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7.4 — The Cardiac Cycle and Cardiac Output
The two ventricles must pump exactly the same volume, beat after beat, for a lifetime. If the left pumped even 1 percent more than the right, the lungs would empty of blood within a few hours; if it pumped 1 percent less, they would flood.
Nothing measures this and nothing corrects it centrally. The matching happens automatically, through a property of muscle itself, and it is the most elegant piece of physiology in the cardiovascular system.
One cycle, in order
At 75 beats per minute, one cycle lasts 0.8 seconds. Systole (contraction) takes about 0.3 seconds and diastole (relaxation) about 0.5.
That ratio matters. The heart spends most of each cycle relaxed, and it fills during that time — and, as Chapter 7.7 covers, the left ventricle also receives its own blood supply during that time. When the heart rate rises, diastole shortens far more than systole, so at very high rates both filling and coronary supply are compromised.
Follow the left ventricle through one cycle.
1. Ventricular filling (diastole). The mitral valve is open, the aortic valve is closed. Blood flows in from the atrium — and about 70 to 80 percent of filling is passive, simply blood running downhill from the atrium because ventricular pressure is near zero.
2. Atrial contraction. The atrium contracts and adds the last 20 to 30 percent — the atrial kick.
This is why losing atrial contraction in atrial fibrillation matters (Chapter 7.3). A healthy person barely notices; someone with a stiff ventricle that fills poorly can be tipped into heart failure by it.
3. Isovolumetric contraction. The ventricle starts to contract. Pressure rises above atrial pressure, so the mitral valve slams shut — this is the first heart sound. But pressure is still below aortic pressure, so the aortic valve is still shut. Both valves are closed, so no blood moves and the volume does not change, which is what "isovolumetric" means. Pressure rises very steeply.
4. Ejection. Ventricular pressure exceeds aortic pressure, the aortic valve opens, and blood is ejected.
5. Isovolumetric relaxation. The ventricle relaxes, pressure falls below aortic pressure, the aortic valve shuts — the second heart sound. The mitral valve has not yet opened. Both closed again, no volume change, pressure falling steeply.
6. The mitral valve opens when ventricular pressure falls below atrial pressure, and filling begins again.
Every valve movement in that list happens because two pressure curves crossed. Nothing opens or closes a valve actively.
The numbers
End-diastolic volume (EDV) — the volume in the ventricle just before it contracts. About 120 ml.
End-systolic volume (ESV) — what remains after ejection. About 50 ml.
Stroke volume (SV) — what was ejected.
SV = EDV - ESV = 120 - 50 = 70\ \text{ml}
Ejection fraction (EF) — the proportion ejected.
EF = \frac{SV}{EDV} = \frac{70}{120} \approx 58\%
Normal ejection fraction is 55 to 70 percent, and it is the single most quoted number in cardiology. Note that the heart never empties — even at maximum effort, a substantial residual volume remains, and that reserve is what allows stroke volume to increase.
Cardiac output (CO) — the volume pumped per minute.
CO = SV \times HR = 70\ \text{ml} \times 75 = 5{,}250\ \text{ml/min} \approx 5\ \text{L/min}
Which is approximately your entire blood volume, every minute, at rest.
In hard exercise, stroke volume can rise to about 120 ml and heart rate to 190, giving:
CO = 120 \times 190 \approx 22.8\ \text{L/min}
Elite endurance athletes reach 35 to 40 L/min, almost entirely through a larger stroke volume — their maximum heart rates are no higher than anyone else's, and often lower.
Cardiac index — cardiac output divided by body surface area, normally 2.5 to 4 L/min/m². Used because a 50 kg person and a 100 kg person need different absolute outputs.
The Frank–Starling mechanism
This is the answer to the matching problem posed at the start.
The principle: the more the ventricle is filled, the more forcefully it contracts, and the more it ejects.
The mechanism is the length–tension relationship from Chapter 6.1. At normal filling volumes, cardiac muscle sarcomeres are shorter than their optimum. Filling the ventricle stretches them toward the optimal overlap of actin and myosin, so more cross-bridges can form and the contraction is stronger.
In cardiac muscle there is a second contribution: stretch also increases the sensitivity of the contractile proteins to calcium, so the same calcium signal produces more force.
Now apply it to the two ventricles. Suppose the right ventricle ejects slightly more than the left on one beat. That extra blood arrives at the left atrium and left ventricle, increasing its filling. The left ventricle is therefore stretched more, contracts more forcefully, and ejects more on the next beat. The imbalance corrects itself within a beat or two.
No sensor, no controller, no nerve. It is a property of the muscle. This is why a denervated transplanted heart works perfectly well, and why the matching is precise over billions of beats.
It also explains the response to standing up, to blood loss, and to intravenous fluids. Give a litre of fluid and venous return increases, filling increases, and stroke volume rises automatically. This is why fluid resuscitation works in shock — you are moving the heart up its Starling curve.
And it explains the limits. In a failing heart, the curve is flattened and shifted down, so the same filling produces less output — and pushing filling higher stops helping and starts causing congestion, with fluid backing up into the lungs. This is exactly why fluid must be given cautiously in heart failure, and why the same litre that saves one patient drowns another.
What determines cardiac output
Three factors for stroke volume, plus heart rate.
Preload — how much the ventricle is stretched before contraction, essentially the end-diastolic volume. More preload, more output, via Frank–Starling. Determined by venous return, blood volume, venous tone, and the calf muscle pump (Chapter 6.6).
Afterload — the pressure the ventricle must overcome to eject. Essentially arterial pressure. More afterload, less output.
This is why treating high blood pressure helps a failing heart — reducing afterload means the ventricle can eject more with the same contractile effort. And it is why aortic stenosis is so damaging (Chapter 7.2): the valve creates an enormous fixed afterload.
Contractility — the intrinsic forcefulness of contraction at a given preload and afterload.
Increased by sympathetic stimulation and adrenaline (via beta-1 receptors, which increase calcium entry), digoxin (Chapter 1.4), and drugs used in intensive care such as dobutamine.
Decreased by beta-blockers, calcium channel blockers, acidosis, hypoxia, and damaged muscle after a heart attack.
Heart rate. Output rises with rate — up to a point. Above about 180 beats per minute, diastole becomes so short that the ventricle cannot fill properly, and stroke volume falls faster than rate rises, so output actually decreases.
This is why a very fast arrhythmia causes collapse even though the heart is beating vigorously. And it is why slowing the rate in fast atrial fibrillation improves the patient — the heart fills better.
Autonomic control
The heart's own pacemaker sets the baseline; the autonomic nervous system adjusts it (Chapter 11.9).
Sympathetic stimulation — noradrenaline on beta-1 receptors. Increases rate, contractility, and conduction speed through the AV node. Response takes a few seconds and lasts tens of seconds, because it works through the second messenger cascade of Chapter 1.8.
Parasympathetic stimulation — the vagus nerve, acetylcholine on muscarinic receptors. Decreases rate and slows AV conduction. Almost no effect on ventricular contractility, because vagal supply to the ventricles is sparse.
Vagal effects are fast — within one beat — and switch off fast, because acetylcholine opens potassium channels directly rather than through a slow cascade.
That difference in speed is directly useful. A vagal manoeuvre — a Valsalva strain, or carotid sinus massage — can terminate a fast rhythm arising above the ventricles by transiently blocking the AV node. A patient blowing hard into a syringe can stop their own tachycardia in seconds, which is a genuinely satisfying piece of applied physiology.
And the same reflexes explain fainting. In a vasovagal faint, a surge of vagal activity slows the heart while sympathetic tone to the blood vessels falls, so blood pressure drops and the brain is briefly underperfused. Lying the person down restores it immediately, because it removes the need to pump uphill — which is why you lie a fainting person flat and raise their legs rather than sitting them up.
Heart failure, in terms of this chapter
Heart failure means the heart cannot deliver enough output for the body's needs at normal filling pressures. The two words that matter are "enough" and "at normal filling pressures", because it can fail in two quite different ways.
Reduced ejection fraction (HFrEF) — the pumping is weak. EF below about 40 percent. Usually from previous heart attack, or dilated cardiomyopathy.
Preserved ejection fraction (HFpEF) — the ventricle is stiff and cannot fill properly, so end-diastolic volume is small even though the percentage ejected is normal. The output is inadequate despite a normal ejection fraction. Associated with hypertension, age, diabetes and obesity, and it accounts for around half of heart failure cases.
HFpEF is harder to treat, because most heart failure drugs improve contraction and the problem here is relaxation. This is an area where the evidence has been genuinely thin until recently, and where SGLT2 inhibitors (Chapter 1.4) have produced the first clear benefits.
The symptoms follow from where the blood backs up.
Left heart failure → blood backs up into the lungs → breathlessness, worse lying flat (orthopnoea, because lying down returns fluid from the legs to the circulation), and waking at night gasping. This is why heart failure patients sleep propped on several pillows, and asking how many pillows someone uses is a real clinical question.
Right heart failure → blood backs up into the systemic veins → swollen ankles, an enlarged tender liver, distended neck veins, and fluid in the abdomen.
Left heart failure is the commonest cause of right heart failure, because the raised pressure passes back through the lungs. Chapter 18.4 covers management.
What the next page fixes
The heart generates the pressure; the vessels distribute it and control where it goes. Chapter 7.5 covers the vessels — why arteries are elastic, why capillaries are one cell thick, why veins hold two thirds of your blood, and how the same total flow is divided between organs that need it and organs that do not.