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A patient with poorly controlled hypertension or a connective-tissue diathesis presents with sudden severe anterior chest or interscapular pain that is maximal at the moment of onset, often described as tearing or ripping, with migration of the pain across territories as the dissection flap propagates. Pulse asymmetry, a new aortic regurgitation murmur, or hypotension after presenting hypertension redirect the differential toward dissection in any chest-pain patient with the demographic profile. Painless dissection occurs in approximately 5-10% of cases (older series sometimes report figures as high as 40% in older, diabetic, or chronically beta-blocked populations), so the absence of tearing pain does not exclude the diagnosis when other dissection features are present.

Chronic hypertension, connective tissue disease, or aging weakens the elastic and collagen scaffolding of the aortic media — cystic medial necrosis is the classic histology in Marfan syndrome. Under shear stress the intima tears, most commonly at the sinotubular junction at the start of the ascending aorta (50–65% of tears) or just distal to the left subclavian artery at the aortic isthmus (20–30%); approximately 90% of intimal tears occur within 10 cm of the aortic valve. Pulsatile blood enters the media and dissects between the intimal and adventitial layers, propagating distally (most often), proximally, or both, to form a false lumen. As the false lumen advances it compresses or shears off the origins of the great vessels, coronaries, spinal arteries, renal arteries, mesenteric arteries, or iliac arteries, producing malperfusion syndromes. Rupture through the adventitia is rapidly fatal; retrograde extension into the pericardium produces tamponade; disruption of the aortic root commissures produces acute aortic regurgitation; and coronary occlusion produces acute myocardial infarction.

This mechanism maps directly onto the bedside picture. The migrating, multi-territory pain pattern reflects the false lumen advancing along the aorta — pain that begins substernal, becomes interscapular, then epigastric, then flank, is dissection until proven otherwise. Pain is maximal at the moment of onset because the tear is a discrete mechanical event, in contrast to ACS, in which pain crescendos over minutes as ischemia evolves. The branch-vessel ischemic findings — stroke, paraplegia, limb ischemia, mesenteric ischemia, AMI — explain why dissection masquerades as so many other diagnoses; locking onto the first explanation misses the unifying diagnosis. An aortic regurgitation murmur with chest pain redirects the differential toward type A dissection involving the aortic root, and hypotension after presenting hypertension suggests rupture, tamponade, or acute severe AR — terminal events that demand immediate operative management. Empiric anticoagulation or thrombolysis is catastrophic in dissection because it expands hemorrhage into the false lumen — the rationale for excluding dissection before treating presumed ACS or stroke when high-risk features coexist.

Aortic dissection follows a bimodal age distribution: a younger peak in patients with connective tissue disorders or congenital aortopathies, and a larger peak after age 50 in patients with chronic hypertension — mean age at presentation is approximately 63 years. Male predominance is approximately 65%; women present at older ages, more often with intramural hematoma, and carry higher in-hospital mortality. The pooled incidence is 2.9 to 4.7 cases per 100,000 persons per year. Acute aortic syndromes — classic dissection, intramural hematoma, and penetrating atherosclerotic ulcer — are uncommon overall, but each missed case carries high mortality. In pregnancy, dissection clusters in the third trimester and early postpartum period and is rare overall but disproportionately fatal. The demographic profile that most often defeats the classic older-hypertensive-male picture is young (<40) patients with Marfan, Ehlers-Danlos, Loeys-Dietz, bicuspid aortic valve, or familial thoracic aortic disease; pregnant or early-postpartum women with connective-tissue disease; recent cocaine or amphetamine use; and deceleration trauma at any age. Chronic hypertension is the single most important risk factor, present in approximately 72% of cases, with systolic blood pressure above 200 mmHg observed in approximately 50% of patients at presentation — the fuller list of predisposing conditions (connective tissue disease, bicuspid aortic valve, family history, prior aortic surgery or dissection, cocaine use, pregnancy, syphilis, trauma) is detailed in the illness script core below.

The base rate of aortic dissection in undifferentiated chest pain is low — far rarer than ACS, GERD, or musculoskeletal pain — but the consequence of a missed diagnosis is catastrophic, so the threshold to consider it stays low; approximately 22% of cases remain undiagnosed prior to death. Pretest probability is anchored to the Aortic Dissection Detection Risk Score (ADD-RS), which stratifies patients with suspected acute aortic syndrome into a 0–3 point score across three categories — high-risk predisposing conditions (Marfan syndrome, family history of aortic disease, known aortic valve disease, recent aortic manipulation, known thoracic aortic aneurysm), high-risk pain features (abrupt onset, severe intensity, ripping or tearing quality), and high-risk exam findings (pulse deficit or limb-to-limb systolic blood pressure differential, focal neurologic deficit with chest/back/abdominal pain, new aortic insufficiency murmur with pain, shock or hypotension) — with one point awarded per category in which any listed feature is present. ADD-RS ≥1 has a pooled sensitivity of approximately 94% for acute aortic syndrome (95% CI 90–96% in a 26,598-patient meta-analysis); the combination of ADD-RS ≤1 plus a negative D-dimer (<500 ng/mL) carries a missed-diagnosis rate of approximately 0.3% in prospective validation and pooled meta-analyses, with combined sensitivity approaching 99–100%. For ADD-RS ≥2, definitive imaging proceeds without reliance on D-dimer. Pretest probability modifies the interpretation of every downstream finding: a "good story" for ACS does not exclude dissection, because the two share risk profiles (older, hypertensive, male) and can coexist when retrograde dissection occludes a coronary ostium.

Painless dissection. A meaningful subset of confirmed dissections present without chest, back, or abdominal pain (approximately 5-10% in modern series; older series sometimes report figures as high as 40% in older, diabetic, or chronically beta-blocked populations). The presenting complaint is one of the dissection's complications: stroke (carotid involvement), syncope (tamponade or aortic-arch propagation), acute limb ischemia, paraplegia (spinal artery occlusion), or new aortic regurgitation murmur. Substitutes for the classic ripping/tearing-pain feature: a focal neurologic or limb-ischemic deficit dominates the presentation.

Stroke-presenting dissection. Frank stroke complicates roughly 5-15% of type A dissections (hemiparesis, dysphasia) when the dissection extends into the carotid arteries — large registries report the lower end and single-center series the higher — part of the broader ~20-30% that present with some neurologic finding (syncope, transient or focal deficit, or coma); type A extension into the carotid producing a focal neurologic deficit specifically is reported in approximately 20% of cases. The temptation is to start tPA — which is catastrophic in a dissection. Substitutes for the classic chest-pain feature: pain may be absent or minor, and the stroke team's tempo can fast-track the patient past the pulse-deficit / blood-pressure-asymmetry findings — or the chest or back pain itself — that would have raised dissection suspicion.

Syncope-only dissection. Pericardial tamponade from a type-A dissection rupturing into the pericardial sac, or cerebral malperfusion from arch-vessel involvement, produces transient hypotension and syncope as the dominant complaint, with chest pain often described after the fact or absent. Substitutes for the classic acute-pain feature: syncope is the entry signal; the pulse deficit, mediastinal widening, and JVD findings are the diagnostic pivots.

Type B dissection presenting as abdominal or flank pain. Descending dissections involving the abdominal aorta may present with epigastric, flank, or back pain that mimics renal colic, mesenteric ischemia, or AAA. Substitutes for the classic ripping-thoracic-pain feature: a more distal pain location with associated visceral findings (oliguria, lactate-elevated mesenteric ischemia).

Malperfusion-mimicking dissection (AMI, paraplegia, limb ischemia). Retrograde extension into the right coronary ostium produces an inferior STEMI pattern; giving aspirin, anticoagulation, and primary PCI without first obtaining aortic imaging is a known catastrophic error. Spinal artery occlusion from a descending dissection produces paraplegia, and limb ischemia — more common with type B dissection — can be the dominant complaint when a subclavian or iliac artery is occluded by the false lumen. Substitutes for the classic chest-pain-with-tearing-quality feature: the presenting complaint is the downstream ischemic event (STEMI, paraplegia, or a pulseless limb), and the unifying aortic process is found only by asking why a patient with a coronary, spinal, or limb occlusion also has chest or back pain.

Heart failure presentation. Acute severe aortic regurgitation from type A dissection produces flash pulmonary edema and a heart-failure-shaped presentation, particularly when the aortic root is involved. Substitutes for the classic tearing-pain feature: dyspnea and pulmonary edema dominate, and the aortic regurgitation murmur — not the pain history — is the pivot that redirects toward dissection.

Pregnancy and postpartum dissection. Dissection clusters in the third trimester and early postpartum period, particularly in women with Marfan syndrome, and is easily missed because the demographic — young, otherwise healthy, pregnant — does not fit the classic older-hypertensive profile. Substitutes for the classic older-hypertensive-male demographic: a young pregnant or postpartum woman, often with an unrecognized connective-tissue disorder, presenting with chest, back, or abdominal pain that is reflexively attributed to a pregnancy-related cause.

Walk-in presentation. Patients who walk in to triage rather than arrive by EMS experience delayed recognition and are at higher risk of misdiagnosis.

The natural history of an untreated type A dissection is dominated by aortic rupture — most often into the pericardium (tamponade) or the left pleural space (massive hemothorax), and almost always rapidly fatal — cardiac tamponade, acute severe aortic regurgitation, and coronary occlusion, usually inferior from right coronary involvement; these terminal events account for the steeply rising hour-by-hour mortality. Cardiac tamponade presents with the Beck triad of hypotension, jugular venous distension, and muffled heart sounds, though pulsus paradoxus may be absent when concurrent acute aortic regurgitation neutralizes the inspiratory pressure swing. Acute severe aortic regurgitation from aortic root disruption produces a physiology distinct from chronic AR — a shorter diastolic murmur, tachycardia (~108 bpm), a narrow pulse pressure (~55 mmHg), a lower systolic blood pressure (~110 mmHg), and a faint or absent S1 from premature mitral valve closure — with flash pulmonary edema and cardiogenic shock following. Medical-management mortality for type A is approximately 58%, compared with approximately 26% surgical mortality; the gap widens with each hour of delay. Branch-vessel malperfusion produces stroke from carotid involvement (approximately 20% of type A cases), paraplegia from spinal artery occlusion, and limb or visceral ischemia from subclavian, iliac, mesenteric, or renal artery compromise.

Type B dissections follow a milder acute course but a chronic-disease trajectory. Pooled medical mortality is approximately 10.7% for uncomplicated type B; complicated type B (refractory pain, refractory hypertension, malperfusion, aneurysmal dilation, or rupture) carries pooled surgical mortality of approximately 29% and is the primary indication for thoracic endovascular aortic repair (TEVAR). Long-term, residual false-lumen patency drives ongoing aortic remodeling and progressive dilation; lifelong tight blood pressure control with beta-blockade is the cornerstone of secondary prevention, and surveillance imaging of the residual aorta is required.

Iatrogenic complications dominate when the diagnosis is missed in its mimicked form. Aspirin, full-dose heparin, or thrombolysis given for a presumed AMI or stroke expands hemorrhage from the false lumen and is rapidly fatal — the rationale for excluding dissection before treating a high-suspicion ACS or stroke when atypical features (pulse deficit, blood-pressure differential, migrating pain, new aortic regurgitation murmur) coexist. Cessation of symptoms in a patient with suspected dissection does not indicate resolution; the false lumen may have re-entered the true lumen, falsely reassuring the clinician while propagation continues.

Aortic dissection lives in the Aortic / great-vessel bucket of the chest pain schema, alongside thoracic aortic aneurysm. It is the must-not-miss diagnosis with the highest acute mortality on the chest-pain differential and is among the six immediate threats — STEMI, tension pneumothorax, aortic dissection, massive PE, cardiac tamponade, and esophageal rupture — that the first-10-minute sweep is built around. The cross-bucket discriminators that pull the workup toward dissection are sudden onset maximal at the moment of onset, tearing or ripping pain quality, migration of pain across territories, blood-pressure differential >20 mmHg between arms, pulse deficit, focal neurologic deficit with chest or back pain, and a new aortic regurgitation murmur with chest pain.

Dissection is also a load-bearing diagnosis well outside the chest-pain schema. Acute severe AR from type A involvement produces flash pulmonary edema and a heart-failure-shaped presentation in the shortness of breath schema. Cerebral malperfusion or tamponade produces syncope without prominent pain. Mesenteric or limb ischemia from descending dissection produces an abdominal-pain or limb-pain presentation. Type A masquerading as inferior STEMI from right-coronary-ostium occlusion is the most catastrophic missed-diagnosis pattern; bilateral blood pressures and a pulse exam precede cath-lab activation when any element of the dissection picture is present in a chest-pain story.

In the back-pain schema the same diagnosis is filed under referred visceral and extra-spinal causes — the bucket for pain generated outside the spine entirely, where the spine itself is innocent and the examination that would localize a mechanical lesion returns normal. Descending dissection refers interscapular and interscapular-to-lumbar pain along the course of the aorta, and it reaches the back-pain differential through the entry gate rather than through any mechanism sort: abrupt tearing pain that is maximal at onset, unaffected by spinal movement or position, and accompanied by a blood-pressure differential between the arms or a new aortic-regurgitation murmur. The discriminator that matters most in this complaint is the one that separates it from the benign majority rather than from its vascular neighbor — pain that ignores what the spine is doing is not coming from the spine, and in an older patient with vascular risk that observation outranks the overwhelming base rate of benign mechanical back pain.

In the altered-mental-status schema the same diagnosis is filed in the parenchymal and vascular bucket on the brain-origin branch, and that placement is where the load-bearing teaching sits: the vessel that has failed is outside the skull, but the deficit is expressed inside it. A stroke syndrome carrying chest or back pain, a blood-pressure differential between the arms, or a new aortic-regurgitation murmur must not be thrombolyzed, which is the reason the stroke pathway asks about chest and back pain before it treats. Dissection reaches a confused patient by two routes — carotid or vertebral malperfusion producing a focal deficit, and tamponade or rupture producing global hypoperfusion with no focal signs at all — and only the first belongs to the bucket it is filed in. The second is carried as a discriminator in fuel and perfusion instead, because a diagnosis may occupy exactly one bucket and the branch that names it has to be the one a learner can reason toward.