Cardiac Cycle — Phases, Valve Events, Heart Sounds, Wiggers Diagram and the Pressure-Volume Loop

StatPearls defines the cardiac cycle as a series of pressure changes within the heart that move blood through the chambers. Depolarisation starts at the SA node, the atria contract together, the impulse pauses briefly at the AV node, and then both ventricles contract together. Mechanical events lag slightly behind electrical ones — on a Wiggers diagram the QRS complex just precedes the rise in ventricular pressure.

Valves make the flow one-way. Because right and left sides behave alike (at very different pressures), the cycle is usually described for the left ventricle.

• Systole = from mitral (and tricuspid) closure to aortic (and pulmonary) closure — ventricular contraction and ejection.
• Diastole = from aortic closure to the next mitral closure — ventricular relaxation and filling.

Ventricular function is divided into four phases: isovolumic contraction, ejection, isovolumic relaxation and filling. Every phase boundary is a valve opening or closing, which happens when the pressure gradient across that valve reverses.

A Wiggers diagram stacks, on a common time axis, aortic pressure, left atrial pressure, left-ventricular pressure, ventricular volume, the ECG and the phonocardiogram. Read it vertically: at any moment you can see which valve is open and which sound is produced.

• S1 coincides with the ventricular pressure curve crossing atrial pressure (mitral closure), just after the QRS.
• Aortic valve opens where LV pressure crosses aortic pressure; LV and aortic curves then run together.
• S2 coincides with the incisura (dicrotic notch) of the aortic pressure curve — A2 and P2 fall on the incisurae of the aortic and pulmonary curves.
• Ventricular volume is highest at end-diastole (EDV) and lowest at end-systole (ESV); the drop between them is the stroke volume.
• On the atrial curve, the a wave follows atrial systole (after the P wave), and the c and v waves follow in ventricular systole.

Because the mitral component dominates S1, changes in S1 intensity mostly reflect forces acting on the mitral valve — left-ventricular contractility, mitral valve structure and the PR interval. S2 has been called the 'key to auscultation of the heart' because its two components and their respiratory behaviour orient you to every other sound.

Timing a murmur against S1 and S2 is the first step in auscultation: a murmur between S1 and S2 is systolic (blood leaving the ventricle — aortic stenosis, mitral regurgitation, HOCM); one after S2 is diastolic (blood entering the ventricle — mitral stenosis, aortic regurgitation). See valvular heart disease and murmurs for the full list.

Normally A2 precedes P2, and the gap widens on inspiration because pulmonary valve closure is delayed (lower pulmonary vascular impedance and more right-sided filling). The two components need more than about 20 ms of separation to be heard as two sounds. A split of more than 0.04 s on expiration is usually abnormal (Clinical Methods).

The mechanism is the 'hangout interval': in the low-impedance pulmonary circulation the pulmonary artery pressure curve lags behind the RV pressure curve by about 30–120 ms, while on the left side the lag is 5 ms or less. Inspiration lowers pulmonary impedance further, prolonging RV ejection and delaying P2, while left-sided ejection shortens slightly and A2 comes a little earlier.

The PV loop plots LV volume on the x-axis and pressure on the y-axis for one beat, so it runs anticlockwise through the four phases: filling along the bottom (rising volume), isovolumic contraction up the right side, ejection across the top (falling volume) and isovolumic relaxation down the left side.

StatPearls notes that, with afterload and contractility constant, a rise in preload moves the loop rightward along the EDPVR, increasing EDV and stroke volume, with a slight rise in ejection fraction. Solaro's analysis shows why afterload matters: when blood is ejected into a stiffer, higher-pressure aorta, the sarcomeres shorten less, so ESV rises and stroke volume falls until EDV increases to compensate. An increase in contractility (e.g. β1-adrenergic stimulation) shifts and rotates the ESPVR to the left, so the ventricle empties to a smaller ESV at the same afterload.

On the Frank–Starling curve the same factors appear as curve shifts: catecholamines (more inotropy) or lower afterload shift the curve up; systolic failure, loss of myocardium after infarction, acute β-blockade or higher afterload shift it down.