Lecture #29: Physiology of Cardiac Cycle Part 2- Loops, Laws, and Cardiac Output

What does the Law of Laplace describe in the ventricle?

The Law of Laplace relates ventricular pressure (P) to tension (T) in the ventricular wall divided by ventricular radius (r); ventricular wall tension is influenced by ventricular pressure and radius.

How does increasing ventricular radius affect wall tension according to the Law of Laplace?

For a given ventricular pressure, increasing ventricular radius increases the wall tension required; therefore, a dilated ventricle has increased wall tension.

What is preload?

Preload refers to ventricular end-diastolic volume (EDV), representing ventricular filling and passive stretch before contraction.

What is afterload?

Afterload is the arterial pressure, such as aortic or pulmonary artery pressure, that the ventricle must overcome to eject blood; it is proportional to arterial pressure.

What is stroke volume (SV)?

Stroke volume is the amount of blood ejected by the heart during each beat.

How is stroke volume calculated?

SV = EDV − ESV, where EDV is end-diastolic volume and ESV is end-systolic volume.

What is cardiac output (CO)?

Cardiac output is the amount of blood pumped by the heart per unit of time.

How is cardiac output calculated?

CO = SV × HR, where stroke volume is expressed in mL/beat and heart rate in beats/min.

What is the relationship between MAP, cardiac output, and total peripheral resistance?

MAP = CO × TPR; changes in cardiac output and total peripheral resistance contribute to maintenance of mean arterial pressure.

What are the major determinants of stroke volume?

Preload, afterload, and myocardial contractility are the major factors regulating stroke volume.

What are the four major phases of the ventricular pressure-volume loop?

Ventricular filling, isovolumetric contraction, ventricular ejection, and isovolumetric relaxation.

What happens during ventricular filling on a pressure-volume loop?

The mitral valve is open and the aortic valve is closed; LV volume increases from ESV toward EDV with relatively little increase in pressure.

What event marks the end of ventricular filling on the PV loop?

Closure of the mitral valve at EDV marks the end of ventricular filling and beginning of isovolumetric contraction.

What happens during isovolumetric contraction on the PV loop?

Both valves are closed, so ventricular pressure rises rapidly while ventricular volume remains constant at EDV.

What causes the aortic valve to open on the PV loop?

The aortic valve opens when LV pressure becomes sufficient to overcome aortic pressure, initiating ventricular ejection.

What happens during ventricular ejection on the PV loop?

The aortic valve is open and the mitral valve is closed; blood leaves the LV, causing ventricular volume to decrease from EDV toward ESV.

What event marks the end of ventricular ejection?

Closure of the aortic valve marks the end of ventricular ejection and the beginning of isovolumetric relaxation.

What happens during isovolumetric relaxation on the PV loop?

Both valves are closed; LV pressure rapidly decreases while ventricular volume remains constant at ESV.

What causes the mitral valve to open on the PV loop?

The mitral valve opens when LV pressure falls sufficiently below left atrial pressure, initiating ventricular filling.

What does the width of the pressure-volume loop represent?

The width of the PV loop represents stroke volume because SV = EDV − ESV.

What does the rightmost point of a normal PV loop represent?

End-diastolic volume (EDV), the maximum ventricular volume immediately before systole and a measure of preload.

What does the leftmost point of a normal PV loop represent?

End-systolic volume (ESV), the volume remaining in the ventricle after ejection.

What does the Frank-Starling law state?

Stroke volume increases as ventricular EDV increases; greater passive ventricular stretch or preload produces greater force of contraction and therefore greater stroke volume.

How does increased preload affect EDV and stroke volume?

Increased preload increases EDV and ventricular stretch, producing a stronger contraction and increased stroke volume through the Frank-Starling mechanism.

How does increased preload affect ESV according to the lecture?

Increased preload increases EDV and stroke volume while ESV remains unchanged because the ventricle generates enough additional force to eject the extra returned blood.

How does venous vasoconstriction affect preload?

Venous vasoconstriction increases venous return, which increases ventricular filling, EDV, ventricular stretch, and therefore preload.

Why is the Frank-Starling mechanism physiologically important?

It allows the heart to eject additional blood returned through the veins and helps prevent pooling of blood in the pulmonary and systemic circulations, including during postural changes.

How does increased afterload affect stroke volume?

Increased afterload decreases stroke volume because the ventricle must overcome a greater arterial pressure to eject blood.

How does increased afterload affect ESV?

Increased afterload decreases stroke volume and increases ESV because more blood remains in the ventricle after systole.

How can hypertension affect afterload and cardiac output?

Hypertension increases arterial pressure and therefore afterload, which can decrease stroke volume and consequently decrease cardiac output.

What chronic cardiac adaptation can result from hypertension?

Chronic hypertension can lead to left ventricular hypertrophy.

What is myocardial contractility?

Contractility is an intrinsic measure of cardiac performance that determines the force of ventricular contraction independent of preload; it can be augmented by factors such as norepinephrine.

How does increased contractility affect stroke volume and ESV?

Increased contractility causes greater ventricular emptying, decreasing ESV and increasing stroke volume.

How does decreased contractility affect stroke volume?

Decreased contractility reduces ventricular emptying, increasing ESV and decreasing stroke volume.

How does norepinephrine affect myocardial contractility?

Norepinephrine increases myocardial contractility, resulting in increased ventricular shortening and stroke volume with decreased ESV.

What initiates cardiac muscle contraction at the cellular level?

Arrival of an action potential increases cytoplasmic Ca²⁺ concentration, which activates cardiac muscle contraction.

What are the two sources of Ca²⁺ used for cardiac muscle contraction?

Ca²⁺ comes from extracellular fluid and the sarcoplasmic reticulum (SR).

How does SERCA contribute to cardiac muscle relaxation?

SERCA, the sarcoplasmic/endoplasmic reticulum Ca²⁺-ATPase, transports cytoplasmic Ca²⁺ back into the sarcoplasmic reticulum.

How does the Na⁺/Ca²⁺ exchanger remove Ca²⁺ from cardiac cells?

The exchanger uses the movement of 3 Na⁺ ions down their electrochemical gradient into the cell to transport 1 Ca²⁺ ion out of the cell against its gradient.

What is the effect of digoxin on the Na⁺/K⁺-ATPase?

Digoxin inhibits the Na⁺/K⁺-ATPase, causing intracellular Na⁺ concentration to increase.

How does digoxin ultimately increase cardiac contractility?

Digoxin inhibits Na⁺/K⁺-ATPase → intracellular Na⁺ increases → the Na⁺/Ca²⁺ exchanger slows → less Ca²⁺ leaves the cell → cytoplasmic Ca²⁺ increases → force of contraction increases.

What is the normal function of the Na⁺/K⁺-ATPase?

It uses ATP to transport K⁺ into the cell and Na⁺ out of the cell against their electrochemical gradients.

How is ejection fraction calculated?

EF (%) = [(EDV − ESV)/EDV] × 100, which is equivalent to (SV/EDV) × 100.

What does ejection fraction represent?

Ejection fraction represents the percentage of end-diastolic ventricular blood volume that is ejected during systole.

How is cardiac output measured using the Fick principle?

Cardiac output = O₂ absorbed by the lungs per minute ÷ arteriovenous O₂ difference; the principle relates whole-body O₂ consumption to the difference between arterial and venous O₂ content.

How does increasing heart rate initially affect stroke volume?

Increasing HR decreases the time spent in diastole, reducing ventricular filling and therefore decreasing stroke volume.

What happens to cardiac output as HR increases to approximately 180–200 bpm?

Cardiac output increases because the increase in HR more than compensates for the decrease in stroke volume.

What happens when HR increases beyond approximately 180–200 bpm?

Both stroke volume and cardiac output decrease because excessive tachycardia markedly reduces diastolic filling time.

Which factors listed in the lecture are directly proportional to myocardial O₂ demand?

Myocardial O₂ demand is directly proportional to contractility, afterload, heart rate, and ventricular diameter/wall tension.

How do preload, afterload, and contractility alter stroke volume?

Increased preload increases SV through Frank-Starling; increased afterload decreases SV and increases ESV; increased contractility increases SV and decreases ESV.