A tear in the inner lining lets blood burrow into the aortic wall and split it apart. Learn the tear-to-false-lumen chain, the pulses that lie, the Stanford fork that decides surgery versus medicine, and why you slow the heart before you drop the pressure.
The Setup
The Wall Splits
Everything about dissection flows from one event: the inner lining tears and high-pressure blood pries the wall apart. Walk that chain once and the whole disease falls into place.
A 58-year-old man with years of poorly controlled high blood pressure feels a sudden, severe, tearing pain that hits hardest at the very first second and shoots straight through to between his shoulder blades. His blood pressure reads 168 over 96 in the right arm and 132 over 80 in the left.
What single mechanism best explains the whole story?
Start with the layers. The aorta is a three-layer pipe: a thin slick inner lining (the intimaThe innermost layer of a blood vessel, a single smooth sheet of cells that the blood glides over.), a thick muscular middle (the mediaThe muscular and elastic middle layer that gives the aorta its strength and stretch. It is the layer that splits in a dissection.), and a tough outer coat (the adventitiaThe outer connective-tissue wall. It is the last barrier before the blood escapes the aorta entirely.). Dissection begins when the inner lining tears.
Now the chain. A weak spot in the lining tears → blood under full arterial pressure jets sideways into the muscular middle layer → that jet peels the layers apart and carves a second channel that should not exist, the false lumen → with every heartbeat the split runs further up or down the aorta. Two things can kill from here. The peeling wall can shear off the mouths of branch arteries (starving the brain, heart, gut, kidneys, or a limb), and the thin outer coat can rupture (bleeding into the chest, the belly, or the sac around the heart).
The force that drives it. What pushes the split forward is not the pressure alone but the steepness of each pulse (written dP/dt), meaning how hard and how fast the left ventricle slams blood into the aorta. Hold that idea. It is the reason the treatment lowers the heart rate first and the pressure second.
One tear, two outcomes. The dashed line is the peeled inner lining (the intimal flap) separating the true channel from the false one. If the split touches the ascending aorta it is a Stanford A and goes to surgery. If it stays in the descending aorta beyond the left subclavian, it is a Stanford B and starts with medicine.
Who tears? The wall fails for one of two reasons: chronic pounding that wears the middle layer thin, or a middle layer that was weak to begin with. Flip each card.
HypertensionTap to flip
The most common causeYears of high pressure batter the media and drive cystic medial degeneration, thinning the layer that holds the aorta together. This is the typical older patient with a long history of poorly controlled blood pressure.
Weak wall, young patientTap to flip
Connective tissue diseaseMarfan, vascular Ehlers-Danlos, and Loeys-Dietz build a faulty media from birth. Suspect dissection in a tall young patient with long limbs, a dislocated lens, or a family history of sudden aortic death.
Valve and aorta defectsTap to flip
Bicuspid valve, coarctation, TurnerA bicuspid aortic valve, aortic coarctation, and Turner syndrome all come with an aorta that is structurally prone to dilate and tear. A bicuspid valve is the classic young-adult setup.
Sudden surgeTap to flip
Acute pressure spikesCocaine and other stimulants, heavy weightlifting, third-trimester pregnancy, and blunt chest trauma (which classically tears the aortic isthmus) can split a wall that was already marginal.
Clinical Images
CT angiogram: intimal flap, true and false lumen · tap
Chest x-ray: widened mediastinum · tap
Gross specimen: blood splitting the wall · tap
At the Bedside
Pain That Tears, Pulses That Lie
Dissection announces itself with a pain unlike a heart attack, and then it reveals where it has traveled through the body it has injured along the way.
The pain has a signature. It is sudden and maximal at the very first instant, unlike the heart attack that builds over minutes. Patients call it tearing or ripping, and it can migrate as the split runs. Location points to the zone: pain felt in the front of the chest suggests the ascending aorta (think type A), while pain that bores into the back between the shoulder blades suggests the descending aorta (think type B).
Then it betrays its path. Each branch the split injures gives a different sign. Tap each one.
Pulse and pressure differential
Tap to reveal
A blood pressure gap greater than 20 mmHg between the two arms, or a weak or missing pulse on one side. The flap has narrowed the artery feeding that limb. This is the single most specific bedside clue.
New diastolic murmur
Tap to reveal
A type A dissection tearing back toward the heart can pull the aortic valve open, producing acute aortic regurgitation: a new blowing murmur after the second heart sound, sometimes with heart failure.
Hypotension with distended neck veins
Tap to reveal
Low pressure, muffled heart sounds, and bulging neck veins is the Beck triad of cardiac tamponade: the dissection has ruptured into the sac around the heart. A type A catastrophe that needs the operating room.
Focal neuro deficit or syncope
Tap to reveal
A flap shearing a carotid artery causes a stroke; a sudden faint can come from tamponade or from the dissection reaching the brain supply. Chest pain plus a new neuro deficit should raise dissection, not just stroke.
Inferior ischemia on the ECG
Tap to reveal
If the split reaches the right coronary artery mouth, the ECG can show an inferior heart attack pattern. This is the trap: the dissection masquerades as the very heart attack you must not treat with clot-busters.
Abdominal or limb ischemia
Tap to reveal
Reaching down the aorta, the flap can starve the gut (severe belly pain with a soft abdomen, the hallmark of mesenteric ischemia), the kidneys (sudden kidney injury), or a leg (a cold, pulseless limb).
From the Attending
The most dangerous version of this disease is the one wearing a heart attack costume. A patient with tearing pain to the back and an inferior pattern on the ECG can have a dissection that crawled into the right coronary. Give clot-busters for that supposed heart attack and you turn a contained tear into a fatal hemorrhage. Before you lyse anyone, check both arm pressures and ask where the pain went.
Confirming It
Confirm Before You Commit
The diagnosis turns on one question before any scan: is the patient stable enough to travel to the scanner, or do you bring the test to the bedside? Then learn the look-alikes.
First, the cheap tests. The chest x-ray classically shows a widened mediastinum (the shadow of the great vessels looks too broad), but a normal film does not rule dissection out. The ECG may be normal, show thickened heart muscle, or mimic an inferior heart attack. A D-dimer is very sensitive: a negative result in a genuinely low-risk patient argues against dissection, but it never substitutes for imaging when suspicion is real.
The imaging fork. Stability decides the test. Try each step before you reveal it.
A 60-year-old with tearing back pain is alert and stable, pressure 150 over 90. Best confirmatory test?
In a stable patient, CT angiography is first: it is fast, it is everywhere, and it shows the intimal flap, the entry tear, and exactly how far the dissection runs (which decides the operation). Stable patient? CT angiography of the whole aorta.
Now the patient is crashing, pressure 78 over 40, too unstable to leave the resuscitation bay. Best test?
An unstable patient does not survive a trip down the hall. Transesophageal echo brings the probe to the bedside, sees the ascending aorta and the valve, and detects tamponade in real time. Unstable patient? Bedside transesophageal echo.
The chest x-ray you got first looks normal, with no widened mediastinum. Does that exclude dissection?
A normal chest x-ray happens in a meaningful slice of real dissections. The film raises suspicion when abnormal but cannot lower it when normal. If the story fits, image definitively no matter what the plain film shows.
Mimic
What separates it
Myocardial infarction
Pain builds over minutes rather than peaking instantly, no arm pressure gap, rising troponin, and ST changes that match one coronary territory. Beware: a type A dissection can cause a true inferior infarct.
Pulmonary embolism
Pleuritic pain worse on breathing, low oxygen, fast heart rate, risk factors such as recent surgery or immobility. CT angiography distinguishes the two.
Esophageal rupture
Boerhaave syndrome after forceful vomiting, with air in the chest wall and a left pleural effusion. The history of retching is the tell.
Pericarditis
Sharp pain better when leaning forward, diffuse ST elevation across many leads, and a scratchy rub. No tearing quality and no pressure differential.
Acute coronary spasm
Transient ST changes that resolve, often nitrate responsive, without the migrating tearing pain or the arm-to-arm gap.
The Plan
Slow the Heart, Then Drop the Pressure
One first move applies to every dissection, and then the Stanford zone decides whether the patient goes to the operating room or to a careful medical drip.
The universal first move. Lower the shearing force on the wall. Give an intravenous beta-blocker first (esmolol or labetalol) to bring the heart rate below 60, and only then add a vasodilator (nitroprusside) to bring the systolic pressure down to 100 to 120. Add opioids for pain, which also calms the sympathetic surge.
From the Attending
Order matters, and here is why. If you reach for the vasodilator first, the pressure drops and the body answers with a reflex tachycardia, a faster, harder pulse that raises dP/dt and shoves the dissection forward. The beta-blocker blunts that reflex before you ever touch the pressure. Rate before pressure. Always.
Then split by Stanford zone.
Type ATap to flip
Surgical emergencyAny involvement of the ascending aorta goes straight to emergency open surgical repair with a graft. Left alone it ruptures into the pericardium, tears the valve, or blocks the coronaries. Medicine alone is not enough.
Type B, uncomplicatedTap to flip
Medical managementA dissection limited to the descending aorta with no complication is managed medically: strict heart rate and blood pressure control in an intensive care unit. Most do well without an operation.
Type B, complicatedTap to flip
InterveneA type B turns surgical when it ruptures, starves an organ or limb (malperfusion), or causes pain or pressure that will not settle on maximal medicine. The modern fix is an endovascular stent graft placed inside the aorta.
Board Trap
Do not give thrombolytics or full anticoagulation to a dissection mistaken for a heart attack, and do not slam in fluids and pressors to chase the low blood pressure of a type A tamponade before the surgeon is ready. The low pressure is a ruptured aorta, not dehydration. The fix for type A is the scalpel, not the fluid bag.
Prove It
Board Walkthrough
Six original clinical vignettes, 5 dealt per round, answer choices shuffled, never repeating within a round. Tap a wrong answer first to see why it almost works, then read the glowing clues.
Medically reviewed by Kaitlyn Cocuzzo, MD and Fatima Ali, DO · Last reviewed June 2026
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