T wave alternans

A 56 year old female with a history of asthma, hypothyroidism, tobacco use, chronic opioid use was found down at home,  found to have subarachnoid hemorrhage, left temporal hematoma with bilateral supraclinoid aneurysms on CTA, s/p embolization. Hospitalization has been complicated by vasospasm, fevers, long QT, and stress induced cardiomyopathy. On hospital day 11 the following EKG was obtained to assess the patient's long QT noted on previous EKGs (500, 516, 620).  

Rate 89, sinus rhythm with sinus p waves, left axis deviation, normal PR, QRS  intervals, prolonged QTc 732. T-wave inversions in I, II, III, aVF, V2-V6. In fact, if you pay attention to the T-wave morphology you will notice polymorphic deep t-waves, alternating in depth and morphology. There are two interesting points from this EKG: 1) T-QT pattern, and 2) T wave alternans. 

T-QT pattern: 

• Large, sometimes global T wave inversions
• T waves may be giant negative; occasionally giant positive
• Prolonged QT
• This is a stereotypical response to a variety of noxious stimuli, most notably acute CNS disorders, catecholamine effect, emotional stress (Tako-Tsubo cardiomyopathy), pulmonary edema, and massive PE. 
• This patient has both acute SAH, as well as catecholamine effect (recent adrenergic stress and pressors). 
• Usually evolves ~24h after the insult. Dr. Littman refers to this as the "day after" EKG. 

T wave alternans: 

• Beat to beat variability in the timing OR morphology of repolarization.
• Indicative of depolarization heterogeneity, which increases susceptibility to ventricular tachyarrythmias. 

Approximately 2 hours after the above EKG, the following rhythm strip was noted on telemetry. 
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Here you see a PVC followed by a compensatory pause, followed by polymorphic VT.  Pauses are frequent triggers of Torsades. The patient went on to experience several sustained, and non-sustained runs of polymorphic VT overnight. She received aggressive Mg & K repletion, defibrillator pads were placed, but patient remained hemodynamically stable and did not require defibrillation or overdrive pacing.  QT decreased and VT resolved. 

Teaching points:

• Acquired long QT is mostly iatrogenic, however not in this case. Other important causes of acquired long QT include acute CNS abnormalities, and acute stress cardiomyopathy. 
• Many medications can prolong QT, notably most psych medications, and antibiotics including quinines, macrocodes, azole antifungals. Electrolyte abnormalities are also often a culprit. 
• T wave alternans is a harbinger of ventricular tachyarrythmias. 
• Patient with prolonged QT need close telemetry monitoring, as well as aggressive K & Mg repletion to the upper limits of normal (K>4, Mg>2). 
• If patient experiences give 2mg MgSO4 IV, can repeat x 1. 
• If Torsades persists after Mg x 2, consider low dose isoproterenol or increasing heart rate by overdrive pacing, or giving a chronotrope such as dobutamine while you pursue emergent cardiology consultation. 
• Overdrive pacing should be transvenous, as opposed to transcutaneous, as there is not 1:1 capture with transcutaneous pacing, and pauses can trigger further episodes of tachyarrythmia. 

References: 
Warraich H, Buxton A, Kociol R. Macroscopic T-wave alternans in a patient with takotsubo cardiomyopathy and QT prolongations. Heart Rhythm. 2014 Oct;11(10):1848-9.
 
Sommargren C, Drew B. Preventing torsades de pointes by careful cardiac monitoring in hospital settings. AACN Adv Crit Care. 2007 Jul-Sep;18(3):285-93