and proximal venous circulation → increased preload
• Venous compliance - i.e. venodilation by NO increases compliance, reducing preload and O2 demand.
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Ventricular Compliance
• Compliance = ΔV/ΔP, but usually we think of it as the inverse of the
slope of passive filling on a PV curve.
• Ventricular compliance is determined by the physical properties of the
tissues making up the ventricular wall and the state of ventricular
relaxation.
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Length Tension Relationship
• Length ∝ tension. When a myocyte is stretched, it’s passive tension
increases (like a stretched rubber band) and it’s active tension
increases (more forceful contraction when electrically stimulated).
This means that increasing preload aka End Diastolic Pressure will
create a bigger End Systolic Pressure (afterload).
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Describe the three possible explanations
for length-dependent activation.
• Increased sarcomere length sensitizes troponin C to calcium.
• Fiber stretching alters calcium homeostasis
• Actin and myosin are brought in closer proximity to each other
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Frank Starling Mechanism
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Afterload
• Afterload- The load against which the heart must contract to eject
blood.
• Left ventricle afterload ~ aortic pressure
• Right ventricle afterload ~ pulmonary artery pressure
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Wall Stress
• La Place Equation: Wall stress, σ, is the average tension each
myocyte must produce to shorten against the intraventricular
pressure. Wall stress is directly proportional to afterload.
• P = intraventricular pressure, r = ventricular radius, h = wall thickness
• Intraventricular pressure is directly proportional to wall stress
• Ventricular chamber dilatation increases wall stress (increased R)
• Hypertrophy decreases wall stress (increased H)
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Afterload and Velocity of Contraction
• Afterload is like the weight that the muscle must lift, so increasing
afterload (force) decreases velocity of contraction.
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Preload and Velocity of Contraction
• Increasing preload increases velocity of contraction for a given
afterload. However, note that the y-intercepts are equal, meaning that
the theoretical max velocity of contraction (what would occur against
zero force) remains the same.
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Afterload and Stroke Volume
• At a given preload, increasing afterload decreases stroke volume.
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What is a normal ejection fraction
•55%
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With changes in preload, EDV will change
and with changes in afterload, ESV will
change.
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Inotropy
• Increased Inotropy Increased Stroke Volume
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Inotropy and ESVPR
• Increased inotropy shifts ESPVR (end systolic pressure volume
relationship) to the left and makes it steeper because the ventricle
can generate increased pressure at any given volume
• Increasing Inotropy also increases stroke volume and ejection fraction
(EF)
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Determinants of Inotropy
• Sympathetic nerve activation: Sympathetic nerves release
norepinephrine which binds to β-1 adrenoceptors on myocytes and
play a role in ventricular and atrial inotropic regulation
• Circulating catecholamines: have positive inotropic effects.
• Afterload: an increase in afterload can cause modest increase in
inotropy by a somewhat unknown mechanism.
• Heart rate: increased heart rate has positive inotropic effects.
• This is due to an inability of the Na+/K+ ATPase to keep up with the sodium influx at
higher frequency of action potential at elevated heart rates leading to an
accumulation of intracellular calcium via sodium calcium exchanger.
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Preload, Afterload and Inotropy
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Dynamic effects of Increased Preload
• Primary change: Increased EDV and SV (right shift, solid red line)
• Secondary change: Increased afterload (due to increased CO and
BP).
• Inotropy is not affected. ESV also increases slightly due to higher
afterload.
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Dynamic effects of Increased Afterload
• An increase in afterload leads to a decrease in SV via an increase in
ESV. The increased ESV inside the ventricle is added to the venous
return, increasing EDV.
• After several beats, a steady state is achieved in which the increase
in ESV is greater than the secondary increase in EDV so that the
difference between the two (SV) is decreased.
• This increase in preload secondary to an increase in afterload
activates the Frank-Starling mechanism, which partially compensates
for the reduction in SV caused by the initial increase in afterload.
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Dynamic effects of Increased Inotropy
• The direct, independent effects of an increase in inotropy are an increase in SV and a decrease in ESV/afterload.
• However, the increased SV increases CO and arterial pressure, which increases afterload on the ventricle.
• Increased afterload tends to increase ESV, which partially offsets the effects of increased inotropy on ESV. With a decrease in ESV from control, less blood remains in the ventricle that can be added to the venous return, so the EDV will be smaller, although this will be partially offset by the tendency of the increased afterload to increase EDV.
• After a new steady state is reached following the increase in inotropy, the net effect is an increases in SV, which is accompanied by a reduction in ESV and a smaller reduction in EDV.
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Myocardial O2 Consumption
• Myocardial oxygen consumption (MVO2) is equal to the coronary blood flow (CBF) multiplied by the amount of oxygen extracted from the blood (the arterial-venous oxygen difference).
• MVO2= CBF * (CaO2 – CvO2)
• CBF= coronary blood flow
• CaO2= arterial oxygen content
• CvO2= venous oxygen content
• The pressure-rate product has been used to estimate myocardial oxygen consumption noninvasively. To find it, you multiply heart rate and systolic arterial pressure (mean arterial pressure is sometimes used instead). This product assumes that the pressure generated by the ventricle is not significantly different than the aortic pressure (i.e. there is no aortic valve stenosis).
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Determinants
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VALVULAR DISEASE
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Mitral Stenosis
• Most common cause: Rheumatic Fever, also calcificic/degenerative and
SLE
• Pathology: Fibrous thickening and calcification of valve leaflets, fusion of
commisures, thickening of chorda tendineae
• Pathophysiology:
• 1. High LA pressure transmitted to pulmonary circulation Dyspnea
• 2. Chronic elevation of RV pressure leads to dilatation Right heart failure
• 3. High LA pressure LA enlargement and atrial fibrillation
• Presentation: Dyspnea, reduced exercise capacity, pulmonary
hypertension, right sided heart failure, JVD, hepatomegaly, ascites,
peripheral edema, compression of recurrent laryngeal nerve, atrial
fibrillation, thromboembolism, infective endocarditis, hemoptysis
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MS Diagnostics
• Auscultation: Right ventricular tap (loud S1), Opening snap following
S2, Diastolic rumble over apex
• EKG: LA enlargement, RVH, A-fib
• Echo: Thickened mitral leaflets and abnormal fusion of commissures
with restricted separation during diastole
• Rx: Diuretics (vascular congestion), β blocker/CaCh Blocker (A-fib),
Anticoagulants (thromboembolism), ACE inhibitors.
• Surgery: Percutaneous Balloon Mitral Valvuloplasty
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Tachycardia and MS
• Increased HR decreased time in diastole even less LV filling
• This leads to a build-up of greater pressure in the LA which backs up
into the pulmonary system
• Beta blockers act to decrease the HR, helping to avoid the worsened
symptoms that accompany tachycardia
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Antibiotic Prophylaxis
• All patients with evidence who have had ARF or evidence of RHD
should be given antibiotic prophylaxis
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Mitral Regurgitation Etiology
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Primary vs. Secondary Causes
Primary mitral regurgitation
• Myxomatous mitral valve: enlarged redundant leaflets bow excessively into LA during systole instead of opposing each other normally
• Endocarditis: leaflet perforation/rupture due to infected chordae tendinae
• Rheumatic heart disease: excessive shortening of chordae tendinae & retraction of leaflets
Secondary mitral regurgitation
• Dilated cardiomyopathy: spatial separation between papillary muscles/mitral annulus stretching
• Ischemic cardiomyopathy: scar/transient dysfunction of papillary muscle
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Mitral Regurgitation
• Pathophysiology: Fraction of LV stroke volume is ejected backward
into LA elevation of LA volume and pressure, reduction of CO and
wall stress on LV during diastole, Frank Starling mechanism elicits
compensatory increase in SV
• Acute MR (chorda rupture) – little compensation in LA size and
compliance High LA pressure
• Pulmonary congestion and edema.
• Chronic MR (Rheumatic valve disease) – LA undergoes
compensatory changes (dilatation) reduced CO
• Weakness and fatigue and potential A-fib
• Eventual deterioration of systolic ventricular function
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MR
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MR Diagnostics
• Auscultation: Loudest at apex
• Chronic MR: Apical holosystolic murmur that radiates to axilla
(have patient clench wrists to enhance murmur), S3 is common
• Acute MR: Decrescendo systolic murmur
• EKG: LA enlargement and signs of LVH
• Echo: Useful to identify structural cause, Doppler can grade severity
• Rx:
• Acute MR: Diuretics (Furosemide), Vasodilators
• Chronic MR: Mitral valve repair over replacement
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Severe MR can be masked by a slightly
elevated ejection fraction!
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Mitral Valve Prolapse
• Common asymptomatic billowing of mitral leaflets into LA during
systole
• Autosomal dominant disorder or related to Marfan’s, Ehlers-Danlos and
other connective tissue diseases
• Accumulation of glycosaminoglycan (dermatan sulfate) in spongiosa layer
with secondary disruption of underlying fibrosa layer.
• Pathophysiology: Principally affects posterior leaflet.
• Usually asymptomatic but can lead to arrythmias
• Chordae may be elongated, thinned, or even ruptured, and the annulus
may be dilated
• Auscultation: Mid-systolic click
• Echo: Shows posterior displacement of mitral leaflets
![Page 290: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/290.jpg)
Aortic Stenosis
• Etiology: Age-related Degenerative Calcific changes, congenital,
rheumatic
• Pathophysiology: LV initially compensates via hypertrophy lower
compliance elevation of diastolic LV pressure
• Angina: due to imbalance of myocardial O2 supply and demand
• Increased muscle mass (hypertrophy)
• Elevated diastolic pressure reduces blood flow
• Exertional Syncope: inability to compensate during exercise
• Congestive Heart Failure: LV may develop contractile dysfunction
overtime leading to increased LA pressure and heart failure
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Why CAD and Degenerative Calcific
Disease may be related.
• Studies have shown that, as in atherosclerosis, the valve tissue of
patients with calcific aortic valve disease display cellular proliferation,
inflammation, lipid accumulation, and increased margination of
macrophages and T lymphocytes.
![Page 292: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/292.jpg)
CRUCIAL SIGNS OF SEVERE AORTIC
STENOSIS
• Pulsus parvus et tardus
• Late-peaking murmur
• Soft or absent A2 sound
• Aortic sclerosis will only show ejection murmur
![Page 293: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/293.jpg)
AS Diagnostics• Auscultation: Right upper sternal border
• 1. Coarse late-peaking systolic ejection murmur
• 2. Reduced aortic component of S2
• 3. Weakened and delayed upstroke of carotid artery pulsations due to obstructed LV outflow
• 4. S4
• Palpation: Suprasternal thrill
• EKG: LV hypertrophy
• Echo: identifies and quantifies degree of stenosis• Normal aortic valve cross sectional area = 3-4 cm2
• Mild AS: <2.0 cm pressure gradient between LV & aorta first appears
• Moderate AS: 1.0-1.5 cm
• Severe obstruction: <1.0 cm
• Rx: Aortic valve replacement• Caution in use of medications!!!
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AR vs. AS
• AS: A coarse, late-peaking systolic ejection murmur at right upper
sternal border
• AR: A blowing murmur in early diastole (diastolic decrescendo) best
heard at lower left sternal border
![Page 295: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/295.jpg)
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AS
![Page 297: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/297.jpg)
Aortic Regurgitation
• Etiology: Abnormalities of leaflets (Congenital, Endocarditis,
Rheumatic), Dilatation of aortic root (Aneurysm, dissection, syphilis,
annuloaortic ectasia)
• Most common cause of Chronic AR – Bicuspid valve
• Pathophysiology:
• Acute AR: LV is of normal size and noncompliant increase in diastolic
pressure transmitted to LA dyspnea/respiratory emergency
• Chronic AR: compensatory adaptation of LV eccentric hypertrophy
reduced aortic diastolic pressure and increased LV stroke volume
(widened pulse pressure) reduced myocardial oxygen supply (angina,
fatigue)
• Presentation: dyspnea, fatigue, sensation of forceful heartbeat
![Page 298: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/298.jpg)
AR: Acute vs. Chronic
• Acute
• Primary: endocarditis
• Secondary: aortic dissection
• Chronic
• Primary
• Bicuspid aortic valve
• Endocarditis
• Inflammatory
• Secondary
• Aortic aneurysm
![Page 299: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/299.jpg)
AR Diagnostics• Auscultation: Left lower sternal border
• 1. Bounding pulse
• 2. Hyper-dynamic LV impulse
• 3. Blowing murmur of AR in early diastole along left sternal border
• 4. Austin Flint murmur (low frequency, mid-diastolic rumbling at cardiac apex)
• 5. WIDE PULSE PRESSURE
• Echo:
• 2D• Leaflet abnormalities
• Enlarged left ventricle
• Dilated ascending aorta
• Doppler• Presence, severity of AR
• Rx: vasodilators to reduce afterload, symptomatic patients should be offered surgery, there are no effective medications and many medications are contraindicated due to disruption of hemodynamics.
![Page 300: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/300.jpg)
AR
![Page 301: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/301.jpg)
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Criteria for Aortic Valve Surgery
• Aortic stenosis
• Patients with severe AS who develop symptoms, or when there is
evidence of progressive LV dysfunction in the absence of symptoms
• Aortic regurgitation
• Symptomatic patients or those who are asymptomatic but have
severe AR and impaired LV contractile function (i.e. ejection fraction
<50%)
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Does Mitral Stenosis or Mitral
Regurgitation cause LV enlargement?
• Mitral regurgitation
• Aortic Regurgitation
![Page 304: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/304.jpg)
Describe the difference in ventricular
hypertrophy between AS and AR
• AS shows concentric hypertrophy (add sarcomeres in parallel to
thicken wall of ventricle) while AR shows eccentric hypertrophy (add
sarcomeres in series to increase diameter of ventricle).
![Page 305: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/305.jpg)
S1
S2
![Page 306: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/306.jpg)
Systolic Murmurs
• Holosystolic
• Mitral regurgitation
• Tricuspid regurgitation
• VSD
• Systolic ejection
• Aortic sclerosis
• Aortic stenosis
• Pulmonary stenosis
• Hypertrophic
cardiomyopathy
![Page 307: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/307.jpg)
Aortic vs. Mitral Stenosis
![Page 308: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/308.jpg)
Murmurs
• Systolic: Aortic or
pulmonary stenosis or
hypertrophic
cardiomyopathy
• Holosystolic: Mitral or
tricuspid regurgitation or
VSD
• Diastolic: Aortic or
pulmonary regurgitation,
mitral stenosis
![Page 309: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/309.jpg)
Etiology of Murmurs
• A murmur is caused by turbulent blood flow. They can result from:
• 1. Flow across a partial obstruction (e.g. aortic stenosis)
• 2. Increased flow through normal structures (e.g. high output state)
• 3. Ejection into a dilated chamber (e.g. dilation of the aorta)
• 4. Regurgitant flow across an incompetent valve
• 5. Abnormal shunting of blood from one vascular chamber to a lower-
pressure chamber
![Page 310: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/310.jpg)
Dynamic Auscultation
• In dynamic auscultation, you listen to the heart when the patient is
lying down, standing and squatting to see the differences in the heart
sounds. When lying down, the LV is at baseline.
• Upon standing → preload drops (↓ venous return)
• Upon squatting → afterload rises (↑ systemic pressure)
• These maneuvers can change when a murmur occurs and can help
differentiate between aortic stenosis and hypertrophic
cardiomyopathy:
• aortic stenosis- will have NO CHANGE w/ dynamic auscultation
• hypertrophic cardiomyopathy- WILL have change w/ dynamic auscultation
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Mechanical vs. Bioprosthetic Valves
• Mechanical
• Impressive durability, with some models functioning well for more than 30 years
• Older mechanical valve models had problems with producing intravascular hemolysis from red blood cell trauma due to their bulky leaflet design, but newer models do not have this issue
• Present foreign thrombogenicsurfaces to circulating blood and thus require lifelong anti-coagulation to prevent thromboembolism
• Bioprosthetic
• Limited durability compared with mechanical valves, and structural failures occur in up to 50% of valves at 15 years
• Valves in the mitral position tend to deteriorate more rapidly
• The main causes of valve damage are leaflet tears and calcification
• Very low rate of thromboembolism and do not require long term anti-coagulation therapy
• Very low rates of subsequent infection
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Patients that need antibiotic prophylaxis
for dental procedures
• Patients with a history of endocarditis
• Patients with prosthetic heart valves
• Patients with a history of recent surgery for a congenital heart disease
• Patients with a history of heart transplant that later developed cardiac
valve abnormalities
![Page 313: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/313.jpg)
Auscultation
![Page 314: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/314.jpg)
Why is there a systolic murmur in aortic
regurgitation
• 1. Valve is abnormal turbulent flow
• 2. Stroke volume is increased by 2 increased flow
![Page 315: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/315.jpg)
Why is diastolic pressure so low in AR?
• By accommodating the large regurgitant volume the aortic diastolic
pressure drops substantially, which in combination with the high LV
stroke volume produces a widened pulse pressure, which is a
hallmark of chronic AR
• Decreased aortic diastolic pressure → decreased coronary artery
perfusion → may produce angina even in the absence of
atherosclerotic disease
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Valve Disease
• Mitral Stenosis
• MCC: Rheumatic Fever
• Sx: dyspnea, RHF, A-fib, Thromboembolism
• Px: Diastolic Murmur: opening snap rumble over apex
• Rx: Diuretics (vascular congestion), B blocker/CaCh Blocker (A-fib), Anticoagulants (thromboembolism), Balloon valvuloplasty
• Mitral Regurgitation
• MCC: Myxomatous degeneration, Rheumatic, Ischemic
• Sx: Acute: dyspnea, pulm. edema, Chronic: Fatigue, A-fib, LV dysfunction
• Px: Apical holosystolic murmur that radiates to axilla
• Rx: Diuretics, Vasodilators, Mitral Valve repair
• CAN BE MASKED BY ELEVATED EF
• Aortic Stenosis
• MCC: Calcific and Rheumatic
• Sx: Angina, exertional syncope, CHF
• Px: Systolic ejection murmur @ RUSB Severe: Pulsus parvus et tardus, Late-peaking murmur, Soft or absent A2 sound
• Rx: ACE inhibitors, diuretics, Beta blockers WITH CAUTION and AVR for symptomatic pts.
• Aortic Regurgitation
• MCC: Bicuspid Valve
• Sx: Acute: dyspnea, pulm. edema, Chronic: Fatigue
• Px: Diastolic murmur (LLSB) + systolic murmur, wide pulse pressure
• Sx: Acute: dyspnea, pulm. edema Chronic: Fatigue, LV dysfunction
• Rx: Vasodilators, USE DRUGS WITH CAUTION, Asymptomatic and symptomatic severe AVR
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HEART FAILURE
![Page 319: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/319.jpg)
![Page 320: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/320.jpg)
Coronary Artery Disease
![Page 321: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/321.jpg)
Restrictive Cardiomyopathy
![Page 322: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/322.jpg)
Pericardial Constriction/Tamponade
![Page 323: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/323.jpg)
Hypertrophic Myopathy
![Page 324: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/324.jpg)
Hypertension/ LV Hypertrophy
![Page 325: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/325.jpg)
Aortic Stenosis
![Page 326: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/326.jpg)
Frank Starling Relationship
![Page 327: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/327.jpg)
2 Types of Heart Failure
• HF with reduced EF: occurs because of impaired myocardial
contractility or pressure overload; systolic dysfunction
• HF with preserved EF: occurs because of impaired early diastolic
relaxation or because of increased stiffness of the ventricular wall;
causes diastolic dysfunction with reduced ventricular filling
![Page 328: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/328.jpg)
![Page 329: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/329.jpg)
Adrenergic System
• The fall in CO is sensed by baroreceptors in the carotid sinus and
aortic arch they decrease their firing, and the signal is sent through
CN IX and X to the cardiovascular control center in medulla
• This results in increased sympathetic outflow to the heart and
peripheral circulation, and parasympathetic tone is diminished.
• The immediate consequences of this are an increased heart rate,
increased ventricular contractility and vasoconstriction, sweating, skin
vasoconstriction, increased renin release, cardiac deterioration
(fibrosis etc.)
![Page 330: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/330.jpg)
Renin-Angiotensin-Aldosterone
• 1) Decreased renal perfusion, 2) Decreased salt delivery to macula
densa, 3) Direct stimulation of juxtaglomerular β2 receptors by
sympathetic nervous system Renin Secretion
• Renin cleaves angiotensinogen to angiotensin, which is cleaved by
ACE to form angiotensin II (a potent vasoconstrictor).
• constricted arterioles and raises total peripheral resistance
• Angiotensin II also increases intravascular blood pressure by
stimulating thirst and increasing aldosterone secretion.
• Aldosterone promotes sodium reabsorption from the distal convoluted
tubule of the kidney, and increases intravascular volume
![Page 331: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/331.jpg)
ADH Secretion
• Increased ADH hormone production: ADH secreted in response to
arterial baroreceptor signaling and increased circulating angiotensin II
• ADH increases intravascular volume by
• 1) Promoting water retention by the distal nephron
• 2) Contributing to systemic vasoconstriction increased LV preload
increased CO
![Page 332: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/332.jpg)
Eccentric vs. Concentric Hypertrophy
• Eccentric hypertrophy: synthesis of new sarcomeres in series with the old, causing myocytes to elongate; wall thickness enlarges proportionally with radius of the ventricular chamber• Caused by chronic chamber dilatation due to volume overload
• Concentric hypertrophy: synthesis of new sarcomeres in parallel with the old, causing myocytes to thicken; wall thickness increases without a proportional increase in chamber radius, which can reduce wall stress substantially• Caused by chronic pressure overload
• Valvular insufficiency: eccentric hypertrophy
• Aortic stenosis: concentric hypertrophy
• Hypertension: concentric hypertrophy
![Page 333: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/333.jpg)
Triggers of Heart Failure
• Fever/Infection: Increased Metabolic Demand
• Pregnancy: Increased Metabolic Demand
• Ischemia: Increased Metabolic Demand
• Acute PE: Increased afterload
• Excess salt intake: Increased blood volume/preload
• Negative inotropic drugs: Reduced contractility
![Page 334: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/334.jpg)
Sx of Heart Failure
• Left• Dyspnea
• Pulmonary congestion and reduced CO
• Orthopnea
• Redistribution of blood to lungs in supine position
• PND
• Gradual reabsorption of peripheral edema in blood volume
• Fatigue
• Decreased CO
• Right• Abdominal Discomfort
• Engorged liver
• Peripheral Edema
• Increased hydrostatic venous pressures
![Page 335: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/335.jpg)
NY Heart Association Criteria
![Page 336: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/336.jpg)
Physical Findings
![Page 337: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/337.jpg)
Chest Radiographic Findings
• Upper-zone vascular redistribution - LA P > 15mmHg
• Kerley-B lines - LA P > 20mmHg• Interstitial edema
• Alveolar opacification - LA P >25-30mmHg• Alveolar edema
• Cardiomegaly - Cardiothoracic ratio of >0.5 on the PA film
• Pleural effusion - fluid into the pleural cavity
![Page 338: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/338.jpg)
Use serum brain natriuretic peptide,
sodium, and creatinine levels to evaluate
the cause of dyspnea and severity of
heart failure.
• BNP: correlates with degree of LV dysfunction and prognosis. If you
have elevated BNP you know dyspnea is due to heart failure and not
other causes (like primary lung diseases) or use as a baseline
indicator.
• Sodium: reduced serum levels reflect activation of the renin-
angiotensin-aldosterone system and alterations in intrarenal
hemodynamics. Less sodium, worse prognosis.
• Creatinine: indicative of renal failure secondary to CHF
![Page 339: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/339.jpg)
Patients with heart failure get low grade
troponin elevation.
Only take real notice if Troponin is > 1.
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Diagnostic Tests
•Ultrasound – tells the ejection fraction
• Below 40% EF, think pathology
• Chest Radiograph
• BNP
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Prognosis: HF pts with preserved EF
have similar rates of hospitalization, in
hospital complications, and mortality as
those with reduced EF
![Page 342: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/342.jpg)
Therapy
• Diuretics:• Furosemide and Bumetanide
• Hydrochlorothiazide and Metolazone
• Spironolactone and Eplerenone
• Vasodilators• Nitrates
• ACE Inhibitors: Lisinopril
• Isorbide dinitrate and Hydralazine
• Inotropics for acute HF• Digoxin and Digitoxin
• PDE Inhibitors• milrinone
• Beta Agonists
• Beta Blockers: Carvedilol
![Page 343: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/343.jpg)
Implantable Defibrillators
• There are cardiac arrhythmias that accompany heart failure, such as
Afib. Conversion to a sinus rhythm is beneficial in these patients.
Ventricular arrhythmias can be lethal and lead to sudden cardiac
death. Patients with heart failure with symptomatic or sustained
ventricular arrhythmias or inducible ventricular tachycardia benefit
more from an implantable ICD than medical treatment.
• Many patients with heart failure have intraventricular conduction
abnormalities that have uncoordinated right and left ventricular
contraction. They benefit from biventricular pacing that stimulates
both ventricles simultaneously to resynchronize them. This is
indicated for patients with advanced systolic dysfunction, a prolonged
QRS complex, and continued heart failure symptoms despite medical
management.
![Page 344: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/344.jpg)
Acute Heart Failure
• Urgent and life threatening symptomology precipitated by certain
triggers
![Page 345: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/345.jpg)
LMNOP Algorithm for Acute
Decompensated Heart Failure• L → Lasix (furosemide) is a diuretic that reduces blood volume and venous
return, therefore, removing blood from the pulmonary circulation and reducing
LV pressures
• M → Morphine reduces respiration, reduces distress, reduces sympathetic
activity (causing vasodilation that reduces resistance and therefore afterload),
and is a vasodilator that helps pool blood in the periphery
• N → Nitrates are vasodilators that reduce venous return, which reduces left
heart pressure, leading to reduced congestion in the pulmonary space
• O → Oxygen
• P → Position (sit upright) will help pool blood in the peripheral lower
extremities rather than in the lungs
![Page 346: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/346.jpg)
CARDIOMYOPATHIES
![Page 347: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/347.jpg)
![Page 348: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/348.jpg)
Types
• Dilated cardiomyopathy: ventricular chamber enlargement with impaired systolic contractile function; only mild increased thickness• Ischemic, idiopathic, infectious (myocarditis), genetic, alcoholic
• Hypertrophic cardiomyopathy: abnormally thickened ventricular wall with abnormal diastolic relaxation but usually intact systolic function; hypertrophy often asymmetrically involving the intraventricular septum
• Restrictive cardiomyopathy: abnormally stiffened myocardium (because of fibrosis or an infiltrative process) leading to impaired diastolic relaxation, but systolic contractile function is normal or near normal; usually without ventricular chamber enlargment
• **LA enlargement is common to all three types of CMP
![Page 349: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/349.jpg)
![Page 350: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/350.jpg)
Dilated Cardiomyopathy Etiology
![Page 351: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/351.jpg)
Ischemic Cardiomyopathy is the cause of
70% of DCM
![Page 352: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/352.jpg)
DCM Pathophysiology
![Page 353: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/353.jpg)
DCM Symptoms and PE
• Sx
• Pulmonary Congestion
• Fatigue
• Dyspnea
• Orthopnea
• PND
• Signs
• Rales
• JVD
• Hepatomegaly
• Edema
• S3
• Mitral Regurgitation Murmur
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DCM Therapy
• Standard Rx for Heart Failure
• ACE inhibitor, diuretic, beta blocker
• Arrhythmia prevention
• Amiodarone
• ICD
• Warfarin for thromboembolic events
• Cardiac transplantation
![Page 355: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/355.jpg)
DCM and Mitral Regurgitation
• 3 Serious Consequences
• 1) Excessive volume and pressure loads are placed on the atria,
causing them to dilate, often leading to atrial fibrillation
• 2) Regurgitation of blood into the left atrium further decreases
stroke volume into the aorta and systemic circulation
• 3) Regurgitant volume returns to the LV during each diastole
leading to an even greater volume load on the dilated LV
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Compensatory Mechanisms of DCM
• 1) Frank–Starling mechanism: ↑ventricular diastolic volume = ↑
stretch of myofibers = ↑ stroke volume
• 2) Neurohormonal activation: sympathetic nervous system = ↑ heart
rate and contractility
• 3) Renin-angiotensin-aldosterone axis: ↓cardiac output = ↓ renal
blood flow
• ↑ renin secreted by kidneys
• ↑peripheral vascular resistance (via angiotensin II)
• ↑ intravascular volume (via aldosterone)
• Help buffer fall in cardiac output
![Page 357: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/357.jpg)
Decompensation in DCM
• 1) Arteriolar vasoconstriction + ↑ systemic resistance
• Difficult for the LV to eject blood in the forward direction
• 2) ↑ intravascular volume
• ↑ ventricular filling pressures pulmonary and systemic congestion
• 3) Chronically ↑ levels of angiotensin II and aldosterone
• Directly contributes to pathological myocardial remodeling and fibrosis
• 4) Ventricular enlargement over time
• Mitral and tricuspid valves may fail to close during systole leading to
valvular regurgitation
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DCM Survival Based on Etiology
• From best to worst survival:
• Peripartum > Idiopathic > Ischemic > HIV
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HCM Etiology
• Genetic
• HCM follows autosomal dominant inheritance with variable
penetrance.
• 100’s of genes all having to do with sarcomere complex
• buzzword favorites: B-myosin heavy chain (B-MHC), cardiac troponin, myosin-
binding protein C
• Random mutant incorporation into sarcomere impairs contractile
function myocyte stress compensatory hypertrophy + fibroblast
proliferation
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Histology of HCM
![Page 361: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/361.jpg)
1/3 of patients with HCM develop outflow
obstruction
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Compare and contrast the LV-Aortic
pressure gradient in patients with HCM
with that seen in severe AS.
• In both HCM with obstruction and aortic stenosis, the LV has to
contract with extra force to overcome the obstruction. So the LV
pressure is higher than the aortic pressure during systole. However, in
aortic stenosis, the “obstruction” is in the aorta, whereas in HCM, the
obstruction is before the aorta, in the outflow tract.
• Post extra systolic potentiation increased force of contraction
• Both show angina and syncope.
![Page 364: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/364.jpg)
HCM Symptoms• Dyspnea:
• Due to elevated diastolic LV pressure, which backs up in to the LA and the pulmonary circulation
• For patients with outflow obstruction, dyspnea is exacerbated by high systolic pressure and mitral regurgitation.
• Angina:
• 1) Narrowing of the small branches of the coronary arteries b/c of the hypertrophied ventricular wall.
• 2) High oxygen demand d/t increased muscle mass.
• Syncope:
• May be caused by arrhythmias, which can develop because of the structurally abnormal myofibers in HCM.
• Orthostatic lightheadedness in patients w/ outflow obstruction:
• Venous return drops d/t gravitational pooling, which causes LV to decrease in size and intensify outflow obstruction transient reduction in CO and cerebral perfusion.
![Page 365: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/365.jpg)
HCM Physical Exam
• Dyspnea
• Angina
• Syncope
• LLSB Systolic Murmur
• S4
• Mitral Regurgitation
![Page 366: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/366.jpg)
HCM Therapy
• Beta Blockers are standard therapy
• Calcium channel antagonists
• Antiarrhythmics
• Amiodarone
• Disopyramide
• No Extreme Physical Exertion
• Pacemaker
• Myomectomy
• Percutaneous septal ablation
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Risks for Sudden Cardiac Death in HCM
• Risk factors:
• Prior ventricular arrhythmias
• History of syncope, especially unexplained episodes
• Family history of sudden death
• Certain high-risk HCM mutations b/c different mutations confer a
vastly different risk
• Extreme hypertrophy of the LV wall (>30 mm)
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Restrictive Cardiomyopathy Etiology
![Page 370: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/370.jpg)
Endomyocardial Biopsy can help to
distinguish between restrictive
cardiomyopathy and constrictive
pericarditis.
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RCM Pathophysiology
![Page 372: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/372.jpg)
RCM Symptoms and PE
• Systemic congestion
• JVD
• Peripheral edema
• Engorged liver
• Fatigue
• Decreased exercise tolerance
• Arrhythmias
• Conduction blocks
• Kussmaul sign
![Page 373: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/373.jpg)
RCM Therapy
• Very poor prognosis
• Salt restriction and cautious use of diuretics
• No vasodilators
• Amyloidosis: chemotherapy, bone marrow stem cell transplantation
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Work Up
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Cardiac Catheterization and MRI
• Use cath for hemodynamics and CAD investigation
• Use MRI for investigating intramuscular/pericardial inflammation
• Cardiac Catheterization
• Patients with angina or possible prior MI
• Inspect coronary arteries for disease
• Confirm pressure changes in uncertain diagnosis
• Elevated diastolic in Dilated CM
• LV pressure gradient in Hypertrophic CM
• Cardiac MRI
• Separate constrictive pericarditis from Restrictive CM
• Diagnose myocarditis
![Page 376: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/376.jpg)
Dilated Cardiomyopathy causes systolic
heart failure and S3 while hypertrophic
and restrictive cardiomyopathy causes
diastolic heart failure and S4
![Page 377: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/377.jpg)
ARRHYTHMIAS
![Page 378: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/378.jpg)
Sinus Bradycardia/SSS
• Rate <60bpm
• Causes• Normal at rest or during sleep
• Depressed automaticity due to ischemic heart disease or cardiomyopathy
• Beta Blockers, Calcium channel blockers
• Hypothyroidism
• High vagal tone in highly trained athletes
• Sx• Usually asymptomatic
• Can result in low CO with dizziness, confusion, or syncope
• Rx• Atropine (anticholinergic)
• Isoproterenol (Beta adrenergic)
• Pacemaker
• Susceptibility to Bradycardia-Tachycardia Syndrome
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Escape Rhythms
• Junctional Escape Rhythm
• Narrow QRS and rate of 40-60bpm
• No normal P waves, but retrograde P waves maybe seen after QRS and
inverted in II, III and avF
• Ventricular Escape Rhythms
• Widened QRS and rate of 30-40bpm
• Can cause RBBB or LBBB
• Sx: often asymptomatic
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AV Blocks• First Degree:
• PR >0.2, with preserved 1:1 relationship of P to QRS
• Usually benign asymptomatic treatment that does not require Rx.
• Second Degree: • Mobitz Type I (Wenckebach): degree of AV delay increases with each beat until a QRS is
dropped.
• Impaired conduction in the AV node with narrow QRS
• Usually benign and temporary
• Rx: Atropine, isoprotenerol or pacemaker
• Mobitz Type II: sudden loss of QRS without lengthening of interval
• Impaired conduction in bundle of His or Purkinje system with wide QRS
• Usually indicates Severe Disease
• Third Degree: Complete Heart Block• MCC: acute MI
• AV dissociation, QRS of normal width or widened
• Lightheadedness and syncope due to slow rate
• Pacemaker almost always necessary
• Slow heart rate does not accommodate exercise
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Supraventricular Arrhythmias
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Sinus Tachycardia
• Rate >100bpm
• Causes
• Increased sympathetic tone and/or decreased vagal tone
• Exercise
• Fever, hypoxemia, hyperthyroidism, hypovolemia, anemia
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APBs
• Causes
• Automaticity or reentry in an atrial focus outside the SA node and are
exacerbated by sympathetic stimulation
• ECG:
• Premature abnormal P wave followed by normal QRS
• Sx:
• Typically asymptomatic, but may cause palpitations
• Rx:
• Beta Blockers
• Address caffeine, alcohol and emotional stress
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Atrial Flutter
• Rapid regular atrial activity at rate of 180-350bpm
• Cause: • Reentry over a large anatomically fixed circuit
• ECG:• Sawtoothed atrial activity
• Sx: • Rate < 100 usually asymptomatic
• Rate > 100 can cause palpitations, dyspnea, weakness
• Antiarrhythmics can worsen condition by increasing ventricular rate
• Predisposition to atrial thrombus formation
• Rx• Electrocardioversion + anticoagulation
• Pacemaker
• 1. Beta blockers/ Calcium Channel blockers/ Digoxin
• 2. Class IA, IC, or III for sinus rhythm and longer term prophylaxis
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Atrial Flutter
![Page 390: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/390.jpg)
Atrial Fibrillation
• Irregularly irregular rhythm of 350-600bpm
• Ventricular rhythm 140-160
• Causes• Multiple wander reentrant circuits within the atria
• Associated with atrial enlargement due to heart failure, hypertension, CAD and pulmonary disease
• ECG:• Discrete P waves are not visible, baseline shows low amplitude undulations punctuated by QRS
complexes and T waves
• Sx• Rapid ventricular rates low CO pulmonary congestion and hypotension
• Stasis risk of thrombus formation
• Rx• Adenosine, Beta blockers/ Calcium channel blockers (digitalis only for ventricular dysfunction)
• Systemic Anticoagulation for at least 3 weeks
• Type IA, IC, III antiarrhythmics or electical cardioversion
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CHA2DS2VAS2
• Algorithm for Anticoagulation
• Congestive Heart Failure
• Hypertension
• >75 (2)
• DM
• Stroke/TIA (2)
• Vascular disease
• >65
• Sex category
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Surgical Procedures for Afib
• Maze procedure: incisions in right and left atria to prevent reentry
circuits
• Percutaneous catheter ablation: left atrium around pulmonary veins is
cauterized to interrupt reentry circuits
• High risk of stroke or tamponade
• Catheter ablation of AV node with insertion of pacemaker
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Paroxysmal Supraventricular
Tachycardias
• 1. Sudden onset and termination
• 2. Atrial rates between 140 and 250 bpm
• 3. Narrow QRS complex
• Cause
• Reentry involving AV node, atrium or accessory pathway
![Page 395: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/395.jpg)
PVSTs
• AVNRT• Slow and Fast AV nodal pathways Reentry
• Regular tachycardia with normal width QRS complexes
• Retrograde inverted P waves in QRS complex
• Presents in teenagers or young adults and is well tolerated
• Rx: Vasalva, IV adenosine
• Preventative Calcium Channer Blockers/Beta blockers
• Catheter ablation
• AVRT – Wolff-Parkinson-White• Shortened PR interval with a delta wave on the upstroke of widened QRS
• Due to conduction through an accessory pathway
• If patient enters AF high risk of VF
• Rx: 1) Cardioversion 2) IA and IC antiarrhythmics (IV procainimide or ibutilide) 3) Ablation
• Caution with beta blockers and calcium channel blockers
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AVNRT
AVRT
![Page 397: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/397.jpg)
Focal Atrial Tachycardia
• Cause:
• Automaticity of atrial ectopic site or reentry
• Digitalis toxicity
• Excess sympathetic tone
• ECG:
• Sinus tachycardia with P wave preceding each QRS but P wave
morphology differs from sinus rhythm
• Rx:
• Vagal maneuvers may have no effect
• Beta blockers, Calcium channel blockers and IA, IC, and III
antiarrhythmics can be effective
• Catheter ablation
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Multifocal Atrial Tachycardia
• Cause
• Abnormal automaticity in several foci within the atria or triggered activity in the setting of pulmonary disease and hypoxemia
• ECG:
• Irregular rhythm with at least 3 P wave morphologies and avg. atrial rate is >100bpm
• Isoelectric baseline distinguishes MAT from AF
• Sx:
• High mortality rate due to underlying disease
• Rx:
• Verapamil
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Ventricular Arrhythmias
![Page 401: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/401.jpg)
VBPs
• Cause:• Ectopic ventricular focus
• Common asymptomatic and benign
• ECG:• Widened QRS complex
• Ectopic beat is not related to a preceding wave
• May appear in repeating patterns
• Sx: • Can be used to track structural heart disease
• Rx: • Symptomatic control using Beta blockers
• ICD in high risk patients
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Ventricular Tachycardia• Series of 3 or more VBPs
• Sustained or nonsustained
• Cause: • Structural heart diesase: MI, heart failure, ventricular hypertrophy, valvular heart disease, long QT
syndrome, congenital cardiac abnormalities
• ECG:• Wide QRS with a rate of 100-200 bpm
• Monomoprphic: reentry circuit due to old infarct or cardiomyopathy
• Polymorphic: QRS complex changes in shape and rate varies• Torsades de Pointes or MI most common causes
• Also consider LQTs and Brugada
• Sx: • Sustained: low CO syncope, pulmonary edema, cardiac arrest
• HEMODYNAMICALLY UNSTABLE!
• Rx: • Electrical Cardioversion
• Amiodarone, Procainimide, Lidocaine
• W/ structural heart disease ICD
• Idiopathic Beta blockers, Calcium channel blockers, Ablation
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VT can be distinguished from SVT by the
width of the QRS complex*
*Except in SVT with aberrancy
SVT is more probable if vagal
maneuvers affect rhythm
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Torsades de Pointes• Cause
• Afterdepolarizations in patients with prolonged QT
• Hypokalemia or hypomagnesemia
• Drugs: Quinidine, Procainimide, disopyramide, sotalol, ibutilide, erythromycin, methadone
• Congenital QT elongation
• ECG:• Polymorphic VT with varying amplitudes of QRS
• Sx: • Lightheadedness or syncope
• Usually self-limited
• Can precipitate Vfib
• Rx:• IV magnesium
• Beta adrenergic stimulating agents or artificial pacemaker to shorten QT
• Beta blockers for congenital long QT decrease sympathetic tone!!!
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Ventricular Fibrillation
• Disordered rapid stimulation of ventricles coordinated contractions
leading to cessation of CO and death
• Cause:
• Initiated by episode of VT which degenerates into multiple smaller
wavelets of reentry
• ECG:
• Chaotic irregular appearance without discrete QRS waveform
• Rx:
• IMMEDIATE DEFIBRILLATION
• IV antiarrhythmics: Amiodarone
• ICD
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REGULATION OF BP
![Page 412: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/412.jpg)
Overview
• SV * HR = CO
• MAP = (SVR*CO) + CVP
• CVP is affected by Blood
volume, Vessel compliance and
Skeletal muscle contraction
![Page 413: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/413.jpg)
Neural Control• Arterial baroreceptors are found in the carotid
sinus and aortic arch. Afferent fibers from the carotid sinus travel in CN IX up to the brainstem and synapse on the nucleus of the solitary tract (NTS). Aortic arch baroreceptors travel to the NTS via the vagus nerve.
• Inhibitory interneurons from the NTS project to other medullary regions containing cell bodies of sympathetic nerves.
• Excitatory interneurons from the NTS project to medullary regions containing cell bodies of parasympathetic/vagal nerve.
• Peripheral baroreceptors respond to stretching of vessel walls by increasing their firing rate. The net result is increased vagal tone, decreased sympathetic tone, and vasodilation.
![Page 414: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/414.jpg)
Regulatory Mechanisms
• Baroreceptors: located in the carotid
sinus and aortic arch
• Monitor stretch
• Influence HR and MAP
• Chemoreceptors: small carotid bodies
located in the external carotid near the
bifurcation with the internal carotid;
aortic bodies in the aortic arch; central
chemoreceptors in the medulla
• Monitor blood PO2, PCO2, or pH
• Influence respiration
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Orthostatic Hypotension
• OH is frequently induced by drugs that lower vascular reactivity and/or impair the CNS (CNS depressants e.g. sleeping pills or alcohol) or by drugs that have alpha-1 adrenergic blocking properties (many antipsychotics, many antidepressants) and by a variety of antihypertensive drugs (examples: ARBs, ACEIs, alpha-1 blockers; especially upon initiation of the treatment (first dose effect)).
• OH is exacerbated by a low blood volume (could be due to bleeding, heat or exercise or consumption of diuretics).
• OH is of special concern in the elderly that have more sluggish baroreflexes and might suffer most from falling.
• OH is common in advanced diabetes. Diabetic neuropathy (DN) produces loss of sensory afferents, especially in the lower limbs
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3 Factors that affect postural hypotension:
Age
Diabetes
Atherosclerosis
![Page 417: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/417.jpg)
Orthostatic MOA• The pooling of blood in the lower part of body reduces central venous pressure
and, the lower central venous pressure reduces right ventricular filling pressure.
• The reduced right ventricular filling causes CO to go down as a consequence of the Frank-Starling effect
• BP = CO * TPR and reactive mechanisms of TPR take time to set in, so there is a rapid drop in BP with standing.
• Baroreceptors sense lowered stretch and reduce firing which increases SNA/decreases PSA vasoconstriction and increased cardiac contractility
• In a hypovolemic state (lack of volume from things such as heat, stress, dehydration): SNS is already working really hard to keep up these mechanisms and cannot compensate
• Fainting is a beneficial mechanism to restore cerebral perfusion
• ** Angiotensin and aldosterone DO NOT contribute
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Low Pressure Baroreceptors
• Low-pressure baroreceptors encode the degree of stretch of
the upper vena cava, the right atrium and the ventricles
• Low-pressure baroreceptors regulate blood volume via release
of ANF and by controlling renal fluid excretion. Their effect is
too slow to contribute to the orthostatic reflex
• By controlling BV they have a role in the long-term adaptations.
• In 0 gravity or bed rest situations, stretch of baroreceptors is
increased as central venous pressure increases, causing a
long term reduction in blood volume. This can lead to
orthostatic hypotension.
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Exercise Regulation
• The cardiovascular responses to exercise are designed to
increase O2 delivery to the more metabolically active
tissues (skeletal muscles and heart)
• The increase in O2 delivery to the muscles occurs via:
• Increased cardiac output
• Vasodilation due to local factors (low pH, K, lactate etc.)
• Increased O2 dumping from Hb due to increased muscle temp.
• Increased O2 dumping from Hb due to increased muscle pCO2
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Beta Blockers and Exercise Capacity
• Beta blockers decrease a person’s exercise capacity
because they reduce the ability to increase sympathetic
innervation.
• This prevents the heart from increasing its HR, SV AND
CO
• Beta blockers don’t have much effect during rest because
there is low endogenous beta-agonist to antagonize.
![Page 421: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/421.jpg)
Pulse Pressure
• Pulse pressure (PP)= systolic P – diastolic P
• Mean blood pressure = diastolic pressure + 1/3 (systolic P
– diastolic P)
• Pulse pressure increases during exercise:
• If stroke volume increases, then why doesn’t diastolic
pressure increase?
• Because of the release of epinephrine in blood
• Because of the increased muscle conductance
• Because of reduced resistance in the pulmonary circulation
• Because of the increased skin blood flow
![Page 422: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/422.jpg)
During exercise, skin blood flow goes
from low to high according to the change
in the body’s core temperature
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Circulatory Shock
• Circulatory Shock is a condition in which decreased blood flow causes decreased tissue perfusion and O2 delivery. Untreated, shock can lead to impaired tissue and cellular metabolism and, ultimately, death.
• Causes:• Decrease in circulating blood volume: Hypovolemic shock
•
• Myocardial impairment: Cardiogenic shock
• Brain impairment: Neurogenic shock
• Leaky capillaries: Septic or anaphylactic shock
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Mechanisms of Compensation
• Activate sympathetic nervous system to stimulate the heart and
constrict systemic vascular beds.
• Increase vasopressin (ADH) and activate the RAAS system to
increase blood volume and reinforce vasoconstriction caused by
sympathetic nervous system.
• Increased lactic acid (acidosis) and stagnant hypoxia (due to
decreased carotid body blood flow) activate chemoreceptors to further
stimulate SNA increased respiratory rate
• Capillary fluid reabsorption can increase intravascular fluid volume, at
the expense of O2 carrying capacity (decreased hematocrit) and
osmotic pressure (dilute plasma proteins)
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Mechanisms of Decompensation• Reduced contractility and SV: coronary artery vasoconstriction → myocardial
hypoxia → myocardial dysfunction
• Vasodilation: prolonged reduction in perfusion to organs→ tissue hypoxia → vasodilation (aka “Sympathetic Escape”) caused by release of vasodilator metabolites by the organs. Eventually hypoxia-induced vasodilation overcomes vasoconstrictive compensatory mechanisms→ BP falls
• Acidosis: prolonged hypotension and hypoxia leads to acidosis as organs begin to generate ATP anaerobically (via lactate) → cardiac and smooth muscle contraction impaired → decreased inotropy and BP
• Cerebral ischemia/hypoxia: enhances sympathetic tone at first, but eventually results in depression of all autonomic outflow → BP falls etc
• Blood viscosity: vasoconstriction→ decreased flow rates in the microvasculature → increased blood viscosity via RBC-RBC adhesion (increased ESR), leukocyte-endothelial adhesion, and platelet-platelet adhesion → disseminated intravascular coagulation → more ischemic damage → worse acidosis & vasodilation
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SYNCOPE
![Page 429: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/429.jpg)
Syncope
• A sudden, transient loss of consciousness (LOC) and postural tone
that fully resolves spontaneously without specific intervention (as in:
CPR, or electrical or chemical cardioversion).
• Pathophysiology
• A transient reduction in cerebral blood flow (CBF), leading to cerebral
hypoperfusion.
• Reduced CBF is usually attributable to cardiovascular and
neurocardiogenic causes.
• Note that even when CBF is normal, a reduced delivery of essential
cerebral nutrients (O2, sugar) can occasionally cause LOC.
![Page 430: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/430.jpg)
Causes
• Orthostasis: decreased blood volume
• Neurogenic: baroreceptor mediated
• Vasovagal (failed baroreceptor reflex in response to standing)
• Carotid Sinus Hypersensitivity (too much baroreceptor activation)
• Situational (Vagus activation due to fear, peeing, pooping, valsalva)
• Bradyarrhythmia: decreased CO decreased MAP
• Tachyarrhythmia: decreased preload decreased SV decreased
MAP
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Etiologies
CausePrevelence Mean
%
Vasovagal 21.2
Orthostatic 9.4
Cardiac 9.5
Seizure 4.9
Medication 6.8
Stroke 4.1
Other 7.5
Unknown 36.6
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Neurocardiogenic Syncope
• Vasovagal:
• Carotid Sinus Hypersensitivity:
• Situational:
![Page 433: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/433.jpg)
Medications that Cause Bradycardia
• Beta Blockers
• Don’t forget the eye drops!
• Calcium Channel Blockers
• Antiarrhythmic Medications
• Digoxin
![Page 434: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/434.jpg)
Medications that Cause Hypotension
• Beta Blockers• Don’t forget the eye drops!
• Calcium Channel Blockers
• Antiarrhythmic Medications
• Digoxin
• ACEI
• ARB
• Opiates
• Benzodiazepines
• Lots More!
![Page 435: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/435.jpg)
Syncope- High Risk Features
• Structural Heart Disease
• VT, VF, Bradyarrhythmia, Valvular Heart Disease
• Symptoms Characteristic of Ischemia or Arrhythmias
• VT, VF
• Abnormal ECG
• VT, VF, Bradyarrhythmias
• Neurologic Disease
• Stroke
• Intracranial hemorrhage
![Page 436: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/436.jpg)
History
• Precipitating factors (micturition, cough, exertion),
• Premonitory symptoms (aura)
• Onset (sudden or slow)
• Associated symptoms (palpitations, chest pain, headache),
• Activity (at rest or with exercise)
• Position (standing, sitting, changing position)
• Other systemic illnesses
• Family history of cardiac illness, arrhythmias, syncope, sudden
death, or pacemaker implantation.
• Medications and recreational drugs
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Carotid Sinus Massage
• R and L carotid independently.
• 5-10 secs of pressure.
• Postive:• >50 mmHg drop in BP
• >3 sec pause
• Contraindications: • Carotid bruits.
• MI, TIA, Stroke within 3 months.
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Treatment
• Orthostatic
• Increase blood volume
• Tachyarrhythmias
• Medical therapy is the primary treatment for SVTs
• Implantable defibrillators are primarily targeted toward VT
• Bradyarrhythmias
• Pacemakers are generally used for bradyarrhythmias.
• Neurocardiogenic
• Pacemakers for carotid sinus hypersensitivity
• Medical therapy in all other cases
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Rx for Neurocardiogenic Syncope
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DIURETICS AND
EDEMATOUS STATES
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Body Fluid Compartments
• The largest compartment by far is comprised of water that is inside of cells – this is the intracellular compartment.
• The extracellular compartment consists of water in the blood vessels (plasma water) and the interstitial space
• The membranes between these distinct spaces are porous to different substances.
• Water moves freely between all compartments; however, sodium movement is highly restricted between the intracellular and extracellular space.
• All body fluid compartments have the same osmolality, that is, the concentration of solutes (electrolytes, proteins, etc.) is the same across all compartments: roughly 290 milliosmoles / liter. However, the concentrations of individual solutes can be very different.
![Page 442: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/442.jpg)
Describe the effect of sodium loading on
extracellular fluid volume.
• Increase of sodium → increase in concentration of sodium for a given
extracellular fluid volume (higher osmolarity) → compensatory
measures: release of arginine vasopressin (AVP / ADH / vasopressin)
→ 1) Increased thirst and 2) Decreased water excretion from kidneys
→ increase in extracellular fluid volume with normal sodium
concentration.
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Describe the renal response to decreased
effective circulating volume.
• Decrease in effective circulating volume → decreased renal perfusion
→ increase RAA system and Arginine Vasopressin (AVP) → 1) Thirst ,
2) Sodium retention, 3) water retention in the kidneys → increase in
ECF volume.
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Describe each variable of Starling’s law.
• Net driving force = (Pcap - Pi) – σ (πcap - πi)
• Pcapis the capillary hydrostatic pressure
• Hydrostatic pressure driving fluid out the capillary.
• Pi is the interstitial hydrostatic pressure
• Hydrostatic pressure in the interstitium that opposes Pcap.
• πcap is the capillary oncotic pressure
• Osmotic pressure exerted by the presence of proteins in the capillary that opposes filtration and promotes reabsorption.
• πi is the interstitial oncotic pressure
• Osmotic pressure exerted by proteins in the interstitium and opposes πcap
• σ is the reflection coefficient of the membrane.
• It is a correction factor used to account for permeability to proteins within capillaries, which lowers the effective oncotic pressure since some of the proteins can diffuse down their gradient.
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Describe how changes in variables of
Starling’s law may promote or inhibit
edema formation
• Promote Edema (increase net driving force)
• Hydrostatic pressure : Increase Pcap or decrease in Pi
• Oncotic pressure: Increase in i or decrease in cap
• Oncotic permeability: Decrease
• Inhibit Edema (decrease net driving force)
• Hydrostatic pressure : Decrease Pcap or increase in Pi
• Oncotic pressure: Decrease in i or increase in cap
• Oncotic permeability: Increase
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Four basic mechanisms of edema
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Describe the mechanism of diuretic
resistance.
• 2 Types:
• Renal Failure
• Increase dose
• DCT Hypertrophy
• Give Thiazide
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Starlings Law and CHF
• Main alteration to Starling’s law is Pcap (hydrostatic capillary pressure)
increases due to low cardiac output & backup of fluid pressure in
veins, venules & capillaries
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Electrolyte Effects of Diuretics
• Delivery of large amounts of sodium to the distal nephron (the
collecting tubule) interferes with normal potassium handling and leads
to potassium wasting.
• Also, blockade of Cl absorption in the medulla alters the electrical
gradient between the tubular lumen and the tubular cells which can
lead to wasting of Magnesium and Calcium.
• Finally, lasix activates the renin-angiotension-aldosterone system.
Increased aldosterone activity results in hypokalemia and enhanced
proton secretion resulting in metabolic alkalosis.
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HYPERTENSION
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Identify the global magnitude and impact
of hypertension on health.
• Approximately 60 million Americans and 1 billion people worldwide
have hypertension.
• 90% of individuals over the age of 55 will develop hypertension in
their lifetime.
• Hypertension is a major risk factor for:
• Coronary artery disease
• Stroke
• Heart failure
• Renal disease
• Peripheral vascular disease
• About 2/3rds of individuals are unaware of their high blood pressure.
Screening is an important aspect of clinical care.
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Maintenance of Blood Pressure
• Short term: Baroreceptor reflex. Baroreceptors in carotid sinus and
aortic arch stretch, send afferent impulse to medulla (CS--
glossopharyngeal, AA--vagus). Tractus solitarius → increase PNS
tone → vasodilate and reduce CO
• Long term: Renin-angiotensin-aldosterone axis regulates Na+ and
intravascular volume.
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SNS Regulation
• The kidneys do not work in isolation
• Extrinsic factors include aldosterone and the sympathetic nervous
system.
• Increased sympathetic nervous system activity produces a right-shift
in the pressure-natriuresis curve
• Sympathetic activity promotes volume expansion via the kidneys by
• (1) Promoting renin release by JGG cells
• (2) Directly stimulating Na reabsorption at the tubules
• (3) Causing decreased renal blood flow via vasoconstriction to
indirectly cause Na reabsorption.
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Major determinants of blood pressure
regulation • Adrenal Gland:
• Control circulating levels of catecholamines and aldosterone
• Kidneys:
• Maintenance of blood volume and electrolyte balance
• The renin–angiotensin–aldosterone axis is an important hormonal regulator. Renin levels in EH patients are above normal
• Heart:
• CO depending on stroke volume, heart rate and contractility
• Blood Vessels contribute to peripheral vascular resistance:
• Sympathetic activity
• Regulation of vascular tone by local factors, including nitric oxide, endothelin, and natriuretic factors
• Contractile vascular smooth muscle
• Autonomic Nervous System:
• Balance of sympathetic and parasympathetic inputs to heart and peripheral blood vessels
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Essential vs. 2° Hypertension
• 90% of Cases are Essential with an unknown cause
• Likely results from multiple defects of blood pressure regulation that
interact with environmental stressors. The regulatory defects may be
acquired or genetically determined and may be independent of one
another.
• Secondary Hypertension: the cause of the high blood pressure
has a definable cause
• More likely if patient develops HTN before age 20 or after age 50
• Often causes BP to rise dramatically
• Often presents abruptly in a patient who was previously normotensive,
rather than gradually progressing over years as in EH
• May have other characteristic abnormalities
• Occurs more sporadically, so may lack a family history
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Hypertension + Hypokalemia
Think Renovascular Hypertension or
Primary aldosteronism
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To distinguish Primary Aldosteronism from
Renal Stenosis, check Renin
In Stenosis Renin will be high, and in
Hyperaldosteronism Renin will be low.
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Do not use ACE Inhibitors with bilateral
renal stenosis
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Criteria for Hypertension
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Basic Patient Evaluation
461
History and physical examination
ECG: look for LVH and LAE, also assess for CAD
Lab tests
Urinalysis: proteinuria/renal dysfunction
BUN and creatinine: renal function
Serum potassium: renal, aldosterone secreting tumor
Blood glucose: metabolic syndrome
Cholesterol: metabolic syndrome
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Initial Laboratory Evaluation of the
Hypertensive Patient
• Urinalysis – evidence of renal damage especially albumin/microalbuminuria
• Blood chemistry for electrolytes and renal function, especially potassium and creatinine with eGFR
• Lipids – LDL, HDL, TG preferably fasting.
• Fasting blood sugar and, if there are concerns about diabetes mellitus, hemoglobin A1c
• ECG
462
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Common Symptoms of Hypertension
• There are no common symptoms of hypertension until
you develop end organ damage!
• Headache
• Epistaxis
• Dizziness
• Palpitations
• None
463
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Hypertensive patients depend on atrial
kick for efficient filling and can often
decompensate into A-fib
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Heart Sequelae
• Left Ventricular hypertrophy
• High arterial pressure increases wall tension
• Typically concentric
• May cause eccentric with chamber dilation
• Diastolic dysfunction pulmonary congestion
• Degree of LVH one of strongest predictors of morbidity
• Systolic dysfunction
• Elevated pressure is too much to handle
• See reduced cardiac output and pulmonary congestion
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Vascular Sequelae
• 1. Smooth muscle hypertrophy
• 2. Endothelial cell dysfunction
• 3. Fatigue of elastic fibers
• Promotes atherosclerosis and ultimately coronary artery disease
• Myocardial infarction/ischemia
• Higher risk of complications: rupture of ventricles, LV aneurysm formation, congestive heart failure
• Formation/rupture of aneurysm
• Post MI
• Abdominal aortic aneurysm
• Aortic dissection
• Weakened aorta wall exposed to high pressure tearing of intima
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Stroke Sequelae
• Hemorrhagic
• Microaneurysms in cerebral parenchymal vessels
• Atherothrombotic
• Portions of atherosclerotic plaque break off and embolize to smaller
vessels
• Intracerebral vessels may be occluded by local plaques also
• LACUNAR INFARCTS
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Renal Sequelae
• Vasculature becomes thickened (hyaline arteriolosclerosis)
• smooth muscle hypertrophy fibrinoid necrosis ischemic atrophy
of tubules
• Malignant hypertension may inflict permanent damage leading to
chronic renal failure
• WITH RENAL FAILURE BP can no longer be regulated
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Retinal Sequelae
• Hypertensive retinopathy
• Acute hypertension leads to hemorrhages, exudation of plasma lipids and
areas of local infarction
• Ischemia of optic nerve blurred vision
• Papilledema from increased ICP
• Arterial sclerosis appears as “copper/silver wiring” in the opthalmoscope
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Hypertensive Retinopathy
Keith Wagner Classification
Grade I – Arteriolar narrowing, tortousity, irregular caliber with copper/silver wiring.
Grade II – Arteriovenous nicking/nipping.
Grade III – flame-shaped and blot. haemorrhages, cotton wool spots and hard exudates.
Grade IV – Papilledema
472
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When to Treat – JNC 7
473
No RF, No TOD At least 1 RF TOD, CCD or DM
No CCD No TOD, CCD, DM (+ or - RF’s)
Prehypertensive
(120-139/80-89)
Stage I
Stage II
(>160/100)***
Life style Life style Drug Rxmodification modification
Life style Life style
mod x 12 m mod x 6m Drug Rx
Drug Rx Drug Rx Drug Rx
(classification based on highest systolic or diastolic BP)
JNC VII. JAMA 2003 or http://www.nhlbi.nih.gov/guidelines/hypertension/
Risk A Risk B Risk C
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Mechanisms of Treatment
• Fundamental concept 1: Recall that BP = CO * TPR, so to reduce
BP, a drug needs to be able to reduce CO or TPR.
• Note that most anti-hypertensives reduce TPR (including diuretics),
but Beta Blockers reduce BP primarily via a reduction in CO.
• Fundamental concept 2: Under normal conditions (no drugs), any
sustained drop in BP is eventually negated by the kidneys via volume
expansion. This is because CO = HR * SV, and an increase in volume
can lead to increased CVP increased preload increased SV.
• Thus, an anti-HTN agent must also be able to reduce the ability of the
kidney to retain fluids.
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6 Important Consequences
• 1. Some degree of volume expansion via renal compensation typically occurs with the antihypertensives that target the heart and blood vessels primarily i.e pure vasodilators > alpha-1 adrenergic antagonists > CCBs.
• 2. The magnitude of the volume expansion depends on their ability to also reset the renal P/natriuresis relationship.
• 3. The addition of a diuretic as second drug (e.g. a thiazide) usually helps to achieve greater reductions in BP.
• 4. All diuretics cause some reduction in plasma volume
• 5. Most other antihypertensive except ACEIs and ARBs cause a small increase in BV (all sympatholytics, CCBs, arteriolar vasodilators).
• 6. ACEIs and ARBs do not increase BV because they are the most effective at resetting the renal pressure natriuresis relationship
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Antihypertensive drugs
• AngII-related drugs: ACEIs = ARBs >> Renin inhibitor• ACE Inhibitors first line
• Diuretics:• 1. Thiazides (and related drugs)
• 2. Potassium-sparing diuretics
• Ca2+ channel blockers• 1. Vascular smooth muscle (VSM)-selective (dihydropyridines)
• 2. Non-selective (diltiazem, verapamil).
• Sympatholytic drugs: • 1. selective α1-adrenergic antagonists
• 2. ß1-adrenergic antagonists
• Aldosterone Receptor Antagonist
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ACE Inhibitors
• Prime consideration in patients with concurrent heart failure, diabetes,
or LV dysfunction.
• MOA: 1) Inhibits Angiotensin Converting Enzyme to inhibit
transformation of angiotensin I to angiotensin II
• Inhibits vasoconstriction and aldosterone production TPR falls and sodium
retention declines
• Decreases degradation of bradykinin vasodilation
• Use: CHF, post MI, Hypertension and diabetic nephropathy,
IMPORTANT FOR DIABETICS!
• SE: Dry cough, hyperkalemia, azotemia, teratogen
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ARBs
• MOA: block Angiotensin II receptor decrease in peripheral
resistance and decrease in effective circulating fluid volume
• Use: Hypertension, CHF, diabetic nephropathy
• SE: NO COUGH, hyperkalemia, teratogen
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Thiazide Diuretics• Thiazide diuretics are the most commonly used diuretics in patients with mild-
moderate HTN with normal renal function.
•
• MOA: They block reabsorption via a Na+/Cl- cotransporter on distal tubule and collecting segment of the renal tubules. • Hydrochlorothiazide, chlorthalidone, indapamide, metolazone
• SE: Elevated triglycerides and glucose, hypokalemia, hyperuricemia, decreased sexual function, metabolic alkalosis. HYPER GLUC + alkalosis and hypokalemia
• Short term effect: reduction in circulatory volume, CO, and mean arterial pressure. The baroreflex kicks in & stimulates sympathetic nervous system, causing transient TPR increase.
• Long term effect: CO returns to normal and TPR decreases. • 1. Baroreceptor resetting and decrease in sympathetic system may cause TPR
reduction
• 2. Thiazide is also a direct smooth muscle relaxant and vasodilation decreases TPR
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Beta Blockers
• MOA: Lower blood pressure by decreasing HR and contractility and
decreasing secretion of renin in the kidney which causes a decrease
of TPR
• B1 and B2 – Propanolol, Nadolol, Pindolol, Timolol
• NOT FOR DIABETICS
• B1 – Metoprolol, atenolol, esmolol, acebutolol, bisoprolol, betaxolol
• Less bronchoconstriction
• A1 and B1 – Labetalol
• Vasodilation
• Use: Hypertension, CAD, tachyarrhythmias, migraines, CHF
• SE: Hypotension, bradycardia, bronchoconstriction, arrhythmias,
sexual dysfunction, fasting hypoglycemia
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α1 and α2 agonists are not commonly
used anymore except for prazosin which
can be used for prostatic hyperplasia.
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Calcium Channel Blockers
• MOA: block voltage gated L-type calcium channels of cardiac and vascular smooth muscles leading to decreased muscle contraction• Decreased myocardial contractility
• Peripheral vasodilation
• Dihydropyridines• Verapamil and Diltiazem
• Use: Hypertension, Prinzmetal angina, Raynaud disease, supraventricular tachycardias
• SE: bradycardia and heart block (verapamil, diltiazem), hypotension, peripheral/pedal edema
• WATCH OUT FOR BETA BLOCKERS bradycardia
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Aldosterone Antagonists
• MOA: Compete for the cytoplasmic aldosterone receptor, inhibiting
the Na+ sensitive channel in the kidney which decreases the lumen
negative potential to drive K+ and H+ ion excretion, thus K+ and H+ are
retained in the circulation. Also shows beneficial cardiac
antiremodeling effects
• Spironolactone, Eplerenone
• Use: Primary or secondary hyperaldostonerism, CHF, and to reduce
loss of potassium caused by other diuretics
• SE: hyperkalemia, antiandrogenic activity (not in eplerenone)
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Lifestyle Modifications
• Low Sodium diet• Limit intake to < 2 gm Na or <5 gm NaCl per day.
• Less Alcohol• Women no more than 1 drink per day, men no more than 2
• Exercise• 30 minutes aerobic activity 3-5x / week
• Weight loss• 10kg loss will lower BP about 10/8 mmHg
• Stress reduction• Meditation, martial arts, prayer reduce stress and BP
• CPAP treatment for sleep apnea• Associated with risk for CAD
• Avoid decongestants (phenylephrine, etc) and NSAIDS (like ibuprofen)• All NSAIDs may raise blood pressure and diminish the antihypertensive efficacy of
all classes of antihypertensive drugs, except calcium channel blockers.
• Treating dyslipidemia will lower BP about 5 mmHg
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Determining Salt Sensitivity
• Salt sensitivity is an independent risk for Cardiovascular Disease
• How to determine salt sensitivity
• Method 1:
• Administer 2 L of normal saline over 4 hours
• Measure BP before infusion, after infusion, and on the next day
• On the second day, give patient diuretic and again remeasure their BP at multiple
timepoints
• Salt sensitivity defined as decrease in MABP >10mmHg on the second day
• Salt Resistant defined as decrease <6 mmg Hg
• Intermediate = 6-9mm Hg
• Method 2:
• Controlled Na+ diet (50 - 250 mmol/day)
• Measure MAP rise of > 4mm Hg
• Controlled Na+ diet (100 – 250 mmol/day)
• Measure MAP rise of >3 mm Hg
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J-Shaped Sodium Curve
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Salt Sensitivity
• 11% Inverse Salt Sensitivity
• 72% Salt Resistant
• 17% Salt Sensitive
• African American and Japanese at high risk
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DEVELOPMENT OF THE
HEART
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Describe the developmental basis of
dextrocardia and atrial septal defects.
• On day 23, the heart tube undergoes a characteristic, right-sided
bending that transforms it into a form referred to as the “cardiac loop”.
• Dextrocardia-This developmental abnormality in which the heart lies on the
right side of the thorax occurs when the heart tube bends to the left instead
of the right.
• Formation of septum primum and secundum occurs as endocardial
cushions begin to fuse.
• Atrial Septal Defect (ASD)-A congenital abnormality caused by either
excessive resorption of tissue around the foramen secundum or
hypoplastic/insufficient growth of the septum secundum.
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List the embryonic structures involved in
the formation of the interventricular
septum.• Most of the interventricular septum is made up of a muscular septum
• Superiorly, the interventricular septum develops in close coordination with the outflow tract and it is during this process that a large portion of congenital heart defects arise.
• Separation of the outflow tract into aortic and pulmonary channels occurs via the aorticopulmonary septum which arises in a spiral pattern, resulting in the twisted configuration of the aorta and pulmonary artery.
• The septum extends inferiorly into the ventricle to form the top part of interventricular septum
• 3 components of IV septum:
• Muscular wall
• Aorticopulmonary septum
• Endocardial cushions (membranous)
• Pathology: VSDs, persistent truncus arteriosus, transposition of the great vessels, tetralogy of Fallot.
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Describe the underlying basis of cyanosis
in congenital heart disease
• Cyanosis occurs when a right-to-left venous shunt mixes venous
blood with systemic blood.
• Deoxygenated/blue blood is being pumped into the systemic
circulation
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Identify adult remnants of the fetal
circulation.
• Closure of the ductus arteriosus
• Occurs immediately after birth by contraction of its muscular wall.
• Muscular contraction mediated by bradykinin released by the lungs during initial inflation.
• Ligamentum arteriosum is your obliterated ductus arteriosus
• Patent ductus arteriosus is a failure in closure seen in pregnancies complicated by rubella or hypoxia.
• Closure of the foramen ovale
• Caused by an increase in pressure in the left atrium
• Pressure changes come with the first breath and press septum secundum against septum primum (LO#1 again) with fusion of the two layers becoming complete around 1 year.
• In first days of life, newborn can reverse closure and shunt blood from right-to-left causing cyanotic period
• Closure of the umbilical arteries
• Occurs within minutes of birth by contraction of the smooth muscle
• Caused by thermal and mechanical stimuli and change in oxygen tension
• Permanent closure through fibrous proliferation • Distal portions converted into the medial umbilical ligaments.
• Proximal converted into vesical arteries to bladder
• Closure of the umbilical vein and ductus venosus
• Occurs shortly after closure of the umbilical arteries
• After obliteration, forms the ligamentum teres in the falciform ligament of the abdominal cavity.
• Obliterated ductus venosum forms the ligamentum venosum
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List in sequence the vessels involved in
bypassing a postductal coarctation of the
aorta.
• Aorta subclavian a internal thoracic artery intercostal arteries
• Or internal thoracic artery→ superior epigastric artery→ inferior
epigastric artery→ external iliac arteries
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CONGENITAL HEART
DEFECTS
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Flow Physiology
• Blood will flow down the path of least resistance
• While a pressure difference will dictate blood flow, blood
will travel to the area of least resistance, even if the
physical pressures are equal.
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Fick Principle
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3 Fetal Structures
• Ductus Venosus: Vascular connection between the placenta and the
heart
• Foramen Ovale: Normal connection between the two atria designed
to allow appropriate shunting
• Ductus Arteriosus: Vascular structure between the PA confluence and
the aorta designed to shunt blood away from the lungs
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Atrial Septal Defect
• 1:1500
• Most commonly occur at foramen ovale, also in ostium primum
• Pathophysiology: High pressure in left ventricle leads to a left-right
directed shunt volume overload and enlargement of RA and RV
• Sx: Typically asymptomatic, dyspnea and fatigue, recurrent lower
respiratory infections
• PE: Systolic impulse at LLSB (RV heave), S2 with widened fixed
splitting pattern
• Dx:
• Enlarged heart on radiograph
• RVH, RAE, and RBB on ECG
• Echo for definitive diagnosis
• Rx: Elective surgical repair with suture closure, synthetic patch or
percutaneous closure device
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In ASD, atria are compliant, so shunting
depends on ventricular pressures and
resistance
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Ventricular Septal Defect
• 1.5-3.5:1000
• Most often in membranous (70%) and muscular (20%) parts of septum
• Pathophysiology: After birth, left-right shunt volume overload on RV, Pulmonary circulation, LA, and LV• Over time can result in chamber dilatation and systolic dysfunction
• Also Eisenmenger Syndrome
• Sx: Large VSDs will cause CHF, tachypnea, poor feeding, failure to thrive and lower respiratory infections• Fall off growth chart after 4 weeks.
• PE: Harsh holosystolic murmur at LSB, systolic thrill
• Dx: • Cardiomegaly and pulmonary vascular markings on radiograph
• LAE, and LVH on ECG
• Echo for definitive diagnosis
• Rx: By age 2 – 50% small VSDs undergo closure, surgical correction within first months for severe disease
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Babies are not symptomatic for the first
few weeks due to slow decrease of
pulmonary vascular resistance
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Patent Ductus Arteriosus
• 1:2500-5000
• Ductus arteriousus typically closes with decrease in PGE1/bradykinin
• Pathophysiology: After birth blood is shunted from aorta to left pulmonary artery LA, LV, and Pulmonary circulation become volume overloaded• Eisenmenger syndrome
• Sx: Large shunts early CHF, tachycardia, poor feeding, slow growth, recurrent lower respiratory infections, Atrial fibrillation, endarteritis
• PE: Continuous machine-like murmur at left subclavicular
• Dx: • Enlarged cardiac silhouette on radiograph, calcification of ductus may be seen
• LAE and LVH on ECG
• Echo for definitive diagnosis
• Rx: High risk of endarteritis even small/asymptomatic PDA is referred for surgical closure, Prostaglandin synthesis inhibitors may be used prior to surgery
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PREMATURITY and rubella are big risk
factors for PDA
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AVSD: most common CHD in Trisomy 21
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Congenital Aortic Stenosis
• 5:10,000, 4X more common in males
• Typically bicuspid leaflet structure is seen
• Pathophysiology: LV systolic pressure increases to pump blood
across valve LVH and aortic dilatation
• Sx: Typically asymptomatic, dyspnea, angina, syncope, fatigue in
adulthood
• PE: crescendo-decrescendo systolic murmur, systolic ejection click
• Dx:
• Enlarged LV and dilated aorta on radiograph
• LVH on ECG
• Echo for definitive diagnosis
• Rx: Transcatheter baloon valvuloplasty for severe cases, often
followed with later repair
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Pulmonic Stenosis
• Congenitally fused valve commissures, fused RV outflow tract or
stenotic pulmonary artery
• Valvular is most common
• Pathophysiology: Increased RV pressure and hypertrophy Right
sided heart failure
• Sx: Mild or moderate: asymptomatic, Severe: dyspnea, exercise
intolerance, abdominal fullness, pedal edema
• PE: Jugular venous a wave, RV heave, crescendo-decrescendo
systolic murmer @ ULSB, widened splitting of S2
• Dx:
• Enlarged RA and RV on radiograph
• RVH on ECG
• Echo for diagnosis
• Rx: Transcatheter balloon valvuloplasty for severe cases
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Aortic Coarctation
• 1:6000
• Discrete narrowing of aortic lumen
• Often with Turner Syndrome or bicuspid valve
• Pathophysiology: LV faces increased afterload diminished flow to lower
extremities LVH, dilatation of intercostal arteries erode ribs
• Sx: Heart failure, differential cyanosis w/ PDA, claudication, upper extremity
hypertension
• PE: weak, delayed femoral pulses, elevated BP in arms or right arm > left
arm
• Dx:
• Notching of ribs on radiograph + indented aorta
• LVH on ECG
• Echo for dx and MRI for severity
• 20 mmHg gradient
• Rx: Prostaglandin infusion to maintain PDA, elective repair in children,
excision and anastomosis or transcatheter procedures
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Conotruncal Malformations
• The Bulbus cordis, or Conus cordis, will become the right ventricle
and the left & right outflow tracts (membranous portion).
• Neural crest cells migrate to the conotruncal area that becomes the
outflow tracts and abnormal migration or proliferation of these cells
can result in congenital malformations of the septum/outflow area.
Neural crest cells are also involved in craniofacial development and,
so, heart malformations are often associated with facial malformations
(22q11 deletions/Velocardiofacial Syndrome/DiGeorge Syndrome)
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Tetralogy of Fallot: CYANOTIC
• 5:10,000, microdeletion 22q11
• Cephalad displacement of infundibular portion of interventricularseptum• VSD
• Subvalvular pulmonic stenosis
• Overriding aorta receives blood from RV and LV
• RVH
• Pathophysiology: Right-Left shunt due to pulmonic stenosis deoxygenated blood to systemic circulation hypoxemia and cyanosis
• Sx: dyspnea, cyanosis, hyperventilation, syncope
• PE: mild cyanosis, clubbing, palpable heave at LLSB, systolic ejection murmur at LUSB
• Dx: Boot shaped heart on radiograph, RVH on ECG, Echo for diagnosis
• Rx: Elective surgical repair @ 6-12 months
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Bundle of His runs in this area and is often
displaced. This puts these children at risk
pre- and post-operatively for dysrhythmia.
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The conotruncal malformations are very
highly associated with 22q11 deletions,
also termed Velocardiofacial Syndrome or
DiGeorge Syndrome
Consists of the findings of the
aforementioned cardiac anomalies,
thymic aplasia and immunodeficiency,
cleft palate, and hypocalcemia
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Transposition of Great Arteries
• 40:100,000, most common in neonates
• Pathophysiology: pulmonary and systemic circulation in
parallel desaturated blood flows to systemic circulation
LETHAL without PDA
• Sx: BLUE
• Dx: RVH on ECG, echo for diagnosis
• Rx: MEDICAL EMERGENCY, prostaglandin infusion,
Jatene procedure (arterial switch)
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Truncus Arteriosus
• If the aorticopulmonary septum truncal swellings fail to fuse, a Ventricular Septal Defect arises.
• A persistent truncus arteriosus results in a common outflow tract that receives blood from both ventricles (deoxygenated from right and oxygenated from left). This is classified as a cyanotic disorder.
• We term this an admixture lesion and it means that in a perfectly balanced world equal parts blue blood mixes with equal parts red blood (Qp=Qs) and the saturations are the average of 100% (normal oxygenated blood) and 70% (normal mixed venous blood) or about 85%
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Eisenmenger Syndrome
• Severe pulmonary vascular obstruction caused by chronic left-right shunting
• Leads to reversal of shunt and systemic cyanosis
• Pulmonary arteriolar media hypertrophies and intima proliferates reducing cross sectional area of vascular bed
• Vessels thrombose increased resistance
• Sx: dyspnea, erythrocytosis, hyperviscosity, fatigue, headaches, stroke, hemoptysis
• PE: cyanosis, clubbing, JV a wave, loud P2
• Dx: • Proximal pulmonary artery dilatation on radiograph, calcification
• RVH and RAE on ECG
• Echo for diagnosis
• Rx: avoidance of strenuous activity, high altitude, peripheral vasodilators, pregnancy, treatment of infections, management of arrhythmias, phlebotomy for erythrocytosis, pulmonary vasodilators
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PATHOLOGY AND
RADIOLOGY
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Benign Cardiac Tumors
• Myxomas are the most common primary cardiac tumor.
• Occur in middle aged patients, more common in women
• Patients may have peripheral embolization of the tumor, obstruction of
an AV valve, or sx of a systemic disease (fever, malaise, etc).
• Typically pedunculated masses located in the LA
• T1-weighted images show a mass with intermediate signal intensity
similar to myocardium. However, this signal may be variable due to
calcifications that are hypointense or hemorrhage that is hyperintense
to myocardium. Myxomas typically enhance heterogeneously.
• Lipomas are the second most common primary cardiac tumor
• Have a high intensity on T1-weighted images that darkens on fat
suppressed sequences.
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Myxoma
• Clinicopathologic:• Most common primary cardiac tumor.
• 90% in atria, 80% on left side. LEFT ATRIUM
• Mean age is 50. ADULTS
• Clinical manifestations:• “Ball-valve” obstruction of “wrecking-ball” destruction of valve.
• Tumor embolization.
• Systemic symptoms due to cytokine production.
• Gross Morphology:• Often at site of fossa ovalis.
• 1-10 cm in size.
• May be sessile or pendunculated, hard or gelatinous texture.
• Microscopic Appearance:• Stellate myoxoma cells embedded in myxomatous mucopolysaccharides substance.
• Prominent vessels, hemorrhage and inflammation common.
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Lipoma
• Pathogenesis: • Benign tumors composed of mature fat cells
• Adults
• Most often occur in left ventricle, right atrium or atrial septum.
• Clinical manifestations:• Typically asymptomatic; incidental finding on imaging.
• May cause ball-valve obstruction or arrhythmias
• Gross Morphology:• May occur in the subendocardium (bulge into the chamber), myocardium (wall
thickening), or subepicardium (bulge into pericardial space).
• Cut section show yellow, glistening, adipose tissue.
• Microscopic Appearance:• Mature adiopose tissue with entrapped myocardium.
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Papillary Fibroelastoma
• Pathogenesis:• Benign tumor of adult.
• Typically occur on valves
• May occur on endocardial surface
• Clincial manifestations:• Often incidental finding.
• May break off and embolize.
• Aortic tumors may prolapse into coronary ostia.
• Gross Morphology: • Compared to sea anemone
• Distinctive cluster of yellow-white hairlike projections covering large portions of valvular surface
• Microscopic Appearance:• Narrow, elongated and branching papillary fronds composed of collagen.
• Lined by endothelium.
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Rhabdomyoma
• Pathogenesis: • Most common cardiac tumor of CHILDREN
• Benign tumor of cardiac myocytes.
• Frequently associated with tuberous sclerosis
• Most commonly occur in ventricles; often multiple.
• Clinical manifestations:• May result in arrhythmias or chamber obstruction
• Natural history is regression.
• Gross Morphology:• Myocardial tumor that may bulge into ventricular chamber.
• Cut section shows tan-white homogenous solid tissue.
• Microscopic Appearance:• Enlarged, atypical myocytes with abundant cleared out cytoplasm (glycogen).
• Cytoplasm strands to connect nucleus to cell membrane (spider cells).
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Cardiac Fibroma
• Pathogenesis: • Typically tumor of CHILDREN, most often in first year of life.
• Benign tumor of fibroblasts; may be locally infiltrative.
• Most often in ventricles (left>right) or ventricular septum.
• Clinical manifestations:• Heart failure, cyanosis, syncope or arrhythmias.
• Gross Morphology:• Myocardial tumor that may bulge into cardiac chamber.
• Nearly always solitary.
• Cut surface is firm, white with whorled appearance.
• Microscopic Appearance:• Bland spindle cell lesion with collagen production.
• May infiltrate into surrounding myocardium.
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Malignant Cardiac Tumors
• Metastatic tumors are the most common tumors found in the heart. The most common cardiac metastases include lung, breast, melanoma, and lymphoma. • Metastases often induce a pericardial effusion.
• Angiosarcoma: the most common primary malignancy of the heart• Usually located in the right atrium.
• Characterized by heterogenous signal on T1-weighted images with areas of elevated signal representing hemorrhage.
• Angiosarcomas demonstrate hyperenhancement after the administration of gadolinium contrast agents.
• Other primary malignant tumors are liposarcoma, leiomyosarcoma, and lymphoma.
• Malignant tumors are more likely to be necrotic, have associated nearby edema, be vascular, demonstrate invasion into adjacent tissues, and have an inhomogeneous appearance.
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Angiosarcoma
• Pathogenesis: • Most common malignant cardiac tumor of ADULTS.
• Usually in RIGHT ATRIUM
• Clinical manifestations:• Arrhythmias, heart block, CHF, angina, or infarction.
• Cardiac tamponade.
• Vast majority are metastatic at presentation.
• Highly aggressive tumor with poor response to therapy.
• Gross Morphology:• Large, infiltrating dark brown, necrotic mass.
• Infiltration of inferior vena cava or tricuspid valve common.
• Microscopic Appearance:• Highly atypical, malignant cells with enlarged nuclei, and prominent nucleloli
• Rudimentary vascular channels.
• Hemorrhage and necrosis.
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Metastatic Tumors
• Direct consequences of tumor:• Pericardial and myocardial metastases
• (melanoma, carcinoma, leukemia/lymphoma).
• A cardiac mass is 40x more likely to be a metastasis than a primary tumor
• Large vessel obstruction
• Pulmonary tumor emboli.
• Indirect consequences of tumor• Nonbacterial thrombotic endocarditis (mucinous adenocarcinoma).
• Carcinoid heart disease (neuroendocrine carcinoma).
• Effect of tumor therapy• Chemotherapy
• (dilated cardiomyopathy).
• Radiotherapy
• (pericarditis, coronary artery disease, restrictive cardiomyopathy).
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Myocarditis
• The most common cause of myocarditis is viral infection
• Coxsackievirus B.
• Inflamed myocardium hyperenhances on early gadolinium enhanced
T1 weighted images due to increased inflow of blood. T2 weighted
images will be bright due to edema.
• Delayed enhanced imaging will demonstrate enhancement in the mid-
myocardium, often in a patchy pattern.
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Necrosis and LGE
• In the case of myocardial necrosis (e.g acute myocardial infarction),
the rupturing of myocytes expands the extracellular space. This
results in a delay transit of contrast media into and out of the
extracellular space. A delay of 12-15 minutes for imaging capture the
contrast media in the abnormal myocardium, resulting in a relative
increase in enhancement of necrotic myocardium as compared to
normal myocardium.
• This same process occurs in areas of myocardial fibrosis, where the
dense collagen fiber results in a slow transit of contrast media in and
out the extracellular space
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Restrictive Cardiomyopathy• Diastolic Heart Failure
• MCC: amyloidosis, hemochromatosis, and sarcoidosis.
• Often difficult to differentiate from constrictive pericarditis, Cardiac MRI is key
• Hypereosinophilic endomyocardial is a type of RCM in which there is extensive endomyocardial fibrosis, often accompanied by an apical thrombus containing eosinophils. The fibrosis itself may be seen as a dark apical rim on gradient echo sequences.
• Sarcoidosis of the heart may appear as focal bright signal in the myocardium on T2 weighted images. Sarcoid granulomas typically demonstrate late hyperenhancement in a patchy midwall and epicardial distribution.
• Amyloidosis involves the myocardium in nearly all cases of primary amyloidosis, but is less common in secondary amyloidosis. The imaging characteristics of cardiac amyloidosis include ventricular wall thickening and DHE. Amyloidosis typically demonstrates extensive midwall DHE. There may be thickening of the atrial septum or right atrial posterior wall as well.
• Hemochromatosis is characterized by iron deposition in tissues throughout the body, including the heart. Iron deposition in the heart is predominantly subepicardial. Due to the paramagnetic nature of the iron deposits, signal loss is seen on both T1 and T2 weighted images.
![Page 534: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/534.jpg)
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Pericarditis
• Pericardial effusion is fluid in the pericardial space.
• Patients can present with pain, dyspnea, pericardial friction rub, and hemodynamic compromise.
• Common causes include neoplasm, uremia, autoimmune disease, inflammation, viral infection, tuberculosis, and hemopericardium.
• Large or rapidly accumulating effusions can cause tamponade.
• Cardiac MRI can be used to characterize pericardial effusions and assess the pericardium
• On spin-echo imaging:• Simple effusions have:
• Low signal intensity on T1-weighted imaging
• High signal intensity on T2-weighted imaging.
• Chylous and hemorrhagic effusions have higher signal on T1
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Constrictive Pericarditis
• Thickened pericardium.
• Etiology: tuberculosis, radiation, viral pericarditis, or prior surgery.
• Diastolic dysfunction due to a non-compliant pericardium
• Symptoms often mimic restrictive cardiomyopathy, MRI is key
• Normal pericardium is less than 3 mm thick. In CP pericardium is often thickened heterogeneously with bi-atrial enlargement.
• A diastolic septal bounce can be seen with constrictive pericarditis.
• Images may show a lack of pericardial slippage during the cardiac cycle due to the tight adhesion between the pericardium and epicardium.
• In effusive constrictive pericarditis, there is both thickening of the pericardium with adhesions to the epicardium as well as loculatedpericardial effusions.
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Aortic Aneurysm
• A vascular aneurysm is a localized abnormal dilation of a blood; most are acquired but they can be congenital.
• Predisposing Factors:• Atherosclerosis and Hypertension
• Cystic Medial Necrosis• Balance of collagen degradation and synthesis is altered.
• Inflammatory cells produce proteolytic enzymes (MMP) which degrades ECM
• Vascular wall is weakened through loss of smooth muscle and elastic fibers.
• Atherosclerotic intimal thickening caused ischemia of inner media.
• Hypertensive changes of vasa vasorum cause ischemia of outer media
• Intrinsic quality of the vascular wall connective tissue is poor
• In some genetic conditions, scaffolding proteins or collagen synthesis are abnormal (Marfan, Ehler-Danlos)
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Cystic Medial Necrosis
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Abdominal Aneurysm
• Abdominal Aortic Aneurysm (AAA): usually atherosclerotic related.
• Most below the renal arteries and above the aortic bifurcation
• Saccular or fusiform
• >5 cm is BAAAADDDD
• Intimal surface of the aneurysm shows severe complicated atherosclerosis with destruction and thinning of the media; frequently contains a laminated, poorly organized mural thrombus that may fill some or all of the dilated segment.
• Clinical consequences of AAA :• Rupture into the peritoneal cavity or retroperitoneal tissues with massive, potentially
fatal hemorrhage
• Obstruction of a branch vessel resulting in ischemic injury of downstream tissues
• Embolism from atheroma or mural thrombus
• Impingement on an adjacent structure
• Presentation as an abdominal mass that simulates a tumor
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Thoracic Aneurysm
• Thoracic Aortic Aneurysm: related to hypertension, tertiary syphilis or
genetic disorders.
• Most are between the aortic valve and innominate artery
• Clinical consequences of thoracic aneurysm :
• Dilatation of aortic root aortic insufficiency
• Respiratory difficulties due to encroachment on the lungs and airways
• Difficulty in swallowing due to compression of the esophagus
• Persistent cough due to irritation of recurrent laryngeal nerves
• Thrombosis, Embolism or Rupture
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Aortic Dissection• Aortic dissection occurs when blood splits the laminar planes of the media to form a blood-
filled channel within the aortic wall.
• Pathogenesis:• Hypertension is the major risk factor
• Arteriosclerosis of vaso vasorum leads to smooth muscle hypertrophy and weakening of wall
• Also due to inherited defects from Marfan syndrome, Ehlers-Danlos syndrome, vitamin C deficiency
• The trigger for dissection is an intimal tear blood flow under systemic pressure dissects through the media, fostering progression of the medial hematoma.
• Gross Morphology:• In the vast majority the intimal tear is found in the ascending aorta within 10 cm of the aortic valve.
• The dissection can extend along the aorta retrograde toward the heart as well as distally
• Spreads along the laminar planes of the aorta, usually between the middle and outer thirds.
• Clinical consequences of aortic dissection:• Rupture through the adventitia causing massive hemorrhage or cardiac tamponade
• Extension of dissection along coronary or cerebral arteries causing myocardial infarction or stroke.
• Compression of spinal arteries resulting in transverse myelitis.
• The dissecting hematoma may reenter the lumen of the aorta through a second distal intimal tear, creating a new vascular channel and forming a “double-barreled aorta” with a false channel.
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Stanford Type A vs. Type B
• Type B is below the brachiocephalic arteries and suggests medical management
• Type A is above the brachiocephalic arteries and suggests surgical intervention
• Medical management: BP and HR control (Beta blockade)
• Surgical: open surgery or endoscopic procedures
• Complications
• Rupture surgical intervention
• Branch organ malperfusion
• Aneurysmal degeneration
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True vs. False Lumen
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True lumen in aortic dissection is typically
smaller.
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PERICARDIAL DISEASE
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Acute Pericarditis Presentation
• Symptoms: Sharp, pleuritic, and positional chest pain in dermatomes
C3-C5 Fever, Non-exertional dypsnea
• PE: Friction rub
• EKG findings
• Abnormal in 90% of patients with acute pericarditis
• Diffuse ST segment elevation
• PR segment depression
• Labs: Lymphocytosis, elevated ESR/CRP
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Etiologies of Pericarditis
Infectious Non-infectious
Viral
•Coxsackie B
•Echovirus
•Influenza
•Varicella
•Mumps
•HepB
•EBV
Post-MI
•Immediately post-MI
•Dressler’s Syndrome
Uremic
Neoplastic
Post-Radiation
Associated with Connective
Tissue Disease
•SLE
•RA
•Systemic Sclerosis
Tuberculous
Non-tuberculous bacterial
(purulent)
•S. pneumo
•S. aureus
Drug-induced
•Procainamide
•Hydralazine
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Rx for Pericarditis
Etiology Treatment
Viral NSAIDs
Colchicine
Steroids
Post-MI (both types) Aspirin
Purulent Catheter drainage, antibiotics
Tuberculous Multi-drug TB treatment
Uremia Dialysis
Neoplastic Palliative
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Pericardial Effusion and Tamponade
• Pericardial effusion is an increase in the fluid in the pericardial space
• Pericardial tamponade occurs when pericardial fluid accumulates under high pressureand severely limits filling of the heart SV and CO decline, leading to hypotensive shock and death
• Physical findings• Beck’s Triad
• Jugular venous distention
• Systemic hypotension
• “Small, quiet heart” on physical exam
• Sinus tachycardia, dyspnea, tachypnea
• Pulsus paradoxus: A decrease in systolic blood pressure of more than 10 mm Hg during normal inspiration.
• Rapid development symptoms of profound hypotension• Confusion
• Agitation
• Slower development of tamponade (e.g., over weeks)• Fatigue due to low CO
• Peripheral edema due to right-sided heart failure
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Water Bottle Heart
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Electrical Alternans on ECG
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Inspiration and Hemodynamics
• Normal hemodynamics• Inspiration → expansion of the thorax → intrathoracic pressure
becomes more negative → increased CVP→ increased RV filling
• Increased RV filling → interventricular septum shifts to the left → decreased LV filling
• Decreased LV filling → decreased SV and decreased systolic BP
• The normal decrease in systolic blood pressure is <10 mm Hg
• Cardiac tamponade• The situation is exaggerated.
• Both ventricles are compressed by the increased fluid in the pericardium, so the bulging of the interventricular septum to the left leads to an even greater decrease in left ventricular volume.
• The decrease in LV filling leads to a decrease in systolic blood pressure >10 mm Hg.
• This is pulsus paradoxus
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Treatment for pericardial tamponade is
pericardiocentesis
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Etiology of Constrictive Pericarditis
• Chronic pericarditis
• Idiopathic
• Post surgical
• Radiation induced
• Tuberculosis
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Constrictive Pericarditis
• Pathophysiology – develops over months to years• Fluid undergoes organization and fusion to the pericardial layers fibrous
scar formation
• Rigid, scarred pericardium inhibits diastolic filling Right sided heart failure
• Impaired filling (reduced preload) decreased SV, CO
• Sx: Fatigue, hypotension, reflex tachycardia
• PE: JVD, hepatomegaly with ascites, peripheral edema, pericardial knock, Kussmaul sign
• Dx:• Chest radiograph – normal or mildly enlarged cardiac silhouette with
calcifications
• ECG – non specific ST and T wave abnormalities, atrial arrhythmias are common
• CT or MRI is superior to echocardiography in assessment of pericardial thickness (pericardial thickness >2mm)
• Definitive diagnosis – cardiac catheterization
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Diastolic Bounce
• The dense, fibrous pericardium restrict normal diastolic filling of the
ventricle. However, unlike restrictive disease, the compliance of the
myocardium is not effected.
• When the ventricle reach a certain volume, the pericardium restricts
further filling and the pressure in the ventricle rapidly rises.
• Since both ventricle are subject to this limitation, the only direction for
pressure to equalize is across the interventricular septum, resulting in
this bouncing motion.
• Distinguishes constrictive pericarditis from effusion
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Cardiac
Tamponade
Constrictive
Pericarditis
Pericardial
calcification Absent Common
Kussmaul’s signAbsent Common
Pulsus paradoxusPresent Rare
Pericardial knockAbsent Common
Atrial fibrillationRare Common
![Page 558: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/558.jpg)
Rx for Constrictive Pericarditis
• Only effective therapy: surgical removal of the pericardium
• Signs and symptoms maybe not resolve immediately
because of associated stiffness of outer walls of the heart,
but “subsequent clinical improvement is the rule in
patients with otherwise intact cardiac function”
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Gross features of Pericarditis
Serous - mild inflammation with small effusion - uremia, autoimmune
Fibrinous - serosanguinous effusion with “bread & butter” fibrin – viral, MI, radiation
Suppurative - pus laden transudate – bacterial
Hemorrhagic - grossly bloody serous effusion - tumor, TB
Caseous - necrotizing caseous necrosis - TB
Fibrinous Hemorrhagic Suppurative
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Microscopic Features of Pericarditis
• Parietal and visceral pericardium shows an infiltration of
white blood cells
• Exudate of fibrin (amorphous eosinophilic material)
admixed with white blood cells.
• Serous - mild inflammation with little to no fibrin,
• Fibrinous – Extensive fibrin and moderate mixed inflammation.
• Suppurative – Abundant neutrophilic inflammation.
• Hemorrhagic – Similar to fibrinous but with blood or hemosiderin
laden macrophages.
• Caseous - necrotizing caseous necrosis with granulomatous
inflammation.
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ENDOCARDITIS
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Bacterial Portals
![Page 563: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/563.jpg)
Predisposing Factors
Structural Other
Rheumatic Heart Disease IV Drug Use
Mitral Valve Prolapse Elderly (>60)
Degenerative Calcific Stenosis Male Predominance
Bicuspid Aortic Valve Poor Dentition
Prosthetic Valves HIV Infection
Congenital Heart Disease Chronic Hemodialysis
Intracardiac Devices Hypercoagulable state
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Single most common bacteria causing
endocarditis?
• Staphylococcus Aureus (31%)
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Classifications of Endocarditis
• Native Valve
• Prosthetic Valve
• Early: Staph
• Late: Strep
• IVDA
• Right sided heart valves
• Nosocomial
• Health care acquired
• Acute vs. Subacute• Acute endocarditis is a hectically febrile illness that rapidly damages cardiac structures,
hematogenously seeds extracardiac sites, and, if untreated, progresses to death within
weeks.
• Subacute endocarditis follows an indolent course; causes structural cardiac damage only
slowly, if at all; rarely metastasizes; and is gradually progressive unless complicated by a
major embolic event or ruptured mycotic aneurysm.
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Bacterial Mechanisms for Survival
• 1. Surface adhesion molecules called microbial surface components recognizing adhesion matrix molecules (MSCRAMMs)• travel to nonbacterial thrombotic endocarditis (NBTE) or injured endothelium
• EXCEPTION: S. aureus – so virulent it does not need injured epithelium
• NOTE on NBTE: often a result of hypercoagulable state → maranticendocarditis (uninfected vegetations seen in patients with malignancy and chronic diseases)
• 2. Other Adherence Mechanisms• Gram positives – fibronectin binding proteins
• S. aureus clumping factor
• streptococci – glucans or FimA
• 3. Ability to survive in bloodstream (gram + more resistant to destruction by complement system)
• 4. Fibrin deposition combines with platelet aggregation and microorganism proliferation to generate an infected vegetation.
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HACEK
• H: Haemophilus aphrophilus
• A: Actinobacillus actinomyetemcomitans
• C: Cardiobacterium hominis
• E: Eikenella corrodens
• K: Kingella kingae
• These are all slow growing, fastidious, gram-negative bacilli that
account for 5-10% of native-valve endocarditis in non-drug using
individuals.
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Pathogenesis
• 1. Endocardial injury
• 2. Focal adherence of platelets and fibrin
• 3. Platelet fibrin nidus becomes colonized with bacteria
• 4. Further activation of coagulation system via extrinsic
clotting pathway and tissue factor
• 5. Adherent monocytes and cytokines
• 6. Activated endothelial cells express further local
deposition of fibronectin
• 7. Bacterial growth occurs within matrix of fibronectin
which shields it from the host immune response
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Clinical Signs
![Page 570: Cardiovascular Review](https://reader034.fdocuments.net/reader034/viewer/2022050907/559f3d541a28ab63748b45fa/html5/thumbnails/570.jpg)
Vegetations• Vegetative lesions are masses of platelets, fibrin, microcolonies of
microorganisms, and scant inflammatory cells
• Vegetation morphology differs with different types of endocarditis
• Rheumatic heart disease; infectious endocarditis; nonbacterial thrombotic endocarditis; Libman-Sacks endocarditis (non-bacterial endocarditis seen in SLE)
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Complications
• CHF develops in 30-40% of patients
• Emboli:
• leading to stroke or encephalopathy
• leading to MI
• leading to renal infarcts and flank pain/ hematuria
• Glomerulonephritis
• Neurologic complications: stroke, encephalopathy, hemorrhagic
infarcts, ruptured mycotic aneurysms, seizures, purulent meningitis
• Heart block: Myocardial abscesses burrow through ventricular septum
and conduction system.
• Chordae rupture leading to severe mitral regurgitation
• Pericarditis: Myocardial abscesses burrow through epicardium.
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Diagnostics
• History: Congenital defects, IV drug use, Hx of valve disease, Hx of valve replacement or repair, prior endocarditis
• PE: Murmurs, Fever, Petetchiae, Osler’s nodes, Janeway lesions, Roth spots, Splenomegaly
• Blood Count: Low HCT and elevated ESR, C-reactive Protein and WBC, Serum Rheumatological Factor
• Blood Cultures
• ECG
• Echocardiogram: TTE or TEE
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Diagnostics: Echocardiography
• Transthoracic echocardiography (TTE) is noninvasive and exceptionally specific
• Cannot image vegetations <2 mm in diameter, and in 20% of patients it is technically inadequate because of emphysema or body habitus.
• TTE detects vegetations in only 65% of patients with definite clinical endocarditis.
• Moreover, TTE is not adequate for evaluating prosthetic valves or detecting intracardiac complications.
• Transesophageal echocardiography (TEE) is safe and detects vegetations in >90% of patients with definite endocarditis
• Studies may be false-negative in 6–18% of endocarditis patients. When endocarditis is likely, a negative TEE result does not exclude the diagnosis but rather warrants repetition of the study in 7–10 days.
• TEE is the optimal method for the diagnosis of PVE or the detection of myocardial abscess, valve perforation, or intracardiac fistulae.
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Dx: Duke Major Criteria• Major Criteria
• 1) Blood culture positive for IE• A.Typical microorganisms consistent with IE from 2 separate blood cultures:
• 1) Viridans streptococci, Streptococcus bovis, HACEK group, Staphylococcus aureus;
• 2) Community-acquired enterococci, in the absence of primary focus; or
• B. Microorganisms consistent with IE from persistently positive blood cultures, defined:• 1) At least 2 positive cultures from blood samples drawn >12 hours apart
• 2) All 3 or a majority of >4 separate cultures of blood
• C. Single positive blood culture for Coxiella burnetii or antiphase I IgG ab titer > 1:800
• 2) Evidence of endocardial involvement
• 3) Echocardiogram positive for IE• A. Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets,
or on implanted material in the absence of alternative anatomic explanation
• B. Abscess
• C. New partial dehiscence of prosthetic valve
• 4) New valvular regurgitation
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Diagnosis: Duke Criteria
• 1. Definitive infective endocarditis
• (1) 2 major criteria
• (2) 1 major criterion and 3 minor criteria
• (3) 5 minor criteria
• 2. Possible infective endocarditis
• (1) 1 major criterion and 1 minor criterion
• (2) 3 minor criteria
• 3. Rejected infective endocarditis
• (1) Firm alternate diagnosis explaining evidence that was attributed to IE
• (2) Resolution of “infective endocarditis syndrome” with antibiotic therapy for 4 days or less
• (3) No pathologic evidence of IE at surgery or autopsy, with antibiotic therapy for 4 days or less
• (4) Does not meet criteria for possible endocarditis
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Vegetations and Therapy
• Vegetations protect bacteria from host defenses and the metabolically
inactive bacteria within them are difficult to kill with antibiotics
• To cure endocarditis, all bacteria in the vegetation must be killed
• This means antimicrobial therapy must be bactericidal and prolonged
• Vegetation size and position can be determined by transthoracic or
transesophageal echocardiography
• Large vegetations (>10 mm in diameter) may indicate surgical removal
• Vegetation obstructing valve may indicate surgical removal
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Subtleties of Endocarditis
• Protean = displaying great diversity or variety
• Symptoms are very nonspecific and endocarditis is rare; however it is
extremely serious. Even though the symptoms are nonspecific, you
can hear a heart murmur in many cases...
• Patients may present with symptoms more indicative of other disease
processes, such as: hematuria, back pain, or bronchitis
• Also, if patients are treated with antibiotics before blood is drawn for
cultures, the ability to grow and identify bacteria may be lost, which is
not good since knowing the causative microorganism is an important
step in diagnosing and treating endocarditis.
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It is difficult to eradicate bacteria from the
vegetation because local host defenses
are deficient and because the largely non-
growing, metabolically inactive bacteria
are less easily killed by antibiotics. To cure
endocarditis, all bacteria in the vegetation
must be killed; therefore, therapy must be
bactericidal and prolonged.
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Antibiotic TherapyOrganism Antibiotic
Susceptible Streptococcus 1) 4 weeks Penicillin
2) 4 weeks Ceftriaxone
3) 4 weeks Vancomycin
4) 2 weeks Penicillin + 2 weeks
Gentamycin
Resistant Streptococcus 1) 4 weeks Penicillin + 2 weeks
Gentamycin
2) 4 weeks Vancomycin
Susceptible Enterococcus 1) 4 weeks Penicillin + 4-6 weeks
Gentamycin
2) 4 weeks Ampicillin + 4-6 weeks
Gentamycin
3) 4 weeks Vancomycin + 4-6 weeks
Gentamycin
Resistant Enterococcus 1) 6 weeks Vancomycin + 6 weeks
Gentamycin
Susceptible Staphylococcus 1) 4-6 weeks Nafcillin + 2 weeks
Gentamycin
Resistant Staphylococcus 1) 6 weeks Vancomycin + 2 weeks
Gentamycin
HACEK 1) 4 weeks Ceftriaxone
2) 4 weeks Amp sulfbactam
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For Culture Negative Endocarditis give 4-
6 weeks Vancomycin + 4-6 weeks
Gentamycin
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Aminoglycoside Synergy
• Aminoglycoside Synergy (source: handout on antibiotics)
• Enterococci are intrinsically resistant to low to moderate levels of
aminoglycosides
• Synergy occurs when enterococci with a low level of
aminoglycoside resistance are exposed to a combination of
aminoglycosides and a ‘cell wall active’ antibiotic (i.e. penicillin,
vancomycin)
• The cell wall-active antibiotic facilitates intracellular uptake of the
aminoglycoside, which then acts bactericidally
• Efficacy in Endocarditis
• Need to kill the bacteria
• Appears to be the only effective bactericidal rx of enterococci
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Surgical Indications
• Class I - Surgery Absolutely Indicated
• Causative organism is resistant or fungal
• In the setting of Congestive Heart Failure
• AV block (burrowing abscess severing conduction system)
• Abscess seen on echo
• Class II - Surgery Possibly Indicated
• Recurrent emboli or persistent vegetations
• Mobile vegetations >10mm in size
• Class III - Surgery Contraindicated/unnecessary
• Uncomplicated prosthetic valves
• Organism sensitive to antibiotic therapy
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Prophylactic Antibiotic Treatment
• Rationale - give to patients who would have adverse outcome if
endocarditis is contracted
• Amoxicillin in pill form 30 minutes before procedure
• Criteria
• Prosthetic valve placed
• Previous endocarditis
• Congenital heart defect
• Unrepaired cyanotic defect
• Repaired defect with placement of prosthetic material (i.e. mesh in ASD)
• Repaired defect with residual deficiency
• Cardiac transplant patients who develop valvulopathy
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Prosthetic Valve Infections
• Prosthetic valve endocarditis (PVE) arising within 2 months of valve
surgery is generally nosocomial, the result of intraoperative
contamination of the prosthesis or a bacteremic postoperative
complication.
• Etiology: Time of onset post-op is related to the likely bacterial source
• Within 2 months - nosocomial (S. aureus, CoNS, facultative gram-
negative bacilli, diphtherioids, fungi)
• 2-12 months - considered a delayed-onset nosocomial infection
• >12 months - organisms similar to community-acquired endocarditis
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Catheter Infections
• Incidence of 1.65 infections per 1,000 central line days in the US
• Frequent source of infection in patient populations that require long-term
catheterization, including hemodialysis, oncology, total parenteral nutrition patients
• Site of catheter infection impacts rate of infection, subclavian the
lowest risk
• Endocarditis complicates 6–25% of episodes of catheter-associated
S. aureus bacteremia
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Mistreated Endocarditis and prior
exposure to antibiotics causes negative
cultures