Physiologic and pathophysiologic function of the heart

Physiologic and Pathophysiologic
Function of the Heart
Prepared and presented by
Marc Imhotep Cray, M.D.
Basic Medical Sciences and
Clinical Knowledge (CK) Teacher

From:
USMLE Step 1 CV Review Tools Cloud Folder

CV Physiology Concepts Schematic
From IVMS Function of the Heart illustrations and Equations Notes

Online reference resource to
the presentation that
follows:

Cardiovascular Physiology
Concepts
Richard E. Klabunde, PhD
Click for enlarged view

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)
 Pressure– Volume Loops: pressure–volume loops provide a tool for
analyzing the cardiac cycle, particularly ventricular function
 Frank– Starling curves: Effects of Cardiac Output, Total Peripheral
Resistance, Contractility, Preload, and Afterload as represented on
the Frank– Starling curve
 Common Valvular Abnormalities
3

Cardiac Output Measurement
 Cardiac output =volume of blood
pumped by each ventricle per
minute. (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)/1000
QT = Cardiac output (L/min)
SV = Stroke volume (mL/min)
HR = Heart rate (beats/min)

 Cardiac output can also be measured
clinically in the cardiac catheterization
laboratory, using a thermodilution
method
 A cold saline solution of known
temperature and volume is injected
into the right atrium.
 The reduction in blood temperature
measured downstream in the
pulmonary artery is a function of
cardiac output.

Example If resting SV is 70 mL and HR is 70 beats/min, then
QT = (70 mL × 70 beats/min)/1000 = 4.9L/min
4

THE FICK PRINCIPLE (1)

 A traditional physiologic method for
calculating cardiac output applies the
Fick principle, which derives blood flow
from variables related to O2
consumption

Example A person consumes 250 mL of O2 per
 Cardiac output can be calculated by
min. Arterial O2 content is 20 mL of O2 per dL
applying the Fick concept to the entire
of blood, and the O2 content of
body, relating total body O2 consumption
mixed venous blood is 15 mL of O2 per dL of
to the difference in O2 content between
blood:
blood in the systemic arteries and the
QT = 250 (mL/min) ÷ (20 mL/dL − 15 mL/dL) =
mixed venous blood sampled from the
50 dL/min
pulmonary artery or the right ventricle
QT = 50 dL / min = 5 L / min
QT = VO2 /(CaO2 − CvO2)
QT = Cardiac output
VO2 = O2 consumption
CaO2 = Arterial O2 content
CvO2 = Mixed venous O2 content
5

THE FICK PRINCIPLE (2)
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 is
measured.
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?

6

During the early stages of
exercise, CO is maintained by↑
HR and ↑ SV During the late
stages of exercise, CO is
maintained by↑HR only (SV
plateaus)
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 2013:553

7

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

Cardiac cycle (2)
Expressed as pressure-volume loop

Source: Tao Le T and Bhushan V, Cardiovascular, IN First Aid for the
USMLE Step 1 2013:556

Phases-left ventricle:
1) Isovolumetric contraction - period
between mitral valve closure and
aortic valve opening; period of
highest 02 consumption
2) Systolic ejection - period between
aortic 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 closure

9

Steps in the Cardiac cycle (3)
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 stroke
volume. 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.
10

Steps in the Cardiac Cycle (4)
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 this
phase.
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).
11

Cardiac output variables
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:
• β1-blockade (↓ cAMP)
• Heart failure (systolic dysfunction)
• Acidosis
• Hypoxia /hypercapnea (↓ PO2 / ↓ PCO2)
• Non-dihydropyridine Ca2+ Channel blockers

12

Preload and afterload
Preload =ventricular EDV
Afterload = 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)

13

Ventricular pressure-volume loop (1)


Generated by plotting ventricular pressure
against ventricular volume at many different
corresponding points during a single cardiac cycle
14

Ventricular pressure-volume loop (2)


EDPVR, end-diastolic pressure-volume relationship;
ESPVR, end-systolic pressure-volume relationship;
SV, stroke volume (EDV - ESV)

15

Left ventricular pressure and volume (3)
 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 occurs
are noted at points A–E

Kibble JD and Halsey CR, CV Physiology, In Medical Physiology
The Big Picture ; McGraw-Hill 2009:144-57
16

Pressure-volume loop (4)
 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 are
noted at points A–E

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

17

Effects of increasing venous return on
LV pressure-volume loops


 This diagram shows the acute
response to an increase in
venous return.
 It assumes no cardiac or
systemic compensation and
that 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 pressurevolume relationship.
18

Factors that Increase Ventricular Preload

Source: Klabunde RE. Cardiovascular Physiology Concepts 2nd Ed.
http://www.cvphysiology.com/textbook.htm
19

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 inotropy
are held constant in this
illustration.
20

Effects of increasing inotropy
on ventricular pressure–volume loops


Increased inotropy shifts the
ESPVR up and to the left,
thereby increasing stroke
volume and decreasing endsystolic volume (ESV).
Decreased inotropy shifts the
end-diastolic pressure–volume
relationship down and to the
right, thereby decreasing stroke
volume and increasing endsystolic volume. Preload and
aortic pressure are held constant
in this illustration.
21

Factors that increase inotropy

Source: Klabunde RE. Cardiovascular Physiology Concepts 2nd Ed.

22

Effects of changes in preload, afterload, and
contractility on the ventricular pressure–volume 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.


Increased preload Increased preload
results in an increase in EDV. This increase
causes an increase in SV (due to FrankStarling relationship), which is reflected as
an increased width of the loop.

23

Changes in the ventricular pressure–volume loop
“Describe each”

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

24

Interdependent effects of changes in preload, afterload, and
inotropy on left ventricular pressure-volume loops (1)

A shows effects of
increasing preload (enddiastolic volume) with
and without a secondary
increase in afterload
(aortic pressure)

25

Interdependent effects of changes in preload, afterload,
and inotropy on left ventricular pressure-volume loops (2)

B shows the effects of
increasing afterload
with and without a
secondary increase in
preload.


26

Interdependent effects of changes in preload, afterload, and
inotropy on left ventricular pressure-volume loops(3)

C shows the effects of
increasing inotropy with
and without secondary
changes in preload and
afterload.


27

Starling curve

Source: Tao Le T and Bhushan V, Cardiovascular, IN
First Aid for the USMLE Step 1 2013:554

Force of contraction is proportional
to end diastolic length of cardiac
muscle fiber
(preload)
↑ contractility with sympathetic
stimulation,
catecholamines, digoxin
↓contractility with
loss of myocardium (MI) ,
β-blockers, calcium channel
blockers
EF↓ in systolic heart failure
28

Wiggers diagram, a correlation of electrical and mechanical
events during the cardiac cycle

Kibble JD and Halsey CR, CV Physiology,
IN Medical Physiology The Big Picture M-H 2009

A phonocardiogram records heart sounds

29

Summary of normal pressures
within the cardiac chambers and great vessels
 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)

Source: Klabunde RE. Cardiovascular Physiology Concepts
2nd Ed., LLW 2012

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

30

NORMAL HEART SOUNDS & COMMON
VALVULAR ABNORMALITIES
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 semilunar
valves. 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 Medical
Physiology The Big Picture McGraw·Hill 2009:144-57

Also see:
Audio-HEART and LUNG Auscultation Sounds mp3s
31

Aortic Stenosis
Systolic murmur of aortic
stenosis
A. Paradoxical splitting of the
second (S2) heart sound
occurs because the aortic
valve (A2) closes later than
the pulmonic valve (P2) due
to prolonged left ventricular
systole
B. Pressure gradient across
the narrowed aortic valve

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

Paradoxical 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)
32

Aortic Stenosis pressure-volume loop

Source: Klabunde, RE,
Ventricular Pressure-Volume Relationship

In aortic stenosis (red loop in figure)
 Left ventricular emptying is impaired because of high
outflow resistance caused by a reduction in the valve orifice
area 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 decrease
in 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.
33

Mitral Insufficiency
Systolic murmur of mitral
insufficiency
A. The early aortic valve (A2)
sound indicates the shortened
systole due to retrograde blood
flow 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

Picture; McGraw-Hill 2009:144-57

34

Mitral Insufficiency pressure-volume loop


mitral valve regurgitation
(red pressure-volume loop in figure)
 As the left ventricle contracts, blood is not only ejected into
the aorta but also back up into the left atrium.
 This causes left atrial volume and pressure to increase
during ventricular systole. During ventricular diastolic
filling, the elevated pressure within the left atrium is
transmitted to the left ventricle during filling so that left
ventricular EDV (and pressure) increases.
 This would cause wall stress (afterload) to increase if it were
not for the reduced outflow resistance because of mitral
regurgitation that tends to decrease afterload during ejection
because of reduced pressure development by the ventricle.
 The net effect of these changes is that the width of the
pressure-volume loop is increased (i.e., SV is increased);
however, ejection into the aorta (forward flow) is reduced.
 The increased ventricular "stroke volume" (measured as the
EDV minus the ESV) in this case includes the volume of blood
ejected into the aorta as well as the volume ejected back into
the left atrium.
35

Aortic Insufficiency
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 of
the closure of the aortic valve.
B. Pathologic runoff of blood
from the aorta into the left ventricle
decreases aortic diastolic blood
pressure 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

36

Aortic regurgitation 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 to
the 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.

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 the
left 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 enddiastolic 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).
37

Mitral Stenosis
Diastolic murmur of mitral stenosis
A. 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). Obstructed
ventricular 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.

Picture McGraw·Hill 2009:144-57

38

Mitral stenosis pressure-volume loop
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 in
cardiac output and aortic pressure.

 This reduction in afterload (particularly
aortic diastolic pressure) enables the endsystolic volume to decrease slightly, but not
enough to overcome the decline in enddiastolic volume.
 Therefore, because end-diastolic volume
decreases more than end-systolic volume
decreases, the stroke volume (shown as the
width of the loop) decreases
39

The End,
Thank you for your attention!!!
Also see companion PowerPoint: Cray MI, RELATIONSHIPS BETWEEN
CARDIAC OUTPUT AND VENOUS RETURN Last updated-11-13

References and suggested reading :
Costanzo LS, Cardiovascular Physiology. In Physiology: with STUDENT
CONSULT Online Access, 5e; Saunders 2013:189-95
Picture McGraw·Hill 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; McGraw·Hill 2013:254-59

40

Physiologic and pathophysiologic function of the heart

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