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CARDIAC TAMPONADE

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The normal pericardium is a fibroelastic sac containing a thin layer of fluid that surrounds the heart. When larger amounts of fluid accumulate (pericardial effusion) or when the pericardium becomes scarred and inelastic, one of three pericardial compressive syndromes may occur (1):

●Cardiac tamponade

●Constrictive pericarditis

●Effusive-constrictive pericarditis

Cardiac tamponade is the result of compression of the myocardium by the contents of the pericardium. This compression is generally caused by fluid but in rare cases may be caused by gas, pus, blood, or a combination of materials (2). Cardiac tamponade is a continuum reflecting the amount of fluid (or other material), its rate of accumulation, and the condition of the heart. The three stages necessary for cardiac tamponade to develop include fluid filling the recesses of the parietal pericardium, fluid accumulating faster than the rate of the parietal pericardium’s ability to stretch, and fluid accumulating faster than the body’s ability to increase blood volume to support right ventricle filling pressures (2).

The final result of these processes is increased pericardial pressure, which causes decreased cardiac compliance and decreased blood flow into the heart, which leads to decreased cardiac output. The most important factor in the development of tamponade is the rate of fluid accumulation (1, 3). The main pathophysiologic derangement of cardiac tamponade is reduced cardiac output. In the United States, malignant disease is the most common cause of pericardial effusion with tamponade (4).

Other causes of pericardial effusions that may result in tamponade include infection, connective tissue disease, heart failure, valvular heart disease, myocardial infarction, uremia, cardiac surgery, trauma and idiopathic (4,2).

Cardiac tamponade symptoms are usually nonspecific. The patient may complain of chest pain, cough or dyspnea (2).

In cardiac tamponade, the ECG classically shows decreasing voltage or electrical alternans, although the latter is rare. Electrical alternans on the ECG is pathognomonic of cardiac tamponade. It is characterized by alternating levels of ECG voltage of the P waves, QRS complexes and T waves, the result of the heart swinging in a large effusion. The chest radiograph may demonstrate an enlarged cardiac silhouette after as little as 200 mL of fluid accumulation (1). This enlarged cardiac silhouette occurs in patients with slow fluid accumulation, compared to a normal cardiac silhouette seen in patients with rapid fluid accumulation and tamponade. Thus, the chronicity of the effusion may be suggested by the presence or absence of an enlarged cardiac silhouette (2).

PATHOPHYSIOLOGY

Limited elasticity of the pericardium  150–200 mL of fluid  pressure in pericardial space  compression of the heart, especially of the right ventricle due to a thinner wall  interventricular septum shifts towards the left ventricle chamber ventricular diastolic filling  stroke  volume (+ venous congestion) cardiac output (5).

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 (5). The outer layer of the heart is made of fibrous tissue (6) which does not easily stretch, so once fluid begins to enter the pericardial space, pressure starts to increase (7).

If fluid continues to accumulate, each successive diastolic period leads to less blood entering the ventricles. Eventually, increasing pressure on the heart forces the septum to bend in towards the left ventricle, leading to a decrease in stroke volume (7). This causes the development of obstructive shock, which if left untreated may lead to cardiac arrest (often presenting as pulseless electrical activity).

3 PHASES OF HEMODYNAMIC CHANGES IN TAMPONADE, AS FOLLOWS:

· 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 (8).

· 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) (8).

· Phase III - A further decrease in cardiac output occurs, which is due to the equilibration of pericardial and left ventricular (LV) filling pressures (8).

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 (9).

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 (9).

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, 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 (9).

Echocardiography is the diagnostic procedure of choice to identify pericardial effusions and cardiac tamponade (4). In the normal pericardium, there is approximately 30–50 mL of fluid between the visceral and parietal pericardium (5, 1). This amount of fluid is usually not visible on ultrasound. The pericardium should appear echogenic. If an effusion is present, an anechoic (dark) space will be evident between the pericardium and the beating heart. With a large or rapidly developing pericardial effusion, this anechoic space surrounding the heart may be associated with diastolic collapse of the right atrium or right ventricle (4, 5). Right atrial collapse is virtually 100% sensitive for cardiac tamponade but is less specific (4).

Duration of right atrial collapse exceeding one-third of the cardiac cycle increases specificity without sacrificing sensitivity. Left atrial collapse is seen in about 25% of patients and is specific for cardiac tamponade (3, 4). Left ventricular collapse is less common due to the muscularity of the left ventricle’s wall (4).

Initial treatment of cardiac tamponade includes intravenous fluids to augment volume to the right ventricle, which increases the filling pressure in an effort to overcome the pressure of pericardial constriction (2). Pericardiocentesis, preferably ultrasound-guided, is the treatment of choice. Enough fluid should be withdrawn to result in hemodynamic stability. If tamponade recurs, pericardiocentesis may be repeated or a drainage catheter can be left in the pericardial space (1, 2). A pericardiotomy may ultimately be necessary. Cardiac tamponade often has a high mortality rate, depending on the severity and nature of the underlying disease, the time course of onset, and the rapidity of diagnosis and successful intervention (2).

Key Teaching Points:

· Cardiac tamponade results from increased pericardial pressure due to a rapidly accumulating pericardial effusion, which causes decreased cardiac compliance and decreased blood flow into the heart, in turn leading to decreased cardiac output.

· The classic triad of cardiac tamponade (hypotension, distended neck veins, and muffled heart

sounds) is seen in less than 40% of patients with cardiac tamponade.

· In cardiac tamponade, the ECG may show evidence of low voltage or electrical alternans,

whereas the chest radiograph may demonstrate an enlarged cardiac silhouette.

· Echocardiography is the study of choice for diagnosing cardiac tamponade; the treatment of

cardiac tamponade is volume augmentation and pericardiocentesis.

Conflicts of interests    None stated by the authors

Financing  None stated by the authors.

REFERENCES:

1. Spodick DH. Acute cardiac tamponade. N Engl J Med 2003; 349:684.

2. Jouriles NJ. Pericardial and myocardial disease. In: Marx JA, Hockberger RS, Walls RM, et

al. (eds). Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th ed. Mosby,

2006;1285–6.

3. Valley VT, Fly CA. Pericarditis and cardiac tamponade. eMedicine Website. Available at

http://www.emedicine.com/ emerg/topic412.htm. Accessed June 26, 2008.

4. Hold BD. Pericardial disease and pericardial tamponade. Crit Care Med 2007;25:S355–64.

5. Hoit BD. Cardiac tamponade. In: Post TW, ed. UpToDate. Waltham, MA:

UpToDate. https://www.uptodate.com/contents/cardiac-tamponade. Last updated May 4,

2016. Accessed December 27, 2016.

6. Patton KT, Thibodeau GA (2003). Anatomy & physiology (5th ed.). St. Louis: Mosby. 

7. Porth, Carol; Carol Mattson Porth (2005). Pathophysiology: concepts of altered health

states (7th ed.). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 978-0-7817-4988-6.

8. Reddy PS, Curtiss EI, Uretsky BF. Spectrum of hemodynamic changes in cardiac

tamponade. Am J Cardiol. 1990 Dec 15. 66(20):1487-91. 

9. Saito Y, Donohue A, Attai S, et al. The syndrome of cardiac tamponade with "small"

pericardial effusion. Echocardiography. 2008 Mar. 25(3):321-7.

Lizzeth Karina Ordóñez Pérez 1

María Virginia Pinzón Fernández 2

Luisa Fernanda Zúñiga-Cerón 3

Jhan Sebastián Saavedra-Torres 4

Carlos Andrés González Idrobo 5

1- Doctor, Universidad del Cauca, Faculty of Health Sciences, Department of Internal Medicine, Health Research Group (GIS) - Popayán - Colombia.

2- Bacteriologist, Esp. Education, Master's Degree in Public Health, PhD candidate in Medical Anthropology, Full Professor at Universidad del Cauca.

3- Student of medicine – Universidad Nacional de Colombia, Faculty of Medicine, Laboratory of the Field Corporation (DLC), Health Research Group (GIS) - Popayán - Colombia.

4 -Student of medicine - Universidad del Cauca, Faculty of Health Sciences, Department of Internal Medicine, Corporación del Laboratorio al Campo (DLC), Health Research Group (GIS) - Popayán - Colombia.

5- Doctor- Medical Cooperative University of Colombia, Faculty of Medicine, Santa Marta - Colombia.