Cardiac Cycle

The cardiac cycle is the sequence of mechanical and electrical events between the start of one heartbeat and the start of the next. For NEET PG, the Wiggers diagram is the single highest-yield figure in cardiovascular physiology — master the timing of pressure curves, valve events, heart sounds, the JVP waveform, and the pressure-volume loop, and a large block of CVS physiology MCQs becomes trivial.

Definition and overview

One cardiac cycle at a resting heart rate of 75/min lasts 0.8 seconds. It is conventionally divided into systole (ventricular contraction, ~0.3 s) and diastole (ventricular relaxation and filling, ~0.5 s). Diastole is therefore longer than systole at rest — clinically important because coronary perfusion of the left ventricle occurs predominantly in diastole, and tachycardia shortens diastole disproportionately, compromising myocardial perfusion.

High-yield: As heart rate rises, diastole shortens far more than systole. This is why tachycardia is dangerous in coronary artery disease and aortic stenosis — less diastolic time for LV coronary filling.

Classification — the phases

The cycle is classically divided into seven phases. A useful framework is the four valve events that bracket them:

1. Atrial systole (atrial contraction; "atrial kick")
2. Isovolumetric (isovolumic) contraction
3. Rapid ejection
4. Reduced (slow) ejection
5. Isovolumetric (isovolumic) relaxation
6. Rapid passive filling
7. Reduced (slow) filling / diastasis

Phases 2–4 are systole; phases 5–7 plus atrial systole are diastole.

Flow of one cycle (valve and pressure logic)

Atrial systole → contributes ~20–25% of LV filling (the rest is passive). Produces the a wave in atrial/JVP tracing and the S4 if pathological → Mitral valve closes when LV pressure exceeds LA pressure (onset of S1) → Isovolumetric contraction: all four valves shut, volume constant, LV pressure rises steeply → Aortic valve opens when LV pressure > aortic pressure (~80 mmHg) → Rapid ejection then reduced ejection → Aortic valve closes when LV pressure falls below aortic pressure (onset of S2, produces the dicrotic notch/incisura in the aortic curve) → Isovolumetric relaxation: all valves shut again, LV pressure falls steeply at constant volume → Mitral valve opens when LV pressure < LA pressure → Rapid filling (may produce S3) → diastasis → next atrial systole.

High-yield: The two isovolumetric phases are the periods when all four valves are closed and ventricular volume is constant. Isovolumetric contraction = LV at end-diastolic volume (EDV); isovolumetric relaxation = LV at end-systolic volume (ESV).

Pressures, volumes and key values

Parameter	Typical value	Note
End-diastolic volume (EDV)	~120–130 mL	Preload indicator
End-systolic volume (ESV)	~50 mL	After ejection
Stroke volume (SV)	~70 mL	SV = EDV − ESV
Ejection fraction (EF)	~60–65%	EF = SV/EDV; <40% = systolic HF
LV systolic pressure	~120 mmHg	Peak ejection
Aortic diastolic pressure	~80 mmHg	Aortic valve opens here
LA pressure (mean)	~5–8 mmHg
RV systolic / PA diastolic	~25 / 10 mmHg	Lower-pressure right side

High-yield: Stroke volume = EDV − ESV and EF = SV/EDV (~60%). Aortic valve opens at ~80 mmHg (= aortic diastolic pressure); mitral valve closes at the start of isovolumetric contraction.

Heart sounds — timing and mechanism

Heart sounds arise from valve closure and the vibration of blood/chamber walls, not valve opening (opening is normally silent unless pathological, e.g. opening snap).

Sound	Cause	Timing	Notes
S1	Mitral + tricuspid closure (M1 then T1)	Onset of systole	Loud in mitral stenosis, short PR
S2	Aortic + pulmonary closure (A2 then P2)	End of systole	Physiological splitting ↑ on inspiration
S3	Rapid ventricular filling	Early diastole	Normal in children/athletes; HF, volume overload in adults
S4	Atrial contraction against stiff ventricle	Late diastole (pre-systolic)	Always pathological; absent in AF

High-yield: S1 marks the beginning of systole; S2 marks the end of systole (beginning of diastole). S3 = rapid filling phase ("ken-tuc-ky" gallop); S4 = atrial systole ("ten-nes-see" gallop). S4 is absent in atrial fibrillation because there is no organised atrial contraction.

Splitting of S2: Normally A2 precedes P2; inspiration increases venous return to the right heart, delaying P2 → physiological (inspiratory) splitting.

• Wide splitting: RBBB, pulmonary stenosis (delayed P2).
• Fixed splitting: atrial septal defect (ASD) — classic.
• Paradoxical (reversed) splitting: LBBB, aortic stenosis (A2 delayed, splitting on expiration).

Jugular venous pulse (JVP) waveform

The JVP reflects right atrial pressure. It has three positive waves (a, c, v) and two descents (x, y).

Wave/descent	Mechanism
a wave	Atrial contraction (atrial systole)
c wave	Tricuspid bulging into RA during isovolumetric contraction (also carotid transmission)
x descent	Atrial relaxation + downward pull of tricuspid annulus during ejection
v wave	Atrial filling against a closed tricuspid valve (late systole)
y descent	Tricuspid opens, rapid atrial emptying into RV

High-yield JVP abnormalities (very frequently asked):

• Absent a wave → atrial fibrillation
• Large/giant a wave → tricuspid stenosis, pulmonary stenosis/hypertension, RV hypertrophy
• Cannon a waves → complete (3rd-degree) heart block, ventricular tachycardia (atrium contracts against closed tricuspid)
• Prominent/giant v wave → tricuspid regurgitation ("cv" or "s" wave)
• Sharp y descent → constrictive pericarditis (Friedreich sign); absent y descent → cardiac tamponade
• Prominent x descent → cardiac tamponade

Mnemonic for cannon a waves — think "AV dissociation": complete heart block and VT. Friedreich's sign = steep y descent in constrictive pericarditis; Kussmaul's sign = paradoxical rise in JVP on inspiration (constrictive pericarditis, RV infarction, tricuspid stenosis).

Pressure–volume (PV) loop

The LV PV loop plots ventricular pressure (y-axis) against ventricular volume (x-axis). Read it counter-clockwise, with four limbs corresponding to the four valve events:

1. Mitral valve opens → diastolic filling (bottom limb, volume rises from ESV to EDV at low pressure).
2. Mitral valve closes → isovolumetric contraction (right vertical limb; pressure rises, volume constant at EDV).
3. Aortic valve opens → ejection (top limb; volume falls from EDV to ESV).
4. Aortic valve closes → isovolumetric relaxation (left vertical limb; pressure falls, volume constant at ESV).

• Width of the loop = stroke volume.
• Area inside the loop = stroke work (external work done by the LV).
• ESPVR (end-systolic pressure–volume relationship): its slope = contractility (Emax); a steeper, leftward-shifted line = increased contractility.
• EDPVR (end-diastolic pressure–volume relationship): reflects ventricular compliance/diastolic stiffness.

High-yield PV loop shifts:

• ↑ Preload: loop widens to the right, EDV ↑, SV ↑ (Frank–Starling).
• ↑ Afterload: aortic valve opens at higher pressure, ESV ↑, SV ↓, loop taller and narrower.
• ↑ Contractility: ESPVR slope ↑, ESV ↓, SV ↑.
• Aortic stenosis: very tall loop (high LV pressure to overcome stenosis).
• Mitral regurgitation: no true isovolumetric contraction phase (blood leaks back into LA), loop loses its sharp left vertical line.

Frank–Starling law: within physiological limits, increased EDV (preload) → increased stroke volume, because greater sarcomere stretch (optimal ~2.2 µm) increases actin–myosin overlap and Ca²⁺ sensitivity. This is the intrinsic, length-dependent mechanism, independent of nervous input.

Timing relationships (ECG ↔ mechanical events)

ECG event	Mechanical correlate
P wave	Atrial depolarisation → atrial systole follows
QRS complex	Ventricular depolarisation → S1 / mitral closure / isovolumetric contraction begin shortly after
T wave	Ventricular repolarisation → S2 / aortic closure near its end
PR interval	AV nodal delay (allows atrial kick before ventricular contraction)

High-yield: S1 occurs just after the QRS; S2 occurs at the end of the T wave. The dicrotic notch (incisura) in the aortic pressure trace corresponds to aortic valve closure (S2).

Special considerations and clinical correlates

• Coronary blood flow: Left coronary flow is maximal in diastole (systolic compression of intramyocardial vessels). Right coronary flow is more even because RV pressure is low. → Tachycardia and AS predispose to subendocardial ischaemia.
• Atrial kick importance: Loss of atrial systole (e.g., atrial fibrillation) reduces filling by ~20% — well tolerated normally but decompensates mitral stenosis and stiff (diastolic dysfunction) ventricles where the kick is critical.
• Mitral stenosis: loud S1, opening snap (after S2), mid-diastolic rumble; short A2–OS interval = severe MS (high LA pressure opens valve early).
• Aortic stenosis: ejection systolic murmur, soft/absent A2, paradoxical S2 splitting, slow-rising "pulsus parvus et tardus", S4.
• Cardiac tamponade: absent y descent (x preserved), pulsus paradoxus, Beck's triad (hypotension, raised JVP, muffled heart sounds).

Recently asked / exam angle

• "All four valves are closed during which phase(s)?" → Isovolumetric contraction and isovolumetric relaxation. A perennial favourite.
• Identify the phase / valve event from a labelled Wiggers diagram — e.g., "point at which aortic valve closes" = dicrotic notch = onset of S2.
• Match the JVP wave to its cause (a = atrial contraction; cannon a = complete heart block/VT; giant v = TR; absent a = AF).
• PV loop manipulation MCQs: "Which change increases ESV?" → increased afterload. "Width of loop represents?" → stroke volume. "Area within loop?" → stroke work.
• Heart sound timing: S4 absent in AF; S2 splitting patterns (fixed = ASD, paradoxical = LBBB/AS).
• Fastest filling phase → rapid (early) passive filling, just after mitral valve opens (corresponds to S3 and the y descent).
• Frank–Starling / contractility questions: ESPVR slope = contractility; preload vs afterload effects on SV.
• Coronary perfusion of LV occurs in diastole — linked to tachycardia and AS clinical scenarios.

Rapid revision

• Cardiac cycle = 0.8 s at HR 75; systole 0.3 s, diastole 0.5 s; diastole shortens more with tachycardia.
• S1 = onset of systole (AV valve closure); S2 = onset of diastole (semilunar valve closure).
• All four valves closed during isovolumetric contraction and relaxation.
• SV = EDV − ESV (~70 mL); EF = SV/EDV (~60%).
• Aortic valve opens at ~80 mmHg; dicrotic notch = aortic valve closure = S2.
• Atrial kick contributes ~20–25% of LV filling; critical in mitral stenosis, lost in AF.
• S3 = rapid filling (volume overload/HF); S4 = atrial contraction against stiff ventricle; S4 absent in AF.
• JVP: a (atrial contraction), c (tricuspid bulge), v (RA filling); cannon a waves = complete heart block/VT; giant v = TR; absent a = AF.
• Fixed split S2 = ASD; paradoxical split = LBBB/AS; wide split = RBBB/PS.
• PV loop: width = stroke volume, area = stroke work, ESPVR slope = contractility.
• Frank–Starling: ↑ preload (EDV) → ↑ stroke volume via optimal sarcomere overlap.
• LV coronary perfusion is maximal in diastole — tachycardia and aortic stenosis cause subendocardial ischaemia.
• Kussmaul sign (inspiratory JVP rise) = constrictive pericarditis/RV infarct; absent y descent = tamponade; steep y (Friedreich) = constriction.