Cardiac Physiology

Core Concepts

Cardiac output: rate × stroke volume

CO = HR × SV. Using commonly taught resting values: 70–75 beats/min × ~70 mL/beat ≈ 5 L/min. Both ventricles pump equal volumes on average, or blood would accumulate on one side. Cardiac reserve is the gap between resting and maximum output; it can rise several-fold during exercise, and reduced reserve is a hallmark of heart disease. The factors trade off: at very high heart rates, diastole shortens, filling time shrinks, and output can actually decrease.

Stroke volume: preload, contractility, afterload

Preload is the stretch of the ventricular muscle at end-diastole — essentially the end-diastolic volume (EDV). The Frank-Starling law of the heart states that, within physiological limits, the more the ventricle is stretched by incoming blood, the more forcefully it contracts — a larger EDV yields a larger stroke volume. This intrinsic property — no nerves required — keeps the two ventricles in balance: whatever one side receives, it pumps out.

Contractility (inotropy) is contraction strength at a given preload — a change in the muscle's performance itself. Sympathetic stimulation (norepinephrine, epinephrine) and calcium increase it (positive inotropy); heart failure reduces it (negative inotropy). More contractility means a smaller end-systolic volume (ESV), hence a larger stroke volume and higher ejection fraction.

Afterload is the pressure the ventricle must overcome to eject — the aortic and pulmonary trunk pressure facing the semilunar valves. Increased afterload (e.g., chronic high blood pressure) makes ejection harder, so stroke volume falls and more blood remains. Afterload is why arterial pressure and cardiac output are linked.

Heart rate: the autonomic nervous system

Heart rate is set by the slope of the SA node's prepotential, which the autonomic nervous system adjusts continuously. The medulla's cardioacceleratory center sends sympathetic fibers to the SA node, AV node, and ventricular muscle; norepinephrine acts on β₁ receptors to increase heart rate (positive chronotropy) and contractility (positive inotropy). The cardioinhibitory center sends vagus fibers to the SA and AV nodes; acetylcholine acts on muscarinic receptors to slow the heart (negative chronotropy), with little direct effect on ventricular contractility. At rest, vagal tone dominates — the heart beats slower than the SA node's intrinsic rate because the vagus applies the brakes. Sympathetic activity also triggers adrenal release of epinephrine and norepinephrine, prolonging the "fight-or-flight" response.

The baroreceptor reflex

Baroreceptors are stretch receptors in the carotid sinuses and aortic arch that monitor blood pressure. When pressure rises, they fire more; the medulla increases parasympathetic and decreases sympathetic output, slowing the heart and reducing contractility — pressure falls back toward normal. When pressure falls (e.g., standing, blood pooling in the legs), they fire less, sympathetic output rises, and the heart speeds up. This classic negative feedback loop is why heart rate jumps when you stand quickly and why blood loss produces a rising heart rate.

Other influences on heart rate and output

Chemoreceptors monitor blood oxygen, carbon dioxide, and pH; strong changes influence heart rate and respiration. Ions matter: elevated extracellular potassium can depress conduction, and calcium supports contraction strength. Temperature, age, fitness, emotions, pain, and the Bainbridge reflex (increased venous return stretches the right atrium, raising heart rate) also play a role. Reference classifications (commonly taught): tachycardia = resting rate above ~100 bpm; bradycardia = below ~60 bpm — population references, not diagnoses.

Common Confusions