Cardiovascular Physiologyarjenh/lect3.pdf · • Mechanical events of the cardiac cycle 5555 2222...

Cardiovascular Physiology

Copyright © 2009 Pearson Education, Inc.

Lectures byJan Machart

University of Texas, Austin

Overview: Cardiovascular System

Ascending arteries

Left atrium

Right atrium

Coronary arteries

PulmonaryveinsPulmonary

arteriesSuperior vena cava

Arms

Lungs

Aorta

Capillaries ArteriesVeins

Head andBrain

Copyright © 2009 Pearson Education, Inc. Figure 14-1

Descending arteries

Abdominal aortaLeft ventricle

HeartRight ventricle

Renalveins

Renalarteries

Hepaticvein

Inferior vena cava

Ascending veins

Venous valve

Trunk

Kidneys

Pelvis andLegs

Liver Digestivetract

Hepatic artery

Hepatic portal vein

Pressure Gradient in Systemic Circulation

• Blood flows down pressure gradients


Pressure Change

• Pressure created by contracting muscles is transferred to blood

• Driving pressure for systemic flow is created by the left ventricle

• If blood vessels constrict, blood pressure


• If blood vessels constrict, blood pressure increases

• If blood vessels dilate, blood pressure decreases

• Volume changes greatly affect blood pressure in CVS

Structure of the Heart

• The heart is composed mostly of myocardium

STRUCTURE OF THE HEART

Superiorvena cava

Aorta

Pulmonaryartery

Copyright © 2009 Pearson Education, Inc. Figure 14-7e–f

Diaphragm

(e) The heart is encased withina membranous fluid-filledsac, the pericardium.

Pericardium

(f) The ventricles occupy the bulk ofthe heart. The arteries and veins allattach to the base of the heart.

vena cava

Rightatrium

Auricle ofleft atrium

artery

Rightventricle

Leftventricle

Coronaryarteryand vein

Structure of the Heart

• The heart valves ensure one-way flowPulmonary

semilunar valve

Rightpulmonary

arteriesSuperior

vena cava

Left pulmonaryarteries

Aorta

Left pulmonaryveins

Copyright © 2009 Pearson Education, Inc. Figure 14-7g

(g) One-way flow through the heartis ensured by two sets of valves.

Right atrium Left atrium

Right ventricle

vena cava veins

Cusp of the AV(bicuspid) valve

Cusp of a right AV(tricuspid) valve

Chordae tendineae

Inferiorvena cava

Papillary muscles

Left ventricle

Descendingaorta

Cardiac Muscle

(a)

Copyright © 2009 Pearson Education, Inc. Figure 14-10(b)

Contractile fibers

Nucleus

Mitochondria

Cardiac muscle cell

Intercalated disk(sectioned)

Intercalated disk

Cardiac Muscle

• Excitation-contraction coupling and relaxation in cardiac muscle

1

2

3

910

2

1

Voltage-gated Ca 2+

channels open. Ca 2+

enters cell.

Ca2+ induces Ca 2+ releasethrough ryanodine

Action potential entersfrom adjacent cell.

ATP NCX

3 Na+

3 Na+

2 K+ Ca2+

Ca2+

ECF

ICF

Ca2+

RyR


4

5

6

7

8

9

10

776

5

8

4

3

2

Ca2+ ions bind to troponinto initiate contraction.

Relaxation occurs whenCa2+ unbinds from troponin.

Na+ gradient is maintainedby the Na +-K+-ATPase.

through ryanodinereceptor-channels (RyR).

Local release causesCa2+ spark.

Ca2+ is pumped backinto the sarcoplasmicreticulum for storage.

Ca2+ is exchanged withNa+ by the NCX antiporter.

Summed Ca 2+ sparkscreate a Ca 2+ signal.

ATP

Sarcoplasmic reticulum(SR)

Myosin

Actin

Relaxation

Ca2+ Ca2+

Ca2+ stores

T-tubule

L-typeCa2+

channel

Ca2+ sparks

Ca2+ signal

Contraction

Ca2+

SR

Myocardial Contractile Cells

• Action potential of a cardiac contractile cell

0

PX = Permeability to ion X

PK and PCa

PNa

PK and PCa

+20

–20

–40

0

1

2

3

Mem

bran

e po

tent

ial (

mV

)


44

0 100 200 300Time (msec)

–60

–80

–100

Phase Membrane channels

Na+ channels open

Na+ channels close

Ca2+ channels open; fast K + channels close

Ca2+ channels close; slow K + channels open

Resting potential

PNa

0

1

2

3

4

Mem

bran

e po

tent

ial (

mV

)

Electrical Conduction in Myocardial Cells

Membrane potentialof autorhythmic cel

Membrane potentialof contractile cell

Cells ofSA node


Contractile cell

SA node

Depolarizations of autorhythmic cellsrapidly spread to adjacent contractilecells through gap junctions.

Intercalated diskwith gap junctions

Electrical Conduction in the Heart 1111

2222

3333

4444

3333

2222

1111

THE CONDUCTING SYSTEMOF THE HEART

SA node

AV node

Internodalpathways

SA node

SA node depolarizes.

Electrical activity goesrapidly to AV node viainternodal pathways.

Depolarization spreadsmore slowly acrossatria. Conduction slowsthrough AV node.

Depolarization movesrapidly through ventricularconducting system to theapex of the heart.


5555

5555

4444

Purkinjefibers

Bundlebranches

AV bundle

AV node

pathwaysDepolarization wavespreads upward fromthe apex.



SA node

AV node

Internodalpathways

SA node


Copyright © 2009 Pearson Education, Inc. Figure 14-18, step 1

Purkinjefibers

Bundlebranches

AV bundle

AV node

pathways


22222222

1111


SA node

AV node

Internodalpathways

SA node



Copyright © 2009 Pearson Education, Inc. Figure 14-18, steps 1–2

Purkinjefibers

Bundlebranches

AV bundle

AV node

pathways


2222

3333

3333

2222

1111


SA node

AV node

Internodalpathways

SA node





Purkinjefibers

Bundlebranches

AV bundle

AV node

pathways


2222

3333

4444

3333

2222

1111


SA node

AV node

Internodalpathways

SA node






4444

Purkinjefibers

Bundlebranches

AV bundle

AV node

pathways


2222

3333

4444

3333

2222

1111


SA node

AV node

Internodalpathways

SA node






5555

5555

4444

Purkinjefibers

Bundlebranches

AV bundle

AV node

pathwaysDepolarization wavespreads upward fromthe apex.

Electrical Conduction

• AV node• Routes the direction of electrical signals • Delays the transmission of action potentials

• SA node• Sets the pace of the heartbeat at 70 bpm


• Sets the pace of the heartbeat at 70 bpm• AV node (50 bpm) and Purkinje fibers (25-40

bpm) can act as pacemakers under some conditions

Einthoven’s Triangle

Electrodes areattached to theskin surface.

Right arm Left arm

I


A lead consists of twoelectrodes, one positiveand one negative.

Left leg

II III

The Electrocardiogram

• Three major waves: P wave, QRS complex, and T wave


Electrical Activity

• Correlation between an ECG and electrical events in the heart

P

R

T

PQ or PR segment:PQ or PR segment:PQ or PR segment:PQ or PR segment:

conduction throughAV node and AVbundle

P wave: P wave: P wave: P wave: atrialdepolarizationSTARTSTARTSTARTSTART

The endThe endThe endThe end

P


P

Q

T

S P

T wave:T wave:T wave:T wave:

ventricularrepolarization

bundle

ELECTRICALEVENTSOF THE

CARDIACCYCLE

Repolarization

P

Q

P

Q

R

P

Q

R

T

S

R waveR waveR waveR waveP

Q

R

S

S waveS waveS waveS wave

Q

R

P

Q waveQ waveQ waveQ wave

Ventricles contract

ST segmentST segmentST segmentST segment

Atria contract

S

Electrical ActivityP wave: P wave: P wave: P wave: atrialdepolarization

ELECTRICALEVENTS

STARTSTARTSTARTSTART

P

Copyright © 2009 Pearson Education, Inc. Figure 14-21 (1 of 9)

EVENTSOF THE

CARDIACCYCLE

Electrical Activity

P



P wave: P wave: P wave: P wave: atrialdepolarization

ELECTRICALEVENTS


P

Atria contract


EVENTSOF THE

CARDIACCYCLE

Electrical Activity

P




ELECTRICALEVENTS


P

Atria contract


EVENTSOF THE

CARDIACCYCLE

P

Q


Electrical Activity

P




ELECTRICALEVENTS


P

Atria contract


EVENTSOF THE

CARDIACCYCLE

P

Q

P

Q

RR waveR waveR waveR wave


Electrical Activity

P




ELECTRICALEVENTS


P

Atria contract


EVENTSOF THE

CARDIACCYCLE

P

Q

P

Q

RR waveR waveR waveR wave


Q

R

P


S

Electrical Activity

P




ELECTRICALEVENTS


P

Atria contract


EVENTSOF THE

CARDIACCYCLE

P

Q

P

Q

RR waveR waveR waveR waveP

Q

R

S


Q

R

P


Ventricles contract


S

Electrical Activity

P






ELECTRICALEVENTS

Repolarization


R

P

Atria contract


EVENTSOF THE

CARDIACCYCLE

P

Q

P

Q

R

P

Q

R

T

S


Q

R

S


Q

R

P


Ventricles contract


S

Electrical Activity

P

Q

R

T

S P






ELECTRICALEVENTS

Repolarization


R


P

Atria contract


EVENTSOF THE

CARDIACCYCLE

P

Q

P

Q

R

P

Q

R

T

S


Q

R

S


Q

R

P


Ventricles contract


S

Electrical Activity

• Comparison of an ECG and a myocardial action potential

(a)(a)(a)(a) The electrocardiogram represents the summedelectrical activity of all cells recorded from the

1 mV

1 sec


electrical activity of all cells recorded from thesurface of the body.

(b)(b)(b)(b) The ventricular action potential is recorded froma single cell using an intracellular electrode.Notice that the voltage change is much greaterwhen recorded intracellularly.

110mV

1 sec

Electrical Activity

• Normal and abnormal electrocardiograms


Mechanical Events

• Mechanical events of the cardiac cycle

5555

2222

1111 Late diastoleLate diastoleLate diastoleLate diastole————both sets ofchambers are relaxed andventricles fill passively.

Atrial systoleAtrial systoleAtrial systoleAtrial systole————atrial contractionforces a small amount ofadditional blood into ventricles.


Isovolumic ventricularIsovolumic ventricularIsovolumic ventricularIsovolumic ventricularrelaxationrelaxationrelaxationrelaxation————as ventriclesrelax, pressure in ventriclesfalls, blood flows back intocusps of semilunar valvesand snaps them closed.


44443333 Isovolumic ventricularIsovolumic ventricularIsovolumic ventricularIsovolumic ventricular

contractioncontractioncontractioncontraction————first phase ofventricular contraction pushes AVvalves closed but does not createenough pressure to open semilunarvalves.

Ventricular ejectionVentricular ejectionVentricular ejectionVentricular ejection————as ventricular pressurerises and exceeds pressurein the arteries, the semilunarvalves open and blood isejected.

S1

S2

Mechanical Events1111 Late diastoleLate diastoleLate diastoleLate diastole————both sets of

chambers are relaxed andventricles fill passively.


Copyright © 2009 Pearson Education, Inc. Figure 14-24, step 1

Mechanical Events

2222





S1

Mechanical Events

2222







S1

S2

Mechanical Events

2222







Ventricular ejectionVentricular ejectionVentricular ejectionVentricular ejection————

as ventricular pressurerises and exceeds pressurein the arteries, the semilunarvalves open and blood isejected.

S1

S2

Mechanical Events

5555

2222




Isovolumic ventricularIsovolumic ventricularIsovolumic ventricularIsovolumic ventricular

relaxationrelaxationrelaxationrelaxation————as ventriclesrelax, pressure in ventriclesfalls, blood flows back intocusps of semilunar valvesand snaps them closed.




Ventricular ejectionVentricular ejectionVentricular ejectionVentricular ejection————

as ventricular pressurerises and exceeds pressurein the arteries, the semilunarvalves open and blood isejected.

S1

S2

Cardiac Cycle

• Left ventricular pressure-volume changes during one cardiac cycle

120

ESVD

Stroke volume EDV = End-diastolicvolumeESV = End-systolicvolume

KEYKEYKEYKEY

Left

vent

ricul

ar p

ress

ure

(mm

Hg)


80

40

0 65 100 135Left ventricular volume (mL)

AB

C

EDV

Onecardiaccycle

Left

vent

ricul

ar p

ress

ure

(mm

Hg)

Wiggers Diagram

P PT

0 100 200 300 400 500 600 700 800

120

AAAA

BBBB

60

90

Time (msec)

Electro-cardiogram

(ECG)

Pressure(mm Hg)

Dicrotic notch

QRScomplex

QRScomplex

Leftventicularpressure

DDDDLeft atrialpressure

30


135

0 CCCC

DDDD

EEEE

FFFF

S1 S2

65

Heart sounds

Leftventricular

volume (mL)

Atrialsystole

Atrialsystole

Atrialsystole

Atrialsystole

Ventricularsystole

Ventricularsystole

Ventriculardiastole

Isovolumicventricularcontraction

Earlyventricular

diastole

Lateventricular

diastole

pressure30

Stroke Volume and Cardiac Output

• Stroke volume• Amount of blood pumped by one ventricle

during a contraction• EDV – ESV = stroke volume

• Cardiac output


• Cardiac output• Volume of blood pumped by one ventricle in a

given period of time• CO = HR × SV• Average = 5 L/min

Sympathetic neurons(NE)

Parasympatheticneurons (Ach)

Integrating center

Efferent path

Effector

Tissue response

Cardiovascularcontrol

center in medullaoblongata

KEYKEYKEYKEY

Autonomic Neurotransmitters Alter Heart Rate


Na+ and Ca 2+ influx

Rate of depolarization

Heart rate

Muscarinic receptorsof autorhythmic cells

K+ efflux; Ca 2+ influx

Hyperpolarizes cell andrate of depolarization

Heart rate

ββββ1-receptors ofautorhythmic cells

Figure 14-27

Stroke Volume

• Frank-Starling law states• Stroke volume increase as EDV increases

• EDV is affected by venous return• Venous return is affected by

• Skeletal muscle pump


• Skeletal muscle pump• Respiratory pump• Sympathetic innervation

• Force of contraction is affected by• Stroke volume• Length of muscle fiber and contractility of heart

Inotropic Effect

• The effect of norepinepherine on contractility of the heart


Stroke Volume and Heart Rate Determine Cardiac Output

determined by

is a function of

determined by

CARDIAC OUTPUTCARDIAC OUTPUTCARDIAC OUTPUTCARDIAC OUTPUT

Heart rateHeart rateHeart rateHeart rate

Rate of depolarizationin autorhythmic cells

Stroke volumeStroke volumeStroke volumeStroke volume

Force of contraction inventricular myocardium


is influenced by

which varies with

increases

increases

aided by

Due toparasympathetic

innervation

Sympatheticinnervation and

epinephrine

Venous returnVenous constriction

End-diastolicvolume

Contractility

Respiratorypump

Skeletal musclepump

Decreases Increases

Summary

• Cardiovascular system—anatomy review• Pressure, volume, flow, and resistance

• Pressure gradient, driving pressure, resistance, viscosity, flow rate, and velocity of flow

• Cardiac muscle and the heart


• Cardiac muscle and the heart• Myocardium, autorhythmic cells, intercalated

disks, pacemaker potential, and If channels

• The heart as a pump• SA node, AV node, AV bundle, bundle

branches, and Purkinje fibers

Summary

• The heart as a pump (continued)• ECG, P wave, QRS complex, and T wave

• The cardiac cycle• Systole, diastole, AV valves, first heart sound,

isovolumic ventricular contraction, semilunar


isovolumic ventricular contraction, semilunar valves, second heart sound, and stroke volume

• Cardiac output• Frank-Starling law, EDV, preload, contractility,

inotropic effect, afterload, and ejection fraction

Blood Flow and the Control of Blood

Pressure


Lectures byJan Machart

University of Texas, Austin

Functional Model of the Cardiovascular SystemElastic arteries

Aorta

Aortic valve

Left heartLeft ventricle

Left atrium

Pulmonary veins

Mitral valve Arteriole withvariable radius

Exchange of


Right heart

Lungs

Right ventricle

Right atrium

Pulmonary arteryPulmonary valve

Tricuspid valve

Capillaries

Venae cavae

Venules

Exchange ofmaterial withcells

Expandable veins

Elastic Recoil in Arteries

1111

22221111

Ventricle contracts.

Semilunar valve opens.Arterioles

Copyright © 2009 Pearson Education, Inc. Figure 15-4a

3333 Aorta and arteries expand andstore pressure in elastic walls.

(a) Ventricular contraction(a) Ventricular contraction(a) Ventricular contraction(a) Ventricular contraction

2222

3333

Pressure Throughout the Systemic Circulation

• Blood pressure is highest in the arteries and decreases continuously as it flows through the circulatory system


Cuff pressure> 120 mm Hg

Cuff pressurebetween 80 and

Inflatablecuff

Pressuregauge

(a)(a)(a)(a)

(b)(b)(b)(b)

Measurement of Arterial Blood Pressure


Stethoscope 120 mm Hg

Cuff pressure< 80 mm Hg

(c)(c)(c)(c)

Figure 15-7

Bloodvolume

Bloodpressure

leads to

triggers

Stimulus

Integrating center

Tissue response

Systemic response

Slow responseFast response

KEYKEYKEYKEY

Blood Pressure


Compensationby

cardiovascularsystem

Vasodilation Cardiac output Excretion of fluid in urineblood volume

Bloodpressureto normal

Compensationby kidneys

Figure 15-9

Factors that Influence Mean Arterial Pressure


Arteriolar Resistance

Copyright © 2009 Pearson Education, Inc. Table 15-2

Distribution of Blood

• Distribution of blood in the body at rest


Blood Flow

• Blood flow through individual blood vessels is determined by vessel’s resistance to flow


Blood Flow

• Flow ∝ 1/resistance

Copyright © 2009 Pearson Education, Inc. Figure 15-15b

Velocity of Blood Flow

• Velocity of flow depends on total cross-sectional area of the vessels


Fluid Exchange at a Capillary

• Hydrostatic pressure and osmotic pressure regulate bulk flow


Fluid Exchange at a Capillary

Arteriole

Netabsorption

Netfiltration

Venule

Copyright © 2009 Pearson Education, Inc. Figure 15-19b

absorption

Lymphvessels

filtration

(b) Relationship between capillaries and lymph vessels(b) Relationship between capillaries and lymph vessels(b) Relationship between capillaries and lymph vessels(b) Relationship between capillaries and lymph vessels

Lymphatic System

Thoracic (left lymph) duct

Axillary lymph nodes

Lymphatics ofmammary gland

Spleen

Pelviclymph nodes

Thoracic duct

Thymus

Right lymph duct

Cervicallymph nodes

Lymphatics ofupper limb

Lumbarlymph nodes


Inguinallymph nodes

Blind-end lymphcapillaries in the tissuesremove fluid and filteredproteins.

Lymph fluid empties into the venous circulation.

Lymphaticsof lower limb

Edema

• Two causes• Inadequate drainage of lymph• Filtration far greater than absorption

• Disruption of balance between filtration and absorption


absorption• Increase in hydrostatic pressure• Decrease in plasma protein concentration• Increase in interstitial proteins

Blood Pressure

• Components of the baroreceptor reflex

Medullarycardiovascularcontrol center

Change inblood

pressure

Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY


Carotid and aorticbaroreceptors

pressure

Parasympatheticneurons

Sympatheticneurons

Veins

Arterioles

Ventricles

SA node

Change inblood

pressure

Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY

Blood Pressure



Change inblood

pressure

Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY

Blood Pressure


baroreceptors

Figure 15-22 (2 of 10)



Change inblood

pressure

Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY

Blood Pressure


baroreceptors

Figure 15-22 (3 of 10)



Change inblood

pressure


Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY

Blood Pressure


baroreceptors

Figure 15-22 (4 of 10)



Change inblood

pressure


Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY

Blood Pressure


baroreceptors

Sympatheticneurons

Figure 15-22 (5 of 10)



Change inblood

pressure


Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY

Blood Pressure


baroreceptors

Sympatheticneurons SA node

Figure 15-22 (6 of 10)



Change inblood

pressure


Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY

Blood Pressure


baroreceptors

Sympatheticneurons SA node

Figure 15-22 (7 of 10)



Change inblood

pressure


Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY

Blood Pressure


baroreceptors

Sympatheticneurons

Ventricles

SA node

Figure 15-22 (8 of 10)



Change inblood

pressure


Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY

Blood Pressure


baroreceptors

Sympatheticneurons

Arterioles

Ventricles

SA node

Figure 15-22 (9 of 10)



Change inblood

pressure


Integrating center

Stimulus

Efferent path

Effector

Sensory receptor

KEYKEYKEYKEY

Blood Pressure


baroreceptors

Sympatheticneurons

Veins

Arterioles

Ventricles

SA node

Figure 15-22 (10 of 10)

Blood Pressure

• The baroreceptor reflex: the response to increased blood pressure


pressure

Figure 15-23

Blood Pressure

• The baroreceptor reflex: the response to orthostatic hypotension


hypotension

Figure 15-24

CVD: Risk Factors

• Not controllable• Sex• Age• Family history

• Controllable


• Controllable• Smoking• Obesity• Sedentary lifestyle• Untreated hypertension

CVD: Risk Factors

• Uncontrollable genetic but modifiable lifestyle• Blood lipids

• Leads to atherosclerosis• HDL-C versus LDL-C

• Diabetes mellitus


• Diabetes mellitus• Metabolic disorder contributes to development of

atherosclerosis

LDL and Plaque

• The development of atherosclerotic plaques (a) Normal arterial wall(a) Normal arterial wall(a) Normal arterial wall(a) Normal arterial wall

(b) Fatty streak(b) Fatty streak(b) Fatty streak(b) Fatty streak

Endothelial cells Elastic connective tissue Smooth muscle cells

Macrophages

Smooth muscle cells

LDL cholesterol accumulates


(b) Fatty streak(b) Fatty streak(b) Fatty streak(b) Fatty streak

(c) Stable fibrous plaque(c) Stable fibrous plaque(c) Stable fibrous plaque(c) Stable fibrous plaque

(d) Vulnerable plaque(d) Vulnerable plaque(d) Vulnerable plaque(d) Vulnerable plaque

A lipid core accumulatesFibrous scar tissue

Smooth muscle cells

Calcifications are depositedwithin the plaque.

Platelets

Macrophages

Hypertension

• The risk of developing cardiovascular disease doubles with each 20/10 mm Hg increase in blood pressure

• Essential hypertension has no clear cause other than hereditary


other than hereditary

Figure 15-26

Hypertension

• Carotid and aortic baroreceptors adapt• Risk factor for atherosclerosis• Heart muscle hypertrophies

• Pulmonary edema • Congestive heart failure


• Congestive heart failure

• Treatment• Calcium channel blockers, diuretics, beta-

blocking drugs, and ACE inhibitors

Myocardial infarction

Decreased oxygen supply to the heart due to blockage of one or more coronary arteries.



Drawing of the heart showing anterior left ventricl e wall infarction



Symptoms:

A person having an acute myocard infarct usually has sudden chest pain (called angina pectoris) that is felt behind the breast bone and sometimes travels to the left arm or the left side of the neck.

Additionally, the person may have shortness of breath, sweating, nausea, vomiting, abnormal heartbeats and anxiety.


Areas of pain


A cardiac troponin rise (as a marker of all heart muscle damage) accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic of MI (WHO).



• Etiology/Prevention:• Lifestyle: smoking, obesity, stress, exercise, …• Diseases: diabetes mellitus, hypertension, lipid disorders, …• Medication: antiplatelet drugs, beta blockers, ACE inhibitors,

statins, other antihypertensive drugs, …


• Treatment angina pectoris: • The most specific medicine to treat angina is nitroglycerin. It is a

potent vasodilator that makes more oxygen available to the heart muscle.

• Beta blockers and calcium channel blockers act to decrease the heart's workload, and thus its requirement for oxygen.


Percutaneous coronary intervention

• During PCI, a cardiologist feeds a deflated balloon or other device on a catheter from the inguinal femoral artery or radial artery up through blood vessels until they reach the site of blockage in the heart and X-ray imaging is used to guide the catheter threading.

• At the blockage, the balloon is inflated to open the artery, allowing blood to flow. • A stent is often placed at the site of blockage to permanently open the artery.


Coronary angiography and angioplasty in acute myocardial infarction

left: RCA closedright: RCA successfully dilated

Coronary artery bypass grafting (CABG), which bypasses stenotic arteries by grafting vessels from elsewhere in the body, is an alternative treatment.


Ischemic heart disease in context of other cardiovascular (related) diseases


EHEALTH

Questions?

and/or


and/or

Blood Pressure Measurement

Cardiovascular Physiologyarjenh/lect3.pdf · • Mechanical events of the cardiac cycle 5555 2222...

Documents

Transcript of Cardiovascular Physiologyarjenh/lect3.pdf · • Mechanical events of the cardiac cycle 5555 2222...