Cardiovascular physiology for FCPS Part 1
Cardiovascular physiology questions come from a short list: the cardiac cycle, action potentials, pressures and volumes, Starling's law, and how blood pressure is controlled. Master the graphs and the numbers.
On this page
What the questions look like
Cardiovascular physiology is one of the most heavily tested areas in Paper 1, and it returns in Medicine & Allied Paper 2. The questions cluster around a few themes:
- what happens at each phase of an action potential or cardiac cycle
- normal values for pressures, volumes and output
- what changes preload, afterload or contractility
- reflex responses to standing, bleeding or exercise
Cardiac action potentials
| Phase | Ventricular muscle | Main current |
|---|---|---|
| 0 | Rapid upstroke | Fast Na⁺ in |
| 1 | Early repolarisation | K⁺ out (transient) |
| 2 | Plateau | Ca²⁺ in (L-type) balanced by K⁺ out |
| 3 | Repolarisation | K⁺ out |
| 4 | Resting potential | K⁺ leak |
Pacemaker cells (SA and AV nodes) have no true resting potential. Phase 4 drifts upwards because of the funny current (If), then calcium channels fire the upstroke. Sympathetic stimulation steepens phase 4. Vagal stimulation flattens it. Ivabradine blocks the funny current.
The long plateau gives cardiac muscle a long refractory period, which is why the heart cannot be tetanised.
The cardiac cycle
| Event | What happens |
|---|---|
| Isovolumetric contraction | All valves shut; pressure rises sharply; S1 just before (mitral and tricuspid closure) |
| Ejection | Aortic valve opens when LV pressure exceeds aortic pressure |
| Isovolumetric relaxation | All valves shut; S2 at the start (aortic and pulmonary closure) |
| Filling | Mitral opens; rapid filling (S3 if pathological), then atrial kick (S4) |
- S3 is normal in children and pregnancy, abnormal in heart failure (volume load).
- S4 means a stiff ventricle (hypertrophy, ischaemia). It is absent in atrial fibrillation.
- JVP waves: a (atrial contraction; absent in AF, giant in complete heart block and tricuspid stenosis), c (tricuspid bulging), x descent, v (venous filling; giant in tricuspid regurgitation), y descent.
Numbers worth knowing
| Measure | Normal value |
|---|---|
| Stroke volume | About 70 mL |
| Cardiac output | About 5 L/min |
| Ejection fraction | About 55–70% |
| Right atrium | 0–5 mmHg |
| Right ventricle | 25/0–5 mmHg |
| Pulmonary artery | 25/10 mmHg |
| Wedge pressure (≈ left atrium) | 6–12 mmHg |
| Left ventricle | 120/5–10 mmHg |
Wedge pressure estimates left atrial pressure. It rises in left heart failure and mitral stenosis, but not in pure right heart disease.
Cardiac output and Starling's law
- Cardiac output = heart rate × stroke volume.
- Stroke volume depends on preload, afterload and contractility.
- Frank–Starling law: a greater end-diastolic stretch gives a stronger contraction, up to a limit.
- Positive inotropes (sympathetic stimulation, digoxin) shift the curve up. Heart failure shifts it down.
- Mean arterial pressure = cardiac output × total peripheral resistance. It is roughly diastolic pressure plus a third of pulse pressure.
Control of blood pressure
- Baroreceptors in the carotid sinus (glossopharyngeal nerve) and aortic arch (vagus) respond to stretch.
- A fall in pressure reduces their firing, so sympathetic tone rises and vagal tone falls: faster heart, stronger contraction, vasoconstriction.
- On standing, blood pools in the legs, venous return drops, and the reflex corrects it within seconds. When it fails, postural hypotension follows.
- Longer-term control is through the kidney: renin–angiotensin–aldosterone, ADH and natriuretic peptides.
- The Bainbridge reflex speeds the heart when atrial stretch increases. The Cushing reflex (hypertension with bradycardia) signals raised intracranial pressure.
Coronary circulation
- Left ventricular coronary flow occurs mainly in diastole, because systolic contraction squeezes the vessels.
- So tachycardia, which shortens diastole, reduces coronary perfusion.
- The heart extracts most of the oxygen from coronary blood even at rest. Extra demand must be met by increasing flow, mainly through local metabolic vasodilatation (adenosine).
Haemorrhage and exercise
- In haemorrhage, heart rate rises and pulse pressure narrows first. Hypotension appears late (after about 30% blood loss in a healthy adult).
- In exercise, cardiac output can rise several-fold. Muscle blood flow increases sharply, systolic pressure rises, and diastolic pressure stays similar or falls because peripheral resistance drops.
Common traps
- The ECG PR interval mainly reflects delay in the AV node.
- QT shortens as heart rate rises, so it is corrected for rate (QTc).
- Hyperkalaemia gives tall peaked T waves. Hypokalaemia gives flat T waves and U waves.
- Afterload for the left ventricle is set mainly by aortic pressure and resistance, not by preload.
How to revise in one week
- Day 1: action potentials and conduction.
- Day 2: cardiac cycle, heart sounds, JVP.
- Day 3: pressures, volumes, cardiac output and Starling.
- Day 4: blood pressure control and reflexes.
- Day 5: regional circulations: coronary, cerebral, skin, muscle.
- Days 6 to 7: haemorrhage, exercise and mixed questions.
Practise these in the FCPS-1 Prep question bank. Cardiovascular questions link to topic reviews with the cycle laid out phase by phase.
Read next: Physiology high-yield · Acid-base and ABGs · Pharmacology high-yield
Frequently asked questions
Which cardiovascular physiology topic is asked most?
The cardiac cycle and its pressures, followed by action potentials and blood pressure control.
Do I need to memorise the Wiggers diagram?
Know what happens at each valve opening and closing, and where the heart sounds fall. That answers most diagram questions without drawing it.
Is ECG interpretation tested in Part 1?
The physiological basis is: what each wave and interval represents and how electrolytes change them. Full clinical ECG reading is more for later exams.