Lab: Cardiac Cycle Practical

This practical session consolidates understanding of the cardiac cycle through physical examination techniques and Wiggers diagram analysis. Clinical examination of the cardiac cycle focuses on correlating observable physical signs with underlying haemodynamic events.

The carotid pulse is palpable between the S1 and S2 heart sounds — during ventricular ejection. Its timing confirms that the pulse follows isovolumetric contraction. The jugular venous pulse (JVP) reflects right atrial pressure changes. The right internal jugular vein is used for JVP assessment because it has a short, direct path to the right atrium (no valves between the vena cava and right atrium). The patient is positioned at 45° with head turned left. JVP waveforms: A wave (atrial contraction), C wave (tricuspid valve bulging into atrium during isovolumetric contraction), V wave (venous filling of atrium during ventricular systole), with X descent (atrial relaxation) and Y descent (AV valve opening).

Diastolic blood pressure represents the lowest aortic pressure — at the instant just before semilunar valve opening (during isovolumetric contraction). Systolic blood pressure represents the peak aortic pressure during mid-ventricular ejection. The incisura (dicrotic notch) on the arterial pressure trace coincides with S2 (semilunar valve closure).

During exercise, diastole is shortened more than systole. The slow mid-diastolic filling phase is preferentially lost. SV is preserved by enhanced venous return (skeletal muscle pump) and stronger atrial contraction. At very high heart rates (e.g. tachyarrhythmia >200/min), diastole becomes so short that ventricular filling is severely impaired → ↓EDV → ↓SV → ↓CO → syncope.

Hypertension increases afterload: the ventricle must generate higher pressure during isovolumetric contraction and ejection to overcome the elevated aortic diastolic pressure. This requires more myocardial work (represented by the larger pressure-volume loop area) and over time leads to left ventricular hypertrophy, increased ischaemic risk, and eventually heart failure. Aortic stenosis narrows the valve orifice, requiring the ventricle to generate supranormal pressures to eject blood — the pressure-volume loop shows elevated peak systolic pressure and delayed opening of the aortic valve.