Aortic dissection occurs when a spontaneous intimal tear develops and blood dissects into the media of the aorta. The tear probably results from the repetitive torque applied to the ascending and proximal descending aorta during the cardiac cycle; hypertension is an important component of this disease process.
Type A dissection involves the arch proximal to the left subclavian artery, and type B dissection occurs in the proximal descending thoracic aorta typically just beyond the left subclavian artery. Dissections may occur in the absence of hypertension but abnormalities of smooth muscle, elastic tissue, or collagen are more common in these patients. Pregnancy, bicuspid aortic valve, and coarctation also are associated with increased risk of dissection.
Blood entering the intimal tear may extend the dissection into the abdominal aorta, the lower extremities, the carotid arteries or, less commonly, the subclavian arteries. Both absolute pressure levels and the pulse pressure are important in propagation of dissection. Aortic dissection is a true emergency and requires immediate control of blood pressure to limit the extent of the dissection. With type A dissection, which has the worse prognosis, death may occur within hours due to rupture of the dissection into the pericardial sac or dissection into the coronary arteries, resulting in myocardial infarction. Rupture into the pleural cavity is also possible. The intimal/medial flap of the aortic wall created by the dissection may occlude major aortic branches, resulting in ischemia of the brain, intestines, kidney, or extremities.
Symptoms and Signs
Severe persistent chest pain of sudden onset radiating down the back or possibly into the anterior chest is characteristic. Radiation of the pain into the neck may also occur. The patient is usually hypertensive. Syncope, hemiplegia, or paralysis of the lower extremities may occur. Intestinal ischemia or kidney injury may develop. Peripheral pulses may be diminished or unequal. A diastolic murmur may develop as a result of a dissection in the ascending aorta close to the aortic valve, causing valvular regurgitation, heart failure, and cardiac tamponade.
A multiplanar CT scan is the immediate diagnostic imaging modality of choice; clinicians should have a low threshold for obtaining a CT scan in any hypertensive patient with chest pain and equivocal findings on ECG.
The CT scan should include both the chest and abdomen to fully delineate the extent of the dissected aorta. MRI is an excellent imaging modality for chronic dissections, but in the acute situation, the longer imaging time and the difficulty of monitoring patients in the MRI scanner make the CT scan preferable. Chest radiographs may reveal an abnormal aortic contour or widened superior mediastinum. Although transesophageal echocardiography (TEE) is an excellent diagnostic imaging method, it is generally not readily available in the acute setting.
Aortic dissection is most commonly misdiagnosed as myocardial infarction or other causes of chest pain such as pulmonary embolization. Dissections may occur with minimal pain; branch vessel occlusion of the lower extremity can mimic arterial embolus.
Aggressive measures to lower blood pressure should occur when an aortic dissection is suspected, even before the diagnostic studies have been completed. Treatment requires a simultaneous reduction of the systolic blood pressure to 100–120 mm Hg and pulse pressure. Beta-blockers have the most desirable effect of reducing the left ventricular ejection force that continues to weaken the arterial wall and should be first-line therapy. Labetalol, both an alpha- and beta-blocker, lowers pulse pressure and achieves rapid blood pressure control. Give 20 mg over 2 minutes by intravenous injection. Additional doses of 40–80 mg intravenously can be given every 10 minutes (maximum dose 300 mg) until the desired blood pressure has been reached. Alternatively, 2 mg/min may be given by intravenous infusion, titrated to desired effect. In patients who have asthma, bradycardia, or other conditions that necessitate the patient’s reaction to beta-blockers be tested, esmolol is a reasonable choice because of its
short half-life. Give a loading dose of esmolol, 0.5 mg/kg intravenously over 1 minute, followed by an infusion of 0.0025–0.02 mg/kg/min. Titrate the infusion to a goal heart rate of 60–70 beats/min. If beta-blockade alone does not control the hypertension, nitroprusside may be added as follows: 50 mg of nitroprusside in 1000 mL of 5% dextrose and water, infused at a rate of 0.5 mL/min for a 70-kg person (0.3 mcg/kg/min); the infusion rate is increased by 0.5 mL every 5 minutes until adequate control of the pressure has been achieved. In patients with bronchial asthma, while there are no data supporting the use of the calcium channel antagonists, diltiazem and verapamil are potential alternatives to treatment with beta-blocking drugs. Morphine sulfate is the appropriate drug to use for pain relief. Long-term medical care of patients should include beta-blockers in their antihypertensive regimen.
B. Surgical Intervention
Urgent surgical intervention is required for all type A dissections. If a skilled cardiovascular team is not available, the patient should be transferred to an appropriate facility. The procedure involves grafting and replacing the diseased portion of the arch and brachiocephalic vessels as necessary. Replacement of the aortic valve may be required with reattachment of the coronary arteries.
Urgent surgery is required for type B dissections if there is aortic branch compromise resulting in malperfusion of the renal, visceral, or extremity vessels. The immediate goal of surgical therapy is to restore flow to the ischemic tissue, which is most commonly accomplished via a bypass. Endovascular stenting of the entry tear at the level of the subclavian artery may result in obliteration of the false lumen and restore flow into the branch vessel from the true lumen. The results, however, are unpredictable and should only be attempted by an experienced team. For acute type B dissections without malperfusion, evidence shows that long-term aortic-specific survival and late aneurysm formation rates are improved with early thoracic stent graft repair. Patients with uncomplicated type B dissections whose blood pressure is controlled and who survive the acute episode without complications may have long-term survival without surgical treatment.