James A. Shaver

Cardiac tamponade: hemodynamic observations in man.

SUMMARY Hemodynamic studies were performed before and after pericardiocentesis in 19 patients with pericardial effusion. Right atrial pressure decreased significantly, from 16 ± 4 mm Hg (mean ± SD) to 7 ± 5 mm Hg in 14 patients with cardiac tamponade. This change was accompanied by significant increases in cardiac output (3.87 ± 1.77 to 7 ± 2.2 I/min) and inspiratory systemic arterial pulse pressure (45 ± 29 to 81 ± 23 mm Hg). The remaining five patients did not demonstrate cardiac tamponade, as evidenced by lack of significant change in these hemodynamic parameters.In all patients with tamponade, right ventricular end-diastolic pressure (RVEDP) was elevated and equal to pericardial pressure; equilibration was uniformly absent in patients without tamponade. During gradual fluid withdrawal in the tamponade group, significant hemodynamic improvement was largely confined to the period when right ventricular filling pressure remained equilibrated with pericardial pressure. In 10 patients with tamponade and pulsus paradoxus, pulmonary arterial wedge pressure (PAW) was equal to pericardial pressure except during early inspiration and expiration when it was transiently less and greater, respectively; however, inspiratory right atrial pressure never fell below pericardial pressure. In these 10 patients, PAW decreased significantly following pericardiocentesis (P < 0.001). In the remaining four patients with tamponade but without pulsus paradoxus, all of whom had chronic renal failure, PAW was consistently higher than pericardial pressure or RVEDP and did not decrease after pericardiocentesis.These data tend to confirm the hypothesis that in patients with tamponade, the venous pressure required to maintain any given cardiac volume is determined by pericardial rather than ventricular compliance. When pericardial compliance determines diastolic pressure in both ventricles, relative filling of the ventricles will be competitive and determined by their respective venous pressures (pulmonary vs systemic), which vary with respiration and alternately favor right and left ventricular filling. This results in pulsus paradoxus. However, if pulmonary arterial wedge pressure is markedly elevated before the onset of tamponade, as in patients with chronic renal failure, then pericardial compliance may only determine right ventricular filling pressure. In such cases, pulsus paradoxus may be absent.

Autonomic Mechanisms in Hemodynamic Responses to Isometric Exercise

Selective autonomic blockade with intravenous propranolol, practolol, atropine, and combined atropine-propranolol was utilized to elucidate the role of the autonomic nervous system in the hemodynamic responses in young adult male volunteers to handgrip sustained at 30% of maximal voluntary contraction for 3 min. The initial 30 s of the tachycardia response was found to be mediated by withdrawal of vagal dominance, as evidenced by blockade of this response by prior atropinization. The mid and late portion of the heart rate response curve was demonstrated to be sympathetic in origin, since it was unaffected by atropine, but was suppressed by combined atropine-propranolol blockade. Sympathetic stimulation appears to be a secondary mechanism for increasing the heart rate, however, as it becomes operative only after the first mechanism of vagal withdrawal has been utilized. This was confirmed by the finding that beta adrenergic receptor blockade alone had little effect on the heart rate response curve. The pressor response to handgrip was accompanied by increased cardiac output and no change in calculated systemic vascular resistance. After propranolol, handgrip resulted in increased peripheral resistance and an equivalent rise in arterial pressure, but no increase in cardiac output. It was concluded that the increase in resistance was the result of sympathetically induced vasoconstriction. This response was shown to be independent of peripheral beta adrenergic receptor blockade by the use of practolol, a cardio-selective beta adrenergic receptor-blocking drug which caused identical hemodynamic responses to those observed after propranolol. Left ventricular ejection time (corrected for heart rate) was prolonged by handgrip. The increased afterload imposed on the left ventricle by sustained handgrip may explain the prolongation of ejection time index. Preejection period was prolonged by SHG after propranolol and shortened after atropine. In addition to confirming the previously defined role of the parasympathetic nervous system, this study delineates the role of the sympathetic nervous system in the heart rate and pressor responses to sustained handgrip.

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 obser...

Reflex heart rate control in man.

Abstract In summary, the relative roles of the parasympathetic and sympathetic nervous systems in baroreceptor reflex heart rate control have been studied in eleven normal young men. These data have been compared to the results of similar studies in a heart transplant subject. The findings indicate that in normal conscious men, reflex parasympathetic stimulation and withdrawal primarily control heart rate responses to changes in blood pressure. Beta-adrenergic activity, while influencing basal heart rate plays little, if any, role in baroreceptor reflex heart rate control. The Valsalva maneuver may be used as an effective measure of parasympathetic integrity but it may not be used as a reliable index of sympathetic integrity. The pharmacologically denervated heart is similar in terms of reflex responses to the surgically denervated heart in conscious man. The heart rate responses to Valsalva maneuver, amyl nitrite inhalation, and phenylephrine infusion should be reliable indices of parasympathetic reinnervation of the transplanted heart should reinnervation occur.

The effect of steady-state increases in systemic arterial pressure on the duration of left ventricular ejection time

The effect of steady-state increases in systemic arterial pressure on the duration of left ventricular ejection time was studied in 11 normal male subjects. Methoxamine, a pressor amine of predominantly vasoconstrictor activity but lacking significant inotropic effect, was administered intravenously resulting in an average increase in mean arterial pressure of 27 mm Hg. Heart rate was held constant by high right atrial pacing, and there was no significant change in cardiac output. During methoxamine infusion, when stroke volume, heart rate, and inotropic state were held constant, left ventricular ejection time increased as mean arterial pressure increased. There was a highly significant correlation between the increase in mean systolic blood pressure and the prolongation of left ventricular ejection time (r = 0.870). In one subject, an increase in mean systolic pressure of 75 mm Hg prolonged left ventricular ejection time 55 msec, producing paradoxical splitting of the second heart sound. The prolongation of left ventricular ejection time during infusion was not blocked by the prior intravenous administration of atropine sulfate or propranolol hydrochloride, thus ruling out both vagal inhibition of the left ventricle and reflex withdrawal of sympathetic tone as its cause. In three subjects, left ventricular end diastolic pressure was measured and found to be significantly increased. This finding suggests that the normal left ventricle maintains a constant stroke volume in the presence of an increased pressure load by the Frank Starling mechanism. This study concludes that arterial pressure must be included as a prime determinant of left ventricular ejection time along with stroke volume, heart rate, and inotropic state in intact man.

Isovolumic relaxation period in hypertrophic cardiomyopathy

Previous reports have demonstrated that patients with hypertrophic cardiomyopathy have a prolonged isovolumic relaxation period as a result of a delay in mitral valve opening, reflecting a reduced rate of fall of left ventricular pressure. This period as measured from the aortic closure sound (A2 on phonocardiogram) to the opening of the mitral valve (on echocardiogram) was determined in 84 patients with hypertrophic cardiomyopathy and compared with findings in 31 normal volunteers. The duration of the isovolumic relaxation period in the 84 patients had a wide range from 0 to 160 ms (mean 71 +/- 32) that was not significantly different from that in normal subjects (63 +/- 11 ms). However, it was possible to identify a group of 15 patients with an extremely short isovolumic relaxation period, 2 standard deviations below the normal range. This shortening was due to a marked delay in aortic closure sound (A2) due to late left ventricular-aortic pressure crossover, as well as early opening of the mitral valve secondary to elevated left atrial pressure, which was confirmed by hemodynamic correlations and digitized echocardiographic data. In this subset of patients, A2 is a poor marker of the onset of rapid left ventricular pressure decline and, thus, the interval from A2 to mitral valve opening is not a valid reflection of left ventricular relaxation. It is concluded that in hypertrophic cardiomyopathy, both the timing and sequence of relaxation are abnormal, as is the rate of relaxation. Furthermore, the isovolumic relaxation period is multifactorially determined and depends not only on the rate of left ventricular pressure decline, but also on the magnitude of the pressure drop from A2 to mitral valve opening. All of these determinants must be kept in mind when the isovolumic relaxation period is used as a measure of left ventricular relaxation.

Sound Pressure Correlates of the Second Heart Sound An Intracardiac Sound Study

The sound pressure correlates of the second heart sound were studied in 22 patients during diagnostic cardiac catheterization. Simultaneous right ventricular and pulmonary artery pressures were recorded with equisensitive catheter-tip micromanometers together with the external phonocardiogram and ECG. In 12 patients having normal pulmonary vascular resistance (group 1), pulmonic closure sound was coincident with the incisura of the pulmonary artery pressure curve which in turn was separated from the right ventricular pressure trace by an interval denoted hangout. The duration of this interval varied (33-89 msec), was independent of pulmonary artery pressure or resistance and was felt to be primarily a reflection of the capacitance of the pulmonary vascular tree. The absolute value of this interval during inspiration was very similar to the splitting interval and, when subtracted from the Q-P2 interval, the remaining interval (QRV) was almost identical to the Q-A2 interval, indicating that the actual duration of right and left ventricular systole is nearly equal. Awareness of the existence of the hangout interval and its hemodynamic determinants offers a reasonable mechanism to explain the audible expiratory splitting of the second heart sound found in patients with idiopathic dilatation of the pulmonary artery following atrial septal defect repair and in one additional patient studied with mild valvular pulmonic stenosis. In nine patients with elevated pulmonary vascular resistance approaching systemic levels (group 2), the absolute value of the hangout interval was markedly reduced (15-28 msec) consistent with the decrease in capacitance of the pulmonary vascular bed and the increased pulmonary vascular resistance known to occur in pulmonary hypertension. In those patients where the duration of right and left ventricular systole were nearly equal, narrow splitting of the second heart sound was present. In those patients where selective prolongation of right ventricular systole occurred, the narrow hangout interval persisted, but the splitting interval was prolonged proportionate to the increased duration of right ventricular systole.

Alterations of right ventricular systolic time intervals by chronic pressure and volume overloading.

Right ventricular (RV) systolic time intervals and hemodynamic parameters were determined by micromanometric techniques in 13 subjects with normal right ventricles (NRV). These data were compared to those of 16 patients with pulmonary hypertension (PH) or predominant pressure overloading and 13 individuals with uncomplicated secundum atrial septal defects (ASD) or predominant volume overloading.In PH, the QP2 interval tends to remain within the normal range due to reciprocal changes in isovolunmic contraction (ICT) and ejection (RVET) times. Elevations of pulmonary artery diastolic pressure are associated with increases in the mean rate of isovolumic pressure rise (MRIPR) (r = 0.84), but the latter change does not fully compensate for the widened ventriculoarterial diastolic pressure dif-splitference and ICT becomes prolonged (P ⩽ 0.001). Factors other than stroke index depression which may contribute to the decreased duration of RVET (P ⩽ 0.001) include tricuspid regurgitation and elevation of pulmonary vascular impedance.In ASD, QP2 is significantly prolonged (P ⩽ 0.025) due to a significant increase in RVET (P ⩽ 0.005). In contrast to NRV, a linear correlation of RVET and stroke index was not present, which suggested an alteration of ejection dynamics in this group. Despite a high incidence of complete or incomplete right bundle branch block, the interval from QRS onset to rapid RV pressure upstroke was not prolonged. This is most probably the result of peripheral bundle branch block of genesis of the QRS pattern by right ventricular hypertrophy.

Hemodynamic Observations after Cardiac Transplantation

Abstract Hemodynamic observations were performed one and six months after cardiac transplantation in a 46-year-old man. Cardiac catheterization revealed normal pressures at rest and a slightly decreased cardiac index. Total cardiac denervation was documented by absence of reflex changes in heart rate during physiologic and pharmacologic stimuli. Intracardiac electrocardiography demonstrated both donor and recipient p waves, the former always controlling the heart rate. Observations during atrioventricular dissociation indicated that the transplanted heart has active atrial transport. The denervated heart responded to the stress of muscular exercise. Cardiac output increased predominantly by increasing stroke volume, although delayed increments in heart rate occurred. After complete beta-adrenergic blockade, the response of the heart rate to exercise was attenuated but not completely blocked. These findings suggest that whereas circulating catecholamines have an important role in cardiac acceleration durin...

Modulation of hemodynamic effects with a converting enzyme inhibitor: Acute hemodynamic dose-response relationship of a new angiotensin converting enzyme inhibitor, lisinopril, with observations on long-term clinical, functional, and biochemical responses

The hemodynamic effects of varying oral doses of the long-acting converting enzyme inhibitor lisinopril were studied in an acute, single-blind, parallel fashion in 55 patients with moderate to severe congestive heart failure. Doses of 2.5, 5.0, and 10 mg produced a significant increase in cardiac index and significant reductions in pulmonary capillary wedge, right atrial, pulmonary arterial, and systemic arterial pressures and systemic vascular resistance. The changes were present up to 24 hours after dosing for most parameters. There was a clear-cut dose-response relationship observed. Forty-seven patients were followed over a 3-month period, during which functional status and exercise tolerance improved. Although 26% showed some evidence of renal dysfunction with lisinopril, these changes could be normalized by decreasing either the lisinopril or the diuretic dose. These data demonstrate that the hemodynamic changes with the long-acting converting enzyme inhibitor lisinopril can be modulated with dose adjustment in patients with congestive heart failure. They also suggest that renal function changes may be normalized by adjustment of either the dose of lisinopril or the diuretic dose.