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A case report of cardiac tamponade is described which did not manifest itself until the patient was allowed to breathe spontaneously. Changes in intrapericardial pressure during spontaneous and controlled ventilation are discussed.
Cardiac tamponade is a rare complication of juvenile rheumatoid arthritis. Three cases seen in the last two years at the Children's Hospital of Philadelphia are reported and compared to four previously reported cases. All three children had systemic-type juvenile rheumatoid arthritis with tachypnea, shortness of breath, and chest pain. Cardiac signs in these children included decreased heart sounds, pericardial friction rub, jugular venous distention, and pulsus paradoxus greater than 12 mm Hg. Roentgenograms of the chest showed cardiomegaly with bilateral pleural effusions. Electrocardiograms showed sinus tachycardia and nonspecific ST-T wave changes. Echocardiograms demonstrated pericardial effusions in all subjects and poor ventricular movements in one child. All three children were treated with short-acting anti-inflammatory drugs and/or prednisone. Pericardiocentesis was performed in two cases. There was no significant morbidity after a mean follow-up of two years.
Clinical examination and transthoracic echocardiography play a vital role in the management of patients with pericardial effusion and cardiac tamponade physiology. We report patients in advanced phase 3 cardiac tamponade with variant clinical and hemodynamic presentations. These atypical cardiac tamponade cases include: A patient with severe aortic valve regurgitation who lacked pulsus paradoxus; a patient with systemic sclerosis without hypotension; and a patient with pulmonary hypertension lacking right heart collapse on echocardiography. Recognition of these atypical clinical and hemodynamic manifestations of cardiac tamponade will avoid undue delay in the treatment.
The effect of acute cardiac tamponade on atrial pressures, plasma atrial natriuretic factor concentration and renin activity, and renal water and electrolyte excretion was studied in pigs loaded intravenously with hydroxyethyl starch and maintained on a continuous intravenous infusion of isotonic saline solution. Saline solution was infused into the pericardial space in 6 anesthetized pigs until a predetermined decrease of 20% in mean arterial pressure was achieved. Another 6 sham-treated pigs served as controls. Tamponade increased atrial intracavitary pressures but decreased atrial transmural (distending) pressures. These changes in atrial pressures were reversed after release of tamponade. Changes in plasma atrial natriuretic factor concentration correlated positively with changes in atrial transmural pressures. Tamponade increased plasma renin activity and decreased urine flow and renal sodium and potassium excretion, and release of tamponade reversed these changes. Thus, the tamponade-induced reduction in atrial distention is associated with hormonal changes, which may contribute to the reductions in diuresis and natriuresis observed in this connection.
Pulsus paradoxus occurs in cardiac tamponade because the output of the left ventricle falls during inspiration. The principal cause for this is reduced filling of the left ventricle during the preceding diastole. The present study examines whether this reduced filling of the left ventricle on inspiration is due to compression by the right heart or due to reduced venous return to the left heart. The effect of pericardial tamponade on hemodynamics and left ventricular and atrial volumes was determined in six experimental animals. The data demonstrate that from the outset pericardial fluid reduces left ventricular end diastolic volume, although initially left ventricular end systolic volume decreases as well. By contrast, pulsus paradoxus is a relatively late phenomenon occurring with severe tamponade and associated with an inspiratory decrease in left atrial and ventricular volumes in the face of a drop in left ventricular filling pressure. Underfilling of the left heart is the most likely cause of this combination of events.
This report describes a case of cardiac tamponade as the initial manifestation of unclassified connective tissue disease (UCTD). A 68-year-old Japanese woman was admitted to hospital because of dyspnea and edema. She had undergone a radical left mastectomy for the treatment of breast cancer 18 years before. On admission, bilateral leg edema, hepatomegaly, and a paradoxical pulse were noted on physical examination. The erythrocyte sedimentation rate was elevated and the C-reactive protein was 2.8 mg/dl. Antinuclear antibodies and anti-SS-A/Ro antibodies were present. The scl-70 and anticentromere antibodies were elevated. Chest radiography showed cardiomegaly. Echocardiography revealed a large pericardial effusion, but the pericardial fluid did not contain malignant cells or bacteria. She did not meet the diagnostic criteria for any known connective tissue diseases, so was diagnosed with cardiac tamponade due to UCTD. Prednisolone (30 mg/day) was administered, which resulted in a gradual resolution of the pericardial effusion. Although connective tissue diseases are known to cause pericardial effusion, cardiac tamponade as the initial manifestation of the disease in the absence of other symptoms is quite rare.
Cardiac tamponade can manifest as profound hypoxemia from intracardiac shunting across a patent foramen ovale. As a consequence, pulmonary embolus can be erroneously diagnosed. As demonstrated in the case described herein, transesophageal echocardiography can be useful in determining the correct diagnosis, especially if transthoracic echocardiography is technically limited. In our patient, the findings on transesophageal echocardiography also helped determine the appropriate treatment. The relative inaccessibility of the pericardial effusion to needle drainage prompted open surgical drainage.
Clinical reports indicate that right ventricular diastolic collapse (RVDC) is associated with cardiac tamponade. To assess the hemodynamic abnormalities associated with RVDC, we studied six chronically instrumented conscious dogs (group A) with two-dimensional echocardiography during cardiac tamponade induced by continuous saline infusion into the pericardial space. We recorded cardiac output (electromagnetic flowmeter), heart rate, respiration, and aortic, intrapericardial, and right atrial pressures. In four additional animals (group B), we recorded right ventricular pressure and placed a hydraulic occluder around the pulmonary artery so that short-term reversible obstruction to right ventricular outflow could be produced. None of the dogs had RVDC when the pericardial space was empty, but all dogs showed RVDC during cardiac tamponade. The appearance of RVDC in group A was associated with a 21% reduction in cardiac output (p less than .01) and no change in mean aortic pressure. Short-term partial pulmonary artery obstruction led to increased right ventricular pressures and a striking reduction in RVDC in early tamponade, suggesting that RVDC is caused by pericardial pressure exceeding right ventricular pressure in early diastole. An additional animal had right ventricular hypertrophy caused by a severe "heart worm" infestation and did not show RVDC during cardiac tamponade. These observations suggest that in the absence of increased resistance to right ventricular outflow or right ventricular hypertrophy, RVDC occurs early in the course of cardiac tamponade and is associated with a hemodynamically important decrease in cardiac output.
Coxsackie virus pericarditis caused cardiac tamponade in a 45-day-old infant with corrected total anomalous pulmonary venous drainage and a hypodynamic left heart. The pathophysiology comprised reduced heart compliance, venous return impairment, acute pulmonary hypertension, and increased airway microvascular permeability. Tracheal edema and external compression caused tracheal lumen narrowing and respiratory failure. Laryngoscopy was difficult because of laryngeal inlet swelling. Endotracheal intubation was accomplished with a 3.0-mm tube. Pericardial cavity evacuation resulted in rapid recovery. A postprocedural chest radiograph revealed tracheal lumen enlargement. Repeated laryngoscopy revealed resolution of upper-airway edema. In infants, large pericardial effusions developing after corrective/palliative heart surgery may cause major airway compromise.
BACKGROUND: Cardiac tamponade due to an intrapericardial infusion is a serious complication of central venous catheterization. CASE REPORT: An infant born at 35 weeks of gestation age, weighing 2300 g, was operated on at H10 for a duodenal stenosis. On day 2, a polyurethane central venous catheter was inserted for parenteral nutrition via his right internal jugular vein. A frank blood return was obtained and a chest X-ray taken 2 hours later showed that the tip into the catheter was in the right ventricle. Four hours after insertion, a sudden deterioration of the infant's status led to tracheal intubation and artificial ventilation on 100% oxygen; no improvement was noted. The heart rate was 135 bpm, but the differential blood pressure was decreased at 68/56 mmHg and there was no blood return on the catheter. Cardiac tamponade was then suspected and immediately confirmed by pericardial tap that yielded 10.5 mL of the infused solution. The catheter tip was then repositioned and a good blood return was obtained. The infant's breathing and hemodynamic status improved dramatically. CONCLUSION: The use of very thin and flexible central venous catheters does not eliminate the risk of perforation of the cardiac chambers. A cardiac tamponade must always be considered in children with a central venous catheter when a sudden deterioration of hemodynamic status is noted.
At present the most frequent cause of cardiac tamponade is neoplasma. A case of a 32-year-old male with recurrent cardiac tamponade caused by pericardium mesothelioma is described. Despite advanced neoplastic process in the pericardium, pleura and mediastinum, neither radiologic examinations of the chest, echocardiography, nor repeated cytologic examination of the pericardial exudate, could establish the etiology of the tamponade. Only after a pericardial window had been performed was it possible to: 1) establish the diagnosis and introduce causal treatment; 2) prevent recurrence of the tamponade; 3) perform cytoreduction of the tumor. It seems that in cases of chronic exudative pericarditis of unknown cause it is proper to perform an early pericardial window as a diagnostic and therapeutic procedure.
The ruptured aortic arch aneurysm with cardiac tamponade is rare and has severely high mortality. We report a case of ruptured aortic arch aneurysm with cardiac tamponade. A 66-year-old man who had syncope attack was transferred to city hospital. Brain computed tomography (CT) showed no significant lesion and he admitted to our hospital for suspecting of aortic dissection. Chest CT showed ruptured aortic arch aneurysm and pericardial effusion. Emergent operation was done on the same day. It was found that the hematoma beneath the tunica adventitia existed at the distal arch and extended to the ascending aorta. Cardiac tamponade was caused by rupture of subadventitial hematoma in pericardial space. Aortic arch replacement was performed using selective cerebral perfusion under deep hypothermia. Postoperatively, he had no cerebral complication and was discharged uneventfully.
Pulsed Doppler echocardiography has been used previously to demonstrate marked changes in transvalvular blood flow velocities during cardiac tamponade in laboratory animals and a small number of patients. To further assess the respiratory changes in transvalvular blood flow during tamponade, pulsed Doppler tracings of flow velocity profiles across all four cardiac valves were recorded during inspiration and expiration in 13 patients during cardiac tamponade, in 6 of the 13 patients after relief of tamponade by pericardiocentesis and in 8 normal control subjects. Flow velocity integrals were calculated for each valve during inspiration and expiration. In the setting of cardiac tamponade, inspiration caused an 85 +/- 46% increase in the flow velocity integral across the pulmonary valve, an 81 +/- 34% increase across the tricuspid valve, a 33 +/- 13% decrease across the aortic valve and a 35 +/- 8% decrease across the mitral valve. These phasic respiratory changes were markedly reduced after relief of tamponade (p less than 0.05 compared with tamponade) and were observed to only a minimal extent in the normal individuals (p less than 0.01 compared with tamponade). The exaggerated respiratory variations in transvalvular flow velocity integrals suggest that Doppler evaluation may be a valuable tool in the diagnosis of cardiac tamponade. Transmitral Doppler indexes of left ventricular filling during cardiac tamponade revealed that inspiration caused a shift to increased filling during late diastole, with a greater contribution of atrial systole to total left ventricular filling. These Doppler indexes did not vary significantly with respiration in the group studied after relief of tamponade or in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVES: The objective of our study was to evaluate the changes in cardiac chamber dimension--longitudinal and transversal axis--in patients with cardiac tamponade after drainage of the pericardial effusion. STUDY DESIGN: This is a five year retrospective study (from 1991 to 1995 inclusive) which evaluates patients with cardiac tamponade from a clinical and electrocardiographic, as well as echocardiographic, point of view. MATERIALS AND METHODS: Thirty-nine consecutive patients with cardiac tamponade were evaluated clinically and by ECG and two-dimensional echocardiography, before and after drainage of the pericardial effusion. The drainage was done by pericardiocentesis alone in 28 cases (72%), pericardiocentesis followed by surgery in seven cases (18%) and surgery alone in four cases (10%). MAIN RESULTS: After drainage we observed a reduction in the diameter of the pericardial effusion from 30.1 +/- 8 to 8.1 +/- 7 mm; the occurrence of jugular vein turgescence decreased from 87% to 5% (p < 0.001) and heart rate also decreased from 100 +/- 20 beats/minute to 79 +/- 17 beats/minute (p < 0.001). Systolic blood pressure increased from 107.8 +/- 20.4 mmHg to 134.6 +/- 20.3 mmHg (p < 0.001). All longitudinal and transversal diameters of the cardiac chambers increased after drainage. The greatest increase was observed in the transversal diameters of the right chambers. CONCLUSIONS: Cardiac tamponade affects both right and left cardiac chambers which are affected in their transversal as well as longitudinal diameters; the effect of compression was more marked in the right chambers and in the transversal diameters.
Localized pericardial effusion leading to cardiac tamponade is seen occasionally in patients after cardiac surgery. This condition may be difficult to diagnose clinically because of unusual presenting symptoms and absence of conventional signs of cardiac tamponade. A case of localized pericardial effusion with presenting symptoms of fever and increasing fatigue is described in this study. The definitive diagnosis was made using transesophageal echocardiography. Surgical drainage of localized effusion resulted in prompt hemodynamic and symptomatic improvement.
We report a case of delayed cardiac tamponade that resulted from pacemaker implantation in the emergency room of a large urban hospital. A 19-year-old male patient with a pacemaker implanted 10 days earlier suffered from delayed perforation of the right ventricle with cardiac tamponade. A review of the literature revealed that cardiac tamponade is a rare complication of pacemaker implantation. Pacemakers should only be implanted by physicians with relevant experience, and emergency room physicians should be aware of the possibility of the associated complications and be prepared to treat them.
Pericarditis complicating cardiac trauma and resulting in tamponade is uncommon. Possible causes include an autoimmune reaction or an inflammatory response to blood entering the pericardium. We present two patients, one with effusive and one with constrictive pericarditis occurring within 2 weeks of a penetrating trauma close to but not directly involving the heart. These cases illustrate the importance of clinical suspicion and aggressive management in the diagnosis and management of such patients.
Since it is very rare that cardiac tamponade due to myocardial rupture caused by infective endocarditis, occurs we are reporting this case. A 62 year old man, who had underlying diseases of pneumoconiosis and hypertensive heart disease, visited Chikuho Rosai Hospital complaining of chest oppression and general fatigue on Feb. 7, 1987. He was diagnosed as having ischemic heart disease by electrocardiogram. Two days later, he suddenly had chills and a fever, and the laboratory data showed leukocytosis and a positive C-reactive protein (CRP). The echo cardiogram showed mitral regurgitation (MR) and aortic regurgitation (AR), but neither vegetation nor pericardial effusion was observed. On Feb. 16, he was admitted with shock, and he died the next day. The blood cultures grew gram-positive cocci, respectively. From the clinical symptoms, chest roentgenogram and electrocardiogram, we suspected a cardiac tamponade. On autopsy findings, though coronary arteries were intact, the aortic valves had severe valvular adhesions, calcifications and hypertrophies. The rupture hole was observed in the left ventricles, which was just under the aortic valve through the pericardiac space. It seemed that he died of a cardiac tamponade due to the outflow of blood from this hole. On histopathologic findings of the cardiac wall, gram-positive cocci and many of neutrophils were observed.