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Cardiac Cycle, Wiggers Diagram, and PV Loops

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Physiology I · 9 min read

The Wiggers diagram and PV loop are the two-language coordinate system for cardiac mechanics. Master them and every valve lesion + drug effect becomes legible.

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Identify the four phases of the cardiac cycle on a Wiggers diagram.
Interpret a PV loop and predict how preload, afterload, and contractility shift it.
Match valve lesions to their characteristic PV-loop patterns.
Apply the loop's geometry to bedside hemodynamic management.

Phases of the cardiac cycle

KeyFour phases per beat.

Isovolumic contraction — mitral closes, aortic still closed, LV pressure climbs without volume change.

Ejection — aortic opens, LV empties; stroke volume leaves.

Isovolumic relaxation — aortic closes, mitral still closed, LV pressure falls without volume change.

Filling — mitral opens, LV fills (passive then active atrial kick).

Diastole is phases 3+4; systole is phases 1+2.

Wiggers diagram of the complete cardiac cycle: aligns LV/aortic/LA pressures, LV volume, ECG, heart sounds across systole and diastole; identifies isovolumetric phases, ejection, filling, and valve events (S1/S2).

Heart sounds S1 and S2 on the cardiac cycle: S1 = mitral+tricuspid closure at systole onset; S2 = aortic+pulmonic closure at end-systole. S2 components A2 precedes P2 with normal physiologic splitting. — Wiggers diagram of the complete cardiac cycle: aligns LV/aortic/LA pressures, LV volume, ECG, heart sounds across systole and diastole; identifies isovolumetric phases, ejection, filling, and valve events (S1/S2).

Wiggers diagram alignment

Five tracings stacked in time

aortic pressure
LV pressure
LA pressure
LV volume
ECG
heart sounds

S1 = mitral closure at start of isovolumic contraction.

S2 = aortic closure at start of isovolumic relaxation.

P wave precedes atrial kick.

QRS precedes LV contraction.

T wave aligns with end of ejection.

Use these landmarks to interpret hemodynamic tracings in real time.

Wiggers diagram: cardiac cycle time-aligned showing aortic, LV, LA pressures, ventricular volume, ECG and heart sounds. Identifies isovolumetric contraction/relaxation, rapid filling, atrial kick.

The normal PV loop

KeyPressure on Y-axis, volume on X-axis, traced counterclockwise.

Four corners

bottom-right (end-diastole, mitral closes)
top-right (start of ejection, aortic opens)
top-left (end-systole, aortic closes)
bottom-left (end of relaxation, mitral opens)

Width = stroke volume.

Area = stroke work.

Slope of end-systolic pressure-volume relationship (ESPVR) = contractility independent of load.

How preload, afterload, contractility shift the loop

KeyIncreased preload — loop shifts right, wider (Frank-Starling).

Increased afterload — loop taller, narrower (lower stroke volume, higher ESP).

Increased contractility — ESPVR slope steeper, end-systolic point shifts up-left (more emptying at same pressure).

Decreased contractility — ESPVR flatter, loop wider with lower stroke work.

Recognizing the pattern tells you which lever to pull intra-op.

Cardiac cycle Wiggers/PV loops - overview/definitions: relates pressures (aorta, LV, LA), volumes, ECG and heart sounds across the cardiac cycle; PV loop integrates these into preload, afterload and contractility.

PV loops in valve lesions

Aortic stenosis — tall, narrow loop

high LV pressure to push past stenosis

concentric hypertrophy

Aortic regurgitation — wide loop

LV dilates to accommodate regurgitant volume

eccentric hypertrophy

Mitral regurgitation — wide loop with reduced isovolumic contraction phase (LV unloads backward through MV early).

Mitral stenosis — small loop

reduced filling limits stroke volume

LA pressure climbs

Normal left ventricular pressure-volume (PV) loop showing four phases: isovolumetric contraction, ejection (aortic valve opens), isovolumetric relaxation, filling (mitral valve opens); ESV ~50 mL, EDV ~120 mL, SV ~70 mL, EF ~58%.

Bedside relevance

KeyPV-loop thinking guides hemodynamic management.

Severe AS hypotension — phenylephrine to preserve coronary perfusion of the hypertrophied LV.

AR — keep HR brisk (less diastolic regurgitant time).

MR — afterload reduction encourages forward flow.

MS — avoid tachycardia (need diastolic filling time).

The drug you reach for matches the loop's geometry, not just the BP number.

Left ventricular pressure-volume loops: normal vs valvular disease. AS - increased systolic pressure, narrow loop; AR - wide loop, increased EDV; MR - reduced ESV, shifted leftward; MS - small loop, low SV; understand preload/afterload alterations.

3D heart anatomy →

Diastolic dysfunction + the stiff ventricle

Diastolic dysfunction (HFpEF, hypertensive heart disease, hypertrophic cardiomyopathy, infiltrative disease) shifts the diastolic portion of the PV loop UP and LEFT — the ventricle is stiff, requiring higher filling pressures for the same end-diastolic volume.

Implications

small reductions in preload cause large drops in stroke volume (preload-dependent)
atrial contraction matters disproportionately (loss of sinus rhythm devastating)
PA wedge pressure no longer reliably reflects LVEDV

Anesthetic strategy

maintain euvolemia (don't dehydrate)
maintain sinus rhythm (cardiovert AF aggressively)
avoid tachycardia (more diastolic filling time needed)
gentle volume + phenylephrine for hypotension

Diastolic dysfunction PV loop (stiff ventricle): upward shift of EDPVR; small loop change with filling pressures, preserved EF but impaired relaxation - HFpEF physiology.

Frank-Starling + the operating-room translation

KeyFrank-Starling: stretch of myocardium during diastole increases force of contraction in the next systole, until overstretch causes decline.

The ascending portion of the curve is preload-responsive — fluid bolus increases CO.

The flat/descending portion is preload-unresponsive — more fluid causes pulmonary edema without CO benefit.

The CURVE shifts depending on contractility: failing heart sits on a flatter curve at the same preload.

Bedside translation: PASSIVE LEG RAISE or 250-500 mL crystalloid bolus — measure CO/SV change predicts whether fluid will help.

Stroke volume variation (SVV) on arterial waveform >10-15% during positive-pressure ventilation suggests preload-responsive.

Frank-Starling: preload-stroke volume relationship. Increased preload (LVEDV) stretches sarcomeres for more forceful contraction up to optimum; flattens in heart failure; informs fluid responsiveness assessment.

⚠ Common pitfalls

Treating preload, afterload, and contractility as independent — they couple through the ventricle's pressure-volume relationship.
Calling diastolic dysfunction a 'small problem' — it's a major driver of OR hypotension in HFpEF.
Dropping HR in mitral stenosis 'to be safe' — tachycardia cuts filling time; both extremes are dangerous.
Reading wedge pressure as LVEDV in diastolic dysfunction — the relationship is no longer linear.

💎 Clinical pearls

Severe AS hypotension: phenylephrine first — preserves coronary perfusion of the hypertrophied LV.
MR benefits from afterload reduction — anesthetic-induced vasodilation can actually help forward flow.
Stroke-volume variation >12% on the A-line during PPV predicts fluid responsiveness.
ESPVR slope = contractility independent of load — that's the conceptual answer to 'how do I assess contractility?'

Recap

Severe AS hypotension: phenylephrine first — preserves coronary perfusion of the hypertrophied LV.
MR benefits from afterload reduction — anesthetic-induced vasodilation can actually help forward flow.
Stroke-volume variation >12% on the A-line during PPV predicts fluid responsiveness.
ESPVR slope = contractility independent of load — that's the conceptual answer to 'how do I assess contractility?'

Mark each section done to complete the module.