INDUCED HYPOTHERMIA AFTER

CPR – DO WE REALLY NEED IT?

NIKOLA BRADIC

CLINIC OF ANESTHESIOLOGY, REANIMATOLOGY

AND INTENSIVE CARE MEDICINE

UNIVERSITY HOSPITAL DUBRAVA

ZAGREB, CROATIA
 AIM

• induced mild hypothermia included in 2005 Guidelines

for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care Recommendations
WHY HYPOTHERMIA AFTER CPR?

• to protect brain after CPR

• better short neurological outcome after CPR (both in-

and out-hospital)

• better outcome after CPR

But, is it everything good and nice
as it looks like with hypothermia?
ADVERSE EFFECTS OF HYPOTHERMIA

• cardiovascular system
• respiratory system
• infection and gastrointestinal function
• renal system
• acid-base disturbances
• hematological disturbances
• adverse effects on drugs
CADRIOVASCULAR EFFECTS

• 80% of all cardiac arrests in alduts caused by

presumed cardiac disease

• more than 60% of adult deaths are from coronary

heart disease
 CADRIOVASCULAR EFFECTS

• in ROSC after VF, myocardium shows huge electrical

and mechanical instability

• this instability may causes refibrillation within short

time after ROSC
 CADRIOVASCULAR EFFECTS

• diferences of normothermic vs hypothermic fibrillating

myocardium

 increased contraction amplitude

 decreased contraction velocity
 decreased median fibrillation frequency
Riishede L, et al. Myocardial effects of adrenaline, isoprenaline and dobutamine at
hypothermic conditions. Pharmacol Toxicol 1990;66(5):354-360
Strohmenger HU, et al. Median fibrillation frequency in cardiac surgery: influence of
temperature and guide to countershock therapy. Chest 1997;111:1560-1564
 CADRIOVASCULAR EFFECTS

• these characteristics of hypothermic heart contribute to

reduced efficiency of electrical counter shock therapy

• these findings observed in both experimental animals

and humans
 CADRIOVASCULAR EFFECTS

• electrophysiological changes associated with ischemia

are similar to those induced by hypothermia

• ischemia may increase the arrhythmogenic potential of

hypothermia

Ujhelyi MR, et al. Defibrillation energy requirements and electrical heterogeneity during total
body hypothermia. Crit Care Med 2001;29(5):1006-1011
 CADRIOVASCULAR EFFECTS

• improving of myocardial perfusion by increasing CPP

may reverse some of electrophysiological changes and
improve CPR outcome

• to improve CPP sometimes it is necessary to use

vasoactive agents
 CADRIOVASCULAR EFFECTS

• during post CPR instability vasoactive agents have

arrhythmogenic effect

• these agents increase myocardial oxygen consumption

• worsen myocardial ischemia

• enlarge infarction zone

 CADRIOVASCULAR EFFECTS

• function of receptors for inotropic and vasoactive drugs

become unresponsible during hypothermia

• action of vasoactive drugs shifts from the heart to the

vasculature

• producing undesirable increase in SVR

 CADRIOVASCULAR EFFECTS

• cooling with surface cooling blankets is slow process

• producing periferal vasoconstriction

• increasing SVR
 CADRIOVASCULAR EFFECTS

• using of large amount of ice-cold (4oC) volume can

decrease core temperature rapidly

• may be very hazardous in patients with unstable heart

function and rhythm
 CADRIOVASCULAR EFFECTS

• large volumes for cooling (40mL/kg) may produce heart

failure because of impaired ventricular function

 consequence of decreased myocardial compliance

 increased left ventricular end-diastolic pressure
 possible mitral valve dysfunction after MI

• large amounts of cold infusions in short time through

central venous catheters may be arrhythmogenic
ADVERSE EFFECTS OF HYPOTHERMIA ON OTHER
ORGANS AND ORGAN SYSTEMS
 RESPIRATORY SYSTEM

• decrease of CO2 production

• respiratory and metabolic alcalosis

• increased incidence of pulmonary infections in patients

on longer mechanical ventilation (VAP)
 INFECTIONS

• hypothermic patients with core temperature just 1.5oC –

2.0oC below normal (35.5oC - 35.0oC) have an
approximately 19% rate of infections vs. 6% rate of
infections for the normothermic patients
 INFECTIONS

• hypothermia increases patients' vulnerability caused

by vasoconstriction and impaired immunity

• incidence of sepsis two times higher in group of

patients randomized to hypothermia than in patients
treated with normothermia (13% vs. 7%)

The hypothermia after cardiac arrest study group. Mild therapeutic hypothermia to improve
the neurological outcome after cardiac arrest. N Eng J Med 2002;346:549-556
 GASTROINTESTINAL DISFUNCTION

• important side effect is insulin resistance

• decreased insulin release

• decreased gastrointestinal motility

• serum amylase and liver enzymes are frequently raised

 GASTROINTESTINAL DISFUNCTION

• metabolic acidosis also occurs as a result of increase in

lactate concentrations

• increased production of free fatty acids, ketones and

glycerol

• in some occasions, these changes can be severe and

pancreatitis can ensue
 RENAL SYSTEM

• increased diuresis results from decreased absorption of

solute in the ascending loop of Henle´

• maintenance of plasma volume

 ELECTROLYTE DISTURBANCES

• intracellular movements of potassium, magnesium and

phosphate during induced hypothermia lead to lowered
serum concentrations

• in re-warming extracellular shift of anions may lead to

increasing plasma concentrations
 HEMATOLOGICAL
• during prolonged induced hypothermia bleeding time
will be lengthened

• reduction in the number and function of platelets

• the coagulation cascade may be impaired

• direct tests such as prothrombin time (PT) and activated

partial thromboplastin time (APTT) may not reflect these
changes, as they are performed at 37oC
 PROLONGED AND ALTERED DRUG EFFECTS

• hypothermia produces significant altered action of many

drugs

• action of many agents used in CPR may be ineffective

or with delayed action

• function of receptors for inotropic and vasoactive drugs

become unresponsible during hypothermia and action
of these drugs shifts from the heart to the vasculature
 PROLONGED AND ALTERED DRUG EFFECTS

• lidocaine has no documented beneficial effects during

hypothermia

• in the state of hypothermia amiodarone had no

beneficial effects on the resuscibilty of the fibrillating
hypothermic heart

Schwarz B, et al. Neither vasopressin nor amiodarone improve CPR outcome in an animal
model of hypothermic cardiac arrest. Acta Anaesthiol Scand 2003;47:1114-1118
 PROLONGED AND ALTERED DRUG EFFECTS

• non-depolarizing muscle relaxants with predictable

half-life in state of hypothermia prolonging their average
action for more than double, with unpredictable time of
action
 CONCLUSIONS

• most of the studies today are orientated exclusively on

the neurological outcome of patients

• most of the studies performed on experimental animals

• lack or very weak evidences of adverse effects of

hypothermia on other organs or organ systems function
 CONCLUSIONS

• from all studies with humans it is not clear which real

time is the best to start with hypothermia to produce
best neuroprotection

• implementation of hypothermia latter than 3 – 8 minutes

after CPR is becoming questionable due to hypoxyc
brain injury
 CONCLUSIONS

• lack of brain monitoring in studies with humans

• role of barbiturates in neuroprotection

• using of induced hypothermia after CPR could be

very dangerous if is not well controlled

• the entire effect could be much more undesirable for

patient than little improvement of neurological outcome