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
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<unk>  rules apply
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
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
In V1 - V3 only
Concave
Discordant with deep S wave
Not more than 2 mm elevated
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
Manifests as persistent ST elevation in territory of old infarct
Q waves should be present in the leads with persistent ST elevation
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)
Types 1 and 2 more commonly give ST elevation
Type 3 has “saddle back” appearance without ST elevation
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<unk>  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<unk> 
In acute presentation, there may be PR elevation and ST depression in aVR only, but this is poorly sensitive
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
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<unk>  from a ruptured plaque and subsequent clot formation in a patient with cocaine toxicity, it is helpful to risk stratify patients with a suspected<unk>  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
STEMI mimics
STEMI equivalents
Cardiac ablation complications
AV blocks
Vincent's angina
Myocardial infarction complications
Torsades de pointes
Scuba diving emergencies