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C.H., a 44-year-old man, was brought to the emer-gency department by paramedics after being

found pulseless and apneic by a passerby. The coldand wet patient was found at a scene littered with beercans and spotted with numerous patches of blood onthe ground. He had been outside all night in ambienttemperatures as low as 35°F (1.6°C). Cardiac monitor-ing by emergency paramedics revealed asystole. Be-cause of the extreme coldness of the man’s body, CPRwas initiated and the patient was transported with noadditional resuscitative efforts by the EMTs.

On arrival at the emergency department, C. H. re-mained pulseless and apneic. The monitor rhythm in-dicated asystole with an occasional polymorphic Pwave. His rectal temperature was less than 84.0°F(28.8°C), the lowest reading found on the ED ther-mometers. His pupils were at 6 mm and nonreactive.No signs of trauma were found, and no obvious sourceof the blood found at the scene was located. Lividitywas noted on the buttocks. C. H. was intubated andgiven ventilatory support, and CPR was continued. In-travenous access was obtained through the externaljugular vein, and intravenous fluids warmed for 1minute in the department microwave were infused.Other rewarming measures included warming blan-kets placed under and over the patient and chemicalwarming packs placed in his armpits and on his groin.An indwelling bladder catheter and nasogastric tubewere inserted; gastric contents and results of a rectalexamination were guaiac negative. Blood specimenswere obtained, as were arterial blood gas values(Table 1). The patient’s temperature was continuous-ly monitored by rectal probe.

The advanced cardiac life support protocol forasystole was followed. One ampule of atropine was

administered intravenously and 1 mg of epinephrine,1:10,000, was given every 5 minutes. Thiamine, 100mg, and 1 ampule of 50% dextrose in water were alsoadministered with no change in baseline rhythm orclinical presentation. As rewarming proceeded, ven-tricular fibrillation was noted on the cardiac monitor,and the patient was consecutively defibrillated with200, 300, and 360 J with no response. A lidocainebolus of 100 mg was given, followed by another shock

at 360 J, and an additional ampule of epinephrine. Athird shock at 360 J resulted in a lapse back into asys-tole. CPR was continued until a rectal probe regis-tered 86.9°F (32°C), 55 minutes after arrival at theemergency department. At that time the physicianterminated the resuscitative effort and pronouncedthe patient dead. However, within minutes, sponta-neous movements of the jaw were noted by the nurse,and C. H. appeared to be trying to swallow. CPR wasimmediately resumed, and a carotid pulse was aus-cultated by Doppler. No blood pressure was palpable,but a spontaneous bradycardic rhythm developed,eventually settling to a junctional bradycardia at 48 to55 beats per minute. A dopamine infusion was start-ed, resulting in a palpable blood pressure. The patientwas transferred to the ICU, where he became hemo-dynamically stable. He recovered consciousness, wasextubated the next morning, and was transferred to astep-down unit 2 days later. He was discharged from

Barbara Carson, Austin, is Staff Nurse, Emergency Department,South Austin Hospital, Austin, Tex.For reprints, write: Barbara Carson, RN, MSN, FNP, CEN, 2619Monarch Dr, Austin, TX 78748.J Emerg Nurs 1999;25:356-60.Copyright © 1999 by the Emergency Nurses Association.0099-1767/99 $8.00 + 0 18/1/97889

Case ReviewSuccessful resuscitation of a 44-year-oldman with hypothermiaAuthor: Barbara Carson, RN, MSN, FNP, CEN, Austin, TexasSection Editor: Patty Campbell, RN, MSN, CCRN, ANP, CS

His rectal temperature wasless than 84.0°F (28.8°C), thelowest reading found on theED thermometers. His pupilswere at 6 mm andnonreactive.

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the hospital 8 days after the incident with no appar-ent deficits.

C. H., a member of the local homeless communi-ty, was known to the ED staff from 2 previous visitsduring the preceding month. He had a history ofseizures and alcohol abuse and had recently beentreated for hyponatremia and a decubitus ulcer on hisbuttocks. C. H. had been admitted to the hospital 1week before this incident but had left against medicaladvice before being transferred from the emergencydepartment to the floor. Social service consultationswere obtained during the previous visits, and shelterresources were made available to C. H. when he wasdischarged after this episode. Whether he followed upwith the resources given is unknown. Two weeksafter this successful resuscitation, C. H. was againfound on the ground, pulseless and apneic. This time,he was pronounced dead at the scene.

DiscussionHypothermia is defined as a core temperature lessthan 95°F (35°C).1,2 Accidental hypothermia is usuallythe result of environmental occurrences—often sud-den immersion in cold water or prolonged exposure tocold environments.1 These exposures may lead to hy-pothermia even in healthy subjects. Children and theelderly are particularly at risk for hypothermia be-cause of their altered thermoregulatory mechanisms.Another high-risk group is the homeless population,whose members are often unable to find shelter dur-ing times of inclement weather. The problem of hy-pothermia in this group is magnified by the use of al-cohol or other drugs. Ethanol is a vasodilator thatproduces anesthetic and central nervous system de-pressant effects.2 Intoxicated persons neither feel thecold nor respond appropriately to it, while increasedblood flow to the dilated peripheral vessels hastensthe loss of heat from the core.2

Body temperatures from 90° to 95°F (32° to 35°C)are classified as mild hypothermia.3 The body re-sponds to this initial cooling by increasing the meta-bolic rate and by shivering in an effort to create heat.Heart rate, cardiac output, and blood pressure all rise.

As the core temperature drops below 93°F (34°C), co-ordination is impaired and mental acuity diminishes,resulting in confusion. Heart rate, respirations, andcardiac output decrease. At 89.6°F (32°C), shiveringceases and the person begins to feel warm as a resultof vasodilation as hypothalamic control of vasocon-striction is lost. The resulting loss of core heat to theperiphery may be exacerbated by paradoxical un-dressing by the confused person. Lethargy follows,and the person soon becomes stuporous.1

As core temperatures fall to 86°F (30°C), the meta-bolic rate decreases, leading to further decreases in

Table 1Selected laboratory values*

Laboratory On Aftervalue admission 3 days

Blood gaspH 6.97 7.42PCO2 45 mm Hg 34 mm HgPO2 458% 63%HCO3 11 mEq/L 22 mEq/LBase excess –20.4 mEq/L –0.6 mEq/LFIO2 100 UnknownChemistrySodium 128 mEq/L 136 mEq/LPotassium 4.0 mEq/L 4.9 mEq/LChloride 94 mEq/L 102 mEq/LCarbon dioxide 19 mg/dL 24 mg/dLGlucose 89 mg/dL 75 mg/dLBUN 14 mg/dL 12 mg/dLCreatinine 0.6 mg/dL 0.7 mg/dLCalcium 8.6 mg/dL 9.3 mg/dLPhosphorus 5.2 mg/dL 4.5 mg/dLMagnesium 2.1 mEq/L 1.6 mEq/LSGOT/AST 41 U/L 48 U/LAlkaline phosphate 104 U/L 83 IU/LAmylase 102 U/L 102 U/LCardiac enzymesCK 494 IU/L 8829 IU/LCKMB 46.8 ng/mL 108.0 ng/mLTroponin I <0.6 ng/mL 4.4 ng/mLCBCWBC 9.2 K/mm3 7.8 K/mm3

RBC 3.30 M/mm3 3.67 M/mm3

Hemoglobin 10.9 g/dL 11.8 g/dLHematocrit 31.9% 35.9%Platelets 360 K/mm3 433 K/mm3

Drug screenAlcohol 106 mg/dLBenzodiazepine Positive

BUN, Blood urea nitrogen; CBC, complete blood cell count;CK, creatine kinase; FIO2, fraction of inspired oxygen; HCO3,bicarbonate; PCO2, partial pressure of carbon dioxide; PO2,partial pressure of oxygen; RBC, red blood cell count;SGOT/AST, serum glutamate oxaloacetate transaminase/as-partate aminotransferase; WBC, white blood cell count.*Not all laboratory values are included.

He was discharged from thehospital 8 days after theincident with no apparentdeficits.

core temperature. Oxygen consumption is half of nor-mal, and cerebral flow may diminish by two thirds.4,5

Pupils appear dilated and nonreactive, and both coughand gag reflexes are depressed. Sinus node depressiondevelops, with a slowing of conduction through theatrial-ventricular nodes. The Osborn (J) wave, a slow,positive deflection at the end of the QRS complex, mayappear on the ECG.2-4 Dysrhythmias may develop, pro-gressing from sinus bradycardia to lethal ventricularfibrillation. At 28°C (82.4°F), pulses and respirationsmay be undetectable. Ventricular fibrillation and asys-tole are common at these temperatures, and acidosismay be moderate to severe. Table 2 summarizes thepathophysiology of hypothermia.

ManagementEmergency departments should review treatmenttechniques and equipment requirements for hy-pothermia before times of need. With the increase inhomelessness in many urban areas, the potential forsevere hypothermia exists, especially in the sun beltstates where people are not well prepared for environ-mental temperature drops. As was found in our emer-gency department, the commonly used oral/rectal or

tympanic temperature probe is ineffective for trackingcore temperatures, which must be continuously moni-tored.2 Determination and monitoring of core tempera-tures are best accomplished by low-reading rectal oresophageal temperature probes.4 A warming blanketwith a rectal probe had to be borrowed from the ICU,and because no fluid warmer was available, fluidswere warmed in the department microwave (a verydangerous practice because of the inability to accu-rately control and measure the temperature of the flu-ids). A radiant warmer also would have been useful butwas not available to our department at that time. Ob-taining these items delayed the rapid warming treat-ment that was desirable in this case.

Recommended management of hypothermiavaries with the degree of severity. Passive rewarmingmeasures such as providing warm, dry clothes andwarm oral fluids and use of isometric exercises areoften sufficient for cases of mild hypothermia.1,3 Thepatient’s thermoregulatory mechanism must be in-tact for passive rewarming to be effective.1,3 Passiverewarming methods are slow and therefore inappro-priate for patients whose cardiovascular system hasbeen compromised.3

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Table 2Summary of stages and pathophysiology of hypothermia

Stage of hypothermia Temperature Presentation Pathophysiology

35°C Shivering General excitation; increased metabolic rate34°C Decreased mentation; decreased Loss of hypothalamic control of vasoconstriction

Mild coordinationAltered judgment Vasodilation occurs

33°C Confusion Loss of core heat to periphery

32°C Feels warmParadoxical undressing Temperature decreasesLethargy

31°C

Moderate30°C Stuporous Oxygen consumption decreased by 50%

Decreased heart rateDecreased respirations Cerebral flow diminished by 66%Decreased cardiac output Metabolic rate decreased

29°C Pupils dilated and nonreactive Core decreased furtherDepression of cough and gag reflex

28°C Arrhythmia sequence:Sinus bradycardia Sinus node depression slows conduction Atrial fibrillation with slow ventric- through atrioventricular node

ular responseSevere 27°C Ventricular fibrillation Tissue hypothermia causes decreased tissue

Asystole metabolismPulse and respiration undetectable Decrease in hepatic function causes toxic

accumulation of drugs in system26°C Acidosis moderate to severe

Modified from Danzl DF. Accidental hypothermia. In: Rosen P, Barkin R, Danzl DF, Hockberger RS, Ling LJ, Markovchick V, et al,editors. Emergency medicine: concepts and clinical practice. 4th ed. St. Louis: Mosby; 1998. p. 966.

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Active rewarming should be initiated for personswith moderate hypothermia who have core tempera-tures of 86°F (30°C) or higher. Active rewarmingmethods include provision of warm water baths,warm blankets, and radiant heat, such as provided byheating blankets or pads or radiant warmers, in addi-tion to the passive interventions of providing warmhumidified oxygen and warm oral fluids if the patientis conscious. Potential complications of active mea-sures include deep-ended hypothermia, also called“core-temperature afterdrop,” which is a deepeningof core hypothermia as peripheral circulation im-proves with vasodilation.1-3 Cold blood returning fromthe periphery to the central circulation paradoxicallymay drop the core temperature and trigger dysrhyth-mias.3 This peripheral vasodilation may result in a rel-ative hypovolemia and hypotension also called “re-warming shock.” Rewarming shock occurs when thebody is unable to maintain a blood pressure becauseof reduced fluid volume and catecholamine depletionfrom prolonged shivering. In addition, active rewarm-ing may result in a washout of lactic acid accumulat-ed in the periphery, causing acidosis.3

Active core rewarming measures may be used formoderate hypothermia and should be instituted whencore temperatures fall below 30°C or if severe cardio-vascular abnormalities exist. The goal of treatment isto maintain or restore cardiac perfusion and maxi-mize oxygenation.4 Intravenous fluids warmed to43°C and warmed oxygen are simple to administer.2

Gentle insertion of a nasogastric tube and an in-dwelling bladder catheter provide access for lavage ofthe gastrointestinal tract and bladder with warmsaline solution. Peritoneal lavage with a potassium-free dialysis solution warmed to 40° to 45°C is possi-ble in most emergency departments. Exchange trans-fusions and extracorporeal rewarming measures areless readily available, and specially trained personnel

are required to operate the equipment used in suchefforts.3 Efforts should concentrate on rewarming thecore; avoiding rapid increases in peripheral tempera-tures will help to prevent short-term complicationssuch as afterdrop and rewarming shock.

Rewarming should proceed no faster than 0.3° to1.2°C per hour in cases of mild hypothermia, but rapidrewarming greater than 3°C per hour is essential incases of cardiovascular instability.4 Oxygen and intra-venous fluids should be warmed and the patient’score temperature constantly monitored. Dependingon availability, this monitoring can be accomplishedwith use of rectal probes, esophageal or endotrachealtube temperatures, or bladder temperatures. Mostrhythm disturbances, such as sinus bradycardia andatrial fibrillation or flutter, will convert spontaneouslywith rewarming. Ventricular fibrillation may be re-fractory to pharmacologic therapy or defibrillation be-fore rewarming.6 It is important to remember that he-patic and renal functions can be impaired in thesepatients, resulting in diminished ability to synthesizeand excrete medications such as lidocaine. This ac-cumulation of drugs in the system may result in toxiclevels. Fifty to one hundred milliliters of 50% dextrosein water should be administered if blood glucose lev-els are low or unavailable.6 In alcohol-related hy-pothermia, 50 to 100 mg of thiamine is administeredintravenously.

Therapies for severe hypothermia must includegentle handling, because rough manipulation of thepatient may precipitate ventricular fibrillation. Incases of cardiac arrest, pulselessness should be as-sessed for 30 to 60 seconds before the initiation of CPR,but CPR should not be withheld in the hypothermicpatient. Three initial defibrillation attempts are recom-mended; if unsuccessful, CPR and rapid rewarmingshould be continued. Defibrillation may be re-attempt-ed when temperatures exceed 30°C.1,4,6

Because of the protective effects of hypothermia,successful rewarming may result in the patient’scomplete recovery. Decreased oxygen requirementsduring severe hypothermia protect the brain andother organs against anoxia and ischemia. Prognosisis directly related to the severity of metabolic acido-sis; a pH of 6.6 or less is a grave predictor of mortali-ty.2 Cardiac laboratory values may continue to riseover the next few days, as occurred in the case ofC. H. These rising isoenzymes occur in response tothe insult to the myocardium during resuscitative ef-forts. The usual criteria for death may not be valid inhypothermic patients; death in hypothermia shouldbe defined as failure to revive with rewarming.1,4 Re-suscitative efforts should continue until core temper-atures are at least 32°C.2,3

Rewarming should proceedno faster than 0.3° to 1.2°Cper hour in cases of mildhypothermia, but rapidrewarming greater than 3°Cper hour is essential incases of cardiovascularinstability.

Health care providers must be cognizant that it ispossible for severely hypothermic patients to surviveeven cardiac arrest with no neurologic deficits. A re-view of pathophysiology, treatment modalities, andgoals may help identify areas where the departmentis unprepared to treat a patient with severe hypother-mia. Equipment used for treatment of hypothermia,such as a core-temperature monitoring system, radi-ant warmers, and intravenous fluid warmers, shouldbe standard in all emergency departments. A clearunderstanding of the natural progression of hypother-mia and appropriate interventions to interrupt thecycle may provide emergency nurses with the oppor-tunity to participate in successful reversals of this po-tentially fatal environmental disorder.

References

1. Leo J, Huether S. Pain, temperature regulation, sleep, andsensory function. In: McCance K, Huether S, editors. Patho-physiology: a basis for disease in adults and children. 3rded. St. Louis: Mosby; 1997. p. 437-8.2. Cohen R, Moelleken B. Disorders due to physical agents.In: Turney L, McPhee S, Papadakas M, editors. Current

medical diagnosis and treatment. 38th ed. Stamford (CT):Appleton & Lange; 1998. p. 1474-77.3. Bessen H. Hypothermia. In: Tintinalli J, Ruiz E, Krome R,editors. Emergency medicine: a comprehensive studyguide. 4th ed. New York: McGraw-Hill; 1996. p. 846-50.4. Decker W, Li J. Hypothermia. In: Danzi D, editor. Emergen-cy medicine. Available from: URL: http://www. emedicine.com5. Weissenberger E. A 17-year old with severe hypothermiaand cardiac arrest from exposure. J Emerg Nurs 1992;18:380-2.6. Cummin R, editor. Advanced Cardiac Life Support. Dallas(TX): American Heart Association; 1997. p. 11-1–11-3.

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This section features actual emergency situationswith particular educational value for the emer-gency nurse. Contributions (4 to 6 typed, double-spaced pages) should include a case summary focused on the emergency care phase, accompa-nied by pertinent case commentary. Submit toPatty Campbell, Section Editor, c/o Managing Editor, 915 Lee St, Des Plaines, IL 60016-6569;phone (847) 460-4044; E-mail: khalm@ena.org.