Therapeutic hypothermia after cardiac arrest in Long QT syndrome: Could it be an adjunctive treatment to prevent dysrhythmias?

Abstract

Therapeutic hypothermia has been used for neuroprotection following cardiac arrest presenting with ventricular tachycardia or ventricular fibrillation regardless of underlying cause. Long QT syndrome is a cause for polymorphic ventricular tachycardia, and we know that therapeutic hypothermia increases the QT interval. We managed a 27-year-old woman, who was 10 weeks post-partum, who collapsed secondary to ventricular fibrillation at home. Bystander cardiopulmonary resuscitation was started with successful resuscitation after a rescue shock from paramedics. On hospital admission, her computerised tomography head, computerised tomography pulmonary angiogram and echocardiography did not show any abnormality. Her baseline electrocardiogram showed prolonged QTc interval of 504 ms without ischaemic changes. After intubation and ventilation, she was treated with therapeutic hypothermia for 48 h. She had a further episode of polymorphic ventricular tachycardia requiring rescue shock just prior to starting therapeutic hypothermia in hospital. No dysrhythmias occurred during therapeutic hypothermia, although the QTc further increased. After stopping the therapeutic hypothermia, she had two further ventricular tachycardia episodes. After commencement of beta blockers, she remained free of arrhythmias, and an implantable cardioverter defibrillator was implanted, she has recovered without any neurological deficit. Ventricular dysrhythmias caused by prolongation of the QT interval during or after therapeutic hypothermia are not well understood. There has been a report of a patient also having ventricular dysrhythmia 2 h after re-warming post therapeutic hypothermia and also a report of arrhythmia free period during therapeutic hypothermia in a long QT syndrome patient; both these features are present in our patient. Re-warming is not usually known to cause any arrhythmias; however, it could be a problem in those with long QT syndrome. Whether therapeutic hypothermia has a place in helping to control ventricular dysrhythmias needs further study.

Summary

Therapeutic hypothermia (TH) can prolong the QT interval on an electrocardiogram (ECG). We report a case in a person with long QT syndrome (LQTS) who had collapsed due to ventricular fibrillation (VF). There was further prolongation of QT with TH, but the patient remained arrhythmia free until the re-warming period. This report indicates that TH can be safe in LQTS despite further prolongation of QT during the cooled period but may be prone to ventricular dysrhythmias in the re-warming period. The protective role for TH in LQTS needs further evaluation.

TH has been used for neuroprotection following cardiac arrest presenting with ventricular tachycardia (VT) or VF regardless of underlying cause. LQTS is one of the known causes for polymorphic VT, and we know that TH increases the QT interval.¹ Whether QTc prolongation secondary to hypothermia is able to induce VT or VF is less well understood. Guidance regarding use of TH in patients presenting with VT/VF and with baseline prolonged QT interval is currently unavailable. Below we present a patient with prolonged QT interval managed with TH that shows possible additional potential benefit of TH in this clinical situation.

A 27-year-old woman, who was 10 weeks post-partum, collapsed secondary to VF at home. Bystander cardiopulmonary resuscitation (CPR) was started with successful resuscitation after a rescue shock (RS) by paramedics. Hospital admission investigations showed a normal computerised tomography (CT) head, CT pulmonary angiogram and echocardiography. Baseline ECG (undertaken on a Philips Pagewriter 300PI) showed prolonged QTc interval of 504 ms (calculated by the software of the machine) without ischaemic changes; this was confirmed by a consultant cardiologist. No other past history or family history of note. She had had a course of metronidazole 2 weeks earlier for retained placental products; previous therapeutics were not confounding factors. The patient was admitted requiring intubation and ventilation and was treated with TH for 48 h. After admission, she had a further episode of polymorphic VT requiring RS just prior to starting TH. No dysrhythmias occurred during TH, and there was an observed increase in the QTc during TH (Figure 1). After stopping the TH, she had two further VT episodes for which she commenced beta blockers, and no amiodarone was given during the admission. An implantable cardioverter defibrillator (ICD) was implanted pre-discharge, and she has recovered without any neurological deficit. No genetic testing has been undertaken.

Figure 1.

Graph showing QTc interval in relation to temperature and episodes of ventricular tachycardia (VT) and introduction of beta blocker (BB).

We present a case of LQTS Schwartz score 4 in a young patient who with modern management had a good outcome. Interestingly, the patient did not have any ventricular dysrhythmias during TH despite further prolongation in the QTc but was prone to ventricular dysrhythmias in the early re-warming period. The mechanisms of temperature change on the ECG are multifactorial, but hypothermia can be associated with hypokalaemia, due to shift of potassium from extracellular to intracellular or extravascular spaces, and hypokalaemia can cause a decrease in the resting membrane potential in ventricular cells, reduce the T wave amplitude and induce QT prolongation.

Whether prolongation of QT interval with hypothermia will cause dysrhythmias is less well understood. Interestingly, Chien-Hua Huang et al.² report about a patient also having ventricular dysrhythmia 2 h after re-warming post TH, and Nishiyama et al.³ also report an arrhythmia free period during TH in a LQTS patient. Re-warming is not known to cause any arrhythmias; however, we observed this to be a problem in our patient who has LQTS. Whether TH has a place in abating ventricular dysrhythmias needs further study.