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Anatomy of the Heart and Pericardium
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The pericardium is an inverted cone-shaped sack surrounding the heart and lying on top of the diaphragm (Figure 36-1). The inner portion, or visceral pericardium, is a single layer of mesothelial cells covering the epicardium. The outer layer is composed of a dense outer fibrous tissue with an inner layer of mesothelial cells known as the parietal pericardium. The fibrous pericardium is attached to the central tendinous portion of the diaphragm inferiorly. Superiorly, the outer fibrous layer blends with the sheath covering the great vessels. Anteriorly, it attaches to the posterior surface of the sternum. Posteriorly, it is attached to the thoracic vertebral column, esophagus, bronchi, and aorta.
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The heart is contained within the pericardial sac (Figure 36-1B). Numerous portions of the heart are exposed behind the anterior chest wall (Figure 36-2). This includes the right ventricle, left ventricle, right atrium, left atrium, aorta, pulmonary artery, and inferior vena cava (IVC). These structures are vulnerable to injury behind the anterior chest wall9,10 (Table 36-1). The surface area that each of these structures contributes to the anterior cardiac silhouette is also listed in this table. These numbers reflect, roughly, the anatomic incidence of injury with cardiac trauma.11 Traumatic injury to any of these structures can result in a pericardial effusion and cardiac tamponade.
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The pericardial cavity is a potential space between the visceral and parietal layers of the pericardium. Up to 50 mL of fluid is normally contained within this space. The fluid acts as a lubricant to the motion of the heart. Accumulation of fluid in the pericardial space requiring drainage can have a variety of etiologies. From a review of several retrospective series, the estimated causes and relative frequencies of pericardial effusions are listed in Table 36-2.12–18
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Cardiac tamponade is a life-threatening condition that must be diagnosed and treated emergently. The diagnosis of cardiac tamponade is primarily clinical. It may easily be overlooked unless a high index of suspicion is maintained in both medical and trauma patients. Sauer and Murdock describe a “danger zone” for penetrating torso trauma19 (Figure 36-3). The superior border is bounded by a line through the sternal notch. The lateral borders are bound by a line through the midclavicle. The inferior border is identified by a line through the epigastric area. Any penetrating injury in the danger zone or through it has the potential to cause a cardiac injury and pericardial tamponade.
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Pathophysiology of Cardiac Tamponade
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The clinical effects of cardiac tamponade occur due to accumulation of fluid under pressure in the pericardial space. This space can become quite large over time. In some chronic disease states, pericardial effusions of 1 to 2 L can occur without signs of cardiac tamponade.14,20 The ability of the pericardial sac to acutely stretch is limited. Estimates of the volume of fluid required to acutely accumulate and produce a cardiac tamponade range from 60 to 200 mL.
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Cardiac tamponade should always be considered as a cause of shock in the medical patient. This includes patients who are taking oral or parenteral anticoagulants, have known cancer, have known pericardial disease, are suspected of having an aortic dissection, or have had a recent myocardial infarction. Cardiac tamponade can also be due to iatrogenic causes, including central venous line placement, transthoracic cardiac pacing, transvenous cardiac pacing, and cardiopulmonary resuscitation.
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The pressure–volume relationship between the size of the pericardial effusion and the pressure imposed on the cardiac chambers is exponential. The initial accumulation of fluid produces little or no clinical effect. The initial physiologic strategies of compensation include an increase in the systemic venous pressure, catecholamine release, and tachycardia. At some point, the ability of the pericardial space to distend and accommodate more fluid is overwhelmed. From this point on, even small amounts of fluid generate significant and increasing pressure on the heart chambers. As the pericardial pressure rises, venous filling of the right heart is drastically impaired. The interventricular septum bulges into the left ventricle. Left ventricular filling becomes compromised from the lack of flow from the right ventricle and the bulging inward of the interventricular septum. Eventually, cardiac perfusion decreases, the heart suffers injury, and the patient goes into a state of shock.
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A progressive decline in cardiac output occurs as pericardial fluid accumulates and intrapericardial pressure increases.21 Initially, the right atrial pressure is greater than the intrapericardial pressure as the body compensates by increasing venous return. This is followed by the equilibration of the right atrial and intrapericardial pressures. Eventually, as the heart chambers cannot achieve a pressure lower than the surrounding pericardial fluid pressure, equilibration of diastolic pressure in each heart chamber occurs and produces the greatest drop in cardiac output. As the intrapericardial pressure continues to increase, the cardiac chambers collapse, resulting in intractable hypotension and death. The disproportionate effects of the later accumulation of small amounts of fluid explain why withdrawal of even a small amount of fluid from the pericardial cavity can produce dramatic temporary improvements in the clinical status of the patient. It also explains why “monitoring” patients for the evolution of cardiac tamponade with central venous pressure lines is dangerous, as the patient will proceed from stable and compensated to profoundly unstable quite suddenly.
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Several clinical findings are associated with cardiac tamponade. Beck's triad of muffled heart sounds, hypotension, and jugular venous distention is associated with cardiac tamponade. Almost all patients with cardiac tamponade will have at least one of these signs. Unfortunately, very few patients with cardiac tamponade will have all three signs. Beck's triad has been found in only up to 40% of patients with cardiac tamponade.22 These findings may be absent if the patient is hypovolemic due to hemorrhage. Restlessness, fatigue, tachycardia, and tachypnea are often present. These can progress to shock, coma, and eventually death.
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Changes in the jugulovenous waveforms may be seen in cardiac tamponade. Instead of the normal systolic X descent and diastolic Y descent, only the systolic X descent occurs in cardiac tamponade. This is a result of the increased diastolic pressure being exerted by the accumulating pericardial fluid. The only time the right heart can fill is during systole, when the internal volume of the heart is reduced. The changes in the jugulovenous waveforms cannot be evaluated in the supine and/or immobilized trauma patient.
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Kussmaul's two signs, paradoxical increase of the jugulovenous pressure during inspiration and pulsus paradoxus, may be seen in patients with cardiac tamponade. Pulsus paradoxus is a drop in systolic blood pressure of ≥10 mmHg during inspiration. To measure this, inflate the blood pressure cuff until the cuff pressure is greater than the patent's systolic pressure. Slowly release the cuff pressure until beats are heard only during expiration. Keep deflating the cuff pressure until beats are heard continuously in both inspiration and expiration. The difference between these two physiologic points is the amount of pulsus paradoxus. This normal physiologic finding is exaggerated by the accumulation of pericardial fluid, forcing the right heart and interventricular septum into the left ventricle.
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Electrocardiographic and radiographic signs of cardiac tamponade are often not present. Changes on the electrocardiogram (ECG) may be present in patients with cardiac tamponade. A pericardial effusion surrounding the heart, if large enough, can result in a “low voltage” ECG tracing. Electrical alternans is a change in the morphology or amplitude of the QRS complexes on the ECG as the heart swings to and fro within the pericardial fluid (Figure 36-4). It may be associated with pericardial tamponade but is not pathognomonic. Pulseless electrical activity (PEA) in the absence of hypovolemia or a tension pneumothorax is highly suggestive of cardiac tamponade. Opinions differ as to the clinical significance of these findings. The finding of an enlarged cardiac silhouette on a chest radiograph may be useful in chronic pericardial effusions but is usually absent or nonspecific in the acute setting.
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Traumatic cardiac tamponade can be caused by a variety of agents and etiologies. This includes bullets, knives, ice picks, displaced fractured ribs, central venous line placement, pacemaker insertion, pericardiocentesis, intracardiac injection, surgery, migrating pins or needles, nails ejected from machinery, and venous bullet embolization. Cardiac tamponade is the most common presentation of penetrating cardiac injuries overall. It occurs in 80% to 90% of stab wounds and 20% of gunshot wounds.11
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Cardiac ultrasound has become the diagnostic procedure of choice to identify cardiac tamponade (Table 36-3). A prospective study showed that bedside ultrasound performed by Emergency Physicians and Trauma Surgeons was 96% accurate and 90% sensitive.23 Cardiac ultrasonography performed on trauma patients can be 98% to 100% accurate and sensitive in diagnosing pericardial fluid and cardiac tamponade.22,24–27 The series of 261 patients had no false negatives. Other studies have demonstrated false-negative rates in the range of 5% to 40%.19,28,29
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Bedside ultrasound can rapidly confirm a suspected pericardial effusion or cardiac tamponade and guide drainage. Blind pericardiocentesis has a complication rate as high as 50%, and an associated mortality.15,16,30 Ultrasound-guided pericardiocentesis can decrease the rate of complications by allowing visualization and avoidance of adjacent anatomic structures. This increased safety factor is supported by multiple studies from the cardiology literature.31–33
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Other ultrasonographic findings in pericardial tamponade include a swinging heart, collapse of the right and left ventricular chambers, and marked inspiratory changes in ventricular dimensions.10 Some authors advocate using transesophageal echocardiography, even in unstable patients, because of its superior imaging when compared to transthoracic echocardiography.34 Other methods of imaging the pericardium include computed tomography (CT), helical CT, and magnetic resonance imaging. These modalities should be used only for stable patients in whom the diagnosis of a pericardial effusion and not cardiac tamponade is being considered.