External Carotid Pulse Research Articles

The use of echocardiography to measure isometric contraction time

The current methods for estimating isometric contraction time were discussed. Ultrasonically derived isometric contraction time, using external carotid pulse tracing, phonocardiogram, and the B-point of the mitral echogram was also measured. Recordings were performed in 10 normal subjects, and 15 patients. Hypertrophic cardiomyopathy (5), congestive cardiomyopathy (6), and ischemic heart disease (4). In 11 patients, the results were correlated with the internal isometric contraction time. The ultrasound isometric contraction time showed good correlation with the internal isometric contraction time (r = 0.92, P < 0.01). The external isometric contraction time showed less correlation with the internal isometric contraction time and was significantly shorter (P < 0.01). The ultrasound isometric contraction time showed a superior discriminating value to the external isometric contraction time for differentiating the normal subjects from the patients' group.

Assessing the severity of aortic stenosis by phonocardiography and external carotid pulse recordings.

Phonocardiograms and carotid pulse tracings were done on a group of 47 patients with all degrees of aortic stenosis and were compared with two groups of normals. Indices evaluated were pre-ejection period, left ventricular ejection time, maximum rate of arterial pulse rise, arterial half rise time (T time) and upstroke time, and timing of the peak intensity of the systolic murmur in relation to the electrocardiographic QRS and first heart sound. The indices most indicative of the presence of aortic stenosis and best correlated with its severity were the ejection time index, the maximal rate of rise of the carotid pulse and the timing of the peak of the systolic murmur. If, in a given case, all three of these indices fall outside of certain limits (ejection time index &gt;0.42 sec, maximum rate of arterial pulse rise &lt;500 mm Hg/sec, and Q wave to peak of murmur &gt;0.19 sec), then severe aortic stenosis is almost invariably present.

Determination of systemic vascular resistance by a noninvasive technic

Measurement of systemic vascular resistance in man currently requires arterial and venous cannulation, so that cardiac output and mean arterial blood pressure may be simultaneously determined. This report describes a noninvasive technic for determining systemic vascular resistance (SVRn), utilizing an ultrasonic method for cardiac output measurement, and a combination of sphygmomanometry and external carotid pulse tracing analysis for determination of mean arterial blood pressure. SVRn was measured by this technic in 18 patients and compared with systemic vascular resistance determined by conventional methods at cardiac catheterization (SVRc). There was excellent correlation, with SVRc = 0.865 SVRn+216 and r = 0.85. The sensitivity of the method was verified in studies on 12 normal subjects in whom SVRn while supine (1235 ± 61 dyne-sec-cm–5, mean ± se) was less than SVRn while standing (1416 ± 81, P < 0.01) and greater than SVRn supine after amyl nitrite inhalation (652 ± 41,P < 0.0001). It is concluded t...

Determination of systemic vascular resistance by a noninvasive technic.

Measurement of systemic vascular resistance in man currently requires arterial and venous cannulation, so that cardiac output and mean arterial blood pressure may be simultaneously determined. This report describes a noninvasive technic for determining systemic vascular resistance (SVR n ), utilizing an ultrasonic method for cardiac output measurement, and a combination of sphygmomanometry and external carotid pulse tracing analysis for determination of mean arterial blood pressure. SVR n was measured by this technic in 18 patients and compared with systemic vascular resistance determined by conventional methods at cardiac catheterization (SVR c ). There was excellent correlation, with SVR c = 0.865 SVR n +216 and r = 0.85. The sensitivity of the method was verified in studies on 12 normal subjects in whom SVR n while supine (1235 ± 61 dyne-sec-cm –5 , mean ± se ) was less than SVR n while standing (1416 ± 81, P &lt; 0.01) and greater than SVR n supine after amyl nitrite inhalation (652 ± 41, P &lt; 0.0001). It is concluded that this noninvasive, simple, and safe technic should prove to be a useful bedside method for routine clinical measurement of systemic vascular resistance.

Midsystolic Carotid Pulse Wave Retraction in Subjects with Prolapsed Mitral Valve Leaflets

Ventriculographic1-2 and echocardiographic3 studies have demonstrated that in some subjects, the syndrome of midsystolic click and late systolic murmur4 is based on late systolic prolapse of mitral valve leaflets. We present here external carotid pulse tracings obtained from patients with angiographically documented prolapse of posterior mitral valve leaflets. All subjects had normal coronary arteriograms; there was no evidence of an aortic subvalvular pressure gradient at rest, during isoproterenol infusion, and after catheter provoked ventricular extrasystoles.

Respiratory variation of left ventricular ejection time in patients with pericardial effusion

Left ventricular ejection times were measured by external carotid pulse tracing in 2 patients with pericardial effusion who had at most only an equivocal paradoxical pulse. Both patients demonstrated a 50 msec variation of ejection time with respiration at a constant heart rate. None of 10 control patients had variation in ejection time of more than 10 msec. These observations confirm the original observations of Weissler et al., who noted variations in left ventricular ejection time in a patient with pericardial effusion; the findings also indicate that such changes may be present when there is no significant paradox during intraarterial pressure recording.

Direct correlation of external systolic time intervals with internal indices of left ventricular function in man.

Direct correlation of externally measured systolic time intervals with internally measured indices was obtained using catheter-tip micromanometers in six patients who had normal coronary arteriograms. Simultaneous recordings were made of central aorta and left ventricular pressure, maximum rate of rise in left ventricular pressure (dp/dt), external carotid pulse, external and internal sound, and electrocardiogram. Acute interventions were used to vary the indices by a variety of mechanisms including changes in contractility, preload, afterload, and heart rate. The initial values and the changes in these values produced by acute interventions are identical for left ventricular ejection time (LVET) whether measured externally (range 175 to 385 msec) or internally (range 169 to 392), r = 0.99. Although the absolute values differed for internally measured isovolumic contraction time (internal ICT), externally measured ICT, and preejection time (PEP), there was good linear correlation between the changes observed in these values following the interventions. Changes in PEP and internal ICT showed excellent linear correlation (r = 0.94) and were also alike in absolute value following the interventions. The interval from the Q wave of the electrocardiogram to rise in left ventricular pressure (electrical-mechanical delay) did not change significantly during these interventions. During a period of spontaneous isorhythmic dissociation there was close tracking between beat-to-beat changes in PEP and internal ICT and between externally and internally measured LVET. Following acute interventions PEP and left ventricular dp/dt changed inversely. Externally measured systolic time intervals have therefore been shown in man to correlate well with directly measured internal indices, both in steady-state conditions and during a series of acute interventions. This convenient and atraumatic method has been shown to be a valid and sensitive measure of myocardial performance.

Systolic time intervals: Relation to severity of coronary artery disease, intercoronary collateralization and left ventricular dyskinesia

In 35 patients total electromechanical systole (Q-S 2), left ventricular ejection period, preejection period, isovolumetric contraction time and preisovolumetric contraction time (Q-S 1) were measured from simultaneous recordings of electrocardiogram, phonocardiogram and external carotid pulse tracing. The severity of coronary artery disease, the existence of intercoronary collateral vessels and the contractility of the left ventricular wall were determined by coronary arteriography and left ventriculography. Group 1, 25 nondigitalized patients, and Group 2, 10 digitalized patients, were further divided into subgroups: patients with triple, double and single coronary artery disease. In addition, separate evaluations were made on patients in Group 1 with left ventricular dyskinesia (10 patients), with intercoronary collaterals (12 patients) and without collaterals (9 patients). In Group 1, significant shortening of left ventricular ejection period (W < 0.025, W = Wilcoxon test) and Q-S 1 (W < 0.05) and significant lengthening of isovolumetric contraction time (W < 0.02) were noted. There was a tendency to shorten the Q-S 2 interval and lengthen the preejection period. In Group 2, digitalis appeared to reverse the influence of coronary artery disease on preejection period, the Q-S 1 interval and isovolumetric contraction time, and to increase the shortening of the Q-S 2, interval (W < 0.05) and left ventricular ejection period (W < 0.05). Left ventricular dyskinesia did not change any of these values. Patients without intercoronary collaterals had significantly shortened Q-S 2 interval, left ventricular ejection period and Q-S 1 interval (W < 0.05, W < 0.0.5 and W < 0.05, respectively). Coronary artery disease, irrespective of the existence of left ventricular dyskinesia and intercoronary collaterals, shortened the left ventricular ejection period and the Q-S 2 interval. The most significant decrease in the Q-S 2 interval occurred in patients without intercoronary collaterals. The prolongation of preejection period was due merely to the lengthening of isovolumetric contraction time, in spite of the masking effect of a shortened Q-S 1 interval. Digitalis may neutralize or even reverse the changes in preejection period, Q-S 1 interval and isovolumetric contraction time due to coronary artery disease.

Unusual hemodynamic findings of diagnostic value in a case of left atrial myxoma ∗

Unusual laboratory findings in a case of left atrial myxoma are presented. The end-diastolic pressure gradient between the left ventricle and wedge position ranged from 0 to 21 mm. Hg with no relation to heart rate or rhythm, respiration, or wedge position. The y descent was slow rather than the usual rapid y descent associated with mobile atrial myxomas. These findings probably were caused by left atrial inflow obstruction rather than outflow obstruction. Pressure transients owing to sudden acceleration and deceleration of the tumor and surrounding blood, with subsequent oscillations of the heart and great vessels, were recorded in the left ventricle, aorta, external carotid pulse, and external phonocardiogram during the phase of isovolumic contraction and during a period beginning with isovolumic relaxation through rapid ventricular filling. These findings, when present, strongly suggest the presence of a mobile atrial tumor.