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CASE SCENARIO

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A 22-year-old man is brought to the emergency department (ED) after an altercation in which he was stabbed in the left chest. On arrival he is diaphoretic, his heart rate is 140 and blood pressure is 80/60. Examination reveals only a puncture wound at the sixth intercostal space, just left of the sternum. Lung sounds are present bilaterally but diminished on the left.

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EPIDEMIOLOGY

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Cardiac injury is uncommon and has a high mortality rate, making it an infrequent but highly lethal injury encountered by the trauma surgeon. Most victims of penetrating cardiac injury (94%) die before reaching the hospital; 50% of those who survive to the hospital will die as well.1 In certain circumstances, for example, after low-velocity injuries, tamponade may prevent lethal exsanguination and improve survival. Among patients presenting to a hospital in South Africa with cardiac stab wounds, those with tamponade had a mortality rate of only 8% versus 34% among those who did not.2 In contrast, patients presenting with cardiac injuries from gunshot wounds and blunt trauma have high mortality, without any observed survival benefit when presenting with tamponade.3,4

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PATHOPHYSIOLOGY

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The pericardium functions to isolate the heart from the rest of the mediastinum. It is a fibrous, relatively inelastic structure surrounding the heart and proximal great vessels, and extends from the central tendon of the diaphragm to the great vessels, and from the sternum to the esophagus. The pericardium forms a sac with an outer parietal layer reflecting upon itself to form the epicardial layer of the heart. Within this sac is roughly 30 to 50 mL of serous fluid that serves to lubricate the heart. Bilateral phrenic nerves run along the lateral aspects of the pericardium anterior to the root of the lungs and innervate the diaphragm.

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Tamponade physiology arises secondary to the poor distensibility of the pericardium. As the pericardium fills with fluid, it reaches a point of inextensibility.4 The amount of fluid within the pericardium is less important than the speed of its accumulation. The pericardium can gradually stretch to accommodate a chronic effusion of 1 L or more without symptoms; however, tamponade can result from the acute accumulation of as little as 60 to 100 mL of blood.5

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Tamponade is a dysfunction of diastolic filling. The inelastic pericardium limits the total intrapericardial volume, and as pericardial fluid volume increases, intracardiac chamber volume must decrease.4 Initially, cardiac output is maintained with compensatory tachycardia, higher filling pressures, and enhanced contractility; however, this will decompensate rapidly with increasing effusions or loss of these mechanisms.6 Tamponade is the endpoint of a continuum of worsening cardiac filling, as higher diastolic pressures are required to overcome the pericardial pressure. Hypotension from low cardiac output follows tachycardia, and ultimately cardiac arrest ensues when intrapericardial and intracardiac pressures equilibrate.7

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