Cardiac Output - MCAT Biology | Premier MCAT Prep

Cardiac Output

6 min read Updated Mar 26, 2026

Cardiac output (CO) answers a simple question: how much blood does the heart pump per minute? It is the single most important measure of the heart’s performance, and the MCAT tests it relentlessly - both the formula itself and the physiological factors that change it. For the physics of blood flow through vessels (Poiseuille’s law, Bernoulli’s equation), see fluid dynamics in physics.

The Core Formula

Think of it this way: the total water flowing out of a pump per minute depends on how much water per squeeze (stroke volume) multiplied by how many squeezes per minute (heart rate). Increase either one, and cardiac output goes up.

Stroke Volume

Stroke volume is the amount of blood ejected from the left ventricle with each heartbeat. It is calculated as:

Ejection fraction (EF) is the percentage of blood ejected per beat: EF = SV/EDV. A normal EF is about 55-70%. An EF below 40% indicates heart failure - the ventricle is not emptying effectively.

The Three Determinants of Stroke Volume

Stroke volume is controlled by three factors. You must know all three:

Diagram showing the factors that determine cardiac output including heart rate and stroke volume, with preload, contractility, and afterload affecting stroke volume — The major factors influencing cardiac output. Stroke volume depends on preload, contractility, and afterload. *Credit: Lumen Learning / OpenStax Anatomy and Physiology, CC BY 4.0*

1. Preload - the degree of stretch on the ventricular wall at the end of diastole. More blood returning to the heart (increased venous return) = more stretch = more preload. Preload is essentially EDV.

2. Afterload - the resistance the ventricle must overcome to eject blood. In the left ventricle, afterload is determined primarily by aortic pressure (or total peripheral resistance). Higher blood pressure = higher afterload = harder for the ventricle to eject = decreased stroke volume.

3. Contractility (inotropy) - the intrinsic strength of contraction, independent of preload. Sympathetic stimulation and epinephrine increase contractility. Contractility increases stroke volume by reducing ESV (the ventricle squeezes more completely).

The Frank-Starling Mechanism

This is arguably the most important concept in cardiovascular physiology for the MCAT.

The Frank-Starling law states: the more the ventricle fills with blood during diastole (greater preload/EDV), the more forcefully it contracts during systole, ejecting a greater stroke volume.

Why? When cardiac muscle fibers are stretched more, actin and myosin filaments reach a more optimal overlap, generating stronger cross-bridge cycling. Up to a point, more stretch = more force.

The physiological power of Frank-Starling: it automatically matches the output of the right and left ventricles. If the right ventricle suddenly pumps more blood to the lungs, more blood returns to the left atrium, increasing left ventricular preload, which increases left ventricular stroke volume. The system is self-balancing.

Autonomic Regulation of Heart Rate

Factor	Effect on HR	Effect on Contractility	Mechanism
Sympathetic stimulation	Increases (chronotropy)	Increases (inotropy)	Norepinephrine on beta-1 receptors
Parasympathetic (vagus)	Decreases	Minimal effect on ventricles	ACh on muscarinic receptors at SA/AV nodes
Epinephrine (adrenal)	Increases	Increases	Circulating catecholamine on beta-1 receptors

Diagram showing sympathetic and parasympathetic nervous system connections to the heart, with the vagus nerve providing parasympathetic input and cardiac accelerator nerves providing sympathetic input — Autonomic innervation of the heart. The vagus nerve (parasympathetic) slows the heart; sympathetic nerves speed it up and increase contractility. *Credit: Lumen Learning / OpenStax Anatomy and Physiology, CC BY 4.0*

A patient loses 1 liter of blood. Using the Frank-Starling mechanism, explain what happens to stroke volume and why.

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Stroke volume decreases. Blood loss reduces total blood volume, which decreases venous return to the heart. Less venous return means less ventricular filling (decreased preload/EDV). By the Frank-Starling mechanism, less stretch on the ventricular wall means weaker contraction and reduced stroke volume.

A patient's cardiac output is 4,900 mL/min and their heart rate is 70 bpm. What is their stroke volume? If their EDV is 130 mL, what is their ejection fraction?

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SV = CO / HR = 4,900 / 70 = 70 mL per beat. ESV = EDV - SV = 130 - 70 = 60 mL. EF = SV / EDV = 70 / 130 = 53.8%. This is at the low end of normal (55-70%), suggesting mildly reduced systolic function.