Physiology · Short notes

Cardiovascular Physiology: Short Notes & Cheat Sheet

The conduction system and ECG, cardiac output and its determinants, blood pressure regulation, heart sounds, cardiac action potentials and RAAS.

Attempt Cardiovascular Physiology MCQs

Short notes

Read these before you attempt the topic's MCQs.

The heart's conduction system

Each part has its own intrinsic rate; the fastest (the SA node) normally controls the heart.

Conduction and the ECG

The SA node (60–100 beats/min) sets the rhythm. The impulse passes to the AV node (which delays it by about 0.1 s), the bundle of His, bundle branches and Purkinje fibres.
P wave: atrial depolarisation. PR interval (0.12–0.20 s): AV conduction. QRS (under 0.12 s): ventricular depolarisation. T wave: ventricular repolarisation.
Atrial repolarisation is hidden in the QRS complex.
Pacemaker cells depolarise slowly in phase 4 through the 'funny' current (If), which ivabradine blocks.
Ventricular action potential: phase 0 sodium in, phase 1 early potassium out, phase 2 plateau with calcium in, phase 3 potassium out, phase 4 rest.

Cardiac output and pressure

Cardiac output = heart rate × stroke volume, about 5 L/min at rest (e.g. 70 beats × 70 mL).
Stroke volume depends on preload (the Frank–Starling law: more stretch, stronger contraction), afterload and contractility.
Ejection fraction = stroke volume ÷ end-diastolic volume; normally about 55–70%.
Blood pressure = cardiac output × total peripheral resistance. Mean arterial pressure ≈ diastolic + one-third of pulse pressure.
Baroreceptors in the carotid sinus (via cranial nerve IX) and aortic arch (via X) adjust heart rate and vessel tone within seconds.

Sounds and hormones

S1 is closure of the mitral and tricuspid valves (start of systole). S2 is closure of the aortic and pulmonary valves (end of systole).
The left ventricle is perfused mainly during diastole, so fast heart rates reduce its blood supply.
RAAS: renin from juxtaglomerular cells turns angiotensinogen into angiotensin I, which ACE (mainly in the lungs) turns into angiotensin II.
Angiotensin II constricts vessels, releases aldosterone and ADH, and stimulates thirst. Atrial natriuretic peptide opposes these effects.

Cheat sheet

High-yield facts in one place. Cover the right-hand column and test yourself.

ECG components

Component	Represents · normal
P wave	Atrial depolarisation
PR interval	AV conduction · 0.12–0.20 s
QRS complex	Ventricular depolarisation · < 0.12 s
T wave	Ventricular repolarisation
QT interval	Whole ventricular activity; varies with rate

Key formulas

Quantity	Formula
Cardiac output	HR × SV (≈ 5 L/min)
Blood pressure	CO × TPR
Mean arterial pressure	DBP + ⅓ (SBP − DBP)
Ejection fraction	SV ÷ EDV (55–70%)

Memory aids

S1 = AV valves shut (Lub), S2 = semilunar shut (Dub): The first heart sound starts systole; the second ends it.

Exam traps

The AV node delays conduction on purpose, to let the ventricles fill.
Atrial repolarisation is not seen separately; it is buried in the QRS.
The left ventricle is perfused in diastole, not systole.
ACE is found mainly in the lungs, not the kidney.

Revised? Now test yourself.

Attempt the Cardiovascular Physiology MCQs while the notes are fresh. Anything you get wrong is saved to your incorrect list for the next revision round.