Pathophysiological Impacts of Hypothermia
Hypothermia produces profound multi-system physiological effects that range from protective metabolic suppression to life-threatening cardiovascular collapse, with the severity and reversibility of these effects directly correlating to the depth and duration of cooling.
Neurological Effects
Cerebral metabolism decreases by approximately 6-7% for each 1°C reduction in core temperature, which forms the basis for hypothermia's neuroprotective properties 1, 2. This metabolic suppression reduces cerebral oxygen requirements and suppresses pathways leading to delayed cell death, including apoptosis, free radical production, and excitatory amino acid release 1.
Progressive cooling produces predictable neurological deterioration 2:
- Patients become confused, uncoordinated, and somnolent as temperature drops 2
- At approximately 30°C, progression to coma occurs 2
- Below 27°C, loss of deep tendon reflexes and pupillary reflexes develops 2
Cardiovascular Effects
The cardiovascular response to hypothermia is biphasic and temperature-dependent 2, 3:
Mild hypothermia (<36°C):
- Increased systemic vascular resistance occurs consistently 1, 4, 5
- Bradycardia develops, which may paradoxically be beneficial (similar to beta-blocker effects, reducing diastolic dysfunction) 1
- Initial increase in sympathetic tone, heart rate, blood pressure, and cardiac output 2
- Myocardial contractility typically increases in most patients, though mild diastolic dysfunction can develop in some 3
Moderate to severe hypothermia:
- Progressive depression of cardiac activity 2, 5
- Clinically significant arrhythmias occur only below 30°C 3
- Decreased cardiac output and arterial pressure 6
Important caveat: The bradycardia induced by mild hypothermia has been associated with good neurological outcomes and should not be aggressively treated 1.
Metabolic and Endocrine Effects
Hypothermia decreases insulin sensitivity and insulin secretion, causing hyperglycaemia that requires insulin treatment 1. This effect is particularly pronounced during therapeutic cooling, with higher blood glucose values, increased variability, and greater insulin requirements compared to normothermia 1.
Decreased clearance of medications occurs, with sedative drugs and neuromuscular blockers reduced by up to 30% at 34°C 1. This has critical implications for sedation protocols and drug dosing.
Renal and Electrolyte Effects
Hypothermia causes cold-induced diuresis initially, followed by decreased glomerular filtration rate with prolonged cooling 4, 5. This biphasic response leads to multiple electrolyte abnormalities 1:
- Hypophosphataemia
- Hypokalaemia
- Hypomagnesaemia
- Hypocalcaemia
The diuresis can lead to dehydration and electrolyte disturbances that further compromise organ function, particularly in patients with underlying cardiac disease 5.
Hematological Effects
Hypothermia impairs platelet function between 33-37°C and affects coagulation factor activity and fibrinogen synthesis below 33°C 2, 5. Despite these laboratory abnormalities, clinical bleeding appears negligible in most studies 1. One registry found increased minor bleeding with combined coronary angiography and mild hypothermia, though this combination was also the best predictor of good outcomes 1.
Respiratory Effects
At 32°C, the medullary respiratory center becomes depressed, leading to 2:
- Decreased minute ventilation
- Increased secretions
- Atelectasis development
Initially, mild hypothermia may increase respiratory rate before this depression occurs 2.
Infectious Complications
Hypothermia impairs immune system function and increases infection rates, particularly pneumonia 1. The incidence of pneumonia is increased with therapeutic hypothermia, though this does not appear to impact overall outcomes 1. Observational data suggest prophylactic antibiotics may reduce pneumonia incidence, and early antibiotic use has been associated with improved survival 1.
Gastrointestinal Effects
Serum amylase concentration commonly increases during hypothermia, though the clinical significance remains unclear 1.
Rewarming Considerations
Rewarming must be performed slowly at approximately 0.25-0.5°C per hour to avoid complications 1. Rapid rewarming can cause 7:
- Cardiac arrhythmias
- Uncontrolled bleeding
- "Rewarming shock"
Rebound hyperthermia after therapeutic hypothermia is associated with increased mortality and worse neurological outcomes 1, making controlled rewarming essential.
Shivering Response
Shivering increases metabolic and heat production, reducing cooling rates 1. Paradoxically, the occurrence of shivering in cardiac arrest survivors undergoing therapeutic hypothermia is associated with good neurological outcome, as it represents a normal physiological response 1.