Cardiac Output Equals Heart Rate Times Stroke Volume

Welcome to the cardiac output lab. I'm Medi, and today we are going to turn the heart into an equation you can actually use. Cardiac output (CO) is the volume of blood your heart pumps per minute. The formula is beautifully simple: CO = HR × SV. Heart rate (HR) is the number of beats per minute, and stroke volume (SV) is the volume of blood ejected per beat, measured in milliliters. At rest, a typical adult has HR ≈ 70 bpm and SV ≈ 70 mL, giving CO ≈ 4,900 mL/min — about 4.9 liters per minute. During intense exercise, HR can climb above 180 bpm and SV can rise to 130 mL or more, pushing CO past 20 L/min. That is a four- to five-fold increase driven by TWO independent levers. Lever 1 — Heart Rate: Your autonomic nervous system controls rate in three sequential steps. First, the parasympathetic branch (vagus nerve) normally keeps a mild brake on the SA node by releasing acetylcholine. Remove the vagal brake and heart rate rises even before sympathetic nerves fire — and before circulating epinephrine from the adrenal medulla joins the response. Second, the sympathetic branch then releases norepinephrine directly onto beta-1 receptors on the SA node, further accelerating the rate (positive chronotropy). Third, the adrenal medulla releases epinephrine (adrenaline) into the bloodstream, sustaining the elevated heart rate during prolonged effort. These three mechanisms act in sequence and involve distinct molecules with distinct sources. Lever 2 — Stroke Volume: Three factors set SV. (1) Preload: the stretch of the ventricle just before contraction, determined by how much blood returns from the veins. More venous return → more stretch → stronger contraction. This is the Frank-Starling mechanism — the heart contracts more forcefully when filled more. (2) Contractility: the intrinsic squeezing power of the myocardium, boosted by sympathetic stimulation independent of preload. (3) Afterload: the pressure the ventricle must overcome to eject blood, primarily determined by aortic/arterial pressure. Higher afterload reduces SV. Here is a useful memory check: if you only increase HR and SV stays fixed, CO rises proportionally. If SV falls (say, from blood loss reducing preload) and HR does not fully compensate, CO drops and organs do not get enough oxygen. The body monitors this moment-to-moment via baroreceptors in the aortic arch and carotid sinus, feeding back to the medulla oblongata, which then adjusts both levers simultaneously. Calculation hint: always convert units first. If SV is given in mL, CO will be in mL/min. Divide by 1,000 to get L/min.