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Aortic dissection<br />

KALANI OLMSTED AND DEBORAH B. DIERCKS<br />

n Agents<br />

n Opioids<br />

n Beta-blockers<br />

n Calcium channel blockers<br />

n Vasodilators<br />

n Evidence<br />

According to panels addressing management of aortic dissection (AD), available<br />

levels of evidence rate no higher than “expert opinion.” 1 Hemodynamic<br />

(anti-impulse) therapy remains the foundation of AD care, and successful<br />

control of blood pressure and heart rate improves patient comfort. However,<br />

in most patients with AD, the inability of anti-impulse therapy to control<br />

severe pain mandates an early role for aggressive analgesia. 2<br />

The first step in AD care, anti-impulse therapy, serves as optimal medical<br />

management and also provides some pain relief. Beta-blockers (e.g. metoprolol,<br />

propranolol, esmolol, labetalol) decrease the force of cardiac contraction<br />

and reduce blood pressure; both of these properties make this class<br />

ideal for minimizing AD progression. 1,3,4 In patients with relative betablocker<br />

intolerance, esmolol’s short half-life renders it the best initial<br />

choice. 1<br />

Ongoing pain after beta-blocker administration usually indicates incomplete<br />

blood pressure control. In such cases, pain relief (and optimal medical<br />

management) is facilitated by vasodilation. The traditional choice is sodium<br />

nitroprusside. Fenoldopam (a dopamine-1 agonist that selectively dilates<br />

arterioles and renal vasculature) may also be used. When AD is accompanied<br />

by cardiac ischemia, the calcium channel blocker nicardipine is indicated;<br />

reflex tachycardia renders nitroglycerin (glyceryl trinitrate) potentially dangerous<br />

as a treatment for chest pain when AD is suspected. 1,3–5<br />

91

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