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PubMed1994

Pneumopericardium: a rare cause of cardiac tamponade in an infant on a positive pressure ventilation.

Cardiac tamponade most commonly results from accumulation of blood, or other fluids, within the pericardial sac. However, rarely air tamponade can lead to tension pneumopericardium and death. Positive pressure ventilation in infants carries a risk of barotrauma and presents as pneumothorax, pneumomediastinum or rarely pneumopericardium. We present an infant with cardiac tamponade due to pneumopericardium to illustrate the classical signs and symptoms, and the management of this rare condition.

Cardiac Tamponade↗

PubMed1990

Increasing atrial pressure during cardiac tamponade does not elevate plasma levels of the peptide ANP in conscious dogs.

1. Factors influencing the release of atrial natriuretic peptide (ANP) are not well understood. We chose a conscious euvolaemic canine model of cardiac tamponade to investigate the roles played by atrial blood pressure, transmural atrial pressure, atrial size, and arginine vasopressin (AVP) on ANP release since during cardiac tamponade the atrial transmural pressure and size decrease as atrial pressure increases. The haemodynamic response to acute cardiac tamponade in conscious dogs differs from that in anaesthetized or convalescent animals. 2. Eighteen mongrel dogs were prepared for the chronic measurement of: ascending aortic blood flow (electromagnetic flowmeter); intrapericardial, right atrial and aortic blood pressures, and the evaluation of right atrial size (two-dimensional echocardiography). After the animals had recovered from surgery, data were collected during progressive cardiac tamponade induced by intrapericardial infusion of warmed saline (20 ml/min) to the point of haemodynamic decompensation. Decompensated cardiac tamponade (DCT) was defined as a decline in mean aortic blood pressure to 70% of the level present when the pericardial space was drained of fluid (baseline) and was produced in all animals within 25 min. Plasma ANP and AVP levels were measured at selected intervals. 3. Cardiac output decreased progressively as intrapericardial pressure, right atrial blood pressure and heart rate increased. Mean aortic blood pressure was well maintained until late in tamponade when it declined rapidly, while atrial transmural pressure and atrial size decreased continuously. These haemodynamic changes were associated with stable ANP plasma levels. There was no significant change in AVP plasma levels from the baseline level of 2.5 +/- 0.4 pg/ml until the point of DCT when they abruptly increased to 117 +/- 36.4 pg/ml. 4. The ability to increase ANP plasma levels was confirmed in a subgroup of animals by noting the response to AVP injection. Although the animals were able to increase plasma ANP levels in response to AVP injection (when intrapericardial pressure was normal) and the plasma AVP level was markedly increased late in tamponade, the time course of plasma AVP elevation could not explain why plasma ANP levels did not decrease as atrial transmural pressure and atrial size declined. 5. Thus, although atrial distention and not simply atrial blood pressure must play a dominant role in stimulating ANP release from the atria, decreased atrial size does not result in lowering of plasma ANP levels below baseline levels in this conscious euvolaemic canine model.

Animals↗

PubMed1992

A case report of purulent pericarditis with cardiac tamponade: echocardiographic findings.

A five year old girl with cardiac tamponade due to purulent pericarditis caused by Staphylococcus aureus was treated successfully with a combination therapy of appropriate antibiotics and surgical open drainage. Right atrial collapse was observed during early systole using two-dimensional echocardiography. This case illustrated the usefulness of echocardiography for early detection and treatment of cardiac tamponade in pediatric patients.

Cardiac Tamponade↗

PubMed1985

Incidence, etiology, diagnosis and treatment of cardiac tamponade in the Negev.

The files of 20 patients who required surgical intervention for cardiac tamponade between May 1976 and June 1983 were reviewed. The most frequently implicated etiological factors were viral or idiopathic (8 of 20 cases). Clinical signs of major importance were: tachycardia, 19 of 20; dyspnea, 17 of 20; and venous engorgement, 17 of 20. Valuable bedside examinations were the pulsus paradoxus for the cardiac tamponade of nontraumatic etiology and the central venous pressure examination for traumatic cardiac tamponade. Echocardiography was the most reliable laboratory examination. All patients were treated surgically either through a left thoracotomy or by the subxiphoid approach. Although both methods were equally effective in controlling this life-threatening condition, the latter technique resulted in a lower rate of postoperative complications.

Adolescent↗

PubMed1988

Mixed venous blood gases are superior to arterial blood gases in assessing acid-base status and oxygenation during acute cardiac tamponade in dogs.

Recent reports using anesthetized ventilator-dependent animal models, have suggested that in certain shock states, a disparity exists between arterial and mixed venous blood gases with regard to acid-base status and oxygenation. In a chronically instrumented unanesthetized canine model of acute cardiac tamponade breathing room air, we studied the effect of a graded decline in cardiac output on arterial and mixed venous pH, PCO2, and PO2. Cardiac tamponade resulted in a profound arterial respiratory alkalosis, whereas mixed venous pH, PCO2, and calculated serum bicarbonate levels remained relatively unchanged. As intrapericardial pressure increased and cardiac output declined, the difference between arterial and mixed venous PCO2 progressively increased. Further, whereas arterial oxygenation improved as cardiac output declined, mixed venous oxygenation steadily worsened. This disparity began early in cardiac tamponade (reductions in cardiac output of 20-40%) long before arterial blood pressure began to fall and progressively worsened as hemodynamic deterioration and lactic acidosis developed. Our findings are consistent with the hypothesis that a reduction in blood flow, resulting in decreased CO2 delivery to the lungs, is the primary mechanism responsible for the difference in pH and PCO2 observed between arterial and mixed venous blood. In this conscious, spontaneously breathing animal model, mixed venous blood gases thus are superior to arterial blood gases in assessing acid-base status and oxygenation, even early in acute cardiac tamponade when the decline in cardiac output is in the range of 20 to 40% and arterial blood pressure has not changed significantly.

Acid-Base Imbalance↗

PubMed1988

Cardiac tamponade and pericardial effusion: respiratory variation in transvalvular flow velocities studied by Doppler echocardiography.

Cardiac tamponade has been associated with an abnormally increased respiratory variation in transvalvular blood flow velocities. To determine whether this finding is consistently present in cardiac tamponade, seven patients were studied prospectively with Doppler echocardiography before and after pericardiocentesis and the results were compared with those found in 20 normal adults and 14 asymptomatic patients with pericardial effusion who did not have definite clinical evidence of tamponade. Doppler ultrasound evaluation included measurement of mitral, tricuspid, aortic, pulmonary and central venous flow velocities, as well as left ventricular ejection and isovolumic relaxation times during inspiration, expiration and apnea. In the patients with severe cardiac tamponade, respiratory variation in transvalvular flow velocities and left ventricular ejection and isovolumic relaxation times were markedly increased compared with values in normal subjects and those obtained after pericardiocentesis. In the 14 asymptomatic patients with pericardial effusion but without overt tamponade, 7 showed respiratory variation in flow velocity similar to that of normal subjects. The other seven patients demonstrated increased respiratory change compared with normal, but less than that in the patients with tamponade. Clinical and hemodynamic data in this latter group suggest that these patients may represent an intermediate stage of pericardial effusion with an element of hemodynamic compromise.

Adult↗

PubMed1984

Cardiac perforation from central venous catheters: survival after cardiac tamponade in an infant.

A 2,210-g infant suffered cardiac tamponade, which resulted from atrial perforation by a central venous catheter. The infant survived due to timely diagnostic and therapeutic intervention. Cardiac tamponade should be suspected in any patient with a central venous catheter whose condition deteriorates suddenly. Immediate chest roentgenogram and echocardiogram may be performed to support the diagnosis; but when the patient's condition is deteriorating, a diagnostic (and therapeutic as well!) pericardiocentesis should be performed without waiting for other diagnostic measures. A review of clinical recognition and diagnostic measures for cardiac perforation and tamponade is presented. Preventive measures to avoid this fatal complication of central venous catheters are suggested, and therapeutic interventions are outlined.

Cardiac Tamponade↗

PubMed1990

Influence of naloxone on response to acute cardiac tamponade in conscious dogs.

During progressive acute cardiac tamponade (CT) in conscious dogs, cardiac output (CO) falls continuously while arterial blood pressure (BP) is well maintained until an abruptly terminal decline. This response is primarily dependent on alpha-adrenergic mechanisms. During hemorrhagic shock, the opioid receptor blocker naloxone increases CO and BP and improves survival perhaps by reversing an opioid-induced cardiovascular depression. We produced 10 episodes of decompensated CT (DCT; 30% decline in BP) by intrapericardial saline infusion (20 ml/min) in five euvolemic conscious dogs. CT resulted in a decrease in CO and BP from base line (3.79 +/- 0.37 l/min and 89.6 +/- 5.2 mmHg, means +/- SE) to DCT (1.35 +/- 0.15 l/min and 57.5 +/- 3.1 mmHg; P less than 0.05). Naloxone (3 mg/kg iv) given at the onset of DCT resulted in a prompt sustained return of BP to base-line levels (P less than 0.05) with no change in CO. Four more animals were studied before and during naloxone (3 mg/kg iv then 0.3 mg.kg-1.min-1 iv). DCT occurred at a higher intrapericardial pressure (20.1 vs. 18.3 mmHg; P less than 0.025) if CT were induced during naloxone treatment than in its absence. Thus naloxone during DCT promptly reversed hypotension with no change in CO and, if present during induction of CT, naloxone allowed slightly higher levels of intrapericardial pressure to be tolerated. Further studies are needed to determine whether naloxone produced these effects solely by its actions on opioid receptors. This study suggests that the interaction between opioid and adrenergic influences plays a role in causing hypotension during CT.

Animals↗

PubMed1992

Occult cardiac tamponade detected by transesophageal echocardiography.

Transesophageal echocardiography is a safe, minimally invasive procedure that should be considered when the diagnosis of cardiac tamponade is a possibility and when conventional methods fail to provide conclusive diagnostic information. In this report, we describe a 74-year-old man in the intensive-care unit whose condition was unstable postoperatively because of an occult loculated pericardial effusion and cardiac tamponade. Routine noninvasive and invasive monitoring, including hemodynamic monitoring and transthoracic echocardiography, failed to confirm definitively the suspected diagnosis of cardiac tamponade. In addition, because of the hemodynamic instability of the patient, transporting him for definitive tests (such as fast computed tomographic scanning of the mediastinum, which could not be performed at the bedside) for assessment of cardiac tamponade was relatively contraindicated. In our patient, the diagnostic information obtained by transesophageal echocardiography may have been lifesaving.

Aged↗

PubMed1983

Cardiac tamponade in Dressler's syndrome. Case report.

A case of Dressler's syndrome with cardiac tamponade is presented. 19 days after an acute lateral myocardial infarction, the patient, 46 years old, was admitted the second time with a characteristic clinical picture of cardiac tamponade. The patient did not receive at any time during his admission an anticoagulant treatment. The clinical diagnosis was supported by fluoroscopic and echocardiographic findings. A pericardiocentesis performed immediately revealed a hemorrhagic pericardial fluid. After withdrawal of 60 ml, the patient's clinical condition improved dramatically and this improvement continued further under treatment with corticosteroids. At the best of our knowledge this is the second case in the literature of Dressler's syndrome with cardiac tamponade and hemorrhagic fluid in a patient not treated with anticoagulants.

Anticoagulants↗

PubMed1994

Accelerated myocardial relaxation in conscious dogs during acute cardiac tamponade.

Eight chronically instrumented conscious dogs were used to test the hypothesis that left ventricular (LV) relaxation is accelerated during cardiac tamponade. The time constant of LV transmural pressure fall was measured before and during intrapericardial (IP) saline infusion (baseline) with and without beta-adrenergic blockade (propranolol 1 mg/kg iv). Heart rate was controlled by atrial pacing. Increasing IP pressure caused a progressive linear decrease in stroke volume before and during beta-blockade in each animal. The time constant of LV transmural pressure fall also decreased continuously with an increase in IP pressure from 26 +/- 7 ms during baseline to 18 +/- 5 ms during severe cardiac tamponade (P < 0.01) before beta-blockade. However, after beta-blockade, the time constant of LV transmural pressure fall was constant over a wide range of IP pressures despite a continuous decrease in LV end-diastolic volume. The time constant of LV transmural pressure fall was not altered by vena caval occlusions that caused the same decrease in LV preload observed during cardiac tamponade. We concluded that despite decreased pump function, LV relaxation was accelerated progressively during graded cardiac tamponade, and this change was dependent not on changes in loading conditions but on an intact beta-adrenergic influence.

Acute Disease↗

PubMed1993

Left ventricular diastolic collapse in regional left heart cardiac tamponade. An experimental echocardiographic and hemodynamic study.

OBJECTIVES: This study was designed to describe the hemodynamic abnormalities associated with the appearance of left ventricular diastolic collapse in the setting of regional left heart cardiac tamponade. BACKGROUND: Cardiac tamponade after heart surgery is frequently associated with localized pericardial effusion. Although right ventricular diastolic collapse and right atrial collapse are reliable echocardiographic findings in patients with circumferential pericardial effusion and tamponade, they are often not present in postoperative patients with localized pericardial effusion and regional left heart tamponade. Left ventricular diastolic collapse has been described in such patients, but the degree of hemodynamic alteration that exists with this finding is not known. METHODS: Acute regional left heart tamponade was produced 14 times in seven spontaneously breathing anesthetized dogs by infusing fluid into an isolated compartment created in the pericardial space adjacent to the left ventricular free wall. Continuous echocardiographic imaging and hemodynamic monitoring of left ventricular, systemic arterial, right atrial, pulmonary capillary wedge and pericardial pressures were performed. Measurements at baseline were compared with those made at the onset of left ventricular diastolic collapse and at decompensated tamponade. RESULTS: Left ventricular diastolic collapse was noted in all 14 episodes of regional tamponade. It occurred when pressure in the left pericardial compartment exceeded left ventricular diastolic pressure by 3.0 +/- 1.9 mm Hg. At the onset of left ventricular diastolic collapse, cardiac output and mean arterial pressure were significantly reduced from the control value (p < 0.05). Systolic hypotension was noted only twice at this stage, respiratory variation in systolic pressure > 10 mm Hg only once. The appearance of this sign was also associated with elevated left heart filling pressures. CONCLUSIONS: Left ventricular diastolic collapse is a reliable sign of regional left ventricular tamponade and is associated with a reduction in cardiac output. This echocardiographic finding usually occurs before the development of arterial hypotension and pulsus paradoxus. Thus, left ventricular diastolic collapse is potentially more reliable than hypotension or pulsus paradoxus in the diagnosis of regional left ventricular tamponade.

Acute Disease↗

PubMed2002

Delayed cardiac tamponade after coronary artery laceration.

Delayed cardiac tamponade after laceration of a coronary artery is unusual and uncommonly reported in the literature. We describe a patient in whom this potentially fatal complication developed 8 days after a stab wound to his chest. In our review of the English language literature we identified only one other report of delayed tamponade after coronary artery laceration.

Adolescent↗

PubMed1990

Efficacy of high-frequency jet ventilation in cardiac tamponade.

To evaluate the effects of high-frequency jet ventilation (HFJV) (f = 60, 120 breaths/min) and conventional mechanical ventilation (CMV) (f = 10, 20) during equivalent conditions of cardiac tamponade, stroke index (SI), intrapericardial pressure (IPP), airway pressure (P(aw)), and cardiac pressures were measured in anesthetized, paralyzed, chest-closed dogs with the same levels of PaCO2. Cardiac tamponade was produced by infusing normal saline into the intrapericardial space to increase IPP to either 8 mm Hg (group 1, n = 8) or 12 mm Hg (group 2, n = 8). Stroke index in group 1 was 7.3 +/- 0.8 during CMV (f = 10), 8.1 +/- 0.7 during CMV (f = 20), 10.9 +/- 1.4 during HFJV (f = 60), and 10.7 +/- 1.2 (mL.beat-1.m-2) during HFJV (f = 120). Stroke index in group 2 was 4.1 +/- 0.7, 5.1 +/- 0.5, 7.2 +/- 0.5, and 6.7 +/- 0.5 (mL.beat-1.m-2), respectively. In both IPP groups, stroke index values during HFJV were significantly higher than during CMV; however, there were no significant differences in mean left and right atrial transmural pressures between HFJV and CMV. Peak IPP, mean P(aw), and peak P(aw) during HFJV were significantly lower than those during CMV. The results indicate that HFJV with lower mean and peak Paw, and with lower mean and peak IPP, can result in higher cardiac output than CMV in cardiac tamponade. Thus, HFJV may be superior to CMV in the clinical management of cardiac tamponade.

Animals↗

PubMed1998

Detecting gastrointestinal hypoperfusion during cardiac tamponade in pigs: a role for nitric oxide tonometry?

OBJECTIVE: To evaluate different techniques and regional approaches for detecting critical reductions in gastrointestinal (GI) perfusion. DESIGN: Laboratory, animal, controlled study. SETTING: University animal research laboratory. SUBJECTS: Thirteen anesthetized, ventilated, juvenile domestic pigs. INTERVENTIONS: Dextran was infused into the pericardial sac to achieve cardiac tamponade that reduced cardiac output to 25% of baseline value. Hemodynamics were invasively monitored, and blood gases were sampled in the systemic and portal circulations. Tonometers were placed in the corpus of the stomach and in the jejunum, 50 cm aboral to the ligament of Treitz. MEASUREMENTS AND MAIN RESULTS: We measured cardiac output, portal venous blood flow, mesenteric oxygen delivery and consumption, systemic and portal venous blood gases and acid-base balance, stomach and jejunal transepithelial potential difference, stomach and jejunal intramucosal pH, arterial plasma concentrations of asymmetric dimethylarginine, and jejunal, intraluminal nitric oxide. One hour of cardiac tamponade decreased mesenteric oxygen delivery and consumption in a linear fashion and resulted in mesenteric acidosis, as evidenced by decreases in pH, standard bicarbonate, oxygen saturation, and PO2 and increases in PCO2. The potential difference in the jejunum decreased earlier than in the stomach, whereas stomach intramucosal pH decreased before jejunal intramucosal pH. Intraluminal nitric oxide in the jejunum was markedly reduced soon after cardiac tamponade. This reduction was accompanied by an increase in arterial plasma concentrations of the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine. Investigated variables were unchanged in control animals. CONCLUSIONS: Both intramucosal pH and potential difference measurements may be used to detect critical reduction in GI perfusion. Regional and temporal differences may reduce the accuracy of these methods. Jejunal tonometry can yield an early nitric oxide measurement that indicates mesenteric low-flow conditions. Jejunal tonometry also yields quantitative information about this modulator of hemodynamic and mucosal barrier function, information that is relevant to GI failure during shock.

Acid-Base Equilibrium↗

PubMed1999

Bloody pericardial effusion in patients with cardiac tamponade: is the cause cancerous, tuberculous, or iatrogenic in the 1990s?

STUDY OBJECTIVES: The decrease in incidence of tuberculosis, along with the increase in invasive cardiovascular procedures, may have changed the frequency of causes of bloody pericardial effusion associated with cardiac tamponade, although this is not yet recognized by medical textbooks. We analyzed the causes of bloody pericardial effusion in the clinical setting of cardiac tamponade in the 1990s; patients' survival; the effect of laboratory results on discharge diagnosis; and how often bloody pericardial effusion is a presenting manifestation of a new malignancy or tuberculosis. DESIGN: Retrospective, observational, single-center study. SETTING: A community hospital. PATIENTS: The charts of all patients who underwent pericardiocentesis for cardiac tamponade and had bloody pericardial effusion were retrospectively reviewed. RESULTS: Of 150 patients who had pericardiocentesis for relieving cardiac tamponade, 96 patients (64%) had a bloody pericardial effusion. The most common cause of bloody pericardial effusion was iatrogenic disease (31%), namely, secondary to invasive cardiac procedures. The other common causes were malignancy (26%), complications of atherosclerotic heart disease (11%), and idiopathic disease (10%). Tuberculosis was detected as a cause of bloody pericardial effusion in one patient and presumed to be the cause in another patient. Bloody pericardial effusion was found to be a presenting manifestation of a newly diagnosed malignancy in two patients. The patients in the idiopathic and iatrogenic groups were all alive and had no recurrence of pericardial effusion at 24 +/- 27 and 33 +/- 21 months after hospital discharge, respectively, whereas 80% of patients with malignancy-related bloody effusions died within 8 +/- 6 months. CONCLUSIONS: In a patient population that is reasonably representative of that in most community hospitals in the United States, the most common cause of bloody pericardial effusion in patients with signs or symptoms of cardiac tamponade is now iatrogenic disease. Of the noniatrogenic causes, malignancy, complications of acute myocardial infarction, and idiopathic disease predominated. Hemorrhagic tuberculous pericardial effusions are uncommon and may likely reflect a low incidence of cardiac tuberculosis in community hospitals in the United States.

Adult↗

PubMed2000

Risk factors for posttransfusion graft versus host disease, mediastinitis, and late cardiac tamponade in heart surgery. Survey of 119 Japanese institutions.

OBJECTIVE: Correlations and risk factors remain to be unclarified for post-heart-surgery posttransfusion graft-versus-host disease, mediastinitis, and late cardiac tamponade caused by deteriorated host-defense mechanisms due to cardiopulmonary bypass both with and without steroid usage. METHODS: We sent questionnaires to 298 Japanese cardiovascular institutions asking for institution profiles, including infection control, steroid use in cardiopulmonary bypass, and prevalence of mediastinitis, late cardiac tamponade, and posttransfusion graft-versus-host disease during 1994. The overall prevalence of posttransfusion graft-versus-host disease since the start of service (from establishment of institution to date) was also requested. RESULTS: The number of pump cases at the 119 institutions responding (40%) were 91.6 +/- 67.9 cases/institution (total = 10,904). The prevalence of mediastinitis was 1.2 +/- 1.8 and that of late cardiac tamponade 1.0 +/- 1.8%. Posttransfusion graft-versus-host disease occurred in 1 of 10,904 patients (0.01%) during 1994 at an institution where steroids and nonirradiated blood were used in surgery. The simple institutional mean prevalence of posttransfusion graft-versus-host disease since establishing institutions was 0.08 +/- 0.13%. Of the 119 institutions surveyed, 86 used steroids in all pump cases (72%); 11 institutions used steroids in a limited number of cases (9%). The institutional mean of methylprednisolone-converted steroid dose was 21.5 +/- 16.4 mg/kg (n = 119). In multivariate regression analysis, operation time (p = 0.005) for mediastinitis, steroid usage (all, limited, or no cases) (p = 0.01) and % aneurysm (p = 0.05) for late cardiac tamponade, and steroid dosage (p = 0.002) for posttransfusion graft-versus-host disease were identified as significant risk factors. CONCLUSION: Our results suggest that massive steroid administration for cardiopulmonary bypass may increase the risk of posttransfusion graft-versus-host disease and late cardiac tamponade, but not mediastinitis.

Aged↗

PubMed2003

Intrapericardial chemotherapy for the management of neoplastic cardiac tamponade.

A young patient with disseminated osteogenic sarcoma presented with cardiac tamponade. She was successfully managed with pericardiocentesis and intrapericardial instillation of cisplatin. There was no reaccumulation of pericardial fluid or recurrence of tamponade until the patient's death 12 months later. Intrapericardial chemotherapy may be effective in the management of cardiac tamponade secondary to malignancy.

Adolescent↗