Cardiac Tamponade

Overview

Practice Essentials 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. Signs and symptoms 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

Diagnosis 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

Management 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.

Background 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. 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).

This anteroposterior-view chest radiograph shows a massive, bottle-shaped heart and conspicuous absence of pulmonary vascular congestion. Reproduced with permission from Chest, 1996: 109:825.

Pathophysiology 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.

Etiology 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]

Epidemiology 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. Sex- and age-related demographics 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.

Prognosis 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]

Clinical Presentation

History Symptoms vary with the acuteness and underlying cause of the tamponade. Patients with acute tamponade may present with dyspnea, tachycardia, tachypnea, decreased urine output, and/or confusion. Cold and clammy extremities from hypoperfusion are also observed in some patients. A comprehensive review of the patient's history usually helps in identifying the probable etiology of a pericardial effusion. The following may be noted:

• Patients with systemic or malignant disease present with weight loss, fatigue, or anorexia

• Chest pain may be the presenting symptom in patients with pericarditis or myocardial infarction

• Musculoskeletal pain or fever may be present in patients with an underlying connective tissue disorder

• A history of renal failure can lead to a consideration of uremia as the cause of pericardial effusion

• Careful review of a patient's medications may indicate that drug-related lupus caused the pericardial effusion

• Recent cardiovascular surgery, coronary intervention, or trauma can lead to the rapid accumulation of pericardial fluid and tamponade [5]

• Recent pacemaker lead implantation or central venous catheter insertion can lead to the rapid accumulation of pericardial fluid and tamponade [13]

• Consider HIV-related pericardial effusion and tamponade if the patient has a history of intravenous (IV) drug abuse or opportunistic infections

• Inquire about chest wall radiation - Ie, for lung, mediastinal, or esophageal cancer

• Inquire about symptoms of night sweats, fever, and weight loss, which may be indicative of tuberculosis

Physical Examination In a retrospective study of patients with cardiac tamponade, the most common symptoms and signs noted by Roy et al were dyspnea, tachycardia, and elevated jugular venous pressure. [14] Evidence of chest wall injury may be present in trauma patients. Tachycardia, tachypnea, and hepatomegaly are observed in more than 50% of patients with cardiac tamponade, and diminished heart sounds and a pericardial friction rub are present in approximately one third of patients. Some patients may present with dizziness, drowsiness, or palpitations. Cold, clammy skin and a weak pulse due to hypotension are also observed in patients with tamponade. Beck triad Described in 1935, this complex of physical findings, also called the acute compression triad, refers to increased jugular venous pressure, hypotension, and diminished heart sounds. These findings result from a rapid accumulation of pericardial fluid. This classic triad is usually observed in patients with acute cardiac tamponade. Pulsus paradoxus Pulsus paradoxus (or paradoxical pulse) is an exaggeration (>12 mm Hg or 9%) of the normal inspiratory decrease in systemic blood pressure. To measure the pulsus paradoxus, patients are often placed in a semirecumbent position; respirations should be normal. The blood pressure cuff is inflated to at least 20 mm Hg above the systolic pressure and slowly deflated until the first Korotkoff sounds are heard only during expiration. At this pressure reading, if the cuff is not further deflated and a pulsus paradoxus is present, the first Korotkoff sound is not audible during inspiration. As the cuff is further deflated, the point at which the first Korotkoff sound is audible during both inspiration and expiration is recorded. If the difference between the first and second measurement is greater than 12 mm Hg, an abnormal pulsus paradoxus is present. The paradox is that while listening to the heart sounds during inspiration, the pulse weakens or may not be palpated with certain heartbeats, while S1 is heard with all heartbeats. A pulsus paradoxus can be observed in patients with other conditions, such as constrictive pericarditis, asthma, severe obstructive pulmonary disease, restrictive cardiomyopathy, pulmonary embolism, rapid and labored breathing, and right ventricular infarction with shock. A pulsus paradoxus may be absent in patients with markedly elevated LV diastolic pressures, atrial septal defect, pulmonary hypertension, aortic regurgitation, low-pressure tamponade, or right heart tamponade. Kussmaul sign This was described by Adolph Kussmaul as a paradoxical increase in jugular venous distention and pressure during inspiration. The Kussmaul sign is usually observed in patients with constrictive pericarditis, but it is occasionally is observed in patients with effusive-constrictive pericarditis and cardiac tamponade. Ewart sign Also known as the Pins sign, this is observed in patients with large pericardial effusions. It is described as an area of dullness, with bronchial breath sounds and bronchophony below the angle of the left scapula. The y descent The y descent is abolished in the jugular venous or right atrial waveform. This is due to an increase in intrapericardial pressure, preventing diastolic filling of the ventricles. Dysphoria Behavioral traits such as restless body movements, unusual facial expressions, restlessness, and a sense of impending death were reported by Ikematsu in about 26% patients with cardiac tamponade. [15] Low-pressure tamponade In severely hypovolemic patients, classical physical findings such as tachycardia, pulsus paradoxus, and jugular venous distention were infrequent. Sagristà-Sauleda et al identified low-pressure tamponade in 20% of patients with cardiac tamponade. [16] They also reported low-pressure tamponade in 10% of large pericardial effusions.

Differential Diagnoses

Diagnostic Considerations

Early diagnosis with a high index of suspicion is necessary to minimize morbidity and mortality from tamponade.

Large pleural effusion

Cases of cardiac tamponade have been reported with large pleural effusions. The increased intrapleural pressure resulting from large pleural effusions can be transmitted to the pericardial space and impair ventricular filling, thus producing the hemodynamic equivalent of cardiac tamponade.

Tension pneumopericardium

The hemodynamic changes in tension pneumopericardium simulate acute cardiac tamponade. Clinically, distant heart sounds, bradycardia, and shifting tympany occur over the precordium, and a characteristic murmur, termed bruit de la roue de moulin, is heard. This is usually observed in infants with mechanical ventilation but is also seen after sternal bone marrow aspiration, penetrating chest wall injury, esophageal rupture, and bronchopericardial fistula.

Rapid and labored breathing

Large decreases in intrathoracic pressure with deep inspirations, often observed during respiratory failure, can accentuate pulsus paradoxus, simulating pericardial tamponade.

Differential Diagnoses

• Cardiogenic Shock

• Constrictive Pericarditis

• Effusive-Constrictive Pericarditis

• Pneumothorax

• Pulmonary Embolism (PE)

Workup

Approach Considerations

As previously stated, prompt diagnosis is key to reducing the mortality risk for patients with cardiac tamponade. Although cardiac tamponade is a clinical diagnosis, further assessment of the patient’s condition and diagnosis of the underlying cause of the tamponade can be obtained through lab studies, imaging studies, electrocardiography, and echocardiography. Echocardiography, for example, can be used to visualize ventricular and atrial compression abnormalities as blood cycles through the heart, while lab studies can demonstrate signs of myocardial infarction, cardiac trauma, and infectious disease. In July 2014, the European Society of Cardiology (ESC) Working Group on Myocardial and Pericardial Diseases released a stepwise scoring system for treating patients with cardiac tamponade. The system is used to identify patients who need immediate pericardiocentesis and patients who can safely be transferred to a specialized institution. [17, 18] According to the guidelines, patients with suspected cardiac tamponade should undergo echocardiography without delay. After diagnosis, patients are scored according to disease etiology, clinical presentation, and imaging findings. A score of 6 or more requires the patient to undergo immediate pericardial drainage. A lower score indicates that drainage can be postponed for up to 12 to 48 hours. [17, 18]

Imaging Studies

Chest radiography findings may show cardiomegaly, a water bottle–shaped heart, pericardial calcifications, or evidence of chest wall trauma. (See the image below.) This anteroposterior-view chest radiograph shows a massive, bottle-shaped heart and conspicuous absence of pulmonary vascular congestion. Reproduced with permission from Chest, 1996: 109:825. A bowed catheter sign on chest radiography in children after central venous catheter insertion may be suggestive of tamponade. [19] CT scanning Gold et al reported compression of the coronary sinus as observed through CT scanning as an earlier marker for cardiac tamponade in 46% of patients. [20] Echocardiography Although echocardiography provides useful information, cardiac tamponade is a clinical diagnosis. 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 - After cardiac surgery, a localized, posterior fluid collection without significant anterior effusion may occur and may readily compromise cardiac output

• Early diastolic collapse of the right ventricular free wall (see the images below)

Early diastolic collapse of right ventricular free wall (subcostal view).

Early diastolic collapse of right ventricular free wall (parasternal short-axis view at aortic valve).

• Late diastolic compression/collapse of the right atrium (see the image below)

Late diastolic collapse of right atrium (subcostal view).

• Swinging of the heart in the pericardial sac

• LV pseudohypertrophy

• Inferior vena cava plethora with minimal or no collapse with inspiration (see the image below)

Dilated inferior vena cava.

• 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

Conditions that may simulate pericardial effusion on 2-D echocardiography include the following:

• A large left pleural effusion

• Any tumor surrounding the heart

• Mitral annular calcification

• A descending thoracic aorta

• A catheter in the right ventricle

• An enlarged left atrium

• An annular subvalvular LV aneurysm

• A bronchogenic cyst

Laboratory Studies The following studies aid in the assessment of patients with cardiac tamponade:

• Creatine kinase and isoenzymes - levels are elevated in patients with myocardial infarction and cardiac trauma

• Renal profile and complete blood count (CBC) with differential - These tests are useful in the diagnosis of uremia and certain infectious diseases associated with pericarditis

• Coagulation panel - The prothrombin time and activated partial thromboplastin time are useful for determining bleeding risk during interventions, such as pericardial drainage and/or the placement of pericardial windows

• Antinuclear antibody assay, erythrocyte sedimentation rate, and rheumatoid factor - Although nonspecific, results from these tests may give clues to a connective tissue disease predisposing to the development of pericardial effusion.

• HIV testing - Approximately 24% of all pericardial effusions are reported to be associated with HIV infection

• Purified protein derivative testing - This is used to diagnose tuberculosis, which is an important and not uncommon cause of pericardial effusion and tamponade.

Electrocardiography With a 12-lead electrocardiogram (see the image below), the following findings suggest, but are not diagnostic for, pericardial tamponade:

• Sinus tachycardia

• Low-voltage QRS complexes

• Electrical alternans - Also observed during supraventricular and ventricular tachycardia

• PR segment depression

A 12-lead electrocardiogram showing sinus tachycardia with electrical alternans. Reproduced with permission from Chest, 1996; 109:825.View Media Gallery

Electrical alternans Alternation of QRS complexes, usually in a 2:1 ratio, on electrocardiographic findings is called electrical alternans. It is caused by movement of the heart in the pericardial space. Electrical alternans is also observed in patients with myocardial ischemia, acute pulmonary embolism, and tachyarrhythmias.

Pulse Oximetry Respiratory variability in pulse-oximetry waveform is noted in patients with pulsus paradoxus. In a small group of patients with tamponade, Stone et al noted increased respiratory variability in pulse-oximetry waveform in all patients. [21] This finding should raise the suspicion for hemodynamic compromise. In patients with atrial fibrillation, pulse-oximetry may aid in detecting the presence of pulsus paradoxus.

Swan-Ganz Catheterization Before or after insertion of the Swan-Ganz catheter, the system must be zeroed after positioning the transducer at the midpoint of the left atrium. Then calibrate the monitoring system. Prior to insertion, test the balloon and flush all of the ports. Then insert the catheter into one of the major veins. At a depth of 20 cm, inflate the balloon and slowly advance the catheter, while continuously monitoring the pressure from the distal lumen. Always deflate the balloon before withdrawing the Swan-Ganz catheter. The waveforms help to indicate the position of the catheter tip if fluoroscopy is not readily accessible. At approximately the 40-50 cm mark, the wedge pressure is usually recorded. Secure the catheter position, and obtain a chest radiograph to confirm the position. In tamponade, near equalization (within 5 mm Hg) of the right atrial, right ventricular diastolic, pulmonary arterial diastolic, and pulmonary capillary wedge pressure (reflecting left atrial pressure) occurs. The right atrial pressure tracings display a prominent systolic x descent and abolished systolic y descent. Boltwood et al described the diastolic equalization of pulmonary capillary and right atrial pressures as predominantly inspiratory; this is known as the inspiratory traction sign. [22] It results from inspiratory traction of the taut pericardium by the diaphragm.

Histologic Findings Occasionally, a pericardial biopsy is performed when the etiology of the pericardial effusion that caused the tamponade is unclear. This is especially useful in cases of tuberculous pericardial effusions, because cultures of the pericardial fluid in these cases rarely yield a positive result for mycobacteria. However, granulomas seen on pericardial biopsy specimens are often seen in patients with tuberculous pericarditis. In general, cytopathologic findings from pericardial fluid and histologic findings from pericardial biopsy specimens depend on the underlying pathology. Cytologic examination identifies the etiopathologic cause of tamponade in about 75% of cases; it is particulalry useful for identifying malignancy-associated effusions. [23]

Treatment & Management

Approach Considerations Cardiac tamponade is a medical emergency that requires urgent drainage of the pericardial fluid. Preferably, patients should be monitored in an intensive care unit. All patients should receive the following:

• Oxygen

• Volume expansion with blood, plasma, dextran, or isotonic sodium chloride solution, as necessary, to maintain adequate intravascular volume - Sagristà-Sauleda et al noted significant increase in cardiac output after volume expansion [24] (see the Cardiac Output calculator)

• Bed rest with leg elevation - This may help increase venous return

Positive-pressure mechanical ventilation should be avoided because it may decrease venous return and aggravate signs and symptoms of tamponade.

Inpatient care After pericardiocentesis, leave the intrapericardial catheter in place after securing it to the skin using sterile procedure and attaching it to a closed drainage system via a 3-way stopcock. Periodically check for reaccumulation of fluid, and drain as needed. The catheter can be left in place for 1-2 days and can be used for pericardiocentesis. Serial fluid cell counts can be useful for helping to discover an impending bacterial catheter infection, which could be catastrophic. If the white blood cell (WBC) count rises significantly, the pericardial catheter must be removed immediately. A Swan-Ganz catheter can be left in place for continuous monitoring of hemodynamics and to assess the effect of reaccumulation of pericardial fluid. A repeat echocardiogram and a repeat chest radiograph should be performed within 24 hours. Consultations Consultations associated with cardiac tamponade can include the following:

• Hemodynamically stable patients - Cardiologist

• Hemodynamically unstable patients - Cardiologist, cardiothoracic surgeon

Activity Initially, the patient should be on bed rest with leg elevation to increase the venous return. Once the signs and symptoms of tamponade resolve, activity can be increased as tolerated. Follow-up A follow-up echocardiogram and chest radiograph should be performed at a monthly follow-up examination to check for recurrent fluid accumulation.

Pericardiocentesis and Pericardiotomy Removal of pericardial fluid, with or without echocardiographic guidance, is the definitive therapy for tamponade and can be done using the following 3 methods. Emergency subxiphoid percutaneous drainage This is a life-saving bedside procedure. The subxiphoid approach is extrapleural; hence, it is the safest for pericardiocentesis performed without echocardiographic guidance. A 16- or 18-gauge needle is inserted at an angle of 30-45° to the skin, near the left xiphocostal angle, aiming towards the left shoulder. When performed emergently, this procedure is associated with a reported mortality rate of approximately 4% and a complication rate of 17%. Echocardiographically-guided pericardiocentesis This is often carried out in the cardiac catheterization laboratory. The procedure is usually performed from the left intercostal space. First, mark the site of entry based on the area of maximal fluid accumulation closest to the transducer. Then, measure the distance from the skin to the pericardial space. The angle of the transducer should be the trajectory of the needle during the procedure. Avoid the inferior rib margin while advancing the needle to prevent neurovascular injury. Leave a 16-gauge catheter in place for continuous drainage. Percutaneous balloon pericardiotomy This can be performed using an approach similar to that for echo-guided pericardiocentesis, with the balloon being used to create a pericardial window for drainage of the pericardial fluid.

Surgical Care in Hemodynamically Unstable Patients For a hemodynamically unstable patient or one with recurrent tamponade, provide care as described below. Surgical creation of a pericardial window This involves the surgical opening of a communication between the pericardial space and the intrapleural space. This is usually a subxiphoid approach, with resection of the xiphoid. However, a left paraxiphoid approach with preservation of the xiphoid has been described. [25] Open thoracotomy and/or pericardiotomy [5] may be required in some cases, and these should be performed by an experienced surgeon. Recurrent cardiac tamponade or pericardial effusion Sclerosing the pericardium This is a therapeutic option for patients with recurrent pericardial effusion or tamponade. Through the intrapericardial catheter, corticosteroids, tetracycline, or antineoplastic drugs (eg, anthracyclines, bleomycin) can be instilled into the pericardial space. Pericardio-peritoneal shunt In some patients with malignant recurrent pericardial effusions, the creation of a pericardio-peritoneal shunt helps to prevent recurrent tamponade. Pericardiectomy Resection of the pericardium (pericardiectomy) through a median sternotomy or left thoracotomy is rarely required to prevent recurrent pericardial effusion and tamponade.

Video-Assisted Thorascopic Procedure In a study of 15 patients with cardiac tamponade, Monaco et al found that a modified, video-assisted thoracoscopic procedure seemed to be a feasible treatment for the condition. [26] Using a right hemithoracic approach, the investigators employed a 15-mm trocar in the fourth right intercostal space of the anterior axillary and a 10-mm trocar in the seventh right intercostal space of the median axillary line. Utilization of a 5-mm optic allowed two instruments, for the optic and for the endoscopic forceps, to be employed simultaneously using one trocar; this left the second trocar available for dissecting scissors. All patients underwent a pericardial resection equal to that achievable via an anterolateral thoracotomy. The pericardial effusion was effectively drained in all patients, with no intraoperative mortality or perioperative morbidity encountered.

Medication

Medication Summary The role of medication therapy in cardiac tamponade is limited.

Cardiovascular, Other Class Summary Beta-1 receptor stimulating agents increase stroke volume and cardiac output.

References

1. Reddy PS, Curtiss EI, Uretsky BF. Spectrum of hemodynamic changes in cardiac tamponade. Am J Cardiol. 1990 Dec 15. 66(20):1487-91. [QxMD MEDLINE Link].

2. Saito Y, Donohue A, Attai S, et al. The syndrome of cardiac tamponade with "small" pericardial effusion. Echocardiography. 2008 Mar. 25(3):321-7. [QxMD MEDLINE Link].

3. Parvez N, Carpenter JL. Cardiac tamponade in Still disease: a review of the literature. South Med J. 2009 Aug. 102(8):832-7. [QxMD MEDLINE Link].

4. Ernst E, Zhang J. Cardiac tamponade caused by acupuncture: a review of the literature. Int J Cardiol. 2011 Jun 16. 149(3):287-9. [QxMD MEDLINE Link].

5. Rylski B, Siepe M, Schoellhorn J, Beyersdorf F. Endoscopic treatment for delayed cardiac tamponade. Eur J Cardiothorac Surg. 2010 Feb. 37(2):490-1. [QxMD MEDLINE Link].

6. Mujovic N, Marinkovic M, Markovic N, et al. Management and outcome of periprocedural cardiac perforation and tamponade with radiofrequency catheter ablation of cardiac arrhythmias: a single medium-volume center experience. Adv Ther. 2016 Oct. 33(10):1782-96. [QxMD MEDLINE Link].

7. Holmes DR Jr, Nishimura R, Fountain R, et al. Iatrogenic pericardial effusion and tamponade in the percutaneous intracardiac intervention era. JACC Cardiovasc Interv. 2009 Aug. 2(8):705-17. [QxMD MEDLINE Link].

8. Hindi Z. Rare purulent cardiac tamponade caused by Streptococcus constellatus in a young immunocompetent patient: case report and review of the literature. Am J Case Rep. 2016 Nov 16. 17:855-9. [QxMD MEDLINE Link].

9. You SC, Shim CY, Hong GR, et al. Incidence, predictors, and clinical outcomes of postoperative cardiac tamponade in patients undergoing heart valve surgery. PLoS One. 2016 Nov 17. 11(11):e0165754. [QxMD MEDLINE Link].

10. Haneya A, Diez C, Kolat P, et al. Re-exploration for bleeding or tamponade after cardiac surgery: impact of timing and indication on outcome. Thorac Cardiovasc Surg. 2015 Feb. 63(1):51-7. [QxMD MEDLINE Link].

11. Le J, Buth KJ, Hirsch GM, Legare JF. Does more than a single chest tube for mediastinal drainage affect outcomes after cardiac surgery?. Can J Surg. 2015 Apr. 58(2):100-6. [QxMD MEDLINE Link].

12. Cornily JC, Pennec PY, Castellant P, et al. Cardiac tamponade in medical patients: a 10-year follow-up survey. Cardiology. 2008. 111(3):197-201. [QxMD MEDLINE Link].

13. Lee YM, Kim HJ, Lee JE, et al. Cardiac tamponade following insertion of an internal jugular vein catheter for hemodialysis. Clin Nephrol. 2009 Sep. 72(3):220-3. [QxMD MEDLINE Link].

14. Roy CL, Minor MA, Brookhart MA, Choudhry NK. Does this patient with a pericardial effusion have cardiac tamponade?. JAMA. 2007 Apr 25. 297(16):1810-8. [QxMD MEDLINE Link].

15. Ikematsu Y. Incidence and characteristics of dysphoria in patients with cardiac tamponade. Heart Lung. 2007 Nov-Dec. 36(6):440-9. [QxMD MEDLINE Link].

16. Sagrista-Sauleda J, Angel J, Sambola A, Alguersuari J, Permanyer-Miralda G, Soler-Soler J. Low-pressure cardiac tamponade: clinical and hemodynamic profile. Circulation. 2006 Aug 29. 114(9):945-52. [QxMD MEDLINE Link].

17. Busko, M. ESC group issues triage strategy to manage cardiac tamponade. Medscape Medical News. July 10, 2014. Available at https://www.medscape.com/viewarticle/828091. Accessed: July 21, 2014.

18. Ristic AD, Imazio M, Adler Y, et al. Triage strategy for urgent management of cardiac tamponade: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J. 2014 Sep 7. 35(34):2279-84. [QxMD MEDLINE Link].

19. Towbin R. The bowed catheter sign: a risk for pericardial tamponade. Pediatr Radiol. 2008 Mar. 38(3):331-5. [QxMD MEDLINE Link].

20. Gold MM, Spindola-Franco H, Jain VR, Spevack DM, Haramati LB. Coronary sinus compression: an early computed tomographic sign of cardiac tamponade. J Comput Assist Tomogr. 2008 Jan-Feb. 32(1):72-7. [QxMD MEDLINE Link].

21. Stone MK, Bauch TD, Rubal BJ. Respiratory changes in the pulse-oximetry waveform associated with pericardial tamponade. Clin Cardiol. 2006 Sep. 29(9):411-4. [QxMD MEDLINE Link].

22. Boltwood C, Rieders D, Gregory KW. Inspiratory tracking sign in pericardial disease. Circulation. 1984. 70(suppl II):103.

23. Petcu DP, Petcu C, Popescu CF, Bataiosu C, Alexandru D. Clinical and cytological correlations in pericardial effusions with cardiac tamponade. Rom J Morphol Embryol. 2009. 50(2):251-6. [QxMD MEDLINE Link].

24. Sagrista-Sauleda J, Angel J, Sambola A, Permanyer-Miralda G. Hemodynamic effects of volume expansion in patients with cardiac tamponade. Circulation. 2008 Mar 25. 117(12):1545-9. [QxMD MEDLINE Link].

25. Motas C, Motas N, Rus O, Horvat T. Left paraxiphoidian approach for drainage of pericardial effusions. Interact Cardiovasc Thorac Surg. 2010 Jan. 10(1):4-5. [QxMD MEDLINE Link].

26. Monaco F, Barone M, David A, et al. [Cardiac tamponade: a modified video-assisted thoracoscopic approach] [Italian]. Chir Ital. 2009 May-Jun. 61(3):321-6. [QxMD MEDLINE Link].

27. Shiota T. Role of echocardiography for catheter-based management of valvular heart disease. J Cardiol. 2017 Jan. 69(1):66-73. [QxMD MEDLINE Link].

28. Khanna S, Maheshwari K. Hemopericardium and acute cardiac tamponade. Anesthesiology. 2018 May. 128(5):1006. [QxMD MEDLINE Link].

29. Lopez PD, Valvani R, Mushiyev S, Visco F, Pekler G. Cardiac tamponade: an unusual presentation of systemic lupus erythematosus. Am J Med. 2018 May. 131(5):e189-e190. [QxMD MEDLINE Link].

30. Appleton C, Gillam L, Koulogiannis K. Cardiac tamponade. Cardiol Clin. 2017 Nov. 35(4):525-37. [QxMD MEDLINE Link].

31. Fernandez Morales A, Iniesta N, Fernandez-Codina A, et al. Cardiac tamponade and severe pericardial effusion in systemic sclerosis: report of nine patients and review of the literature. Int J Rheum Dis. 2017 Oct. 20(10):1582-92. [QxMD MEDLINE Link].

32. Chen X, Miao Q, Yu Y, et al. Blunt trauma-induced pericardial tamponade after video-assisted thoracoscopic surgery. Ann Thorac Surg. 2018 Nov 24. [QxMD MEDLINE Link].

33. Doukky R, Improvola G, Shih MJ, et al. Usefulness of oximetry paradoxus to diagnose cardiac tamponade. Am J Cardiol. 2018 Nov 6. [QxMD MEDLINE Link].