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PubMed1992

Loculated pericardial effusion and cardiac tamponade late after cardiac surgery.

A case of loculated pericardial effusion diagnosed by chest roentgenogram and subsequent echocardiogram is presented. This effusion was unusual in its late appearance after thoracotomy and its discrete location which resulted in hemodynamic embarrassment. Subsequent cultures demonstrated an infected pericardial space and septicemia.

Adult↗
PubMed1980

Cardiac tamponade.

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Cardiac Tamponade↗
PubMed1993

Atypical presentations and echocardiographic findings in patients with cardiac tamponade occurring early and late after cardiac surgery.

Cardiac tamponade, a potentially lethal complication following cardiac surgery, may present either early or late postoperatively and may be difficult to diagnose due to atypical clinical, hemodynamic, or echocardiographic findings. To determine the frequency and clinical features of postoperative cardiac tamponade, we performed a review of 510 consecutive patients who underwent cardiac surgery. The incidence of postoperative cardiac tamponade was 2.0 percent (10/510 patients) and occurred following valvular, bypass, and aortic surgery. Nine of ten patients had either atypical clinical, hemodynamic, and/or echocardiographic findings. The diagnosis of tamponade was made 1 to 30 days (mean = 8.5 days) postoperatively. Presenting symptoms were often mild and nonspecific. Classic signs including hypotension, pulsus paradoxus greater than 12 mm Hg, and elevated jugular venous pressure were present in 7, 6, and 5 patients, respectively. Right heart hemodynamics revealed elevated and equalized diastolic pressures in three of six patients. Two-dimensional echocardiography revealed selective compression of the left ventricle (LV) (four patients), right ventricle (RV) (one patient), left atrium (LA)/RV (one patient), LA/LV (one patient), LA/LV/RV (one patient), all four chambers (one patient), and no diastolic collapse of any chamber (one patient). There was often an absence of anterior pericardial fluid (six patients) with tethering of a portion of the RV to the chest wall anteriorly (five patients). Coagulation parameters were "supratherapeutic" in only three of eight patients who were receiving systemic anticoagulants at the time of diagnosis. The initial diagnosis was confused with congestive heart failure in one patient, pulmonary embolism in three patients, acute myocardial infarction in two patients, and sepsis in one patient. Eight of ten patients survived; all of these patients underwent surgical removal of fluid and/or hematoma in the operating room. We conclude that postoperative tamponade after cardiac surgery may have varied clinical and hemodynamic presentations, often due to selective chamber compression by loculated fluid or clot. Due to its frequently atypical features and presentation that may simulate other disorders, the diagnosis of tamponade should be considered whenever hemodynamic deterioration or signs of low output failure occur in the postcardiotomy patient.

Adult↗
PubMed1987

Ventricular performance related to transmural filling pressure in clinical cardiac tamponade.

In clinical cardiac tamponade, open-catheter intrapericardial pressure (IPP) may be used to estimate left ventricular transmural filling pressure (TMFP). However, it has been suggested recently that right atrial pressure (RAP) is superior to IPP in assessing true extracardiac pressure during pericardial drainage. In 10 patients with subacute cardiac tamponade, pulmonary wedge pressure (PWP), RAP, and IPP were measured along with indexes of systolic function. To test the relative merits of IPP and RAP in assessing true pericardial pressure, three TMFP estimates were analyzed: TMFP1 = (PWP - IPP); TMFP2 = (PWP - 1/3 RAP - 2/3 IPP); and TMFP3 = (PWP - RAP). An accurate TMFP presumably should increase during pericardiocentesis and correlate with left ventricular stroke work. In addition, to test the role of preload variation in pulsus paradoxus, respiratory variation in TMFP was analyzed. In the initial tamponade state, RAP and IPP were essentially equal, so all three TMFP estimates gave equivalent results. For instance, TMFP1 averaged 4 +/- 2 mm Hg but fell to 0.2 +/- 1.3 mm Hg during inspiration (p less than .001 vs expiration) and showed beat-by-beat correlation with pulse arterial pressure. After intermediate pericardiocentesis (280 +/- 160 ml), the IPP of 6 +/- 3 mm Hg fell significantly below the RAP of 10 +/- 3 mm Hg (p less than .001), but with a 570 +/- 320 ml residual effusion suggesting continued IPP measurement accuracy. By complete pericardiocentesis (810 +/- 430 ml) there was a significant increase in TMFP1 to 8 +/- 4 mm Hg (p less than .05 vs tamponade) but not in the TMFP3 of 1 +/- 3 mm Hg. Encompassing tamponade and pericardiocentesis data, left ventricular stroke work index showed positive correlation with TMFP1 (r = .59) and TMFP2 (r = .52) but not with TMFP3. Thus cardiac tamponade often may be diagnosed with a TMFP averaging well above zero, and diastolic equalization of PWP, RAP, and IPP may be a predominantly inspiratory finding ("inspiratory tracking"). This supports the role of preload variation in the genesis of pulsus paradoxus. On the other hand, true pericardial pressure may fall substantially below RAP in the course of pericardial drainage. This may be reconciled with the concept that normal pericardial pressure nearly equals RAP by hypothesizing an increased pericardial capacity in subacute tamponade so that pericardiocentesis produces a state analogous to removal of normal pericardial constraint.

Cardiac Tamponade↗
PubMed2006

Pericardial hydatid cyst presenting with cardiac tamponade.

Cases of cardiac hydatid cyst disease are uncommon, occurring in approximately 0.5% to 2% of patients with hydatid disease. Most cardiac hydatid cysts are located in the left ventricle and interventricular septum. Cardiac involvement may have serious consequences. Both the disease and its surgical treatment carry a high complication rate, including rupture leading to cardiac tamponade, anaphylaxis and also death. In the present report, a 10-year-old girl with cardiac tamponade secondary to a pericardial hydatid cyst is described.

Cardiac Tamponade↗
PubMed1992

Usefulness of right ventricular indices in early diagnosis of cardiac tamponade.

Early diagnosis of postoperative cardiac tamponade is impeded by its clinical similarity to left ventricular failure. Moreover, the hemodynamic changes necessary to diagnose cardiac tamponade are detected by conventional monitoring technique only after clinical compromise. Early signs of cardiac tamponade and left ventricular failure were studied with emphasis on right ventricular function in anesthetized dogs. One group (n = 20) had cardiac tamponade produced by incrementally increasing pericardial pressure (2 to 20 mm Hg), and another group (n = 20) had acute left ventricular failure produced by successive ligation of the anterior descending coronary artery at the lower, middle, and upper thirds. Besides standard hemodynamic measurements, right ventricular function was examined with a rapid-response thermodilution catheter. During cardiac tamponade, cardiac output, right ventricular ejection fraction, right ventricular stroke volume, and right ventricular end-diastolic volume were significantly decreased from baseline values after a pericardial pressure of 8 mm Hg or more (p less than 0.05). Right atrial and pulmonary arterial pressures were not significantly elevated until 14 and 20 mm Hg of pericardial pressure, respectively. Although cardiac function in the left ventricular failure group was reduced after each ligation, right ventricular ejection fraction remained unchanged. This study suggests that right ventricular indices may facilitate earlier diagnosis of cardiac tamponade with greater accuracy.

Animals↗
PubMed2002

Diagnosis, management, and clinical outcome of cardiac tamponade complicating percutaneous coronary intervention.

Cardiac tamponade is an uncommon but life-threatening complication of percutaneous coronary intervention (PCI). The purpose of the present study was to characterize the incidence, management, and clinical outcome associated with this complication. We analyzed a prospective database of 25,697 PCIs performed at William Beaumont Hospital (Royal Oak, Michigan) between October 1993 and December 2000. Cardiac tamponade was observed in 31 of 25,697 PCI procedures (0.12%). Cardiac tamponade was diagnosed in the catheterization laboratory in 17 of 31 patients (55%), and 14 patients (45%) had a delayed presentation (mean time from PCI 4.4 hours). Cardiac tamponade was twice as frequent after use of atheroablative devices compared with percutaneous transluminal coronary angioplasty and stenting (0.26% vs 0.11%, p <0.05). All patients with immediate cardiac tamponade had coronary artery perforation. In 11 of 14 patients with delayed tamponade (79%), no actual site of perforation could be identified. A moderate or large pericardial effusion was observed in 20 patients, and 9 had small effusions without typical echocardiographic features of tamponade. Pericardiocentesis was performed in 30 patients; 19 patients (61%) were treated successfully with aspiration alone, but 12 patients (39%) required further emergency surgical intervention. In-hospital complications included death (42%), emergency surgery (39%), myocardial infarction (29%), and transfusion (65%). Cardiac tamponade is an uncommon but important complication of PCI and is associated with high mortality and morbidity. Most cases are recognized in the catheterization laboratory, but delayed cardiac tamponade may occur and must be considered as a cause of late hypotension after PCI.

Aged↗
PubMedDate not supplied

A case with acute leukemia presenting with cardiac tamponade.

Pericardial effusions and cardiac tamponade are rare and severe complications of leukemia. They often develop during the radiation therapy, chemotherapy, or infections in the course of leukemia. However, some cases present with pericardial effusion and tamponade. We report a three-year-old girl who was admitted with cardiac tamponade and needed urgent pericardiocentesis. Clinical evaluation and laboratory results revealed myeloid markered-T cell acute lymphoblastic leukemia (ALL) and pericardial invasion. She is the youngest patient with cardiac tamponade who was diagnosed acute lymphoblastic leukemia in the English-language literature.

Cardiac Tamponade↗
PubMed1986

Total peripheral resistance during cardiac tamponade: adrenergic and angiotensin roles.

During progressive cardiac tamponade in conscious dogs, cardiac output falls continuously while arterial blood pressure is maintained until cardiovascular decompensation by increases in total peripheral resistance (TPR). Plasma renin activity (PRA) is known to increase at decompensation. We hypothesized that the increase in TPR during cardiac tamponade was mediated by alpha-adrenergic and renin-angiotensin mechanisms. Twelve adult dogs were instrumented to measure cardiac output (electromagnetic flow probe), aortic and right atrial blood pressures, and intrapericardial pressure (IPP). TPR was calculated as the conscious euvolemic animals underwent cardiac tamponade induced by intrapericardial saline infusion at 20 ml/min. Six dogs underwent cardiac tamponade in the control condition (no medications) and during independent alpha- and beta-adrenergic and angiotensin-converting enzyme (ACE) inhibition. PRA and angiotensin II (ANG II) were measured during control tamponade. We found that TPR increased continuously to levels of greater than 200% of base line as IPP rose during cardiac tamponade (P less than 0.01). This increase in TPR was unaffected by beta-adrenergic or ACE blockade but was blunted by alpha-adrenergic blockade. PRA and ANG II increased only at decompensated tamponade (P less than 0.05) when arterial blood pressure had fallen by 30%. These changes in PRA and ANG II during tamponade were not altered by beta-blockade in six separate animals. We conclude that cardiac tamponade stimulates renin release and ANG II generation by a non-beta-receptor-mediated mechanism. The increase in TPR during cardiac tamponade is primarily dependent on alpha-adrenergic mechanisms, with a limited late contribution from the renin-angiotensin system.

Angiotensin II↗
PubMed2002

Simultaneous malignant hypertension and cardiac tamponade.

Malignant hypertension and cardiac tamponade are uncommon but potentially life-threatening medical emergencies. Both conditions may be associated with collagen vascular diseases, such as systemic lupus erythematosus. We report a case of acute cardiac tamponade associated with malignant hypertension secondary to lupus nephritis. Immediately after pericardiocentesis, blood pressure declined substantially. Although malignant hypertension is seen with modest frequency in patients with systemic lupus erythematosus, true cardiac tamponade is a less common complication of lupus serositis. Acute, simultaneous presentation of both life-threatening entities and the hemodynamic course have not been described.

Adult↗
PubMed2000

Cardiac tamponade due to post-cardiac injury syndrome in a patient with severe haemophilia A and HIV-1 infection.

An 18-year-old man with severe haemophilia A (FVIII:C < 1%) and human immunodeficiency virus 1 (HIV-1) infection was admitted to the hospital with fever and chest pain for 7 days. Eight weeks prior to his admission he had an accident for which he underwent, at another hospital, clinical and laboratory examination that revealed bone fractures of the nose cavity, and he was given factor VIII concentrates for seven days due to nasal bleeding. On admission, chest roentgenogram showed a large cardiac silhouette and echocardiography confirmed the presence of a large quantity of pericardial fluid. A presumptive diagnosis of the post-cardiac injury syndrome was made and he was given anti-inflammatory drugs plus infusion of recombinant factor VIII concentrate (35 units kg-1 b.i.d.). On the seventh day he exhibited cardiac tamponade for which he underwent subxiphoid pericardiotomy with drainage of approximately 1500 mL of bloody exudate. He had an uncomplicated recovery and 10 days later he left hospital. He was given a continuous prophylactic treatment of 15 units kg-1 of recombinant FVIII every 2 days for 6 months, and 30 months after this episode the patient is free of any symptom.

Adolescent↗