A 74-year-old man arrives at the emergency ward (EW) at 2:31 AM. Gripping his chest, he complains of an intense tearing pain. Medical history is significant for poorly controlled hypertension, hyperlipidemia, and gout. Surgical history is significant for a right hip replacement and cholecystectomy. Vital signs are blood pressure—left: 188/124 mm Hg, right: 125/110 mm Hg; pulse 124/minute; and respirations 24/minute. Physical exam is remarkable for slight confusion, no jugular venous elevation, bilateral basilar rales, holodiastolic diastolic murmur, unremarkable abdomen, and no pedal edema. Pulses are unequal with the right radial pulse obviously weaker than the left radial pulse. Left pedal pulse is weaker than right pedal pulse. The patient has a 14-gauge intravenous catheter in the left forearm. Electrocardiogram shows ST-segment elevation in the inferior leads with a baseline sinus tachycardia. Chest film demonstrates widening of the mediastinum, and a computed tomography (CT) scan confirms a type A dissection extending to the iliac bifurcation. Now, you get paged to the EW to assist with management! Strap in and hold on because you’re in for a ride! Forget about getting any sleep for the rest of the night because this patient needs to go to the operating room pronto! Establish arterial monitoring in the left radial artery, reduce the systolic blood pressure to 110 mm Hg, order some blood, and get a quick transthoracic or transesophageal echocardiogram to assess for cardiac tamponade and to determine the mechanism of his aortic insufficiency, which the holodiastolic murmur tipped you off to. Get a lot of help because time is of the essence in these cases, and even when you do your job just right, the patient can still have a bad outcome.

Dissections of the ascending aorta, representing 60% to 70% of all aortic dissections, are true life-threatening emergencies. They involve a tear of the intimal wall of the aorta, creating a false channel. Due to the high aortic pressures and shear stress created by pulsatile perfusion, the dissection flap can continue to dissect in its proximal or distal extent (often in a spiral manner) and potentially compromise blood flow to multiple vital organs.

Risk factors for aortic dissection include congenital unicuspid or bicuspid aortic valve, aortic aneurysm, collagen vascular disorders (e.g., Marfan
syndrome), cocaine use, chest trauma, and chronic, uncontrolled hypertension. Aortic dissection usually occurs in patients of ages 30 to 80 years, with the peak occurrence in the sixth and seventh decades of life. It affects men more frequently than women. The Stanford classification of aortic dissection designates type A as involving the ascending aorta, while type B refers to dissections that do not involve the ascending aorta. Furthermore, using the DeBakey classification of aortic dissection, a type I (involves the entire aorta), type II (involves only the ascending aorta), or type III (involves only the descending aorta) designation can better clarify which aortic segments are involved.

The most common presentation (80% of patients) is chest pain described as “ripping,” “tearing,” “sharp,” “stabbing,” or “pressurelike.” There may be pulse deficits in the extremities, suggesting limb ischemia or systemic hypoperfusion. Aortic dissection resulting in cardiac tamponade (i.e., commonly from aortic root rupture into the transverse pericardial sinus) may produce jugular venous elevation and systemic hypotension; complete cardiovascular collapse is also possible. If the dissection causes severe aortic insufficiency, signs of congestive heart failure (e.g., pulmonary edema) may be present.

Diagnosis of ascending aortic dissection is commonly made by CT, magnetic resonance imaging with angiography (sensitivity 94%-100% and specificity of 95%-100% for all dissections), aortic angiography, or transesophageal echocardiography (TEE) (sensitivity 78%-100% for type A). TEE is a particularly useful diagnostic modality to rule out cardiac tamponade, both for a more detailed analysis of the extent of the dissection and for determining the mechanism/severity of aortic insufficiency (if present). Intraoperatively, TEE can help identify both the true and false aortic lumens, which will facilitate the arterial cannulation required for the initiation of cardiopulmonary bypass (CPB). Any attempt to perform a preoperative diagnostic TEE must be made in conjunction with an experienced cardiac anesthesiologist because inadequate sedation and blunting of sympathetic autonomic outflow could result in immediate aortic rupture with unrecoverable hemodynamic collapse.

The mortality rates associated with Stanford type A dissections are approximately 1% to 2% per hour, in the first 48 hours, following initial onset of symptoms. This increases to 60% in the first 6 days and 74% by 2 weeks, and by 6 months, the trend levels off near 91%. The complications associated with type A dissection are listed in Table 145.1. The high degree of morbidity and mortality is usually related to involvement of the coronary ostia, dissection into the aortic root causing severe aortic insufficiency, and proximal dissection causing cardiac tamponade. The dissection can also cause rupture into either atria or the right ventricle.

Acute medical management is directed at control of systemic blood pressure to reduce the shear stress or change in pressure over time (ΔP/Δt) transmitted
to the aortic wall. Although there has not been any pressure range proven to be best, a pressure of 100 to 110 mm Hg systolic is the generally accepted goal. This pressure will likely maintain adequate organ perfusion while minimizing the risk of aortic rupture.