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Cardiac tamponade secondary to perforation of a hepatic amoebic abscess developed six years after the patient had visited an area where Entamoeba histolytica is endemic. He was treated with metronidazole and imipenem, emergency percutaneous catheter drainage, and open surgical drainage.
Cardiac tamponade is an emergency situation. Diagnosis is to be suspected when an elevation of systemic venous pressure, a decline in systemic arterial pressure and a clinical context of neoplasia or recent acute pericarditis are associated. Transthoracic echocardiogram is the gold-standard of diagnosis, and allows the accurate diagnosis of a large pericardial effusion: precise localisation and haemodynamic evaluation are needed before therapeutic decision. Pericardiocentesis is the only appropriate treatment. Surgical procedure, or less traumatic echo-guided pericardiocentesis, provide rapid haemodynamic relief of symptoms. Prognosis is determined by aetiology.
Cardiac tamponade is a frequent cause of death in acute myocardial infarction--in as many 23%. It is encountered in particular in the 7th and 8th decade, in patients with a first infarction which is frequently situated in the anterior wall of the left ventricle. 93% of the patients have obvious ECG manifestations of Q infarction. The diagnosis of cardiac tamponade is easy when during an acute terminal attack slow activity on the ECG tracing is found without a haemodynamic response and the pulse on the great arteries is not palpable even after external cardiac massage. In 80% the onset of cardiac tamponade is very sudden. The presence of shock or cardiac failure makes the diagnosis of cardiac tamponade more difficult. As to investigated indicators, in the development of cardiac tamponade the systemic pressure--systolic as well as diastolic--on admission or during hospitalization, may play a part. The patients have a less marked coronary sclerosis, fibrosis of the cardiac muscle is less frequently present. Previous necroses of the heart muscle may have probably a certain protective effect on the development of cardiac tamponade. Anticoagulants obviously do not influence the development of cardiac tamponade.
BACKGROUND: Cardiac tamponade after cardiac surgical procedures is often associated with hemodynamically significant localized pericardial effusions. The localized collection of pericardial effusion in the postoperative period and the atypical presentation of cardiac tamponade limit the use of conventional clinical and echocardiographic signs usually seen with a circumferential pericardial effusion. Observation of left ventricular diastolic collapse in the echocardiogram of a patient with postoperative regional cardiac tamponade prompted us to explore the frequency of this sign in regional cardiac tamponade. METHODS AND RESULTS: We retrospectively analyzed the echocardiograms of 18 patients with postoperative cardiac tamponade for the following echocardiographic findings: right atrial collapse, right ventricular diastolic collapse, left atrial collapse, and left ventricular diastolic collapse. Three of the 18 patients had circumferential pericardial effusion, and 15 had loculated pericardial effusion; in 10, the effusion was predominantly posterior, and in the other five, it extended laterally or inferiorly. The conventional echocardiographic signs of cardiac tamponade such as right atrial collapse, right ventricular diastolic collapse, and left atrial collapse were present in only 3, 1, and 3 of these 15 patients, respectively, but all exhibited left ventricular diastolic collapse. Increasing pressure within the compartment of a loculated pericardial effusion reaching the limit of pericardial distensibility and consequent transient reversal of transmural left ventricular pressure during diastole are most likely the basis for diastolic collapse of the thick-walled ventricle in a setting of regional cardiac tamponade. CONCLUSIONS: We conclude that left ventricular diastolic collapse is a frequent sign of regional cardiac tamponade and could be a useful marker of tamponade in postoperative patients.
OBJECTIVE: To investigate the effectiveness of X-ray and echocardiography (ECHO) as a diagnostic tool for cardiac tamponade in adult cardiac surgery patients. METHODS: Thirty five coronary artery bypass and graft surgery patients who developed cardiac tamponade at Cleveland clinic foundation, were included in this study. Their diagnosis was confirmed at the time of re-exploration in the operating room. These patients were followed retrospectively for demographics, X-ray and echocardiography findings. Abnormal and enlarged cardiac silhouette which was different from first postoperative X-ray was used as radiological criteria for tamponade while echocardiographic diagnosis was left to the discretion of cardiologist. RESULTS: Twenty four males (69%) and 11 (31%) females with an average age of 60.7 +/- 15.2 years were included in this study. Only 7 (20%) patients met our criteria for radiological diagnosis of tamponade. All 35 patients showed pericardial effusion on ECHO while cardiac tamponade was present in 30 (86%) patients. Tamponade developed on an average on 4th postoperative day. CONCLUSION: Radiological diagnosis of cardiac tamponade based on changes in cardiac silhouette provide limited information while ECHO is a reliable diagnostic tool when combined with clinical findings.
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Cardiac tamponade is an important complication after cardiac surgery, yet little has been published on the echocardiographic diagnosis of this situation. The two-dimensional echocardiograms of 11 patients who required surgical relief of cardiac tamponade complicating cardiac surgery were therefore reviewed. Four had nonloculated pericardial effusions surrounding both ventricles. The other seven patients had a loculated posterior pericardial effusion; in three of these the effusion altered left ventricular posterior wall contour so that it was concave toward the effusion in the long-axis view; in two, a strikingly abnormal motion of the left ventricular posterior wall was noted, such that the width of the posterior pericardial space diminished in systole and widened abruptly in early diastole. The quantity of pericardial contents (fluid, blood or clot) evacuated surgically was smaller than usually encountered in patients with tamponade due to various "medical" conditions. Thus, unlike tamponade with other pericardial effusions, tamponade after cardiac surgery is due to a pericardial effusion that is smaller in volume, often loculated posteriorly and associated with certain unique two-dimensional echocardiographic features.
Patients with cardiac tamponade usually have significant hypotension; hypertension is rare. Before administering any medication during tamponade one must consider the complex physiology and compensatory mechanisms of cardiac compression [1]. We observed both an accentuation of pulsus paradoxus and retrospectively recognized fluctuations of left-ventricular function after progressively rising arterial blood pressure had been lowered.
BACKGROUND: In cardiac tamponade cardiac output falls, but peripheral vascular resistance increases, so that systemic blood pressure may be maintained at normal or near-normal levels. We recently observed a patient with cardiac tamponade whose blood pressure was markedly elevated. METHODS: To determine the frequency of elevated blood pressure in patients with cardiac tamponade and their hemodynamic characteristics, we studied 18 consecutive patients with cardiac tamponade from a variety of causes using right heart catheterization. RESULTS: Six of the 18 patients had systolic arterial blood pressures ranging from 150 to 210 mm Hg (mean [+/- SD], 176 +/- 26) and diastolic pressures ranging from 100 to 130 mm Hg (mean, 113 +/- 14). All six had previously been hypertensive. After pericardiocentesis there was a significant decrease in blood pressure (to 139 +/- 13 mm Hg systolic, P less than 0.05; and 83 +/- 6 mm Hg diastolic, P less than 0.01) and peripheral vascular resistance (from 2150 +/- 588 to 1207 +/- 345 dyn.sec.cm-5, P less than 0.01). Cardiac output increased in all six. The other 12 patients, 3 of whom had a history of hypertension, had significant increases in cardiac output and systolic blood pressure (from 119 +/- 13 to 127 +/- 7 mm Hg, P less than 0.05) after pericardiocentesis, whereas peripheral vascular resistance decreased. Both groups had similar degrees of cardiac tamponade, as indicated by measurements of cardiac output and intrapericardial, right atrial, and pulmonary-artery wedge pressures. CONCLUSIONS: Elevated blood pressure may occur in some patients with cardiac tamponade who have preexisting hypertension. Moreover, blood pressure may fall after pericardiocentesis in patients who have elevated blood pressure associated with tamponade.
Cardiac actinomycosis occurs in less than 2 percent of the patients with infections due to Actinomyces israelii. We describe the findings in a patient with acute cardiac tamponade who survived through pericardial drainage and aggressive medical therapy. Although uncommon, this disorder is important to recognize because it is curable with current medical and surgical therapy.
Experimental cardiac tamponade was induced in anesthetized dogs by injection of isotonic solution of sodium chloride into the pericardium via a polyethylene catheter which was implanted before. Myocardial contractility was continuously recorded by using analog and digital computers. The pressure rise in the pericardium was accompanied by a significant growth of myocardial contractility indices. However, the increase in myocardial contractility under experimental cardiac tamponade did not make for complete compensation of cardiac pump function failure caused by restriction of the heart blood content on dilatation.
Whether cardiac tamponade causes myocardial ischemia and whether volume resuscitation can improve coronary perfusion pressure and myocardial blood flow were studied by hemodynamic responses to three blood infusions of 15 ml/kg in dogs with left ventricular hypovolemia produced by cardiac tamponade (N = 10) or hemorrhage (N = 10). Coronary perfusion pressure decreased to 37 +/- 2 mm Hg with tamponade and 39 +/- 1 mm Hg with hemorrhage, causing significant blood flow decreases in both ventricles. Myocardial oxygen extraction increased significantly in both groups without affecting lactate extraction. Volume resuscitation after hemorrhage progressively restored hemodynamic variables to baseline values. Volume resuscitation after tamponade did not increase stroke volume, whereas it increased coronary sinus pressure to 19.2 +/- 1.0 mm Hg (p less than 0.05). Coronary perfusion pressure increased to 53 +/- 5 mm Hg following the first infusion (p less than 0.05), but exhibited no further improvement. Tamponade did not produce myocardial ischemia. Coronary perfusion pressure and blood flow were not restored to baseline values with volume resuscitation since coronary sinus pressure rose incrementally with each volume infusion.
Fatal cardiac tamponade is a well recognised complication of the use of central venous catheters in neonatal patients. There is controversy over optimum catheter tip position to balance catheter performance against risk of adverse events. We report a series of five cases of tamponade occurring in one neonatal unit over a 4-year period, related to catheter tip placement in the right atrium. Right atrial catheter angulation, curvature or looping (CA) was present in all five cases on plain radiograph. It was frequently seen in other patients over the same period. Review of the literature indicates that CA was present in 6 of the 11 previous cases where the presence or absence of CA can be determined. Where right atrial catheter tip placement is accepted, clinicians should be aware of this characteristic catheter configuration, which is a major risk factor for cardiac tamponade. We recommend that catheter tips should not be placed in the right atrium to avoid risk of tamponade.
Acute cardiac tamponade was created in a large animal model in an effort to investigate the hemodynamic and oxygen transport variables during the inflation of the pneumatic antishock garment (PASG) to two different pressures (60 and 80 mm Hg). Inflation of PASG to either pressure under these conditions had no significant effects on filing pressures to the right or left heart, cardiac index, arterial blood gases, oxygen delivery, indexed pulmonary, and systemic vascular resistances. We conclude in this animal model of acute cardiac tamponade that no beneficial or harmful effects were demonstrated during the application and inflation of the pneumatic antishock garment to 60 or 80 mm Hg.
Primary cardiac angiosarcoma is a rare tumor associated with a poor prognosis. We report a case of a 59-year-old woman with right atrial angiosarcoma presenting with cardiac tamponade due to right atrial perforation. She underwent urgent surgical resection of the tumor. However, the patient died 68 days after surgery due to local recurrence. An effective treatment for cardiac angiosarcoma has not yet been established. However, more aggressive treatment with a combination of surgery, radiation, chemotherapy and IL-2 should be considered.
Primary cardiac angiosarcoma is a rare disease of difficult diagnosis and poor prognosis frequently associated with recurring hemopericardium. We report the case of a 30-year-old female with a right atrial angiosarcoma and spontaneous rupture to the pericardial cavity, who was diagnosed during an emergency exploratory thoracotomy, whose indication was cardiac tamponade. This is the 8th case reported in the literature. Clinical findings are discussed and a literature review is provided.
A case of a neonate with a life-threatening cardiac tamponade due to cardiac tumour is presented. Pericardiocentesis was performed and 300 ml of purulent fluid was evacuated. Pericardial drainage was undertaken. Six months later cardiac tamponade recurred and was again successfully treated with pericardial drainage. A subsequent 10-month follow-up was uneventful. Diagnosis and treatment of cardiac tumours associated with pericardial effusion are discussed.