Cooling off on Therapeutic Hypothermia: Long QTc during Therapeutic Hypothermia
– An Underreported phenomenon
Chima-Okereke, Chidinma MD; Cosgriff, JoAnne MD
Yale Primary Care Internal Medicine Residency Program, New Haven and Waterbury, Connecticut
Background
Case 1 Description
Case 2 Description
Since the advent of therapeutic hypothermia (TH), it has proven
to be an invaluable weapon in the neuroprotection armory in
patients that suffer witnessed cardiac arrest secondary to
ventricular tachycardia or fibrillations.
A 31 year old woman with a chronic tracheostomy for sleep apnea
presented in the ED from home after an aborted cardiac arrest.
An initial rhythm of ventricular tachycardia was noted by EMS and
she received a shock from the defibrillator with the return of
spontaneous circulation at home.
She was unresponsive on arrival and therapeutic hypothermia
protocol initiated. At presentation, her longest QT interval was 382
ms and corrected by the Bazett formula, her QTc was 429ms. As
she reached goal temperature at 33°C, her QT/QTc increased to
700/639ms.
A 77 year old man with a history of coronary artery disease
experienced a witnessed cardiac arrest while out for coffee with
friends. He received bystander CPR and was shocked twice by an
AED with the resumption of a perfusing rhythm.
Since it’s introduction in 2002 with the ILCOR Guidelines,
therapeutic hypothermia with cooling to 32-34°C for up to 24
hours has become an essential tool in helping protect the brain of
comatose patients following witnessed VT or VF cardiac arrest.
In the ED, cardiac catheterization showed a 99% ostial proximal
LAD stenosis which was stented. His initial HR was 80 and
QT/QTC interval was 378/444. ECGs performed every 5-6 hours
showed QT/QTc of 692/557 and sinus bradycardia at 37 bpm at
goal temperatures. Cooling was halted after 18 hours and his
QT/QTc shortened to 298/438 after he was rewarmed.
These two cases illustrate that bradyarrythmias and QTc
prolongation during therapeutic hypothermia is not a rare event.
A recent systemic review demonstrated that in patients treated
with therapeutic hypothermia, 40% showed an improved
neurological outcome at 6 months compared with 28% in the
normothermia group1. However this does not come without risk.
Hypothermia is known to facilitate arrhythmogenic cardiovascular
and electrophysiological effects.
ECGs were performed every 3-5 hours and she developed
marked sinus bradycardia to the 30s and wide QRS complexes.
Cooling was halted and rewarming begun at 20 hours after which
her QT/QTc shorted to 508/508 and hear rate improved at
normothermia.
Objectives


Indeed one study noted QTc prolongation (>460ms) in all patients
undergoing therapeutic hypothermia who previously had normal
QTc intervals2. The question remains whether this QTc
prolongation leads to an increased incidence of Torsades de
Pointes (TdP) or ventricular fibrillation. A small prospective study
confirms the increased QTc prolongation buts notes only 8%
progress onto VT with no increased incidence of life threatening
arrhythmias in the TH group3.
However as QTc prolongation is linked to TdP and other serious
arrhythmias, we advocate frequent ECG monitoring .
Graphs of QTc changes with TH
Learning Points
We will suggest that extreme QTc prolongation is a very real
and under-reported adverse effect of therapeutic hypothermia
that has the possibility of inducing refibrillation.
 Therapeutic Hypothermia (TH) can lead to QTc prolongation.
 Extreme QTc prolongation carries the risk of Torsades de
Pointe s(TdP), ventricular fibrillation and sudden death.
We propose that measures should be taken to incorporate
frequent periodic electrocardiogram (ECG) QTc monitoring into
Therapeutic Hypothermia protocols.
 However one small demonstrated no higher incidence of life
threatening arrhythmias in the mild TH group but further study
is needed as serious bradycardia and pauses were seen in
these 2 case studies.
QTc in milliseconds

We report on two case studies of patients who underwent
therapeutic hypothermia using the Arctic Sun cooling system
following cardiac arrest that resulted extreme QTc
prolongation.
Case 2: EKG at normothermia QT/QTc 378/444ms
Literature Review
Case 2: EKG at 33 degrees C QT/QTc 692/557ms
 We recommend incorporating into therapeutic hypothermia
protocols ECG monitoring at intervals of 4-6 hours as patients
approach goal temperatures in light of the potentially
arrhythmogenic effects of hypothermia.
 Opportunities for further study: In our cases, cooling was
stopped and rewarming began when QTc became extremely
prolonged. Is there is a role for preventing further cooling and
monitoring QTcs for the remaining of the cooling period?
References
1. Walters JH, Morley PT, and Nolan JP. The role of hypothermia in post-cardiac arrest
patients with return of spontaneous circulation: A systematic review. Resuscitation. 2011
May;82(5):508-16.
2. Khan JN, Prasad N, Glancy JM et al. QTc prolongation during therapeutic hypothermia:
are we giving it the attention it deserves? Europace (2010) 12, 266–270
Example of the Arctic Sun system used for the Therapeutic Hypothermia protocol
3. Storm C, Hasper D, Nee J, et al. Severe QTc prolongation under mild hypothermia
treatment and incidence of arrhythmias after cardiac arrest--a prospective study in 34
survivors with continuous Holter ECG. Resuscitation. 2011 Jul;82(7):859-62.