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**What are the common causes of these

valvular lesions:

Mitral Stenosis

Mitral Insufficiency

Aortic Stenosis

Aortic Insufficiency

Mitral stenosis --- rheumatic heart disease (RHD)

Mitral insufficiency --- mitral valve prolapse

Aortic stenosis (AS) --- calcification of valves (normal or

bicuspid)

Aortic insufficiency --- dilation of ascending aorta, most

commonly due to aging or hypertension

What are congenital bicuspid AVs prone to? calcification, IE, CoA (narrowing), and aortic dissection

What is myxomatous degeneration, and

which condition is it most commonly

associated with?

Myxomatous degeneration refers to a pathological

weakening of connective tissue. The term is most often

used in the context of mitral valve prolapse, which is

known more technically as "primary form of myxomatous

degeneration of the mitral valve."

What condition does this describe: one or

both leaflets is (are) enlarged, hooded or

tent-like, and floppy?

mitral valve prolapse

what are common sequelae of Rheumatic

heart disease (RHD)?deforming fibrosis of AV and/or MV

In what disease would you see an Aschoff

body?RHD (acute only)

What is an Anitschkow cell? what disease

do you see them in?

activated macrophage -- RHD (acute only)

(fyi - nuclear chromatin within cell forms a central

irregular ribbon resembling a caterpillar)

*what disease (& where) do you see a

"fishmouth" valve?Chronic RHD causing mitral stenosis (looking from LV)

What is another term for IE? what can cause

it?

bacterial endocarditis, even though can be caused by

fungi, rickettsiae, or Chlamydia

vegetations (offending agent + thrombotic

debris) are common to RHD, IE, NBTE, and

LSE (Libman-Sacks Endocarditis)... which

both sides: LSE (inflmmatory - Lupus linked)

chordae: IE

one has vegetation that affects both sides of

the leaflets? which can affect cordae?

what are verrucae? where do they typically

form?

Small wart-like projections (verrucae) appear along the

lines of closure

** What is carcinoid syndrome?

Carcinoid syndrome is a group of symptoms associated

with carcinoid tumors -- tumors of the small intestine,

colon, appendix, and bronchial tubes in the lungs.

These tumors release too much of the hormone

serotonin, as well as several other chemicals that cause

the blood vessels to open (dilate).

Does carcinoid syndrome usually affect the

L or R heart? why?

Right - first exposure to bioactive substances released by

carcinoid tumors, also serotonin is deactivated when it

passes through the lungs before reaching the left heart.

What is the most common cause of calcific

aortic stenosis?aging

*myxomatous valves are common to MV

prolapse, what substance is more abundant

in these valves? and what color do they stain

(Movat)?

proteoglycans - blue/green

what is the initial infection that leads to

Rheumatic fever?

group A b-hemolytic strep infection, usually pharyngeal

(RHD is an immune mediated disease)

what is the cardiac implication of long term

RHD?

Deforming fibrosis of AV and/or MV which may not

present clinically until years later

* which valve disease are verrucae most

commonly seen in?RHD

Can endocarditis invade the endocardium

and lead to the destruction of the underlying

tissue?

yes, often

FYI* The endocardium is the innermost layer of tissue that

lines the chambers of the heart. Its cells are

embryologically and biologically similar to the endothelial

cells that line blood vessels.

The endocardium underlies the much more voluminous

myocardium, the muscular tissue responsible for the

contraction of the heart. The outer layer of the heart is

termed epicardium and the heart is surrounded by a

small amount of fluid enclosed by a fibrous sac called the

pericardium.

what is another term for nonbacterial

thrombic endocarditis (NBTE)? * what

type of patients does this most commonly

occur in?

- marantic endocarditis

- Occurs in debilitated patients (e.g. cancer)

Deposition of small noninfected, loosely attached masses

of fibrin, platelets, and other blood components on valves

Often associated with hypercoagulable state, as in

mucinous adenocarcinoma

what type of patients does Libman-Sacks

Endocarditis most commonly occur in?LSE - lupus (predisposed to clotting)

* what do carcinoid tumors secrete? serotonin

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Standard EKG

small box = 1mm or 40ms, big box = 5mm or 200ms, Pwave = < 100ms

wise and < 3mm high and upright in I/II/aVF and inverted in aVR, 120 < PR

< 200, 60 < QRS < 100?, Q < 3mm, QT < 420?, T wave upright in I/II and

inverted in aVR, T wave </= 5mm in limb leads

prominent U waves in..."hypokalemia, hypercalcemia, digitalis therapy, thyrotoxicosis (U waves

best seen in V3)

hypothermia EKG findings"J wave (osborn wave), conduction delays (PR, QRS, QT prolongation),

dysrhytmias like sinus brady or a-fib with SVR

J wave broad upright deflection at end of upright QRS (EKG sign in hypothermia)

hypokalemia EKG findings U wave, QT prolongation, torsades

hyperkalemia EKG findingshyperacute T waves, prolonged PR interval, widened QRS, sine wave,

Vfib

hypocalcemia EKG findings QT prolongation, torsades

torsades cause QT prolongation (hypokalemia, hypocalcemia, hypomagnesemia,

hypothermia, class IA/IC antidysrhythmics, TCAs)

hypercalcemia EKG

findingsQT shortening

hypomagnesemia EKG

findingsQT prolongation, torsades

digitalis therapy EKG

findingssagging ST, QT shortening (most prominent in lateral leads)

digitalis toxicity EKG

findings

"bigeminal and multiform PVCs are most common, paroxysmal atrial

tachycardia with AV block is pathognomonic

digitalis toxicity symptomsflu-like syndrome (malaise, anorexia, n/v/d), visual changes (yellow/green

halos around objects), MS changes

digitalis toxicity treatmentactivated charcoal, Fab fragments, correct electrolyte disturbances that

may contribute to dig toxicity, lidocaine to control tachydysrhythmias

multifocal atrial tachycardiairregularly irregular, narrow QRS, >/= 3 different P wave morphologies in

one lead

PAC vs PJC vs PVC

"PACs have noncompensatory pause (PJCs/PVCs have compensatory),

PJCs/PVCs have inverted P waves when present (PACs have upright P

waves), PVCs have wide QRS (narrow QRS in PACs/PJCs)

Vtach definition 3 or more consecutive PVCs at rate > 120

Hs and Ts of

PEA/asystole/vfib/vtach

hypovolemia, hypoxia, hypothermia, hypo/hyperkalemia, acidosis, tension

pneumo, tamponade, MI/PE, toxin

incomplete vs complete

BBBcomplete = QRS > 120ms, incomplete = QRS 90-110ms

RBBB QRS > 120, RSR' in V1, wide S waves in I/V5-6

LBBB QRS > 120, Wide R in V5-6, LAD

AV blocks1st degree = PR prolongation, 2nd degree = dropped beats (type 1 vs type

2), 3rd degree (AV dissociation)

1st degree AV block PR prolongation (> 200ms)

2nd degree type 1 AV

blockprogressive PR prolongation to dropped beat

2nd degree type 2 AV random dropped beats (no PR prolongation)

block

3rd degree AV block complete AV dissociation

Wolf-Parkinson-White

syndrom

pre-excitation through bundle of kent (atria to ventricle accessory pathway)

resulting in delta wave, PR shortening, wide QRS

Lown-Ganong-Levine

syndrome

pre-excitation through James fibers (atria to His bundle accessory

pathway) resulting in PR shortening without delta wave/QRS widening

AVNRT treatment"vagal maneuvers then adenosine then synchronized cardioversion if

stable (go directly to cardioversion if unstable)

types of a-fibfirst episode, paroxysmal (recurrent), persistent (recurrent, > 7days),

permanent (recurrent, > 1yr)

CHADS2 score risk of stroke in pt with a-fib - CHF, HTN, Age > 75, DM, prior stroke or TIA

a-fib/a-flutter treatment

if unstable - cardioversion, if stable but symptomatic - control rate first

(BB/CCB unless EF < 40 then use dig/amio) then cardiovert (DC or amio),

must perform TEE or anticoagulate with heparin x3wks before

cardioversion if a-fib > 48hrs

how to reveal a-flutter give adenosine

VT treatment

"if stable - medical cardioversion (lido, amio, procainamide or Mg), if

unstable - electrical cardioversion then medical maintinance, if pulseless -

defibrillation/epi/lido

Vfib/pulseless VT treatment defibrillation, epi, lido/amio

PEA/asystole treatment epi, search for Hs/Ts

first degree AV block

treatmentnothing

second degree mobitz 1

treatmentnothing if asymptomatic, if symptomatic use atropine or transcu pacing

second degree mobitz 2

treatment

transcu pacing bridge to transvenous pacing (usually happens in acute

anteroseptal MI)

third degree AV block

treatment

treat like mobitz 1 if narrow (usually inferior wall MI), if wide treat like

mobitz 2 (usually anteroseptal MI)

WPW if unstable use cardioversion, if stable depends on ortho vs antidromic - if

narrow complex (orthodromic) treat as SVT

(vagal/adenosine/cardioversion) but if wide complex (antidromic) treat with

procainamide (although will look like VT so will probably use lido first)

pacemaker lettersfirst letter - champer paced, second letter - chamber sensed, third letter -

response to sensing of electrical activity

pts who present with

atypical MIselderly, DM, women, alcoholics, spinal cord disease

serum markers in acute MI

myoglobin - rises first (2-3 hrs) but nonspecific to cardiac muscle, CK -

rises within ~6hrs but nonspecific, CKMB - rises within ~6hrs and fairly

specific, tropinin T/I - rise within ~6hrs and are very specific but remain

elevated for weeks

acute MI treatmentIV/O2/monitor, aspirin/clopidogrel/heparin, morphine(if pain)/NTG(unless

inferior MI or sildenafil), abciximab?, lytics/cath, BB/ACE (within first 24hrs)

MI and AV block

association

anterior MI associated with mobitz 2 (can decompensate to complete heart

block) while inferior MI associated with type 1 or mobitz 1 AV block

ACPE CXR signs cephalization of pulmonary vasculature, vascular congestion, Kerly B lines

normal PAWP ~10mmHg

ACPE treatment

IV/O2/monitor, NTG/furosemide, consider nitroprusside (if need more

preload/afterload reduction), consider dobutamine/norepinephrine (if low

BP or decreased CO), consider CPAP/intubation (if poor ox/vent)

Kussmaul's signincreased JVD on inspiration - sign of poor RV filling (constrictive

pericarditis, restrictive CMP, cardiac tamponade etc)

gallopsS3 (ventricular gallop) = diastolic filling of dilated ventricle; S4 (atrial

gallop) = atrial kick against stiff ventricle

AS vs HOCM murmursAS murmur increases with squatting; HOCM murmur increases with

valsalva (decreased LVEDP)

HOCM ECG findings LVH/LAE, septal Q waves

Wells criteriaassesses PE risk, low risk can be r/o with D-dimer (there is also a Wells

score for DVT)

DVT treatment heparin or lytics (if limb is in danger)

Vichows triad venostasis, hypercoaguability, vessel wall injury

PE triaddyspnea, pleuritic chest pain, hemoptysis (uncommon);

dyspnea/CP/tachypnea (almost always present)

PE treatment heparin or lytics (if hemodynamically unstable)

where does pericarditis

pain radiate to?left trapezius muscle ridge

convex vs concave ST

segments

STEMIs have convex ST segments while pericarditis has concave ST

segments

pulsus paradoxusdecrease in inspiratory (relative to expiratory) blood pressure > 10mmHg;

or the absence of radial pulse during inspiration; sign cardiac tamponade

cardiac tamponade findings

class triad - hypotension, JVD, distant heart sounds (late findings); narrow

pulse pressure, pulsus paradoxus and kussmaul's sign are earlier; low

voltage or electrical alternans on EKG and waterbottle heart on CXR

hypotension and distended

neck veins differential

tension pneumo (look for tracheal deviation), cardiac tamponade (get

echo), massive PE (get echo to look for dilated RV), acute RV MI, SVC

syndrome

myocarditis what do i need to know here? how to diagnose/screen? how to treat?

most common

pericarditis/myocarditis

viruses

cocksakie A/B, echovirus

myocarditis treatmnet supportive (apparently no NSAIDs?), IVIG has some promise

endocarditis signsOsler nodes, Janeway lesions, Roth spots, splinter hemorrhages,

conjunctival hemorrhages

thoracic aortic aneurysm

risk factors

hypertension (THE BIG ONE!), conective tissue disorders (ehlers-danlos,

marfans, lupus, giant cell arteritis, cystic medial necrosis), trauma, syphilis,

and many more...

pathophysiology of aortic

dissection

intimal tear --> blood into media --> seperation of media from adventitia (or

splitting the media depending on source)

hallmark of aortic

dissectionunequal or abscent pulses between extremeties

aortic dissection CXR

findings

mediastinal widening (> 8cm), calcium sign (extension of aortic shadow >

5mm beyond calcified intima), double density, tracheal deviate (to right),

elevated right main stem bronchus and depressed left main stem

bronchus, apical capping

aortic dissection treatmentcontrol BP, HR, dP/dT (metoprolol/nitroprusside), surgery if involve

ascending aortica (type A)

where is a AAA mass felt epigastric puslitile (potentially tender) mass

hypertensive emergency

treatment

nitroprusside is default (reduce MAP by 30% in first hour), nicardipine if

SAH (decreases vasospasms), nitroglycerine if AMI (decreases coronary

steal)

calcium channel blockersdihydropyridines vasodilate (amlodipine, nicardipine), nondihydropyridines

are negative chronotropes (diltiazem > verapamil

hypertensive urgency vs

emergencyurgency = DBP > 115 while emergency = end organ damage

mitral valve prolapse

murmur

late apical systolic with midsystolic click; decreasing LVEDP (valsavla,etc)

moves click closer to S1 and increases length of murmur

mitral valve prolapse

pathophysiology

commonly secondary to myxomatous degerneration of mitral valve leaflets

and cordae tendoneae (usually seen in women)

mitral stenosis etiology usually rheumatic heart disease

mitral stenosis murmur diastolic with early diastolic opening snap

mitral regurgitation etiologyif chronic - RHD, if acute - MI with cordae tendoneae rupture, if MVP -

myxomatous degeneration

mitral regurgitation murmur apical systolic radiating to axilla (after midsystolic click if MVP)

aortic stenosis etiologyif young - congenital bicuspid valve, if old - calcific stenosis, if also MV

disease - RHD

aortic stenosis murmur basal systolic radiating to carotids with opening click

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Tyrosine to dopa enzyme tyrosine hydroxylase

tyrosine hydroxylase inhibitor metyrosine

Dopamine transporter VMAT (transports into synaptic vesicle

blocks dopamine uptake by VMAT reserpine

Allows NE reuptake NE transporter

blocks NE transporter Cocaine, tricyclic antidepressants

Inhibits SNAPs and VAMPs Guanethadine, Bretylium

alpha 1 receptor activates which G protein Gq (IP3 and DAG)

Beta and alpha 2 receptors activate which G protein

beta receptors activate Gs proteins and

increase adenylyl cyclase and cAMP

alpha 2 receptors activate Gi proteins and

decrease adenylyl cyclase and cAMP

Heart has which receptor and effectBeta 1: increases heart rate, increases heart

contractility, speeds AV node conduction

hypotension treated w/ which autonomic drug class adrenergic agonist

Shock treated w/ which autonomic drug class adrenergic agonist

hemistasis treated w/ which autonomic drug class adrenergic agonist

acute heart failure treated w/ which autonomic drug

classadrenergic agonist

chronic hypertension or hypertensive emergencies

treated w/ which autonomic drug classadrenergic beta antagonist

angina treated w/ which autonomic drug class adrenergic antagonist

cardiac arrhythmias treated w/ which autonomic drug

classadrenergic beta antagonist

chronic heart failure treated w/ which autonomic drug

classadrenergic beta antagonist

ID epinephrine

beta 1 agonist

beta 2 agonist

alpha 1 agonist

ID NEbeta 1 agonist

alpha 1 agonist

ID isoproterenol beta 1 agonist

beta 2 agonist

ID Dopamine

beta 1 agonist

D1 agonist

alpha 1agonist

ID dobutamine

beta 1 agonist

beta 2 agonist

alpha 1 agonist

id Ephedrine beta 1 agonist (treats bronchospasm)

ID pheynlephrine alpha 1 agonist

ID midodrinealpha 1 agonist (treats orthostatic

hypotension)

epinephrine general effect

potent vasodilator and cardiac stimulant

Leads to increased stroke volume, heart rate,

and cardiac output

Epi beta 1 effect

β1-receptors induce positive inotropic and

chronotropic actions (increase in pulse rate,

increase in the rate and force of cardiac

contraction through B-1 receptors)

epi alpha effectα-receptors cause vasoconstriction in

vascular beds (including kidney)

epi beta 2 effectActivates β2-receptors in skeletal muscle

blood vessels and liver which leads to dilation

Isoproterenol general effect potent vasodilator, increase cardiac output

isoproterenol receptor and effect

beta receptor agonist

fall in DIASTOLIC blood pressure; systolic

remains same

Lowers peripheral mean arterial pressure

dopamine activates which receptors, whereActivates D1-receptors in vascular beds

Activates β1-receptors in heart

Low dose dopamine activate D1 in renal and vascular beds = local

vasodilatation, renal blood flow and glomerular

filtration = diuresis

(< 2 µg/kg/min)

mid dose dopamine

activate cardiac beta1-receptors (direct and

indirect) = increased heart rate, cardiac

contractility and stroke volume = increased

cardiac output

(2-10 µg/kg/min)

high dose dopamine

activates systemic α-receptors =

vasoconstriction = increased systemic

resistance (may mimic epinephrine)

primary hypertension treated by blocking and

mechanism

alpha 1

lower peripheral vascular resistance

α1 receptors determine arteriolar and venous

tone of vascular smooth muscle

chronic hypertension, ischemic heart disease and

arrhythmias treated by blocking and mechanism

beta

Lowers BP causing negative inotropic and

chronotropic effects

action of alpha 1 receptor

vasoconstriction of vascular smooth muscle

(arterioles and veins) [responsible for BOTH

arteriolar and venous tone]

increases production of IP3 and DAG =

increase in intracellular Ca ions

action of alpha 2 receptor

Inhibition of NE release and vasoconstriction

of coronary and renal arterioles [responsible

for BOTH arteriolar and venous tone]

decreases production of cAMP = inhibits

further release of NE

action of beta 2 receptor

Vasodilation of vascular smooth muscle

(arterioles except in skin and cerebral)

bronchodilation

glycogenolysis (liver)

action of beta 1 receptor inc heart rate, contractility

speeds up AV node conduction

Increases renin release

increases NE release

stimulates lipolysis

alpha agonist actionlower sympathetic outflow from the brain =

decrease in BP and HR

alpha antagonist actionlower peripheral resistance and blood

pressure

Epinephrine reversal

the fall in blood pressure produced by

epinephrine when given following blockage of

α-adrenergic receptors (alpha antagonist)

you will see a lower peripheral resistance and

a drop in blood pressure

clonidine

alpha 2 agonist

Decreases HR and reduces peripheral

vascular resistance = decreases cardiac

output

Reduces arterial pressure, decreases RENAL

vascular resistance and maintains renal blood

flow

very lipid soluble (enters CNS)

Prazosin, Terazosin, Doxazosin (-azosins)

highly selective alpha 1 antagonist

Relaxes arteriole and venous vascular smooth

muscle; produces less reflex tachycardia

management of hypertension (more effective

when used w/ diuretic or beta blocker)

adverse effects of -azosinsorthostatic hypotension, syncope, dizziness,

tolerance

Which -azosin is most water solubleterazosin, higher bioavailability and longer

t1/2 life compared to prazosin and doxazosin

which -azosins are used to treat BPH terazosin and doxazosin

key adverse effects of alpha antagonist Postural hypotension - d/t antagonism of

sympathetic nervous system stimulation of α1-

receptors in venous smooth muscle

(after first dose of -azosins)

Reflex tachycardia - result of exposure to

nonselective α-antagonists when BP is lower

than normal (the release of norepinephrine

activates primarily β-receptor as a result of

agents that block α2-presynaptic receptors)

Beta blocker action and types

Competitively block catecholamines and β-

agonists at the receptor

Most are pure antagonists

Some are partial agonists

Few are inverse agonists

NOT always SPECIFIC to Beta 1. (dose

dependent, diminishes at higher

concentrations)

pharmokinetics of beta blockers

low bioavailability EXCEPT: betaxolol,

penbutolol, pindolol, and sotalol

avg half life 3 to 10 hours EXCEPT: esmolol

(10 min)

most are metabolized well EXCEPT: nadolol

which is excreted unchanged

effects of beta blockers

Negative inotropic and chronotropic effects

Slowed atrioventricular conduction with an

incr. PR interval

Opposed β2-mediated vasodilation which May

lead to a rise in peripheral resistance d/t

unopposed α-receptor mediated effects

When to use beta blockers (clinical applications)

Hypertension

Glaucoma

Migraine

Thyrotoxicosis

Arrhythmia prophylaxis after MI

Supraventricular tachycardias

Angina pectoris

Propanolol properties beta blocker

extensive first pass metabolism (low

bioavailability)

very lipid soluble (crosses BBB)

treatment of hypertension, angina and

arrhythmias, myocardial infarction, and

congestive heart failure

propanolol indications

treatment of hypertension, angina and

arrhythmias, myocardial infarction, and

congestive heart failure

propanolol adverse effects

decreased glycogenolysis and decreased

glucagon secretion, fatigue and exercise

intolerance

bronchoconstriction, diabetes, peripheral

vascular disease

metoprolol properties

beta 1 selective blocker (safer for patients

who experience bronchoconstriction with

propanolol)

CYP2D6 metabolism

treatment of hypertension, stable angina,

acute myocardial infarction and chronic heart

failure

metroprolol indicationshypertension, stable angina, acute myocardial

infarction and chronic heart failure

Esmolol IV

Ultra-short acting beta 1-antagonist

Gets metabolized by esterases in RBC

Peak effect occurs within 6-10 min

Block lasts ~20 min post-infusion

Clinical Indications: supraventricular

arrhythmias, arrhythmias associated with

thyrotoxicosis, perioperative hypertension and

myocardial ischemia in acutely ill pts

Adverse Effects: hypotension, diaphoresis

Safe to use in critical ill patients

Esmolol IV indications supraventricular arrhythmias, arrhythmias

associated with thyrotoxicosis, perioperative

hypertension and myocardial ischemia in

acutely ill pts

Pindolol, Acebutolol

Partial β-agonists with intrinsic sympathetic

activity (ISA)

Exhibiting low level agonist activity while

acting as a receptor site antagonist

Pindolol is a non-selective β-blocker

Acebutolol β1-blocker

indicated for hypertension, angina, patients

that show bradycardia

pindolol, acebutolol indicationshypertension, angina, patients that show

bardycardia

Labetalol

Reversible antagonist (also has α1-receptor

antagonist properties)

2 isomers one is a potent β-blocker and one is

a potent α-blocker

Clinical Indications: Hypertension,

hypertensive emergencies and congestive

heart failure

Hypotension is less than with other α-blockers

Does not alter serum lipid or blood glucose

levels

Adverse Effects: hypotension, syncope

labetalol indicationsHypertension, hypertensive emergencies and

congestive heart failure

carvedilol

Non-selective β-receptor antagonist; has

some capacity to block α1-receptors

Stronger ability to antagonize catecholamines

at β-receptor

Antioxidant properties

Contributes to clinical benefit in chronic heart

failure

Racemic mixture with stereoselective

metabolism: (R)-carvedilol

avoid beta blockers in patients with asthma

nodal dysfunction (SA or AV)

diabetes

beta blockers WITHOUT Intrinsic sympathetic activity

(adverse effects)

increased triglycerides in plasma

lower HDL cholesterol

beta receptor blockers WITH ISA have little

effect on blood lipids

how to discontinue beta blockers

taper off 2 weeks to avoid tachycardia,

hypertension, and/or ischemia

NEVER STOP ABRUPTLY

Stimulating β1 receptors will do what to the force and

rate of contraction of the heart?Increase

Stimulating M receptors will do what to the force and

rate of contraction of the heart?Decrease

Stimulating α1 receptors will cause most arteries to do

what?Vasoconstrict

Stimulating α2 receptors will cause veins to do what? Vasoconstrict

Stimulating β2 receptors will cause arteries in skeletal

muscle to do what?vasodilate

this drug can be used to treat reflex vagal discharge or

hyperactive carotid sinus reflexesatropine (M2 antagonist)

this drug can cause a decrease in blood pressure as

peripheral vascular resistance and venous return are

decreased.

mecamylamine (ganglionic blocker)

This drug increases peripheral resistance, diastolic and

systolic BP. it is an agonist at β1 and α receptors.Norepinephrine (AKA. Levarterenol)

This drug can be used in the treatment of shock

Adverse Effects - precipitation of angina, cardiac

arrhythmias and myocardial ischemia

Norepinephrine (AKA. Levarterenol)

The overall effects of this drug include

-Increased cardiac contractility, decreased peripheral

resistance (due to balance between α-mediated

vasoconstriction and β2 mediated vasodilation)

-Little change in heart rate and does not require a

Dobutamine

greater oxygen demand on myocardium

Dobutamine

receptor/action?

Primarily considered β1 selective synthetic

catecholamine, but has activity at both α and β

receptors

Clinically prepared as a racemic mixture

(+) isomer is a potent β1 agonist and an α1

antagonist (partial agonist)

(-) isomer is a potent α1 agonist (causes

significant vasoconstriction when given alone)

This drug is used for heart failure NOT ACCOMPANIED

BY hypotension

-Useful only short-term due to receptor downregulation

Adverse Effects - tachyarrhythmias ventricular

arrhythmias

Dobutamine

This drug is contraindicated in the elderly (start at low

dose)

Drug Interactions - MAOIs may cause hypertension

Dobutamine

Phenylephrine

receptor/action?

α-agonist (favors α1 over α2)

used for hypotension, supraventricular

tachycardia

This drug can be used to raise BP and terminate

episodes of supraventricular tachycardia

Adverse Effects - hypertension, reflex bradycardia,

hypertension headaches

phenylephrine (α-agonist)

Phenylephrine

Contraindications and drug interactions

Contraindications - hypertension, within 14

days of MAOIs

Drug Interactions - MAOIs

This drug is used in the treatment of orthostatic

hypotension due to impaired autonomic nervous system

function (chronic)

It increases peripheral resistance

Midodrine; a prodrug hydrolyzed to

desglymidodrine (α1-receptor agonist)

Adverse effects, contraindications and drug interactions Adverse Effects - Supine hypertension, urinary

of Midodrine

urgency, retention, polyuria, dysuria

Contraindications - pheochromocytoma,

thyrotoxicosis, persistent and significant

supine hypertension, severe organic heart

disease and acute renal failure

Drug Interactions - β-blockers, Ca2+ channel

blockers, digoxin

This drug

-Activates α and β receptors

-Enhances the release of norepinephrine from

sympathetic neurons

-Stimulates heart rate and cardiac output and increases

peripheral resistance

-Ultimately raises BP (both systolic and diastolic)

Ephedrine

This drug is used to treat idiopathic orthostatic

hypotension & anesthesia-induced hypotensionEphedrine

Adverse Effects - hypertension, arrhythmias, insomnia

Contraindications - cardiac arrhythmias, elderly

(crosses BBB causing confusion), diabetes, thyroid

dysfunction, seizures

Drug Interactions - MAOIs --> increased hypertension

Ephedrine

This drug:

Reduces peripheral resistance decreasing blood

pressure

Reduces RENAL vascular resistance

May also reduced heart rate and cardiac output

α-methyldopa

Pro-drug metabolized centrally to α-methyl-

norepinephrine which stimulates α2 receptors

This drug is used to treat pregnancy-related

hypertension

α-methyldopa

Pro-drug metabolized centrally to α-methyl-

norepinephrine which stimulates α2 receptors

Which drug?

Adverse Effects: sedation (at onset), lactation due to

increased prolactin secretion (both men and women),

α-methyldopa

Pro-drug metabolized centrally to α-methyl-

norepinephrine which stimulates α2 receptors

impotence

Positive Coomb's test in 10 - 20% of pts. after 1-yr

-Complicates cross-matching of blood for transfusion

-Can cause hemolytic anemia

Potential for serious hepatotoxicity, hemolytic anemia,

hepatitis and drug fever

This drug binds covalently to α receptors (primary

action; irreversible blockade for ~ 2 days)

-Also inhibits the reuptake of released norepinephrine

by presynaptic adrenergic nerve terminals. This block

impairs the normal feedback inhibition of norepinephrine

release increasing the baroreceptor reflex increase in

heart rate (an undesired side effect of the non-selective

α antagonists)

-Also blocks histamine, acetylcholine and serotonin

receptors (at higher doses)

phenoxybenzamine

this drug is used to treat Pheochromocytoma

Adverse Effects: orthostatic hypotension and reflex

tachycardia, nasal stuffiness, inhibition of ejaculation

Phenoxybenzamine

Attenuates catecholamine induced

vasoconstriction

-Reduces BP when sympathetic tone is high

(upright position or low blood volume)

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Terms Definitions

What is a positive stress testFlat or Down sloping St-segment depression >1 mm occurring 80 msec

after j point

When to stop a stress testSt segment depression > 2 mm, ventricular tachycardia, drop in SBP >

15, chest pain, dyspnea, lightheadedness

Stress test of choice with a

LBBB or ventricular pacing?Myocardial perfusion imaging with adenosine,NOT exercising!

Know the algorithm for stress

testingSee page 5-3,figure 5-1

When to not use doutamine

for stressHistory of VT, severe HTN, Low BP, poor echo images

When to not use adenosine

for stress

Bronchospasm, severe valvular dysfunction, severe carotid stenosis,

2nd degree heart block, theophylline dependent

Normals for PA catheter

pressuresRA <7, RV 30/7, PCWP 3-11

PA cath findings in

tamponade or restrictive

pericarditis

Diastolic pressures elevated and equalized in all chambers, low BP

PA cath findings with RV AMIElevated RA and PA pressures, decreased or nl PCWP, hypotension,

and inferior MI. R side is decompensated, cannot fill L side of the heart

PA cath findings in

cardiogenic shockElevated PCWP, RA pressure, and decreased SBP/cardiac output

PA cath findings in mitral

stenosis with RV failureElevated RA, PA (very elevated), PCWP, nl SBP

PA cath findings in pulmonary

HTNElevated PA, RA pressures, nl PCWP, SBP

Pulsus paradoxus

decrease in systolic BP of more than 10mmHg with normal inspiration;

palpated as weakened pulse with inspiration along with more heart

contractions to pulse beats

What conditions give you

pulsus paradoxus?Constrictive or restrictive pericarditis, asthma, tension pneumothorax

What gives you pulsus

bisferiens (two systolic peaks

per cycle)

Aortic regurgitation, HOCM

What causes pulsus alternans Severe LV dysfunction

What causes pulsus tardus Aortic stenosis

How do positional maneuvers -standing/valsalva - decreased cardiac filling, decreases most murmurs

affect blood flow and murmurs

except MVP and HOCM

-squatting/ lying down - increase cardiac volume, increased murmurs

except MVP, HOCM

-sustained handgrip - increases systemic resistance, decreases murmur

in HOCM, AS

What causes a physiologic

split S2

Increased blood volume in the RV prolongs systole and delays

pulmonary valve closure

What causes a fixed split S2Pulmonary stenosis, PE, LV pacer, RBBB, MR (early AV closure), ASD,

RV failue

What causes a paradoxic split

S2LBBB, RV pacing, HOCM

What causes an S3? Rapid LV filling - acute ventricular decompensation, severe AR or MR

KNOW - S3 with LV

dysfunction is a poor

prognostic factor

...

What causes a S4?

Decreased ventricular compliance during atrial contraction - ischemic

heart dz, AS, MR, HOCM, hypertrophic or diabetic cardiomyopathy,

HTN heart dz, concentric LVH

Can you have a S4 with atrial

fibrillation?No - no atrial contraction

What are the parts of the

venous waveform?

A wave - atrial contraction

X descent - atria relax, RV fills rapidly

Bottom of x descent is TC valve closure

V wave - ventricle contacting against closed TC valve

Y descent - TC valve opens, passive emptying into ventricle

What gives elevated a and v

wavesPulmonary HTN, RV infarction

Large r side v waves Septal rupture

Large v waves TR (right), MR (left)

Rapid x and y descentConstrictive pericarditis, restrictive cardiomyopathy, tamponade (x

descent only, loss of y descent)

Large a waves TS,severe RVH (on right), MS

Cannon a waves AV disassociation - complete heart block, ventricular pacing

Slow Y descent Delayed atrial emptying - TS

Most important prognostic

factor with CADDegree of LV dysfunction

Causes of resting ST

elevation

MI, pericarditis, LV aneurysm, LBBB, ventricular pacing, LVH, early

repolarization

Hibernating myocardium

myocardium near the infarction may be underperfused but not necrotic-

the metabolism of the cells adapts to low energy supplies and are

nonfunctional until perfusion is restored

Reperfusion injury

the re-establishment of blood flow after a coronary artery is blocked,

which may further damage the heart tissue due to the formation of

oxygen free radicals

Stunned myocardiumprolonged post ischemic dysfunction, salvaged by reperfusion, several

days

Giving nitrates causes severe

decompensation in a IWMI pt.

What happened?

Pt had R side infarction as well, the preload reduction from the nitrate

now meant little flow getting to the L side of the heart

St segment elevation during a

stress signifies what?Coronary artery spasm

NSTEMI have _____ initial

mortality, but have the _____

one year mortality as a STEMI

Lower, Same

NSTEMI have a higher risk of

these vs. STEMIPersistent angina, reinfarction, and death within several months

MI without chest pain is more

likely to happen in theseElderly, diabetics, women

MR due to papillary muscle

rupture is most common with

MI in this region

Inferior

VSD is more likely with MIs

hereAnterior, inferior

Types of arrythmias with Junctional escape, Mobitz I, and they are usually temporary

IWMI

Types of arrythmias with

AWMI

,Mobitz II, BBB. More of the myocardium

Is involved

After 12 hrs., pt has no more

CP, nl trop and EKG. What's

next

Stress test. If nl, can dc

What do all Pts with ACS get

Continuous EKG, ASA, NTG prn for pain or continuous IV gtt if

continued ischemia or HTN, oxygen if sats < 90, morphine is pain not

better with NTG, B-blocker, ACE if still with HTN or LV dysfunction

Contraindications for B-

blockers

Bradycardia, hypotension, 2nd or 3rd degree AVB, pulmonary edema,

asthma. NOT DM

When to use non-

dihydropyridne CCBs in ACS

Contraindications to B blockers, continued ischemia, but NO LV

dysfunction

What anticoagulant to use

with ACS

Enoxaparin good, but have to stop 12-24 hrs before CABG

Fondaparinux is increased risk of bleeding, do not use if going to do PCI

- increased risk of catheter thrombosis and coronary complications

If using Fondaparanux and decide to do PCI, change to heparin or

bivalirudin

What are the platelet P2Y12

receptor blockersClopidogrel or plavix, ticlodipine or Ticlid, prasugrel or effident

When to use clopidogrel with

ACS

All Pts if proven ACS, hold until after CABG or PCI, or for those

intolerant of ASA for conservative treatment

Prasugrel vs clopidogrel Faster onset, more anti platelet activity, more risk of bleeding

GP IIb/IIIa inhibitors, action

and use

Abciximab, eptifibatide, tirofiban, limifiban

Block platelet aggregation

Use in any ACS pt going to cath for probable PCI

When to use fibrinolytics in

ACS

Not with UA/NSTEMI - increases mortality

Use in STEMI, new LBBB if no contraindications and immediate PCI not

available

What to give pt with

UA/NSTEMI

Anti-platelet therapy (plavix) - use at least 1 yr with drug eluting stent, up

to a year even without stent

Lipid and BP control

DC NSAIDs except ASA

ASA, O2, B-blocker, nitrate prn

Heparin, enoxaparin, Fondaparanux, or bilavirudin

Monitor

Gp IIa/IIIb (abciximab, etc) if immediate PCI planned

NO FIBRINOLYTICS!

When to do urgent PCI with

UA/NSTEMI

CHF or hemodynamic instability, recurrent or refractory angina, life

threatening arrythmias

When to use invasive therapy

within 48 hrs with UA/NSTEMI

elevated troponin, dynamic ST changes, DM, GFR < 60, EF < 40%,

Early post-MI angina, PCI in last 6 months, prior MI, prior CABG,

intermediate/ high risk score

When to use conservative

therapy with UA/NSTEMI

no indications for invasive therapy, good response to initial treatment,

low risk post-ACS stress testing. Has the same 1 yr mortality

Cocaine/ meth use and

UA/NSTEMI

give NTG and CCBs

If no better, do cath

If cath not available, give fibrinolytics

No cath is no ST/T changes, negative stress, and negative biomarkers

Anti-platelet therapy after

UA/NSTEMI

no stent - ASA 75-162mg lifelong + Clopidogrel x 1-12 month

Bare metal stent - ASA 162-325 x 1 mo, then 75-162 for life +

Clopidogrel x 1 mo-1 yr

Drug eluting stent - ASA 162-325 x 3-6 mo, then 75-162 for life +

Clopidogrel x 1 yr minimum

Initial therapy for STEMI/new

LBBB MI

Same as NSTEMI, but can use fibrinolytics if PCI not available within 90

minutes of ER arrival

EKG findings with posterior

MIST depression in V1, V2, tall R waves in V1+2

PCI vs. fibrinolytics

Better outcome if experienced practictioner, done within 12 hrs of

symptoms, 90 minutes from ER; substantially better patency of infarcted

vessels

When to use fibrinolytic

therapy

ST elevation in 2+ contiguous lead, new LBBB, under 75 yo, within 12

hrs of symptoms, no capabilty to do PCI

Contraindications to

fibrinolytic therapy

absolute - previous hemorhhagic CVA, cerebrovacular event in last yr,

intracranial neoplasm, active internal bleeding, suspected aortic

dissection

Relative - persistent BP > 180/110, remote CVA, INR > 2-3, bleeding

disorders, recent (2-3 wks) major trauma, non-compressible venous

puncture, previous exposure to streptokinase or antistreplase,

pregnancy, active peptic ulcer, chronic HTN

This class of drugs interacts

with Clopidogrel and should

be carefully watched

PPI's - interfere with Plavix metabolism, increases levels

What vessel for RV infarct

and IWMIRAD; if RV is also infarcted, much worse prognosis

Triad of RV infarct in setting

of IWMIHoTN, clear lung fields, elevated JVD; also often have Kussmauls sign

R heart cath findings of RV

infarctelevated PA pressure > 10 + > 80% of PCWP

Treatment for RV infarctAvoid nitrates and preload agents, fluid support, may need inotropic

support with dobutamine

AVB and bradycardia are

most common with this MI

IWMI. If with AWMI, it means a large part of the intraventricular

myocardium is destroyed, is with high mortality, and usually require

permanent pacer

Indications for temporary

pacing with MI

Asystole, symptomatic bradycardia (sinus brady or AVB with

hypotension not responsive to atropine), complete AVB, Mobitz type II

Mechanical complicatons of

MI's

1. Papillary muscle rupture - IWMI, 3-7 days out, short early systolic

murmur, sudden onset of shock. Dx with echo, treat with urgent CT

surgery

2. VSD - 3-7 days out, anterioseptal MI, sudden shock, loud holosystolic

murmur. Oxygen step up 10% from RA to PA on RHC. Dx with echo, tx

with urgent CT surgery. High mortality

3. Free wall rupture of LV - 3-7 days out, large AWMI, usually elderly

HTN women. Sudden syncope, neck veins engorged, tamponade. Few

survive with urgent surgery

ICD's post MI - indications EF < 35%, baseline episodes of VT

What affects HDLincreases - exercise, small amounts of EtOH, niacin, estrogens

Decreases - tobacco, andogens

True/false - cholesterol levels

are accurate around the time

false - can be falsely low for up to 2 months

of MI/ surgery

Indications for CABG

1. significant LMA or LMA equivalent (proximal LAD + proximal LCA)

2. 3 vessel disease - survival benefit even greater with EF<50

3. 2 vessel + prox LAD + EF <50% or ischemia on non-invasive testing

4. 1-2 vessel dz w/o significant prox LAD, but have a lareg area of viable

myocardium and high risk stress

5. Can use PCI for others

CABG improves survival in

which groups

1. L main dz or L main equivalent (2 vessel, one is LAD)

2. 3 vessel with LV dysfunction

3. DM

Does not improve survival in 1-2 vessel dz, but does improve symptoms

Stent vs. angioplasty

Less plaque dissection

Less elastic recoil

Lower restenosis rate

Restenosis rates

Angioplasty- 30-50% on 6 mo

Bare metal stent - 25%

Drug eluting stent - 5%

Causes of PAD

Arteriosclerosis (risks DM, smoking)

Arteritis (CTD, Takayasu's)

Trauma

Buerger's disease (males <30, smokers, affects wrists, hands)

Entrapment

Best test for functional

imparement in PADpre and post exercise ABI

Non-invasive tx of PAD

1. Exercise

2. Stop smoking

3. Pletal (Cilostazol) - cannot use with grade III or IV CHF

4. Pentoxyfylline (Trental)

S/Sx spontaneous internal

carotid dissection

Unilateral HA, TIA or dilated pupil, unilateral neck pain in a HTN pt.,

cholesterol emboli on fundoscopy

No treatment needed (occasionally needs stent or anticoagulation

Risks for Thoractic aortic

aneurysm

HTN, cystic medial necrosis, bicuspid aortic valve, coarctation of the

aorta, 3rd trimester of pregnancy, Marfan's syndrome

Side effects of proximal TAA Aortic regurgitation, hemopericardium, MI from involvement of the

coronary artery takeoff. Presents as severe anterior chest pain and inter

scapular pain

Treatment of TAA dissection

Decrease BP with B Blockers, nitroprusside

Surgery for all ascending TAA due to risk of complications

Surgery for descending if persistent pain, evidence of end-organ

damage (renal insufficiency, limb compromise)

Size for TAA surgery 5.5 for ascending, 5.0 if Marfans, 6.5 for descending

Surgery for AAA

Monitor with q6mo CT or US if <5.5 cm

Surgery if larger or if increase in size >0.5cm every 6 months

Do cardiac testing pre op if two or more cardiac risks. Heart issues

cause 70% of the mortality

Classification of endocarditis

1. Acute vs. subacute

2. Native valve vs. prosthetic valve vs. assc. with IVDU vs. culture

negative

Bugs with endocarditis

Acute - S. aureus, broup B strep, gram negatives

Sub-acute - strep (60-80% of all), enterococcus (older men post GU

surgery), staph epi

Types of bugs in IVDU and

prosthetic valve endocarditisS. aureus, S epi, gram negs

Physical findings with

endocarditis

new murmur, Oslers nodes (painful, fingers), Janeway lesions

(nontender, palms, soles), splinter hemorrhages, Roth spots

when to replace prosthetic

valve with endocarditis

Less than 2 months from surgery, valve ring infection, myocardial

penetration (new HB or BBB)

Indications for surgery in

endocarditis

CHF, extension into the myocardium, perivalvular abscess, failure of

medical therapy, large vegetation with septic emboli

Indications for endocarditis

prophylaxis

Prosthetic valves, H/O endocarditis, congential HD (unrepaired cyanotic

CHD, repair within 6 months, repair with residual defects), cardiac

transplant with valve lesions

Drugs for endocarditis

prophylaxis

Dental - Amox, Amp, Cefazolin, Ceftriaxone; allergic - Clinda, Azithro,

Clarithro

GU/ GI - not needed!

Respiratory tract procedures, skin or muscle infection - staph, strep

coverage

Jones criteria for rheumatic

fever

Major criteria, Major: Carditis, Polyarthritis, Chorea, Erythema

marginatum, Subcutaneous nodules

Minor: Arthralgia, Fever, Elevated Acute Phase Reactants, Prolonged

PR, Previous History of Group A Strep Infeciton or rheumatic Fever.

2 Major or 1 major 2 Minor

Aortic stenosis info

Etiol - age related calific degeneration or bicuspid valve

S/Sx - LV failure, syncope, angina

Exam - slow upstroke to pulse (pulsus tardus), sustained apical impulse,

diamond shaped SEM at RUSM with radiation to neck, S4 gallop,

decreased or absent S2 (AV doesn't move well), ejection click

Have a higher rate of CAD, so cath before fixing

Severe AS = area < 1.0 cm, gradient >50

Treat all symptomatic pts with AoVR

Post AovR, anticoagulation to INR 2-3 (2.5-2.5 with MVR)

Chronic aortic regurgitation

info

Etiol - valve deformity (bifid, rheumatic fever, endocarditis, degenerative

valve dz) or abnormal aortic root (Marfans, senile aortic dz, giant cell

arteritis, relapsing polychondritis, syphilis)

Causes LV volume overload ->LVH -> LV dysfunction

Exam - decrescendo diastolic high pitched blowing murmur, RUSB (root

dz) or LUSB (leaflet dz), wide bounding pulse (water hammer), can give

low pitched rumble (Austin-Flint) with flow against mitral valve; Becker's

sign (pulsatile retinal arteries), de Musset's sign (bobbing head with

pulse)

Treatment of aortic regurg

Vasodilators (ACE, ARB, diuretics)

Surgery if symptomatic, LV end systolic dimension > 55mm, LV end

diastolic dimension > 75mm, EF <55%

Acute AR

Sx - severe pulm edema, low cardiac output, no bounding arterial pulse

(low EF). If significant AR and CHF without a reversable cause, usually

require immediate surgery

Mitral Stenosis info

Usually from rheumatic fever. Often have a fib. Can have CHF, usually

have pulm HTN. Hemoptysis from pulm congestion

Exam - diastolic murmur, low pitched rumble, accentuated S1, diastolic

opening snap

CXR - triad of prominent pulm art vascularity, enlarged LA, nl LV

Increased fluid state in pregnancy can cause acute exacerbation. Can

use heparin if a fib, cardioversion, procainamine, digoxin, verapamil

Treatment for MSValvotomy or surgical replacement if symptomatic, asx with pulm HTN

(>50 rest, >60 exercising)

Chronic mitral regurgitation

Causes - rheumatic HD, annulus dilation from LVH, endocarditis,

ischemic papillary muscle

Presentation - steady systolic murmur, often a fib, wide split S2, s3 if

severe

Treatment - diuretics, afterload reduction; surgery if symptoms, asx with

EF < 65%, LV enlargement with LVESD>45, a fib, pulm HTN. Prefer

repair to replacement

Mitral valve prolapse

Causes - weak papillary muscles, myxomatous leaflets

Sx - none (do NOT get dyspnea, panic attacks, palps, CP, etc)

Exam - midsystolic click with late murmur if MR. Click louder and earlier

if standing or valsalva

No treatment

Acute mitral regurg

Presents with pulmonary edema

Native valve - from flail leaflet (MVP, endocaditis), papillary muscle

ischemia or rupture, chordae tendinae rupture

Prosthetic valve - from tissue valve rupture, mechanic valve closure

problem (thrombus), paravalvular vegetation

Exam - decrescendo apical systolic murmur, nl size LA on echo, large L

side v waves

Rx - afterload resuction, diuresis; IABP; often need surgery

Tricuspid stenosis

Causes - rheumatic fever, congenital, endocarditis, carcinoid syndrome

(usually with TR as well)

Exam - diastolic murmur, LSB, increase with inspiration, giant a wave;

ascites, edema; EKG - tall peaked P waves in II and V1

Treatment - treat underlying, surgery

Tricuspid regurgitation

Causes - functional RV dilation from end stage LV failure, submassive

PE, pulmonary HTN, rheumatic HD, endocarditis (drug users, staph

sometimes candida), carcinoid, congenital (Ebstein's anomoly)

Exam - holosystolic LLSB murmur, parasternal heave; liver pulsations,

ascites, edema; large v waves

Dx with echo

Tx - treat underlying, rarely needs surgery except candida

Pulmonic stenosis Usually congenital, does not progress, rarely from rheumatic HD or

carcinoid; with Noonan's syndrome (low set ears and hairline)

Exam - ejection click, jugular a wave

May need balloon valuloplasty

Pulmonic regurgitation

usually from pulmonary HTN, can be congenital, rheumatic,

endocarditis.

Occasionally see with WPW, PSVT

Prognostic factors after valve

surgeryEF, symptoms, type of surgery

Three mechanisms for

arrhythmias

reentry, triggered, automaticity. Reentry is most common in PVC, SVT

(2/3rds of cases), A flut/fib, VT.

Automaticity - accelerated ectopic rhythims

Triggered RVOT VT - triggered by exercise or adrenergic stimuli

Sick sinus syndrome

Any combo of SA node problems (sinus brady/ pause/ arrest, tachy

brady)

Good prognosis

Indication for pacer - symptomatic, pt with tachyarrhythmias who

treatment would cause bradycardia

Treatment for atrial flutter

Rarely seen in healthy hearts. tx: 1. Drugs to slow impulse conduction

(BB, CCB, digitalis) 2. Conversion with antiarrhythmic drug (ibutilide,

quinine, procainamide, flecanide, propafenone); 3. Cardioversion; 4.

temporary pacing wire; 5. radiofrequency catheter ablation (to destroy

the reenterant pathway)

Anticoagulate if chronic

Cardioversion in A fib

prefer electrical except <48 hr with EF <40, then give amiodarone

Immediate cardioversion if 1. AF with RVR + ischemia, HoTN, CHF,

angina 2. Preexcitation with RVR or hemodynamically unstable, 3.

Severe symptoms

If slow a fib, put in temporary pacer first - likely has nodal dz, may go

into asystole

Pharmacologic cardioversion

drugs for A fib

If > 7 days: 1st Dofetilide; next choices - amio, ibutilide

< 7 days: 1st line - dofetilide, flecanide, ibutilide, or propafenone; 2nd

line - amio

Maintenance drugs in a fib No or minimal HD: flecanide, propafenone, sotalol. If ineffective, use

amio, dofetilide, ablation

CHF, EF< 35%: amio, dolfetilide; fails - ablation

CAD - dolfetilide, sotalol; fails - amio, ablation

HTN with LVH - amio; fails - ablation

HTN, no LVH - flecanide, propafenone, sotalol; fails - amio, ablation,

dolfetilide

Chronic anticoagulation

decision in a fib

Based on CHADS2 score:

C- CHF (1 pt)

H - HTN (1 pt)

A - Age >75 (1 pt)

D - DM (1 pt)

S - stroke or TIA in past (2 pt)

0 pts - ASA; 1 pt - either ASA or warfarin; 2+ pt - warfarin

Multifocal atrial tachycardia

info

Seen with pulmonary dz, especially on theophylline; also low K, Mg

If due to theophylline and cannot stop theoph, rx with diltiazem or

verapamil

Digoxin can worse it - avoid

Rx with ablation or pacing if refractory

Findings with WPW PR<0.12, QRS > 0.12, delta waves

Treatment of WPW

Narrow complex tachy - vagal, cardioversion, procainamide, verapamil,

adenosine

A fib/ flut - usually wide complex - avoid dig, verapamil, B-blockers - can

cause preferential conduction down accesory pathway and incite VF.

Treat with Procainamide or shock if unstable

Can cure with ablation

Treat PVC's?

If structurally normal heart, no - even if couplets, lots of them

Can use B-blocker, should get 80% reduction to call it effective

If H/O MI, EF< 40%, PVC's, especially sequential, are at high risk for

sudden death

DDX of wide complex

tachycardia

VT, SVT with aberrant conduction; WPW, SVT with LBBB, severe

hyperkalemia

EKG changes indicating VT

1. Severe L axis deviation;

2. QRS >0.14 in RBBB, >0.16 in LBBB (usually <0.12 if SVT with

aberrancy);

3. AV disassociation, disassociated P waves (cannon a waves);

4. QR or QS in V6 with LBBB or R axis dev with a LBBB;

5. Fusion beats; 6. Rate > 100; 7. capture beats

Treatment of monomorphic Stable - procainamide or amiodarone

VT

Unstable - shock

Unstable and refractory to cardioversion - IV amio or procainamide

VTwith MI - amio first, can use lidocaine

Treatment of polymorphic VT

same as monomoprhic except:

IV B-blocker if ischemia cannot be excluded

IV amio if no prolonged QT

Cath if ischemia suspected

RVOT VTInduced by exercise

Treat with B-blockers

Causes of torsades

Usually preceded by prolong QT interval, U wave

Causes - quinidine, procainamide, class Ia antiarrhythmics, dofetilide,

class III antiarrhythmics (sotalol), tricyclics, hypokalemia,

hypomagnesemia

Treatment of torsadesIncrease atrial rate (isoproterenol), overdrive pacing, MgSulfate if others

contraindicated (MI, severe ischemic HD), shock is last resort

Rhythms to avoid verapamil

with

A fib/ flut with WPW

Wide complex tachycardia

B-Blockers - both negative chronotropes and inotropes

Indications for ICD

VT with structural HD (esp HCM)

VT and cannot correct CAD

VT with EF < 30%

Indications for pacers

Symptomatic bradycardia

Complete HB

Mobitz II after AWMI

Side effects of quinidine

cinchonism (tinnitus), hemolytic anemia, sudden death(quinidine

syncope) due to QT prolongation, torsade/polymorphic ventricular

tachycardia; fever, rash, ITP, psychosis

Side effects of DisopyramideProlonged QT, QRS, torsades; (anticholinergic and vagolytic) urinary

retention, dry mouth, constipation

Side effects of procainamide

agranulocytosis, lupus (does NOT affect kidneys) with high ANA; also

QT prolongation with torsades/ventricular tachycardia; caution with CHF

- slight myocardial depressant

Side effect of Lidocaine seizures

Side effect of tocainide aplastic anemia

Side effects of amiodarone

corneal microdeposits, optic neuritis, pulmonary fibrosis (severe, fatal in

10%),bluish skin discoloration, photosensitivity, hypothyroids or

hyperthyroids, elevated INRs in warfarin patients, may elevate digoxin

levels; no hematologic effects

Evaluation for

neurocardiogenic syncope

1st episode, young, no suspected HD - observe

Infrequent episodes - tilt table, psych eval

Frequent episodes - continuous ambulatory EKG (event monitor)

Tx - B blockers

Types of cardiomyopathies Hypertrophic, restrictive, dilated

HCM is associated with which

bad occurrence

Sudden cardiac death, likely due to ventricular arrhythmia. Only cure is

transplant. Most frequent in young pts with familial form

Problem in HCM

LVH, especially in the basal ventricular septum, occasionally concentric

See diastolic dysfunction; can see Q waves - pseudoinfarct (also can

see with WPW)

Present with exercise induced syncope or severe dyspnea

Exam with HCM

Harsh, non-radiating aortic midsystolic murmur, increases with Valsalva,

decrease with handgrip; bifid pulse - strong upstroke, then falls off as it

obstructs later in systole

EKG - nl, can have inf to lat Q waves from the hypertrophy, with nl to

high voltage from LVH (if low voltage, consider infiltrative CM - amyloid)

Work up for HCM

Echo with doppler

Exercise nuc stress

Holter to look for ventricular arrhythmias

Risk factors for sudden death

in HCM

Septal thickness >30mm

H/O syncope

Fam hx sudden death in 1st degree relative

NSVT/VT on holter

Failure to increase SBP on treadmill test (<10mm)

Treatment for HCM Surgery (septal myotomy) - decreased symptoms, no change in SCD

risk

B-blocked, Verapamil - improve sx

Amiodarone if high risk for SCD (familial)

RV pacing - can improve obstruction in some pts

Avoid anything that decreases LV volume - diuretics, nitrates, volume

depletion (can us diuretics very carefully if in CHF)

Restrictive CM

Causes - amyloidosis, sarcoidosis, hemochromatosis, lipid storage

diseases

Echo - thickened myocardium, may have granularity

MUST differentiate from constrictive pericarditis - identical s/sx, but

pericarditis is quickly treated with good results, restrictive CM is

irreversable

Treatment - diuretics. Avoid digoxin unless a fib

Dilated CM

Causes - idiopathic (usually viral), alcohol, cocaine, amphetamines,

organic solvents, chemo, late hemochromatosis, possibly selenium or

carnitine deficiency

Sx - R & L HF, slow onset over months. Can form mural thrombi with

arterial embolization. Slow, steady progression to death in 3 years

Rx - anticoagulate for thrombus risk, treat HF sx as usual - diuretics, B-

blockers, ACE/ARB

NYHA CHF classes

I - no limitation in activity

II - slight limitation with activity, no sx at rest

III - marked limitation of activity, comfortable at rest. Sx with even slight

activity

IV - sx at rest

ACC/AHA stages for HF

A - at risk for HF, no structural dz

B - structural dz, but no s/sx HF

C - structural dz with s/sx

D - Marked sx at rest

ACC/AHA stage A CHF -

definition, goal, meds

Def: at risk for HF - includes HTN, ASHD, DM, metabolic syndrome,

cardiotoxins, FH of cardiomyopathy

Goal - treat disorder, exercise, discourage alcohol/ illicit drug use

Drugs - ACE/ARB for all

ACC/AHA stage B - definition,

goal, meds

Def - structural HD, no s/sx of HF - includes prior MI, LV remodeling

from LVH, low EF, asx valvular dz

Goals - same as stage A

Tx - ACE/ARB + B-blockers, ICD if indicated

ACC/AHA stage C - definition,

goal, meds

Def - structural HD with s/sx HF - dyspnea, fatigue, decreased exercise

tolerance

Goals - like A/B, add dietary salt restriction

Rx - ACE/ARB + BB + diuretics. May need aldactone, ARBs with ACE,

dig, hydralazine/nitrate combo. BiV pacing +/or ICD as needed

ACC/AHA stage D HF -

definition, goal, meds

Def - marked sx at rest despite max therapy; frequently hospitalized

Goals - A/B/C + discuss end of life care

Meds - same as C. Discuss hospice vs. extraordinary measures

(transplant, chronic inotropes, permanent mechanical support -

ventricular assist device, experimental treatments)

Poor prognosis in CHFLow EF, hyponatremia, high BUN, hypokalemia, hypo/hyperMg, high

norepinephrine and catacholamine levels

BNP in restrictive CM vs.

constrictive pericarditisElevated in RCM, nl in CPC

Diastolic dysfunction

Causes - ischemia, sever concentric LVH, HCM, diabetic CM

CO is normal, HF develops from decreased relaxation/ increased

stiffness of ventricle

Elevated LVEDP, RVEDP, tachycardia, s4

Effects of ACE/ARB in CHFincrease cardiac output, decrease LV filling, vasodilation, decrease

tachycardia, decrease incidence of VT/VF, prolong survival

B-blockers in HFdecrease remodeling, arrythmias. Coreg decreases mortality 65%,

metoprolol + bisoprolol 35%

Diuretics in HF Help fluid control, symptom control, but no improvement in mortality

Spironolactone/ Eplerenone

in HFeffective only with class III/IV, do decrease mortality

Digoxin in HF

effective only in sever systolic failure - stage C or later; use after other

standard therapies, EF <40, class II/III/IV

Resets baroreceptors, dampens renin-angiotensin effects

Improves symptoms, decreases hospitalization, no effect on mortality

Nitrates + hydralazine in HF Use in class III/IV, african american, still symptomatic despite other txs

Anticoagulation in HF start if EF<25% due to risk of mural thrombus

Meds in severe HF Dopamine - only for renal effects. Higher dose - vasoconstriction,

tachycardia

Dobutamine - inotropic, but no vasoconstriction

Milrinone (Primacor)- inotrope, vasodilator - short term use in HF

Nesiritide (natrecor) - BNP -improves clinical status, decreased PCWP/

PA pressure, improved stroke volume, no increase in HR

Hydralazine+NTG - afterload and preload reduction

CABG - only if acute MR, papillary muscle rupture

Transplant in HF Only at end stage - 65% 5 yr survival, 55% 10 yr

High output failure causesperipheral shunting (AV fistula, severe hepatic hemangioma, Pagets),

low SVR (sepsis), hyperthyroidism, Beriberi, carcinoid, anemia

Effects of azotemia on

diuretics

Avoid spironolactone and triamterene - causes hyperkalemia

Thiazides ineffective

Lasix usually works, higher doses needed

Treatment of acute pulmonary

edema

Sit with legs dangling (decrease venous return)

100% O2, morphine

Lasix - venodilation before diuresis

Digoxin - contraindicated if WPW, severe concentric LVH, restrictive CM

IV NTG/ nitroprusside if BP>100

Dobutamine if BP <90

Aminophyline - occasionally used to improve repiratory muscle function

Causes of non-constrictive

pericarditis

Idiopathic (90%, likely viral), TB, CT diseases, sepsis, renal failure,

cancer, MI (dressler syndrome autoimmune, 1-2 wks after MI),

procainamide, hydralazine

Presentation of pericarditis

severe CP, pleuritic, better leaning forward, fever, tachycardia;

pericardial friction rub (not always)

EKG - diffuse, concave upsloped ST elevation, occasionally depressed

PR in II

Transient increase in CKMB

Treatment for pericarditis

Stop/ treat cause

NSAID's

Steroids only if not idiopathic - higher risk of relapse; definitely use if TB

Colchicine

Causes of constrictive

pericarditis

Usually idiopathic, open heart surgery, radiotherapy, coccidiomycosis,

TB

Exam with constrictive

pericarditis

Loud presystolic knock just after s2 (due to rapid early diastolic LV

filling), pulsus paradoxus

Kussmaul sign - heart encapsulated, can't accomodate extra blood in

inspiration, so don't get usual drop in JVD with inspiration, can actually

increase

Large R sided x+y descent due to brisk collapse of the jugular during

diastole

Kussmauls & large x+y descent are HALLMARKS

Imaging with constrictive

pericarditis

CXR - calcification of pericardium - seem best in lateral over R ventricle

- pathognomic for this

CT/MRI/ echo - measures thickness of pericardium - >5mm suggest this

Treatment for constrictive

pericarditispericardectomy. Fixes problem in 50%

Recurrent pericarditis

problem is chest pain

Does NOT progress to constrictive pericarditis

Rarely gives arrythmias

NSAIDs, colchicine, steroids to treat

Pericardectomy not as effective, only use if other options fail

Best imaging modality for

pericardial effusionCT or MRI are better than echo, and can see small pockets of fluid

When to surgically drain

pericardial effusion

traumatic hemopericadium, post surgical effusion, bacteria or TB

suspected as cause

Hallmarks of tamponade

1. Hypotension and muffled heart sounds

2. Pulsus paradoxus

3. JVD with no collapse during diastole

Ostium secundum ASD

Most common CHD found in adults; SEM at LSB (increased flow across

pulm valve)

occ diastolic murmur (flow across tricuspid valve) and a fixed split S2

(RVH)

enlarged RV on CXR and shunt vasculature

RAD and/or RBBB on ECG, can see A fib

Tx: surgical closure or percutaneous closure (do if > 2:1 left to right

(pulmonic/systemic) shunt

Pulmonic HTN is considered a contraindication to surgery

Ostium primum ASD

loud pansystolic murmur 2/2 MR or TR (regurg because ostium is low

on septum, interfering with function of AV valves or L mitral valve).

ECG has left axis and RBBB

Surgery fixes problem

Eisenmenger syndrome is a contraindication to surgery

Sinus venosus ASD SV: Sup septal area ~ CS: Inf septal area, close to Coronary Sinus,

rare; assc with anomalous pulmonary venous return

Patent ductus arteriosus

Usually asymptomatic

Continuous "machinery" murmur LUSB

CXR with calcification of ductus arteriosus

Develop differential cyanosis - clubbed toes, nl fingers, pulmonary HTN

Consider Eisenminger syndrome if develops pulm HTN

Surgical or percutaneous closure

Ventricular septal defect

Most common CHD in kids, uncommon in adults

80% close in 1st year of life

Large VSD's require surgery

Coarctation of the aorta

bicuspid AoV in 70%

Delayed femoral/ brachial pulse

Upper body HTN, HTN aneurysmal dilations, rupture in circle of willis

CXR - rib notching

Amonalous coronary artery suspect with exertional CP or syncope in a young healthy individual

Causes of sudden cardiac

death in exercising young

people

HCM - 36%

Coronary anomalies

Primary pulm HTN

Eisenmenger syndrome

When the left to right shunts cause pulmonary hypertension, vascular

hypertrophy, and eventually shift the L=>R shunt to a R=>L shunt, and

cause late cyanosis. Heart-lung transplant is only cure

Pulm HTN

Includes sporadic idiopathic - young women, refractory, death in 5-10

yrs

Tx - CCBs, sildenafil, heart lung transplant

Pregnancy heart issues

Contraindication to pregnancy - pulm HTN, eisenmengers

Watch closely - secundum ASD, AoS, dilated CM

Bed rest - AoS, dilated CM

Causes of LAD L anterior hemiblock, so a marker of CAD

Causes of RAD

nl in kids, young adults

L posterior hemiblock, RVH, acute or chronic RV overload (pulm HTN,

PE, pulm stenosis)

If an adult has RAD, work it up!

Formula for QTc QT/square root of RR, all in seconds. Nl 340-430 msec

Estimate by 40% of RR

Causes of prolonged QT

Tricyclic OD, hypocalcemia, hypomagnesemia, hypokalemia, starvation,

CNS insult, Type Ia (quinidine, procainamide), III (amiodarone, sotalol)

antiarrhythmics, non sedating antihistamines + EES, azoles,

ketoconazole, liquid protein diet

Causes of short QT digitalis, hypercalcemia

Retrograde P waveneg in II, pos in aVR - ectopic AV focus in the inferior atrium or AV

junction

RAE findings

Causes - RA enlargement, hypertrophy, overload)

nl P width (<0.12)

Peaked P in II, V1

LAE findings

increased L side of the wave, so wave >0.12, wide P wave, shortened

PR interval

notched P in II, increase neg portion in V1

Peaked T waves

hyperkalemia

Hyperacute MI

intracerebral hemorrhage

V1, V2 in evolving MI

Focally flipped T waves

Ischemia

V1-2 with RBBB, RVH, RV HTN, LVH

Lateral leads (I, aVL, V6) with LBBB

Precordial leads in LVH with strain

Diffuse flipped T's in

pericarditis

Diffuse ischemia, post resuscitation

Metabolic abnormalities

Intracerebral hemorrhage

U waves

Best seen just after T in V2-3

If prominent, risk for torsades - hypokalemia, bradycardia, digitalis,

amiodarone

Negative U wave - caused by ischemia, HTN, AV valve dz, RVH. See in

60% on ant MI, 30% of IWMI

ST elevation causes

MI, prinzmetals angina, pericarditis

Less seen in ICH, early repolarization, HCM, LVH, LBBB, cocaine

abuse, myocarditis, hypothermia

ST depression causes

Subendocardial ischemia

Posterior MI (V1-2)

Reciprocal depression in V1-2 in some IWMI

LVH with LV strain

isolated RV infarction (ST elevation V1, depression in V2)RVH

sometimes in V1

Digitalis toxicity

Hypokalemia

Criteria for LVH

Q in V1+ R in V6 >35

R in V5+R in V6 >25-35

If LAD, use S in III>15

RVH RAD + ST depression + flipped T in V1-2

LBBB criteria

QRS = 120-180

RR' in V6, SS' in V1

T opposite of mean QRS vector in anterioseptal and lateral leads

RBBB criteria

QRS >120

delayed depolarization of RV - RSR' or RR' in V1, slurred S in V5-6

Flipped T in V1, sometimes V2

LAFB criteria

LAD -45 to -90 degrees

Large S in inferior leads

Dominant R in I

No other causes of LAD (LBBB)

Poor R wave progression

LPFB criteria

Small Q, large R in inf leads

Small R in I, large S in I, aVL

R axis +80-+140 degrees

Order of changes with MI

T inversion - ischemia

ST changes - injury

Q waves - cell death

All 13 termsPrint new! Export Combine

Terms Definitions

What does the QRS represent depolarization of two simultaneously contracting

ventricles

What does the P wave represent atria depolarization

What does the T wave represent ventricular repolarization

How long should the PRI be 0.12 - 0.20 s

How long should the QRS be < 0.12 s

Where are positive and negative leads placed

on Bipolar leads I, II and II

Lead I - Right Arm is negative - Left Arm is positive

Lead II - Right Arm is negative - Left Leg is positive

*Lead III - Left Arm is negative - Left Leg is positive

How much is the small box 0.04 s

How much is the large box 0.20 s

What is the 1st positive deflection following

the P waveR wave

What is the 1st negative deflection following

the P waveQ wave

Pathological Q wavePathological Q wave is > 0.04 s or deeper than 1/3 of

the total height of the QRS complex

To be considered significant, S-T segment

has to be >> 1 mm or one small box

What does QT interval represent ventricular depolarization and repolarization