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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/8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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=sharing8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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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Cardiac Output Measurement
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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Cardiac Output Measurement
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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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
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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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
Source: Klabunde, RE, Ventricular Pressure-Volume Relationship
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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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
Source: Klabunde, RE, Ventricular Pressure-Volume Relationship
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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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
Source: Klabunde, RE, Ventricular Pressure-Volume Relationship
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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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
Source: Klabunde, RE, Ventricular Pressure-Volume Relationship
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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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Factors that increase inotropy
22
Source: Klabunde RE. Cardiovascular Physiology Concepts 2ndEd.
http://www.cvphysiology.com/textbook.htm
ff f h l d f l d d
http://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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)
Source: Klabunde, RE, Ventricular Pressure-Volume Relationship
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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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.
Source: Klabunde, RE, Ventricular Pressure-Volume Relationship
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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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.
Source: Klabunde, RE, Ventricular Pressure-Volume Relationship
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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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
http://www.cvphysiology.com/textbook.htm
NORMAL HEART SOUNDS & COMMON
http://www.cvphysiology.com/textbook.htmhttp://www.cvphysiology.com/textbook.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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=sharing8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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Aortic Stenosis
32
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.
Source: Klabunde, RE,
Ventricular Pressure-Volume Relationship
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.htm8/14/2019 Physiologic and Pathophysiologic Function of the Heart: Cardiac Cycle Graphs, Curves, Loops and CO Calculations
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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
Source: Klabunde, RE,
Ventricular Pressure-Volume Relationship
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,
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