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INTRODUCTION

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Cardiac tamponade is a clinical syndrome in which fluid accumulates within the pericardial sac, leading to increased pericardial pressures that compress the chambers of the heart and restrict cardiac filling. Cardiac tamponade can be caused by myocardial infarction, myocarditis, cardiac surgery, Dressler’s syndrome, dissecting aortic aneurysms, and iatrogenic trauma that may occur during percutaneous coronary intervention, electrophysiology studies, and cardiopulmonary resuscitation. Blunt and penetrating trauma may rapidly lead to hemopericardium and subsequently acute tamponade. Pericardial effusions, which can lead to tamponade physiology, also have a variety of etiologies: infection, malignancy, autoimmune, uremia, and collagen vascular disease, among others.

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There are several subtypes of cardiac tamponade:

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  • Acute cardiac tamponade, often resulting from trauma or medical procedures, can rapidly progress to cardiogenic shock in minutes to hours.

  • Subacute cardiac tamponade is usually caused by chronic pericardial effusions, such as those seen in patients with malignancy or renal failure, though most effusions are deemed idiopathic. They develop over days to weeks, allowing for gradual expansion of the pericardial sac. Patients may initially be asymptomatic. However, once the pericardial pressure reaches a critical threshold, patients experience dyspnea, chest fullness, peripheral edema, and fatigue.

  • Regional cardiac tamponade occurs when there is compression of a portion of the heart, often caused by a localized hematoma or loculated effusion after pericardiotomy or myocardial infarction. Because only certain regions of the heart are compressed, the typical signs of cardiac tamponade may be absent.

  • Low-pressure cardiac tamponade is uncommon. It occurs in severely hypovolemic patients due to hemorrhage, hemodialysis, or overdiuresis and is characterized by low filling pressures (intracardiac and pericardial diastolic pressures of approximately 6–12 mmHg). Clinical findings commonly associated with cardiac tamponade, such as elevated heart rate, jugular venous distention, and pulsus paradoxus, are rarely seen. Although some patients are critically ill, most present in a stable condition.

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PATHOPHYSIOLOGY

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In cardiac tamponade, the rapid accumulation of fluid in the pericardial sac transmits intrathoracic pressure to the cardiac muscle that decreases cardiac filling. Tamponade is a spectrum of hemodynamic abnormalities of varying severity. It is not all-or-nothing obstructive shock. Pathophysiologic changes include the following:

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  • Increased intrapericardial pressure → compression of all heart chambers

  • Decreased ventricular compliance → decreased left ventricular filling

  • Decreased systemic venous return → decreased right ventricular filling

  • Decreased stroke volume → low cardiac output

  • Equalization of all cardiac filling pressures with the intrapericardial pressure

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Compensatory efforts of the sympathetic nervous system and circulatory systems to maintain cardiac output include tachycardia and peripheral vasoconstriction (increased systemic vascular resistance).

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Ventricular interdependence refers to the interaction between the right and left ventricles that occurs throughout the cardiac cycle. When a healthy individual inspires, thoracic pressure decreases, causing two major effects on blood flow to the heart. First, there is increased venous return to the right heart. Second, as a result of decreased pulmonary vascular pressure, there is a ...

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