J D O'Toole

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.

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.

The mechanism of splitting of the second heart sound in atrial septal defect.

The mechanism underlying the width of splitting of the second heart sound (S,) was investigated in 27 patients with ostium secundum atrial septal defect (ASD), all of whom had significant left to right shunting. Micromanometer catheters were used to record simultaneous high fidelity right ventricular (RV) and pulmonary arterial (PA) pressures. Electrocardiogram and external phonocardiograms were recorded simultaneously with pressures. QP, QA, and Q-RV intervals were measured from the onset of the Q-wave of the ECG to the onset of P, A, and to the downstroke of the RV pressure trace at the level of the pulmonary incisura, respectively. The width of splitting of the second heart sound (A,-P, interval) and hangout (HO) intervals were derived by subtracting QA, from QP, and Q-RV from QP, respectively. The patients were divided into three groups. There were 14 patients in group I (normotensive ASD) with sinus rhythm and normal PA pressure (mean<21 mm Hg); in group II (hyperkinetic pulmonary hypertension) there were seven patients with sinus rhythm and elevated PA pressure (mean PA>23 mm Hg) and group III consisted of six patients with atrial fibrillation. For normotensive ASD, A,-P, and hangout intervals correlated well (r=0.91) and were essentially equal. QA, and Q-RV intervals were also approximately equal, indicating that the electromechanical interval was essentially equal for right and left ventricles (LV). In hyperkinetic pulmonary hypertension the hangout interval was relatively narrow as compared to group I (P < 0.001) and the splitting interval varied from narrow to wide, depending upon the relative durations of Q-RV and QA,. The QA, indices tended to be within normal limits, suggesting that the duration of Q-RV was the major determinant of the width of splitting. In atrial fibrillation, HO was fixed and narrow; A,-P, and Q-RV intervals were directly related to preceding cycle length. Thus, an understanding of the mechanism of splitting of the second heart sound in ASD must reflect the HO interval as well as the relative durations of RV and LV electromechanical systoles.

Sound pressure correlates of the Austin Flint murmur. An intracardiac sound study.

Mitral valve motion and pressure correlates of the Austin Flint murmur (AFM) were investigated in nine patients with aortic regurgitation using high fidelity catheter tip micromanometers and the mitral valve echocardiogram (MVE). External phonocardiography demonstrated a mid-diastolic murmur (MDM) in eight subjects and a presystolic murmur (PSM) in five. Maximum intensity of both AFM components was found in the left ventricular (LV) inflow tract; the murmur was not recordable in the left atrium (LA). In two patients, an apparent AFM was recorded in the intracardiac phonocardiogram when absent externally. Only one subject had a significant late diastolic “reversed” or LV to LA gradient; in this patient, presystolic mitral regurgitation was shown angiographically but no PSM was present and MVE revealed absence of atriogenic mitral valve re-opening. In two subjects, a PSM disappeared from the external phono when a “reversed” gradient occurred during the diastolic pause following a ventricular premature systole; this LV to LA gradient was associated with diastolic mitral regurgitation recordable in the left atrial phono. In two patients, LV inflow phono showed the MDM to begin 80–120 msec after the aortic second sound and during the D to E phase of the MVE. The rate of early diastolic mitral valve closure in patients (152±24 mm/sec) was not significantly different from 13 normals (232 i 30 mm/sec). With regard to the genesis of the AFM, the present study concludes: 1) diastolic mitral regurgitation plays no role, and 2) antegrade mitral valve flow is required but simultaneous retrograde aortic flow may also be necessary.

Delayed Postoperative Cardiac Tamponade: Diagnosis and Management

Symptoms and signs of decreased cardiac output associated with an elevated venous pressure should alert one to the possibility of delayed cardiac tamponade. Enlargement of the cardiothoracic ratio shown by serial roentgenograms and demonstration of significant pericardial effusion by echocardiogram or radionuclide angiocardiography support the diagnosis. Erratic response of the prothrombin time to administration of warfarin and abnormal results of liver function test are additional clues to its diagnosis. Right heart catheterization documents the presence of tamponade and excludes other diagnostic considerations. Operative decompression of the pericardial space can be accomplished by pericardicentesis, subxiphoid pericardiotomy, median sternotomy, or thoracotomy. Hemodynamic observations following the relief of tamponade assure that an adequate therapeutic procedure has been performed.

The contribution of tricuspid valve closure to the first heart sound. An intracardiac micromanometer study.

The sound-pressure correlates of the second high frequency component of a split first heart sound (S,) were investigated in 27 patients. An external phonocardiogram was recorded with high fidelity sound and pressure from the left and right atria in 21 patients, from the pulmonary artery in 14 of these, and from the central aorta in 11. In the remaining six patients, high fidelity recordings from the central aorta and right-sided chambers were obtained with an external phonocardiogram. The external component of S, that coincided with a left atrial C wave and “internal sound” was defined as M1. In those cases where the left atrial pressure was not recorded, this component could be identified by a low frequency transient in the central aortic pressure trace. The other external high frequency component of S, that was synchronous with a separate right atrial C wave and “internal sound” was defined as T,; with two exceptions, M, preceded T1. The two exceptions which caused rever-sal of this order, so that T1 preceded M, were due to chronic left bundle branch block and mitral stenosis. In both cases, T, was shown to be distinctly separated from the upstroke of pressure rise in the central aorta. This finding was also demonstrated in three cases of right bundle branch block and one case with aortic valvular disease. The usual asynchrony of ventricular contraction was altered by induction of ventricular premature systoles; the separation of externally identifiable M, and T1 components and their internal markers was predictably altered by this maneuver. The occurrence of T1 was variable in relation to the upstroke of the pulmonary artery pressure, which suggests that it is not related to pulmonic ejection. It is concluded that micromanometrically recorded right and left atrial C waves can serve as markers for externally recordable M, and T, components of the first heart sound. In addition, T, is frequently an externally recordable and audible event.

Endocarditis due to six entrapped pacemaker leads and concomitant recurrent coronary arteriosclerosis

A case of endocarditis associated with six entrapped endocardial pacer leads is presented. Because of many failed attempts at removing them by conservative measures, cardiopulmonary bypass was needed; concomitant redo coronary bypass grafts were done. To our knowledge, this represents a unique case, the like of which has not been reported previously. Salient features of management are discussed.

Pressure and sound correlates of the mitral valve echocardiogram in mitral stenosis

SUMMARY The pressure and sound correlates of the mitral valve echocardiogram (MVE) were investigated in 10 patients with mild to moderate mitral stenosis using high fidelity catheter tip micromanometers. Slow and rapid phases of the MVE anterior motion at the time of opening are associated with the slow and rapid phases of the left atrial y descent. The slow MVE motion and the slow y descent begin during isovolumic left ventricular relaxation when left ventricular pressure still exceeds left atrial pressure. The rapid MVE anterior motion and the rapid y descent begin with pressure crossover. Posterior motion of the MVE at the time of closure also occurs in two phases. After the onset of left ventricular pressure rise at end-diastole, a slow posterior motion is associated with a rising left atrial c wave. Rapid posterior motion begins with pressure crossover and is completed near the peak of the c wave. The fall in left atrial pressure during valve opening can be related to movement of the mitral valve away from the left atrium with the fall in left ventricular (LV) pressure. During valve closure, the rising left atrial (LA) pressure can be related to the ascent of the mitral valve toward the left atrium. Both the mitral component of the first heart sound and the opening snap occur at points of maximum MVE excursion and after LVLA pressure crossover.

Surgical Treatment of Acute Aortic Regurgitation in Infective Endocarditis

During a six-year period 15 consecutive patients with isolated aortic regurgitation due to infective endocarditis were encountered. None had prior significant aortic valve disease. Elective valve replacement was performed in 13 patients; emergency operation was needed in only 1 patient because of intractable pulmonary edema. One patient died suddenly from acute heart block while undergoing medical treatment. Preoperative cardiac catheterization studies in 10 of the 14 patients revealed gross elevations of left ventricular end-diastolic pressure, pulmonary hypertension, depressed cardiac output, and 3 to 4+ aortic regurgitation. There was 1 early and 1 late postoperative death, both due to systemic embolism, yielding an overall surgical mortality of 14%. After a mean follow-up of 18 months, 10 of the 11 patients are in New York Heart Association Functional Class I. Most patients with acute aortic regurgitation secondary to infective endocarditis have clinically observable congestive heart failure and will eventually require valve replacement. If congestive heart failure can be stabilized by a medical regimen, a course of antibiotic therapy can be administered and elective valve replacement can be performed. The time taken for preoperative antibiotic treatment is not associated with irreversible myocardial damage sufficient to influence the results of operation.