What are the perioperative management options for traumatic hemopericardium?

What are the perioperative management options for traumatic hemopericardium?

Traumatic hemopericardium can develop after both blunt and penetrating chest injuries. Unlike chronic effu-sions, in which as much as 600 mL of pericardial fluid may not cause hemodynamic depression, even small accumula-tions of blood following acute injury result in cardiac tam-ponade with significant hypotension and even cardiac arrest. Inflow occlusion of the atrioventricular valves, resulting from external compression by pericardial blood, leads to decreased ventricular filling, especially in the right heart. As a relatively small amount of acute fluid accumu-lation can cause major hemodynamic changes, evacuation of even a small amount of blood from the pericardium usually restores the blood pressure. Thus, hypotensive patients who may have cardiac tamponade may benefit from pericardiocentesis. Transthoracic echocardiography (TTE) or, in intubated patients without suspected esophageal injury, TEE can aid in diagnosing as well as evacuating the pericardial blood. Diastolic collapse, defined as approxima-tion of the left ventricular walls during diastole, is a sign of tamponade and is associated with a reduction in systemic blood pressure of 15–20% or more. During evacuation, simultaneous imaging of the needle and the pericardial sac prevents cardiac perforation. The clinical signs that are char-acteristic of chronic cases are virtually useless in acute trau-matic tamponade. Beck’s triad (cervical venous distention, hypotension, and muffled heart sounds) is seen in less than 50% of cases of traumatic tamponade. Agitation, combat-iveness, and cool vasoconstricted extremities are seen in patients with cardiac tamponade, but they are also present in patients with hypovolemic shock. Paradoxical inspiratory distention of the neck veins (Kussmaul’s sign) is characteris-tic of cardiac tamponade, but it may be extremely difficult to demonstrate in the acutely traumatized patient.

Paradoxical pulse, although not specific for cardiac tamponade, is probably the most reliable clinical sign in these circumstances. It refers to a greater than 10 mmHg decline in the systolic arterial pressure during inspiration with the patient breathing spontaneously, and is simply an exaggeration of the normal 3–6 mmHg respirophasic variation. This sign lacks specificity, since it can also occur in patients with uncomplicated hypovolemia. Furthermore, its absence does not exclude cardiac tamponade. A concur-rent septal defect, severe left ventricular failure, or aortic regurgitation may preclude a paradoxical pulse.

Two synergistic mechanisms during inspiratory reduc-tion of intrathoracic pressure are responsible for the devel-opment of paradoxical pulse: (1) increase in transmural aortic pressure and thus in left ventricular afterload and underfilling of the left ventricle because of leftward displacement of the interventricular septum. The increased venous pressure during inspiration in normovolemic patients makes the paradoxical pulse more obvious because it increases right ventricular filling and thus enhances the leftward septal shift. In hypovolemic trauma patients, however, right ventricular filling and thus the septal shift are limited, rendering pulsus paradoxus less perceptible. Equalization of elevated intrapericardial and right ventric-ular filling pressures is an inevitable phenomenon in com-pensated cardiac tamponade. With further accumulation of blood, these pressures rise toward the left ventricular dias-tolic pressure. With diastolic underfilling, cardiac output becomes rate dependent. A decrease in heart rate may result in catastrophic hypotension and cardiac arrest. Severe cardiac tamponade can also produce a reduction in coro-nary blood flow but myocardial ischemia and decreased contractility are unlikely, probably because of a propor-tional decrease in myocardial work resulting from decreased systemic blood pressure and stroke volume.

Associated injuries often overshadow the clinical manifes-tations of cardiac tamponade even when the classical signs of this entity are evident. Thus it is important to be familiar with the ancillary diagnostic findings of this readily treat-able emergency. Radiographic findings are not helpful. Cardiomegaly is unlikely to be present in traumatic cardiac tamponade and is nonspecific. Electrocardiographic (ECG) findings are also not specific, although elevation of the ST segment and diminished QRS voltage may be observed if significant pericardial blood accumulates. Electrical alter-nans (the phasic alteration of R wave amplitude) may be more specific but can also occur in patients with tension pneumothorax. Total electrical alternans (phasic alteration of P and R wave amplitudes), although rare, is considered a pathognomonic sign. As mentioned, echocardiography is the most reliable diagnostic tool for this entity. Of the four sites examined during a focused abdominal sonographic study (FAST) the first involves exploration of the pericardium via a subxiphoid window. Transthoracic and transesophageal views can also be used. The ultrasound may demonstrate not only pericardial blood and its volume but also right ventric-ular diastolic collapse. Diastolic collapse may be absent in patients with a hypertrophic right ventricle or in those with high intraventricular pressures from tricuspid regurgitation.

Management priorities depend on pre-existing cardiac conditions, the type and extent of associated injuries, intravascular volume, the quantity of pericardial blood, and patient cooperation. If the severity of associated injuries permits, pericardiocentesis with echocardiographic guidance or surgical drainage and intravascular volume restoration should precede any anesthetic. Unlike pleural blood, pericar-dial blood clots easily. Thus it may be possible to drain only a fraction of the pericardial fluid, but even this amount will produce significant hemodynamic improvement.

Any drug that decreases myocardial contractility or pro-duces peripheral vasodilation may precipitate hemodynamic depression. The classical anesthetic induction agent is ketamine, but even with this drug the blood pressure may deteriorate. Positive-pressure ventilation should be carefully maintained with low airway pressures and without positive end-expiratory pressure (PEEP). In most instances of major trauma with pericardial tamponade, invasive monitoring other than an arterial line may be difficult to place. But, if present, a pulmonary artery catheter can be helpful; equalization of cardiac chamber pressures, the cardiac output, and any response to therapeutic intervention can be observed. Bradycardia during direct laryngoscopy or surgical manipulation should be avoided at all cost.