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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.
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)
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
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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: Tao Le T and Bhushan V, Cardiovascular, IN First Aid for the USMLE Step 1 2013:256
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Generated by plotting ventricular pressure against ventricular volume at many different corresponding points during a single cardiac cycle
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EDPVR, end-diastolic pressure-volume relationship; ESPVR, end-systolic pressure-volume relationship; SV, stroke volume (EDV - ESV)
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Kibble JD and Halsey CR, CV Physiology, In Medical Physiology The Big Picture ; McGraw-Hill 2009:144-57 16
Kibble JD and Halsey CR, CV Physiology, In Medical Physiology The Big Picture McGraw-Hill 2009:144-57
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Effects of changes in preload, afterload, and contractility on the ventricular pressurevolume loop
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.
Source: Klabunde, RE, Ventricular Pressure-Volume Relationship
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.
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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)
A shows effects of increasing preload (enddiastolic volume) with and without a secondary increase in afterload (aortic pressure)
Source: Klabunde, RE, Ventricular Pressure-Volume Relationship
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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.
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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.
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Starling curve
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) , -blockers, calcium channel blockers
Source: Tao Le T and Bhushan V, Cardiovascular, IN First Aid for the USMLE Step 1 2013:554
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
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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) 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 2nd Ed., LLW 2012 http://www.cvphysiology.com/textbook.htm
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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
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)
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Kibble JD and Halsey CR, CV Physiology, In Medical Physiology The Big Picture; McGraw-Hill 2009:144-57
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
Kibble JD and Halsey CR, CV Physiology, In Medical Physiology The Big Picture; McGraw-Hill 2009:144-57
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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
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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.
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.
Kibble JD and Halsey CR, CV Physiology, In Medical Physiology The Big Picture McGrawHill 2009:144-57
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This leads to a decrease in stroke volume by the Frank-Starling mechanism and a fall in cardiac output and aortic pressure.
Source: Klabunde, RE, Ventricular Pressure-Volume Relationship
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
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