Table 1: Human physiology changes in extreme heat and cold.
Body systems | Extreme cold | Extreme heat |
Cardiovascular | • Peripheral vasoconstriction with blood shift to central circulation • In early hypothermia: ○ Increased inotropism and chronotropism ○ Increased cardiac output and blood pressure • At late hypothermia: ○ Decreased chronotropism and inotropism ○ Decreased cardiac output and blood pressure • ECG disturbances (bradycardia, heart block and prolongation of PR, QRS and QT intervals) |
• Peripheral vasodilatation with blood shift from central to peripheral circulation • Decreased blood pressure and in severe cases, shock • Hyperdynamic circulation: Tachycardia and increased cardiac output • ECG disturbances (prolonged QT interval, rhythm disturbances, conduction defects and ST segment changes) |
Respiratory | • In early hypothermia: ○ Hyperventilation • At late hypothermia: ○ Hypoventilation • Hypercapnia and pulmonary acidosis, secondary to hypoventilation • Decreased: ○ Ciliary motility ○ Lung compliance ○ Thorax elasticity • Increased: ○ Bronchorrhea ○ Noncardiogenic pulmonary edema • Alterations in diaphragm and intercostal muscles contractility |
• Thermal-hyperpnea (increases in tidal volume and frequency of breathing) • Hypocapnia and pulmonary alkalosis, secondary to hyperventilation • Brain heat dissipation secondary to respiratory evaporation |
Neuromuscular | • Great activation of sympathetic nervous system • At first, blood flow to the brain increases but starts decreasing steadily • Increased muscular tremor to produce heat at early stages • Decreased nerve conduction: ○ Decreased sensitivity ○ Decreased deep tendon reflexes |
• Great activation of sympathetic nervous system • At first, blood flow to the brain increases but starts decreasing as temperature rises • Increased blood-brain-barrier permeability • Muscular weakness and cramps • Neurologic dysfunction to irreversible neuronal damage |
Digestive | • Gastrointestinal organs injury secondary to hypoperfusion: ○ Splenic and hepatic insult. Decreased function of the last • Decreased intestinal motility, leading to ileus and internal organs distention • Mucosal damage and erosions in stomach, duodenum, ileum and colon • Pancreatitis secondary to hypothermic-related serum amylase elevations |
• Gastrointestinal organs injury secondary to hypoperfusion: • Hepatic insult with consequent enzymes elevations • Intestinal injury may lead to diarrhea |
Hematologic | • Clinical manifestations of thrombocytopenia • Increased disseminated intravascular coagulation • Increased prothrombin time • Increased hemoconcrentation and hence, hematocrit • Spleen contraction increases circulating erythrocytes • Increased leukopenia • Increased bone marrow supression • Increased blood viscosity |
• Clinical manifestations of thrombocytopenia • Increased disseminated intravascular coagulation • Increased prothrombin time • Early removal of red blood cells from circulation |
Renal | • Increase of cold diuresis • Mild degree of renal insufficiency due to renal vasoconstriction |
• Oliguria • Renal injury and insufficiency due to direct thermal damage and hypoperfusion (dehydration and blood shift to the skin) • Activation of the renin-angiotensin-aldosterone system |
Integumentary | • Increased cutaneous vasoconstriction • Decreased sweat production by eccrine sweat glands • Increased non-shivering thermogenesis through brown adipose tissue |
• Increased cutaneous vasodilatation • Increased sweat production by eccrine sweat glands with the consequent loss of water and electrolytes |