CVR Physiotherapy

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Cardiac anatomy and physiology for physiotherapists

Chapter 1 is revision, but every cardiac answer leans on it: which artery feeds which wall (ECG leads in MI cases), why a fast heart rate starves the heart muscle, why stroke volume rises with training, why patients faint when stood up after bed rest. Learn these links rather than isolated facts.

Syllabus
Ch 1(b) Cardiac anatomy and physiology
Priority
Foundation. Not asked on its own in 2016–2026; underpins the cardiac pages.
Asked as
Not asked 2016–2026
Usual split
Revision; possible 3-mark definitions or diagrams
Checked against
Standard physiology and anatomy texts (Guyton and Hall). Full list under Sources.
Content checked
19 October 2026. Next review due October 2027.
My revision

1Anatomy: chambers, valves and coronary arteries

  • The heart lies in the middle mediastinum; the apex beat is normally in the left 5th intercostal space in the mid-clavicular line.
  • Right side (right atrium → tricuspid valve → right ventricle → pulmonary valve → lungs) pumps at low pressure; left side (left atrium → mitral valve → left ventricle → aortic valve → body) pumps at high pressure, so the left ventricular wall is the thickest.
  • Pericardium: a two-layered sac; fluid in it (effusion, tamponade) restricts filling.
Coronary arteries and what they supply
ArterySuppliesBlocked: ECG leads
Left main → left anterior descending (LAD)Front wall of the left ventricle, front two-thirds of the septum, apexV1–V4 (anteroseptal)
Left main → circumflexSide and back of the left ventricle, left atriumI, aVL, V5–V6 (lateral)
Right coronary artery (RCA)Right atrium and ventricle, inferior wall of the left ventricle, back of the septum; the SA node in most people and the AV node in most (right-dominant) heartsII, III, aVF (inferior); watch for slow heart rhythms and heart block

Veins drain into the coronary sinus. Nerves: sympathetic (β1) speeds the heart and strengthens contraction; the vagus (parasympathetic) slows it.

2Conduction system

How each heartbeat spreads

SA node to atria to AV node to bundle of His to Purkinje fibres The SA node in the right atrium fires 60 to 100 times a minute. The impulse spreads through the atria, which contract and make the P wave. The AV node delays it by about 0.1 second so the ventricles can fill, seen as the PR interval; it can pace at 40 to 60 a minute if the SA node fails. The bundle of His divides into right and left bundle branches. Purkinje fibres spread the impulse through the ventricles, which contract and make the QRS; the ventricles can pace at 20 to 40 a minute. SA node (right atrium) natural pacemaker, 60–100 a minute Atria contract P wave AV node delay of about 0.1 s lets the ventricles fill (PR interval) backup pacemaker 40–60 a minute Bundle of His right and left bundle branches Purkinje fibres → ventricles contract QRS; backup pacemaker 20–40 a minute
The T wave is ventricular recovery (repolarisation). When the higher pacemakers fail, the lower ones take over at slower rates: this is why complete heart block gives a slow pulse.

3Cardiac cycle and heart sounds

  • Systole (contraction): isovolumetric contraction, then ejection. Diastole (relaxation): isovolumetric relaxation, then filling (rapid filling, then atrial contraction tops it up).
  • Typical pressures: left ventricle 120/0–10 mmHg, aorta 120/80; right ventricle 25/0–5, pulmonary artery 25/10.
  • S1 ("lub"): mitral and tricuspid valves close (start of systole). S2 ("dub"): aortic and pulmonary valves close (start of diastole); it splits on breathing in.
  • S3: rapid filling into a failing, dilated ventricle (heart failure; can be normal in the young). S4: atrial contraction into a stiff ventricle (hypertension, ischaemia).
  • The left ventricle's own blood supply flows mainly in diastole, because contraction squeezes the coronary vessels. At rest diastole is about two-thirds of each beat; a fast heart rate shortens it, so less blood reaches the heart muscle while it needs more. This is why tachycardia brings on angina and why beta-blockers help.

4Cardiac output and its regulation

TermMeaningTypical value
Cardiac output (CO)Heart rate × stroke volumeAbout 5 L/min at rest; about 20–25 L/min in maximal exercise in fit young adults
Stroke volume (SV)End-diastolic volume − end-systolic volumeAbout 70 mL at rest
Ejection fraction (EF)SV ÷ end-diastolic volumeAbout 55–70%; 40% or below is reduced (heart failure grades on the valve and heart failure page)
PreloadStretch of the ventricle before it contracts (filling)Raised by venous return: muscle pump, breathing, lying down
AfterloadResistance the ventricle pumps againstRaised by high BP and aortic stenosis
ContractilityStrength of contraction at a given stretchRaised by sympathetic drive; lowered by heart muscle damage
  • Frank–Starling law: the more the ventricle is filled (stretched), the more strongly it contracts, up to a limit. A failing heart sits on a flatter curve.
  • Blood pressure = cardiac output × total peripheral resistance. Mean arterial pressure ≈ diastolic + one-third of (systolic − diastolic); for 120/80, about 93 mmHg.
  • Baroreceptor reflex (carotid sinus and aortic arch): a fall in BP on standing quickly raises heart rate and narrows vessels. After bed rest, with some drugs and with autonomic damage it fails, giving postural hypotension.
  • Myocardial oxygen demand rises with heart rate, BP, wall tension and contractility. Heart rate × systolic BP (the rate–pressure product) is a bedside guide; angina appears at a fairly fixed product for each patient.

Responses to exercise and training are on the exercise physiology card.

5Physiology behind physiotherapy decisions

PhysiologyWhat it means in practice
Coronary flow in diastole; rate–pressure productKeep exercise below the heart rate that brings on angina; long warm-up; avoid sudden bursts
Valsalva raises chest pressure then BP swingsBreathe out on effort; no breath-holding in resistance training
Coronary territoriesInferior MI (RCA): watch for slow heart rate and heart block during mobilisation
Frank–Starling and the failing heartLower intensity, interval training, watch weight gain and breathlessness (fluid)
Baroreceptor reflexSit up in stages after bed rest; check postural BP
Muscle pump and venous returnAnkle pumps against DVT and swelling; cool down slowly so blood does not pool in the legs
Autonomic control of heart rateHeart rate is unreliable with beta-blockers, pacemakers and after transplant: use RPE

6Exam corner

Not asked on its own in the 20 papers (2016–2026). The ECG localisation table is used in MI cases (W20, W22, S25: changes in II, III and aVF mean an inferior MI).

Test yourself

3 mWhy does tachycardia worsen myocardial ischaemia?

The heart muscle is perfused mainly in diastole; a fast rate shortens diastole, so supply falls while demand (rate × pressure) rises.

MCQST elevation in II, III and aVF usually means a block in the:A. LADB. Circumflex onlyC. Right coronary arteryD. Left main

C. Inferior wall, usually the right coronary artery.

MCQCardiac output at rest is about:A. 1 L/minB. 5 L/minC. 15 L/minD. 25 L/min

B. About 70 beats × 70 mL ≈ 5 L/min.

 Sources

  1. MUHS BPTh syllabus (2012), CVR Ch 1.
  2. Hall JE, Hall ME. Guyton and Hall Textbook of Medical Physiology (cardiac cycle, output, regulation).
  3. Standard anatomy texts (Gray's Anatomy; Chaurasia) for coronary anatomy.
  4. Structure and classical content: Hillegass (2022), chapters on cardiovascular anatomy and physiology.

Educational notes for exam preparation. Not medical advice.

Version 1. Content checked 19 October 2026. Next review October 2027.