2010 ACLS Guidelines
history of hypothermia and review (Chest 2008;133;1267-1274)
Hypothermia review article Bernard SA, Buist M, Induced hypothermia in critical care medicine: a review. Crit Care Med 2003;31:2041-51.
Major clinical trials have been done using mild therapeutic hypothermia following cardiac arrest. The Hypothermia after Cardiac Arrest Study Group performed the largest randomized clinical trial of hypothermia . In this multicentered trial with blinded assessment of outcome, adult patients who remained comatose after suffering cardiac arrest from ventricular fibrillation were randomized to therapeutic mild hypothermia and normothermic groups after ROSC. The arrest was of presumed cardiac etiology, estimated down time no longer than 15 min and time to ROSC no more than 60 min from the time of collapse. Patients in the hypothermic group had an external cooling device applied and set to a target temperature of 32?34°C. The temperature was maintained for 24 h followed by passive rewarming over 8 h. All patients were intubated, sedated and paralyzed. Standard critical care was delivered to both groups and the temperature was continuously monitored by bladder catheter. Only 8% of all patients in cardiac arrest were eligible for the study with 275 patients entered . For patients in the hypothermic group, it took 105 min to initiate cooling measures. The median time to achieve the target temperature of 32?34°C was 8 h. Outcome was assessed at 6 months and 55% (75/136) of patients had a favorable neurologic outcome in the hypothermic group compared with 39% (54/137) in the normothermic group (P = 0.009). After adjustment for all the baseline variables, the risk ratio was 1.47 (95% CI 1.09?1.82). The overall 6-month mortality was also significantly better in the hypothermic compared with the normothermic group (41% versus 55%; P = 0.02). Although sepsis was more commonly seen in the hypothermic group, there was no overall difference in complications between the two groups . The other major randomized controlled trial was performed by Barnard et al.  for adult patients with out-of-hospital cardiac arrest from ventricular fibrillation. Patients with ROSC were randomized to hypothermic and normothermic groups. All patients were intubated, sedated and paralyzed and received standard critical care treatment. Patients in the hypothermic group were cooled with ice packs as soon as possible with the goal of reaching a core temperature of 33°C. This temperature was maintained for 12 h when the patients were actively rewarmed over 8 h. Outcome was assessed at discharge and 49% (21/43) of patients in the hypothermic group had a good neurologic outcome compared with 26% (9/34) in the normothermic group (P = 0.046). The odds ratio for a good outcome was 5.25 (confidence interval (CI) 1.47?18.76; P = 0.011). The mortality was 51% in the hypothermic group and 68% in the normothermic group (P = 0.145) . In a small feasibility study using a helmet device to induce hypothermia, Hachimi-Idrissi et al.  studied 30 patients who were unconscious following ROSC after cardiac arrest with asystole or pulseless electrical activity. It took 3 h for the patients to reach the target temperature of 34°C. Three of 16 patients in the hypothermia group and one of 14 patients in the normothermic group left the hospital alive. No adverse effects due to hypothermia treatment were noted. Holzer et al. [11?] did a metaanalysis of mild therapeutic hypothermia for comatose patients with ROSC after cardiac arrest. They found that more patients in the hypothermia group had favorable neurologic outcome than the normothermic group with a risk ratio of 1.68 (96% CI 1.29?2.07). The number needed to treat for one additional patient to have a favorable neurologic outcome was six with a 95% CI of 4?13.
ILCOR for therapeutic hypothermia after card arrest cool 32-34 C for 12-24 hours if ROSC after v. fib arrest (Circ 2003;108:118)
and probably in other rhythms as well
30 cc/kg of 4° C (39° F) crystalloid over 30 minutes (Resus 2003;56:9-13) and (Crit Care Med 2005;33(12):2744)
1500 cc of NS or NS and colloid over 30-60 minutes, then 500cc Q10 minutes if temp still >33.5
(resus 2003;57:231) Review (Crit Care Med 2003;31(7):2041) probably most effective method is 30-40 cc/kg of 4 C fluid
Practical Aspects (Inten Care Med 2004;30:757)
Meta-analysis: (Hypothermia for neuroprotection after cardiac arrest: Systematic review and individual patient data meta-analysis Crit Care Med 2005;33(2):414-418)
Great review on how to get it done (CJEM 2005;7(1): )
suitable patients: v-fib/v-tach with motor score of 4 or less not due to other conditions except hypoxic/ischemic encephalopathy
sedate morphine 2-5 mg/hr and propofol 1-3 mg/kg/hr
cooling blanket above and below the patient with ice packs in groin/armpits
desired temp 33 + – 5 C
The protocol for shivering prophylaxis and treatment follows. All patients will receive treatments #1 and #2. All other treatments will be initiated sequentially if shivering occurs in the study protocol. All are standard, currently used treatments for the prevention and treatment of shivering in hypothermic individuals: 1) Acetaminophen 650mg every 4 hours orally or per nasogastric tube or rectum 2) Meperidine 1 mg/kg pre-cooling loading dose given orally or intravenously, if the patient is not intubated and has no other contraindications. Maximum dose of 100mg. if the dose is >50mg then the doses are divided into two and separated by 30 minutes. (This has been without complication in patients treated so far.) 3) Combined stocking/glove/face warming (heated gel pack for hands and feet and warmed oxygen mask/face tent) 4) Buspirone 30 mg. every 8 hrs orally or per nasogastric tube 5) Meperidine, either orally or intravenously, 0.5 to 1.0 mg/kg every 30 minutes to effect or sedation (maximum 1500mg/day) 6) If the patient is intubated or there is a known seizure history, propofol is initiated intravenously with 5 micrograms/kg/minute until effect (maximum 2000 mg/day). For any associated nausea, ondansetron is the recommended anti-emetic with an initial dose of 4mg IV and then 8 mg PO/NG every 8 hours, as needed.
Intensive Care Med. 1983;9(5):275-7. Related Articles, Links Serum potassium levels during prolonged hypothermia. Koht A, Cane R, Cerullo LJ. Hypokalemia (mean serum potassium 2.3 +/- 0.4 mEq/l) was observed in six hypothermic patients (30 degrees – 32 degrees C) with head injuries or brain hypoxia. In the first three patients, potassium was administered to maintain serum levels above 3.5 mEq/l and on rewarming after 48 h of hypothermia hyperkalemia (peak serum potassium = 7.1 +/- 0.5 mEq/l) associated with cardiac arrhythmias developed. The remaining three patients received sufficient potassium to approximately replace measured losses during the hypothermic period. These patients did not become hyperkalemic on rewarming. Clinically insignificant sinus bradycardia, premature atrial contractions and junctional rhythms were seen during hypothermia with hypokalemia. We conclude that hypothermia produces hypokalemia by a shift of potassium from the extracellular to intracellular or extra vascular spaces. Potassium therapy during controlled hypothermia in the range 30 degrees – 32 degrees C should only replace measured losses. Consider prophylaxis with broad spectrum abx, cold limits immune response and allows easier reproduction of bacteria
Tylenol may make hypothermia easier and overcome impulse to fever (Stroke 2002;33(1):134) The two NEJM studies
NEJM 2002;346(8):549 and 557
Meta-Analysis (Crit Care Med 2005;33(2):414)
Prospective Study of iced NS (Crit Care Med 2005;33(12):2744)
Practical Aspects (Inten Care Med 2004;30:757)
How to get it done (CJEM 2005;7(1):42)
Prelim study of iced crystalloid (Resus 2003;56:9)
Review (Crit Care Med 2003;31(7):2041)
Resus 2007 73:46 cold infusions get patients cold, but alone do not keep patients cold
Effects of hypothermia on drug metabolism (Crit Care Med 2007;35:2196)
Another hypothermia series (Anaesthesia 2008;63:15)
1. shivering from hypothermia is self explanatory. We paralyze for visible shivering but recognize we could be missing some. 2. delayed (Lance Adams) action myoclonus is a problem long after leaving ICU. 3. early postanoxic myoclonus (of which status myoclonus is a subtype) is uniformly associated with poor outcome in my experience and my discussions with colleagues. 4. seizures, which more often are misdiagnosed myoclonus, are diagnosed and treated just as in other settings. I cannot remember the last time I saw postanoxic seizures within 24h, although I am sure I have seen it, but I can easily remember 2 status myoclonus patients, the last of which developed profound metabolic acidosis and rhabdomyolysis when we stopped the paralytics.
ketamine may have a role (Anesth Analg 2008;106:120)
for arrest 32-34
for other uses 35.5 is probably a good goal
Each liter of iced saline cools ~0.8-12 C
Baumgardner et al. Anesth Analg 89:163?169
Rajek et al Anesthesiology 93(3):629 ? 637
Bernard et al. Resuscitation 56(1):9-13
Virkkunen et al. Resuscitation 62(3):299-302
Polderman Crit Care Med 2005;33:2744
goal is to reach target in 2 hours
SR shows NNT for leaving hospital with good neuro is 6 (Crit Care Med 2005;33:414) (95% CI 4-13)
they still talk about empiric 30 cc/kg
36 ? 35 ºC Tachycardia < 35 ? 32 ºC Bradycardia < 33 ºC ECG – inc PR, wide QRS, Inc QT < 30 ºC Increased risk of fatal arrhythmias ? Hemodynamic effects Decrease in CO by 25% (coupled to VO2) < 35 ? 32 C: mild increase in MAP (?cold-pressor? response) ? Treatment is non-specific, supportive care Plt dysfunction and thrombocytopenia from clumping?
Can use thrombolytics, anticoagulation, antiplatelets (COOL MI, Bernard et al.)
can cause hyperglycemia and metabolic acidosis (? RTA)
Perform ABGs at pt’s temperature
If done at normal temp, you will overestimate PaO2 and Overestimate PaCO2
20% increase in baseline WBC
Look at temperature of water to know if it is a fever
occurs at 36, should stop at 34
Bedside Shivering Assessment Scale (BSAS):
0 ? None: No Shivering
1 ? Mild: Shivering localized to neck/thorax, maybe seen only as artifact on ECG or felt by palpation
2 ? Moderate: Intermittent involvement of the upper extremities +/- thorax
3 ? Severe: Generalized shivering or sustained upper/lower extremity shivering
treat with cutaneous vasodilation
Mg INfusions goal Mg 3.0 mg/dL
Central alpha receptor mechanism
buspirone 30 mg po q 8
demerol 0.5-1 mg /kg / hr
dexmedetomidine 0.2-1.5 mcg/kg/hr
Propofol <5 mg/kg/hr
APAP 975 mg PO
Buspirone 30 po q 8
start with mg 0.5-1 g/hr until 3-4 mg/dL
fentanyl or demerol
last shot is paralyze
Mg Study (Zwefler et al 2004)
vasodilation can cause dramatic hemodynamic changes
rebound increase in ICP
bring up < 0.25 C/hr
rebound fever universal (setpoint?)
from lecture by Neeraj Badjatia
Bedside Shivering Assessment (BSAS)
0-None, no shivering. Must not have shivering on EKG or palpation.
1-Mild-localized to neck/thorax. May only be noticed on palpation or EKG.
2-Moderate-intermittent involvement of upper extremities +/- thorax
3-Severe-generalized shivering or sustaine dupper extremity shivering
All patients receive
Acetaminophen 650 mg PO Q 6 hours unless contraindication
Buspirone 30 mg PO Q 8 hours
If BSAS > 1
Fentanyl Drip (titrate as per EHCED drip sheet)
If still BSAS > 1
Propofol Drip (titrate as per EHCED drip sheet)
If BSAS still > 1 after titration of sedation/opioid
Nimbex 0.15 mg/kg IV Q 1 hour
Paralysis should only be necessary under extraordinary circumstances
Physiological Effects of Hypothermia
Ventricular arrhythmias (HT patients are more susceptible to atrial and ventricular fibrillation).
Myocardial depression, bradycardia
Increased SVR, decreased CO, decreased contractility (Hypothermia has a negative chronotropic effect on pacemaker tissue, which may lead to bradycardia or AV block).
Increased PR, QRS, QT intervals
(Hypothermia may cause repolarization abnormalities, producing ST segment elevation and TWI).
Decreased RR (Hypoventilation, suppression of cough, and mucociliary reflexes associated with hypothermia may lead to hypoxemia, atelectasis and pneumonia.)
Shift in oxyhemoglobin dissociation curve to the left (less oxygen is released from oxyhemoglobin to the tissues)
Decreased cough & Increased secretions
Decreased basal metabolic rate (Hypothermia inhibits insulin release from pancreas, but glucose levels remain normal in mild HT because shivering increased glucose utilization. Shivering increases metabolic rate, Co2 production, o2 consumption and myocardial work).
Decreased drug biotransformation
Decreased tissue perfusion
Decreased motility, liver function, insulin release
Decreased renal plasma flow
Decreased urine output
Increased specific gravity
Increased blood viscosity (hemoconcentration)
Decreased muscular tone
Adapted from Burns, S. (2001). Revisiting Hypothermia; A Critical Concept. Critical Care Nurse, 21 (2), 83-86
Physiology og Hypothermia (Br J Anaes 1959;31:96)
water temp <5 c =active cooling water temp >20 C indicates no or minimal cooling If <10 for prolonged period of time, consider cultures and antibiotics causes ileus and asymptomatic elevation of amylase. Enteral feeding should be held during cooling Mild prolongation of Pt and Ptt but all thrombolytics, antiplt, and anticoag can be given if clinically indicated causes insulin resistance Is our vent air heated, if so, can it be turned Correct K to 3.4, no higher ref for BSAS Neurocrit Care 2007;6:213 write stephan for lipase added to labs absence of brainstem reflexes, consider not doing hypothermia columbia uses not following commands They give demerol 25 mg as their first shivering response
Use Mag for shivering, 1 g/hr
Journal of Applied Physiology, Vol 69, Issue 1 376-379
Determination of esophageal probe insertion length based on standing and sitting height
The following equations were derived to predict the placement of the esophageal probe at the T8/T9 level based on standing height: L (CM) = 0.228 x (standing height) – 0.194, and sitting height: L (cm) = 0.479 x (sitting height) – 4.44.
Management following resuscitation from cardiac arrest: recommendations from the 2003 Rocky Mountain Critical Care Conference
Canadian Journal of Anesthesia 52:309-322 (2005)
- Induce hypothermia [bladder or esophageal temperature 32 to 34°C within four hours of return of spontaneous circulation (ROSC)] and maintain for 24 hr if the patient fulfills the following criteria after a witnessed ventricular fibrillation or witnessed ventricular tachycardia arrest:
– Interval < 15 min from collapse to resuscitation attempt
– ROSC achieved within 60 min of arrest Exclusions to this approach include hypotension (mean arterial pressure < 60 mmHg for more than 30 min after ROSC), response to voice after ROSC, and Glasgow coma score > 9. OVERALL EVIDENCE GRADE: B Induction of hypothermia COULD be extended to patients with pulseless electrical activity or asystolic arrests if they have witnessed arrests with collapse-resuscitation attempt intervals < 15 min and they achieve ROSC within 60 min. This is an extrapolation and has NOT been studied in randomized controlled trials. OVERALL EVIDENCE GRADE: E
- Hyperthermia should not be tolerated. Temperatures over 38°C should be reduced. OVERALL EVIDENCE GRADE: B
- Consider treatment of temperatures over 37°C during the first 72 hr after ROSC with active cooling and/or pharmacologic means such as acetaminophen and/or non-steroidal antiinflammatory drugs (NSAID). OVERALL EVIDENCE GRADE: D
- If the patient is hypothermic on presentation rewarming should be gradual and final temperature should not exceed 37°C. OVERALL EVIDENCE GRADE: B
- Serum magnesium level and potassium levels should be normalized. OVERALL EVIDENCE GRADE: E
- Replace peripheral or central lines placed without proper sterile techniques during the cardiac resuscitation. OVERALL EVIDENCE GRADE: E
- Identify and manage complications resulting from cardiopulmonary resuscitation. OVERALL EVIDENCE GRADE: E
- Administer deep vein thrombosis prophylaxis if systemic anti-coagulation is not required. OVERALL EVIDENCE GRADE: A
TABLE III Neurologic care recommendations
- Elevate head of bed at least 30° and maintain in the midline position for first 24 to 48 hr OVERALL EVIDENCE GRADE: C
- Document neurologic evaluation shortly after return of spontaneous circulation (ROSC) and at 6 hr, 12 hr, 24 hr, 36 hr, 48 hr, and 72 hr after ROSC. This assessment cannot be done in patients who are anesthetized/paralyzed or hypothermic and should not be attempted if these are ongoing. The following minimum findings should be documented at each assessment:
- Motor response to pain (central and peripheral);
- Pupillary eye signs (light response; corneal; occulocephalic);
- Glasgow coma scale
- Ability to breathe or trigger ventilator.
OVERALL EVIDENCE GRADE: E
- If sedation is needed short lasting agents are preferred. Sedation should be with fentanyl/midazolam or with propofol. Sedation should be interrupted daily unless the patient is paralyzed for hypothermia treatment. OVERALL EVIDENCE GRADE: B
- Benzodiazepines (lorazepam, midazolam, diazepam) should be administered acutely to treat seizure activity if it occurs. Phenytoin (or its prodrug fosphenytoin) is indicated to prevent the recurrence of seizures (20 mg·kg?1 loading dose). Pentobarbital, midazolam, or propofol infusions may be required if seizure activity continues despite additional doses of phenytoin or lorazepam. OVERALL EVIDENCE GRADE: A
- Frequent myoclonus should be treated with oral clonazepam or iv midazolam. If this is not successful valproic acid, propofol or newer anticonvulsant drugs can be tried. OVERALL EVIDENCE GRADE: E
- If best neurologic response 72 hr after ROSC is not better than withdrawal to painful stimuli, the prognosis is dismal. Intensive medical support should be withdrawn and palliative care provided. This assumes that barbiturates, neuromuscular blockers and/or other potent sedative agents have not been administered and that there is no other reason except anoxic brain damage from the arrest to explain the neurologic findings. OVERALL EVIDENCE GRADE: D
- Routine computed tomography (CT) scan of the head is not indicated. Head CT scan should be done if there are definite indications. These include signs of raised intracranial pressure or lateralizing signs. Magnetic resonance imaging of the brain can be considered as part of a research protocol to assess the contribution of this technique to outcome prediction. OVERALL EVIDENCE GRADE: E
- The use of somatosensory evoked potentials should be considered as part of a protocol to assess its contribution to prognostication. Routine electroencephalogram (EEG) is not indicated but EEG should be used if there are concerns about ongoing seizure activity. OVERALL EVIDENCE GRADE: C
- Glasgow outcome scores must be recorded to evaluate outcome at appropriate intervals. OVERALL EVIDENCE GRADE: E
TABLE IV Respiratory care recommendations
- FIO2 adjusted to give PaO2 over 100 mmHg for the first 24 hr (SaO2 of 99?100%). OVERALL EVIDENCE GRADE: E
- If mechanically ventilated use positive end-expiratory pressure (PEEP) of 5 cm H2O. More PEEP may be applied to maintain PaO2 over 100 mmHg if FIO2 is over 0.6 OVERALL EVIDENCE GRADE: E
- If mechanically ventilated pCO2 should be 35 to 40 mmHg for the first 24 hr. Hyperventilation should not be used routinely. Patients may be hyperventilated if there are objective signs of acutely increasing intracranial pressure. Hyperventilation below 35 mmHg should not be used to compensate for metabolic acidosis. OVERALL EVIDENCE GRADE: C
- pH on arterial blood gases should be between 7.30 to 7.45 and buffer infusion can be used if the presence of metabolic acidosis results in sustained pH below 7.30. In this instance attempts should be made to ensure that filling pressures and cardiac output are assessed and augmented if inadequate. OVERALL EVIDENCE GRADE: E
TABLE V Cardiac care recommendations
- Rapidly measure and monitor mean arterial pressure (MAP) by inserting an arterial line. OVERALL EVIDENCE GRADE: E
- Maintain normotension (MAP 80?100 mmHg; or normal for the patient) after the cardiac arrest for the first 24 hr. OVERALL EVIDENCE GRADE: D
- Hypotension should be managed with vasopressors and inotropes if volume infusion is ineffective or pulmonary edema limits further administration of volume. OVERALL EVIDENCE GRADE: E
- Consideration should be given to obtaining cardiac index over 2.5 L·min?1·m2 before large doses of alpha adrenergic agents are used. A pulmonary artery catheter or alternate cardiac output measurement device should be considered if large doses of vasopressors or inotropes are in use. OVERALL EVIDENCE GRADE: E
- Assessment of central pressures and cardiac output should be considered if metabolic acidosis is persistent or increasing after the return of spontaneous circulation or if vasopressors or inotropes are required for more than two or three hours. OVERALL EVIDENCE GRADE: E
- If there is evidence of acute coronary syndrome then anticoagulation, platelet inhibition, beta blockers, and angiography/angioplasty should be used according to the American Heart Association guidelines. OVERALL EVIDENCE GRADE: A
- After the correction of electrolyte deficiencies and active ischemia, amiodarone should be used if there is recurrent non-sustained ventricular tachycardia or sustained ventricular tachycardia/fibrillation. OVERALL EVIDENCE GRADE: B
TABLE VI Gastrointestinal care recommendations
- Blood glucose levels should be controlled for the duration of the intensive care unit (ICU) stay. Blood glucose should be measured at least every four hours initially. Serum glucose should be 5 to 8 mmol·L?1 and insulin infusions used to rapidly achieve this range. Hyperglycemia (glucose > 8 mmol·L?1) should not be tolerated. OVERALL EVIDENCE GRADE: D
- Consideration should be given to administration of non-hypotonic iv glucose solutions (D5NS) over the first 24 hr if insulin infusions are used unless enteral/parenteral nutrition is being delivered. OVERALL EVIDENCE GRADE: E
- Enteral (preferred) or parenteral feeding should be started within 48 hr of return of spontaneous circulation. OVERALL EVIDENCE GRADE: E
- Pharmacologic gastrointestinal prophylaxis should be initiated (H2 blocker, sucralfate, or proton pump inhibitor) in ICU patients who have a coagulopathy, or who are expected to be intubated for over 48 hr. Prophylaxis may be discontinued after gastric feeds are established. OVERALL EVIDENCE GRADE: A
PCI and hypothermia (Crit Care Med 2008;36:1780)
References: NEJM 2002 – HACA (Mild Hypothermia after Cardiac Arrest) 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2005;112 [Suppl I]:IV-84-IV-88. Bernard, S., Gray, T., Buise, M., Jones, B., Silvester, M., Gutteridge, M., Smith, K. (2002). Treatment of Comatose Survivors of Out-Of ?Hospital Arrest with Induced Hypothermia. New England Journal of Medicine, 346 (8), 557-563. Burns, S. (2001). Revisiting Hypothermia; A Critical Concept. Critical Care Nurse, 21 (2), 83-86 Hypothermia after Cardiac Arrest Study Group, (2002). Mild Therapeutic Hypothermia to Improve Neurologic Outcome After Cardiac Arrest. New England Journal of Medicine, 346 (8), 549-556. Ginsberg MD. Hypothermic Neuroprotection in Cerebral Ischemia. In Primer on Cerebrovascular Diseases. 1997:272-275. Ginsberg MD, Sternau LL, Globus MY, Dietrich WD, Busto R. Therapeutic modulation of brain temperature: relevance to ischemic brain injury. Cerebrovasc Brain Metab Rev 1992; 4:189-22. Holzer M, Bernard SA, Hachimi-Idrissi S, Hypothermia for neuroprotection after cardiac arrest: systematic review and individual patient data meta-analysis. Crit Care Med. 2005 Jun;33(6):1449-52. Nolan J, Morley P, Vanden Hoek T, Therapeutic hypothermia after cardiac arrest. An advisory statement by the Advanced Life Support Task Force of the International Liason Committee on Resuscitation (ILCOR). Resuscitation 2003;57:231-235. Mayer SA, Sessler DI. Therapeutic Hypothermia. New Tyork: Marcel-Dekker, 2005. Polderman KH. Application of therapeutic hypothermia in the ICU: opportunities and pitfalls of a promising treatment modality – Part 2: Practical aspects and side effects. Intensive Care Med 2004; 30: 757-769. Cooling with IV Saline Bernard S, Buist M, Monteiro O, Induced Hypothermia using large volume, ice-cold intravenous fluid in comatose survivors of out-of-hospital cardiac arrest: a preliminary report. Resuscitation 2003;56:9-13. Kim F, Olsufka M, Longstreth WT, Pilot Randomized Clinical Trial of Prehospital Induction of Mild Hypothermia in Out-of-Hospital Cardiac Arrest Patients with a Rapid Infusion of 4 °C Normal Saline. Circulation 2007;115;3064-3070. Polderman K, Rijnsburger E, Peerdeman S, Induction of hypothermia in Patients with various types of neurologic injury with use of large volumes of ice-cold intravenous fluid. Crit Care Med 2005;33:2744-2751. Shivering Alfonsi P, Sessler D, Dumanoir B. The effects of meperidine and sufentanil on the shivering threshold in postoperative patients. Anesthesiology 1998;89:43-8. Doufas AG., Lin CM., Suleman MI., Dexmedetomidine and meperidine additively reduce the shivering threshold in humans. Stroke 2 003 May;34(5):1218-23. Mokhtarani M, Maghoub A, Morioka N. Buspirone and meperdine synergistically reduce the shivering threshold. Anesth. Analg. 2001;93:1223-9.
These references have been selected for relevance to hypothermia but are by no means inclusive of the literature. Please forward suggestions for additional references through the “contact us” option from the homepage. Click on the following references to be linked to their abstracts.
- Abella, B.S., et al., Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey. Resuscitation, 2005. 64(2): p. 181-6.
- Arrich J; The European Resuscitation Council Hypothermia After Cardiac Arrest Registry Study Group. Clinical application of mild therapeutic hypothermia after cardiac arrest. Crit Care Med. 2007 Feb 19.
- Bartels M, Tjan DH, Reussen EM, van Zanten AR. Therapeutic hypothermia after prolonged cardiopulmonary resuscitation for pulseless electrical activity. Neth J Med. 2007 Jan;65(1):38-41.
- Bernard, S.A., et al., Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med, 2002. 346(8): p. 557-63.
- Busch M, Soreide E, Lossius HM, Lexow K, Dickstein K. Rapid implementation of therapeutic hypothermia in comatose out-of-hospital cardiac arrest survivors. Acta Anaesthesiol Scand. 2006 Nov;50(10):1277-83
- Eisenburger, P., et al., Therapeutic hypothermia after cardiac arrest. Curr Opin Crit Care, 2001. 7(3): p. 184-8.
- Green RS, Howes DW. Stock your emergency department with ice packs: a practical guide to therapeutic hypothermia for survivors of cardiac arrest. CMAJ. 2007 Mar 13;176(6):759-62.
- HACA, Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med, 2002. 346(8): p. 549-56.
- Hachimi-Idrissi, S., et al., Mild hypothermia induced by a helmet device: a clinical feasibility study. Resuscitation, 2001. 51(3): p. 275-81.
- Holzer, M., et al., Hypothermia for neuroprotection after cardiac arrest: systematic review and individual patient data meta-analysis. Crit Care Med, 2005. 33(2): p. 414-8.
- Holzer M, Mullner M, Sterz F, Robak O, Kliegel A, Losert H, Sodeck G, Uray T, Zeiner A, Laggner AN. Efficacy and safety of endovascular cooling after cardiac arrest: cohort study and Bayesian approach. Stroke. 2006 Jul;37(7):1792-7.
- Hovdenes J, Laake JH, Aaberge L, Haugaa H, Bugge JF. Therapeutic hypothermia after out-of-hospital cardiac arrest: experiences with patients treated with percutaneous coronary intervention and cardiogenic shock. Acta Anaesthesiol Scand. 2006 Dec 15. PMID: 17181536
- ILCOR Advisory Statement. Therapeutic Hypothermia After Cardiac Arrest: An Advisory Statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation.
- Kliegel, A., et al., Cold simple intravenous infusions preceding special endovascular cooling for faster induction of mild hypothermia after cardiac arrest–a feasibility study. Resuscitation, 2005. 64(3): p. 347-51.
- Laver SR, Padkin A, Atalla A, Nolan JP. Therapeutic hypothermia after cardiac arrest: a survey of practice in intensive care units in the United Kingdom. Anaesthesia. 2006 Sep;61(9):873-7.
- Merchant RM, Abella BS, Peberdy MA, Soar J, Ong ME, Schmidt GA, Becker LB, Vanden Hoek TL. Therapeutic hypothermia after cardiac arrest: Unintentional overcooling is common using ice packs and conventional cooling blankets. Crit Care Med. 2006 Dec;34(12 Suppl):S490-S494.
- Merchant RM, Soar J, Skrifvars MB, et al: Therapeutic hypothermia utilization among physicians after resuscitation from cardiac arrest. Crit Care Med 2006; 34:1935?1940.
- Nagao K, Mukoyama T, Kikushima K, Watanabe K, Tachibana E, Iida K, Tani S, Watanabe I, Hayashi N, Kanmatsuse K. Resuscitative Value of B-Type Natriuretic Peptide in Comatose Survivors Treated With Hypothermia After Out-of-Hospital Cardiac Arrest due to Cardiac Causes. Circ J. 2007 Mar;71(3):370-6.
- Nolan, J.P., et al., Therapeutic hypothermia after cardiac arrest: an advisory statement by the advanced life support task force of the International Liaison Committee on Resuscitation. Circulation, 2003. 108(1): p. 118-21.
- Oddo M, Schaller MD, Feihl F, Ribordy V, Liaudet L. From evidence to clinical practice: effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest. Crit Care Med. 2006 Jul;34(7):1865-73
- Olivecrona GK, Gotberg M, Harnek J, van der Pals J, Erlinge D. Mild hypothermia reduces cardiac post-ischemic reactive hyperemia. BMC Cardiovasc Disord. 2007 Feb 26;7(1):5
- Pestel, Gunther J; Kurz, Andrea. Hypothermia – it’s more than a toy. Current Opinion in Anaesthesiology. April 2005; 18(2):151-156.
- Scott BD, Hogue T, Fixley MS, Adamson PB. Induced hypothermia following out-of-hospital cardiac arrest; initial experience in a community hospital. Clin Cardiol. 2006 Dec;29(12):525-9.
- Sunde K, Pytte M, Jacobsen D, Mangschau A, Jensen LP, Smedsrud C, Draegni T, Steen PA. Implementation of a standardised treatment protocol for post resuscitation care after out-of-hospital cardiac arrest . Resuscitation. 2007 Apr;73(1):29-39.
- Sunde K, Dunlop O, Rostrup M, Sandberg M, Sjoholm H, Jacobsen D. Determination of prognosis after cardiac arrest may be more difficult after introduction of therapeutic hypothermia. Resuscitation. 2006 Apr;69(1):29-32.
- Wolfrum S, Radke PW, Pischon T, Willich SN, Schunkert H, Kurowski V. Mild therapeutic hypothermia after cardiac arrest-A nationwide survey on the implementation of the ILCOR guidelines in German intensive care units. Resuscitation. 2007 Feb;72(2):207-13.
Cerebral Circulation Disorders
Return of cardiac function does not automatically restore normal cerebral circulation. Depending on the duration of the ischemic period, cerebral vessel dysfunction develops, which likely contributes to neuronal damage. Experimentally, different phenomena can be distinguished. First, reperfusion fails completely in circumscribed areas of the brain (no-reflow phenomenon).22?24 These areas increase with the duration of ischemia.22,24 No-reflow is probably caused by capillary congestion because of edema of endothelium and perivascular glia,25 blood cell sludging,26,27 leukocyte adhesion,25,28 and disseminated intravascular coagulation.26,29?31
Local no-reflow is paralleled by global cerebral hyperemia during the early period of reperfusion.32,33 This is probably caused by the accumulation of metabolites such as adenosine, lactate, or hydrogen ions during ischemia,12 which are potent vasodilators. However, within the first hour after reperfusion, reactive hyperermia is followed by a global reduction in cerebral blood flow (delayed hypoperfusion).32?34 This phenomenon is probably caused by cerebral vasospasms because of dysfunctional nitric oxide and endothelin metabolism.35?37
Resuscitation. 2010 Jan;81(1):117-22. Epub 2009 Nov 13. Hypocalcemia following resuscitation from cardiac arrest revisited. Youngquist ST, Heyming T, Rosborough JP, Niemann JT.Department of Surgery, Division of Emergency Medicine, University of Utah Medical Center, 30 North 1900 East 1C026, Salt Lake City, UT 84132, United States. email@example.comOBJECTIVE: Hypocalcemia associated with cardiac arrest has been reported. However, mechanistic hypotheses for the decrease in ionized calcium (iCa) vary and its importance unknown. The objective of this study was to assess the relationships of iCa, pH, base excess (BE), and lactate in two porcine cardiac arrest models, and to determine the effect of exogenous calcium administration on post-resuscitation hemodynamics. METHODS: Swine were instrumented and VF was induced either electrically (EVF, n=65) or spontaneously, ischemically induced (IVF) with balloon occlusion of the LAD (n=37). Animals were resuscitated after 7 min of VF. BE, iCa, and pH, were determined prearrest and at 15, 30, 60, 90, 120 min after ROSC. Lactate was also measured in 26 animals in the EVF group. Twelve EVF animals were randomized to receive 1g of CaCl(2) infused over 20 min after ROSC or normal saline. RESULTS: iCa, BE, and pH declined significantly over the 60 min following ROSC, regardless of VF type, with the lowest levels observed at the nadir of left ventricular stroke work post-resuscitation. Lactate was strongly correlated with BE (r=-0.89, p<0.0001) and iCa (r=-0.40, p<0.0001). In a multivariate generalized linear mixed model, iCa was 0.005 mg/dL higher for every one unit increase in BE (95% CI 0.003-0.007, p<0.0001), while controlling for type of induced VF. While there was a univariate correlation between iCa and BE, when BE was included in the regression analysis with lactate, only lactate showed a statistically significant relationship with iCa (p=0.02). Post-resuscitation CaCl(2) infusion improved post-ROSC hemodynamics when compared to saline infusion (LV stroke work control 8+/-5 gm vs 23+/-4, p=0.014, at 30 min) with no significant difference in tau between groups. CONCLUSIONS: Ionized hypocalcemia occurs following ROSC. CaCl(2) improves post-ROSC hemodynamics suggesting that hypocalcemia may play a role in early post-resuscitation myocardial dysfunction. Copyright 2009 Elsevier Ireland Ltd. All rights reserved. PMID: 19913975 [PubMed – in process]
One Groups Hypothermia Protocol (anesth anal 110 1328)
Studies showing quicker is better in animals (Neurosurg 1996;38:542, Crit Care Med 1993;21:1348, Crit Care Med 2005;33:1340)