No abstract

No abstract

Large changes in stroke volume and peripheral vascular resistance were induced by varying the heart rate and by intra-aortically infusing acetylcholine or angiotensin II in six dogs with heart block and electromagnetic flowmeters chronically implanted around their ascending aortas. Changes in stroke volume, aortic and atrial pressures, and systemic resistance were monitored continuously for 3-6 hours under morphine-pentobarbital anesthesia. The characteristics of diastolic pressure decay at heart rates ranging from 60 beats/min to 200 beats/min and during transient periods of asystole were studied, especially with reference to the distortions caused by reflected pressure waves. The diastolic phase of pressure pulses recorded over a segment of the thoracic aorta several centimeters long centered about 4 cm cephalad to the dorsal insertion of the diaphragm could be closely approximated by a straight line on a semilogarithmic scale. Under the conditions of these experiments, changes in the slope of that line and of its reciprocal, the time constant, correlated well with concomitant variations in peripheral vascular resistance. This relationship appears to be of practical value for continuous monitoring of systemic resistance directly from the diastolic segments of pressure pulses recorded from the lower thoracic aorta. KEY WORDSatrial-ventricular pacing dog vasoactive drugs peripheral vascular resistance central aortic pressure decay • The contour of the arterial pressure pulse varies dramatically during its transmission down the arterial tree, and the pressure decay during diastole is generally not a monotonic function of time (1-4). However, a relatively smooth diastolic pressure decay has been described for aortic pressure pulses recorded near the dorsal insertion of the diaphragm (5, 6); this observation has been confirmed repeatedly in our laboratory. An initial objective of this study was to determine how uniformly an approximately monotonic diastolic decay of the aortic pressure pulse could be recorded from this particular site in the aorta in different dogs and during widely different hemodynamic conditions. Secondarily, a time-independent method of characterizing this pressure decay, presumably caused by drainage of blood from the large arteries to the periphery, was sought. If such a time-independent characterization could be established, it would allow extrapolation into the immediately preceding or subsequent systolic periods of the decrement in aortic pressure due to peripheral flow. If possible, this extrapolation would provide a means of "correcting" aortic pressures during systole for the drainage of blood from the great arteries during ventricular ejection. This increment in aortic pressure due to ventricular ejection might be directly related to individual values of stroke volume by, at worst, a small number of calibration factors or, at best, a single easily determined constant multiplier.When pressure pulses were recorded from the above-mentioned specific aortic location in preliminary experiment...

SUMMARY Present methods for measurement of stroke volume from die aortic pressure pulse are not suitable for beat-to-beat determinations during non-steady state conditions because these methods assume that each systolic ejection is equal to the peripheral runoff during the same beat We bare tested a new method which allows determination of an aortic pressure-volume conversion factor over a wide range of pressures during transient changes in stroke volume and infusions of vasoactive drugs in 6 dogs with chronically implanted aortic electromagnetic flowmeters. Each aortic diastolic pressure decay is approximated by an exponential the time constant of which is used to calculate the pressure loss during systole due to blood flow into the periphery. The total increment in aortic pressure due to systolic ejection, if there were no flow from the aorta during systole, then is calculated. The total systolic increment (AP 3V ) is assumed to describe the pressure-volume characteristics during systole and is related to stroke volume by a constant multiplier that is derived from the indicator-dilution measurements of cardiac output. The values for beat-to-beat variations that were determined by use of the aortic electromagnetic flowmeter and by this aortic pressure pulse method were found to be within the range of measurement errors of stroke volume determined from individual aortic electromagnetic flow pulses.