Cardiac Physiology Quiz to Master Heart Function Basics

Cardiac output equals heart rate multiplied by stroke volume. If heart rate is 70 beats per minute and stroke volume is 70 milliliters per beat, cardiac output equals 4900 milliliters per minute or 4.9 liters per minute. This formula directly quantifies total blood pumped each minute. Other combinations mix unrelated variables that do not represent systemic blood flow, making them physiologically incorrect representations of cardiac performance.

Mean arterial pressure equals cardiac output multiplied by peripheral resistance. For example, if cardiac output is 5 liters per minute and resistance equals 18 mmHg per liter per minute, MAP approximates 90 mmHg. This reflects steady perfusion pressure across systemic circulation. Other formulas ignore vascular resistance or stroke determinants, failing to capture the hemodynamic interaction necessary to maintain adequate organ blood flow under varying physiological conditions.

Stroke volume equals end-diastolic volume minus end-systolic volume. If EDV equals 120 milliliters and ESV equals 50 milliliters, stroke volume becomes 70 milliliters. This subtraction represents actual ejected blood volume per beat. Adding or reversing values would produce negative or inflated numbers. Physiologically, only the difference between filled volume and residual volume accurately represents mechanical ejection efficiency during systole in a functioning ventricle.

Ejection fraction equals stroke volume divided by end-diastolic volume. Using EDV of 120 milliliters and SV of 70 milliliters, ejection fraction equals 58 percent. This ratio measures pumping efficiency rather than total volume. Dividing EDV by ESV exaggerates output, while multiplication distorts proportional meaning. Clinically, normal ejection fraction ranges from 55 to 70 percent, making this calculation essential for assessing systolic performance quantitatively.

The first heart sound occurs when atrioventricular valves close at onset of systole. As ventricular pressure exceeds atrial pressure, mitral and tricuspid valves shut, preventing regurgitation. This abrupt tension generates audible vibration. Opening valves does not create sufficient turbulence for sound production. Timing corresponds with isovolumetric contraction phase, making valve closure mechanically and acoustically responsible for the first heart sound heard during auscultation.

The second heart sound results from closure of aortic and pulmonic valves at end of systole. When ventricular pressure falls below arterial pressure, semilunar valves snap shut, preventing backflow. This produces distinct acoustic vibration. Opening valves generates smoother laminar flow without sharp sound. The timing corresponds with onset of isovolumetric relaxation, marking completion of ventricular ejection and separation of systolic and diastolic phases clearly.

When ventricular pressure is lower than atrial pressure, atrioventricular valves open, allowing passive ventricular filling. Pressure gradients drive blood from atria into ventricles. If ventricular pressure were higher, valves would close. Semilunar valves remain closed because arterial pressure exceeds ventricular pressure during filling. This phase increases end-diastolic volume, directly influencing preload and stroke volume through the Frank-Starling relationship in healthy myocardium.

After atrial contraction, ventricular contraction begins. Atrial systole tops off ventricular volume, increasing EDV slightly before pressure rises sharply in ventricles. Once ventricular pressure exceeds atrial pressure, AV valves close. Isovolumetric contraction follows immediately before ejection occurs. This sequence ensures maximal preload and coordinated timing between chambers, optimizing stroke volume and preventing backward blood movement during early systolic pressure development.

LaPlace’s Law states that wall tension equals pressure multiplied by radius divided by wall thickness. As ventricular radius increases, more tension is required to generate identical pressure. For example, doubling radius doubles required tension if thickness remains constant. This explains why dilated hearts must work harder and why hypertrophy can temporarily compensate by increasing wall thickness to normalize tension demands.

Increased preload raises end-diastolic volume, stretching myocardial fibers. According to Frank-Starling mechanism, greater stretch enhances cross-bridge formation and calcium sensitivity, increasing stroke volume. For instance, raising EDV from 110 to 130 milliliters increases fiber length and force generation proportionally. This intrinsic regulation allows heart output to match venous return without external neural input, preserving circulatory balance during exercise or volume expansion.

Increased afterload means ventricles pump against higher arterial pressure. More blood remains after contraction, increasing end-systolic volume. For example, elevated systemic resistance raises residual volume from 50 to 70 milliliters, reducing effective ejection. Wall tension rises according to LaPlace’s Law. Chronic afterload elevation can trigger hypertrophy as compensation. Immediate effect is reduced emptying efficiency and higher mechanical workload on myocardium.

Cardiac muscle has a prolonged absolute refractory period due to sustained calcium influx during plateau phase. This prevents summation and tetanus. If contractions overlapped, relaxation would be incomplete, eliminating filling time and cardiac output. The refractory duration nearly equals contraction time, ensuring rhythmic cycles. Skeletal muscle differs because it has shorter refractory periods allowing summation, which would be fatal in cardiac tissue.

Sympathetic stimulation increases calcium influx through L-type channels and enhances calcium release from sarcoplasmic reticulum. Elevated intracellular calcium increases cross-bridge cycling and force generation. If calcium entry rises by even small percentages, contractile strength increases measurably. Beta-adrenergic activation also speeds relaxation through faster calcium reuptake, improving efficiency and increasing cardiac output during stress or exercise conditions.

Calcium-induced calcium release occurs when calcium entering through L-type channels triggers ryanodine receptors on sarcoplasmic reticulum to release additional calcium. This amplifies contraction strength. A small extracellular influx produces larger intracellular release. Without this mechanism, contraction would be weak. The amplification ensures sufficient calcium binds troponin, initiating cross-bridge cycling and coordinated myocardial contraction during each action potential.

Purkinje fibers conduct rapidly because of their large diameter and strong inward sodium current. Larger diameter reduces internal resistance, increasing conduction velocity according to cable theory. Rapid sodium influx accelerates depolarization slope. Combined, these features allow near-simultaneous ventricular activation, optimizing synchronized contraction and maximizing stroke volume efficiency compared to slower conduction pathways within ordinary myocardial fibers.