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The mammalian heart is a four-chamber muscular pump that delivers blood through two circulations in series: a pulmonary loop carrying deoxygenated blood to the lungs for gas exchange, and a systemic loop carrying oxygenated blood to every tissue of the body. It contracts approximately 70 times per minute throughout life — close to three billion beats in a typical lifespan — generating its own electrical activation from a specialised pacemaker, coordinating contraction through a hierarchical conduction system, and regulating its output through autonomic, hormonal and intrinsic mechanisms. The cardiac cycle is the second-by-second sequence of pressure, volume and valve events that links chamber contraction to forward blood flow. This lesson examines heart anatomy, the cardiac cycle, the intrinsic conduction system, the regulation of cardiac output, and the clinical consequences of conduction and contractile failure. The heart is the central engine of mass transport — Section 3.3 lessons 5–7 cover its anatomy, physiology and vessels — and it is the most exam-relevant single organ in Section 3.3.
This lesson maps to AQA 7402 Section 3.3.4 — Mass transport in animals (refer to the official AQA specification document for exact wording). The specification requires that students understand the general structure of the mammalian heart and the events of the cardiac cycle, including pressure and volume changes, the operation of valves, and the regulation of cardiac output. The cardiac cycle is one of the most reliably examined topics in AQA A-Level Biology.
The heart is divided by a muscular septum into a right side (pulmonary pump) and a left side (systemic pump). Each side has two chambers: a thin-walled atrium receiving venous return, and a thick-walled ventricle ejecting blood into an artery. The four chambers, four valves, and two great vessels form a precisely choreographed unit.
flowchart LR
VC[Venae cavae<br/>deoxygenated systemic return] --> RA[Right atrium]
RA -->|tricuspid valve| RV[Right ventricle<br/>thin wall, low pressure]
RV -->|pulmonary semilunar valve| PA[Pulmonary artery]
PA --> LU[Lungs<br/>gas exchange]
LU --> PV[Pulmonary veins]
PV --> LA[Left atrium]
LA -->|bicuspid mitral valve| LV[Left ventricle<br/>thick wall, high pressure]
LV -->|aortic semilunar valve| AO[Aorta]
AO --> BODY[Systemic tissues]
BODY --> VC
The double circulation arrangement — pulmonary and systemic in series, sharing a single pump — is the mammalian and avian innovation. Reptiles and amphibians have variably mixed single or three-chamber arrangements; fish have a single-circulation, two-chamber heart. The advantage of double circulation is that systemic blood pressure can be high (driving rapid tissue perfusion) without exposing the delicate pulmonary capillary bed to that pressure.
The left ventricular wall is approximately three times thicker than the right because it must generate systemic arterial pressures (~120 mmHg systolic) against the high resistance of the systemic circulation, whereas the right ventricle generates only the pulmonary arterial pressure (~25 mmHg systolic) against the low-resistance pulmonary bed. Both ventricles eject the same stroke volume (~70 mL in an adult) per beat — a mass-balance requirement of a series circulation — but at very different pressures.
Two atrioventricular (AV) valves separate atria from ventricles. On the right is the tricuspid valve (three cusps); on the left is the bicuspid or mitral valve (two cusps). Each valve cusp is anchored by chordae tendineae (tendinous cords) to papillary muscles projecting from the ventricular wall. During ventricular contraction, the papillary muscles contract first, taking up slack in the chordae and preventing the valve cusps from being pushed backward (prolapsing) into the atrium under the rising ventricular pressure. Failure of this system — for instance, papillary muscle rupture after a myocardial infarction — produces acute mitral regurgitation and cardiogenic shock.
Two semilunar valves separate ventricles from arteries: the pulmonary semilunar valve between right ventricle and pulmonary artery, and the aortic semilunar valve between left ventricle and aorta. Each has three cusps shaped like half-moons (hence the name). They lack chordae tendineae; their cusps are passively pushed open by ventricular ejection and passively closed by the back-pressure of the arterial blood column when ventricular pressure falls below arterial pressure.
The valves are not actively opened or closed by muscle — they are passive, pressure-gated structures. They open whenever upstream pressure exceeds downstream pressure and close whenever the opposite holds. This is the most commonly misunderstood point in AQA cardiac cycle questions.
The heart muscle itself is supplied by the coronary arteries, the first branches off the aorta as it leaves the heart. The left coronary artery divides into the left anterior descending and circumflex branches; the right coronary artery supplies the right atrium and ventricle and (in most people) the AV node. Coronary blood flow is highest during ventricular diastole — paradoxically, because ventricular wall contraction during systole compresses the intramural coronary vessels and reduces flow. Heart muscle is therefore vulnerable to ischaemia when diastole is shortened (tachycardia) or when coronary arteries are stenosed (coronary artery disease). Occlusion of a coronary artery causes myocardial infarction — death of the muscle downstream.
A complete cardiac cycle lasts ~0.8 s at a resting heart rate of 75 bpm and divides into three phases.
Both atria contract simultaneously, raising atrial pressure ~5 mmHg above ventricular pressure. The AV valves are already open (they have been open throughout late diastole as venous return passively filled the ventricles); the atrial contraction adds the final ~20–25 % of ventricular filling — the "atrial kick". In healthy young people at rest, the atrial kick is a small contributor (most filling has already occurred passively); in older patients with stiff ventricles or atrial fibrillation, it becomes critical.
Ventricular muscle contracts. Ventricular pressure rises rapidly. As soon as ventricular pressure exceeds atrial pressure, the AV valves snap shut — producing the first heart sound, "lub". For a brief moment (~0.05 s) both AV and semilunar valves are closed; the ventricle is an isolated chamber whose pressure rises without volume change (isovolumetric contraction). When ventricular pressure exceeds arterial pressure (~80 mmHg for the aorta in late diastole), the semilunar valves open and blood is ejected into the aorta and pulmonary artery. Ventricular pressure peaks at ~120 mmHg in the left ventricle, ~25 mmHg in the right. Ejection slows as ventricular pressure begins to fall.
Ventricular muscle relaxes. Ventricular pressure falls. When ventricular pressure drops below arterial pressure, the semilunar valves snap shut — producing the second heart sound, "dub". Briefly, both AV and semilunar valves are again closed (isovolumetric relaxation) and ventricular pressure falls without volume change. When ventricular pressure drops below atrial pressure, the AV valves open passively and ventricular filling begins. Atria fill passively from the great veins throughout diastole, and the cycle then begins again with the next atrial systole.
| Phase | LA pressure | LV pressure | LV volume | Valves |
|---|---|---|---|---|
| Atrial systole | ~10 mmHg | ~5 mmHg rising to ~10 | 130 mL (end-diastolic) | AV open, SL closed |
| Isovolumetric contraction | falls | rising 10 → 80 mmHg | 130 mL (constant) | All closed |
| Ejection | falls then rises | 80 → 120 → 100 mmHg | 130 → 60 mL | AV closed, SL open |
| Isovolumetric relaxation | rises | 100 → 5 mmHg | 60 mL (constant) | All closed |
| Filling | high then falls | 5 mmHg | 60 → 130 mL | AV open, SL closed |
The volume change per beat (130 − 60 = 70 mL) is the stroke volume. The fraction ejected (70/130 ≈ 54 %) is the ejection fraction, a key clinical metric — values below ~50 % indicate systolic heart failure.
The heart generates its own electrical activation independently of any external nerve input. The mechanism is the myogenic property of cardiac muscle and a hierarchy of specialised conducting tissues.
flowchart TD
SAN[Sinoatrial node<br/>right atrium<br/>~70 bpm intrinsic rate<br/>pacemaker]
SAN -->|atrial myocardium<br/>spreads across atria| AVN[Atrioventricular node<br/>~0.1 s delay]
AVN --> BH[Bundle of His<br/>septum]
BH --> LB[Left + right bundle branches]
LB --> PF[Purkinje fibres<br/>ventricular endocardium]
PF --> VM[Ventricular myocardium<br/>contracts simultaneously]
The electrocardiogram records the electrical events of the cycle at the body surface. The three principal waves are:
Atrial repolarisation is buried within the QRS complex and is not normally seen. The PR interval reflects AV nodal conduction time; lengthening indicates AV block. The QRS duration reflects ventricular depolarisation speed; widening indicates bundle branch block. The ST segment reflects ventricular plateau (Ca²⁺-driven phase); elevation or depression indicates ischaemia.
Cardiac output (CO) = stroke volume (SV) × heart rate (HR). A resting adult has CO ≈ 70 mL × 70 bpm ≈ 5 L min⁻¹; during vigorous exercise this can rise to 25–35 L min⁻¹. Both terms can be regulated.
The sympathetic nervous system (cardioaccelerator nerves) releases noradrenaline at the SA node, binding β₁-adrenergic receptors and accelerating spontaneous depolarisation; HR rises. The parasympathetic nervous system (vagus nerve, CN X) releases acetylcholine at the SA node, binding muscarinic M₂ receptors and slowing depolarisation; HR falls. At rest, parasympathetic tone dominates: the intrinsic SA rate of ~100 bpm is reduced to ~70 bpm by tonic vagal inhibition. During exercise, vagal withdrawal raises HR rapidly, followed by sympathetic activation that drives further increases.
The American physiologist Walter Cannon (paraphrase) described the integrated sympathetic response to stress — "fight or flight" — in which adrenal medullary adrenaline, sympathetic nerve activity and parasympathetic withdrawal jointly raise heart rate, cardiac output and blood pressure. This is synoptic with course 6 (nervous coordination — autonomic NS) and course 7 (homeostasis — adrenaline).
Two factors regulate stroke volume.
The two factors combine: during exercise, increased venous return raises preload (Frank–Starling), while sympathetic activation raises both contractility and heart rate. Cardiac output rises severalfold without intervention from the conscious brain.
Disruption of the conduction system produces clinically important arrhythmias.
Artificial pacemakers are battery-powered devices implanted under the skin with leads extending into the right atrium and/or ventricle. They sense intrinsic activity and pace when intrinsic activity fails, restoring physiological rate and AV coordination. Modern pacemakers also serve as implantable cardioverter-defibrillators (ICDs) that can deliver a shock if they detect ventricular fibrillation.
Specimen question modelled on the AQA paper format. Not a past-paper item.
Discuss how the structure and function of the mammalian heart, the intrinsic conduction system, and the autonomic nervous system are integrated to deliver appropriate cardiac output during rest and during sustained vigorous exercise. Your answer should refer to ion channels, valve mechanics, the Frank–Starling relationship, and the synoptic links to nervous coordination and homeostasis. [25 marks]
AO breakdown. AO1 (10 marks) — recall of heart anatomy, conduction system, autonomic transmitters, and Frank–Starling. AO2 (8 marks) — application to rest vs exercise scenarios. AO3 (7 marks) — synoptic integration of ion channels, valve mechanics, and homeostatic regulation.
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