Acute Aortic Syndromes and Dissection

Acute aortic dissection is a true can’t-miss — uncommon, lethal, and a great mimic of ACS. Getting it wrong in the other direction is also dangerous: treat a dissection as an MI and anticoagulate, and you can kill the patient. Recognition, the right first moves, and anticipating the complications matter enormously.

• •Classic dissection — an intimal tear creates a true and a false lumen.
• •Intramural hematoma (IMH) — blood within the aortic wall without an obvious intimal flap; managed like dissection by location.
• •Penetrating atherosclerotic ulcer (PAU) — an atherosclerotic ulcer eroding into the wall, usually in older patients.
• •All three are graded by whether they involve the ASCENDING aorta — that single fact drives the surgery-vs-medical decision.

• •Sudden, severe, “tearing” or “ripping” chest or interscapular back pain, often maximal at onset; pain may migrate.
• •Pulse or blood-pressure differential between arms; a new aortic regurgitation murmur; syncope.
• •Malperfusion signs: stroke/focal deficit, limb ischemia, mesenteric or renal ischemia; cardiac tamponade (type A).
• •Risk factors: hypertension (most common), connective-tissue disease (Marfan, Loeys-Dietz, Ehlers-Danlos), bicuspid aortic valve, prior aortic disease/surgery, cocaine, pregnancy.

• •CT angiography of the aorta is the usual first test for the stable patient (fast, very sensitive and specific).
• •TEE is the alternative, especially in the unstable patient who can’t leave the resuscitation area; MRI is mainly for stable follow-up.
• •A normal CXR does NOT exclude it (a widened mediastinum is suggestive but ~10–20% can look normal); D-dimer is an adjunct, not a substitute for imaging when suspicion is high.
• •Troponin can be positive if the dissection involves a coronary — don’t let that anchor you on ACS.

• •Stanford type A — involves the ascending aorta: SURGICAL emergency (risk of rupture, tamponade, AR, coronary involvement).
• •Stanford type B — descending aorta only (distal to the left subclavian): usually MEDICAL (anti-impulse) management unless complicated.
• •DeBakey: I (ascending + arch ± descending), II (ascending only), III (descending only). DeBakey I and II behave like Stanford A; III behaves like Stanford B.

Goal: reduce aortic wall shear by lowering heart rate AND blood pressure — target HR <60 and SBP ~100–120 with adequate perfusion/mentation. Doses are typical adult starting points; your protocol governs.

• •Give an IV β-blocker FIRST to control rate — esmolol ~500 mcg/kg load then ~50 mcg/kg/min titrated, OR labetalol 20 mg IV then repeat/escalate.
• •If a β-blocker is truly contraindicated, use a non-dihydropyridine CCB (diltiazem or verapamil) for rate control.
• •THEN add a vasodilator (nicardipine or nitroprusside) only if SBP is still high — never before rate control.
• •Adequate analgesia (pain drives catecholamines and BP).

• •Type A: tamponade, acute aortic regurgitation, coronary involvement (classically the RIGHT coronary → inferior MI pattern), stroke, and rupture.
• •Any location: malperfusion of a branch vessel — mesenteric, renal, limb, or spinal cord.
• •Hypotension in a dissection patient is ominous — think tamponade, rupture, or severe acute AR, and reconsider before reflexively giving pressors.

• •Type A → emergent open surgical repair.
• •Uncomplicated type B → medical anti-impulse therapy and BP control, monitored.
• •Complicated type B (malperfusion, rupture/impending rupture, refractory pain or hypertension, rapid expansion) → TEVAR (endovascular) or surgery.

• •Anchoring on ACS and anticoagulating/giving antiplatelets in an undiagnosed dissection.
• •Giving a vasodilator BEFORE a β-blocker → reflex tachycardia increases shear stress.
• •Being reassured by a normal CXR or relying on D-dimer to exclude it when suspicion is high.
• •Reflexively giving pressors for hypotension without considering tamponade/rupture/severe AR.
• •Missing the pulse/BP differential or the new AR murmur.