Time domain analysis of the arterial pulse in clinical medicine

Abstract

The arterial pulse at any site is created by an impulse generated by the left ventricle as it ejects blood into the aorta, together with multiple impulses travelling in the opposite direction from reflecting sites in the peripheral circulation. The compound wave at any site depends on the pattern of ventricular ejection, the properties of large arteries, particularly their stiffness (which determines rate of propagation) and the distance to and impedance mismatch at reflecting sites. Physicians are familiar with waveform analysis in the time domain, as in the electrocardiogram (ECG) where the principal features are explicable on the basis of atrial depolarisation followed by ventricular depolarisation, then repolarisation. Effects of cardiac functional and structural disease can be inferred from the ECG. It is more difficult to make similar interpretations from the pulse waveform and clinicians usually use this only to count heart rate, extremes of the pressure pulse to express systolic and diastolic pressure, and (sometimes) time from wave foot to incisural notch to measure time of systole and diastole. More information can be gleaned from the shape of the arterial pressure wave through consideration of the factors which create it-on stiffening of large arteries with age, effects of drugs on smallest arteries, and changes in such arterial properties on left ventricular load and function. Such is a major challenge to future physicians. It is aided by better and more accurate methods for measuring flow and diameter as well as pressure waveforms, and by appropriate use of other analytic techniques such as analysis of the pulse in the frequency domain.

Augmentation Index, Left Ventricular Contractility, and Wave Reflection

“…Our findings of a significant negative correlation between heart rate and AIx in response to ␤-adrenergic stimulation are consistent with previous studies that have induced tachycardia by vasoactive drugs (nitroglycerine), 12 ventricular pacing, 25 and atrial or atrio-ventricular pacing. 13,26 Interestingly, the shapes of the radial and derived central waveforms after dobutamine infusion in this current study (Figure 3) are comparable with those found during high heart rates provoked by disparate mechanisms, including pacing, 26 junctional tachycardia, 33 and peak exercise. 34 As heart rate increases, there is a concomitant reduction in the ejection duration, as well as the diastolic portion of the cardiac cycle, with a proportionally greater reduction in the diastolic phase.…”

Non-invasive monitoring of central blood pressure by electrical impedance tomography: first experimental evidence

“…Further development work needs to be done to be able to measure aortic EIT-PTT values at even higher and lower blood pressures and also during mechanical ventilation and spontaneous breathing. Future studies including additional cardiovascular maneuvers such as NO administration and cold stress need to be performed in order to assess the sensitivity of the proposed EIT-PTT parameter to vasomotion phenomena [7].…”

Pulse Wave Analysis of the Aortic Pressure Waveform in Severe Left Ventricular Systolic Dysfunction

“…[1][2][3] Both the forward and reflected pressure waves are related to LV ejection wave amplitude. Additionally, the forward traveling wave is affected by central (elastic) arterial stiffness and peak LV ejection, whereas the reflected wave is affected by the elastic properties of the entire arterial tree, transmission velocity of the forward and reflected waves, and distance to the major reflecting site.…”