First examine the radial pulse: note the rate, the volume, the character, the rhythm and the vessel wall; if the right side is difficult to detect, check and compare it with the left (figure 39a,b).
The rate is between 60 and 80 in fit individuals. In healthy young subjects the rate varies with the respiratory cycle (sinus arrhythmia); this becomes less noticeable with age.
A low volume pulse may indicate low stroke volume. A bounding pulse suggests a large pulse pressure, as seen in a number of conditions, such as pregnancy, thyrotoxicosis, anemia, ateriovenous fistulae, Paget’s disease and chronic respiratory failure.
The rhythm in health is sinus rhythm, and beat-to-beat variation is not usually detectable. Irregular rhythms may be caused by the presence of atrial fibrillation (irregularly irregular pulse, usually obvious when the pulse is rapid), or may be caused by the presence of atrial or ventricular premature beats. With ventricular premature beats, there is usually a compensatory pause immediately after the premature beat, and the very next beat is likely to be a larger pulse volume. When these variations occur in health they can be eliminated by exercise.
The character of the pulse is best determined by examining the carotid pulse (figure 40). This enables you to see and analyse the wave form. A slow rising pulse suggests aortic outflow obstruction due to either aortic stenosis or subvalvular aortic stenosis.
The anacrotic pulse (due to slow ejection of blood from the left ventricle in aortic stenosis) can be combined with a collapsing pulse to produce the bisferiens pulse.
A collapsing pulse (figure 41), characterised by a rapid up and down stroke, may occur when there is significant aortic regurgitation, a patent ductus arteriosus or an arteriovenous malformation. This ‘water-hammer’ pulse is felt by your palm placed around the wrist.
In pulsus paradoxus, deep inspiration lowers the pulse volume (rather than the normal increase) and this may occur with constrictive pericarditis, pericardial tamponade and severe asthma. The latter is caused by abnormal movement of the septum, occluding the cavity of the left ventricle during systole.
In assessment of the jugular venous pulse, remember that the surface marking of the internal jugular vein is a line passing from just behind the angle of the jaw to the depression between the sternal and clavicular heads of the sternomastoid muscle. The patient should be at an angle of 45 degrees, with their head turned slightly away from the midline. Look just deep to the sternomastoid muscle: in health, the pulsation is barely visible. In heart failure or pericardial constriction, the jugular venous pulse is elevated.
It can be difficult to distinguish between a venous and arterial pulsation in the root of the neck. Press lightly over the internal jugular vein, in the root of the neck, to obliterate the venous pulse, the arterial pulsation can then be observed independently (figure 42).
Another technique to identify the jugular pulse, is to apply light pressure over the liver, this expels more blood into the right side of the heart. The manoeuvre exaggerates a raised jugular venous pulse (hepatojugular reflex – figure 43). Non-pulsatile elevation of venous pressure is suggestive of superior vena caval obstruction.
When there is an abnormality of the venous pulse, try to synchronise it with the arterial pulse by compressing the contralateral carotid pulse. In this way, you can time the systolic waves of tricuspid regurgitation and the occasional cannon wave, typical of complete heart block.
Occasionally flutter waves may be seen and, if there is a 2:1 block, the venous wave moves twice as fast as the carotid rate. The ACXVY components of a normal venous pulse are a textbook rather than a clinical phenomenon.