AorticDissection

Type A + Type B · complete reference · Stanford classification · full doses · Full Card

Symptoms / Associated Sx

• Abrupt-onset tearing or ripping chest/back pain — maximal at onset (distinguishes from ACS which builds gradually); anterior chest pain = ascending involvement; interscapular back pain = descending; radiation to abdomen or flanks = distal propagation to abdominal aorta or iliac arteries

• BP differential >20 mmHg between arms (30–40% sensitivity — absence does NOT exclude); pulse deficit (subclavian/carotid involvement); pallor and diaphoresis; Horner syndrome (superior cervical ganglion compression by hematoma)

• Type A complications: new AR murmur (aortic root/annular involvement — wide pulse pressure, diastolic decrescendo murmur); syncope (cardiac tamponade from hemopericardium — Beck triad); inferior STEMI pattern (RCA ostium involvement — DO NOT give lytics); neurologic deficits (carotid artery involvement — hemiplegia, aphasia)

• Type B complications: lower extremity ischemia (iliac involvement); renal ischemia (renal artery — rising Cr, oliguria); mesenteric ischemia (SMA involvement — abdominal pain, lactate rise, peritoneal signs); spinal cord ischemia (intercostal arteries — paraplegia)

Neg

• Pt denies substernal pressure-quality chest pain radiating to the left arm or jaw building over minutes with diaphoresis and no BP differential between arms — argues against ACS as primary diagnosis (ACS pain is crescendo; dissection pain is maximal at onset; if any dissection features present, obtain CTA before anticoag or thrombolytics — giving lytics or heparin to a dissection patient is fatal)

• Pt denies pleuritic sharp chest pain worsening with inspiration and lying flat, improved by leaning forward, with audible friction rub and diffuse saddle-shaped ST elevation without reciprocal changes — argues against pericarditis (dissection does not cause PR depression; dissection pain is tearing/ripping/back-predominant; pericarditis lacks BP differential)

• Pt denies acute onset dyspnea + pleuritic chest pain + tachycardia + hypoxia + signs of DVT without any back pain or BP differential — argues against PE as the primary diagnosis (CT-PA can be obtained simultaneously with CTA aorta if both are in the differential; obtain CXR first — widened mediastinum tilts toward dissection)

• Pt denies reproducible musculoskeletal pain with chest wall palpation, with no BP differential and no tearing quality — argues against MSK etiology (dissection commonly presents with sudden severe back pain that can be misattributed to musculoskeletal causes; maintain high suspicion for dissection in any sudden-onset severe back pain in hypertensive patients)

Social History (SHx)

• HTN severity and duration (present in 70–80%; poorly controlled HTN = most important modifiable risk factor); Marfan syndrome features (tall stature, arm span > height, lens dislocation [ectopia lentis], high-arched palate, pectus excavatum, joint hypermobility — prophylactic aortic repair when root >5 cm or >4.5 cm with family hx rupture); bicuspid aortic valve (known or suspected)

• Cocaine or methamphetamine use (acute catecholamine surge → severe HTN → shear force); prior aortic surgery or cardiac catheterization (iatrogenic dissection); pregnancy (3rd trimester — ↑circulating volume + ↑wall stress + hormonal changes → medial degeneration); family history of aortic aneurysm/dissection or sudden cardiac death; connective tissue disease (Ehlers-Danlos Type IV — COL3A1; Loeys-Dietz)

Main Etiology

• Hypertensive medial degeneration (~70%): chronic HTN → cystic medial necrosis → ↓elastin + ↑collagen → intimal vulnerability → tear → hematoma tracking in media → false lumen; most common in elderly hypertensive men

• Connective tissue disease: Marfan syndrome (FBN1 mutation — fibrillin-1 deficiency → medial degeneration; most common genetic cause; prophylactic surgery at root >5 cm); Loeys-Dietz syndrome (TGFBR1/2 — more aggressive; operate at >4.2 cm or smaller); Ehlers-Danlos Type IV (COL3A1 — most lethal; surgery often not feasible)

• Bicuspid aortic valve aortopathy: independent of valve stenosis/regurgitation; dilated aortic root + ascending aorta; ↑dissection risk even with normally functioning valve

• Other: aortitis (Takayasu arteritis — young Asian women; giant cell arteritis — elderly; inflammatory destruction of media); iatrogenic (post-PCI, post-CABG, post-valve surgery); blunt deceleration trauma; cocaine/amphetamines

RF

• HTN (strongest modifiable — 70–80% of all dissections), age 60–80, male sex (3:1), Marfan/Loeys-Dietz/Ehlers-Danlos IV, bicuspid AoV, prior aortic aneurysm (>5 cm ascending or >5.5 cm descending = elective repair threshold), cocaine/methamphetamines, prior cardiac surgery, pregnancy (3rd trimester), family history aortic dissection or aneurysm, Turner syndrome

Data

• CTA chest/abdomen/pelvis with IV contrast — gold standard and first-line imaging (intimal flap separating true and false lumen; false lumen usually larger with slower flow; extent of dissection — ascending vs descending; branch vessel involvement [carotid, subclavian, renal, SMA, iliac]; pericardial effusion/hemopericardium; aortic root diameter; contrast leak = impending rupture; perform CTA BEFORE any anticoag/thrombolytics/vasodilators if dissection suspected)

• ECG immediately (inferior STE = RCA ostium involvement by dissection flap — this mimics inferior STEMI exactly; DO NOT give thrombolytics without CTA if tearing pain or BP differential; normal or non-specific in 30% of dissections; LVH from chronic HTN)

• CXR portable (widened mediastinum >8 cm = sensitivity 60%, specificity 90%; pleural effusion L > R in Type B; loss of aortic knob; calcium sign [separation of intimal calcification >1 cm from outer aortic wall]; cannot exclude dissection with normal CXR — CTA required)

• BP measurement bilateral both arms simultaneously (>20 mmHg differential = subclavian involvement in dissection; 30–40% sensitivity; right arm cuff may underestimate BP if right subclavian involved — use left arm for drug titration in this case)

• TEE (transesophageal echo) (sensitivity 99% for Type A; useful if patient too hemodynamically unstable for CTA; identifies: intimal flap, true/false lumen, AR severity, pericardial effusion, tamponade, LV function, regional wall motion; blind spot in distal ascending aorta due to bronchus interposition)

• TTE bedside (rapid screening: pericardial effusion = tamponade; AR; LV function; cannot definitively exclude dissection — TEE or CTA required for diagnosis)

• BMP (Cr — renal artery involvement; malperfusion; contrast risk; K+ — arrhythmia risk; glucose — stress response; CO2 — metabolic acidosis from mesenteric ischemia)

• Lactate serial (mesenteric malperfusion — rising lactate + abdominal pain + acidosis = surgical emergency for Type B with SMA involvement)

• T&S + 4 units pRBC on hold + FFP for all Type A pre-op; CBC; coagulation studies (baseline before surgery); troponin (if inferior STE pattern — elevated from RCA ischemia, not plaque rupture)

DDx

ACS/STEMI (crescendo pressure CP + arm/jaw radiation — CTA before ANY lytics or anticoag if BP differential or tearing quality; RCA ostium dissection mimics inferior STEMI exactly) · PE (pleuritic CP + hypoxia + tachycardia + DVT signs — CT-PA; dissection excluded first if widened mediastinum) · Pneumothorax (sudden unilateral chest pain + absent breath sounds — CXR distinguishes) · Pericarditis (pleuritic positional CP + friction rub + diffuse saddle ST↑ + PR↓ — no BP differential; no tearing quality) · Aortic aneurysm leak/rupture (known aneurysm + severe abdominal/back pain — CTA; hemodynamic instability = OR immediately)

Home Meds

• Hold immediately: all anticoagulants (warfarin [Coumadin], DOACs, heparin — ↑hemorrhage into false lumen); antiplatelet agents (aspirin [Bayer], clopidogrel [Plavix]); thrombolytics absolutely contraindicated if dissection confirmed or suspected

• Hold vasodilators without beta-blockade (nitrates, hydralazine [Apresoline], amlodipine [Norvasc] alone — reflex tachycardia → ↑dP/dt → dissection propagation); esmolol (Brevibloc) or labetalol (Trandate) must be established first

• Continue: existing beta-blockers at reduced dose once hemodynamics stabilized and esmolol/labetalol infusion running

Plan

• Immediate — CTA chest/abdomen/pelvis with contrast before any treatment: rule out dissection before anticoag, lytics, or vasodilators; simultaneous IV access ×2 + arterial line placement; blood type and crossmatch; call cardiac surgery and ICU immediately upon clinical suspicion — do not wait for imaging

• Anti-impulse therapy — esmolol (Brevibloc) FIRST (both Type A and B): 500 mcg/kg IV bolus over 1 min → 50 mcg/kg/min → titrate up to 200 mcg/kg/min; target HR <60 bpm (↓dP/dt = rate of pressure rise = primary driver of shear force propagating the dissection); establish HR target before adding vasodilator; pure vasodilator without beta-blockade causes reflex tachycardia → ↑dP/dt → extension of dissection | The sequence is non-negotiable: esmolol [Brevibloc] FIRST to ↓HR → then nitroprusside [Nipride] to ↓SBP; reversing this order is the most common and most dangerous treatment error in aortic dissection

• Vasodilator (once HR <60 established):

  • Nitroprusside (Nipride) 0.3–0.5 mcg/kg/min IV → titrate to SBP <120 mmHg (arterial line required; cyanide toxicity if >72h or high dose — check thiocyanate level; antidote hydroxocobalamin [Cyanokit] 5 g IV); target SBP <120 + HR <60 within 20 minutes

  • OR labetalol (Trandate) 20 mg IV → 40–80 mg IV q10 min (max 300 mg/24h) → 2 mg/min infusion (provides both alpha- and beta-blockade in one agent; acceptable alternative when esmolol + nitroprusside combination complex to manage)

  • Nicardipine (Cardene) 5–15 mg/hr IV: alternative vasodilator if nitroprusside not available or renal dysfunction; less preferred as lacks anti-impulse properties

• Type A dissection (ascending aorta ± arch involved) — emergent cardiac surgery:

  • Immediate cardiothoracic surgery consult upon CTA diagnosis; transfer to OR as quickly as possible; mortality 1–2% per hour without surgery; untreated in-hospital mortality ~50% at 48h

  • Pre-op: arterial line right radial (left subclavian may be involved in flap); central venous access; 4 units pRBC + 4 units FFP crossmatched; foley; NPO; anesthesia consult

  • Tamponade from hemopericardium: pericardiocentesis as bridge only if patient in extremis — may paradoxically worsen by releasing tamponade effect on bleeding false lumen; temporize; OR is the definitive treatment

  • RCA ostium involvement (inferior STE on ECG): PCI after surgical repair if ST elevation persists; do NOT give thrombolytics

  • Severe AR from root dissection: emergent surgery with aortic root replacement (Bentall procedure) or valve-sparing root replacement

• Type B dissection (descending aorta, distal to left subclavian) — medical management unless complicated:

  • Uncomplicated Type B: medical anti-impulse + vasodilator therapy; ICU; oral transition when SBP stable: metoprolol succinate (Toprol-XL) 50–200 mg PO daily + amlodipine (Norvasc) 5–10 mg PO daily; target SBP <120/80 long-term

  • Complicated Type B (TEVAR indicated): malperfusion syndrome (limb ischemia, renal ischemia [rising Cr + oliguria], mesenteric ischemia [abdominal pain + ↑lactate + peritoneal signs]); refractory pain despite adequate BP control; uncontrolled HTN; rapid false lumen expansion; aortic rupture; TEVAR = thoracic endovascular aortic repair (stent-graft deployed percutaneously); vascular surgery urgently

• Pain control: IV morphine (MSIR) 2–4 mg IV q4–6h PRN or IV fentanyl (Sublimaze) 25–50 mcg IV q1–2h PRN; pain indicates ongoing dissection — adequate analgesia required; persistent or worsening pain despite good BP control → repeat CTA (propagation or impending rupture)

• Monitoring: continuous arterial line (radial — use right arm unless right subclavian involved); bilateral arm BP measurements q1h; Foley (UO ≥0.5 mL/kg/hr — renal malperfusion marker); serial neuro checks q1–2h (carotid/spinal cord involvement); continuous telemetry; serial CTA Type B at 24–48h, 1 week, 1 month

• PT/OT eval and treat — strict bed rest Type A pre-op and immediate post-op; Type B strict bed rest until pain-free ×48h and BP stable on PO medications; gradual mobilization; avoid straining, Valsalva, isometric exercise (↑intrathoracic pressure → ↑aortic wall stress)

• Trend daily: BP bilateral arms q1h → q4h once stable (SBP target <120 mmHg); HR (target <60 bpm); pain score (↑pain = propagation or rupture → repeat CTA immediately); UO q1h; Cr (renal malperfusion); lactate (mesenteric ischemia); neuro checks; nitroprusside (Nipride) thiocyanate level if >72h; serial CTA per protocol

• Escalation triggers: Type A confirmed on CTA → OR immediately · tamponade (Beck triad + hemodynamic collapse) → pericardiocentesis bridge → OR · Type B with malperfusion (limb ischemia + rising Cr + mesenteric ischemia + ↑lactate) → vascular surgery + TEVAR urgently · persistent/worsening pain despite SBP <120 + HR <60 → repeat CTA (propagation or rupture) · new neuro deficit → CTA + neurology + vascular surgery · refractory HTN Type B → add nicardipine (Cardene) IV 5–15 mg/hr · nitroprusside (Nipride) cyanide toxicity (lactic acidosis + AMS + ↑thiocyanate) → stop nitroprusside + hydroxocobalamin (Cyanokit) 5 g IV

• Discharge (Type B medically managed): metoprolol succinate (Toprol-XL) 50–200 mg PO daily + amlodipine (Norvasc) 5–10 mg PO daily; home SBP target <120/80 (home BP monitor twice daily); serial CTA aorta surveillance: 1 month, 3 months, 6 months, then annually (false lumen thrombosis = favorable; expansion >5 mm/year = consider TEVAR); avoid heavy lifting (>20 lbs), isometric exercise, contact sports; genetic testing for Marfan/Loeys-Dietz/Ehlers-Danlos if suspected; first-degree family member screening; smoking cessation; vascular surgery f/u 2–4 weeks; return precautions: sudden severe chest/back pain + new neurologic deficit + pulse differential → 911 immediately

⚠ Red Flags

• Thrombolytics in Type A dissection mimicking inferior STEMI (RCA ostium involvement) → massive aortic hemorrhage → death; always screen for dissection (tearing quality, BP differential, CXR mediastinum) before any lytic therapy in inferior STEMI — 30-second screen can prevent a fatal error

• Pure vasodilator without beta-blockade in dissection (nitroglycerin or hydralazine alone) → reflex tachycardia → ↑dP/dt → propagation of dissection distally; esmolol (Brevibloc) or labetalol (Trandate) MUST be established before or simultaneously with vasodilator

• Tamponade from Type A hemopericardium — pericardiocentesis removes tamponade effect on bleeding false lumen; may paradoxically worsen hemorrhage; only appropriate as a brief bridge to OR in extremis; never a substitute for surgical repair

• Type B malperfusion syndrome missed (rising Cr + limb ischemia + abdominal pain + rising lactate) → irreversible end-organ damage; TEVAR window narrows with time; urgent vascular surgery consultation at first sign of malperfusion

• Anticoagulation in dissection (heparin for presumed ACS) → ↑hemorrhage into false lumen → ↑risk of rupture; hold all anticoag until CTA confirms or excludes dissection

Senior IM Resident Pearls

• Pain at maximal intensity at onset = dissection until proven otherwise: ACS pain crescendos; dissection pain is maximal the instant it starts; this single feature is the most powerful differentiator in the history; "worst pain of my life at the very second it started" = get CTA

• Anti-impulse before vasodilator — always: esmolol (Brevibloc) 500 mcg/kg bolus → infusion to HR <60 BEFORE nitroprusside (Nipride); dP/dt (rate of pressure rise) — not peak pressure — is the primary driver of shear force; ↓HR ↓dP/dt more than ↓BP alone; pure vasodilator = reflex tachycardia = ↑dP/dt = propagation; labetalol (Trandate) IV achieves both effects with one drug

• Stanford classification dictates management: Type A (any ascending involvement) = emergent surgical repair — no exceptions; Type B (distal to left subclavian) = medical management unless complicated (malperfusion, refractory pain, rapid expansion, rupture); this classification must be made immediately from CTA report

• Marfan syndrome surveillance: prophylactic aortic repair at root diameter >5 cm (or >4.5 cm with family hx of dissection/rupture or rapid expansion); losartan (Cozaar) 50–100 mg PO daily (↓TGF-β signaling → ↓aortic root growth rate; COMPARE-Marfan 2023); beta-blocker (atenolol [Tenormin] or metoprolol [Toprol-XL]) lifelong; avoid contact sports + heavy weightlifting; annual CTA or MRA aorta

• Common mistake — normal CXR used to exclude dissection: CXR sensitivity for dissection is only 60%; a normal CXR does NOT exclude aortic dissection; CTA is required in any patient with sudden severe chest or back pain + HTN history or connective tissue disease features; do not be falsely reassured by normal CXR

• Common mistake — confusing inferior STEMI and Type A dissection: RCA ostium involvement produces ST elevation in II/III/aVF indistinguishable from inferior STEMI on ECG; if the patient has tearing back pain, BP differential, or widened mediastinum → CTA first; thrombolytics in this scenario = death; activate STEMI protocol only after dissection is confidently excluded