Cardiac Anatomy and Physiology

The heart is a fist-sized muscular pump that beats roughly 100,000 times a day and moves about 7,000 litres of blood, yet almost never rests. To understand cardiology at all — arrhythmias, heart failure, valve disease, myocardial infarction — you first have to understand the healthy heart as a piece of engineering: four chambers, four valves, its own blood supply, a mechanical pumping cycle, and an electrical system that orchestrates every beat. Get this foundation right and the rest of cardiology becomes logical rather than a list to memorise.

This page ties the anatomy directly to the physiology, and then to the electrocardiogram (ECG), so that when you look at a tracing you can picture exactly what the muscle is doing.

Learning Objectives

• Identify the four chambers and four valves of the heart and describe the direction of blood flow through them.
• Trace the coronary circulation and predict which region of myocardium is at risk when a given artery occludes.
• Describe the phases of the cardiac cycle and relate pressures, volumes, valve events, and heart sounds.
• Explain the cardiac conduction system and why the atrioventricular (AV) node introduces a deliberate delay.
• Map each wave and interval of the ECG onto the underlying electrical event in the heart.
• Appreciate the historical experiments (Harvey, Einthoven) that established modern cardiac science.

Quick Answer

The heart has four chambers: two thin-walled atria that receive blood and two thick-walled ventricles that eject it. Deoxygenated blood enters the right atrium, passes the tricuspid valve into the right ventricle, and is pumped through the pulmonary valve to the lungs; oxygenated blood returns to the left atrium, crosses the mitral valve into the left ventricle, and is ejected through the aortic valve to the body. The heart supplies itself through the right and left coronary arteries. Each beat is a coordinated cycle of filling (diastole) and ejection (systole) driven by an electrical impulse that starts in the sinoatrial (SA) node, pauses at the AV node, and spreads through the His–Purkinje system. The ECG is a surface recording of that electrical wave: the P wave is atrial depolarisation, the QRS complex is ventricular depolarisation, and the T wave is ventricular repolarisation.

Where It Came From

For most of history, no one knew blood circulated. The Greek physician Galen (2nd century AD) taught that the liver continuously manufactured blood, which the tissues consumed like fuel, and that blood seeped from the right side of the heart to the left through invisible pores in the septum. This model went essentially unchallenged for about 1,400 years — an extraordinary example of authority outlasting evidence.

The revolution came from William Harvey, an English physician who published De Motu Cordis ("On the Motion of the Heart and Blood") in 1628. Harvey's genius was quantitative. He estimated the volume ejected per beat and multiplied by the heart rate, showing that the heart pumps far more blood in an hour than the body could possibly manufacture from food. The only logical conclusion was that the same blood must circulate in a closed loop — out through the arteries, back through the veins. He demonstrated one-way flow with a simple experiment: compressing an arm vein and watching that the valves permitted blood to move only toward the heart. Harvey could not see the capillaries linking arteries to veins (Marcello Malpighi found them under the microscope in 1661), but he had proved circulation by reasoning from measurement — the birth of cardiac physiology as a science.

The second landmark was electrical. Physiologists in the 19th century knew the heart produced tiny currents, but these were too faint and fast to record reliably. Willem Einthoven, a Dutch physiologist, solved this around 1901–1903 by inventing the string galvanometer, a device sensitive enough to capture the heart's electrical signal from the body surface. He named the deflections P, Q, R, S, and T (starting mid-alphabet, partly to leave room for corrections), defined the three limb leads (Einthoven's triangle), and correlated waveforms with cardiac events. His work earned the 1924 Nobel Prize and created the ECG — still, a century later, the first test ordered for chest pain anywhere in the world. The need driving both men was the same: to replace speculation about the beating heart with objective, reproducible measurement.

Chambers, Walls, and the Direction of Flow

The heart is really two pumps side by side, working in series. The right heart handles the pulmonary circuit (to the lungs, a low-pressure system); the left heart handles the systemic circuit (to the whole body, a high-pressure system).

Blood flow follows one continuous path:

1. Deoxygenated blood returns from the body via the superior and inferior venae cavae into the right atrium.
2. It crosses the tricuspid valve into the right ventricle.
3. The right ventricle ejects it through the pulmonary valve into the pulmonary arteries to the lungs.
4. Oxygenated blood returns via the pulmonary veins to the left atrium.
5. It crosses the mitral valve into the left ventricle.
6. The left ventricle ejects it through the aortic valve into the aorta and the systemic circulation.

The wall thicknesses tell a physiological story. The atria are thin because they only need to nudge blood into the ventricles a short distance. The right ventricle is moderately thick because pulmonary pressures are low (around 25/10 mmHg). The left ventricle is by far the thickest, roughly three times the right, because it must generate systemic pressures (around 120/80 mmHg) to perfuse the entire body. This is why the left ventricle is the chamber that "fails" most conspicuously in hypertension and why its muscle is the most vulnerable to ischaemia.

The Four Valves: One-Way Doors

Valves ensure flow goes forward only. There are two atrioventricular (AV) valves between atria and ventricles, and two semilunar valves at the ventricular outflows.

• Tricuspid valve (right AV): three leaflets, between right atrium and right ventricle.
• Mitral valve (left AV): two leaflets ("bicuspid"), between left atrium and left ventricle.
• Pulmonary valve (semilunar): right ventricle to pulmonary artery.
• Aortic valve (semilunar): left ventricle to aorta.

The AV valves are tethered by thin cords, the chordae tendineae, to papillary muscles in the ventricular wall. When the ventricle contracts, the papillary muscles tense the cords and stop the leaflets from being blown backward into the atrium (prolapse). This is clinically vital: after a myocardial infarction, a papillary muscle can rupture, causing sudden, severe mitral regurgitation and acute pulmonary oedema.

A useful memory aid for auscultation: valves are best heard downstream of where they sit. Aortic — right 2nd intercostal space; Pulmonary — left 2nd space; Tricuspid — lower left sternal border; Mitral — 5th space, midclavicular line (the apex). "APT M" from top to apex.

Coronary Circulation: The Heart Feeds Itself

The myocardium is too thick to get oxygen by diffusion from the blood inside the chambers, so it has its own arteries. The right and left coronary arteries arise from the aorta just above the aortic valve (from the aortic sinuses).

• The left main coronary artery quickly divides into the left anterior descending (LAD) — supplying the anterior wall, most of the interventricular septum, and the apex — and the left circumflex (LCx) — supplying the lateral and posterior left ventricle.
• The right coronary artery (RCA) supplies the right ventricle, the inferior wall, and in most people the SA and AV nodes.

Because each artery supplies a defined territory, an ECG can localise an infarct. A worked example: a 58-year-old man with crushing chest pain shows ST elevation in leads V1–V4. Those are the anterior leads, so the culprit is almost certainly the LAD — sometimes nicknamed "the widow-maker" because it feeds so much muscle. By contrast, ST elevation in leads II, III, and aVF points to the inferior wall and the RCA; watch such patients for bradycardia and heart block, because the RCA also feeds the conduction nodes.

One more physiological subtlety: the left ventricle is perfused mainly during diastole, because in systole the contracting muscle squeezes its own coronary vessels shut. This is why very fast heart rates (which shorten diastole) or very low diastolic blood pressure can worsen cardiac ischaemia.

The Cardiac Cycle: Pressures, Volumes, and Sounds

The cardiac cycle is the sequence of events in one heartbeat, divided into diastole (relaxation and filling) and systole (contraction and ejection). Blood always moves down pressure gradients, and valves open or close passively when the pressure on one side exceeds the other.

Walk through the left heart:

1. Ventricular filling (diastole). The mitral valve is open; blood flows from left atrium to ventricle passively. Late in diastole the atrium contracts (the "atrial kick"), topping off the ventricle. The ventricle now holds its end-diastolic volume (about 120 mL).
2. Isovolumetric contraction. The ventricle starts contracting; pressure rises and slams the mitral valve shut — this makes the first heart sound, S1 ("lub"). Both valves are momentarily closed, so volume is fixed while pressure climbs steeply.
3. Ejection (systole). When ventricular pressure exceeds aortic pressure, the aortic valve opens and blood is ejected. About 70 mL leaves (the stroke volume), leaving an end-systolic volume of ~50 mL.
4. Isovolumetric relaxation. The ventricle relaxes; pressure falls below aortic pressure, so the aortic valve snaps shut — the second heart sound, S2 ("dub"). Again both valves closed, volume fixed.
5. Ventricular pressure falls below atrial pressure, the mitral valve reopens, and filling begins again.

Two quick derived numbers students are always asked: Ejection fraction = stroke volume ÷ end-diastolic volume = 70 ÷ 120 ≈ 58% (normal is roughly 55–70%). Cardiac output = stroke volume × heart rate ≈ 70 mL × 70 beats/min ≈ 4,900 mL/min, close to 5 L/min at rest.

The heart sounds are simply valves closing: S1 = AV valves closing (start of systole), S2 = semilunar valves closing (end of systole). Extra sounds (S3, S4) and murmurs are variations on this theme — a murmur is turbulent flow through a narrowed (stenotic) or leaky (regurgitant) valve.

The Conduction System and Why the AV Node Delays

The heart does not need the brain to beat — it generates its own rhythm through specialised pacemaker and conducting tissue.

• Sinoatrial (SA) node, in the right atrium, is the natural pacemaker (~60–100 beats/min). It fires spontaneously and sets the rate.
• The impulse spreads across both atria, causing them to contract, and converges on the atrioventricular (AV) node.
• The AV node deliberately slows conduction (a delay of ~0.1 second). This pause lets the atria finish emptying into the ventricles before the ventricles contract — the timing that makes the atrial kick useful.
• From the AV node the signal races down the bundle of His, splits into the right and left bundle branches, and fans out through the Purkinje fibres, which deliver the impulse rapidly to the ventricular muscle so it contracts almost as a unit, from apex upward.

If the SA node fails, lower tissues can take over but at slower intrinsic rates (AV junction ~40–60/min; ventricular escape ~20–40/min) — the physiological basis of "escape rhythms" and why complete heart block produces a dangerously slow pulse.

How the ECG Reflects the Heart

The ECG records the summed electrical activity of the heart from electrodes on the skin. Each feature corresponds to a mechanical/electrical event:

ECG feature	Electrical event	Mechanical correlate
P wave	Atrial depolarisation	Atria contract
PR interval	SA to AV conduction (includes AV delay)	Time for atria to fill ventricles
QRS complex	Ventricular depolarisation	Ventricles contract
ST segment	Ventricles fully depolarised (plateau)	Ejection
T wave	Ventricular repolarisation	Ventricles relax

Notice there is no visible wave for atrial repolarisation — it is small and buried inside the large QRS. The PR interval is essentially the AV nodal delay made visible; if it lengthens, conduction through the AV node is slowing (first-degree heart block). A wide QRS means the ventricles are being activated slowly or abnormally (e.g. a bundle branch block, where one bundle is broken and the impulse spreads muscle-to-muscle instead of through Purkinje fibres). ST-segment elevation signals acute injury, classically myocardial infarction. This direct mapping — Einthoven's legacy — is why the ECG remains the single most informative bedside cardiac test.

Real-World Applications

• Chest pain triage. An ECG in the first minutes localises an infarct (anterior LAD vs inferior RCA) and guides emergency angioplasty. Minutes of muscle saved translate directly into survival and preserved ejection fraction.
• Heart failure. Understanding stroke volume and ejection fraction underpins the distinction between reduced-EF failure (weak pump) and preserved-EF failure (stiff ventricle that fills poorly) — different diseases with different treatments.
• Valve disease. Auscultation locations and cycle timing let a clinician distinguish, for example, aortic stenosis (a systolic murmur) from mitral regurgitation at the bedside before any imaging.
• Pacemakers. When the SA or AV node fails, an artificial pacemaker substitutes for the conduction system — a direct engineering translation of the physiology.
• Everyday relevance. Why athletes have slow resting pulses (high vagal tone on the SA node), why caffeine can cause palpitations, and why fainting can follow a sudden drop in cardiac output all follow from this material.

Common Mistakes

1. "The left side of the heart carries deoxygenated blood." Wrong — it is the reverse. The right heart handles deoxygenated (venous) blood going to the lungs; the left heart handles oxygenated blood going to the body. The confusion arises because on a diagram the patient's left is on the viewer's right. Always orient anatomy to the patient, not the page.
2. "The QRS complex is when the ventricles relax." No. QRS is ventricular depolarisation, which triggers contraction. The T wave is repolarisation (relaxation). Mislabelling this reverses the entire timing of the cardiac cycle.
3. "Valves open and close because muscles pull them." Valves are passive. They open and close purely because of pressure differences across them. The chordae tendineae only prevent prolapse; they do not actively open the leaflets. Thinking of valves as motor-driven leads to wrong predictions about murmurs.
4. "Coronary arteries fill during systole, like the rest of the body." The left ventricle is perfused mainly in diastole, because systolic contraction compresses its own vessels. This is a favourite exam trap and explains why tachycardia worsens ischaemia.

Comparison and Connections

Feature	Right ventricle	Left ventricle
Circuit served	Pulmonary (lungs)	Systemic (body)
Pressure generated	Low (~25/10 mmHg)	High (~120/80 mmHg)
Wall thickness	Thinner	~3x thicker
Outflow valve	Pulmonary	Aortic

Systole vs diastole: systole = contraction/ejection (S1 marks its start); diastole = relaxation/filling (S2 marks its start). Diastole is normally longer at rest, which is fortunate because it is when the coronaries fill.

Depolarisation vs contraction: depolarisation is the electrical trigger (what the ECG shows); contraction is the mechanical response that follows a few milliseconds later. They are linked but not identical — a heart can be electrically active yet mechanically failing (pulseless electrical activity), a critical concept in resuscitation.

Practice Questions

Recall

Q: Name the valve between the left atrium and left ventricle, and state how many leaflets it has. A: The mitral (bicuspid) valve, with two leaflets.

Understanding

Q: Why does the AV node deliberately delay the impulse? A: The ~0.1 s delay allows the atria to finish contracting and completely fill the ventricles (the atrial kick) before the ventricles contract. Without it, atria and ventricles would contract together and ventricular filling would suffer, reducing stroke volume.

Application

Q: A patient shows ST elevation in leads II, III, and aVF. Which artery is likely occluded, and what conduction complication should you watch for? A: These are inferior leads, so the right coronary artery (RCA) is the likely culprit. Because the RCA usually supplies the SA and AV nodes, watch for bradycardia and AV block.

Analysis

Q: A patient's ejection fraction is 30% with an end-diastolic volume of 150 mL. Calculate the stroke volume and explain what this suggests. A: Stroke volume = EF × EDV = 0.30 × 150 = 45 mL (low). A dilated ventricle (high EDV) with a low EF ejecting little blood indicates systolic heart failure — a weak, enlarged pump. Cardiac output can only be maintained by raising heart rate, which is unsustainable.

FAQ

Is the heart on the left side of the chest? Mostly central, but it points and sits slightly left, with its apex (the tip of the left ventricle) in the left 5th intercostal space — which is why the apex beat and heart sounds are felt/heard on the left.

How can the heart keep beating outside the body or after brain death? Because the SA node generates its own rhythm (automaticity). The nervous system modulates rate but does not initiate the beat, so an isolated heart with oxygen and nutrients will continue beating for a time.

What actually makes the "lub-dub" sound? Valves closing, not opening. "Lub" (S1) is the AV valves (mitral and tricuspid) closing at the start of systole; "dub" (S2) is the aortic and pulmonary valves closing at its end. The sounds are the abrupt deceleration of blood and vibration of the closed leaflets.

Why is the left ventricle so much thicker than the right? It must generate far higher pressure to push blood through the entire body's resistance (systemic circulation), whereas the right ventricle only pushes blood a short distance through the low-resistance lungs.

If the ECG shows normal waves, does that mean the heart is pumping? Not necessarily. The ECG shows electrical activity only. In pulseless electrical activity, the electrical signal is present but the muscle is not generating an effective pulse — which is why we always check a pulse, not just the monitor.

Quick Revision

• Four chambers: right/left atria (receive), right/left ventricles (pump); left ventricle is thickest.
• Flow: body → RA → tricuspid → RV → pulmonary valve → lungs → LA → mitral → LV → aortic valve → body.
• Coronaries: LAD (anterior/septum), LCx (lateral), RCA (inferior + usually the nodes). LV perfuses in diastole.
• Cycle: diastole fills, systole ejects; S1 = AV valves close, S2 = semilunar valves close.
• Key numbers: EDV ~120 mL, SV ~70 mL, EF ~55–70%, CO ~5 L/min.
• Conduction: SA node → atria → AV node (delay) → bundle of His → bundle branches → Purkinje fibres.
• ECG: P = atrial depolarisation, QRS = ventricular depolarisation, T = ventricular repolarisation; PR = AV delay.
• History: Harvey proved circulation by measurement (1628); Einthoven invented the ECG (~1901–1903).

Related Topics

Prerequisites

• Cardiology overview
• Basic anatomy of the thorax (see ../../1._Anatomy/index.md)
• Cardiovascular physiology fundamentals (see ../../2._Physiology/index.md)

Related Topics

• Electrocardiography and rhythm interpretation (within this branch)
• Coronary artery disease and myocardial infarction (within this branch)
• Heart failure and ejection fraction (within this branch)

Next Topics

• Interpreting the 12-lead ECG in detail
• Valvular heart disease and murmurs
• Arrhythmias and the conduction system