Cardiovascular

Aortic dissection: classification, diagnosis, and management

Clinical Overview and When to Suspect Aortic Dissection

— Peak incidence 60–70 years; men > women 2:1, but women present later with worse outcomes

— Hypertension is the dominant risk factor (~70% of cases)

— Connective tissue disease: Marfan, Loeys-Dietz, vascular Ehlers-Danlos, Turner syndrome

— Bicuspid aortic valve, prior cardiac surgery, coarctation

— Cocaine/methamphetamine use (catecholamine surge), severe weightlifting Valsalva

— Pregnancy (third trimester/peripartum, especially with Marfan or aortic root >40 mm)

— Inflammatory aortitis (giant cell, Takayasu), syphilis, blunt deceleration trauma

— Stanford A: involves ascending aorta ± arch ± descending → surgical emergency

— Stanford B: distal to left subclavian only → typically medical, unless complicated

— DeBakey I: ascending + arch + descending; II: ascending only; III: descending only

— Acute (<14 days), subacute (14–90 days), chronic (>90 days)

— Abrupt severe chest/back/abdominal pain (tearing, ripping, migrating)

— Pulse deficit, BP differential >20 mmHg between arms, or focal neuro deficit

— Widened mediastinum on CXR or new aortic regurgitation murmur

Board pearl: Any patient with chest pain plus a neurologic deficit, syncope, limb ischemia, or new diastolic murmur — think dissection before thrombolysing a "stroke" or "STEMI." Missed dissection given tPA is a classic malpractice scenario tested on Step 3.

Definition: Intimal tear allowing pulsatile blood to enter the aortic media, creating a false lumen that propagates antegrade or retrograde, with risk of rupture, malperfusion, tamponade, or aortic regurgitation.

Epidemiology and risk factors:

Classification systems:

When to suspect — the high-pretest-probability triad:

Aortic Dissection Detection (ADD) Risk Score (0–3): predisposing conditions, pain features, exam findings. Score ≥2 mandates urgent imaging.

Presentation Patterns and Key History

— Sudden, maximal at onset (unlike MI's crescendo) — described as "tearing," "ripping," "sharp" in ~50%

— Anterior chest pain suggests type A; interscapular/back pain suggests type B

— Migratory pain that tracks downward as the dissection propagates is highly specific but uncommon

— Abdominal pain suggests visceral malperfusion (mesenteric, renal)

— Coronary ostia (usually RCA) → inferior STEMI pattern; never thrombolyse before excluding dissection in an inferior MI with disproportionate pain or unequal pulses

— Carotid → stroke, altered mental status, Horner syndrome

— Spinal arteries → paraplegia, anterior cord syndrome

— Subclavian → arm ischemia, BP differential

— Mesenteric → "pain out of proportion," lactic acidosis

— Renal → flank pain, oliguria, AKI, refractory HTN

— Iliofemoral → cold pulseless leg

— Pericardium → tamponade (leading cause of death in type A)

— Onset timing (instantaneous vs gradual)

— Maximal intensity at start?

— Migration of pain location?

— History of HTN, connective tissue disease, family history of dissection/sudden death

— Cocaine/stimulant use, recent heavy lifting

— Pregnancy status

— Prior aortic surgery or aneurysm

Key distinction: MI pain crescendos and is exertional; dissection pain is maximal at onset and migrates. Pulmonary embolism causes pleuritic pain with dyspnea, not tearing pain. A patient with "the worst pain of my life" plus BP asymmetry has dissection until proven otherwise — even if the troponin is positive.

Pain characteristics (the linchpin of the history):

Associated symptoms by branch involvement:

Syncope: occurs in ~10%, suggests tamponade, stroke, or rupture — high-mortality marker.

Painless dissection: ~5–15%, more common in elderly, diabetics, prior aortic surgery, Marfan; presents as syncope, stroke, or heart failure.

Key history questions to ask:

Physical Exam Findings and Hemodynamic Assessment

— Hypertension in 70% of type B and ~35% of type A (catecholamine surge, renal malperfusion)

— Hypotension/shock in type A → suggests tamponade, aortic rupture, or severe AR; ominous

— Pseudohypotension: measuring BP in a limb supplied by a compressed/dissected artery — always check bilateral arm and leg pressures

— Interarm systolic BP differential >20 mmHg in ~30%

— Pulse deficit in any extremity raises mortality

— Document radial, brachial, femoral, dorsalis pedis bilaterally

— New early diastolic decrescendo murmur of AR at left sternal border → proximal dissection disrupting valve coaptation

— Muffled heart sounds, JVD, pulsus paradoxus → tamponade (Beck triad)

— S3 or pulmonary crackles → acute LV failure from severe AR

— Focal deficits (carotid involvement) — mimics stroke

— Hoarseness (recurrent laryngeal nerve compression — Ortner sign)

— Horner syndrome (sympathetic chain)

— Paraplegia (spinal artery compromise)

— Pleural effusion (usually left, from inflammatory exudate or hemothorax)

— Abdominal tenderness with peritonism if mesenteric malperfusion

— Cold mottled limb, absent femoral pulse

— Superior vena cava syndrome (rare, from compression)

Step 3 management: On initial assessment, simultaneously cycle bilateral arm BPs, palpate all four extremity pulses, auscultate for AR, and check for tamponade physiology. Document these findings before imaging — they drive the ADD score and pre-test probability, which determines whether you proceed to CTA emergently or pursue alternative diagnoses. Pseudohypotension can falsely reassure; if one arm reads 80/50 and the other 180/100, treat the higher pressure as the true aortic pressure.

Vital signs — two opposite patterns:

Pulse and BP asymmetry:

Cardiac auscultation:

Neurologic exam:

Other findings:

Diagnostic Workup — Initial Labs, ECG, and Chest X-Ray

— Often nonspecific (LVH from chronic HTN, nonspecific ST-T changes)

— Inferior STEMI in ~5% when dissection involves RCA ostium — critical pitfall; reflexive thrombolysis is catastrophic

— Low voltage or electrical alternans suggests pericardial effusion/tamponade

— Widened mediastinum (>8 cm on supine AP) — ~60% sensitive

— Abnormal aortic contour, loss of aortic knob

— Calcium sign: intimal calcium displaced >1 cm from outer aortic shadow

— Left pleural effusion, tracheal deviation, depressed left mainstem bronchus

— A normal CXR does NOT exclude dissection (~10–20% normal)

— CBC, BMP (creatinine for contrast risk and renal malperfusion), LFTs, lactate

— Troponin — may be positive from coronary ostial involvement or demand

— Type and crossmatch ≥4 units PRBCs

— Coagulation panel (PT/INR/PTT) — needed before surgery

— Lipase if abdominal pain to rule out alternatives

— D-dimer: highly sensitive (~97%); <500 ng/mL in low-risk patient (ADD score 0–1) can argue against dissection per ADvISED protocol, but not stand-alone; never use D-dimer to rule out a high-pretest patient

— Bedside TTE can detect pericardial effusion, dilated aortic root, intimal flap in ascending aorta

— Excellent for rapid triage in unstable patient before CT

Board pearl: A patient with chest pain, inferior ST elevations, and an interarm BP differential — do NOT give heparin/tPA/ticagrelor. Order an emergent CTA chest first. Giving antiplatelet/anticoagulation to a dissection patient before recognition is a high-yield Step 3 patient-safety vignette and a sentinel event.

ECG (obtain within 10 minutes of arrival):

Chest X-ray (PA and lateral if patient stable):

Initial labs (send all simultaneously):

Point-of-care ultrasound (POCUS):

Diagnostic Workup — Confirmatory Imaging

— First-line confirmatory test in hemodynamically stable patients

— Sensitivity and specificity >95%

— Defines: entry tear location, true vs false lumen, extent (Stanford A vs B), branch vessel involvement, malperfusion, pericardial blood, rupture

— ECG-gated CTA reduces motion artifact at aortic root

— Limitations: contrast nephrotoxicity, radiation, requires patient transport

— Preferred when patient is too unstable to transport, in pregnancy (no radiation), or with severe contrast allergy/AKI

— Sensitivity >95% for type A; can identify intimal flap, AR mechanism, pericardial effusion, coronary involvement

— Can be performed in the OR or ED at bedside

— Operator-dependent; blind spot at distal ascending aorta/proximal arch

— Highest accuracy but slow — reserved for stable patients, chronic dissection, or follow-up

— Useful in renal failure (avoid gadolinium if eGFR <30) and pregnancy

— Screening only; sensitive for proximal ascending dissection and complications (tamponade, AR) but misses descending dissection; never use to rule out

— Historical gold standard; now reserved for endovascular intervention planning

Step 3 management: In a hemodynamically unstable patient with high suspicion — go to bedside TEE and concurrently activate cardiothoracic surgery; don't waste minutes in the CT scanner. In a stable patient with moderate-to-high suspicion — CTA chest/abdomen/pelvis is the move. If creatinine is elevated, weigh contrast risk against the near-100% mortality of missed type A dissection — always image first, dialyze later.

CT angiography (CTA) of chest/abdomen/pelvis with contrast:

Transesophageal echocardiography (TEE):

MRA (magnetic resonance angiography):

Transthoracic echo (TTE):

Aortography:

Risk Stratification and First-Line Management Logic

— Confirmed Stanford A → emergent cardiothoracic surgery consult; mortality rises 1–2% per hour untreated

— Confirmed Stanford B, uncomplicated → medical management in ICU, BP/HR control

— Complicated type B (malperfusion, rupture, refractory pain/HTN, rapid expansion) → TEVAR (thoracic endovascular aortic repair)

— Two large-bore IVs, arterial line (right radial preferred — left subclavian may be dissected), Foley

— Type and cross 4–6 units PRBCs

— NPO, head-of-bed elevation

— Adequate analgesia with IV opioids (fentanyl/morphine) — reduces sympathetic surge

— HR <60 bpm (reduces dP/dt — the shear force on aortic wall)

— SBP 100–120 mmHg (or lowest tolerated maintaining end-organ perfusion: mentation, urine output ≥0.5 mL/kg/hr)

— Achieve rate control BEFORE vasodilator to prevent reflex tachycardia and increased shear stress

— Antiplatelets, anticoagulants, thrombolytics — bleed risk into false lumen

— Sole use of hydralazine or pure vasodilators (reflex tachycardia)

— Inotropes (increase dP/dt) unless tamponade physiology

— Suspect tamponade, rupture, severe AR

— Fluid resuscitation cautiously; pericardiocentesis only as bridge (can worsen by increasing dP/dt)

— Definitive: emergent surgery

CCS pearl: Order set on the CCS case — "IV access ×2, cardiac monitor, arterial line, type and cross 4 units, NPO, esmolol drip, nicardipine drip, fentanyl PRN, urine output monitoring, CT surgery consult STAT, ICU admission." Advance the clock only after these are placed. Re-check BP and HR every 5–10 minutes until targets met.

Immediate triage decision tree:

ABC stabilization while awaiting surgery:

Hemodynamic targets:

Avoid:

In hypotensive type A:

Pharmacotherapy — First-Line Regimen

— Esmolol: load 500 mcg/kg over 1 min, then 50–200 mcg/kg/min infusion — titratable, short half-life (~9 min), preferred in unstable patients

— Labetalol: 20 mg IV bolus, then 20–80 mg q10min or 0.5–2 mg/min infusion — combined α/β blockade, useful when HR and BP need simultaneous control

— Metoprolol: 5 mg IV q5min ×3, then PO transition once stable

— Target HR <60 bpm

— Nicardipine: 5 mg/hr IV, titrate by 2.5 mg/hr q5–15min, max 15 mg/hr — preferred when beta-blocker insufficient

— Clevidipine: rapid-acting dihydropyridine, 1–2 mg/hr, titratable

— Sodium nitroprusside: 0.25–10 mcg/kg/min — potent but requires concurrent beta-blockade (avoids reflex tachycardia); risk of cyanide toxicity with prolonged use or renal failure

— Diltiazem or verapamil IV for rate control

— In cocaine-related dissection: avoid pure beta-blockade (unopposed α); use labetalol or phentolamine + diltiazem

— IV fentanyl or morphine — reduces sympathetic tone, helps achieve hemodynamic targets

— Pain control is therapy, not just comfort

— Reverse anticoagulation (4-factor PCC for warfarin, idarucizumab for dabigatran, andexanet/PCC for factor Xa inhibitors)

— Hold antiplatelets if possible; surgery proceeds regardless if life-threatening

Board pearl: Beta-blocker before vasodilator — always. A vasodilator alone (nitroprusside, hydralazine) causes reflex tachycardia and increases aortic wall shear stress (dP/dt), propagating the dissection. This sequence is a perennial Step 3 question stem.

Step 1: Heart rate control with IV beta-blocker FIRST

Step 2: Add vasodilator if SBP still >120 mmHg after rate control

If beta-blocker contraindicated (severe asthma, decompensated HF, high-grade AV block, cocaine-induced):

Analgesia:

Pre-operative considerations:

Procedures and Definitive Management

— Median sternotomy, cardiopulmonary bypass, deep hypothermic circulatory arrest for arch involvement

— Replace ascending aorta ± hemiarch ± total arch with graft

— Aortic valve management: resuspension if leaflets intact; root replacement (Bentall) if root involved or in connective tissue disease

— Coronary reimplantation if ostia involved

— Operative mortality: 15–30%; without surgery: ~50% at 48 hours, ~90% at 1 month

— Uncomplicated: medical therapy (beta-blocker + ARB/ACEi long-term); 30-day mortality ~10%

— Complicated (malperfusion, rupture, refractory pain/HTN, rapid aortic expansion, false lumen >22 mm): TEVAR — endovascular stent graft covering primary entry tear

— TEVAR mortality lower than open repair (~5–10%); reduces aortic-related mortality at 5 years vs medical alone in selected uncomplicated patients (INSTEAD-XL data)

— Branch vessel stenting or fenestration for malperfusion

— Pericardial window/drainage for tamponade — avoid full pericardiocentesis which can precipitate rupture; controlled drainage only as bridge

— Strict BP control (SBP <120, ideally <110)

— Continue IV antihypertensives, transition to oral when extubated

— Monitor for paraplegia (spinal cord ischemia — consider CSF drainage), stroke, renal failure, bowel ischemia

— Daily neuro and vascular exams

Step 3 management: Order sequence — confirm type A → call CT surgery → consent for emergent repair → continue esmolol/nicardipine drip → cross 6 units PRBCs, 4 FFP, 1 platelets → transport to OR. For type B uncomplicated → ICU admission, BP/HR drip titration, serial CTA at 48–72h to assess stability before transitioning to oral regimen.

Stanford Type A — emergent open surgical repair:

Stanford Type B — management by complication status:

Adjunct procedures:

Post-procedure ICU care:

Special Populations — Elderly and Renal/Hepatic Impairment

— Higher prevalence of painless or atypical presentations (syncope, CHF, altered mentation)

— Type A surgical mortality rises to 30–40%; nonetheless, age alone is not a contraindication to surgery — frailty, functional status, and comorbidities matter more

— Shared decision-making essential; involve family/surrogate early

— Endovascular repair (TEVAR) increasingly used even for selected type A in prohibitive surgical risk

— Contrast-induced nephropathy risk with CTA — do not delay diagnosis; pre-hydrate with isotonic saline if possible, but the diagnostic and therapeutic urgency overrides nephroprotection

— TEE is a contrast-free alternative when feasible

— Avoid gadolinium MRA if eGFR <30 (nephrogenic systemic fibrosis risk)

— Adjust nicardipine — minimal renal adjustment; nitroprusside accumulates thiocyanate/cyanide in renal failure — limit duration to <24–48 hr or avoid

— Beta-blockers: esmolol minimally renally cleared (preferred); metoprolol hepatic; atenolol renally cleared (avoid)

— Reduced metabolism of labetalol, metoprolol — start lower doses

— Coagulopathy from synthetic dysfunction — correct with FFP/vitamin K before surgery

— Higher perioperative mortality with cirrhosis (MELD score predictive)

— Review home antihypertensives — many can be resumed/uptitrated after stabilization

— Statin continuation reduces long-term aortic-related mortality

— Avoid NSAIDs (renal, BP, bleeding)

Board pearl: In an elderly patient with syncope, hypotension, and a new diastolic murmur but no chest pain, painless type A dissection with tamponade is on the differential. Don't be falsely reassured by absence of "tearing pain" — order POCUS and CTA. A normal D-dimer is less reliable in the elderly due to age-related elevation.

Elderly (>75 years):

Chronic kidney disease:

Hepatic impairment:

Polypharmacy considerations:

Special Populations — Pregnancy and Genetic Aortopathies

— Highest risk in third trimester and early postpartum (hormonal aortic wall changes, hyperdynamic state, increased cardiac output)

— Underlying substrate often present: Marfan, Loeys-Dietz, vascular Ehlers-Danlos, bicuspid aortic valve, Turner syndrome

— Marfan with aortic root >40 mm → counsel against pregnancy or recommend prophylactic root repair pre-conception

— Beta-blockers (labetalol, metoprolol) safe in pregnancy; avoid atenolol (fetal growth restriction); ACEi/ARBs contraindicated

— Imaging: TEE or MRA preferred to minimize fetal radiation; if CTA needed for life-threat, do it

— Management: type A in viable pregnancy (≥28 wk) → cesarean delivery followed immediately by aortic repair; <28 wk → repair with fetus in utero if possible (high fetal loss)

— Marfan syndrome (FBN1): prophylactic root replacement at aortic root ≥50 mm (or ≥45 mm with risk factors: rapid growth >3 mm/yr, family history of dissection, planned pregnancy)

— Loeys-Dietz (TGFBR1/2): repair at ≥42 mm (more aggressive — earlier dissection)

— Vascular Ehlers-Danlos (COL3A1): notoriously friable vessels — avoid surgery if possible; medical management

— Bicuspid aortic valve aortopathy: repair at ≥55 mm (or ≥50 mm with risk factors)

— First-degree relatives → screen with TTE and consider genetic testing

— Rare; almost always associated with genetic syndrome or trauma

— Lower threshold for imaging when chest/back pain in known aortopathy

Key distinction: Type B dissection in pregnancy — manage medically if uncomplicated (labetalol, nicardipine). Type A — surgery is non-negotiable; both maternal and fetal survival depend on prompt repair.

Pregnancy-associated dissection:

Genetic aortopathies — screening and prophylaxis:

Pediatric dissection:

Complications and Adverse Outcomes

— Aortic rupture — leading cause of death; into pericardium (tamponade), pleura (hemothorax), mediastinum, retroperitoneum

— Cardiac tamponade — Beck triad, pulsus paradoxus, electrical alternans; mortality of type A

— Acute severe aortic regurgitation — flash pulmonary edema, cardiogenic shock

— Coronary malperfusion → MI (usually inferior, RCA ostium)

— Stroke — carotid involvement; ~5–10% of type A

— Spinal cord ischemia → paraplegia; ~2–5%, higher with extensive descending repair

— Mesenteric ischemia → lactic acidosis, peritonitis, bowel necrosis

— Renal malperfusion → AKI, refractory hypertension

— Limb ischemia → may require fenestration or stenting

— Post-implantation syndrome after TEVAR (fever, leukocytosis, self-limited)

— Pneumonia, VTE, ICU-acquired weakness

— Wound infection, mediastinitis post-sternotomy

— Recurrent laryngeal nerve injury → hoarseness

— Aneurysmal degeneration of residual dissected aorta — most common late complication; requires lifelong surveillance imaging

— Anastomotic pseudoaneurysm

— Progressive aortic regurgitation requiring valve replacement

— Endoleak after TEVAR (types I–V; type I and III require reintervention)

— Recurrent dissection (especially in connective tissue disease)

— Chronic kidney disease, chronic limb ischemia

— Untreated type A: 50% at 48 hr, 80% at 2 weeks

— Operated type A: 15–25% in-hospital

— Type B medical: ~10% at 30 days; complicated TEVAR: ~10–15%

Board pearl: A patient post-type A repair returns weeks later with hoarseness and a left pleural effusion — think expansion of residual false lumen or anastomotic pseudoaneurysm, not pneumonia. Image with CTA.

Early (within hours to days):

Intermediate (days to weeks):

Late (months to years):

Mortality benchmarks:

When to Escalate — ICU, Consults, and Triage

— Any confirmed or strongly suspected aortic dissection → call cardiothoracic surgery (for type A) or vascular surgery (for type B)

— Hemodynamic instability, tamponade physiology → activate massive transfusion protocol, OR

— Stroke + chest pain → do not activate stroke alert with tPA until dissection excluded

— Continuous arterial line monitoring, q5–15 min BP/HR titration

— Frequent neuro checks, distal pulse checks, urine output

— Serial labs (lactate, creatinine, troponin, hemoglobin)

— Cardiac monitoring for arrhythmias, ischemia

— Cardiothoracic surgery (type A)

— Vascular surgery / endovascular specialist (type B, TEVAR planning)

— Cardiology (AR assessment, perioperative)

— Anesthesia (high-risk perioperative)

— Nephrology if AKI or contrast considerations

— Neurology if stroke/spinal cord ischemia

— Genetics if young patient or syndromic features

— Community ED without CT surgery → stabilize hemodynamics, initiate esmolol/nicardipine, transfer emergently to tertiary center with aortic program

— Do not delay transfer for additional imaging if diagnosis confirmed

— Air vs ground transport based on distance and stability; pressurization considerations in air transport are not clinically significant for dissection

— Hemodynamically stable on oral regimen for ≥24–48 hr

— Pain controlled, no malperfusion, normalizing labs

CCS pearl: On the CCS, after confirming type A — sequence is "CT surgery consult STAT, anesthesia consult, ICU admit, blood bank notify, OR booking." Failing to call surgery promptly costs points and lives. For type B, "vascular surgery consult, ICU admit, esmolol drip, nicardipine drip, serial CTA at 48 hr."

Immediate (within minutes) escalation triggers:

ICU admission criteria — essentially all acute dissections:

Multidisciplinary consults:

Transfer considerations:

Step-down/floor transfer (post-acute):

Key Differentials — Other Aortic and Vascular Mimics

— Hemorrhage within aortic media without intimal tear or false lumen flow

— Considered part of acute aortic syndrome spectrum; treated similarly to dissection by location (type A → surgery, type B → medical)

— CTA: crescentic high-attenuation aortic wall thickening without contrast in wall

— Can progress to overt dissection or regress

— Ulceration of atheroma penetrating internal elastic lamina, usually descending aorta in elderly with severe atherosclerosis

— Risk of pseudoaneurysm, rupture

— Management: BP control, TEVAR if symptomatic or enlarging

— Thoracic or abdominal aortic aneurysm rupture — shares risk factors (HTN, smoking)

— Triad of AAA rupture: hypotension, pulsatile abdominal mass, back/flank pain

— CTA distinguishes; management is emergent vascular repair (open or EVAR)

— Deceleration mechanism (MVC, fall from height); typically at aortic isthmus (distal to left subclavian, near ligamentum arteriosum)

— Widened mediastinum on CXR after trauma → CTA mandatory

— Giant cell, Takayasu, infectious — can present with chest/back pain, elevated inflammatory markers; chronic course distinguishes

— Young patient with HTN, BP differential between arms and legs, rib notching

— Young women, peripartum; mimics ACS; coronary angiography diagnoses

Key distinction: IMH, PAU, classic dissection, and contained rupture form the "acute aortic syndrome" spectrum — all share clinical features and require the same initial workup (CTA) and hemodynamic management. Treatment branches by location and complication, not by which specific entity.

Intramural hematoma (IMH):

Penetrating atherosclerotic ulcer (PAU):

Aortic aneurysm rupture/leak:

Traumatic aortic injury:

Aortitis:

Coarctation with dissection:

Spontaneous coronary artery dissection (SCAD):

Key Differentials — Non-Aortic Mimics

— Substernal pressure, diaphoresis, exertional onset; ECG ST changes; troponin rise

— Crucial pitfall: dissection can cause inferior STEMI — always check BP differential and consider CTA before thrombolysis in atypical features

— Diagnostic clue: dissection pain is maximal at onset; MI pain crescendos

— Pleuritic chest pain, dyspnea, tachycardia, hypoxia

— D-dimer elevated in both — not discriminating

— CTA chest catches both; PE shows filling defects in pulmonary arteries

— Sudden pleuritic pain, dyspnea, unilateral absent breath sounds

— CXR or POCUS diagnoses; tension PTX needs immediate decompression

— After forceful vomiting; chest/back pain, subcutaneous emphysema, Hamman crunch

— Left pleural effusion (mimics dissection); CT esophagram diagnoses

— Pleuritic, positional pain; pericardial friction rub; diffuse ST elevation with PR depression

— Epigastric/RUQ pain; lipase, LFTs, ultrasound differentiate

— Reproducible with palpation; no systemic features

— Hypertensive emergency with MI — overlaps; manage both BP and ischemia, but rule out dissection first if features suggest

Board pearl: The deadly six causes of acute chest pain: MI, aortic dissection, PE, tension pneumothorax, pericardial tamponade, esophageal rupture. Initial workup (ECG, CXR, POCUS, troponin, D-dimer) should screen for all six. A "negative" workup that didn't include vascular imaging in a high-pretest patient is incomplete.

Acute myocardial infarction (STEMI/NSTEMI):

Pulmonary embolism:

Pneumothorax (especially tension):

Esophageal rupture (Boerhaave syndrome):

Pericarditis/myocarditis:

Acute cholecystitis, pancreatitis, perforated ulcer:

Musculoskeletal pain, costochondritis:

Pulmonary causes: pneumonia, pleurisy

Acute coronary syndrome with severe HTN:

Secondary Prevention and Long-Term Pharmacotherapy

— Target SBP <120 mmHg, HR <60 bpm (more stringent than general HTN guidelines)

— First-line: beta-blocker (metoprolol succinate, atenolol, bisoprolol, carvedilol) — reduces dP/dt and aortic wall stress; mortality benefit

— Second agent: ARB or ACEi — ARBs (losartan) particularly favored in Marfan (TGF-β antagonism, though clinical benefit modest beyond BP control)

— Calcium channel blocker (amlodipine, diltiazem) if beta-blocker not tolerated or for adjunct BP control

— Avoid hydralazine monotherapy and direct vasodilators that cause reflex tachycardia

— High-intensity statin (atorvastatin 40–80, rosuvastatin 20–40) — reduces aortic-related events and ASCVD mortality

— Smoking cessation (essential — accelerates aortic disease)

— Avoid heavy isometric exercise, weightlifting, Valsalva-inducing activities

— Avoid stimulants (cocaine, amphetamines, high-dose decongestants)

— Aerobic exercise OK at moderate intensity; avoid competitive contact sports

— Weight management, low-sodium diet (DASH)

— Limit alcohol

— Generally avoided unless separate indication (mechanical valve, AF, recent stent); decision individualized

— Index case <60 yr or with syndromic features → genetic testing

— First-degree relatives → TTE screening with periodic surveillance

Step 3 management: Discharge med list for post-dissection patient — beta-blocker (titrated to HR <60), ARB or ACEi (titrated to SBP <120), high-intensity statin, smoking cessation counseling. Document BP and HR targets explicitly in discharge instructions. Schedule first follow-up within 2 weeks, repeat CTA at 1, 3, 6, and 12 months, then annually.

Lifelong BP control — the cornerstone:

Statin therapy:

Lifestyle modifications:

Antiplatelet/anticoagulation:

Genetic counseling and family screening:

Follow-Up, Monitoring, and Counseling

— CTA (or MRA) chest/abdomen/pelvis at 1 month, 3 months, 6 months, 12 months, then annually for life

— More frequent if rapid expansion (>5 mm/yr) or symptoms recur

— MRA preferred long-term to reduce cumulative radiation, especially in young patients

— Document maximal aortic diameters at standard levels (root, ascending, arch, descending, abdominal)

— First post-discharge visit within 1–2 weeks — BP/HR check, medication titration, wound assessment

— Aortic specialty clinic (cardiology + vascular surgery) every 3–6 months in year 1, then annually

— Home BP monitoring with log; teach proper technique

— Residual aortic diameter ≥55 mm (≥50 mm in connective tissue disease)

— Rapid expansion >5 mm/yr (>3 mm/yr in CTD)

— New malperfusion, refractory pain, endoleak (type I or III)

— Symptomatic aneurysmal degeneration

— Supervised, low-to-moderate intensity aerobic program

— Avoid resistance training >50% 1-rep-max, Valsalva maneuvers, contact sports

— Encourage walking, stationary cycling, swimming

— PTSD and anxiety common after life-threatening event — screen and refer

— Address driving restrictions per state law during recovery

— Sexual activity counseling (resume when can climb 2 flights of stairs without symptoms)

— Travel: avoid high-altitude or extreme exertion in first 3 months; commercial flight typically OK after 2–4 weeks if stable

Board pearl: A post-dissection patient at 6-month follow-up has SBP averaging 135 mmHg at home. Don't accept this — uptitrate beta-blocker and ARB to target <120. Inadequate BP control is the leading driver of late aortic events and need for reintervention.

Surveillance imaging schedule:

Outpatient clinic visits:

Reintervention thresholds:

Cardiac rehabilitation:

Psychosocial counseling:

Ethical, Legal, and Patient Safety Considerations

— Type A dissection patient often has impaired capacity (pain, sedation, shock, stroke)

— Obtain emergency surrogate consent from spouse/next of kin per state hierarchy

— If no surrogate available and delay is life-threatening, two-physician emergency consent under doctrine of presumed consent

— Document capacity assessment and surrogate identification clearly

— Among top sources of malpractice in emergency medicine

— Common errors: anchoring on MI/musculoskeletal diagnosis, failure to check bilateral BPs, premature discharge after "negative" troponin

— Mitigation: structured use of ADD risk score, mandatory bilateral BP documentation, low threshold for CTA in high-risk patients

— Giving tPA to misdiagnosed dissection patient (presenting as stroke or STEMI) is a sentinel event requiring institutional root-cause analysis

— Stroke protocols increasingly include BP-differential check and rapid aortic imaging in select patients

— Handoff between ED → ICU → OR → step-down → outpatient is a high-risk transition

— Use structured handoff (SBAR, I-PASS) including hemodynamic targets, drip rates, surgical plan

— Medication reconciliation at every transition — beta-blocker and ARB must not be missed at discharge

— In elderly with poor functional status or severe comorbidities, surgery may be futile

— Discuss goals of care, palliative options early; involve palliative care team

— Document DNR/POLST status; honor patient values

— Driver fitness reporting may be required if syncope or neurologic deficits; state-dependent

— Duty to inform patient about implications for first-degree relatives; offer cascade screening

Step 3 management: A 78-year-old with type A dissection and dementia arrives without family. Activate surgery, attempt to reach surrogate, document urgency. Do not delay life-saving repair pending consent if patient lacks capacity and surrogate unreachable — emergency exception applies. Update family ASAP and document thoroughly.

Informed consent in the unstable patient:

Diagnostic error and missed dissection:

Thrombolytic catastrophe:

Transition-of-care safety:

End-of-life considerations:

Mandatory reporting:

Genetic disclosure:

High-Yield Associations and Rapid-Fire Facts

Board pearl: Memorize the "BP first" trap reversed — HR first, then BP. Beta-blocker → vasodilator. This single concept generates multiple Step 3 questions per cycle.

Marfan syndrome — FBN1 mutation; tall, arachnodactyly, ectopia lentis (upward), aortic root dilation; pregnancy high-risk; repair at root ≥50 mm

Loeys-Dietz — TGFBR1/2; hypertelorism, bifid uvula, cleft palate, arterial tortuosity; repair at ≥42 mm

Vascular Ehlers-Danlos — COL3A1; thin translucent skin, easy bruising; avoid surgery if possible (friable vessels)

Turner syndrome (45,X) — bicuspid AV, coarctation, aortic dilation; screen with TTE

Bicuspid aortic valve — associated aortopathy independent of valve dysfunction

Tertiary syphilis — ascending aortic aneurysm/aortitis (vasa vasorum endarteritis)

Cocaine/methamphetamine — acute catecholamine surge; avoid pure beta-blockers (unopposed α)

Pregnancy — third trimester/peripartum, especially with underlying aortopathy

Giant cell arteritis — thoracic aortic aneurysm/dissection (10–20% develop late aortic disease) — screen annually

Takayasu arteritis — young Asian females, pulseless disease

Aortic Dissection Detection (ADD) Risk Score — predisposing condition, pain features, exam (each scores 1 point; ≥2 → image)

D-dimer — sensitive (~97%) but not specific; useful in low-risk rule-out only

Calcium sign on CXR — intimal calcium displaced >1 cm from outer aortic wall

Beck triad — hypotension, JVD, muffled heart sounds (tamponade)

Ortner syndrome — hoarseness from recurrent laryngeal nerve compression

DeBakey I/II/III vs Stanford A/B — Stanford simpler and management-relevant

Type A mortality — 1–2% per hour untreated; surgical mortality 15–25%

Right radial arterial line preferred — left subclavian often dissected

dP/dt — the shear force on aortic wall; lowered by beta-blockade

Cyanide toxicity — long-duration nitroprusside in renal failure

TEVAR — first-line for complicated type B; reduces aortic-related mortality at 5 years

Annual CTA/MRA — lifelong surveillance after acute event

Board Question Stem Patterns

— 65-year-old man with sudden severe chest pain radiating to back, BP 180/100 right arm, 130/80 left arm, inferior ST elevations on ECG. Next best step? → CTA chest, NOT thrombolytics. Initiate esmolol first.

— Confirmed type B dissection, BP 200/110, HR 95. Best initial pharmacologic step? → IV esmolol (or labetalol); add nicardipine after HR controlled. Wrong answer: nitroprusside alone.

— Tall young man with pectus excavatum, lens dislocation, aortic root 48 mm at routine echo. Next step? → Beta-blocker, ARB, surveillance imaging; surgical referral at ≥50 mm (or with risk factors). Genetic counseling.

— 28-week-pregnant woman with Marfan, sudden severe chest pain, widened mediastinum. Best imaging? → TEE or MRA (avoid radiation if possible); if life-threat → CTA. Management: delivery + emergent repair if type A.

— Elderly diabetic with syncope, new diastolic murmur, hypotension. Diagnosis to consider? → Type A dissection with tamponade. Order POCUS, then CTA or TEE.

— Patient 1 month after type B dissection on labetalol with home SBP averaging 140. Best action? → Uptitrate; add ARB; verify CTA scheduled at 3 months.

— Cocaine-related chest pain with dissection features. Avoid? → Pure beta-blocker (unopposed α). Use? → Labetalol, phentolamine, benzodiazepines.

— Acute hemiparesis, chest pain, BP differential. Next step before tPA? → CTA to exclude dissection.

— Mesenteric malperfusion; lactate elevated. Action? → Surgical/endovascular fenestration or stenting.

— First-degree relative of dissection victim. Recommendation? → TTE screening, consider genetic testing if syndromic.

Step 3 management: Recognize the "diastolic murmur + chest pain + BP differential" triad — it's nearly pathognomonic on a question stem.

Pattern 1 — The "MI" that isn't:

Pattern 2 — Beta-blocker before vasodilator:

Pattern 3 — The Marfan patient:

Pattern 4 — Pregnant Marfan:

Pattern 5 — Painless dissection:

Pattern 6 — Post-discharge follow-up:

Pattern 7 — The wrong drug:

Pattern 8 — Stroke alert pitfall:

Pattern 9 — Pulse deficit + abdominal pain:

Pattern 10 — Family screening:

One-Line Recap

Aortic dissection is a time-critical acute aortic syndrome where CTA confirms the diagnosis, Stanford A goes emergently to surgery while Stanford B is medically managed (TEVAR if complicated), and IV beta-blockade precedes vasodilator to lower dP/dt with targets of HR <60 and SBP <120, followed by lifelong BP control, statin, surveillance imaging, and family screening.

Board pearl: The four highest-yield concepts — (1) rate before pressure in pharmacotherapy, (2) Stanford A = surgery, B = medical unless complicated, (3) bilateral BP and pulse exam is mandatory, (4) lifelong surveillance and HR/BP targets <60 and <120 drive long-term survival. Master these, and you'll answer nearly every dissection question on Step 3 correctly — and more importantly, you'll catch the diagnosis at 3 AM when the patient's life depends on it.

Recognize: Sudden tearing chest/back pain + pulse or BP differential + new diastolic murmur or neurologic deficit → ADD score, then CTA (or TEE if unstable). Never thrombolyse atypical inferior STEMI without excluding dissection.

Stabilize: IV esmolol or labetalol to HR <60 first, then nicardipine or nitroprusside to SBP <120. Analgesia with fentanyl reduces sympathetic surge. Two large-bore IVs, arterial line (right radial), type and cross, ICU.

Definitive treatment: Stanford A → emergent open repair (mortality climbs 1–2% per hour untreated). Uncomplicated Stanford B → medical therapy. Complicated Stanford B (malperfusion, rupture, refractory pain, rapid expansion) → TEVAR.

Long-term: Beta-blocker + ARB/ACEi to SBP <120 / HR <60, high-intensity statin, smoking cessation, exercise restrictions (no heavy lifting/Valsalva), surveillance CTA at 1/3/6/12 months then annually. Genetic counseling and first-degree-relative screening when syndromic features or age <60.