EKGs are a simple, cheap modality that can give an emergency physician quite a bit of information. Sometimes, in a busy ER, this information can be very subtle and almost overlooked without a second thought. A perfect example of this is a New Tall T-wave in lead V1 (NTTV1). This finding can be a normal variant, but can also be a precursor to badness.
Takotsubo Cardiomyopathy was first described in Japan in 1990 and in the United States in 1998. It was named after an octopus trap (“tako-tsubo”) due to the shape of the trap being similar to the appearance of the left ventricular (LV) apical ballooning that occurs in this condition. Why is this condition so important to know? It can mimic acute coronary syndrome and most patients go to the emergency department because they are worried they are having an acute myocardial infarction.
It is well known that primary percutaneous coronary intervention (PPCI) is the gold standard in STEMI treatment and that decreased door-to-balloon time has better patient outcomes. Guidelines recommend that the interval between arrival at the hospital and intracoronary balloon inflation (door-to-balloon time) should be 90 minutes or less.
ECG interpretation is one of the most important skills to master as an emergency physician, and its interpretation can be very complex and frustrating. ECG manifestations can be very subtle, and sometimes the earliest and only ECG change seen will be reciprocal changes alone. To further complicate this, many patients have the atypical symptoms of nausea/vomiting, weakness, or shortness of breath and not chest pain.
Brugada Syndrome is an abnormal ECG (Right Bundle Branch Block Pattern with coved ST elevation over the right precordial leads of V1-V3), which leads to ventricular fibrillation (VF) and sudden cardiac death (SCD) in patients with structurally normal hearts. It has been recognized as a clinical entity since 1992. Why should all ED physicians know about this entity? Although a rare syndrome, it is often mistaken as a STEMI and more importantly the clinical spectrum can be asymptomatic to SCD.
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Torsades de pointes is a polymorphic form of ventricular tachycardia. Why does this occur? What does it characteristically look like? Why is this an important form of ventricular tachycardia to differentiate from the more classic monomorphic ventricular tachycardia? View this short 9 minute video on QT intervals and Torsades de Pointes.
Augmented leads (aVR, aVF, and aVL) were developed to derive more localized information looking at the right, lower, and left part of the heart respectively. Specifically, lead aVR obtains information from the right upper side of the heart. It also gives reciprocal information on the left lateral side of the heart, which is already covered by leads aVL, I, II, V5, and V6. This is the main reason lead aVR has become forgotten.