Aortic Dissection and Hypertensive Emergency

In depth

The one-page summary above is what the PDF prints. These sections go further.

Acute aortic syndromes: mechanism and classification

In dissection, an intimal tear lets blood split the media lengthwise, creating a false lumen separated from the true lumen by a flap. The dissection propagates mostly distally, sometimes back toward the root, and a breach of the adventitia is rupture. Medial degeneration is the substrate, driven by hypertension in most adults and by Marfan, Loeys-Dietz or vascular Ehlers-Danlos syndrome, a bicuspid valve or familial disease in younger patients; other triggers are stimulants, prior aortic procedures, and pregnancy from the third trimester to 12 weeks postpartum (2022 ACC/AHA).

Wall stress rises with pressure and radius and falls with wall thickness (Laplace), but the force of each ejection (dP/dt) and the number of beats drive a tear forward. Type A kills through tamponade, acute aortic regurgitation, coronary occlusion (usually the right coronary, mimicking an inferior STEMI) and stroke; either type can rupture or cause branch malperfusion. Untreated type A is still quoted at 1–2% mortality per hour (2022 ACC/AHA); among 5,611 IRAD patients it was 0.5% per hour (23.7% at 48 h) with medical care and 4.4% at 48 h when surgery was intended (Harris 2022). Uncomplicated type B carries about 10% 30-day mortality; with malperfusion or rupture, 25% by day 30.

Intramural hematoma (IMH) is blood in the media without a visible tear or flowing false lumen: crescentic or circular wall thickening over 5 mm, bright on non-contrast CT. It is 6–23% of acute aortic syndromes in the West and 26–44% in Asia; under 10% resolve and 16–47% progress to dissection. A penetrating atherosclerotic ulcer (PAU) is a plaque ulcerating through the internal elastic lamina, usually in the descending aorta of people over 70; it is 2–7% of cases and can lead to IMH, dissection, pseudoaneurysm or rupture (2022 ACC/AHA).

Recognition: ADD-RS, D-dimer and imaging

Pain is abrupt and worst at onset, more often called sharp or stabbing than tearing (2022 ACC/AHA). In IRAD's first 464 patients only 31.6% had an aortic regurgitation murmur, 15.1% a pulse deficit and 12.4% a normal chest x-ray (Hagan 2000). Measure BP in both arms and both legs: a difference over 20 mm Hg suggests a compromised branch.

• High-risk conditions: Marfan or other connective tissue disease, family history of aortic disease, known aortic valve disease or thoracic aneurysm, recent aortic manipulation
• High-risk pain: chest, back or abdominal pain that is abrupt, severe, or ripping or tearing
• High-risk exam: pulse deficit or SBP difference, focal deficit with pain, new aortic regurgitation murmur with pain, hypotension or shock
• ADD-RS gives 1 point per category: 0 is low, 1 moderate and 2–3 high risk (2022 ACC/AHA)

In ADvISED (Nazerian 2018, 1,850 patients), D-dimer under 500 ng/mL was 96.7% sensitive and 64% specific, and ADD-RS ≤1 with a negative D-dimer missed 3 of 924 patients (0.3%). Use it only to rule out at low or moderate risk; a score of 2–3 goes straight to CT angiography (Class 1), ECG-gated for the root and with a non-contrast phase for IMH. TEE and MRI are alternatives (Class 2a); TTE shows effusion and regurgitation but cannot exclude dissection.

Anti-impulse therapy in depth

Anti-impulse therapy cuts the force and number of ejections first, then the pressure, with an arterial line in an ICU (2022 ACC/AHA, Class 1). Targets: heart rate 60–80 and SBP under 120 mm Hg, or the lowest pressure that keeps brain, kidneys and gut perfused (Class 1). The ESC 2019 position paper and many exam items use a heart rate of 60 or less. None of these numbers comes from a randomized trial.

An IV beta-blocker comes first (Class 1). A vasodilator alone triggers reflex tachycardia and a steeper upstroke, so it is added only if BP stays high after rate control (Class 1): nicardipine or clevidipine, or nitroprusside, which is fastest but releases cyanide above about 2 mcg/kg/min (label). Esmolol (half-life about 9 min) wears off in minutes if it is not tolerated; labetalol treats rate and pressure in one drug but lasts hours, so an overshoot persists (ESC 2019). If beta-blockers are contraindicated, IV diltiazem or verapamil controls rate (Class 2a). IV opioids are part of the therapy because pain drives rate and pressure; ketorolac can raise BP and harm the kidneys (2022 ACC/AHA).

Long-term oral beta-blockade after any acute aortic syndrome is Class 1, with ARBs or ACE inhibitors added to reach goal (2022 ACC/AHA).

Surgery, TEVAR or medical therapy

Type A needs immediate surgical consultation and repair (2022 ACC/AHA, Class 1); in IRAD, operative mortality fell from 25% to 18% (1995–2013) while medical mortality stayed at 57%. On bypass, the surgeon resects the entry tear and replaces the ascending aorta with an open distal (hemiarch) anastomosis under hypothermic circulatory arrest with cerebral perfusion, extending into the arch only for an arch tear or aneurysm; the valve is resuspended if its leaflets are normal, and the root is replaced when destroyed, aneurysmal or genetically weak. A nonhemorrhagic stroke favors operating (mortality 25–27% vs 76% medically), and transfer of stable patients to a center doing at least 7 dissection repairs a year is reasonable (Class 2a).

Uncomplicated type B starts with medical therapy (Class 1). Complicated type B (rupture or growing periaortic hematoma, malperfusion, extension including retrograde type A, enlarging lumens, intractable pain or uncontrolled hypertension) needs repair: TEVAR for rupture when anatomy suits (Class 1) and endovascular over open repair for other complications (Class 2a). The stent graft seals the primary entry tear so flow returns to the true lumen and the false lumen can thrombose; fenestration or branch stents treat residual malperfusion.

TEVAR may be considered for uncomplicated type B with high-risk features (Class 2b) such as aortic diameter over 40 mm, false lumen over 20–22 mm, an entry tear over 10 mm or on the lesser curve, bloody pleural effusion, imaging-only malperfusion, or refractory pain or hypertension. The best timing is unknown. INSTEAD (2009, 140 stable patients) showed no 2-year survival difference but remodeling in 91.3% with TEVAR vs 19.4% without; by 5 years TEVAR had lowered aorta-specific mortality (6.9% vs 19.3%) and progression (27.0% vs 46.1%), not all-cause mortality (INSTEAD-XL 2013).

IMH is managed like dissection of the same type: urgent repair if complicated, prompt surgery for type A (or medical care for high-risk patients without high-risk imaging, Class 2b), medical therapy for type B. PAU is repaired when it ruptures, sits in the ascending aorta with IMH, or causes persistent pain. Elective cases that need left subclavian coverage are revascularized first (Class 1); without it the left arm reads low.

Malperfusion and spinal cord protection after TEVAR

Malperfusion is dynamic when the pressurized false lumen squeezes the true lumen and the flap drapes over a branch ostium; restoring true-lumen flow usually fixes it. It is static when the dissection extends into the branch and narrows or clots it, which needs a branch stent (2022 ACC/AHA). Imaging shows malperfusion in up to 25% of type A; the clinical syndrome raised mortality to 30.5% from 6.2%, and mesenteric malperfusion to 63.2%. For gut ischemia, repairing the aorta first or reperfusing the gut first are both reasonable (Class 2a).

The anterior spinal artery depends on segmental intercostal and lumbar arteries, the largest usually the artery of Adamkiewicz (left side, T8–L2; De Paulis 2022), plus subclavian-vertebral and hypogastric collaterals. Risk rises with long coverage, coverage near T8–L2, left subclavian coverage, prior AAA repair, hypotension and anemia. Spinal cord injury follows 2–15% of thoracoabdominal repairs, open or endovascular, and can appear up to 2 weeks later, usually after hypotension, arrhythmia or bleeding (2022 ACC/AHA).

Spinal cord perfusion pressure is MAP minus CSF pressure. CSF drainage is Class 1 for high-risk open thoracoabdominal repair: in Coselli 2002 (extent I–II), draining to 10 mm Hg or less for 48 h cut paraplegia or paraparesis from 13.0% to 2.6%, though an earlier trial showed no benefit. For TEVAR the evidence is observational; centers drain all extensive repairs, only high-risk patients, or only for rescue. Protocols vary; typical ones keep CSF pressure about 10 mm Hg (8–12), cap drainage near 15–20 mL/h, hold MAP 80–90 for 48 h, then clamp for 24 h and remove the drain if the legs stay strong (Spratt 2022, De Paulis 2022).

1. New leg weakness: call the surgeon and raise MAP above 100 mm Hg with volume and vasopressors; cardiovert tachyarrhythmias
2. Drain CSF: lower the pressure setting, or have a drain placed
3. Transfuse to hemoglobin above 10 g/dL (2022 ACC/AHA Table 20)

Abdominal aortic aneurysm rupture

An AAA is an abdominal aorta over 3.0 cm, usually infrarenal. Repair is recommended at 5.5 cm in men and 5.0 cm in women, or for symptoms at any size (2022 ACC/AHA); women rupture at smaller diameters. Rupture kills 80–90% overall, most before reaching hospital. Bleeding into the retroperitoneum can be contained for hours, while free rupture into the peritoneum is rapidly fatal. The triad of pain, hypotension and a pulsatile mass is often incomplete, and the pain passes for renal colic or back strain; an aorta over 3 cm on bedside ultrasound in a hypotensive patient with pain is rupture until proven otherwise.

• Permissive hypotension: an SBP that keeps the patient mentating, typically 60–90 mm Hg (2022 ACC/AHA, Class 2a); blood products early, little crystalloid
• CT if stable, to plan EVAR (Class 1); EVAR over open repair when anatomy suits (Class 1)
• EVAR under local anesthesia when possible (Class 2a): induction removes the catecholamine drive and can cause collapse, so prep and drape first

IMPROVE (2014, 613 patients) found no 30-day difference with an endovascular-first strategy (35.4% vs 37.4%) and a possible benefit in women (OR 0.44); survival favored EVAR between 90 days and 3 years (HR 0.57). After repair, watch for abdominal compartment syndrome (bladder pressure over 20 mm Hg with new organ dysfunction), colon ischemia (bloody or frequent stools, rising lactate), AKI, leg ischemia and, after EVAR, endoleak.

Hypertensive emergency: autoregulation and pace

A hypertensive emergency is BP over 180/120 with new or worsening target-organ damage; without damage it is severe hypertension (formerly urgency), managed with oral drugs. How fast BP rose matters more than the number. An abrupt rise in resistance injures endothelium (fibrinoid necrosis, microangiopathy), and ischemia plus pressure natriuresis activate renin, raising resistance further (ESC 2019).

Brain, heart and kidney hold flow steady across a range of pressures that chronic hypertension shifts right. Strandgaard (1976) found the lower limit of cerebral autoregulation at a MAP of 113 mm Hg in untreated severe hypertension (resting 145) and 73 in normotensive controls (resting 98): in both, about 20–25% below resting pressure, the basis of the 25% rule. Dropping below that floor causes watershed stroke, MI, AKI and blindness. Above the upper limit, forced vasodilation causes hyperperfusion and vasogenic edema, mostly posterior where sympathetic innervation is sparse (PRES).

The 2017 ACC/AHA pace for most emergencies: no more than 25% in the first hour, then 160/100–110 over 2–6 h, then normal over 24–48 h. Worked example: 220/130 is a MAP of about 160; a 25% drop is a MAP of 120, about 170/95, which still looks high and is correct. MAP falls over 50% have caused stroke and death (ESC 2019). Pressure natriuresis leaves many patients volume-depleted, so the first vasodilator dose can overshoot; small saline boluses correct it, and diuretics are for congestion only.

Treating numbers alone harms: in noncardiac inpatients, treating high readings was associated with more AKI (10.3% vs 7.9%) and myocardial injury (1.2% vs 0.6%) (Rastogi 2021). Look first for pain, urinary retention, anxiety and missed home doses; short-acting nifedipine is not used.

Drug choice by syndrome, preeclampsia and pheochromocytoma

Preeclampsia is placental: antiangiogenic factors injure maternal endothelium, causing hypertension, HELLP, pulmonary edema, PRES and eclampsia, sometimes first after delivery. Treat SBP ≥160 or DBP ≥110 persisting 15 min within 30–60 min (ACOG PB 222) with IV labetalol (10–20 mg, then 20–80 mg every 10–30 min, maximum 300 mg), IV hydralazine (5 mg, then 5–10 mg every 20–40 min, maximum 20 mg) or immediate-release oral nifedipine (10–20 mg, repeated in 20 min). ESC 2019 aims for under 160/105 and no longer recommends hydralazine, which ACOG still lists. Magnesium (4–6 g load, 1–2 g/h until 24 h after delivery) prevents seizures but does not lower BP; reflexes vanish above about 9 mg/dL and breathing fails near 12, and calcium gluconate 10%, 10 mL IV over 3 min, treats toxicity.

Pheochromocytoma crises follow tumor handling, anesthesia induction, high-dose steroids, metoclopramide or a beta-blocker given without alpha-blockade, causing severe or swinging BP, arrhythmias, catecholamine cardiomyopathy, pulmonary edema and lactic acidosis. Give phentolamine 5 mg IV, repeated as needed (label), or nicardipine, clevidipine or nitroprusside, and add esmolol only after alpha-blockade; labetalol has accelerated hypertension in case reports (ESC 2019). Elective patients get 7–14 days of alpha-blockade with salt and fluids, aiming for under 130/80 seated (Endocrine Society 2014). After resection expect hypotension and, within hours, rebound hypoglycemia.

Nursing monitoring

• Arterial line for titration (Class 1 in aortic syndromes); cuffs can under-read pressures above 180/100 by up to 50/30 mm Hg (Demiselle 2026).
• BP every 5 min while titrating; document the times of the first dose and of reaching each target.
• On beta-blockade, watch for heart block, bronchospasm and heart failure.
• Hourly neuro checks, with leg strength and sensation for 48–72 h after TEVAR or with descending dissection.
• Recurrent, migrating or changing pain means extension or impending rupture; a new diastolic murmur, muffled tones, pulsus paradoxus or rising CVP points to the root or pericardium.
• Four-limb pulses with Doppler, abdominal exam, lactate trend and hourly urine output (flag under 0.5 mL/kg/h); 12-lead ECG with any change in pain.
• Lumbar drain: hourly pressure, volume and color at a consistent zero; clamp for repositioning and transport.
• Nitroprusside: protect from light, watch lactate and acid–base for cyanide. Clevidipine: aseptic handling, discard 12 h after puncture, no egg or soy allergy. Peripheral nicardipine: new site every 12 h.
• Overlap oral agents before stopping infusions; give opioids, anxiolysis and stool softeners; keep infusions and arterial monitoring running during transfer.

Exam pearls

• Stanford A (ascending involved) means emergency surgery; B is medical unless complicated.
• DeBakey I: ascending through the arch and beyond; II: ascending only; III: descending only.
• Beta-blocker before vasodilator: heart rate 60–80 (many items say under 60) and SBP under 120 within an hour.
• Hypotension in dissection: tamponade, rupture, acute aortic regurgitation, coronary occlusion, or a falsely low arm.
• Inferior STEMI or stroke with back pain or a pulse deficit: exclude dissection before heparin or lytics.
• New leg weakness after TEVAR: raise MAP, drain CSF, transfuse to hemoglobin over 10 and call the surgeon.
• Ruptured AAA: permissive hypotension (mentating, SBP 60–90) and EVAR when anatomy allows.
• Hypertensive emergency: no more than 25% in the first hour, except dissection, preeclampsia, pheochromocytoma and stroke.
• Magnesium toxicity: patellar reflexes go first, then breathing; give calcium gluconate.
• Pheochromocytoma: alpha-blockade before any beta-blocker. Nitroprusside: cyanide above 2 mcg/kg/min and raised ICP.