Use of hypothermia in the intensive care unit

Table 1 Potential therapeutic effects of hypothermia

Effect	Mechanism	Onset and duration of effect
Improved energy balance	Reduced cerebral metabolism for O2 and glucose. O2 consumption reduced 5%-6%/1 °C between 22-37 °C and ATP hydrolysis decreased by a similar rate	Hours to d. Metabolism may begin to increase after 24 h
	Reduced ATP demand and promotes glycolytic production of ATP. Net increase ATP
	Decreased mitochondrial dysfunction
	Improved recovery of high-energy phosphate compounds upon improvement of perfusion demand and following rewarming
Anti-epileptic effect	Attenuation of [K+]ex increases with resulting decrease in Ca2+ influx. Temps between 31%-33% have demonstrated decreased duration, amplitude, and frequency of ictal discharges	Hours to days. This anti-epileptic effect may continue for a period of time following rewarming
	Increased duration between depolarizations with slowing return of membrane potential
	Decreased synthesis, reuptake, and release of excitatory neurotransmitters including glutamate
Neuro-protective	Reduced CNS edema-Improves BBB and energy reserve for membrane pumps via better energy balance	Hours to days
	Prevent/reduce apoptosis-Hypoxia/ischemia can induce apoptosis and calpain-mediated proteolysis. HT mitigates the initiation of these processes	Hours to weeks
	Intracellular alkalinization	Hours to days
	Less Excitotoxicity-Ca++ accumulation precedes neuronal damage in sensitive brain regions. Excessive pre-synaptic release of glutamate activates NMDA and non-NMDA post-synaptic receptors with resulting Ca++ entry and release of intracellular Ca++ stores. This [Ca++]in increases activates Ca++ dependent enzymes producing cell injury. Decreased release of glutamate may reduce mitochondrial dysfunction, DNA damage, and decreased activation of kinases and excitotoxic cascades	Minutes to 72 h
	Anti-oxidant effects-30%-40% decrease in Krebs cycle metabolites with shunting to Pentose Phosphate Pathway occurs. This shunting of metabolites may result in increased NADPH/NADH, improved glutathione reduction, peroxide detoxification, and reduced membrane peroxidation	Hours to days
	Suppression of inflammatory reaction and impaired leukocyte function	First hour to first week
	Improved microcirculation, improving CBF and reducing cerebral edema	Hours to days

Adapted from[65,73,74,93,149,201]. Number in right column refer to numbered entry in “mechanisms” column. ATP: Adenosine triphosphate; BBB: Blood-brain barrier; HT: Hypothermia; NADPH: Nicotinamide adenine dinucleotide phosphate; CBF: Cerebral blood flow.

Table 2 Qualitative description of Electroencephalogram pattern

Malignant EEG Patterns	Benign EEG Patterns
Non-reactive background	Generalized slowing
Burst-suppression associate with generalized epileptic activity	Mixed α-theta frequencies
Diffuse periodic complexes on a non-reactive background	Reactive background
Generalized suppression to < 20 mV	Continuous rhythm
Status epilepticus

EEG: Electroencephalogram.