|CARDIOVASCULAR [79, 230, 267]||• Initial vasoconstriction (effect blocked by ethanol). Vasoconstriction fails <24 °C .||• Failed vasoconstriction means the patient becomes poikilothermic i.e. dependent on ambient temperature.|
|• Cardiac conduction is affected by cold and changes in pH and PaO2 . Initial tachycardia due to shivering  subsides as temperature drops due to decreased spontaneous depolarization of pacemaker cells leading to linear fall in pulse rate (~50 % at 28 °C) . Any ECG rhythm is possible. Commonly at <32 °C, sinus bradycardia, prolonged QTc. J waves (not pathognomonic for hypothermia) best seen in leads I & V6 [79, 269–272]. Likelihood of VF is high <28 °C .||
• Bradycardia is atropine unresponsive .|
• A “relative” tachycardia inconsistent with patient’s temperature means something else is going on e.g. occult trauma.
• Be prepared for any rhythm but expect it to be resistant to treatment until the heart rewarms.
• Normal rhythm resumes on rewarming.
|• Cardiac output falls to 45 % at 25 °C .||• Hypotension is the norm.|
|• After rewarming, mean arterial pressure, contractility, and cardiac output are decreased, especially if alcohol ingested before cooling .||• More prolonged depression of cardiac function after rewarming|
|CENTRAL NERVOUS SYSTEM||
• Reflexes become increasingly sluggish as body temperature falls and become absent ≈ 28–30 °C [230, 274].|
• Pupils become dilated and cease reacting to light at ≈ 28 °C .
• EEG shows burst suppression ≈ 22 °C and becomes isoelectric ≈ 18–20 °C [79, 275].
• The level of consciousness should be consistent with the core temperature. A significant discrepancy suggests an alternative diagnosis.|
• All the effects of hypothermia make it very hard to diagnose death by the usual criteria while the patient is still cold
|RESPIRATORY||• Tidal volume, respiratory rate, pulmonary compliance and thoracic elasticity decrease . The respiratory rate may only be five breaths per minute when the body temperature is <30 °C . Sensitivity to CO2 is attenuated, although the hypoxic drive is maintained to deeper levels of hypothermia . Cough reflex is obtunded, ciliary activity is reduced and secretions are more viscous.||
• An irregular respiratory pattern can be mistaken for agonal breathing leading to premature institution of CPR.|
• The likelihood of a chest infection is increased.
|• Oxygen consumption and carbon dioxide production fall by about 50 % at 30 °C ||• Reduced CO2 production means it is easy to inadvertently hyperventilate hypothermic patients. Hyperoxia is also possible.|
|RENAL & METABOLIC||• Cold diuresis, partly due to the relative central hypervolaemia resulting from peripheral vasoconstriction , but also from a reduction in ADH release and resistance to its effects . Alcohol will further increase the diuresis.||• Severely hypothermic patients are dehydrated. This becomes particularly important during rewarming as the consequent opening up of the peripheral circulation will lead to a rapid fall in BP.|
|• Hyperglycaemia is common due to catecholamine-induced glycogenolysis, decreased insulin release and inhibition of insulin transport [79, 267].||• Hyperglycaemia can exacerbate the diuresis.|
|• Glomerular filtration rate falls as cardiac output and hence renal blood flow fall . At low temperatures, tubular capacity for H+ secretion is reduced, and hence there is a renal component of the acidosis .||• This makes the interpretation of acid-base more complex.|
|• Hypokalaemia commonly occurs with hypothermia .||
• If potassium replacement is given excess to the losses, hyperkalaemia may occur on rewarming [276, 277].|
• Severe initial hyperkalaemia is a marker of acidosis and cell death and is therefore a sign of poor prognosis 
|HAEMATOLOGY||• Haematocrit increases by about 2 % for every 1 °C decline in temperature .||• A normal haematocrit in a moderately or severely hypothermic patient suggests pre-existing anaemia or blood loss .|
|COAGULATION||• Platelet function and coagulation enzyme activity are reduced .||• Coagulopathy is likely and increases with decreasing core temperature. At temperatures below 33 °C coagulopathy significantly increases mortality in patients with concomitant trauma .|