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Although cardiac tamponade is a known complication of malignancy, it is rarely the initial manifestation. We report a 46-year-old male who presented with malignant cardiac tamponade 6 months prior to the definitive diagnosis of primary pericardial mesothelioma. A thorough literature search has not revealed a similar care.
Cardiac tamponade complicating catheter ablation of atrial fibrillation (AF) occurs in approximately 1% of pulmonary vein isolation (PVI), and up to 6% of linear ablation procedures. We reviewed 348 consecutive AF ablation (including repeat) procedures over 1 year, which all included PVI, with additional linear lesions at the mitral isthmus in 73%, and cavotricuspid isthmus (CTI) in 76%. An irrigated-tip ablation catheter was used, with power limited to 25-35 W for PVI and 45-60 W for linear lesions. Tamponade occurred in seven men and three women (2.9% of the population) during the creation of linear ablation lesions. Mechanical perforations occurred in two patients, and "popping" during radiofrequency (RF) energy delivery at the mitral isthmus in six, and at the CTI in two patients. Peak RF power was significantly higher in patients with than without tamponade (53 +/- 4 W vs 48 +/- 7 W; P = 0.02), and was greater than 48 W in all cases of "popping." In the following year, RF power for linear ablation was limited to </=42 W. Among 398 procedures, tamponade occurred in four patients (1.0%; P = 0.047 vs first year), three from "popping" and one from mechanical trauma. Procedural success rate remained the same despite reduction of power. Risk of tamponade was highest during linear ablation, mainly associated with high energy delivery and "popping." Reducing the energy limited, though did not eliminate this complication.
Cardiac tamponade linked to parenteral nutrition is a rare complication, but often fatal. This clinical study describes a case in which this complication occurs, with a review of literature on the subject and several recommendations for prevention and treatment.
Postoperative cardiac tamponade due to localized compression of the atria occurred in a 64-year-old man after aortic valve replacement and repair of an ascending aortic dissection. The clinical findings were subtle and the echocardiographic findings were unusual. Color Doppler flow imaging assisted in making the diagnosis of localized atrial compression.
To investigate the pathophysiology of cardiac tamponade, the hemodynamics of 77 consecutive patients with greater than 150 ml of pericardial effusion were studied. Patients were classified into 3 groups based on the equilibration of intrapericardial with right atrial and pulmonary arterial wedge pressures (mm Hg): group I (n = 16), intrapericardial pressure was less than right atrial and pulmonary arterial wedge pressures; group II (n = 13), intrapericardial pressure was equilibrated with right atrial but not pulmonary arterial wedge pressures; group III (n = 48), intrapericardial pressure was equilibrated with right atrial and pulmonary arterial wedge pressures. Pericardiocentesis produced the following changes: group I--significant (p less than 0.03) decreases in intrapericardial pressure (7 +/- 2 mm Hg), right atrial pressure (3 +/- 2 mm Hg), pulmonary arterial wedge pressure (2 +/- 2 mm Hg), and the inspiratory decrease in arterial systolic pressure (3 +/- 4 mm Hg) but no significant change in cardiac output; group II--significant (p less than 0.02) decreases in intrapericardial pressure (11 +/- 5 mm Hg), right atrial pressure (6 +/- 4 mm Hg), pulmonary arterial wedge pressure (4 +/- 5 mm Hg), and inspiratory decrease in arterial systolic pressure (8 +/- 7 mm Hg), and increase in cardiac output (1.1 +/- 1.2 liters/min); group III--significant (p less than 0.001) decreases in intrapericardial pressure (16 +/- 7 mm Hg), right atrial pressure (9 +/- 4 mm Hg), pulmonary arterial wedge pressure (8 +/- 5 mm Hg), inspiratory decrease in arterial systolic pressure (17 +/- 11 mm Hg), and increase in cardiac output (2.8 +/- 1.5 liters/min). The changes after pericardiocentesis in all parameters were significantly (p less than 0.05) greater in group III than in groups I or II except for the change in right atrial pressure, which was not significantly different in groups II versus III. The changes after pericardiocentesis indicate pericardial effusion caused the greatest abnormalities in group III but also caused significant abnormalities of pressure and flow in group II and of pressure alone in group I.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac tamponade is a life-threatening process that must be diagnosed and treated in a timely fashion. As blood fills the pericardial sac, right ventricular filling is impeded and cardiac output is diminished, ultimately leading to cardiovascular collapse. Fortunately, emergency ultrasonography has improved the way we manage these patients today. In this report, we discuss a patient with hypotension and tachycardia who was found to have a massive loculated posterior pericardial effusion with impending cardiac tamponade. The diagnosis and appropriate treatment of this patient were rapidly ascertained with the use of bedside echocardiography. We review the literature on emergency ultrasonography, and consider the numerous instances in which emergency echocardiography can be life-saving.
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Late cardiac tamponade (LCT) is a poorly studied life threatening complication after operation on the heart. Two cases of LCT developing 18 and 47 days after an operation are described. With consideration for the literature, the authors discuss the causes of LCT, the peculiarities of its clinical course, the diagnosis and treatment. A poor prognosis in LCT is an indication for early active surgical tactics. Puncture of the pericardium with its drainage, as well as pericardiotomy performed through an epigastric approach or by thoracotomy or by means of median sternotomy are effective methods for the management of this menacing complication.
A 2994 g infant suffered cardiac tamponade from an infusion of total parenteral nutrition through an indwelling central venous catheter. The infant survived as a result of early diagnosis and aggressive therapeutic intervention. Cardiac tamponade secondary to central venous catheterisation is rare, but potentially lethal. Possible mechanisms are direct puncture by the catheter tip, or osmotic injury from the use of hypertonic solutions. To avoid this complication, the catheter tip should be prevented from entering the right atrium and its position should be checked periodically by chest X ray. Cardiac tamponade should be considered in any patient with a central venous catheter whose clinical condition deteriorates suddenly. Diagnostic or therapeutic pericardiocentesis should be employed as the first measure and time should not be wasted on other diagnostic procedures.
The first case of spontaneous cardiac tamponade caused by wire suture for sternotomy closure is presented. The proper analysis of bloody pericardial fluid, including simultaneous aspirate and venous hematocrit, oxygen content, and coagulation studies, is emphasized. In addition, the causes of acute hemopericardium are reviewed. Spontaneous cardiac tamponade as a potential late complication of cardiac surgery should be considered in the postoperative patient who presents with pericarditis or a sudden change in cardiac status.
Screw-in atrial pacing leads are widely used. Cardiac tamponade is a complication. An 81-year-old woman with advanced atrioventricular block underwent permanent pacemaker implantation and subsequently developed cardiac tamponade. At surgery, the lead-tip screw was found penetrated through the right atrium but not through the pericardium. The source of bleeding was confirmed to scratching the inner pericardial membrane by the screw tip. Although cardiac tamponade due to perforation and leakage is known, tamponade caused by the trauma of an atrial screw on the pericardium with resultant ooze is less well described.
INTRODUCTION: Patients with lung adenocarcinoma often suffer from metastatic pericardial effusion that may eventually cause cardiac tamponade. Recurrence of pericardial effusion is frequent after pericardial drainage and therapy for the prevention of fluid reaccumulation is still controversial. We evaluated the safety and effectiveness of the intrapericardial infusion of cisplatin, a substance with antineoplastic and sclerosing properties, after pericardiocentesis in patients with lung adenocarcinoma and malignant cardiac tamponade. METHODS: Twenty-five patients (19 males and 6 females, median age 55 years) with lung adenocarcinoma confirmed by cytological examination and cardiac tamponade were studied. All patients underwent subxiphoid pericardiocentesis through catheter insertion, under electrocardiographic, echocardiographic and haemodynamic guidance. After the malignant aetiology of the pericardial effusion had been confirmed by cytological examination, cisplatin was instilled (10 mg in 20 ml normal saline) into the pericardial cavity during three consecutive days. Clinical and echocardiographic evaluation was performed every month thereafter. RESULTS: Pericardial fluid of 350-1700 ml was removed (median 750 ml) and was haemorrhagic in 80% of the cases. Paroxysmal atrial fibrillation was detected in three patients (12%) and non-sustained ventricular tachycardia in two (8%). None of the patients had hypotension or retrosternal pain. One patient suffered from significant pericardial effusion reaccumulation (4%). Laboratory findings were not influenced by systemic drug absorption in any patient. Transthoracic echocardiographic study revealed pericardial thickening without physiology of constriction in 4 patients (16%). After pericardiocentesis, the mean survival period overall was 4.5 months (range 3-92 weeks), and mortality was attributed to widespread disease (respiratory failure). CONCLUSIONS: Intrapericardial administration of cisplatin is safe and effective in preventing the reaccumulation of malignant pericardial effusion in the majority of patients with lung adenocarcinoma.
Pericardial effusion is not infrequent as a manifestation of hypothyroidism, however, cardiac tamponade is exceptional in these patients. We report a case of a female patient with cardiac tamponade that in the forward workshop was diagnosed of primary hypothyroidism. A brief presentation of clinical history is reported. The literature's review emphasizes the rarity of this case, the importance of the knowledge of triggering factors to establish a precious diagnosis and satisfactory clinical evolution with hormonal treatment without recurrences of the cardiac tamponade after pericardiocentesis is performed, although the resolution of the pericardial effusion is usually slow.
The value of a newly described echocardiographic sign for the detection of cardiac tamponade was retrospectively evaluated in 91 patients. M-mode echocardiograms were reviewed in 86 patients, 36 of whom had concurrent two-dimensional echocardiographic examinations; in five patients, only two-dimensional echocardiography was performed. Cardiac tamponade was clinically present in 17 patients, 14 of whom had abnormal posterior motion of the right ventricular free wall in early diastole. Two of the 17 patients with tamponade had equivocally abnormal motion and one had normal wall motion. The patient with normal wall motion was later proved to have predominantly constrictive pericardial disease. In all cases, the abnormal wall motion reverted to normal after a definitive drainage procedure. Two-dimensional echocardiography confirmed that the abnormal right ventricular wall motion represented a true collapse of the right ventricular cavity in early diastole. Of the 69 patients without clinical cardiac tamponade, only seven had abnormal right ventricular wall motion. Detection of abnormal diastolic right ventricular free wall motion may be a sensitive indicator or a hemodynamically significant pericardial effusion. Conversely, the presence of normal motion of the right ventricular free wall appears to be a reliable indicator that the pericardial effusion is exerting little effect on overall cardiac function.
Late cardiac tamponade is a rare but serious complication following open-heart surgery. It occurred in 9 (0.8%) of 1 094 consecutive patients 6 to 13 (median 8) days after operation. Six patients had undergone valve replacement and three coronary bypass surgery. All were on anticoagulant medication postoperatively (median TT index 7%). Early symptoms of cardiac tamponade were nausea and general malaise (present in all 9 cases), whereas classical signs of tamponade such as arterial hypotension and distended neck veins appeared late. The cardiac silhouette was radiographically enlarged in all cases, but this finding was seldom diagnostic. Computed tomography gave the surest diagnosis and permitted quantitative assessment of the fluid in the pericardium. Pericardial needle puncture was effective in temporarily relieving the tamponade, but insertion of a tube by the subxiphoid approach gave definitive drainage.
We report a case of profound hypotension, after induction of general anaesthesia, that resulted from unexpected cardiac tamponade. The differential diagnosis was complicated by the absence of any evidence to indicate that there was significant direct chest injury. Many of the recognised clinical signs of cardiac tamponade were absent, in particular, there was no compensatory tachycardia, and heart rate remained stable despite severe hypotension before surgical drainage of the pericardium. The possible aetiology and pathophysiology is discussed. It is suggested that after major trauma, cardiac tamponade should be considered as a possibility even in the absence of significantly abnormal cardiovascular signs, evidence of direct chest injury, or an abnormal chest X ray.
The onset of right ventricular diastolic collapse has been shown to be a very sensitive and specific sign of cardiac tamponade in both clinical and conscious canine studies, and is associated with a decline in cardiac output of about 20%. To determine if blood flow to critical regions was affected at the time of onset of right ventricular diastolic collapse, seven unanesthetized, chronically instrumented dogs were studied during cardiac tamponade induced by the intrapericardial infusion of warm saline solution. Aortic blood pressure, heart rate, and cardiac output (electromagnetic flowprobe) were recorded at baseline (drained pericardial space) and at the onset of right ventricular diastolic collapse as seen on two-dimensional echocardiography. Regional blood flow was measured with radionuclide-labeled microspheres. Despite the expected decline in cardiac output, there was no significant change in cardiac, renal, or cerebral cortical blood flow at the onset of right ventricular diastolic collapse. Therefore, this noninvasive marker of early cardiac tamponade begins before vital organ perfusion is compromised, thus strengthening its clinical value.
Although neoplastic involvement of the pericardium frequently is present postmortem, cardiac manifestations before death are uncommon, and cardiac tamponade as the initial presentation of cancer is rare. In this study, a malignancy was first recognized in eight of 23 patients (35 percent) who presented with cardiac tamponade. Seven of these eight patients had lung and one patient thyroid carcinoma. The prognosis of these eight patients was poor with seven of eight patients dead within a mean of seven weeks (range 2.5 to 16). Overall, pericardial fluid cytology demonstrated a specific diagnosis of malignancy in 14 of 19 patients (74 percent). Earlier recognition of the possibility of malignancy may allow initiation of appropriate local or systemic treatment to lessen the probability of cardiac tamponade and improve survival. We recommend that all patients who present with tamponade have cytology performed on the pericardial fluid, even if malignancy is not suspected initially.