Cardiac cycle
Cardiac Cycle, Heart Sounds, JVP and Pressures: FCPS Part 1 Physiology
Cardiac cycle phases, heart sounds, S2 splitting, JVP waves, pressures and ejection fraction for FCPS Part 1, all explained by pressure gradients. Covers S3 and S4, loud and variable S1, pulse deficit in AF, pulsus paradoxus and aortic stenosis syncope.
The core idea
Valves have no muscle of their own. They open when the pressure behind them exceeds the pressure in front and close when the gradient reverses. Work out which chamber has the higher pressure and every phase, heart sound and JVP wave follows.
The phases (left heart)
| Phase | Valves | What happens | ECG |
|---|---|---|---|
| Atrial systole | Mitral open, aortic shut | Atrium tops up the ventricle (last 10–20% of filling; more at fast rates and in stiff ventricles); lost when there is no P wave (AF) | After the P wave |
| Isovolumetric contraction | Both shut | Ventricular pressure rises steeply with no volume change; S1 at its start | Just after QRS |
| Rapid ejection | Aortic opens when LV pressure exceeds aortic (about 80 mmHg) | Most of the stroke volume leaves; aortic pressure peaks | ST segment |
| Reduced ejection | Aortic open | Ejection slows | T wave |
| Isovolumetric relaxation | Both shut | Pressure falls with no volume change; S2 at its start | After T |
| Rapid filling | Mitral opens | About two-thirds of filling; S3 if present | |
| Diastasis | Mitral open | Slow filling; first to shorten as heart rate rises |
- Ventricular systole runs from the QRS to the end of the T wave.
- Dicrotic notch: when the ventricle relaxes, aortic pressure exceeds ventricular pressure, blood briefly flows backwards towards the valve and the aortic valve snaps shut; the brief rebound makes the notch on the aortic pressure trace.
- At 75 beats/min a cycle lasts 0.8 s (systole 0.3, diastole 0.5). If heart rate doubles, the cycle halves to about 0.4 s, mostly at the expense of diastole, which is why tachycardia impairs filling and coronary perfusion.
Heart sounds
| Sound | Cause | Timing | Clinical meaning |
|---|---|---|---|
| S1 | Mitral and tricuspid closure | Start of isovolumetric contraction | Loud in mitral stenosis with mobile cusps; soft once calcified |
| S2 | Aortic (A2) then pulmonary (P2) closure | Start of isovolumetric relaxation | Higher frequency and shorter than S1 |
| S3 | Vibration of the ventricular wall and blood during rapid filling into a large compliant ventricle | Early diastole | Normal in children, athletes, pregnancy; heart failure or MR in older adults |
| S4 | Atrial contraction into a stiff ventricle | Late diastole, just before S1 | LVH, hypertension, aortic stenosis, acute MI; absent in AF |
- Loud S1 in mitral stenosis: the high left atrial pressure holds the cusps wide open until the ventricle contracts, so they close from a wide position with force. Once the valve calcifies and stiffens, S1 becomes soft.
- Variable S1 in complete heart block: atria and ventricles beat independently, so the PR interval varies. When atrial contraction happens just before ventricular systole, the leaflets are wide open and S1 is loud; when it happened long before, the leaflets have drifted nearly closed and S1 is soft. Variable leaflet position at the onset of systole explains the sign; occasional cannon a waves appear when the atrium contracts against a shut tricuspid valve.
- Hypertensive patient with S4 who develops AF: the S4 disappears because it needs effective atrial contraction. If a question describes AF, an S4 cannot be present.
| Splitting of S2 | Cause |
|---|---|
| Physiological, widens on inspiration | Negative intrathoracic pressure increases venous return to the right heart, prolonging RV ejection and delaying P2 |
| Wide but still varies | Right bundle branch block, pulmonary stenosis |
| Fixed | Atrial septal defect |
| Paradoxical (narrows on inspiration) | Left bundle branch block, severe aortic stenosis |
The jugular venous pulse
| Wave | Cause | Abnormal |
|---|---|---|
| a | Right atrial contraction | Absent in AF; giant in tricuspid stenosis or pulmonary hypertension; cannon a waves in complete heart block and VT |
| c | Tricuspid valve bulging into the atrium during right ventricular isovolumetric contraction | |
| x descent | Atrial relaxation; valve ring pulled down | |
| v | Atrial filling against the closed tricuspid valve | Large v waves in tricuspid regurgitation |
| y descent | Tricuspid opens, atrium empties | Steep in constriction; blunted in tamponade |
Pulse findings explained
- Pulse deficit in AF: the apical rate (140) exceeds the radial rate (100) because beats after a very short cycle follow too little filling; they eject too small a stroke volume to produce a palpable radial pulse. Count the rate at the apex.
- Pulsus paradoxus: an inspiratory fall in systolic pressure of more than 10 mmHg. In tamponade the fixed pericardial volume means that the inspiratory increase in right ventricular filling pushes the septum left and reduces left ventricular filling and stroke volume. Kussmaul sign (JVP rising on inspiration) suggests constrictive pericarditis.
- Aortic stenosis: slow-rising (plateau) pulse, ejection systolic murmur at the right second intercostal space radiating to the carotids. On exertion, muscle vasodilatation lowers peripheral resistance, but the fixed outflow obstruction stops cardiac output rising, so blood pressure and cerebral perfusion fall: exertional syncope. Angina arises from hypertrophy with limited coronary reserve.
Exam trap Avoid strong vasodilators in severe aortic stenosis; output cannot rise to compensate.
Pressures worth knowing (mmHg)
| Chamber | Pressure |
|---|---|
| Right atrium | 0–5 (mean) |
| Right ventricle | 25/0–5 |
| Pulmonary artery | 25/10 (mean about 15) |
| Pulmonary capillary wedge (left atrium) | 8–12 |
| Left ventricle | 120/5–10 |
| Aorta | 120/80 |
- The wedge pressure estimates left atrial and so left ventricular filling pressure, except in mitral stenosis.
Volumes and ejection fraction
- Stroke volume = end-diastolic volume minus end-systolic volume; ejection fraction = SV ÷ EDV (normal 55–70%).
- Worked example: cardiac output 5.6 L/min at 70 beats/min gives SV = 5,600 ÷ 70 = 80 mL; with EDV 160 mL, EF = 80 ÷ 160 = 50%.
The pressure–volume loop
One loop is one beat: filling (bottom), isovolumetric contraction (right), ejection (top), isovolumetric relaxation (left). The area is stroke work.
- More preload widens the loop to the right; stroke volume rises.
- More afterload makes it taller and narrower; end-systolic volume rises.
- More contractility lowers end-systolic volume; stroke volume rises.
Remember Valves follow pressure; isovolumetric means all valves shut.
Related bedside fact
- An S1Q3T3 pattern with sudden breathlessness after delivery suggests pulmonary embolism; CT pulmonary angiography is the investigation of choice.
How FCPS asks about this
- Phase with both valves shut: isovolumetric contraction and relaxation.
- Maximum aortic pressure: rapid ejection; aortic valve opens at the start of ejection.
- S3 timing: rapid filling phase (two-thirds of filling); S4 needs atrial contraction, lost in AF.
- Loud S1: mitral stenosis with mobile cusps; variable S1 with slow regular pulse: complete heart block.
- Apical rate above radial rate in AF: short-cycle beats eject too little to be felt.
- Systolic fall of 18 mmHg on inspiration with effusion: pulsus paradoxus.
- Exertional syncope in aortic stenosis: fixed outflow cannot raise output.
Test yourself on this topic
5 of the 33 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
In an ICU patient, a balloon-tipped pulmonary artery catheter is wedged in a small pulmonary artery branch, and the pressure recorded is 22 mmHg. Which of the following pressures does this mainly estimate?
Answer: Left atrial pressure
When the balloon occludes a pulmonary artery branch, flow stops in that segment, so the catheter tip is connected by a static column of blood through the capillaries and pulmonary veins to the left atrium. The wedge pressure therefore approximates left atrial pressure, and in the absence of mitral stenosis, left ventricular end-diastolic pressure. Normal values are about 6–12 mmHg; a value of 22 mmHg suggests raised left-sided filling pressure and a risk of pulmonary oedema.
Wedge pressure
- Balloon stops flow
- Static column to the left atrium
- Estimates LA and LVEDP
- Normal 6–12 mmHg
Remember The wedge looks through the lungs to the left atrium.
Exam trap In mitral stenosis the wedge pressure overestimates LV end-diastolic pressure.
Why the other options are wrong
- Right atrial pressure Measured by a central venous catheter.
- Pulmonary artery systolic pressure Measured with the balloon deflated.
- Right ventricular end-diastolic pressure Right-sided; the wedge looks forward to the left heart.
- Pulmonary capillary oncotic pressure Oncotic pressure is not measured by a catheter.
A 28-year-old who injects drugs has fever and a pansystolic murmur at the left lower sternal edge that is louder on inspiration. His neck veins show a large wave that rises with each systole and his liver pulsates. Which JVP finding is this?
Answer: Giant v waves (TR)
Right-sided endocarditis in people who inject drugs most often affects the tricuspid valve. When the tricuspid valve leaks, the right ventricle pushes blood back into the right atrium and great veins during systole. The normal v wave, which reflects atrial filling against a closed tricuspid valve, becomes a large systolic wave (sometimes called a cv wave) that coincides with the carotid pulse, and the liver can pulsate. Right-sided murmurs become louder on inspiration because venous return to the right heart increases (Carvallo's sign). Cannon a waves are intermittent and caused by the atrium contracting against a closed valve; giant a waves occur when the atrium contracts against resistance, as in tricuspid stenosis or pulmonary hypertension.
JVP waves
- a = atrial contraction
- v = atrial filling; giant v in TR
- Cannon a = complete heart block
- Right-sided murmurs louder on inspiration
Remember TR fills the neck in systole.
Exam trap Cannon a waves (CHB) and giant v waves (TR) are both big waves; timing and regularity separate them.
Why the other options are wrong
- Cannon a waves (heart block) Cannon a waves are irregular and occur when atrium and ventricle contract together.
- Giant a waves (TS) Giant a waves are presystolic, from atrial contraction against a stenosed valve.
- Steep y descent (constriction) A steep y descent is a diastolic finding in constriction.
- Absent a waves (AF) Absent a waves fit AF but do not explain a large systolic wave.
A 30-year-old woman has progressive exertional breathlessness. There is a left parasternal heave, and the pulmonary component of the second heart sound is loud and palpable in the left 2nd intercostal space. What is the most likely cause of the loud P2?
Answer: Raised pulmonary artery pressure
The loudness of a valve closure sound depends on the pressure that snaps the valve shut. In pulmonary hypertension, high diastolic pressure in the pulmonary artery closes the pulmonary valve forcefully, giving a loud, sometimes palpable P2, and the right ventricle hypertrophies, producing a parasternal heave. Pulmonary stenosis does the opposite: low post-valve pressure and a stiff valve give a soft, delayed P2. Causes of pulmonary hypertension include mitral stenosis, chronic lung disease, thromboembolism and idiopathic arterial disease.
Loud P2
- Closure loudness tracks closing pressure
- Pulmonary hypertension: loud P2
- Plus RV heave
- Pulmonary stenosis: soft P2
Remember Loud, palpable P2 with a heave: pulmonary hypertension.
Exam trap In thin young people P2 may be heard at the apex normally; loudness must be judged at the pulmonary area.
Why the other options are wrong
- Pulmonary valve stenosis Gives a soft, delayed P2 with an ejection murmur.
- Raised left ventricular pressure Would affect A2, not P2.
- Aortic valve sclerosis Affects the aortic component, heard in the right 2nd space.
- Severe tricuspid regurgitation May follow pulmonary hypertension but does not itself make P2 loud.
A 68-year-old man with atrial fibrillation has no a waves in his JVP. Which of the following cardiac cycle phases has been lost?
Answer: Atrial systole
The a wave of the JVP is caused by right atrial contraction, which pushes blood into the ventricle at the end of diastole and briefly back into the great veins. In atrial fibrillation there is no coordinated atrial contraction, so the a wave disappears, the P wave is absent on ECG and S4 cannot occur. Loss of this atrial 'kick', normally 15–25% of filling, can reduce cardiac output, especially in stiff ventricles.
JVP in AF
- a wave = atrial contraction
- AF: no a wave, no P wave
- No S4 in AF
- Lost atrial kick cuts filling
Remember No atrial systole, no a wave.
Exam trap Large a waves suggest a stiff right ventricle or tricuspid stenosis; absent a waves suggest AF.
Why the other options are wrong
- Isovolumetric contraction Still occurs; gives the c wave from tricuspid bulging.
- Rapid ventricular filling Still occurs passively; linked with the y descent and S3.
- Isovolumetric relaxation Still occurs after valve closure.
- Reduced ejection Still occurs; ventricular function is intact.
A 72-year-old has exertional chest pain and fainted while climbing stairs. He has a slow-rising pulse and an ejection systolic murmur radiating to the carotids. Why does exertion cause syncope?
Answer: Fixed outflow cannot raise output
In severe aortic stenosis the narrowed valve limits stroke volume. During exercise, muscle vasodilatation lowers systemic resistance, but cardiac output cannot rise enough, so blood pressure falls and brain perfusion drops, causing syncope. The thick ventricle needs more oxygen while coronary perfusion is reduced, causing angina. Symptomatic severe aortic stenosis needs valve replacement.
Aortic stenosis symptoms
- Angina, syncope, breathlessness
- Slow-rising pulse, narrow pulse pressure
- Exercise: fixed output
- Symptomatic: valve replacement
Remember Fixed valve, fixed output: faints on effort.
Exam trap Avoid strong vasodilators in severe aortic stenosis.
Why the other options are wrong
- Mitral valve prolapses Not the lesion.
- Coronary arteries dilate too much Not the mechanism.
- Pulmonary pressure falls Not the mechanism.
- Heart rate falls during exercise Heart rate rises.
Where this sits in the CPSP syllabus
- Paper 1: Cardiovascular system, Cardiac cycle, heart sounds and pressures
- Surgery & Allied, Paper 2: Cardiovascular system, Cardiac cycle, heart sounds and pressures
- Medicine & Allied, Paper 2: Cardiovascular system, Cardiac cycle, heart sounds and pressures