In the clinical assessment of the arterial pulse, it is worth remembering the following points:
1. The three features of the arterial pulse that should be diligently sought for are the amplitude, the upstroke, and the pulse contour abnormalities.
2. Other features include the determination of rate, rhythm, pulse deficit, symmetry, radio-femoral delay, bruits, and specifically looking for the peripheral signs of aortic regurgitation when indicated.
3. Palpation of the carotid arterial pulsation is necessary to determine the pulse upstroke and for the detection of abnormal contours. The amplitude may bejudged by palpation of the carotid as well as the more peripheral vessels.
4. The amplitude of the pulse is assessed by determining the displacement felt by the palpating fingers. The displacement is dependent on the change in tension in the artery between diastole and systole. The amplitude of the pulse must be judged as to whether it is normal, low, or increased.
5. The low-amplitude (the low-volume) pulse usually indicates low momentum of ejection due to decreased stroke volume and low pulse pressure as seen in significant obstructive lesions of the outflow or the inflow tracts (severe aortic or mitral stenoses), poor ventricular pump function as in severe cardiomyopathy or heart failure, and severe reductions in left ventricular filling as in cardiac tamponade or significant loss in the blood volume or the extracellular fluid volume.
6. In severe systemic hypertension with excessive vasoconstriction, the peripheral pulse amplitude may be poor due to decreased change in radius and wall tension.
7. If the pulse amplitude is considered increased or exaggerated ("bounding pulses"), then conditions associated with large stroke volume and low peripheral resistance must be considered. These include aortic regurgitation and aortic regurgitation mimickers (aortic sinus with a communication to a low-pressure chamber such as the right atrium, aorto-pulmonary window, and persistent ductus arteriosus).
8. The pulse amplitude will also be exaggerated in conditions associated with vasodilatation and low peripheral resistance, since in these states (e.g., septic states, drugs causing vasodilatation, arterio-venous communications congenital or iatrogenic or due to pathological processes in systemic organs as in cirrhosis of the liver, chronic renal disease, chronic pulmonary disease, Paget's disease, and beriberi) the diastolic pressure in the vessel is low and therefore the change in tension is better appreciated.
9. In patients with combined aortic stenosis and regurgitation where both are significant, the amplitude of the carotid pulsation often would reflect the aortic stenosis, whereas the aortic regurgitation will show its effects on the amplitude more peripherally such as in the popliteal arteries.
10. In the elderly with decreased compliance of the large arteries, ejection of normal stroke volume may cause significant systolic hypertension. The pulse amplitude will be high due to rapid pulse wave velocity caused by the increased stiffness and reduced compliance of the arteries, resulting in increased augmentation of central systolic and pulse pressures due to reflection. In fact, even the presence of aortic stenosis may be masked in such patients.
11. The upstroke of the pulse is best assessed over the carotid artery. The normal rate of rise is felt as a sharp tap by the palpating finger. The delayed upstroke is felt as a gentle sustained push. In some, the sensation may be jagged, simulating a "thrill" or "shudder." A normally rising carotid pulse rules out significant fixed aortic stenosis. The delayed carotid upstroke, on the other hand, is indicative of fixed left ventricular outflow obstructive lesions. Rare exceptions are, of course, elderly patients. Delayed upstroke may be masked in the elderly with stiff aorta where the pressure rise may be steep due to the decreased compliance of aorta. The elderly may also have a hump on the upstroke due to an exaggerated anacrotic shoulder mimicking a delayed upstroke without the presence of any significant aortic stenosis.
When the amplitude of the pulse is low as in low stroke output, then the rate of the rise of the pulse is often difficult to judge.
12. When the upstroke of the pulse is thought to be brisk or rapid and if the pulse amplitude is normal or low, then conditions associated with rapid left ventricular ejection such as hypertrophic cardiomyopathy with or without subvalvular dynamic muscular obstruction must be considered. If the upstroke is brisk and the pulse amplitude is normal, then rapid ejection with normal stroke volume as in significant mitral regurgitation must be considered.
13. Bifid pulse contours or pulsus bisferiens must lead one to consider hypertrophic cardiomyopathy with possible obstruction as well as combined aortic regurgitation and stenosis where the aortic regurgitation is more dominant and hemody-namically significant than the aortic stenosis. In hypertrophic cardiomyopathy with obstruction, amplitude of the pulse is low while the upstroke will be brisk and the initial peak will be brisk and taller than the late peak. In combined aortic stenosis and regurgitation with bisferiens, the amplitude will be large and the upstroke will be relatively normal. The second peak will be larger than the first peak.
14. Exaggerated dicrotic wave may occasionally be the cause of a bifid pulse contour. The second impulse in this instance will occur in diastole as timed by auscultation. The exaggerated dicrotic wave is usually associated with low momentum of ejection, usually the result of low stroke volume as in severe heart failure, cardiomyopathy, and cardiac tamponade. In these instances, the pulse amplitude will be expected to be low.
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