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Acute aortic syndrome and dissection

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Acute aortic syndrome

Abrupt severe chest, back or abdominal pain with syncope, pulse or pressure asymmetry, new aortic regurgitation, neurological deficit, limb or visceral ischaemia, pericardial effusion or shock is a time-critical aortic emergency.

Action: Call the aortic team immediately, monitor invasively, give analgesia and carefully titrated anti-impulse therapy when haemodynamics allow, and obtain ECG-gated CTA from neck to pelvis without delaying immediate surgery for confirmed type A disease.

Synopsis

Recognize acute aortic syndromes, confirm anatomy rapidly, initiate safe anti-impulse care, and route type A, type B and malperfusion emergencies.

  • Suspect acute aortic syndrome with abrupt severe chest, back or abdominal pain plus aortic disease, pulse deficit, new regurgitation, neurological deficit or shock.
  • Stanford type A involves the ascending aorta and needs immediate surgery; type B begins distal to the left subclavian artery without ascending involvement.
  • Complicated type B means rupture or impending rupture, malperfusion, persistent or recurrent pain, uncontrolled hypertension or disease progression and usually needs urgent intervention.

Key red flags

Hypotension in suspected dissection can mean rupture, tamponade, severe aortic regurgitation, myocardial ischaemia or organ malperfusion; do not reflexively give antihypertensives.

Any ascending aortic involvement is Stanford type A and requires immediate cardiothoracic surgical management, irrespective of where the entry tear lies.

Persistent pain, refractory hypertension, rapid expansion, rupture, shock or cerebral, coronary, mesenteric, renal, spinal or limb malperfusion makes type B dissection complicated.

A normal chest radiograph, non-specific ECG or low-risk isolated symptom does not exclude acute aortic syndrome when pre-test probability remains high.

Thrombolysis or routine anticoagulation for presumed myocardial infarction, stroke or pulmonary embolism can be catastrophic when dissection remains plausible.

Abrupt maximal pain

Severe chest, interscapular, abdominal or migrating pain reaches maximum intensity rapidly and may track with propagation.

Proximal complication

New diastolic murmur, pulmonary oedema, myocardial ischaemia, pericardial effusion or tamponade suggests ascending involvement.

Malperfusion syndrome

Stroke, paraplegia, abdominal pain with lactate rise, oliguria, pulse loss or acute limb ischaemia signals branch compromise.

Complicated type B

Persistent pain, uncontrolled hypertension, rupture signs, rapid expansion or organ ischaemia converts medical surveillance into an urgent intervention pathway.

Investigation priorities

01
First-line: ECG-gated CT angiography from neck to pelvisFirst stepFirst line

Confirm AAS and map entry, extent, branches, rupture and access.

Management branches

Worked caseRoute pain with neurological deficit

A patient develops abrupt chest pain, transient hemiparesis and unequal arm pressures.

  1. Recognize high pre-test probability from abrupt pain, neurological deficit and pressure asymmetry; call the cardiothoracic aortic service during ABCDE stabilization.
  2. Obtain bilateral observations where safe, arterial access, ECG, cross-match and focused echo, while arranging ECG-gated CTA from neck to pelvis without laboratory delay.

Key medicines

Intravenous labetalolGive 50 mg intravenously over at least 1 minute with the patient supine; if necessary repeat 50 mg at 5-minute intervals until satisfactory response, to a maximum cumulative 200 mg. Continuously monitor pressure and pulse and stop escalation once the anti-impulse target or a safety limit is reached.Do not give in cardiogenic shock, hypotension, uncontrolled or incipient heart failure, sick-sinus syndrome, second- or third-degree heart block, bradycardia below 45–50 beats per minute, or a history of wheeze or asthma. Stop further dosing for hypotension, important bradycardia, block, bronchospasm or worsening low-output or organ perfusion; tamponade, rupture, severe regurgitation and malperfusion require definitive correction rather than forced targets.
Intravenous nicardipine infusionOnly after beta blockade or alternative rate control, start continuous intravenous nicardipine at 3–5 mg/hour for 15 minutes; increase by 0.5–1 mg/hour every 15 minutes to response, maximum 15 mg/hour, then reduce progressively to 2–4 mg/hour maintenance while the target remains necessary.Never give as an unopposed bolus or first anti-impulse drug because reflex tachycardia can increase shear. Use a controlled pump with continuous pressure monitoring; halve the dose or stop for systemic hypotension or reflex tachycardia, and stop or retarget if neurological, spinal, renal, mesenteric or limb perfusion worsens. It is contraindicated in severe aortic stenosis, unstable angina, compensatory hypertension and within 8 days of myocardial infarction; use lower, cautious titration in older adults and hepatic or renal impairment.
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Sources and review status5 sources · checked 12 Sept 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 12 Sept 2026; clinical approval remains outstanding.

Authoring stateRapid draftClinical stateAwaiting reviewJurisdictionUnited Kingdom