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. MUCH OF OUR

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 isovolumic 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 difference and ICT becomes prolonged (P less than 0.001). Factors other than stroke index depression which may contribute to the decreased duration of RVET (P less than 0.001) include tricuspid regurgitation and elevation of pulmonary vascular impedance. In ASD, QP2 is significantly prolonged (P less than 0.025) due to a significant increase in RVET (P less than 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.

SUMMARY The genesis of gallop sounds was investigated in 12 patients by simultaneous measurement of external apexcardiographic (ACG) and left ventricular (LV) pressure, dP/dt, and sound using infinite time constant piezo-resistive pressure transducers with identical sensitivity and frequency responses. Absolute intensity of internal and external sound was quantified. The external transducer was applied to the chest wall with a pressure of 200-400 mm Hg. Six patients had a third heart sound (S,), eight had a fourth heart sound (S4) and one patient had a summation gallop. Left atrial (LA) pressure, dP/dt, and sound were also recorded in one S.and four S4 patients. The dP/dt of the rapid filling wave (RFW) and "a" wave of both apexcardiogram and left ventricle were measured. Similar data were obtained in 10 control patients without gallop sounds.The intensity of gallop sounds was uniformly greater over the chest wall than inside the left ventricle or left atrium. In addition, the dP/dt of RFW and "a" wave tended to be higher in the apexcardiogram than the left ventricle of control patients. Also, the dP/dt of the LV RFW in S, patients and "a" wave in S4 patients tended to be higher than ihose in control subjects, but there was overlap. The dP/dt of ACG filling waves in patients with gallop sounds was significantly greater (p < 0.01) than the respective filling wave of the left ventricle. The ACG dP/dt of the RFW in all S, patients and "a" wave in all S, patients was increased above the maximal values of the respective ACG filling waves in the control subjects.The data suggest that the higher intensity of gallop sounds and the higher dP/dt of the filling waves over the chest cannot be caused by passive transmission of sound or pressure changes in the left ventricle. Therefore, we postulate that the greater vibratory energy of gallop sounds recorded over the precordium is caused by the impact of the heart on the chest wall. The strength of the impact is a function of several interacting mechanisms, including the momentum transfer and coupling between the heart and the chest wall.SINCE POTAIN'S original description of gallop sounds in 1885,1 several mechanisms have been proposed to explain their genesis. From studies using phonocardiograms in association with the apexcardiograms with short-time constants, Benchimol et al. concluded that the third heart sound (S3) occurs at the peak of the rapid ventricular filling wave (RFW), and that the fourth heart sound (S4) appears at the peak of the "a" wave of the ACG.'On the basis of these findings and hemodynamic observations made by means of fluid-filled catheters, several investigators proposed that the S3 is caused by the sudden deceleration of the RFW and that the S4 was produced by an exaggerated "a" wave generated by the left atrium in an attempt to fill a noncompliant left ventricle.3-' However, Arevalo et al." found in animals that the S3 occurs when left ventricular (LV) pressure ceases to fall during relaxation. At this instant, the dP/dt of LV pressure is almost 0 ...

SUMMARY Documented cardiac tophi are rare and have not previously been reported to cause clinically manifest valvular disease. A 31-year-old male with complex cyanotic congenital heart disease (Taussig-Bing anomaly) and secondary tophaceous gouty arthritis is described. Terminally, he presented with clinical evidence of a brain abscess and a new semilunar regurgitant murmur. Two-dimensional echocardiography suggested vegetative lesions as the cause of the murmur. The patient was treated for infective endocarditis. At autopsy, the cause of the semilunar regurgitant murmur was shown to be sterile tophi located along the line of pulmonary valvular coaptation. Tophaceous deposits were also present in the mitral valve.ALTHOUGH clinically evident valvular heart disease may have many causes, gout has not previously been reported as one of them. Tophi are frequently observed in the periarticular tissues, skin, subcutaneous tissues and kidneys, but their presence in other anatomic sites is rare.' Only five documented cases of macroscopic urate deposits in the heart have been reported.26 In each, the mitral valve was involved, but clinically manifest valvular disease attributable to the tophi was not described. The unique aspect of the present case was the occurrence of cardiac semilunar leaflet tophi leading to a regurgitant murmur. no growth. During the next 2 days, he had grand mal seizures beginning on the right side. The patient was transferred to Presbyterian-University Hospital, where physical examination revealed a temperature of 37.2°C, marked peripheral and central cyanosis, 4 + digital clubbing and tophi over the interphalangeal joints of the left hand, right thumb, olecranon bursae and external ear. A grade IIVI basal systolic ejection murmur radiated to the carotids; a grade IIINVI early decrescendo blowing murmur was audible along the left sternal border, lasting two-thirds of diastole and radiating to the apex. The liver and spleen were firm and palpable 8 cm and 6 cm below their respective costal margins. He was oriented to person only; a central left seventh cranial nerve paresis and bilateral Babinski signs were present. Laboratory data disclosed a hemotocrit of 67%, leukocyte and platelet counts of 8500 and 20,000/mm3, respectively, an arterial Po2 of 31 mm Hg and a uric acid of 15.2 mg/ dl. A spinal tap yielded clear fluid that was unremarkable on laboratory examination. Two-dimensional echocardiography disclosed dense echoes in the region of a semilunar valve. Case ReportThe patient was begun on chloramphenicol, gentamicin and cefazolin as empiric therapy for presumed endocarditis with a brain abscess. A CAT scan subsequently demonstrated a contrast-enhanced ring lesion in the left temporal region consistent with such an abscess. Renal insufficiency supervened associated with development of anemia and a further fall in platelet count. On the seventh hospital day, the patient developed erythema, swelling and pain in the right knee; arthrocentesis revealed class II fluid and intracellular crystals consi...

seven normal volunteers (group 1) and six patients with pulmonary hypertension of diverse etiology (group 2) using catheter-tip micromanometers. In group 1 subjects, inspiratory widening of this interval was found to average 27.2 msec, of which 7.6 ± 2.7 msec (1 SD) or 27 + 7% was due to a decrease in the Q-A2 interval. The major contribution of Q-P2 interval prolongation was divided into two components: a) Q-O was measured from the onset of the QRS to the onset of the rapid descent of the right ventricular (RV) negative dp/dt, which was felt to reflect the duration of RV electromechanical systole, b) O-P2 or Q-P2 -Q-0. Increase in the Q-O interval accounted for only 7.7 ± 5.0 msec or 28 ± 12% of the total IA. The major single component of IA was the increase in O-P2 which averaged 11.9 ± 3.0 msec. Five of six group 2 patients demonstrated significant respiratory change in Q-P2 intervals. In contrast to group 1 subjects, however, this was accomplished primarily via increases in the duration of RV electromechanical systole. The O-P2 interval is felt to primarily reflect the impedance characteristics of the pulmonary vascular bed. It is concluded that physiologic splitting of the second heart sound in normal subjects is most probably due to an inspiratory decrease in impedance of the pulmonary bed rather than the traditional explanation of prolongation of RV systole secondary to an increase in venous return. When the normal impedance characteristics of this bed are lost, as in pulmonary hypertension, IA must occur primarily via increases in the duration of RV systole. The inspiratory delay from the conclusion of RV systole to the occurrence of P2 is attributed to the inertiance of the RV stroke mass.