Hemodynamic effects of isoproterenol and norepinephrine in acute cardiac tamponade.

The hemodynamic effects of isoproterenol infusion, 0.5 mug/kg per min were evaluated in eight intact anesthetized dogs during cardiac tamponade. During tamponade, the mean of pericardial pressures was increased from - 1.5 to 12.5 mm Hg, and the mean of right atrial pressures was increased from 1 to 12.4 mm Hg. Mean cardiac output fell from 144.8 to 44.8 ml/kg per min (P < 0.001), and rose to 105.6 ml/kg per min (P < 0.001) with isoproterenol. Mean cardiac stroke volume fell from 20.3 to 6.1 ml during tamponade (P < 0.001) and rose to 12.1 ml with isoproterenol (P < 0.001). The heart rate increased from 193.3 beats/min during tamponade to 217.5 beats/min with isoproterenol (P < 0.05). During isoproterenol infusion, the mean right atrial pressure and mean pericardial pressure decreased significantly. With cardiac tamponade, the mean blood pressure fell from 157.5 to 126.1 mm Hg (P < 0.01) and did not change significantly with isoproterenol, 11 additional animals were studied with norepinephrine infusion during tamponade. There were no consistent hemodynamic effects with infusions of 0.5 and 1 mug/kg per min. With norepinephrine 2, 5, and 10 mug/kg per min cardiac output rose in some experiments. Isoproterenol infusion increased the cardiac output during tamponade principally by increasing cardiac stroke volume and to a lesser degree by increasing the heart rate. It is postulated that the increased stroke volume resulted from an increased ejection fraction with greater decrease in end-systolic than end-diastolic ventricular volume. These effects are consistent with the known positive inotropic, peripheral vasodilator, and positive chronotropic effects of isoproterenol.

Hemodynamic effects of phenoxybenzamine in anesthetized dogs.

Our studies demonstrated that phenoxybenzamine, 10 mg/kg, administered intravenously to intact anesthetized dogs, produced an immediate and significant increase of heart rate and cardiac output. In heart-lung preparations, phenoxybenzamine had no effect or a negative cardiac inotropic effect, hence these actions were not related to direct cardiac action or to release of myocardial norepinephrine stores. Serial estimations of arterial blood catecholamines after phenoxybenzamine showed an increase of epinephrine and norepinephrine; the peak values of these catecholamines did not correlate well with the maximum cardiac output responses. Ganglionic blockade largely eliminated the early cardiac effects of phenoxybenzamine, hence its action did not appear to be upon peripheral terminals of postganglionic sympathetic or parasympathetic nerves. Phenoxybenzamine was found to have antivagal actions which might account for some of the delayed cardiac acceleration. When beta adrenergic receptor blockade was induced by sotalol, the cardiac effects of phenoxybenzamine were largely eliminated. Baroreceptor denervation prevented the increase of cardiac output after phenoxybenzamine. These observations are consistent with the concept that the increase of cardiac rate and output produced by phenoxybenzamine is principally mediated by baroreceptor reflexes acting through sympathetic cardiac nerves or circulating catecholamines.

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.

Influence of acute right ventricular dysfunction on cardiac tamponade.

Echocardiographic and hemodynamic data were measured in nine closed chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, 15 mm Hg) before and after production of diffuse acute ischemic right ventricular dysfunction. Right ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (mean diameter +/- SD 54 +/- 4 microns) and caused a significant increase in right atrial pressure (7.6 +/- 1.4 vs. 1.6 +/- 1 mm Hg, p less than 0.001) and cross-sectional areas of both the right atrium (8.3 +/- 0.3 vs. 5.6 +/- 0.2 cm2, p less than 0.001) and right ventricle (8.8 +/- 0.4 vs. 5.7 +/- 0.4 cm2, p less than 0.001). Right atrial and ventricular collapse required a significantly larger pericardial effusion and pericardial pressure after right ventricular infarction than before. Mean aortic pressure had fallen 1.9 +/- 2% and 6.5 +/- 6.9% at the time of right atrial collapse (p = NS before vs. after right ventricular dysfunction) and 3 +/- 4.1% and 20.1 +/- 20.8% at the time of right ventricular collapse (p less than 0.03) before and after right ventricular dysfunction, respectively. In the presence of ischemic right ventricular dysfunction, echocardiographic signs of cardiac tamponade are less sensitive and occur later in the hemodynamic progression of cardiac tamponade. Pulsus paradoxus with cardiac tamponade was not prevented by coexisting ischemic right ventricular dysfunction.

Regional cardiac tamponade: a hemodynamic study.

In 10 dogs, atrial tamponade, ventricular tamponade and then combined atrioventricular (AV) tamponade were produced at 10, 15 and 20 mm Hg intrapericardial pressure. Cardiac output decreased significantly at each level of cardiac tamponade; the changes in cardiac output and mean aortic pressure were comparable with atrial and ventricular tamponade. Combined atrial and ventricular tamponade produced significantly greater increases of right and left atrial pressure and significantly greater decreases of cardiac output than did either atrial or ventricular tamponade. During atrial tamponade only, a significant pressure gradient developed between the venae cavae and the right atrium. Compression of both ventricles by tamponade has a much greater hemodynamic effect than does compression of either ventricle alone. Compression of the entire heart has a greater hemodynamic effect than does compression of the atria alone or the ventricles alone. Compression of the great veins has a potential effect in tamponade, demonstrable when the ventricles could fill normally.

Recurrent acute pericarditis: follow-up study of 31 patients.

Thirty-one patients with recurrent pericarditis were observed for periods of 2 to 19 years. Twenty-four had idiopathic pericarditis; four had postoperative or posttraumatic pericarditis, two had postinfarction pericarditis and one had recurrent pericarditis after anticoagulant-induced intrapericardial bleeding. In 24 patients (Group I), recurrences were documented by electrocardiographic changes, echocardiographic evidence of pericardial fluid or a pericardial rub as well as chest pain. In seven patients (Group II), recurrences were documented only by increased white blood cell count, increased erythrocyte sedimentation rate or fever in addition to pain. In 19 patients, the duration of the active or recurrent process was 5 years or more; in 7, it was 8 years or more. Three patients had cardiac tamponade in the initial attack; none had tamponade during recurrences. No patient developed congestive heart failure, constrictive pericarditis or cardiac arrhythmias with recurrences. Immunoelectrophoresis showed normal findings or minor deviations in 11 patients studied; B cell and T cell lymphocyte counts were normal in 10 patients and showed minor deviations in 3. Antinuclear antibody studies were normal in 19 of 22 patients and positive in low titer in 2. Most patients required adrenal steroid therapy for pain relief; steroid withdrawal was often difficult. Pericardiectomy was done in nine patients; in only two was this followed by clear-cut relief. In this group of 31 patients, 22 of whom were observed for 5 years or more, recurrent attacks of chest pain were the only major disabling feature of their pericarditis.

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.

Hemodynamic and regional blood flow distribution responses to dextran, hydralazine, isoproterenol and amrinone during experimental cardiac tamponade.

Four different interventions were examined in dogs with cardiac tamponade. Infusion of 216 to 288 ml saline solution into the pericardium reduced cardiac output from 3.5 +/- 0.3 to 1.7 +/- 0.2 liters/min as systemic vascular resistance increased from 4,110 +/- 281 to 6,370 +/- 424 dynes . s . cm-5. Left ventricular epicardial and endocardial blood flows were 178 +/- 13 and 220 +/- 12 ml/min per 100 g, respectively, and decreased to 72 +/- 14 and 78 +/- 11 ml/min per 100 g with tamponade. Reductions of 25 to 65% occurred in visceral and brain blood flows and in a composite brain sample. Cardiac output during tamponade was significantly increased by isoproterenol, 0.5 microgram/kg per min intravenously; hydralazine, 40 mg intravenously; dextran infusion or combined hydralazine and dextran, but not by amrinone. Total systemic vascular resistance was reduced by all interventions. Left ventricular epicardial flow was increased by isoproterenol, hydralazine and the hydralazine-dextran combination. Endocardial flow was increased by amrinone and the combination of hydralazine and dextran. Right ventricular myocardial blood flow increased with all interventions except dextran. Kidney cortical and composite brain blood flows were increased by both dextran alone and by the hydralazine-dextran combinations. Blood flow to small intestine was increased by all interventions as was that to large intestine by all except amrinone and hydralazine. Liver blood flow response was variable. The most pronounced hemodynamic and tissue perfusion improvements during cardiac tamponade were effected by combined vasodilation-blood volume expansion with a hydralazine-dextran combination. Isoproterenol had as dramatic an effect but it was short-lived. Amrinone was the least effective intervention.

Hemodynamic efficacy of rapid saline infusion and dobutamine versus saline infusion alone in a model of cardiac rupture.

Despite recent reports describing survival after cardiac rupture, the effectiveness of circulatory support while awaiting definitive surgical treatment is controversial. To assess the efficacy of volume expansion and pharmacologic support in cardiac tamponade due to cardiac rupture, a model of hemorrhagic cardiac tamponade was developed and treatment with rapid saline infusion and dobutamine was compared with rapid saline infusion alone in 15 closed chest dogs. A right ventricular wound of reproducible size was produced by deflating an aortic valvuloplasty balloon that had previously been passed by way of the internal jugular vein into the pericardial space and through a stab wound in the right ventricular free wall. Hemodynamic values were compared at baseline, during tamponade and after a rapid infusion (1 liter at 100 ml/min) of either saline solution alone or saline solution plus dobutamine (20 micrograms/kg per min). Atrial and pericardial pressures increased significantly in both groups. Mean arterial pressure, cardiac output and stroke volume increased with combined saline and dobutamine infusion to values similar to those at baseline (91 +/- 19%, 114 +/- 43% and 94 +/- 37% of baseline, respectively). In contrast, saline infusion alone caused a small increase in cardiac output but failed to significantly increase mean arterial pressure or stroke volume (76.8 +/- 14.2%, 55 +/- 18% and 51 +/- 17% of baseline, respectively). Combined rapid infusion of saline solution and dobutamine infusion has a more beneficial hemodynamic effect and may be more effective than rapid saline infusion alone in resuscitating patients with hemorrhagic cardiac tamponade due to cardiac rupture.

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.

Effects of pericardiectomy on canine pulmonary blood volume during hypervolaemia.

STUDY OBJECTIVE: The aim was to determine the effect of the pericardium on the pulmonary blood volume response to intravascular volume loading. DESIGN: Changes in pulmonary lung volume were measured from radioactive counts over the lung during radionuclide ventriculography. Baseline measurements, and repeat measurements after infusion of 21 ml.kg-1 of the dog's own blood, were made both before and after a pericardiectomy. SUBJECTS: Ten closed chest, anaesthetised dogs were studied. MEASUREMENTS AND MAIN RESULTS: Prior to and following pericardiectomy, volume loading produced equivalent and significant increases in left atrial, mean pulmonary artery, and right atrial pressures (all p less than 0.05). Before pericardiectomy, radionuclide lung counts increased from 1606(SEM 348) to 1870(402) with volume loading, corresponding to a 16% rise in lung counts from baseline (p less than 0.05). Following pericardiectomy, a similar volume load did not result in a significant rise in lung counts [1588(245) to 1697(255), 9%, p = 0.16], but was accompanied by an increase in left ventricular diastolic volume, from 39.7(6.6) to 58.7(6.4) ml, p less than 0.05, and a decrease in systemic vascular resistance index, from 122,600(14,600) to 86,600(10,000) dynes.s.cm-5 x kg, p less than 0.05. CONCLUSIONS: These data support the concept that removal of the pericardium is accompanied by reduced pulmonary blood volume overload in response to intravascular volume loading. The mechanism appears to be related to improved left ventricular diastolic filling, perhaps the result of diminished ventricular interaction, and to redistribution of excess intravascular volume from the pulmonary to the systemic circuit.

Electrocardiographic diagnosis of right ventricular infarction.

The electrocardiographic findings in 11 cases of acute right ventricular infarction associated with acute left ventricular inferior wall myocardial infarction are described. The diagnosis of right ventricular infarction was proved by autopsy findings in five cases and supported by hemodynamic data in the other six. Ten of the 11 patients had typical electrocardiographic changes of acute inferior myocardial infarction and one had that of inferior wall injury. Transient S-T segment elevation was present in one (lead V1) or more of the right precordial leads in eight cases. In the absence of other explanations for the S-T segment elevation, acute right ventricular infarction was most likely the cause. Therefore, when acute inferior myocardial infarction is accompanied by S-T segment elevation in the right precordial leads, the coexistence of right ventricular infarction should be suspected. The sensitivity and specificity of this electrocardiographic sign are yet to be determined.

Constrictive pericarditis: new aspects.

The current status of constrictive pericarditis is reviewed with regard to its etiology, physical signs, electrocardiographic findings, and hemodynamic features. Angiographic aspects are also presented. The role and limitations of M-mode echocardiography in this disease are emphasized. The value of other noninvasive studies such as measurement of systolic time intervals, myocardial scanning, and high-speed echocardiography is described. Emphasis is placed on the invasive and noninvasive methods that may be useful in separating restrictive cardiomyopathy from constrictive pericarditis. Methods of treatment, indications for pericardial resection, and the current operative results are commented on briefly.

Indications for surgical replacement of the mitral valve. With particular reference to common and uncommon causes of mitral regurgitation.

Mitral valve replacement is considered when there is severe mitral stenosis, severe mitral insufficiency or a combination of the two. Ordinarily, surgical replacement is considered only for patients who are in functional classes III or IV and do not respond to medical management. Patients with symptomatic mitral stenosis should be treated with mitral commissurotomy whenever possible. Patients selected for commissurotomy should have a pliable valve, no other major valve dysfunction, sinus rhythm, no systemic embolism and good left ventricular function. Early operation is not ordinarily required. Mitral insufficiency may require mitral valve replacement in six rather common settings: rheumatic disease, rupture of mitral chordae tendineae, postinfarction rupture of a papillary muscle, intractable infective endocarditis, floppy mitral valve and malfunction of a prosthetic valve. Rupture of mitral chordae tendineae can usually be recognized from the history, physical examination, echocardiogram and angiocardiogram. Severe left ventricular papillary muscle dysfunction is usually due to cardiac infarction, and occurs within the first 9 days of infarction. When only a papillary muscle tip is ruptured the patient may survive long enough for a mitral valve replacement. In infective endocarditis, operation is more often needed because of congestive heart failure than because of refractory infection. Evidence of mitral stenosis or insufficiency in a patient with a previously implanted prosthetic valve usually indicates an urgent need for study and early operation. Uncommon causes of mitral incompetence that may require valve replacement are endocardial fibroelastosis, Marfan's syndrome, calcified mitral anulus, osteogenesis imperfecta, methysergide-induced heart disease and carcinoid heart disease.

Electrocardiographic changes and cardiac arrhythmias in patients receiving psychotropic drugs.

Eight patients had cardiac manifestations that were life-threatening in five while taking psychotropic drugs, either phenothiazines or tricyclic antidepressants. Although most patients were receiving several drugs, Mellaril (thioridazine) appeared to be responsible for five cases of ventricular tachycardia, one of which was fatal in a 35 year old woman. Supraventricular tachycardia developed in one patient receiving Thorazine (chlorpromazine). Aventyl (nortriptyline) and Elavil (amitriptyline) each produced left bundle branch block in a 73 year old woman. Electrocardiographic T and U wave abnormalities were present in most patients. The ventricular arrhythmias responded to intravenous administration of lidocaine and to direct current electric shock; ventricular pacing was required in some instances and intravenous administration of propranolol combined with ventricular pacing in one. The tachyarrhythmias generally subsided within 48 hours after administration of the drugs was stopped. Five of the eight patients were 50 years of age or younger; only one clearly had antecedent heart disease. Major cardiac arrhythmias are a potential hazard in patients without heart disease who are receiving customary therapeutic doses of psychotropic drugs. A prospective clinical trial is suggested to quantify the risk of cardiac complications to patients receiving phenothiazines or tricyclic antidepressant drugs.

Pericarditis caused by Histoplasma capsulatum.

Sixteen patients with pericarditis caused by Histoplasma capsulatum were studied. Fourteen were less than 30 years old, and no patient had an underlying illness or was receiving immunosuppressive therapy. All patients experienced a flu-like prodromal illness lasting from 2 weeks to 4 months. Pneumonitis or hilar adenopathy, or both, was found in 12; pleural effusion, uncommon in primary pulmonary histoplasmosis, was found in seven patients. Pericardial fluid, pleural fluid and bone marrow cultures yielded no growth. All patients demonstrated a fourfold or greater change in complement-fixing antibody titers. No patient had disseminated disease, and only one required treatment with ampholericin B. The illness ran a protracted course, and in six patients symptomatic pericarditis recurred. Ultimately all recovered. Ten patients were restudied 6 months to 12 years after recover. Only one patient had pericardial calcification, and none had constrictive pericarditis. This form of granulomatous pericarditis, unlike that caused by Mycobacterium tuberculosis, appears to carry a good prognosis.

Right heart catheter lesions: any significance?

In order to determine whether endocardial lesions that developed in relation to an indwelling catheter in the right heart had any significance or characteristics, a study with clinicopathologic correlations was performed in which a total of 57 hearts were found to have right heart endocardial lesions at necropsy. Some of our findings fall within the range of results of various similar studies, e.g., clinical backgrounds and incidence in which these lesions occur. However, others do not; pulmonary embolism was preexisting and coexisting rather than attributable to the heart lesions. Right heart lesions occur significantly more often (P less than 0.01) in patients who received a right heart catheter than those who did not. The morphologic features of these endocardial lesions are sufficiently characteristic to indicate not only that an intracardiac catheter had been present but even what type of catheter it was. Infective endocarditis was found in seven catheterized patients. This process has a tendency to involve valves transmurally, indicating possible need for prosthetic valve replacement if any patients were to survive the underlying disease. Traumatic perforation of the endocardium was uncommon. With the aid of careful indications and strict adherence to guidelines, the risk of fatality from these lesions is extremely unlikely.

Recurrent pericarditis.

The most common background for recurrent pericarditis is that of acute nonspecific pericarditis. Relapsing pericarditis also may follow cardiac trauma, cardiac operations, myocardial infarction, and intrapericardial bleeding. The exact recurrence rate after initial attacks of idiopathic pericarditis is unknown but appears to be in the range of 15% to 32%. The mechanism of recurrent pericarditis is uncertain. An autoimmune response has been proposed, but this concept is unproved. Yoneda and coworkers, in a case of pericarditis due to coxsackie B virus, found no rise in antibody titer to this virus during recurrences. The prognosis, except for disabling pain and malaise, is good, and constrictive pericarditis, chronic myocardial disease, and cardiac tamponade are unusual complications. Although constrictive pericarditis may follow an initial attack of idiopathic pericarditis, it was reported in neither two other series of patients with relapsing pericarditis nor in this series. Cardiac tamponade has been reported as an occasional complication of relapses but did not occur in our patients. None of our patients died. Most patients with recurrent pericarditis respond to adrenal steroid therapy, but many times there is difficulty in weaning the patient from the drug. Because it is suspected that adrenal steroids may prolong attacks and promote tendency to further recurrences, initial therapy should be offered with aspirin or NSAIDs, and adrenal steroid therapy should be used only when there is no response to these agents. Recurrences may take place over a period lasting as long as 15 years, and patients with as many as 19 recurrences have been described.(ABSTRACT TRUNCATED AT 250 WORDS)

Constrictive pericarditis: its history and current status.

The diagnosis of constrictive pericarditis remains a challenge because it is often mimicked by restrictive cardiomyopathy. The last few years have seen numerous advances in our ability to differentiate between these two conditions which often have similar physical findings and hemodynamics. This review begins with a brief history of constrictive pericarditis; this is followed by an extensive discussion of newer etiologies, and then the classical clinical history and physical examination findings are described. Radiologic, electrocardiographic, and angiographic findings are discussed. The hemodynamics of constrictive pericarditis are reviewed. Recent results of echocardiographic and echo-Doppler investigations are presented. Emphasis is placed upon the limitations of M-mode echocardiography in the diagnosis of constrictive pericarditis. The value of echocardiographic Doppler studies of mitral and tricuspid flow velocity patterns, as well as of those in the pulmonary veins and hepatic veins, is described. Nuclear ventriculograms and angiocardiograms tend to show more rapid ventricular filling in constrictive pericarditis than in restrictive cardiomyopathy. Although only a small number of patients has been studied, these evaluations seem to have merit in separating restrictive cardiomyopathy from constrictive pericarditis. The role of computed tomography scanning and magnetic resonance imaging studies of pericardial thickness in confirming the presence of constrictive pericarditis is discussed. Abnormal pericardial thickening (> 3 mm) confirms the diagnosis of constrictive pericarditis, but only if the characteristic hemodynamic pattern is present. The usefulness of endomyocardial biopsy in recognizing specific varieties of restrictive cardiomyopathy is presented.(ABSTRACT TRUNCATED AT 250 WORDS)