STEMI mimics: Difference between revisions
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==Background== | ==Background== | ||
*ST segment elevation | *ST segment elevation is myocardial injury until proven otherwise | ||
*When STEMI is unlikely, | **1mm in two contiguous leads or Left Bundle Branch Block (LBBB) configuration meeting Sgarbossa criteria | ||
* | *When STEMI is unlikely based on symptoms and demographics, consider other etiologies of ST elevation | ||
**Serial EKGs helpful in observing evolution of STEMI pattern | |||
***Only 72% of patients with STEMI receive diagnosis in first 1.5h <ref>Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-hospital outcomes for STEMI patients presenting with non-diagnostic initial ECG: A report from the Aheadache mission: lifeline program. Am Heart J. 2013; 165(1):50–56.</ref> | |||
==Mnemonic== | ==Mnemonic== | ||
The mnemonic “ELEVATION”, can help you remember STEMI mimics | The mnemonic “ELEVATION”, can help you remember STEMI mimics | ||
*'''E'''lectrolytes (Hyperkalemia) | *'''E'''lectrolytes ([[Hyperkalemia]]) | ||
*'''L'''eft Bundle Branch Block | *[[LBBB|'''L'''eft Bundle Branch Block]] | ||
*'''E'''arly Repolarization | *[[early repolarization|'''E'''arly Repolarization]] | ||
*'''V'''entricular Hypertrophy (Left) | *[[LVH|'''V'''entricular Hypertrophy]] (Left) | ||
*'''A'''neurysm (Ventricular) | *[[LV aneurysm|'''A'''neurysm (Ventricular)]] | ||
*'''T'''hailand (Brugada Syndrome) | *'''T'''hailand ([[Brugada Syndrome]]) | ||
*'''I'''nflammation (Pericarditis) | *'''I'''nflammation ([[Pericarditis]]) | ||
*'''O'''sborne (J) Waves | *'''O'''sborne (J) Waves ([[hypothermia]]) | ||
*'''N'''on-Ischemic Vasospasm | *[[coronary artery vasospasm|'''N'''on-Ischemic Vasospasm]] | ||
==ELEVATION== | ==ELEVATION== | ||
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*Synonymous with J-point elevation (though not to be confused with a J-wave) i.e. elevation of the point where the QRS usually meets the isoelectric line | *Synonymous with J-point elevation (though not to be confused with a J-wave) i.e. elevation of the point where the QRS usually meets the isoelectric line | ||
*Some studies suggest an increased risk of VF in these patients, though the lifetime risk remains unclear | *Some studies suggest an increased risk of VF in these patients, though the lifetime risk remains unclear | ||
*Elevation in this case should be concave and greatest in precordial leads | |||
===[[Left ventricular hypertrophy (LVH)|Ventricular Hypertrophy (Left Ventricular Hypertrophy)]]=== | ===[[Left ventricular hypertrophy (LVH)|Ventricular Hypertrophy (Left Ventricular Hypertrophy)]]=== | ||
*LVH typically with ‘strain’ pattern | *LVH typically with ‘strain’ pattern | ||
*ST elevation should be: | |||
**In V1 - V3 only | |||
**Concave | |||
**Discordant with deep S wave | |||
**Not more than 2 mm elevated | |||
===[[Left ventricular aneurysm|Aneurysm (Ventricular Aneurysm)]]=== | ===[[Left ventricular aneurysm|Aneurysm (Ventricular Aneurysm)]]=== | ||
*After | *After MI, walls of ventricles can become aneurysmal | ||
*Q waves | **Manifests as persistent ST elevation in territory of old infarct | ||
* | **Q waves should be present in the leads with persistent ST elevation | ||
*[[Takotsubo cardiomyopathy]] (broken heart syndrome) | *Echo is required for the final confirmation | ||
*[[Takotsubo cardiomyopathy]] (broken heart syndrome) presents similarly | |||
===[[Brugada syndrome|Thailand (Brugada Syndrome)]]=== | ===[[Brugada syndrome|Thailand (Brugada Syndrome)]]=== | ||
* | *Cardiac sodium channel mutation (usually SCN5A) first described in Thailand in 1992 | ||
*May be responsible for 4-5% of all sudden cardiac deaths | *May be responsible for 4-5% of all sudden cardiac deaths | ||
*3 described ECG types | *3 described ECG types: | ||
* | **Types 1 and 2 more commonly give ST elevation | ||
**Type 3 has “saddle back” appearance without ST elevation | |||
*Can be pharmacologically unveiled (ex: antiarrhythmics such as sodium channel blockers), precipitated by illness or fever, or be intermittent (will commonly see an incomplete RBBB pattern) | |||
===[[Pericarditis|Inflammation (Pericarditis)]]=== | ===[[Pericarditis|Inflammation (Pericarditis)]]=== | ||
* | *Diffuse ST elevation | ||
* | **In acute presentation, there may be PR elevation and ST depression in aVR only, but this is poorly sensitive | ||
*In acute | *PR depression classically taught as EKG sign of pericarditis but may only occur in viral pericarditis | ||
*Consider the diagnosis of STEMI in favor of pericarditis when: there is ST depression anywhere (except for V1, aVR), ST elevation height in III>II, there is a convex/horizontal ST elevation morphology, or when there are new Q waves | *Consider the diagnosis of STEMI in favor of pericarditis when: there is ST depression anywhere (except for V1, aVR), ST elevation height in III>II, there is a convex/horizontal ST elevation morphology, or when there are new Q waves | ||
*If predominantly inferior elevation, depression in aVL is very sensitive for STEMI<ref>Bischof JE, Worrall C, Thompson P, et al. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med. 2016; 34(2):149-154.</ref> | *If predominantly inferior elevation, depression in aVL is very sensitive for STEMI<ref>Bischof JE, Worrall C, Thompson P, et al. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med. 2016; 34(2):149-154.</ref> | ||
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===[[Cocaine chest pain|Non-Ischemic Vasospasm]]=== | ===[[Cocaine chest pain|Non-Ischemic Vasospasm]]=== | ||
*True ST elevation, in the sense that the ST elevation pattern is that of an injury current, but has a different mechanism and a different management | *True ST elevation, in the sense that the ST elevation pattern is that of an injury current, but has a different mechanism and a different management | ||
*Cocaine-induced ST elevation secondary to vasospasm should be treated with | *Cocaine-induced ST elevation secondary to vasospasm should be treated with benzodiazepines and nitrates as needed | ||
*While it is possible to have a STEMI from a ruptured plaque and subsequent clot formation in a patient with cocaine toxicity, it is helpful to risk stratify patients with a suspected STEMI by age, risk-factors, etc | *While it is possible to have a STEMI from a ruptured plaque and subsequent clot formation in a patient with cocaine toxicity, it is helpful to risk stratify patients with a suspected STEMI by age, risk-factors, etc | ||
*It may be impossible to tell by surface ECG (and therefore without a left heart catheterization) if the ST elevation is due to cocaine toxicity or due to plaque rupture | *It may be impossible to tell by surface ECG (and therefore without a left heart catheterization) if the ST elevation is due to cocaine toxicity or due to plaque rupture | ||
Latest revision as of 16:49, 26 September 2019
Background
- ST segment elevation is myocardial injury until proven otherwise
- 1mm in two contiguous leads or Left Bundle Branch Block (LBBB) configuration meeting Sgarbossa criteria
- When STEMI is unlikely based on symptoms and demographics, consider other etiologies of ST elevation
- Serial EKGs helpful in observing evolution of STEMI pattern
- Only 72% of patients with STEMI receive diagnosis in first 1.5h [1]
- Serial EKGs helpful in observing evolution of STEMI pattern
Mnemonic
The mnemonic “ELEVATION”, can help you remember STEMI mimics
- Electrolytes (Hyperkalemia)
- Left Bundle Branch Block
- Early Repolarization
- Ventricular Hypertrophy (Left)
- Aneurysm (Ventricular)
- Thailand (Brugada Syndrome)
- Inflammation (Pericarditis)
- Osborne (J) Waves (hypothermia)
- Non-Ischemic Vasospasm
ELEVATION
Electrolytes (Hyperkalemia)
- T waves are peaked without any concave-down (tombstone) ST elevation
- T waves of hyperkalemia should be tall, symmetrical, pointed, and narrow
- Untreated hyperkalemia will progress to a sinuventricular rhythm or a sine wave
Left Bundle Branch Block
- LBBB as well as any LBBB configuration (ex: RV pacing) can result in ST segment elevation, usually < 5mm
- Use Sgarbossa Criteria to determine if there is a concurrent infarct
- In addition, may look for Cabrera’s sign or Chapman’s sign if infarct is suspected, though both are specific but poorly sensitive
- RBBB does not typically give ST elevation, therefore in cases of RBBB, the usual STEMI rules apply
Early Repolarization
- Normal variant often seen in young athletes
- Synonymous with J-point elevation (though not to be confused with a J-wave) i.e. elevation of the point where the QRS usually meets the isoelectric line
- Some studies suggest an increased risk of VF in these patients, though the lifetime risk remains unclear
- Elevation in this case should be concave and greatest in precordial leads
Ventricular Hypertrophy (Left Ventricular Hypertrophy)
- LVH typically with ‘strain’ pattern
- ST elevation should be:
- In V1 - V3 only
- Concave
- Discordant with deep S wave
- Not more than 2 mm elevated
Aneurysm (Ventricular Aneurysm)
- After MI, walls of ventricles can become aneurysmal
- Manifests as persistent ST elevation in territory of old infarct
- Q waves should be present in the leads with persistent ST elevation
- Echo is required for the final confirmation
- Takotsubo cardiomyopathy (broken heart syndrome) presents similarly
Thailand (Brugada Syndrome)
- Cardiac sodium channel mutation (usually SCN5A) first described in Thailand in 1992
- May be responsible for 4-5% of all sudden cardiac deaths
- 3 described ECG types:
- Types 1 and 2 more commonly give ST elevation
- Type 3 has “saddle back” appearance without ST elevation
- Can be pharmacologically unveiled (ex: antiarrhythmics such as sodium channel blockers), precipitated by illness or fever, or be intermittent (will commonly see an incomplete RBBB pattern)
Inflammation (Pericarditis)
- Diffuse ST elevation
- In acute presentation, there may be PR elevation and ST depression in aVR only, but this is poorly sensitive
- PR depression classically taught as EKG sign of pericarditis but may only occur in viral pericarditis
- Consider the diagnosis of STEMI in favor of pericarditis when: there is ST depression anywhere (except for V1, aVR), ST elevation height in III>II, there is a convex/horizontal ST elevation morphology, or when there are new Q waves
- If predominantly inferior elevation, depression in aVL is very sensitive for STEMI[2]
Osborn (J) wave
- Hypothermia, usually <30 C is associated with the presence of Osborn J waves
- Positive deflections at the J point.
- Bradycardia (including AV block) and atrial fibrillation are also common in moderate and severe hypothermia
- Hypothermic patients are at risk for VF
Non-Ischemic Vasospasm
- True ST elevation, in the sense that the ST elevation pattern is that of an injury current, but has a different mechanism and a different management
- Cocaine-induced ST elevation secondary to vasospasm should be treated with benzodiazepines and nitrates as needed
- While it is possible to have a STEMI from a ruptured plaque and subsequent clot formation in a patient with cocaine toxicity, it is helpful to risk stratify patients with a suspected STEMI by age, risk-factors, etc
- It may be impossible to tell by surface ECG (and therefore without a left heart catheterization) if the ST elevation is due to cocaine toxicity or due to plaque rupture
See Also
References
- ↑ Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-hospital outcomes for STEMI patients presenting with non-diagnostic initial ECG: A report from the Aheadache mission: lifeline program. Am Heart J. 2013; 165(1):50–56.
- ↑ Bischof JE, Worrall C, Thompson P, et al. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med. 2016; 34(2):149-154.
