Cardiac Tamponade
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Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. The condition is a medical emergency, the complications of which include pulmonary edema, shock, and death.
Symptoms vary with the acuteness and underlying cause of the tamponade. Patients with acute tamponade may present with dyspnea, tachycardia, and tachypnea. Cold and clammy extremities from hypoperfusion are also observed in some patients. Other symptoms and signs may include the following:
Elevated jugular venous pressure
Pulsus paradoxus
Chest pressure
Decreased urine output
Confusion
Dysphoria
See Clinical Presentation for more detail.
Prompt diagnosis is key to reducing the mortality risk for patients with cardiac tamponade. Although echocardiography provides useful information, cardiac tamponade is a clinical diagnosis. Echocardiography can be used to visualize ventricular and atrial compression abnormalities as blood cycles through the heart. The following may be observed with 2-dimensional (2-D) echocardiography:
An echo-free space posterior and anterior to the left ventricle and behind the left atrium
Early diastolic collapse of the right ventricular free wall
Late diastolic compression/collapse of the right atrium
Swinging of the heart in the pericardial sac
Left ventricular pseudohypertrophy
Inferior vena cava plethora with minimal or no collapse with inspiration
A greater than 40% relative inspiratory augmentation of blood flow across the tricuspid valve
A greater than 25% relative decrease in inspiratory flow across the mitral valve
See Workup for more detail.
Removal of pericardial fluid is the definitive therapy for tamponade and can be done using the following three methods:
Emergency subxiphoid percutaneous drainage
Pericardiocentesis (with or without echocardiographic guidance)
Percutaneous balloon pericardiotomy
The role of medication therapy in cardiac tamponade is limited.
See Treatment and Medication for more detail.
Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. The condition is a medical emergency, the complications of which include pulmonary edema, shock, and death. (See Pathophysiology, Etiology, and Prognosis.)
The overall mortality risk depends on the speed of diagnosis, the treatment provided, and the underlying cause of the tamponade. Untreated, the condition is rapidly and universally fatal (see the image below). (See Presentation, Workup, Treatment, and Medication.)
The pericardium, which is the membrane surrounding the heart, is composed of 2 layers. The thicker parietal pericardium is the outer fibrous layer; the thinner visceral pericardium is the inner serous layer. The pericardial space normally contains 20-50mL of fluid.
Reddy et al describe 3 phases of hemodynamic changes in tamponade, as follows [1] :
Phase I – The accumulation of pericardial fluid impairs relaxation and filling of the ventricles, requiring a higher filling pressure; during this phase, the left and right ventricular filling pressures are higher than the intrapericardial pressure
Phase II – With further fluid accumulation, the pericardial pressure increases above the ventricular filling pressure, resulting in reduced cardiac output (see the Cardiac Output calculator)
Phase III – A further decrease in cardiac output occurs, which is due to the equilibration of pericardial and left ventricular (LV) filling pressures
Pericardial effusions, which cause cardiac tamponade, can be serous, serosanguineous, hemorrhagic, or chylous.
The underlying process for the development of tamponade is a marked reduction in diastolic filling, which results when transmural distending pressures become insufficient to overcome increased intrapericardial pressures. Tachycardia is the initial cardiac response to these changes to maintain the cardiac output.
Systemic venous return is also altered during tamponade. Because the heart is compressed throughout the cardiac cycle due to the increased intrapericardial pressure, systemic venous return is impaired and right atrial and right ventricular collapse occurs. Because the pulmonary vascular bed is a vast and compliant circuit, blood preferentially accumulates in the venous circulation, at the expense of LV filling. This results in reduced cardiac output and venous return.
The amount of pericardial fluid needed to impair diastolic filling of the heart depends on the rate of fluid accumulation and the compliance of the pericardium. Rapid accumulation of as little as 150mL of fluid can result in a marked increase in pericardial pressure and can severely impede cardiac output, [2] whereas 1000 mL of fluid may accumulate over a longer period without any significant effect on diastolic filling of the heart. This is due to adaptive stretching of the pericardium over time. A compliant pericardium can allow considerable fluid accumulation over a long time period without hemodynamic compromise.
For all patients, malignant diseases are the most common cause of pericardial tamponade. Among etiologies for tamponade, Merce et al reported the following incidence rates:
Malignant diseases – 30-60% of cases
Uremia – 10-15% of cases
Idiopathic pericarditis – 5-15%
Infectious diseases – 5-10%
Anticoagulation – 5-10%
Connective tissue diseases – 2-6%
Dressler or postpericardiotomy syndrome – 1-2%
Tamponade can occur as a result of any process that causes pericarditis. Pericarditis can result from the following [3] :
Human immunodeficiency virus (HIV) infection
Infection – Viral, bacterial (tuberculosis), fungal
Drugs – Hydralazine, procainamide, isoniazid, minoxidil
Postcoronary intervention – Ie, coronary dissection and perforation
Acupuncture [4]
Postcardiac percutaneous procedures – Including mitral valvuloplasty, atrial septal defect (ASD) closure, left atrial appendage occlusion
Trauma to the chest
Cardiovascular surgery – Postoperative pericarditis [5]
Postmyocardial infarction – Free wall ventricular rupture, Dressler syndrome
Connective tissue diseases – Systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis
Radiation therapy to the chest, radiofrequency ablation [6]
Iatrogenic [7] – After sternal biopsy, transvenous pacemaker lead implantation, pericardiocentesis, or central line insertion
Uremia
Anticoagulation treatment
Idiopathic pericarditis
Complication of surgery at the esophagogastric junction – Eg, antireflux surgery
Pneumopericardium – Due to mechanical ventilation or gastropericardial fistula
Hypothyroidism
Still disease
Duchenne muscular dystrophy
Type A aortic dissection
Streptococcus constellatus infection (very rare; only 3 cases in the literature) [8]
In patients undergoing heart valve surgery, cardiac tamponade has been associated with any amount of pericardial effusion at the first postoperative transthoracic echocardiography as well as with mechanical valve replacement of the aortic or mitral valve. [9]
The incidence of cardiac tamponade is 2 cases per 10,000 population in the United States. Approximately 2% of penetrating injuries are reported to result in cardiac tamponade.
In children, cardiac tamponade is more common in boys than in girls, with a male-to-female ratio of 7:3. In adults, cardiac tamponade appears to be slightly more common in men than in women. A male-to-female ratio of 1.25:1 was observed at the author’s referral center, based on the International Classification of Diseases (ICD) code 423.9. However, a male-to-female ratio of 1.7:1 was observed at another level 1 trauma center.
Cardiac tamponade related to trauma or HIV is more common in young adults, whereas tamponade due to malignancy and/or renal failure occurs more frequently in elderly individuals.
Cardiac tamponade is a medical emergency. The prognosis depends on prompt recognition and management of the condition and the underlying cause of the tamponade. Untreated, cardiac tamponade is rapidly and universally fatal.
Haneya et al retrospectively (2005-2011) evaluated the impact of timing and indication of reexploration for bleeding or tamponade following cardiac surgery in 209 patients and found that reexploration was associated with higher rates of mortality and morbidity. [10] Multivariate analysis indicated it was the adverse effects of reexploration (eg, blood loss, transfusion requirements) rather than the procedure itself that were independent risk factors for death. Adverse outcomes were more likely in those whose reexploration was delayed and who suffered from cardiac tamponade. [10]
In a separate study, Le et al indicated that following cardiac surgery, there is no advantage for the use of multiple mediastinal chest tubes over a single chest tube in preventing return to the operating room for bleeding or tamponade. [11]
In addition to treatment for the tamponade, all patients should also receive treatment for the condition’s underlying cause in order to prevent recurrence.
In a study of patients with cardiac tamponade, Cornily et al reported a 1-year mortality rate of 76.5% in patients whose tamponade was caused by malignant disease, compared with 13.3% in patients with no malignant disease. The investigators also noted a median survival of 150 days in patients with malignant disease. [12]
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Chakri Yarlagadda, MD, FACC, FSCAI, FASNC, CCDS Director of Cardiac Rehabilitation, St Elizabeth Youngstown Hospital; Radiation Safety Officer, Mercy Health Cardiology
Chakri Yarlagadda, MD, FACC, FSCAI, FASNC, CCDS is a member of the following medical societies: American College of Cardiology, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions
Disclosure: Nothing to disclose.
Terrence X O’Brien, MD, MS, FACC Professor of Medicine/Cardiology, Director, Clinical Cardiovascular Research, Medical University of South Carolina College of Medicine; Director, Echocardiography Laboratory, Veterans Affairs Medical Center of Charleston
Terrence X O’Brien, MD, MS, FACC is a member of the following medical societies: American College of Cardiology, American Heart Association, American Society of Echocardiography, Heart Failure Society of America, South Carolina Medical Association
Disclosure: Nothing to disclose.
Russell F Kelly, MD Assistant Professor, Department of Internal Medicine, Rush Medical College; Chairman of Adult Cardiology and Director of the Fellowship Program, Cook County Hospital
Russell F Kelly is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.
Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC, FCCP is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx Clinical Trials + honoraria; Bayer Grant/research funds Consulting
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
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