35. Cold-defense and cold-induced disorders

Page created on March 23, 2019. Last updated on April 19, 2022 at 16:58

Introduction

The human “core” body temperature is relatively stable. It lies around 36.5 – 37.5°C, but it fluctuates with the circadian rhythm, changes in the ovulatory cycle, during exercise and after food intake. The outer surface temperature varies mainly according to the conditions of the environment.

Regulations of the body temperature relies on information coming from warm-sensitive and cold-sensitive thermoreceptors at different points in the body. The hypothalamus is the part of the brain that is mainly responsible for interpretation and processing of this thermal information.

The effector part of temperature regulation involves partly behavioural changes like putting on more clothes or undressing, seeking out sunlight or shade, and partly autonomic mechanisms. These autonomic mechanisms include:

• Shivering thermogenesis
• Non-shivering thermogenesis (uncoupling in brown adipose tissue)
• Skin vasodilation and vasoconstriction
• Piloerection – erection of the small hairs on the skin
• Sweating

Many factors can passively alter the body temperature:

• Exogenous factors
  • Temperature
  • Humidity
  • Wind
• Endogenous factors
  • Thyroid hypofunction/hyperfunction
  • Decreased sweating ability
  • Decreased metabolism during tissue hypoxia

Unless there are disorders of the cold-defence or warm-defence will these passive factors not alter the body temperature significantly, unless the factors are severe.

The brain (mainly hypothalamus) works by assigning a “set point” temperature (T_set) that the core temperature (T_c) should equal. When the core temperature has shifted away from the set point temperature will the body actively use its available mechanisms to either decrease or increase the core temperature so that it is equal to the T_set again. By balancing heat loss and heat production can the hypothalamus ensure a stable core temperature.

Notably, alcohol and sedatives disturb the thermal sensation and therefore impairs the hypothalamus’ ability to regulate temperature correctly.

Cold defence

The body’s defence against cold involves shivering and non-shivering thermogenesis, piloerection (to create a layer of insulating air) and peripheral vasoconstriction. The peripheral vasoconstriction withholds blood from the cold environment and instead redirects it to the internal organs.

Disorders of cold defence

A disorder of the cold defence means that you have a greater tendency to develop hypothermia in an environmental temperature where otherwise healthy persons would be normothermic. Our cold-defence isn’t unlimited; even the healthiest athletes will develop hypothermia in sufficiently cold environments.

A disorder of cold defence can be due to:

• Defective cold-sensation
  • Alcohol
  • Sensory neuropathies
• Defective effectors
  • Starvation
  • Exhaustion
  • Hypoxia
• Defective central regulatory system
  • Old age
  • Infants
  • Narcotics
  • Alcohol
• Decreased insulation
  • Low body fat

The body responds to a cold environment by causing the skeletal muscles to contract in small movements, called shivering (shivering thermogenesis). It will also induce non-shivering thermogenesis, which involves uncoupling the H⁺ gradient from ATP synthesis in the mitochondria. Used energy will then be used to produce heat instead of ATP.

If the body doesn’t have the energy to perform shivering or non-shivering thermogenesis will the main effectors of cold defence be impaired. This can occur for example during starvation or exhaustion.

Autonomic control of cold-defence involves the sympathetic nervous system. From this we can deduce that in countries with seasons of varying temperature, the sympathetic activity is generally higher during the winter months. Indeed, Finnish studies have described increased cardiovascular mortality during the winter months, either from AMI, arrhythmias or thromboembolic episodes, all of which can be attributed to the increased sympathetic activity.

Hypothermia

The book uses other temperature ranges. These ranges are taken from other sources, like Amboss, BMJ best practice, Harrison’s Principles of Internal Medicine, Color Atlas of Pathophysiology and Rosen’s emergency medicine.

When the core temperature is 32 – 35°C there is mild hypothermia. Around 33°C will shivering thermogenesis start to decrease. Confusion sets in. The decreased shivering will further impair the cold defence. There is muscle weakness and uncoordinated movements.

When the core temperature is 28 – 32°C there is moderate hypothermia. At this point has shivering completely stopped, causing the core temperature to plummet. Circulation (heart rate) and respiration decrease, and consciousness further deteriorates.

When the core temperature is below 28°C there is severe hypothermia. Ventricular fibrillation or asystole sets in. Coma develops. The patient may die from cardiac arrest.

At low temperatures is metabolism slowed down, so tissues’ energy and oxygen need decreases. For this reason, people who suffer cardiac arrest while hypothermic have better chance of surviving if they eventually receive CPR and proper treatment than people who suffer cardiac arrest while normothermic. A common saying says “you aren’t dead until you are warm and dead”, indicating that hypothermic, seemingly dead people may be actually still be alive and salvageable.

Re-warming a hypothermic person should be performed cautiously by slowly warming the trunk while continuously monitoring the circulation, respiration and salt/water balance. Failing to do this properly may cause circulatory shock or so-called “afterdrop”. Afterdrop involves a further and critical fall of core temperature as cold blood returns from the periphery if the body is re-warmed too quickly. Circulatory shock may develop as the peripheral tissues’ energy and O₂ requirement increases as body temperature increases.