EMCrit.org

Post ROSC Care & Induced Hypothermia

web site with tons of resources

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 [12]. 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 [12].

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 [12].

The other major randomized controlled trial was performed by Barnard et al. [16] 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) [16].

In a small feasibility study using a helmet device to induce hypothermia, Hachimi-Idrissi et al. [17] 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

Further:

(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)

Shivering?

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)

Temp:

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

Combined Approach

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

Shivering

occurs at 36, should stop at 34

treat with cutaneous vasodilation

BAIR hugger

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

Antishivering protocol

APAP 975 mg PO

Buspirone 30 po q 8

persistent

start with mg 0.5-1 g/hr until 3-4 mg/dL

fentanyl or demerol

precedex

add propofol

last shot is paralyze

Mg Study (Zwefler et al 2004)

Rewarming

vasodilation can cause dramatic hemodynamic changes

SIRS syndrome

rebound increase in ICP

rebound hyperkalemia

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

and

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

Cardiovascular	Ventricular arrhythmias (HT patients are more susceptible to atrial and ventricular fibrillation).
	Myocardial depression, bradycardia
	Angina
	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).
Respiratory	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
Metabolic	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
GI	Decreased motility, liver function, insulin release
	Ileus
	Stress ulceration
Renal	Decreased renal plasma flow
	Decreased urine output
	Increased specific gravity
	Decreased ADH
Hematologic	Increased blood viscosity (hemoconcentration)
	Platelet dysfunction
Neurologic	Confusion
	Decreased LOC
	Depressed reflexes
	Decreased muscular tone
	Coma

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.

Post-ROSC Care

Management following resuscitation from cardiac arrest: recommendations from the 2003 Rocky Mountain Critical Care Conference

Canadian Journal of Anesthesia 52:309-322 (2005)

General Care

1. 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

2. Hyperthermia should not be tolerated. Temperatures over 38°C should be reduced.
   OVERALL EVIDENCE GRADE: B
3. 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
4. If the patient is hypothermic on presentation rewarming should be gradual and final temperature should not exceed 37°C.
   OVERALL EVIDENCE GRADE: B
5. Serum magnesium level and potassium levels should be normalized.
   OVERALL EVIDENCE GRADE: E
6. Replace peripheral or central lines placed without proper sterile techniques during the cardiac resuscitation.
   OVERALL EVIDENCE GRADE: E
7. Identify and manage complications resulting from cardiopulmonary resuscitation.
   OVERALL EVIDENCE GRADE: E
8. Administer deep vein thrombosis prophylaxis if systemic anti-coagulation is not required.
   OVERALL EVIDENCE GRADE: A

TABLE III Neurologic care recommendations

TABLE IV Respiratory care recommendations

TABLE V Cardiac care recommendations

TABLE VI Gastrointestinal care recommendations