Noble O. Fowler

Cardiac tamponade in medical patients.

We reviewed the cases of 56 medical patients with cardiac tamponade who were treated at the University of Cincinnati. A paradoxic arterial pulse was critical in the diagnosis because most patients did not have a small quiet heart, and blood pressure was often well maintained. Fifty-two of 55 patients had enlarged cardiac silhouette by chest radiogram; heart sounds were diminished in 19 patients; arterial systolic pressure was ⩾ 100 mm Hg in 35, and arterial pulse pressure was ⩾ 40 mm Hg in 27.Echocardiograms in 23 patients showed abnormally increased right ventricular dimensions and decreased left ventricular dimensions during inspiration, except in one patient with left ventricular dysfunction. The causes of cardiac tamponade were metastatic tumor in 18 patients, idiopathic pericarditis in eight and uremia in five; five cases of tamponade occurred after heparin administration in acute cardiac infarction. Myxedema and dissecting aneurysm each caused tamponade in two patients. Pericardiocentesis relieved tamponade initially in 40 of 46 patients; however, two suffered fatal complications. Pericardial resection was done in 18, including 12 of these 46.

Unreliability of conventional electrocardiography monitoring for arrhythmia detection in coronary care units

To evaluate the reliability of conventional coronary care unit electrocardiographic monitoring, a study was made of 31 consecutive patients with uncomplicated verified acute myocardial infarction. All patients were monitored routinely with conventional equipment, and at the same time the electrocardiogram for each patient was recorded continuously on electromagnetic tape and stored for later analysis by an automated arrhythmia detection system. All patients studied were within 24 hours of the onset of chest pain and on entry into study all were free of shock, heart block, bundle branch block, severe heart failure or an existing arrhythmia. By conventional monitoring, premature ventricular contractions were recognized in 64.5 percent of patients compared with 100 percent using the automated detection system (P <0.01). The corresponding percentages for recognition of premature atrial contractions were 45.2 vs. 96.8 percent (P < 0.001); serious ventricular arrhythmias, 16.1 vs. 93.5 percent (P <0.001); multifocal premature ventricular contractions, 6.5 vs. 87.1 percent (P < 0.001); and consecutive premature ventricular contractions, 13.0 vs. 77.5 percent (P < 0.001), respectively. The delay from the time of first occurrence as detected by the automated system to recognition by the conventional monitoring system averaged 18 hours for premature ventricular contractions, 10 hours for serious ventricular arrhythmias and 23 hours for premature atrial contractions. The on-line use of an automated arrhythmia detection system in the coronary care unit is suggested if further improvement in the elimination of arrhythmias as a primary cause of death after myocardial infarction is to be achieved. The presence of serious ventricular arrhythmias in virtually all patients after myocardial infarction suggests that prophylactic antiarrhythmic agents be used in this setting; however, none of the presently available antiarrhythmic agents have been shown to reduce mortality when given prophylactically following myocardial infarction.

Coronary and Myocardial Actions of Angiotensin

In the dog heart-lung preparation, single injections of 40 μg angiotensin II produced consistently a biphasic response. Initial impairment of cardiac function was observed with decrease of cardiac output and of ventricular force, and with increase of atrial pressures. After 10 to 20 seconds, there was a positive inotropic effect, with an increase of cardiac output and of ventricular force, and a decrease in atrial pressures. Responses were comparable in reserpinized and nonreserpinized preparations. Tachyphylaxis to angiotensin was found consistently in the heart-lung preparation, with a regular decrease in response following second and third injections. A positive inotropic action of angiotensin II was demonstrated in the cat papillary muscle preparation. These studies demonstrated that angiotensin has a direct cardiac action, namely a positive inotropic effect. This action probably does not depend upon myocardial stores of catecholamines. When the left anterior descending coronary artery of the dog was perfused with blood at a constant flow, single intracoronary injections of angiotensin (1.0 μg) consistently increased coronary resistance (6% to 92%). Continuous intracoronary infusion of angiotensin increased coronary vascular resistance when blood concentrations were as low as 0.42 μg/ liter. No evidence of initial cardiac depression or of increased coronary vascular resistance was found after norepinephrine. It is concluded that the initial impairment of cardiac performance following angiotensin is caused at least in part by decreased coronary blood flow. Caution is suggested in the use of angiotensin in the treatment of human shock because of its action upon the coronary circulation.

M-mode echocardiography in constrictive pericarditis

M-mode echocardiograms from 40 patients with proven constrictive pericarditis and 40 subjects without evidence of cardiac disease were reviewed for features previously described in constrictive pericarditis. In this large series, no single feature of the M-mode echocardiogram could be considered diagnostic, although a pattern of normal left ventricular size and systolic function, mild left atrial dilation, flattened diastolic left ventricular posterior wall motion and abnormal septal motion was found in most patients. It is concluded that the M-mode echocardiogram can provide findings suggestive of constrictive pericarditis but must be used in conjunction with hemodynamic and other studies to establish the diagnosis.

Transmural ventricular pressures in experimental cardiac tamponade.

Experimental cardiac tamponade was produced in open-chest dogs. Left and right ventricular systolic pressures fell when intrapericardial pressure was increased only a few millimeters of mercury. Negative diastolic transmural pressures of 1 to 6 mm. Hg developed in the left ventricle and negative diastolic transmural pressures of 2 to 8.5 mm. Hg developed in the right ventricle. In some instances the period of right ventricular systolic ejection was greatly abbreviated at higher levels of intrapericardial pressure.

Antibiotic Levels in Pericardial Fluid

An experimental model was designed to study the ability of antibiotics to enter the pericardial compartment. Noninfected and infected pericardial fluid and serum antibiotic activities were determined in adult mongrel dogs before and at intervals after antibiotic administration. After the administration of penicillin G, methicillin, cephaloridine, streptomycin, or gentamicin, clinically adequate antibiotic levels in the noninfected pericardial fluid were obtained within 1 h, and these levels approached or exceeded the serum levels within 2-4 h. Antibiotic levels obtained from infected dog pericardial fluids were higher than those from noninfected animals. Patients serum and pericardial fluid antibiotic levels were measured after penicillin G, penicillin V, cephalothin, and gentamicin administration. We have found, both in the canine and human studies, that pericardial antibiotic levels taken at least 2 h after antibiotic administration are almost identical to those in the blood.

Evaluation of Bretylium Tosylate for the Treatment of Premature Ventricular Contractions

In a controlled setting bretylium tosylate was evaluated for efficacy, toxicity, onset, and duration of action in eight patients with frequent premature ventricular contractions (PVC). Four patients received a single im dose of bretylium, 4 mg/kg, with before and after control days; the other four patients received bretylium, 2 and 4 mg/kg, on different days with before and between control days. PVC were quantified from stored continuous ECG tape recordings by an automated arrhythmia-detection system. Five patients had 50% or more reduction of PVC frequency with bretylium 4 mg/kg, and one with 2 mg/kg. Bretylium 4 mg/kg but not 2 mg/kg reduced mean PVC frequency by half beginning at the sixth hour and continuing for 12 hours. Hypotension began within 1 hour. Maximum fall in mean supine blood pressure was 17/6 mm Hg with 2 mg/kg, and 25/12 mm Hg with 4 mg/kg. Plasma bretylium concentration was maximum at about 1 hour with a mean elimination half-life of 10 hours. A controlled quantitative method for evaluation of antiarrhythmic drugs in man demonstrated that bretylium can be effective in suppressing PVC frequency. The dissociation between hypotensive and antiarrhythmic effects of bretylium suggested that its antiarrhythmic effect was independent of adrenergic neuronal blockade.

Cardiac tamponade in left ventricular dysfunction.

Echocardiographic and hemodynamic data were measured in closed-chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, and 15 mm Hg) before and after production of diffuse ischemic left ventricular dysfunction. Left ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (54 +/- 3.9 mm diameter). Changes in left atrial pressure with cardiac tamponade were influenced by coexisting left ventricular dysfunction. Left atrial pressure increased with tamponade and was equal to pericardial pressure before left ventricular dysfunction was produced. However, after left ventricular dysfunction was produced, left atrial pressure was significantly higher than pericardial pressure before tamponade, but it fell toward pericardial pressure when tamponade was produced. Pulsus paradoxus (greater than 10 mm Hg) was present in all animals with cardiac tamponade before left ventricular dysfunction but in only one animal afterward. During each level of tamponade, the inspiratory fall of aortic systolic pressure was greater before than with left ventricular dysfunction. The slope of the linear regression between pericardial pressure and millimeters of mercury of inspiratory fall in aortic systolic pressure was significantly greater before than with left ventricular dysfunction (0.74 +/- 0.12 versus 0.32 +/- 0.12, p less than 0.05). Left ventricular dysfunction caused a leftward and upward shift of the pericardial pressure-volume relation. As a result, right atrial and ventricular collapse occurred with significantly smaller volumes of pericardial fluid after than before left ventricular dysfunction. We conclude that pulsus paradoxus may be absent in cardiac tamponade with coexisting left ventricular dysfunction and unequal filling pressures. Echocardiographic signs of cardiac tamponade may occur with small effusions in the presence of left ventricular dysfunction.

Cardiac tamponade: A comparison of right versus left heart compression

It has been postulated that in cardiac tamponade, the hemodynamic effects of compression of the right heart chambers and great veins are more important than are the effects of left heart compression. In 10 anesthetized dogs with surgically compartmented pericardium, the hemodynamic effects of right atrial and right ventricular compression were compared with the hemodynamic effects of left atrial and left ventricular compression. The effects of right heart compression, left heart compression, and then effects of combined right and left heart compression, were compared at three levels of intrapericardial pressure: 10, 15 and 20 mm Hg. Aortic mean pressure decreased significantly at each level of intrapericardial pressure with right-sided tamponade but not with left-sided tamponade. Left atrial mean pressures decreased significantly with right-sided tamponade and increased with left-sided and combined tamponade. Right atrial mean pressures increased significantly with right-sided and combined tamponade, but not with left-sided tamponade. Heart rate increased significantly with each of the three varieties of tamponade. Cardiac output and stroke volume, which decreased with each variety of tamponade, were significantly lower during right-sided than during left-sided tamponade. Combined tamponade lowered stroke volume more than did right-sided tamponade, and lowered cardiac output more at 15 and 20 mm Hg intrapericardial pressure. It is concluded that, in this preparation, right-sided cardiac compression has more important hemodynamic effects than does left-sided compression. However, left-sided tamponade still makes a significant contribution to the total hemodynamic picture of cardiac tamponade.

Adrenal Medullary Secretion During Hypoxia, Bleeding, and Rapid Intravenous Infusion

This study reports the effect of hypoxia, of lowering blood pressure by bleeding, and of rapid infusion upon adrenal secretion in anesthetized dogs. Adrenal norepinephrine-like substances (NEL) were measured in adrenal venous blood by means of a bio-assay method, using the rabbit aortic strip. In 10 of 11 dogs breathing 7.1 per cent O2 in N2, the left adrenal NEL output was augmented 1.5 to 6.6 times control levels. The increased adrenal medullary secretion during hypoxia was not dependent upon a fall in systemic arterial blood pressure and was not associated with an increase of 17-hydroxycorticosteroid output. In five dogs bled to a blood pressure of 80 to 90 mm. Hg, left adrenal NEL output was augmented 2.9 to 7.4 times control levels. In 11 animals in which the blood pressure was lowered to 40 to 50 mm. Hg by bleeding, left adrenal NEL output was augmented 1.8 to 17 times control levels. Seven dogs were made anemic and hypervolemic by rapid infusion of 1,125 to 1,900 ml. normal saline or Krebs solution. Cardiac outputs were increased more than 200 per cent in six, and considerable dilution anemia was produced. However, left adrenal NEL outputs fell to values ranging from 14 to 50 per cent of control. During rapid infusions, output of adrenal 17-OHCS increased 18.5 to 92 per cent. It is concluded that increased adrenal medullary secretion did not participate in the increase of cardiac output observed in these seven animals.