Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO...

8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations

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Prepared and presented byMarc Imhotep Cray, M.D.

Basic Medical Sciences and

Clinical Knowledge (CK) Teacher

Physiologic and PathophysiologicFunction of the Heart

From:

USMLE Step 1 CV Review Tools Cloud Folder
https://drive.google.com/folderview?id=0B-tlCbPSHvfZcHUyQUVLRmxkVjA&usp=sharinghttps://drive.google.com/folderview?id=0B-tlCbPSHvfZcHUyQUVLRmxkVjA&usp=sharinghttp://www.imhotepvirtualmedsch.com/


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Online reference resource to

the presentation thatfollows:

Cardiovascular Physiology

Concepts

Richard E. Klabunde, PhD

Click for enlarged view

CV Physiology Concepts SchematicFrom IVMS Function of the Heart illustrations and Equations Notes
http://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htmhttps://docs.google.com/file/d/0B-tlCbPSHvfZVy1WaVhYVmRlcDQ/edit?usp=sharinghttps://docs.google.com/file/d/0B-tlCbPSHvfZVy1WaVhYVmRlcDQ/edit?usp=sharinghttps://drive.google.com/file/d/0B-tlCbPSHvfZdXM3eWwzMkRVTmM/edit?usp=sharinghttps://drive.google.com/file/d/0B-tlCbPSHvfZdXM3eWwzMkRVTmM/edit?usp=sharinghttps://drive.google.com/file/d/0B-tlCbPSHvfZdXM3eWwzMkRVTmM/edit?usp=sharinghttps://drive.google.com/file/d/0B-tlCbPSHvfZdXM3eWwzMkRVTmM/edit?usp=sharinghttps://docs.google.com/file/d/0B-tlCbPSHvfZVy1WaVhYVmRlcDQ/edit?usp=sharinghttp://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htmhttps://docs.google.com/file/d/0B-tlCbPSHvfZVy1WaVhYVmRlcDQ/edit?usp=sharing


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TOPICS DISCUSSION OUTLINE

The physiologic function of the heart can be represented in several

ways:

Cardiac output as measured using the Fick principle

Cardiac Cycle (Wiggers diagram)

PressureVolume Loops: pressurevolume loops provide a tool foranalyzing the cardiac cycle, particularly ventricular function

FrankStarling curves: Effects of Cardiac Output, Total Peripheral

Resistance, Contractility, Preload, and Afterload as represented onthe FrankStarling curve

Common Valvular Abnormalities

3


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Cardiac Output Measurement

4

Cardiac output =volume of blood

pumped by each ventricle perminute. (N5L/min)

Cardiac output (QT) is regulated by

autonomic nerves and hormones

through changes in heart rate (HR)or stroke volume (SV)

In adults, cardiac output is usually

expressed in liters per minute:

QT = (SV HR)/1000QT= Cardiac output (L/min)

SV= Stroke volume (mL/min)

HR= Heart rate (beats/min)

Example If resting SV is 70 mL and HR is 70 beats/min, then

QT= (70 mL 70 beats/min)/1000 = 4.9L/min

Cardiac output can also be measured

clinically in the cardiac catheterizationlaboratory, using a thermodilution

method

A cold saline solution of known

temperature and volume is injectedinto the right atrium.

The reduction in blood temperature

measured downstream in the

pulmonary artery is a function of

cardiac output.


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THE FICK PRINCIPLE (1)

5

A traditional physiologic method for

calculating cardiac output applies theFick principle, which derives blood flow

from variables related to O2

consumption

Cardiac output can be calculated by

applying the Fick concept to the entirebody, relating total body O2 consumption

to the difference in O2 content between

blood in the systemic arteries and the

mixed venous blood sampled from the

pulmonary artery or the right ventricle

QT = VO2 /(CaO2 CvO2)QT = Cardiac output

VO2 = O2 consumption

CaO2 = Arterial O2 content

CvO2 = Mixed venous O2 content

Example A person consumes 250 mL of O2 per

min. Arterial O2 content is 20 mL of O2 per dL

of blood, and the O2 content of

mixed venous blood is 15 mL of O2 per dL of

blood:

QT = 250 (mL/min) (20 mL/dL 15 mL/dL) =

50 dL/min

QT = 50 dL / min = 5 L / min


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THE FICK PRINCIPLE (2)

6

The Fick principle for measuring cardiac

output is expressed by the following

equation:

The equation is solved as follows:

1. O2 consumption for the whole body ismeasured.

2. Pulmonary vein [O2] is measured in a

peripheral artery.

3. Pulmonary artery [O2] is measured in

systemic mixed venous blood

For example, a 70-kg man has a resting O2

consumption of 250 mL/min, a peripheral

arterial O2 content of 0.20 mL O2/mL of blood,

a mixed venous O2 content of 0.15 mL

O2/mL of blood, and a heart rate of 72

beats/min.

What is his cardiac output? What is

his stroke volume?


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7

During the early stages of

exercise, CO is maintained by

HR and SV During the late

stages of exercise, CO is

maintained byHR only (SVplateaus)

If HR is too high, diastolic filling

is incomplete and CO(e.g.,

ventricular tachycardia)

Source: Tao Le T and Bhushan V, Cardiovascular, In First Aid for the

USMLE Step 1 2013:253


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Cardiac cycle(1)

The seven phases of the cardiac

cycle are

(1) atrial systole;

(2) Isovolumetric contraction;

(3) rapid ejection;(4) reduced ejection;

(5), isovolumetric relaxation;

(6) rapid filling; and

(7) reduced filling.

Source: Klabunde, RE, Ventricular Pressure-Volume Relationship 8
http://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htm


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Cardiac cycle (2)

Expressed as pressure-volume loop

9

Phases-left ventricle:1) Isovolumetric contraction - period

between mitral valve closure and

aortic valve opening; period of

highest 02 consumption

2) Systolic ejection - period betweenaortic valve opening and closing

3) Isovolumetric relaxation - period

between aortic valve closing and

mitral valve opening

4) Rapid filling- period just after

mitral valve opening

5) Reduced filling- period just before

mitral valve closureSource: Tao Le T and Bhushan V, Cardiovascular, IN First Aid for the

USMLE Step 1 2013:256


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Stepsin the Cardiac cycle (3)

10

1 2 (isovolumetric contraction)

On excitation, the ventricle contracts and

ventricular pressure increases. The mitral valve

closes when left ventricular pressure is greater

than left atrial pressure. Because all valves are

closed, no blood can be ejected from the

ventricle (isovolumetric).

2 3 (ventricular ejection)The aortic valve opens at point 2 when

pressure in the left ventricle exceeds pressure

in the aorta. Blood is ejected into the aorta,

and ventricular volume decreases. The volume

that is ejected in this phase is the strokevolume. Thus, stroke volume can be measured

graphically by the width of the pressure

volume loop. The volume remaining in the left

ventricle at point 3 is ESV.


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Stepsin the Cardiac Cycle (4)

11

3 4 (isovolumetric relaxation)At point 3, the ventricle relaxes. When

ventricular pressure decreases to less than

aortic pressure, the aortic valve closes.

Because all of the valves are closed again,

ventricular volume is constant during thisphase.

4 1 (ventricular filling)

Once left ventricular pressure decreases to

less than left atrial pressure, the mitral (AV)

valve opens and filling of the ventricle

begins. During this phase, ventricular volume

increases to about 140 mL (the end-diastolic

volume).


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Cardiac output variables

12

Stroke Volume is affected by Contractility, Afterload, and Preload

SV when preload, afterload , or contractility

Contractility (and SV) with :

Catecholamines (activity of Ca2+ pump in sarcoplasmic reticulum)

intracellular Ca2+

extracellular Na+ ( activity of Na+/Ca2+ exchanger)

Digitalis ( blocks Na+-K+ pump intracellular Na+ Na+/Ca2+exchanger activity intracellular Ca2+)

Contractility (and SV) with:

1-blockade (cAMP)

Heart failure (systolic dysfunction)

Acidosis

Hypoxia /hypercapnea ( PO2 / PCO2)

Non-dihydropyridine Ca2+ Channel blockers


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Preload and afterload

13

Preload =ventricular EDVAfterload= mean arterial pressure

(proportional to peripheral resistance)

Venodilators (e.g., nitroglycerin) Preload.

Vasodilators (e.g., hydralazine) Afterload (arterial)

Preload with :

Exercise (slightly)

blood volume (e.g., overtransfusion) Excitement (sympathetic activity)


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Ventricular pressure-volume loop (1)

Generated by plotting ventricular pressure

against ventricular volume at many different

corresponding points during a single cardiac cycle

Source: Klabunde, RE, Ventricular Pressure-Volume Relationship

14


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Ventricular pressure-volume loop (2)

EDPVR, end-diastolic pressure-volume relationship;

ESPVR, end-systolic pressure-volume relationship;

SV, stroke volume (EDV - ESV) 15



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Left ventricular pressure and volume (3)

16

Correlation between changes in left

ventricular pressure (upper panel )

and left ventricular volume (lower

panel ) during a single cardiac cycle

Landmark events of valve opening

and closure and the point where

peak systolic blood pressure occursare noted at points AE

Kibble JD and Halsey CR, CV Physiology, In Medical Physiology

The Big Picture; McGraw-Hill 2009:144-57


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Pressure-volume loop (4)

17

Left ventricular pressure is

plotted as a function of left

ventricular volume

Landmark events of valve

opening and closure and the

point where peak systolic

blood pressure occurs arenoted at points AE

Kibble JD and Halsey CR, CV Physiology, In Medical Physiology The Big

Picture McGraw-Hill 2009:144-57


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Effects of increasing venous return on

LV pressure-volume loops

This diagram shows the acuteresponse to an increase in

venous return.

It assumes no cardiac or

systemic compensation andthat aortic pressure remains

unchanged

Increased venous return

increases end-diastolic volume

(EDV) but it normally does not

change ESV; therefore, stroke

volume (SV) is increased.

ESPVR, end-systolic pressure-

volume relationship. 18



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Factors that Increase Ventricular Preload

19

Source: Klabunde RE. Cardiovascular Physiology Concepts 2ndEd.

http://www.cvphysiology.com/textbook.htm
http://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htm


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Effects of changes in afterload

(PAo) LV pressure-volume loops

Increased aortic pressure solid

red loop) decreases stroke

volume (width of loop) and

increases end-systolic volume

(ESV), whereas decreased

aortic pressure (AO dashed red

loop) increases stroke volume

and decreases end-systolic

volume. Preload and inotropyare held constant in this

illustration.

20



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Effects of increasing inotropy

on ventricular pressurevolume loops

Increased inotropy shifts theESPVR up and to the left,

thereby increasing stroke

volume and decreasing end-

systolic volume (ESV).Decreased inotropy shifts the

end-diastolic pressurevolume

relationship down and to the

right, thereby decreasing stroke

volume and increasing end-

systolic volume. Preload and

aortic pressure are held constant

in this illustration.

21



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Factors that increase inotropy

22

Source: Klabunde RE. Cardiovascular Physiology Concepts 2ndEd.


ff f h l d f l d d


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Effects of changes in preload, afterload, and

contractility on the ventricular pressurevolume loop

23

Increased preload Increased preload

results in an increase in EDV. This increase

causes an increase in SV (due to Frank-

Starling relationship), which is reflected as

an increased width of the loop.

Increased afterload results from an

increase in aortic pressure, which leads to

a decrease in SV. This decreases the width

of the loop.

Increased contractility Increased

contractility leads to the ventricle

developing greater tension during systole

and increases the SV.

Source:Klabunde,RE,V

entricularPressure-Volum

eRelationship
http://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htm


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Changes in the ventricular pressurevolume loop

Describe each

24

Source: Costanz LS. Cardiovascular Physiology IN BRS Physiology 5th ed. LLW, 2012


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Interdependent effects of changes in preload, afterload, and

inotropy on left ventricular pressure-volume loops (1)

25

Ashows effects of

increasing preload (end-

diastolic volume) withand without a secondary

increase in afterload

(aortic pressure)



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Interdependent effects of changes in preload, afterload,

and inotropy on left ventricular pressure-volume loops (2)

26

Bshows the effects of

increasing afterload

with and without a

secondary increase in

preload.



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Interdependent effects of changes in preload, afterload, and

inotropy on left ventricular pressure-volume loops(3)

27

C shows the effects of

increasing inotropy with

and without secondary

changes in preload and

afterload.



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Starling curve

28

Force of contraction is proportional

to end diastolic length of cardiacmuscle fiber

(preload)

contractility with sympathetic

stimulation,

catecholamines, digoxin

contractility with

loss of myocardium (MI) ,

-blockers, calcium channel

blockersSource: Tao Le T and Bhushan V, Cardiovascular, IN

First Aid for the USMLE Step 1 2013:554

EF in systolic heart failure

Wi di l i f l i l d h i l


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Wiggers diagram, a correlation of electrical and mechanical

events during the cardiac cycle

29A phonocardiogram records heart sounds

Kibble JD and Halsey CR, CV Physiology,

IN Medical Physiology The Big Picture M-H 2009


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Summary of normal pressures

within the cardiac chambers and great vessels

30

The higher of the two pressure values(expressed in mm Hg) in the right ventricle

(RV), left ventricle (LV), pulmonary artery (PA),

and aorta (Ao) represent the normal peak

pressures during ejection (systolic pressure)

WHEREAS

The lower pressure values represent normal

end of diastole pressure (ventricles) or the

lowest pressure (diastolic pressure) found in

the PA and Ao. Pressures in the right atrium(RA) and left atrium (LA) represent average

values during the cardiac cycle

Source: Klabunde RE. Cardiovascular Physiology Concepts

2ndEd., LLW 2012


NORMAL HEART SOUNDS & COMMON


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NORMAL HEART SOUNDS & COMMON

VALVULAR ABNORMALITIES

31

A. First (S1) and second (S2) heart

sounds.

B. Physiologic splitting of S2. S1 is caused

by the closure of the

atrioventricular valves; S2 is caused by

the closure of the semilunarvalves. Physiologic splitting mainly results

from the delayed closure

of the pulmonic valve on inspiration. M1,

mitral valve closure; T1,tricuspid valve closure; A2, aortic valve

closure; P2, pulmonic valve

closure.

Kibble JD and Halsey CR, CV Physiology, In MedicalPhysiology The Big Picture McGrawHill 2009:144-57

Also see:

Audio-HEART and LUNG Auscultation Sounds mp3s

A i S i
https://drive.google.com/folderview?id=0B3Sb6jVcZDpKNGppMDZEQnlRVGM&usp=sharinghttps://drive.google.com/folderview?id=0B3Sb6jVcZDpKNGppMDZEQnlRVGM&usp=sharinghttps://drive.google.com/folderview?id=0B3Sb6jVcZDpKNGppMDZEQnlRVGM&usp=sharinghttps://drive.google.com/folderview?id=0B3Sb6jVcZDpKNGppMDZEQnlRVGM&usp=sharinghttps://drive.google.com/folderview?id=0B3Sb6jVcZDpKNGppMDZEQnlRVGM&usp=sharinghttps://drive.google.com/folderview?id=0B3Sb6jVcZDpKNGppMDZEQnlRVGM&usp=sharinghttps://drive.google.com/folderview?id=0B3Sb6jVcZDpKNGppMDZEQnlRVGM&usp=sharing


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Aortic Stenosis

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Systolic murmur of aortic

stenosisA. Paradoxical splitting of the

second (S2) heart sound

occurs because the aortic

valve (A2) closes later thanthe pulmonic valve (P2) due

to prolonged left ventricular

systole

B. Pressure gradient across

the narrowed aortic valveParadoxical splitting of S2 occurs when closure of

the aortic valve is delayed, causing P2 to occur first,

followed by A2. The most notable causes are aortic

stenosis (which prolongs left ventricular systole) and

left bundle branch block (which delays the onset of

left ventricular contraction)

Kibble JD and Halsey CR, CV Physiology, In Medical

Physiology The Big Picture; McGraw-Hill 2009:144-57


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Aortic Stenosis pressure-volume loop

33

In aortic stenosis (red loop in figure)

Left ventricular emptying is impaired because of high

outflow resistance caused by a reduction in the valve orificearea when it opens.

This high outflow resistance causes a large pressure gradient

to occur across the aortic valve during ejection, such that

the peak systolic pressure within the ventricle is greatly

increased.

This leads to an increase in ventricular afterload, a decreasein stroke volume, and an increase in end-systolic volume.

Stroke volume (width of pressure-volume loop) decreases

because the velocity of fiber shortening is decreased by the

increased afterload (see force-velocity relationship).

Because end-systolic volume is elevated, the excess residual

volume added to the incoming venous return causes the

end-diastolic volume to increase.

This increases preload and activates the Frank-Starling

mechanism to increase the force of contraction to help

the ventricle overcome, in part, the increased outflow

resistance.

Source: Klabunde, RE,

Ventricular Pressure-Volume Relationship


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Mitral Insufficiency

34

Systolic murmur of mitralinsufficiency

A. The early aortic valve (A2)

sound indicates the shortened

systole due to retrograde bloodflow into the left atrium

B. The large atrial v wave due

to regurgitation of blood from

the left ventricle into the left

atrium during systole

Kibble JD and Halsey CR, CV Physiology, In Medical Physiology The BigPicture; McGraw-Hill 2009:144-57


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Aortic Insufficiency

36

Diastolic murmur of aortic

insufficiency.A. Sound intensity of the murmur

decreases during diastole as a

function of aortic blood

pressure. S1 is the first heart

sound; A2 indicates timing ofthe closure of the aortic valve.

B. Pathologic runoff of blood

from the aorta into the left ventricle

decreases aortic diastolic bloodpressure and increases left

ventricular filling, increasing stroke

volume and systolic blood pressure.

Kibble JD and Halsey CR, CV Physiology, In Medical Physiology The

Big Picture McGraw-Hill 2009:144-57


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Aortic regurgitation pressure-volume loop

37

In aortic valve regurgitation

(red loop in figure)

Aortic valve does not close completely at end of

systolic ejection. As the ventricle relaxes during

diastole, blood flows from the aorta back into the

ventricle so the ventricle immediately begins to fill

from the aorta.

Once the mitral valve opens, filling occurs from theleft atrium; however, blood continues to flow from

the aorta into the ventricle throughout diastole

because aortic pressure is higher than ventricular

pressure during diastole.

This greatly enhances ventricular filling so that end-

diastolic volume is increased as shown. The increased end-diastolic volume (increased

preload) activates the Frank-Starling mechanism to

increase the force of contraction, ventricular peak

(systolic) pressure, and stroke volume (as shown by

the increased width of the pressure-volume loop).

As long as the ventricle is not in failure,

end-systolic volume may only be increased

a small amount (as shown in figure) due tothe increased afterload (ventricular wall

stress). If the ventricle goes into systolic

failure, then end-systolic volume will

increase by a large amount and the peak

systolic pressure and stroke volume (net

forward flow into aorta) will fall.




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Mitral Stenosis

38

Diastolic murmur of mitral stenosisA. An opening snap (OS) is a unique

sound that is characteristic of mitral

stenosis.

The sound produced by obstructed flow

through the mitral valve is described as

a presystolic murmur (PSM). Obstructedventricular filling may delay closure of

the mitral valve (M1) relative

to closure of the tricuspid valve (T 1).

B. Obstruction of the mitral valve causes

a sustained increase in left atrial

pressure.

Kibble JD and Halsey CR, CV Physiology, In Medical Physiology The BigPicture McGrawHill 2009:144-57


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Mitral stenosis pressure-volume loop

39

Mitral stenosis

(red pressure-volume loop in figure)

Impairs left ventricular filling so that there

is a decrease in end-diastolic volume

(preload)

This leads to a decrease in stroke volume by

the Frank-Starling mechanism and a fall incardiac output and aortic pressure.

This reduction in afterload (particularly

aortic diastolic pressure) enables the end-

systolic volume to decrease slightly, but not

enough to overcome the decline in end-diastolic volume.

Therefore, because end-diastolic volume

decreases more than end-systolic volume

decreases, the stroke volume (shown as the

width of the loop) decreases



The End


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References and suggested reading :

40

Costanzo LS, Cardiovascular Physiology. In Physiology: with STUDENT

CONSULT Online Access, 5e; Saunders 2013:189-95

Kibble JD and Halsey CR, CV Physiology, In Medical Physiology The Big

Picture McGrawHill 2009:144-57

Klabunde RE, Ch. 4-Cardiac Function and Ch. 5-Vascular Function. In

Cardiovascular Physiology Concepts.2e; LLW 2011:60-120

Tao Le T and Bhushan V, Cardiovascular, In First Aid for the USMLE Step 1

2013;McGrawHill 2013:254-59

The End,

Thank you for your attention!!!Also see companion PowerPoint: Cray MI, RELATIONSHIPS BETWEEN

CARDIAC OUTPUT AND VENOUS RETURN Last updated-11-13
http://www.scribd.com/doc/184182328/RELATIONSHIPS-BETWEEN-CARDIAC-OUTPUT-AND-VENOUS-RETURNhttp://www.scribd.com/doc/184182328/RELATIONSHIPS-BETWEEN-CARDIAC-OUTPUT-AND-VENOUS-RETURNhttp://www.scribd.com/doc/184182328/RELATIONSHIPS-BETWEEN-CARDIAC-OUTPUT-AND-VENOUS-RETURNhttp://www.scribd.com/doc/184182328/RELATIONSHIPS-BETWEEN-CARDIAC-OUTPUT-AND-VENOUS-RETURNhttp://www.scribd.com/doc/184182328/RELATIONSHIPS-BETWEEN-CARDIAC-OUTPUT-AND-VENOUS-RETURN

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