Resuscitation 47 (2000) 317–320

Case report

Successful defibrillation in profound hypothermia(core body temperature 25.6°C)

Richard Thomas a,*,1, Chris J. Cahill b

a Department of Anaesthetics, Royal Hospital Haslar, Gosport, Hampshire, PO12 2AA, UKb Department of Accident and Emergency Medicine, Queen Alexandra Hospital, Southwick Hill Road, Cosham, Portsmouth PO6 3LY,

Hampshire, UK

Received 19 May 2000; received in revised form 26 June 2000; accepted 26 June 2000

Abstract

We report a case of successful defibrillation in a severely hypothermic patient with a core body temperature of 25.6°C asmeasured oesophageally. Ventricular fibrillation is a recognised life threatening arrhythmia in severely hypothermic patients. Thetraditional wisdom is that this arrhythmia is refractory to defibrillation at temperatures below 28°C. © 2000 Elsevier ScienceIreland Ltd. All rights reserved.

Keywords: Hypothermia; Defibrillation; Ventricular fibrillation

www.elsevier.com/locate/resuscitation

1. Introduction

Accidental hypothermia is associated with bothbenign and malignant cardiac arrhythmias [1].Cardiac arrest, secondary to ventricular fibrillationis the commonest cause of death in accidentalhypothermia in man [2–4], and in experimentalanimals [5]. Hypothermia itself induces character-istic electrophysiological and mechanical alter-ations in the heart that predispose toarrhythmogenesis [6]. Progression to pre-terminalor fatal arrhythmia may be precipitated by fluidmaldistribution, continued body cooling of thebody or anything but the most gentle handling ofthe casualty [7]. It is recognised that defibrillationof severely cold myocardium is difficult [8]. Thismay be due to the decrease in fibrillation threshold

observed as cardiac temperature falls [9]. Part ofthe rationale behind rapid rewarming techniquessuch as extra-corporeal bypass is to raise the deepbody temperature above such a ‘fibrillationthreshold’. Extra-corporeal bypass techniques arebeyond the facilities and capabilities of somehospitals.

2. Case report

An 82-year-old female was found lifeless in herunheated living room by her neighbours at 09:00h. Ambient air temperature was 13°C. Her generalpractitioner attended 10 min later, and found herapnoeic, blue, apparently lifeless and commencedconfirmation of death. Heart sounds were heard,and a faint carotid pulsation was detected at a rateof 25 beats per min (bpm). Basic life support wascommenced and an ambulance was called to thescene. By 09:31 h the ambulance had arrived,tracheal intubation and artificial ventilation with

* Corresponding author. Present address: West Court, 14 WestStreet, Titchfield, Fareham, P014 4DH, UK. Tel.: +44-1329-843580;fax: +44-13256-354224.

1 Now of: Department of Anaesthetics, North Hampshire HospitalBasingstoke, Hampshire, RG 24 9NA, UK.

0300-9572/00/$ - see front matter © 2000 Elsevier Science Ireland Ltd. All rights reserved.PII: S0300-9572(00)00254-9

R. Thomas, C.J. Cahill / Resuscitation 47 (2000) 317–320318

100% oxygen had been instituted. Intravenous ac-cess was obtained and 1.0 mg of atropine adminis-tered as the ECG demonstrated sinus bradycardiaof 30 bpm. Non-invasive blood pressure (NIBP)was unrecordable.

Transfer to the emergency department took 30min. On arrival the Glasgow coma scale was 3/15,heart rate 36 bpm, with a spontaneous respiratoryrate of five per min. Her pupils were small andnon-reactive. Her peripheral circulation was inade-quate as demonstrated by very prolonged capillaryrefill time and unrecordable NIBP. Blood glucosewas 8.6 mmol/l. On transfer to the resuscitationtrolley she developed pulseless ventricular tachy-cardia at 10:00 h. This reverted to a junctionalbradycardia of 30 to 50 beats per min with a single200J DC shock. Atropine 0.5 mg and 500 mls ofwarmed colloid were administered. Junctional rateincreased to 65 and NIBP to 80/50 mmHg. Initialarterial blood gas analysis revealed an acidosis ofmixed respiratory and metabolic aetiology.

An oesophageal thermocouple thermometer re-vealed a core temperature of 25.6°C. Rectal andtympanic membrane temperature measurementsconfirmed this. Passive re-warming was com-menced and she was artificially ventilated.

She developed ventricular fibrillation at 10:24 h.After two 200J DC shocks, one 360J DC shockand 1.0 mg of adrenaline this reverted to a junc-tional bradycardia of 55 bpm. NIBP was 90/55mmHg.

En route to the intensive therapy unit (ITU),frequent multifocal ventricular ectopic beats oc-curred. On arrival in ITU at 1038, her observa-tions were NIBP 70/30 mmHg, heart rate 45 bpmand oesophageal temperature 25.3°C. Radial arte-rial and right internal jugular central venous ac-cess was obtained and invasive monitoring wascommenced shortly after arrival in the ITU. Inva-sive blood pressure (IBP) was 70/30mmHg and anadrenaline infusion was commenced. Externalwarming with a forced air device was used. Shewas ventilated to maintain an arterial carbon diox-ide tension of 5 kPa.

Initial progress on ITU was satisfactory. At1200 her cardiovascular parameters were stablewith adrenaline infusion of 0.14 micrograms/kgper min: IBP 130/80 mmHg, heart rate 70 in sinusrhythm, and central venous pressure of 7 mmHg.Oesophageal temperature had risen to 27°C and adiuresis of 0.5 ml/kg per h was measured. On

re-warning, she developed several benign supra-ventricular arrhythmias.

Her past medical history included idiopathicepilepsy, diagnosed in 1956 and treated with phe-nobarbitone, treated hypothyroidism and radicalvulvectomy for carcinoma. She had a history ofdepression and, in 1994 she had taken phenobarbi-tone in a deliberate overdose.

Twelve hours after admission, she had beenwarmed to 36°C, weaned off adrenaline andstarted on dopexamine to maintain an adequateblood pressure and urine output. Sinus rhythmpersisted once her core body temperature hadreached 30°C. Her core body temperature hadincreased by approximately 1°C per h. Satisfactorygas exchange was maintained on a F1O2 of 0.3. Nosedation had been administered.

A computerised tomography (CT) scan of herbrain performed the next morning was unremark-able. After 24 h of normothermia, her circulationremained stable with satisfactory gas exchangeand normal acid-base variables. Bowel soundswere present and urine output adequate. Howevershe had shown no signs of wakening, with apersistently low Glasgow coma scale (3/15), fixedpupils and weakly positive cough reflex. It was feltthat significant cerebral damage had occurred. Shestarted to deteriorate with worsening gas ex-change. Consultation with close family memberssupported a decision not to escalate treatment.Later the following day she became bradycardicand ultimately asystolic. Death was confirmed 56h from admission.

Coroner’s post mortem examination revealedacute bronchiolitis on a background of chronicgranulomatous lung disease. The following bio-chemical analyses on admission samples were onlyavailable after death: thyroid function was withinnormal limits and elevated phenobarbitone levelsof 115 mg/l (therapeutic range 15–40 mg/l) everpresent.

3. Discussion

Successful defibrillation occurred at a core tem-perature below 26°C. Published literature [10–14]and resuscitation texts [15–17] comment on thedifficulty of defibrillating cold myocardium. A re-cent case report of successful defibrillation at acore temperature of 25.9°C [18] confirms that our

R. Thomas, C.J. Cahill / Resuscitation 47 (2000) 317–320 319

experience is not unique and therefore indicatesthe potential value of attempting defibrillation insuch circumstances.

Primary hypothermia may occur with normalthermoregulation but overwhelming exposure tocold. Hypothermia may also occur with mild tomoderate cold exposure but abnormal thermoreg-ulation. Humans enjoy the survival advantages ofhomeothermy and defend a relatively narrowrange of body temperature primarily by be-havioural means [19]. Hence it can be appreciatedthat any condition adversely affecting the abilityto regulate body temperature can result in suchsecondary hypothermia. Examples include hypopi-tuitarism, myxoedema, alcohol or drug intoxica-tion, phenothiazine therapy, head injury andcerebral neoplasm [20].

Mortality from hypothermia is very high in theelderly population, and associated with coexistentillness [21,22]. This contrasts the experience ofaccidental hypothermia in young adults and chil-dren where good functional recovery is possibledespite prolonged resuscitation [23–28].

This case report is an example of a specialresuscitation situation and specific guidance rele-vant to hypothermic cardiac arrest is taught aspart of the Advanced Life Support syllabus [15].We feel, however, that the following points areworth stressing.1. The principles of basic and advanced life sup-

port apply to the hypothermic patient. In par-ticular, despite theoretical difficulties ofsuccessfully defibrillating myocardium below30°C, three initial shocks should be given asper the ventricular fibrillation protocol.

2. The diagnosis of death may be difficult andmajor arteries should be palpated for at least 1min before concluding that cardiac output isabsent. Death should only be pronounced oncea patient has been warmed above 33°C, orattempts to raise the core temperature havefailed.

3. Re-warming using a forced air device requiresa spontaneous cardiac output to be effective.

4. Great care is needed in the handling of thehypothermic patient. Even trivial physical dis-turbances can precipitate compromisingarrhythmias.

5. Ventricular fibrillation can be precipitated byintubation. Pre-oxygenation may help to pre-vent this complication.

6. Chest compressions should be commenced ifcardiac output is absent. This intervention mayresult in ventricular fibrillation that may berefractory to cardioversion. In this circum-stance, rapid care rewarming in parallel withcontinuing cardiopulmonary resuscitation isnecessary until defibrillation becomes effective.

7. As a general guide patients should be re-warmed at a rate which accords with the rapid-ity of onset of their hypothermia. This casereport illustrates a management approach ofslow re-warming in an elderly patient who hadan insidious onset of hypothermia.

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