Updated July 2026 · 7 min read
Part of the ICU Emergencies Hub — browse every related guide in one place.
A patient who did well after a heart attack a few weeks ago comes back with chest pain, and the first fear in everyone's mind is another MI. But this pain is different — it is sharp, it stabs when they take a deep breath, and it eases when they lean forward. There is a low-grade fever, and the troponin is not doing what a re-infarction would do. This is Dressler syndrome, an immune-driven inflammation of the sac around the heart that surfaces weeks after cardiac injury, and recognizing it keeps a patient from being rushed back to the cath lab for the wrong reason.
When heart muscle is damaged — by an infarct, by the trauma of open-heart surgery, or by other injury — proteins from the injured tissue are exposed to the immune system in a way they normally are not. In susceptible patients the immune system mounts a delayed reaction against the pericardium, treating the heart's own lining as something to attack. Because it is an immune process rather than a mechanical or ischemic one, it takes time to develop; the classic window is a few weeks after the event, which is exactly why it fools people. The patient has moved past the acute phase, gone home or to a step-down setting, and then returns with what looks alarmingly like a repeat heart attack but is in fact inflammation of the sac around the heart.
| Feature | Dressler (pericarditis) | Re-infarction (ischemia) |
|---|---|---|
| Timing | Weeks after the index event | Any time, often abrupt |
| Pain quality | Sharp, pleuritic; worse deep breath & lying flat, better leaning forward | Pressure/heaviness, not positional |
| Fever | Low-grade fever common | Not typical |
| Exam | Pericardial friction rub | No rub |
| Labs | High inflammatory markers (ESR/CRP), leukocytosis | Rising troponin in an ischemic pattern |
| Effusion | Pericardial effusion common | Not the defining feature |
The three findings that most strongly point toward Dressler rather than another coronary event are the positional, breathing-related nature of the pain, a friction rub heard on auscultation, and the weeks-later timing with fever and elevated inflammatory markers. None of this means ischemia can be dismissed — the team still rules out a coronary cause — but the nurse who notices "this pain gets better when he sits up and leans forward" is handing the team the clue that reframes the whole picture.
Dressler syndrome is treated as the inflammatory condition it is. Anti-inflammatory therapy is the backbone: NSAIDs (often high-dose aspirin, particularly relevant given the recent MI) and colchicine, which reduces both symptoms and the chance of recurrence; corticosteroids are generally reserved for cases that do not respond or when other agents cannot be used. Most patients improve, though recurrences can happen and some need a longer course. The nurse administers and monitors these medications — NSAIDs carry gastrointestinal and renal considerations, and colchicine has its own gastrointestinal side effects and dose adjustments in kidney disease — while managing the patient's pain and reassuring them that the plan is anti-inflammatory, not another intervention on the arteries.
Beyond medications, the nurse keeps a close eye on the trend: is the pain settling, is the fever coming down, are inflammatory markers falling, and — most importantly — is any effusion stable or growing? Repeat echocardiography is often used to follow the fluid, and the nurse's serial vital signs and physical assessment are what catch a quietly enlarging effusion before it tips into tamponade. Clear discharge teaching matters too: the patient should know this can recur, should understand their medication schedule, and should know which symptoms — worsening breathlessness, lightheadedness, recurrent chest pain — mean they need to be seen again.
Explore related ICU cardiac emergencies: cardiac tamponade, acute aortic dissection, fulminant myocarditis, and spontaneous coronary artery dissection (SCAD).
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