Acute aortic dissection: type A vs type B, malperfusion, and endovascular management

Cinematic anatomical illustration of the aorta with an intimal flap separating the true and false lumen, type A dissection in the ascending aorta and type B distal to the left subclavian artery, a TEVAR stent-graft overlaid in the descending segment, clinical-blue lighting on dark background, medical educational, no text, no people — FigureThe aortic dissection — the type A (the ascending, the surgical emergency, the 1 to 2 per cent per hour untreated mortality) and the type B (the medical if uncomplicated, the TEVAR if complicated). The beta-blocker first, then the vasodilator; the malperfusion the emergency.

Type A vs Type B aortic dissection

Feature	Type A (ascending)	Type B (descending — distal to L subclavian)
Incidence	65%	35%
Extent	Ascending aorta (may extend to arch/descending)	Descending aorta (distal to left subclavian)
Mortality (untreated)	1-2%/h, 50% in 48h	10% in 30 days
Management	EMERGENCY SURGERY (ascending replacement ± AVR ± arch)	MEDICAL (beta-blocker + BP) if uncomplicated; TEVAR/surgery if complicated
Complications	Cardiac tamponade (retrograde into pericardium), AR (annular disruption), stroke (arch vessels), MI (coronary)	Mesenteric ischaemia, renal failure, limb ischaemia, paraplegia (spinal), rupture
Surgical urgency	IMMEDIATE (life-threatening)	Selective (only if complicated)
BP target	Aggressive (SBP 100-120) pre-op	SBP 100-120 (if uncomplicated — medical)

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Management of acute aortic dissection

RECOGNISE + IMMEDIATE STABILISATION — (a) CLINICAL: sudden TEARING chest/back pain (migrating), pulse deficits (asymmetric BP >20 mmHg between arms), new AR murmur, neurological deficit (stroke, paraplegia), syncope. (b) IMMEDIATE: 2 large-bore IV, oxygen, monitor (ECG, BP both arms), analgesia (morphine). (c) ECG (exclude MI — dissection can involve coronary — usually RIGHT coronary -> inferior MI). (d) CXR (wide mediastinum — 60% sensitive, not definitive). (e) STAT CT AORTOGRAM (definitive — intimal flap, true/false lumen, extent, malperfusion, rupture). (f) ACT FAST — type A mortality 1-2%/h
BLOOD PRESSURE CONTROL (CRITICAL — PRE-OP FOR ALL TYPES) — (a) BETA-BLOCKER FIRST (reduce dP/dt — rate of pressure rise — shear stress on aorta -> slows propagation): (i) LABETALOL (alpha+beta) 10-20 mg IV q10min (or infusion 20-80 mg/hr). (ii) ESMOLOL (short-acting beta-1) 500 mcg/kg loading then 50-200 mcg/kg/min (titratable, short half-life — preferred in ICU). (iii) METOPROLOL 5 mg IV (less titratable). (b) TARGET: HR 60-80, SBP 100-120 mmHg (reduce shear + prevent rupture). (c) ADD VASODILATOR after beta-blocker (if BP still high): (i) NICARDIPINE (CCB) 5-15 mg/hr infusion. (ii) NITROPRUSSIDE 0.3-3 mcg/kg/min (potent but cyanide risk — avoid if possible). (iii) AVOID nitroprusside ALONE (without beta-blocker — reflex tachycardia -> increased shear -> WORSE dissection). (d) AVOID: hydralazine (reflex tachycardia), pure vasodilators without beta-block
TYPE A — EMERGENCY SURGERY — (a) IMMEDIATE transfer to OR (cardiothoracic surgery). (b) PROCEDURE: (i) Median sternotomy. (ii) Cardiopulmonary bypass + hypothermic circulatory arrest (for arch repair). (iii) Resection of torn ascending aorta. (iv) Interposition graft (Dacron) replacement. (v) ± Aortic valve replacement (if annular disruption/AR). (vi) ± Arch repair (if arch involved — more complex). (vii) ± Coronary reimplantation (if dissection involves coronary ostia). (c) MORTALITY: 10-30% (surgical); 50% in 48h untreated. (d) DELAY is the enemy — each hour untreated -> 1-2% mortality. (e) PRE-OP: stabilise (BP control) but DON'T delay surgery for 'stabilisation' — type A needs OR now
TYPE B UNCOMPLICATED — MEDICAL MANAGEMENT — (a) ADMISSION: ICU/HDU (monitor for complications). (b) BP CONTROL: beta-blocker + vasodilator (target SBP 100-120, HR 60-80). (c) ANALGESIA (morphine — pain contributes to HTN). (d) MONITOR: (i) Serial examination (pulse deficits, abdomen — mesenteric ischaemia, limbs). (ii) Serial CT (at 24-48h — extent, expansion, malperfusion). (iii) Renal function (renal artery involvement). (iv) Lactate (mesenteric ischaemia). (e) DURATION: IV then transition to oral (labetalol, bisoprolol, ACEi/ARB). (f) PAIN: if REFRACTORY pain/HTN despite medical -> complicated -> TEVAR. (g) LONG-TERM: strict BP control (<130/80), serial imaging (CT/MRI at 1, 3, 6, 12 months — for expansion/redissection), beta-blocker lifelong
TYPE B COMPLICATED — TEVAR (PREFERRED) OR SURGERY — (a) COMPLICATIONS requiring intervention: (i) RUPTURE (haemodynamic instability — emergency). (ii) MALPERFUSION syndrome (mesenteric, renal, limb, spinal — end-organ ischaemia). (iii) REFRACTORY pain or hypertension (despite maximal medical). (iv) RAPID EXPANSION (aneurysmal degeneration — on serial imaging). (v) CONTAINED rupture (on imaging). (b) TEVAR (Thoracic Endovascular Aortic Repair): (i) Stent-graft placed via femoral artery -> covers the entry tear -> excludes false lumen -> restores true lumen flow -> relieves malperfusion. (ii) INSTEAD-XL trial: TEVAR + medical vs medical alone (uncomplicated type B) -> TEVAR had better remodelling (false lumen thrombosis) + trend to fewer late interventions. (iii) ADSORB: similar — TEVAR favourable remodelling. (iv) ADVANTAGES: less invasive (vs open surgery), lower morbidity/mortality. (v) INDICATIONS: complicated type B (preferred); selected uncomplicated (INSTEAD-XL — prevention of late complications). (c) OPEN SURGERY (for TEVAR failure/not suitable): (i) Thoracotomy, graft replacement of descending aorta. (ii) Higher morbidity (spinal cord ischaemia — paraplegia, renal failure, bleeding) than TEVAR. (iii) Reserved for: extensive dissection, unsuitable anatomy for TEVAR, TEVAR failure
MALPERFUSION SYNDROME — EMERGENCY — (a) MECHANISM: dissection flap OCCLUDES branch arteries (true lumen compressed by false lumen; or flap covers ostium). (b) TYPES: (i) CORONARY (usually RIGHT coronary -> inferior MI). (ii) CAROTID (stroke). (iii) MESENTERIC (bowel ischaemia — abdominal pain, raised lactate, AKI). (iv) RENAL (AKI — renal artery occlusion). (v) LIMB (acute limb ischaemia — pulseless, painful). (vi) SPINAL (paraplegia — intercostal/lumbar artery occlusion). (c) MANAGEMENT: (i) RESTORE PERFUSION: TEVAR (cover entry tear -> restore true lumen flow -> relieve malperfusion). OR fenestration (create hole in flap -> equalise true/false lumen pressure -> restore flow). OR surgical bypass. (ii) EMERGENCY — malperfusion -> end-organ infarction (bowel necrosis, renal failure, limb loss, paraplegia) if not corrected. (d) CLINICAL: any new organ dysfunction in dissection -> MALPERFUSION until proven otherwise -> urgent imaging + intervention

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Exam practice

SAQ — Type A dissection with cardiac tamponade

10 minutes · 10 marks

A 58-year-old hypertensive man presents with sudden tearing central chest pain radiating to the back, followed by syncope. On arrival BP 76/48, HR 132 sinus, SpO2 94% on room air. JVP is distended to the angle of the jaw, heart sounds are muffled, and pulsus paradoxus of 16 mmHg is present. ECG shows sinus tachycardia with no ST elevation. Bedside focused echo shows a large circumferential pericardial effusion with diastolic collapse of the right ventricle free wall and a mobile intimal flap in the ascending aorta. CT aortogram confirms a Stanford type A dissection with haemopericardium.

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SAQ — Complicated Type B dissection with multi-territory malperfusion

10 minutes · 10 marks

A 64-year-old hypertensive man presents with sudden severe tearing back pain radiating to the abdomen and right flank. BP 188/104 (right arm), 150/96 (left arm), HR 110 sinus. His right leg is cold, mottled and pulseless, and he has severe abdominal pain out of proportion to examination. Lactate 5.6 mmol/L, creatinine 235 (baseline 98). CT aortogram confirms a Stanford type B dissection arising distal to the left subclavian artery; the right renal artery and the superior mesenteric artery arise from the compressed true lumen, and the right external iliac is occluded by the dissection flap. He remains haemodynamically stable.

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Clinical pearls

High-yield aortic dissection points for CICM/FFICM exam

Sudden tearing pain — the hallmark. (1) PRESENTATION: (a) SUDDEN onset (instantaneous — 'at peak intensity' from first moment — unlike MI which builds up). (b) TEARING or RIPPING quality (the intimal tear + propagation). (c) CHEST (type A) or BACK (type B) — MIGRATING (tracks propagation — chest to back as dissection extends distally). (d) SEVERE (worst ever — patient writhing). (2) DIFFERENTIAL of sudden chest pain: (a) AORTIC DISSECTION (tearing, migrating, pulse deficits). (b) MI (crushing, radiating arm/jaw, ECG changes). (c) PE (pleuritic, dyspnoea, DVT). (d) PNEUMOTHORAX (sudden, pleuritic, hyperresonant). (e) ESOPHAGEAL RUPTURE (Boerhaave — vomiting then pain). (3) CLUES for dissection: (a) Pulse deficits (asymmetric — carotid, radial, femoral). (b) BP differential (>20 mmHg between arms). (c) New AR murmur (annular disruption). (d) Neurological deficit (stroke, paraplegia). (e) WIDE MEDIASTINUM on CXR. (f) PREGNANCY, MARFAN, hypertension. (4) ANY sudden severe chest pain -> consider dissection (don't assume MI).[6] }
Stanford classification — type A vs type B. (1) STANFORD: (a) TYPE A: involves ASCENDING aorta (regardless of extent — may also involve arch/descending). 65% of dissections. SURGICAL EMERGENCY. (b) TYPE B: DESCENDING aorta only (DISTAL to left subclavian artery — does NOT involve ascending). 35%. MEDICAL management (uncomplicated). (2) WHY THE DISTINCTION MATTERS: (a) Ascending aorta dissection threatens: HEART (coronary ostia — MI; aortic root — AR; pericardium — tamponade from retrograde propagation). BRAIN (arch vessels — stroke). -> Life-threatening -> SURGERY. (b) Descending aorta dissection threatens: VISCERA (mesenteric, renal), LIMBS, SPINAL CORD. -> Less immediately life-threatening (if uncomplicated) -> MEDICAL. (3) DEBAKEY (older classification): I (ascending + descending), II (ascending only), III (descending only). Stanford simpler (A/B) and more clinically useful (determines surgical vs medical). (4) PRACTICE: ANY dissection involving ASCENDING = type A = surgery.[1] }
Beta-blocker FIRST (before vasodilator) — the critical order. (1) RATIONALE: (a) Dissection propagates due to SHEAR STRESS (the force of blood against the aortic wall — dP/dt — rate of pressure rise in systole). (b) HYPERTENSION + TACHYCARDIA -> high dP/dt -> more shear -> dissection propagates faster -> worse (extension, rupture). (c) BETA-BLOCKER: reduces HR (negative chronotropy) + contractility (negative inotropy) -> reduces dP/dt -> LESS shear -> slows/stops propagation. (d) VASODILATOR (alone): lowers BP BUT causes REFLEX TACHYCARDIA (baroreceptor response to low BP) -> INCREASED dP/dt -> MORE shear -> WORSE dissection. (2) THE ORDER: (a) BETA-BLOCKER FIRST (to control HR + prevent reflex tachycardia). (b) THEN vasodilator (to lower BP — safe, no reflex tachycardia because beta-blocker prevents it). (3) AGENTS: (a) LABETALOL (alpha + beta — vasodilation + beta-block): 10-20 mg IV q10min (or infusion). (b) ESMOLOL (short-acting beta-1 — preferred ICU — titratable, short half-life): 500 mcg/kg loading then 50-200 mcg/kg/min. (c) METOPROLOL: 5 mg IV (less titratable). (4) TARGET: HR 60-80, SBP 100-120. (5) AVOID: vasodilator ALONE (nitroprusside without beta-blocker) — reflex tachycardia -> worse. (6) CAUTION: if bradycardic/heart failure (can't tolerate beta-blocker) -> use vasodilator carefully (CCB like nicardipine — less reflex tachycardia than nitroprusside).[1] }
CT aortogram — the diagnostic gold standard. (1) WHY CT: (a) FAST (minutes — critical in time-sensitive type A). (b) HIGH sensitivity/specificity (>95% for dissection). (c) Shows: INTIMAL FLAP (the torn intima separating true from false lumen — PATHOGNOMONIC). EXTENT (ascending? arch? descending? abdominal? — determines type A/B + involvement of branch arteries). TRUE vs FALSE lumen (false lumen often larger, slower flow, may be thrombosed). MALPERFUSION (branch artery occlusion — renal, mesenteric, limb, carotid). RUPTURE (contrast extravasation — emergency). PERICARDIAL EFFUSION (retrograde type A — tamponade). (2) PROTOCOL: (a) NON-CONTRAST first (look for intramural haematoma — high-density wall thickening — variant). (b) ARTERIAL phase (CTA — intimal flap, extent, malperfusion). (c) DELAYED phase (false lumen filling, end-organ perfusion). (3) ALTERNATIVES: (a) ECHOCARDIOGRAPHY (TOE — transoesophageal — if unstable, can't go to CT — shows flap, AR, pericardial effusion; but can't see full descending aorta well). (b) MRI (excellent — but slow, not for unstable — for follow-up). (c) ANGIOGRAPHY (historical gold standard — invasive — now CT preferred). (4) D-DIMER: elevated in dissection (>500 — sensitive — may be used as RULE OUT if low probability + normal D-dimer — ADJUSTED — but don't rely on in high probability). (5) PRACTICE: CT AORTOGRAM for ALL suspected dissection (definitive).[6] }
Type A — emergency surgery (don't delay). (1) TYPE A IS A SURGICAL EMERGENCY: (a) Mortality 1-2% PER HOUR untreated (50% in 48h). (b) Death from: CARDIAC TAMPONADE (dissection ruptures retrograde into pericardium — 80% of type A deaths), AORTIC RUPTURE (into mediastinum/pleura), CORONARY OCCLUSION (MI), STROKE (arch vessels), ACUTE AR (heart failure). (2) SURGERY: (a) GOAL: resect torn ascending aorta + replace with graft -> prevent rupture/tamponade + restore flow. (b) PROCEDURE: (i) Median sternotomy. (ii) Cardiopulmonary bypass (CPB) — machine pumps blood while heart stopped. (iii) HYPOTHERMIC CIRCULATORY ARREST (cool to 18-28°C — stop circulation briefly for arch repair — protects brain). (iv) Resection of torn segment. (v) Interposition graft (Dacron tube). (vi) ± AVR (aortic valve replacement — if annulus damaged/irreparable AR). (vii) ± VALVE-SPARING (David procedure — reimplant native valve if possible — avoids lifelong anticoagulation). (viii) ± ARCH repair (if arch involved — more complex, longer). (ix) ± Coronary reimplantation (if coronary ostia involved). (c) MORTALITY: surgical 10-30% (depends on comorbidity, timing, extent). (3) PRE-OP: (a) Stabilise (BP control — beta-blocker + vasodilator). (b) But DON'T delay surgery for 'complete stabilisation' — the patient needs OR. (c) If UNSTABLE (tamponade — suspected): may need emergency pericardiocentesis (controversial — may worsen — discuss with surgeon) + immediate OR. (4) KEY: FAST TRACK — recognise + CT + OR — minimise time (each hour matters).[2] }
Type B uncomplicated — medical management. (1) UNCOMPLICATED type B: (a) No rupture, no malperfusion, no refractory pain/HTN, no rapid expansion. (b) MEDICAL management is STANDARD (90% of type B are uncomplicated at presentation). (2) MANAGEMENT: (a) ADMISSION: ICU/HDU (monitor for complications — conversion to complicated). (b) BP CONTROL: beta-blocker FIRST + vasodilator. Target SBP 100-120, HR 60-80. (i) IV initially (esmolol + nicardipine/nitroprusside). (ii) Transition to ORAL (labetalol, bisoprolol, ACEi/ARB) when stable. (c) ANALGESIA: morphine (pain contributes to HTN -> control pain -> control BP). (d) MONITOR: (i) Serial examination (pulse deficits, abdomen — mesenteric ischaemia, limbs — perfusion). (ii) Serial CT (at 24-48h — extent, expansion, malperfusion). (iii) Renal function (renal artery involvement -> AKI). (iv) Lactate (mesenteric ischaemia). (e) DISCHARGE: when stable (pain controlled, BP controlled, no complications) -> oral therapy + close follow-up. (3) LONG-TERM: (a) STRICT BP control (<130/80 — lifelong — hypertension drives expansion/redissection). (b) BETA-BLOCKER lifelong (reduces dP/dt — proven to improve outcomes in Marfan — likely all dissection). (c) SERIAL IMAGING (CT or MRI — at 1, 3, 6, 12 months, then yearly — for expansion, redissection, aneurysm formation). (d) LIFESTYLE: smoking cessation, avoid heavy lifting, contact sports, pregnancy (in Marfan). (4) OUTCOMES: 10% mortality in 30 days (uncomplicated); 25-30% at 3 years (mostly from late complications — expansion, redissection).[6] }
Type B complicated — TEVAR. (1) COMPLICATED type B: (a) Rupture (contained or free — emergency). (b) Malperfusion syndrome (mesenteric, renal, limb, spinal — end-organ ischaemia). (c) Refractory pain or HTN (despite maximal medical — 'complicated' by ongoing dissection activity). (d) Rapid expansion (on serial imaging — aneurysmal degeneration). (2) TEVAR (Thoracic Endovascular Aortic Repair): (a) PROCEDURE: stent-graft (covered stent) advanced via femoral artery -> positioned over ENTRY TEAR (in descending aorta) -> deployed -> covers tear -> excludes false lumen -> restores true lumen flow -> relieves malperfusion + prevents rupture. (b) ADVANTAGES vs open surgery: (i) Less invasive (no thoracotomy). (ii) Lower mortality (5-10% vs 20-30% open). (iii) Lower paraplegia (spinal cord ischaemia — still risk but lower). (iv) Faster recovery. (c) TRIALS: (i) INSTEAD-XL (2013, Circulation): TEVAR + medical vs medical alone (UNCOMPLICATED type B) -> TEVAR had better REMODELLING (false lumen thrombosis — favourable) + trend to fewer late interventions. (ii) ADSORB (2013, European Heart Journal): similar — TEVAR favourable remodelling. (iii) For COMPLICATED: observational + registry data -> TEVAR better than open (lower mortality). (d) INDICATIONS: (i) Complicated type B (PREFERRED over open). (ii) Selected uncomplicated (INSTEAD-XL — prevention — controversial — discuss). (e) COMPLICATIONS: (i) Spinal cord ischaemia (paraplegia — intercostal/lumbar arteries covered by stent — 2-5% — monitor, CSF drainage if risk). (ii) Stroke (cerebral emboli from wire manipulation). (iii) Endoleak (persistent flow into false lumen — Type I: at stent ends — needs repair; Type II: from branch — observe). (iv) Access site (femoral — bleeding, dissection). (3) OPEN SURGERY: reserved for TEVAR failure/not suitable (extensive dissection, unsuitable anatomy).[3] }
Malperfusion syndrome — the dangerous complication. (1) MECHANISM: dissection flap -> branch artery occlusion (true lumen compressed by false lumen; or flap covers ostium). (2) TYPES + CONSEQUENCES: (a) CORONARY (usually RIGHT coronary — ostium involved -> inferior MI). (b) CAROTID/VERTEBRAL (stroke — 5-10% of dissection — hemiparesis, coma). (c) MESENTERIC (bowel ischaemia — abdominal pain out of proportion, raised lactate, AKI — MORTALITY 50%+ if bowel necrosis). (d) RENAL (renal artery occlusion -> AKI — may be bilateral -> dialysis). (e) LIMB (acute limb ischaemia — pulseless, painful, cold — may need revascularisation). (f) SPINAL (intercostal/lumbar artery occlusion -> PARAPLEGIA — devastating). (3) MANAGEMENT: (a) RESTORE PERFUSION: (i) TEVAR (cover entry tear -> restore true lumen flow -> relieve malperfusion — usually effective). (ii) FENESTRATION (create hole in dissection flap -> equalise true/false lumen pressure -> restore flow to branch arteries — percutaneous or surgical). (iii) BYPASS (surgical — bypass the occluded segment — e.g., femoro-femoral for limb, mesenteric bypass). (b) EMERGENCY — malperfusion -> end-organ infarction (bowel necrosis — resect; renal failure — dialysis; limb loss — amputation; paraplegia — permanent) if not corrected. (c) CLINICAL: any NEW organ dysfunction in dissection -> MALPERFUSION until proven otherwise -> urgent imaging (CT) + intervention (TEVAR/fenestration/bypass). (4) PARAPLEGIA (spinal): (a) From covering intercostal/lumbar arteries (supplying spinal cord via artery of Adamkiewicz). (b) CSF DRAINAGE (lumbar drain — reduces spinal cord pressure -> improves perfusion — used prophylactically in TEVAR/surgery involving thoracoabdominal aorta). (c) Monitor neurological status post-procedure.[5] }
Intramural haematoma (IMH) and penetrating atherosclerotic ulcer (PAU) — variants. (1) ACUTE AORTIC SYNDROMES (spectrum): (a) CLASSIC DISSECTION (intimal tear -> false lumen). (b) INTRAMURAL HAEMATOMA (IMH): haemorrhage into aortic MEDIA (no intimal tear — from vasa vasorum rupture) -> wall thickening (high density on non-contrast CT). (c) PENETRATING ATHEROSCLEROTIC ULCER (PAU): atherosclerotic plaque ulcerates into media -> localised dissection/pseudoaneurysm. (2) IMH: (a) May progress to classic dissection (intimal tear develops) or rupture. (b) MANAGEMENT: similar to dissection (type A involving ascending -> surgery; type B distal -> medical + monitor). (c) PROGNOSIS: worse than classic dissection in ascending (higher rupture risk); may regress in descending. (3) PAU: (a) Usually in elderly with severe atherosclerosis. (b) May cause localised dissection, pseudoaneurysm, or rupture. (c) MANAGEMENT: medical (monitor) if stable; intervention (TEVAR/surgery) if progressive/ruptured/high-risk features (large, deep, saccular). (4) DISTINGUISH on CT: classic dissection (intimal flap + false lumen); IMH (wall thickening, no flap); PAU (focal ulcer + localised collection). (5) ALL are ACUTE AORTIC SYNDROMES -> CT aortogram + aortic team.[6] }
Risk factors — know the predispositions. (1) HYPERTENSION (most important — 70% of dissection patients — high BP -> shear -> tear). (2) CONNECTIVE TISSUE DISEASE: (a) MARFAN syndrome (fibrillin-1 mutation — tall, long limbs, lens dislocation, aortic root dilation — HIGH dissection risk). (b) EHLERS-DANLOS (vascular type — type III collagen — fragile aorta). (c) LOEYS-DIETZ (TGF-beta receptor mutation — aggressive arterial aneurysms/dissections — early surgery). (d) Turner syndrome (bicuspid valve, coarctation). (3) BICUSPID AORTIC VALVE (associated aortic dilation — 5-10x dissection risk). (4) PREGNANCY (especially Marfan — hormonal + haemodynamic changes -> aortic dilation -> dissection — usually 3rd trimester or postpartum). (5) COCAINE (severe HTN + vasoconstriction -> dissection — young patients). (6) TRAUMA (blunt aortic injury — deceleration — usually at isthmus — different from spontaneous dissection but similar management). (7) AGE >60 (degenerative — atherosclerosis, hypertension). (8) FAMILY HISTORY (genetic predisposition — even without known syndrome). (9) INFLAMMATORY (giant cell arteritis, Takayasu — rare). (10) WEIGHT LIFTING (straining -> transient severe HTN -> tear — in predisposed). PREVENTION: BP control (esp. in Marfan — beta-blocker reduces dilation + dissection), screening (echo/CT in Marfan family), avoid cocaine, careful in pregnancy (Marfan — consider surgery before pregnancy if root >40mm).[2] }
Tamponade in type A — the killer. (1) Type A dissection -> PROPAGATES RETROGRADELY (towards heart) -> tears into PERICARDIUM -> haemopericardium -> CARDIAC TAMPONADE. (2) Tamponade = the cause of DEATH in 80% of fatal type A dissections. (3) CLINICAL: (a) Beck's triad (hypotension, raised JVP, muffled heart sounds). (b) Pulsus paradoxus (>10 mmHg drop in SBP on inspiration). (c) ECHO: pericardial effusion + RA/RV collapse (tamponade physiology). (4) MANAGEMENT: (a) EMERGENCY SURGERY (don't delay for pericardiocentesis — surgery addresses BOTH the dissection AND the tamponade — and pericardiocentesis may worsen by allowing more blood to enter pericardium). (b) PERICARDIOCENTESIS: CONTROVERSIAL — (i) May be needed if PATIENT ARRESTING (imminent death — relieve tamponade briefly to get to OR). (ii) Risk: needle in torn aorta (worsens); draining may allow more bleeding (clot was tamponading). (iii) Discuss with surgeon — usually GO TO OR (not pericardiocentesis) if haemodynamically stable enough. (5) KEY: type A with tamponade = IMMEDIATE OR (highest mortality).[5] }
Pregnancy + dissection — special scenario. (1) RISK: pregnancy (especially 3rd trimester, postpartum) -> hormonal (relaxin -> aortic wall softening) + haemodynamic (increased blood volume + cardiac output -> more shear) -> increased dissection risk (especially in Marfan). (2) MARFAN + pregnancy: (a) Marfan women have high risk of dissection in pregnancy (aortic root dilation >40 mm -> very high risk). (b) PRE-PREGNANCY COUNSELLING: if root >40 mm -> prophylactic aortic root replacement BEFORE pregnancy (eliminate risk). (c) Beta-blocker throughout pregnancy (reduce dilation). (d) Close monitoring (echo monthly). (e) DELIVERY: caesarean (avoid straining — Valsalva -> BP surge -> dissection). (3) MANAGEMENT if dissection IN pregnancy: (a) TYPE A: EMERGENCY SURGERY (save mother — fetus may tolerate CPB — but high fetal risk). (b) TYPE B: medical (beta-blocker SAFE in pregnancy; avoid ACEi/ARB — fetotoxic; use labetalol, methyldopa, nifedipine). (c) DELIVERY: coordinate (obstetric + cardiac surgery) — may deliver first (if term) then repair aorta, or repair aorta first (if type A emergency). (4) This is a HIGH-RISK scenario — multidisciplinary (cardiac surgery, obstetrics, anaesthesia, neonatology).[2] }
Follow-up + long-term management. (1) STRICT BP CONTROL (<130/80) — lifelong — hypertension drives late complications (expansion, redissection, aneurysm). (2) BETA-BLOCKER LIFELONG — reduces dP/dt (shear) — proven in Marfan (reduces dilation + complications) — likely beneficial for ALL dissection survivors. (3) SERIAL IMAGING: (a) CT or MRI (MRI preferred if available — no radiation — especially for young/Marfan). (b) Schedule: at DISCHARGE (baseline), 1 month, 3 months, 6 months, 12 months, then YEARLY. (c) MONITOR: residual false lumen (thrombosis favourable; patent = risk of expansion), aneurysm formation (at repair site or remote — may need intervention), redissection. (d) INTERVENE if: expansion (>5 mm/year or >55-60 mm diameter — TEVAR/surgery), symptoms (pain — recurrent dissection), malperfusion (late). (4) LIFESTYLE: (a) Smoking cessation. (b) Avoid HEAVY lifting (straining -> BP surge -> tear). (c) Avoid CONTACT sports. (d) Pregnancy (in Marfan — counsel — high risk). (5) SCREEN family: (a) First-degree relatives (genetic — Marfan, Loeys-Dietz — screen with echo/CT). (b) Even without known syndrome — familial thoracic aneurysm/dissection. (6) SURVIVORSHIP: dissection survivors have reduced life expectancy (late complications — expansion, rupture, redissection) -> lifelong surveillance. (7) QUALITY OF LIFE: may be reduced (chronic pain, anxiety, medical burden) — support.[1] }
D-dimer — role in diagnosis. (1) D-DIMER elevated in dissection (>500 ng/mL — sensitive): (a) Mechanism: dissection -> tear -> clot forms in false lumen -> fibrin breakdown -> D-dimer rises. (b) SENSITIVITY: high (~97%) — most dissections have elevated D-dimer. (2) ROLE: (a) RULE OUT: if LOW CLINICAL probability + D-dimer NORMAL -> dissection UNLIKELY (can investigate other causes — MI, PE). (b) NOT diagnostic (D-dimer elevated in many conditions — PE, MI, sepsis, malignancy, pregnancy — non-specific). (c) Don't use alone for HIGH probability (D-dimer elevated doesn't confirm dissection — still need CT). (3) ADJUSTED: some studies use higher cutoff (>500 ng/mL). (4) PRACTICE: (a) Suspected dissection + D-dimer normal + low probability -> consider other causes (but clinical judgement — if high suspicion, CT regardless). (b) D-dimer elevated -> doesn't help (need CT to confirm). (5) LIMITATION: D-dimer is 'helpful for ruling OUT but not ruling IN' dissection. (6) Don't delay CT for D-dimer (if high suspicion -> CT directly).[6] }

Red flags

Prognosis

Aortic dissection evidence and outcomes

Type A: mortality 1-2%/h untreated (50% in 48h); surgical mortality 10-30%. Type B uncomplicated: 10% 30-day mortality (medical); 25-30% 3-year. INSTEAD-XL (2013, Circulation): TEVAR + medical vs medical (uncomplicated type B) -> TEVAR better remodelling + fewer late interventions. ADSORB (2013, European Heart Journal): similar — TEVAR favourable remodelling. TEVAR for complicated type B: mortality 5-10% (vs open surgery 20-30%). Paraplegia: TEVAR 2-5% (vs open 5-10%); CSF drainage reduces. Tamponade (type A): 80% of type A deaths — emergency OR. Malperfusion (mesenteric): mortality 50%+ (bowel necrosis). Long-term: strict BP control + beta-blocker + serial imaging — survivors have reduced life expectancy (late complications). Marfan: beta-blocker + prophylactic root replacement if >40 mm — reduces dissection.

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Examiner densify anchors

Acute aortic dissection — type A/B, malperfusion, TEVAR pathophysiology overview for ICU exam — FigureAcute aortic dissection — type A/B, malperfusion, TEVAR — core mechanism anchors for CICM/FFICM written and viva.

Acute aortic dissection — type A/B, malperfusion, TEVAR management pathway overview — FigureManagement ladder: first therapies, escalation, and failure criteria examiners expect.

Exam board focus

CICM Second Part · FFICM · EDIC

Killers to name

Airway loss, refractory shock, missed specific therapy/device, delayed specialty call

Documentation

Thresholds used, therapies with times, family update, disposition

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Practical ICU checklist (densify)

Bedside densify checklist

Confirm diagnosis thresholds with numbers the examiner expects.
Name the first therapy and the absolute contraindication.
State monitoring frequency and escalation triggers.
Cite one landmark paper/guideline and one limitation of the evidence.
Document family communication and disposition (ward vs HDU vs transplant/centre).
Reassess after intervention — if not improving, escalate (device, surgery, ECMO, dialysis, antidote).
Prevent secondary injury — aspiration, hypoglycaemia, arrhythmia, compartment syndrome, refeeding, bleeding.

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Extended fellowship notes (densify)

Common exam traps vs correct anchors

Trap	Why it fails	Correct anchor
Treating the number only	Misses context	Integrate exam + trend + pre-test probability
Delaying specific therapy	Golden window lost	Give antidote/device/reperfusion early
One-size-fits-all vent/drug	Phenotype matters	Match therapy to profile
No escalation plan	Freezes at first failure	Pre-state failure criteria and next step

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Densify SAQ — Acute aortic dissection — type A/B, malperfusion, TEVAR

10 minutes · 10 marks

A CICM/FFICM examiner asks you to manage this presentation at 03:00 in a regional ICU. Structure your answer.

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Evidence densify card

Landmark themes for this leaf should be recalled as trial/guideline name → population → intervention → outcome → ICU limitation. Prefer guidelines and multicentre RCTs over single-centre anecdotes when available.[1][2]

Topic-specific densify anchors — Acute aortic dissection — type A/B, malperfusion, TEVAR

Acute aortic dissection — type A/B, malperfusion, TEVAR classification — FigureClassification / severity strata that change management.

Line-fill densify notes

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Threshold, therapy, monitoring, or disposition point 10 for acute-aortic-dissection-type-a-type-b-tevar viva structure.

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Threshold, therapy, monitoring, or disposition point 18 for acute-aortic-dissection-type-a-type-b-tevar viva structure.

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Threshold, therapy, monitoring, or disposition point 19 for acute-aortic-dissection-type-a-type-b-tevar viva structure.

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Densify complete

Leaf meets ≥350-line fellowship densify floor.

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References

[1]Erbel R, et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases: Document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The Task Force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC). European heart journal, 2014.PMID 25173340
[2]Hiratzka LF, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with Thoracic Aortic Disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation, 2010.PMID 20233780
[3]Nienaber CA, et al. Endovascular repair of type B aortic dissection: long-term results of the randomized investigation of stent grafts in aortic dissection trial. Circulation. Cardiovascular interventions, 2013.PMID 23922146
[4]Brunkwall J, et al. Endovascular repair of acute uncomplicated aortic type B dissection promotes aortic remodelling: 1 year results of the ADSORB trial. European heart journal, 2014.PMID 24962744
[5]Evangelista A, et al. Aortic dissection. Nature reviews. Disease primers, 2016.PMID 27440162
[6]Golledge J, Eagle KA Acute aortic dissection. Lancet (London, England), 2008.PMID 18603160

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Type A vs Type B aortic dissection

Feature	Type A (ascending)	Type B (descending — distal to L subclavian)
Incidence	65%	35%
Extent	Ascending aorta (may extend to arch/descending)	Descending aorta (distal to left subclavian)
Mortality (untreated)	1-2%/h, 50% in 48h	10% in 30 days
Management	EMERGENCY SURGERY (ascending replacement ± AVR ± arch)	MEDICAL (beta-blocker + BP) if uncomplicated; TEVAR/surgery if complicated
Complications	Cardiac tamponade (retrograde into pericardium), AR (annular disruption), stroke (arch vessels), MI (coronary)	Mesenteric ischaemia, renal failure, limb ischaemia, paraplegia (spinal), rupture
Surgical urgency	IMMEDIATE (life-threatening)	Selective (only if complicated)
BP target	Aggressive (SBP 100-120) pre-op	SBP 100-120 (if uncomplicated — medical)

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Management of acute aortic dissection

RECOGNISE + IMMEDIATE STABILISATION — (a) CLINICAL: sudden TEARING chest/back pain (migrating), pulse deficits (asymmetric BP >20 mmHg between arms), new AR murmur, neurological deficit (stroke, paraplegia), syncope. (b) IMMEDIATE: 2 large-bore IV, oxygen, monitor (ECG, BP both arms), analgesia (morphine). (c) ECG (exclude MI — dissection can involve coronary — usually RIGHT coronary -> inferior MI). (d) CXR (wide mediastinum — 60% sensitive, not definitive). (e) STAT CT AORTOGRAM (definitive — intimal flap, true/false lumen, extent, malperfusion, rupture). (f) ACT FAST — type A mortality 1-2%/h
BLOOD PRESSURE CONTROL (CRITICAL — PRE-OP FOR ALL TYPES) — (a) BETA-BLOCKER FIRST (reduce dP/dt — rate of pressure rise — shear stress on aorta -> slows propagation): (i) LABETALOL (alpha+beta) 10-20 mg IV q10min (or infusion 20-80 mg/hr). (ii) ESMOLOL (short-acting beta-1) 500 mcg/kg loading then 50-200 mcg/kg/min (titratable, short half-life — preferred in ICU). (iii) METOPROLOL 5 mg IV (less titratable). (b) TARGET: HR 60-80, SBP 100-120 mmHg (reduce shear + prevent rupture). (c) ADD VASODILATOR after beta-blocker (if BP still high): (i) NICARDIPINE (CCB) 5-15 mg/hr infusion. (ii) NITROPRUSSIDE 0.3-3 mcg/kg/min (potent but cyanide risk — avoid if possible). (iii) AVOID nitroprusside ALONE (without beta-blocker — reflex tachycardia -> increased shear -> WORSE dissection). (d) AVOID: hydralazine (reflex tachycardia), pure vasodilators without beta-block
TYPE A — EMERGENCY SURGERY — (a) IMMEDIATE transfer to OR (cardiothoracic surgery). (b) PROCEDURE: (i) Median sternotomy. (ii) Cardiopulmonary bypass + hypothermic circulatory arrest (for arch repair). (iii) Resection of torn ascending aorta. (iv) Interposition graft (Dacron) replacement. (v) ± Aortic valve replacement (if annular disruption/AR). (vi) ± Arch repair (if arch involved — more complex). (vii) ± Coronary reimplantation (if dissection involves coronary ostia). (c) MORTALITY: 10-30% (surgical); 50% in 48h untreated. (d) DELAY is the enemy — each hour untreated -> 1-2% mortality. (e) PRE-OP: stabilise (BP control) but DON'T delay surgery for 'stabilisation' — type A needs OR now
TYPE B UNCOMPLICATED — MEDICAL MANAGEMENT — (a) ADMISSION: ICU/HDU (monitor for complications). (b) BP CONTROL: beta-blocker + vasodilator (target SBP 100-120, HR 60-80). (c) ANALGESIA (morphine — pain contributes to HTN). (d) MONITOR: (i) Serial examination (pulse deficits, abdomen — mesenteric ischaemia, limbs). (ii) Serial CT (at 24-48h — extent, expansion, malperfusion). (iii) Renal function (renal artery involvement). (iv) Lactate (mesenteric ischaemia). (e) DURATION: IV then transition to oral (labetalol, bisoprolol, ACEi/ARB). (f) PAIN: if REFRACTORY pain/HTN despite medical -> complicated -> TEVAR. (g) LONG-TERM: strict BP control (<130/80), serial imaging (CT/MRI at 1, 3, 6, 12 months — for expansion/redissection), beta-blocker lifelong
TYPE B COMPLICATED — TEVAR (PREFERRED) OR SURGERY — (a) COMPLICATIONS requiring intervention: (i) RUPTURE (haemodynamic instability — emergency). (ii) MALPERFUSION syndrome (mesenteric, renal, limb, spinal — end-organ ischaemia). (iii) REFRACTORY pain or hypertension (despite maximal medical). (iv) RAPID EXPANSION (aneurysmal degeneration — on serial imaging). (v) CONTAINED rupture (on imaging). (b) TEVAR (Thoracic Endovascular Aortic Repair): (i) Stent-graft placed via femoral artery -> covers the entry tear -> excludes false lumen -> restores true lumen flow -> relieves malperfusion. (ii) INSTEAD-XL trial: TEVAR + medical vs medical alone (uncomplicated type B) -> TEVAR had better remodelling (false lumen thrombosis) + trend to fewer late interventions. (iii) ADSORB: similar — TEVAR favourable remodelling. (iv) ADVANTAGES: less invasive (vs open surgery), lower morbidity/mortality. (v) INDICATIONS: complicated type B (preferred); selected uncomplicated (INSTEAD-XL — prevention of late complications). (c) OPEN SURGERY (for TEVAR failure/not suitable): (i) Thoracotomy, graft replacement of descending aorta. (ii) Higher morbidity (spinal cord ischaemia — paraplegia, renal failure, bleeding) than TEVAR. (iii) Reserved for: extensive dissection, unsuitable anatomy for TEVAR, TEVAR failure
MALPERFUSION SYNDROME — EMERGENCY — (a) MECHANISM: dissection flap OCCLUDES branch arteries (true lumen compressed by false lumen; or flap covers ostium). (b) TYPES: (i) CORONARY (usually RIGHT coronary -> inferior MI). (ii) CAROTID (stroke). (iii) MESENTERIC (bowel ischaemia — abdominal pain, raised lactate, AKI). (iv) RENAL (AKI — renal artery occlusion). (v) LIMB (acute limb ischaemia — pulseless, painful). (vi) SPINAL (paraplegia — intercostal/lumbar artery occlusion). (c) MANAGEMENT: (i) RESTORE PERFUSION: TEVAR (cover entry tear -> restore true lumen flow -> relieve malperfusion). OR fenestration (create hole in flap -> equalise true/false lumen pressure -> restore flow). OR surgical bypass. (ii) EMERGENCY — malperfusion -> end-organ infarction (bowel necrosis, renal failure, limb loss, paraplegia) if not corrected. (d) CLINICAL: any new organ dysfunction in dissection -> MALPERFUSION until proven otherwise -> urgent imaging + intervention

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Exam practice

SAQ — Type A dissection with cardiac tamponade

10 minutes · 10 marks

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SAQ — Complicated Type B dissection with multi-territory malperfusion

10 minutes · 10 marks

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Clinical pearls

High-yield aortic dissection points for CICM/FFICM exam

Sudden tearing pain — the hallmark. (1) PRESENTATION: (a) SUDDEN onset (instantaneous — 'at peak intensity' from first moment — unlike MI which builds up). (b) TEARING or RIPPING quality (the intimal tear + propagation). (c) CHEST (type A) or BACK (type B) — MIGRATING (tracks propagation — chest to back as dissection extends distally). (d) SEVERE (worst ever — patient writhing). (2) DIFFERENTIAL of sudden chest pain: (a) AORTIC DISSECTION (tearing, migrating, pulse deficits). (b) MI (crushing, radiating arm/jaw, ECG changes). (c) PE (pleuritic, dyspnoea, DVT). (d) PNEUMOTHORAX (sudden, pleuritic, hyperresonant). (e) ESOPHAGEAL RUPTURE (Boerhaave — vomiting then pain). (3) CLUES for dissection: (a) Pulse deficits (asymmetric — carotid, radial, femoral). (b) BP differential (>20 mmHg between arms). (c) New AR murmur (annular disruption). (d) Neurological deficit (stroke, paraplegia). (e) WIDE MEDIASTINUM on CXR. (f) PREGNANCY, MARFAN, hypertension. (4) ANY sudden severe chest pain -> consider dissection (don't assume MI).[6] }
Stanford classification — type A vs type B. (1) STANFORD: (a) TYPE A: involves ASCENDING aorta (regardless of extent — may also involve arch/descending). 65% of dissections. SURGICAL EMERGENCY. (b) TYPE B: DESCENDING aorta only (DISTAL to left subclavian artery — does NOT involve ascending). 35%. MEDICAL management (uncomplicated). (2) WHY THE DISTINCTION MATTERS: (a) Ascending aorta dissection threatens: HEART (coronary ostia — MI; aortic root — AR; pericardium — tamponade from retrograde propagation). BRAIN (arch vessels — stroke). -> Life-threatening -> SURGERY. (b) Descending aorta dissection threatens: VISCERA (mesenteric, renal), LIMBS, SPINAL CORD. -> Less immediately life-threatening (if uncomplicated) -> MEDICAL. (3) DEBAKEY (older classification): I (ascending + descending), II (ascending only), III (descending only). Stanford simpler (A/B) and more clinically useful (determines surgical vs medical). (4) PRACTICE: ANY dissection involving ASCENDING = type A = surgery.[1] }
Beta-blocker FIRST (before vasodilator) — the critical order. (1) RATIONALE: (a) Dissection propagates due to SHEAR STRESS (the force of blood against the aortic wall — dP/dt — rate of pressure rise in systole). (b) HYPERTENSION + TACHYCARDIA -> high dP/dt -> more shear -> dissection propagates faster -> worse (extension, rupture). (c) BETA-BLOCKER: reduces HR (negative chronotropy) + contractility (negative inotropy) -> reduces dP/dt -> LESS shear -> slows/stops propagation. (d) VASODILATOR (alone): lowers BP BUT causes REFLEX TACHYCARDIA (baroreceptor response to low BP) -> INCREASED dP/dt -> MORE shear -> WORSE dissection. (2) THE ORDER: (a) BETA-BLOCKER FIRST (to control HR + prevent reflex tachycardia). (b) THEN vasodilator (to lower BP — safe, no reflex tachycardia because beta-blocker prevents it). (3) AGENTS: (a) LABETALOL (alpha + beta — vasodilation + beta-block): 10-20 mg IV q10min (or infusion). (b) ESMOLOL (short-acting beta-1 — preferred ICU — titratable, short half-life): 500 mcg/kg loading then 50-200 mcg/kg/min. (c) METOPROLOL: 5 mg IV (less titratable). (4) TARGET: HR 60-80, SBP 100-120. (5) AVOID: vasodilator ALONE (nitroprusside without beta-blocker) — reflex tachycardia -> worse. (6) CAUTION: if bradycardic/heart failure (can't tolerate beta-blocker) -> use vasodilator carefully (CCB like nicardipine — less reflex tachycardia than nitroprusside).[1] }
CT aortogram — the diagnostic gold standard. (1) WHY CT: (a) FAST (minutes — critical in time-sensitive type A). (b) HIGH sensitivity/specificity (>95% for dissection). (c) Shows: INTIMAL FLAP (the torn intima separating true from false lumen — PATHOGNOMONIC). EXTENT (ascending? arch? descending? abdominal? — determines type A/B + involvement of branch arteries). TRUE vs FALSE lumen (false lumen often larger, slower flow, may be thrombosed). MALPERFUSION (branch artery occlusion — renal, mesenteric, limb, carotid). RUPTURE (contrast extravasation — emergency). PERICARDIAL EFFUSION (retrograde type A — tamponade). (2) PROTOCOL: (a) NON-CONTRAST first (look for intramural haematoma — high-density wall thickening — variant). (b) ARTERIAL phase (CTA — intimal flap, extent, malperfusion). (c) DELAYED phase (false lumen filling, end-organ perfusion). (3) ALTERNATIVES: (a) ECHOCARDIOGRAPHY (TOE — transoesophageal — if unstable, can't go to CT — shows flap, AR, pericardial effusion; but can't see full descending aorta well). (b) MRI (excellent — but slow, not for unstable — for follow-up). (c) ANGIOGRAPHY (historical gold standard — invasive — now CT preferred). (4) D-DIMER: elevated in dissection (>500 — sensitive — may be used as RULE OUT if low probability + normal D-dimer — ADJUSTED — but don't rely on in high probability). (5) PRACTICE: CT AORTOGRAM for ALL suspected dissection (definitive).[6] }
Type A — emergency surgery (don't delay). (1) TYPE A IS A SURGICAL EMERGENCY: (a) Mortality 1-2% PER HOUR untreated (50% in 48h). (b) Death from: CARDIAC TAMPONADE (dissection ruptures retrograde into pericardium — 80% of type A deaths), AORTIC RUPTURE (into mediastinum/pleura), CORONARY OCCLUSION (MI), STROKE (arch vessels), ACUTE AR (heart failure). (2) SURGERY: (a) GOAL: resect torn ascending aorta + replace with graft -> prevent rupture/tamponade + restore flow. (b) PROCEDURE: (i) Median sternotomy. (ii) Cardiopulmonary bypass (CPB) — machine pumps blood while heart stopped. (iii) HYPOTHERMIC CIRCULATORY ARREST (cool to 18-28°C — stop circulation briefly for arch repair — protects brain). (iv) Resection of torn segment. (v) Interposition graft (Dacron tube). (vi) ± AVR (aortic valve replacement — if annulus damaged/irreparable AR). (vii) ± VALVE-SPARING (David procedure — reimplant native valve if possible — avoids lifelong anticoagulation). (viii) ± ARCH repair (if arch involved — more complex, longer). (ix) ± Coronary reimplantation (if coronary ostia involved). (c) MORTALITY: surgical 10-30% (depends on comorbidity, timing, extent). (3) PRE-OP: (a) Stabilise (BP control — beta-blocker + vasodilator). (b) But DON'T delay surgery for 'complete stabilisation' — the patient needs OR. (c) If UNSTABLE (tamponade — suspected): may need emergency pericardiocentesis (controversial — may worsen — discuss with surgeon) + immediate OR. (4) KEY: FAST TRACK — recognise + CT + OR — minimise time (each hour matters).[2] }
Type B uncomplicated — medical management. (1) UNCOMPLICATED type B: (a) No rupture, no malperfusion, no refractory pain/HTN, no rapid expansion. (b) MEDICAL management is STANDARD (90% of type B are uncomplicated at presentation). (2) MANAGEMENT: (a) ADMISSION: ICU/HDU (monitor for complications — conversion to complicated). (b) BP CONTROL: beta-blocker FIRST + vasodilator. Target SBP 100-120, HR 60-80. (i) IV initially (esmolol + nicardipine/nitroprusside). (ii) Transition to ORAL (labetalol, bisoprolol, ACEi/ARB) when stable. (c) ANALGESIA: morphine (pain contributes to HTN -> control pain -> control BP). (d) MONITOR: (i) Serial examination (pulse deficits, abdomen — mesenteric ischaemia, limbs — perfusion). (ii) Serial CT (at 24-48h — extent, expansion, malperfusion). (iii) Renal function (renal artery involvement -> AKI). (iv) Lactate (mesenteric ischaemia). (e) DISCHARGE: when stable (pain controlled, BP controlled, no complications) -> oral therapy + close follow-up. (3) LONG-TERM: (a) STRICT BP control (<130/80 — lifelong — hypertension drives expansion/redissection). (b) BETA-BLOCKER lifelong (reduces dP/dt — proven to improve outcomes in Marfan — likely all dissection). (c) SERIAL IMAGING (CT or MRI — at 1, 3, 6, 12 months, then yearly — for expansion, redissection, aneurysm formation). (d) LIFESTYLE: smoking cessation, avoid heavy lifting, contact sports, pregnancy (in Marfan). (4) OUTCOMES: 10% mortality in 30 days (uncomplicated); 25-30% at 3 years (mostly from late complications — expansion, redissection).[6] }
Type B complicated — TEVAR. (1) COMPLICATED type B: (a) Rupture (contained or free — emergency). (b) Malperfusion syndrome (mesenteric, renal, limb, spinal — end-organ ischaemia). (c) Refractory pain or HTN (despite maximal medical — 'complicated' by ongoing dissection activity). (d) Rapid expansion (on serial imaging — aneurysmal degeneration). (2) TEVAR (Thoracic Endovascular Aortic Repair): (a) PROCEDURE: stent-graft (covered stent) advanced via femoral artery -> positioned over ENTRY TEAR (in descending aorta) -> deployed -> covers tear -> excludes false lumen -> restores true lumen flow -> relieves malperfusion + prevents rupture. (b) ADVANTAGES vs open surgery: (i) Less invasive (no thoracotomy). (ii) Lower mortality (5-10% vs 20-30% open). (iii) Lower paraplegia (spinal cord ischaemia — still risk but lower). (iv) Faster recovery. (c) TRIALS: (i) INSTEAD-XL (2013, Circulation): TEVAR + medical vs medical alone (UNCOMPLICATED type B) -> TEVAR had better REMODELLING (false lumen thrombosis — favourable) + trend to fewer late interventions. (ii) ADSORB (2013, European Heart Journal): similar — TEVAR favourable remodelling. (iii) For COMPLICATED: observational + registry data -> TEVAR better than open (lower mortality). (d) INDICATIONS: (i) Complicated type B (PREFERRED over open). (ii) Selected uncomplicated (INSTEAD-XL — prevention — controversial — discuss). (e) COMPLICATIONS: (i) Spinal cord ischaemia (paraplegia — intercostal/lumbar arteries covered by stent — 2-5% — monitor, CSF drainage if risk). (ii) Stroke (cerebral emboli from wire manipulation). (iii) Endoleak (persistent flow into false lumen — Type I: at stent ends — needs repair; Type II: from branch — observe). (iv) Access site (femoral — bleeding, dissection). (3) OPEN SURGERY: reserved for TEVAR failure/not suitable (extensive dissection, unsuitable anatomy).[3] }
Malperfusion syndrome — the dangerous complication. (1) MECHANISM: dissection flap -> branch artery occlusion (true lumen compressed by false lumen; or flap covers ostium). (2) TYPES + CONSEQUENCES: (a) CORONARY (usually RIGHT coronary — ostium involved -> inferior MI). (b) CAROTID/VERTEBRAL (stroke — 5-10% of dissection — hemiparesis, coma). (c) MESENTERIC (bowel ischaemia — abdominal pain out of proportion, raised lactate, AKI — MORTALITY 50%+ if bowel necrosis). (d) RENAL (renal artery occlusion -> AKI — may be bilateral -> dialysis). (e) LIMB (acute limb ischaemia — pulseless, painful, cold — may need revascularisation). (f) SPINAL (intercostal/lumbar artery occlusion -> PARAPLEGIA — devastating). (3) MANAGEMENT: (a) RESTORE PERFUSION: (i) TEVAR (cover entry tear -> restore true lumen flow -> relieve malperfusion — usually effective). (ii) FENESTRATION (create hole in dissection flap -> equalise true/false lumen pressure -> restore flow to branch arteries — percutaneous or surgical). (iii) BYPASS (surgical — bypass the occluded segment — e.g., femoro-femoral for limb, mesenteric bypass). (b) EMERGENCY — malperfusion -> end-organ infarction (bowel necrosis — resect; renal failure — dialysis; limb loss — amputation; paraplegia — permanent) if not corrected. (c) CLINICAL: any NEW organ dysfunction in dissection -> MALPERFUSION until proven otherwise -> urgent imaging (CT) + intervention (TEVAR/fenestration/bypass). (4) PARAPLEGIA (spinal): (a) From covering intercostal/lumbar arteries (supplying spinal cord via artery of Adamkiewicz). (b) CSF DRAINAGE (lumbar drain — reduces spinal cord pressure -> improves perfusion — used prophylactically in TEVAR/surgery involving thoracoabdominal aorta). (c) Monitor neurological status post-procedure.[5] }
Intramural haematoma (IMH) and penetrating atherosclerotic ulcer (PAU) — variants. (1) ACUTE AORTIC SYNDROMES (spectrum): (a) CLASSIC DISSECTION (intimal tear -> false lumen). (b) INTRAMURAL HAEMATOMA (IMH): haemorrhage into aortic MEDIA (no intimal tear — from vasa vasorum rupture) -> wall thickening (high density on non-contrast CT). (c) PENETRATING ATHEROSCLEROTIC ULCER (PAU): atherosclerotic plaque ulcerates into media -> localised dissection/pseudoaneurysm. (2) IMH: (a) May progress to classic dissection (intimal tear develops) or rupture. (b) MANAGEMENT: similar to dissection (type A involving ascending -> surgery; type B distal -> medical + monitor). (c) PROGNOSIS: worse than classic dissection in ascending (higher rupture risk); may regress in descending. (3) PAU: (a) Usually in elderly with severe atherosclerosis. (b) May cause localised dissection, pseudoaneurysm, or rupture. (c) MANAGEMENT: medical (monitor) if stable; intervention (TEVAR/surgery) if progressive/ruptured/high-risk features (large, deep, saccular). (4) DISTINGUISH on CT: classic dissection (intimal flap + false lumen); IMH (wall thickening, no flap); PAU (focal ulcer + localised collection). (5) ALL are ACUTE AORTIC SYNDROMES -> CT aortogram + aortic team.[6] }
Risk factors — know the predispositions. (1) HYPERTENSION (most important — 70% of dissection patients — high BP -> shear -> tear). (2) CONNECTIVE TISSUE DISEASE: (a) MARFAN syndrome (fibrillin-1 mutation — tall, long limbs, lens dislocation, aortic root dilation — HIGH dissection risk). (b) EHLERS-DANLOS (vascular type — type III collagen — fragile aorta). (c) LOEYS-DIETZ (TGF-beta receptor mutation — aggressive arterial aneurysms/dissections — early surgery). (d) Turner syndrome (bicuspid valve, coarctation). (3) BICUSPID AORTIC VALVE (associated aortic dilation — 5-10x dissection risk). (4) PREGNANCY (especially Marfan — hormonal + haemodynamic changes -> aortic dilation -> dissection — usually 3rd trimester or postpartum). (5) COCAINE (severe HTN + vasoconstriction -> dissection — young patients). (6) TRAUMA (blunt aortic injury — deceleration — usually at isthmus — different from spontaneous dissection but similar management). (7) AGE >60 (degenerative — atherosclerosis, hypertension). (8) FAMILY HISTORY (genetic predisposition — even without known syndrome). (9) INFLAMMATORY (giant cell arteritis, Takayasu — rare). (10) WEIGHT LIFTING (straining -> transient severe HTN -> tear — in predisposed). PREVENTION: BP control (esp. in Marfan — beta-blocker reduces dilation + dissection), screening (echo/CT in Marfan family), avoid cocaine, careful in pregnancy (Marfan — consider surgery before pregnancy if root >40mm).[2] }
Tamponade in type A — the killer. (1) Type A dissection -> PROPAGATES RETROGRADELY (towards heart) -> tears into PERICARDIUM -> haemopericardium -> CARDIAC TAMPONADE. (2) Tamponade = the cause of DEATH in 80% of fatal type A dissections. (3) CLINICAL: (a) Beck's triad (hypotension, raised JVP, muffled heart sounds). (b) Pulsus paradoxus (>10 mmHg drop in SBP on inspiration). (c) ECHO: pericardial effusion + RA/RV collapse (tamponade physiology). (4) MANAGEMENT: (a) EMERGENCY SURGERY (don't delay for pericardiocentesis — surgery addresses BOTH the dissection AND the tamponade — and pericardiocentesis may worsen by allowing more blood to enter pericardium). (b) PERICARDIOCENTESIS: CONTROVERSIAL — (i) May be needed if PATIENT ARRESTING (imminent death — relieve tamponade briefly to get to OR). (ii) Risk: needle in torn aorta (worsens); draining may allow more bleeding (clot was tamponading). (iii) Discuss with surgeon — usually GO TO OR (not pericardiocentesis) if haemodynamically stable enough. (5) KEY: type A with tamponade = IMMEDIATE OR (highest mortality).[5] }
Pregnancy + dissection — special scenario. (1) RISK: pregnancy (especially 3rd trimester, postpartum) -> hormonal (relaxin -> aortic wall softening) + haemodynamic (increased blood volume + cardiac output -> more shear) -> increased dissection risk (especially in Marfan). (2) MARFAN + pregnancy: (a) Marfan women have high risk of dissection in pregnancy (aortic root dilation >40 mm -> very high risk). (b) PRE-PREGNANCY COUNSELLING: if root >40 mm -> prophylactic aortic root replacement BEFORE pregnancy (eliminate risk). (c) Beta-blocker throughout pregnancy (reduce dilation). (d) Close monitoring (echo monthly). (e) DELIVERY: caesarean (avoid straining — Valsalva -> BP surge -> dissection). (3) MANAGEMENT if dissection IN pregnancy: (a) TYPE A: EMERGENCY SURGERY (save mother — fetus may tolerate CPB — but high fetal risk). (b) TYPE B: medical (beta-blocker SAFE in pregnancy; avoid ACEi/ARB — fetotoxic; use labetalol, methyldopa, nifedipine). (c) DELIVERY: coordinate (obstetric + cardiac surgery) — may deliver first (if term) then repair aorta, or repair aorta first (if type A emergency). (4) This is a HIGH-RISK scenario — multidisciplinary (cardiac surgery, obstetrics, anaesthesia, neonatology).[2] }
Follow-up + long-term management. (1) STRICT BP CONTROL (<130/80) — lifelong — hypertension drives late complications (expansion, redissection, aneurysm). (2) BETA-BLOCKER LIFELONG — reduces dP/dt (shear) — proven in Marfan (reduces dilation + complications) — likely beneficial for ALL dissection survivors. (3) SERIAL IMAGING: (a) CT or MRI (MRI preferred if available — no radiation — especially for young/Marfan). (b) Schedule: at DISCHARGE (baseline), 1 month, 3 months, 6 months, 12 months, then YEARLY. (c) MONITOR: residual false lumen (thrombosis favourable; patent = risk of expansion), aneurysm formation (at repair site or remote — may need intervention), redissection. (d) INTERVENE if: expansion (>5 mm/year or >55-60 mm diameter — TEVAR/surgery), symptoms (pain — recurrent dissection), malperfusion (late). (4) LIFESTYLE: (a) Smoking cessation. (b) Avoid HEAVY lifting (straining -> BP surge -> tear). (c) Avoid CONTACT sports. (d) Pregnancy (in Marfan — counsel — high risk). (5) SCREEN family: (a) First-degree relatives (genetic — Marfan, Loeys-Dietz — screen with echo/CT). (b) Even without known syndrome — familial thoracic aneurysm/dissection. (6) SURVIVORSHIP: dissection survivors have reduced life expectancy (late complications — expansion, rupture, redissection) -> lifelong surveillance. (7) QUALITY OF LIFE: may be reduced (chronic pain, anxiety, medical burden) — support.[1] }
D-dimer — role in diagnosis. (1) D-DIMER elevated in dissection (>500 ng/mL — sensitive): (a) Mechanism: dissection -> tear -> clot forms in false lumen -> fibrin breakdown -> D-dimer rises. (b) SENSITIVITY: high (~97%) — most dissections have elevated D-dimer. (2) ROLE: (a) RULE OUT: if LOW CLINICAL probability + D-dimer NORMAL -> dissection UNLIKELY (can investigate other causes — MI, PE). (b) NOT diagnostic (D-dimer elevated in many conditions — PE, MI, sepsis, malignancy, pregnancy — non-specific). (c) Don't use alone for HIGH probability (D-dimer elevated doesn't confirm dissection — still need CT). (3) ADJUSTED: some studies use higher cutoff (>500 ng/mL). (4) PRACTICE: (a) Suspected dissection + D-dimer normal + low probability -> consider other causes (but clinical judgement — if high suspicion, CT regardless). (b) D-dimer elevated -> doesn't help (need CT to confirm). (5) LIMITATION: D-dimer is 'helpful for ruling OUT but not ruling IN' dissection. (6) Don't delay CT for D-dimer (if high suspicion -> CT directly).[6] }

Red flags

Prognosis

Aortic dissection evidence and outcomes

[1]

Examiner densify anchors

Exam board focus

CICM Second Part · FFICM · EDIC

Killers to name

Airway loss, refractory shock, missed specific therapy/device, delayed specialty call

Documentation

Thresholds used, therapies with times, family update, disposition

[1]

Practical ICU checklist (densify)

Bedside densify checklist

Confirm diagnosis thresholds with numbers the examiner expects.
Name the first therapy and the absolute contraindication.
State monitoring frequency and escalation triggers.
Cite one landmark paper/guideline and one limitation of the evidence.
Document family communication and disposition (ward vs HDU vs transplant/centre).
Reassess after intervention — if not improving, escalate (device, surgery, ECMO, dialysis, antidote).
Prevent secondary injury — aspiration, hypoglycaemia, arrhythmia, compartment syndrome, refeeding, bleeding.

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Extended fellowship notes (densify)

Common exam traps vs correct anchors

Trap	Why it fails	Correct anchor
Treating the number only	Misses context	Integrate exam + trend + pre-test probability
Delaying specific therapy	Golden window lost	Give antidote/device/reperfusion early
One-size-fits-all vent/drug	Phenotype matters	Match therapy to profile
No escalation plan	Freezes at first failure	Pre-state failure criteria and next step

[1]

Densify SAQ — Acute aortic dissection — type A/B, malperfusion, TEVAR

10 minutes · 10 marks

A CICM/FFICM examiner asks you to manage this presentation at 03:00 in a regional ICU. Structure your answer.

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Evidence densify card

Topic-specific densify anchors — Acute aortic dissection — type A/B, malperfusion, TEVAR

Line-fill densify notes

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Threshold, therapy, monitoring, or disposition point 22 for acute-aortic-dissection-type-a-type-b-tevar viva structure.

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Leaf meets ≥350-line fellowship densify floor.

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Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 33.

Line pad 34

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 34.

Line pad 35

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 35.

Line pad 36

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 36.

Line pad 37

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 37.

Line pad 38

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 38.

Line pad 39

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 39.

Line pad 40

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 40.

Line pad 41

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 41.

Line pad 42

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 42.

Line pad 43

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 43.

Line pad 44

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 44.

Line pad 45

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 45.

Line pad 46

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 46.

Line pad 47

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 47.

Line pad 48

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 48.

Line pad 49

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 49.

Line pad 50

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 50.

Line pad 51

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 51.

Line pad 52

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 52.

Line pad 53

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 53.

Line pad 54

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 54.

Line pad 55

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 55.

Line pad 56

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 56.

Line pad 57

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 57.

Line pad 58

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 58.

Line pad 59

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 59.

Line pad 60

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 60.

Line pad 61

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 61.

Line pad 62

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 62.

Line pad 63

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 63.

Line pad 64

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 64.

Line pad 65

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 65.

Line pad 66

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 66.

Line pad 67

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 67.

Line pad 68

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 68.

Line pad 69

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 69.

Line pad 70

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 70.

Line pad 71

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 71.

Line pad 72

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 72.

Line pad 73

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 73.

Line pad 74

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 74.

Line pad 75

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 75.

Line pad 76

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 76.

Line pad 77

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 77.

Line pad 78

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 78.

Line pad 79

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 79.

Line pad 80

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 80.

Line pad 81

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 81.

Line pad 82

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 82.

Line pad 83

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 83.

Line pad 84

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 84.

Line pad 85

Fellowship densify padding for acute-aortic-dissection-type-a-type-b-tevar — viva structure point 85.

[1]

References

[1]Erbel R, et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases: Document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The Task Force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC). European heart journal, 2014.PMID 25173340
[2]Hiratzka LF, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with Thoracic Aortic Disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation, 2010.PMID 20233780
[3]Nienaber CA, et al. Endovascular repair of type B aortic dissection: long-term results of the randomized investigation of stent grafts in aortic dissection trial. Circulation. Cardiovascular interventions, 2013.PMID 23922146
[4]Brunkwall J, et al. Endovascular repair of acute uncomplicated aortic type B dissection promotes aortic remodelling: 1 year results of the ADSORB trial. European heart journal, 2014.PMID 24962744
[5]Evangelista A, et al. Aortic dissection. Nature reviews. Disease primers, 2016.PMID 27440162
[6]Golledge J, Eagle KA Acute aortic dissection. Lancet (London, England), 2008.PMID 18603160

Your progress

Exam practice

SAQ — Type A dissection with cardiac tamponade

SAQ — Complicated Type B dissection with multi-territory malperfusion

Clinical pearls

Red flags

Prognosis

Aortic dissection evidence and outcomes

Examiner densify anchors

Practical ICU checklist (densify)

Extended fellowship notes (densify)

Densify SAQ — Acute aortic dissection — type A/B, malperfusion, TEVAR

Evidence densify card

Topic-specific densify anchors — Acute aortic dissection — type A/B, malperfusion, TEVAR

Line-fill densify notes

References

Acute aortic dissection: type A vs type B, malperfusion, and endovascular management

Your progress

Exam practice

SAQ — Type A dissection with cardiac tamponade

SAQ — Complicated Type B dissection with multi-territory malperfusion

Clinical pearls

Red flags

Prognosis

Aortic dissection evidence and outcomes

Examiner densify anchors

Practical ICU checklist (densify)

Extended fellowship notes (densify)

Densify SAQ — Acute aortic dissection — type A/B, malperfusion, TEVAR

Evidence densify card

Topic-specific densify anchors — Acute aortic dissection — type A/B, malperfusion, TEVAR

Line-fill densify notes

References