METABOLISM AND

THERMOREGULATION

Fasilitator : Ronny Lesmana, dr., MKes., PhD

KELOMPOK 6
RIEZA NURDINSYAH H (BEDAH ANAK)
ANDRI PRATAMA K (UROLOGI)
ILHAM RIZKY ERNAWAN (BEDAH SARAF)
JONI PUTRA (BEDAH MULUT)
 THERMOREGULATION
• Process of transfer and transformation of Heat
Energy

• To maintain balance between Heat Production

& Heat Loss

• Homeostasis requires stable temperature of

98.6°F  37 degree Celsius
HEALTHY HUMANS ARE
HOMEOTHERMIC
• Body temperature (BT)  maintained within a
narrow range, despite changes in environmental
conditions, physical activity and other influencing
factors

• Core temperature  Normal core temperature

36.1-37.0 ºC

• Surface temperature of the skin and extremities

can vary  30°C - 40°C
 BT measurement
• Orally (0.3 to 0.5°C higher than the surface
temperature)
• Rectally (0.5 to 1°C higher than the surface
temperature)
• Axillary (arm-pit) (0.5 to 1°C lower than the
surface temperature)
• Tympanic membrane (TM)
* Measures radiant heat energy from the TM
and nearby ear canal
HUMAN
THERMOREGULATION
THERMOREGULATION
Control Mechanism
• Hypothalamus
• Peripheral thermoreceptors

Thermosensitive neurons in
hypothalamus balance heat
production and dissipation
MECHANISMS OF HEAT LOSS
BODY TEMPERATURE REGULATION

• Activated by cold exposure

• Reflex vasoconstriction
• Stimulation of the hypothalamic nuclei
• Heat preservation mechanism
• Shivering
• Autonomic and endocrine responses
• Adaptive behaviors
Thermoregulation of human body
Heat regulation in humans
 Core body
temperature Increase Body Temperature
>37°C

Thermoreceptors

Hypothalamus
nerves Muscles of
Sweat skin arteriole
glands walls relax
Muscles increase Skin arteries dilate
reduce secretion More blood to the
activity skin.
More radiation &
conduction of heat

More water covers the

skin.
More evaporation
Less heat generated
 Core body
temperature
<37°C
Decrease Body Temperature

Thermoreceptors Hypothalamus
nerves
nerves Muscles of
skin arteriole
Muscles Sweat walls
glands constrict Skin arteries
shivering constrict
decrease
Less blood to the
secretion skin.
Less radiation &
conduction of heat

Less water covers the

More heat skin.
generated Less evaporation
Increase Body Temperature
Vasoconstriction: Arterioles get
smaller to reduce blood going to skin,
keeping the core warm.
Shivering: Rapid contraction and
relaxing of skeletal muscles. Heat
produced by respiration.
Piloerection: Hairs on skin stand up
(trapping more air) and decreasing
heat loss.
Curling up: reduces heat loss,
decreases surface area.
Decrease Body Temperature
Vasodilation: arterioles dilate (widen)
so more blood enters the skin
capillaries and heat is lost.
Sweating: Glands secrete sweat which
removes heat when water evaporates.
Pilorelaxation: Hairs on skin flatten
(trapping less air) and increasing heat
loss.
Stretching Out: By opening up, the
body has a larger surface area.
 IMPAIRED THERMOREGULATION
Trauma or Neoplastic lesions,
Central
degenerative processes, congenital
Acute spinal cord transection (loss of
Peripheral
peripheral vasoconstriction)
DKA, uremia, hypoglycemia, sepsis,
Metabolic
pancreatitis
Narcotics (stops shivering response)
barbituarates, benzodiazepines, anti-
Medications
seizure meds, anti-psychotics and
sedative, NSAIDS
HYPOTHERMIA
Accidental Hypothermia

• Body’s core temperature unintentionally

drops below 35ºC (95ºF)
Primary Hypothermia

• Due to environmental exposure, no

underlying medical condition causing
disruption of temperature regulation.
Secondary Hypothermia

• Low body temperature resulting from a

medical illness, e.g., trauma.
FACTORS PREDISPOSING TO HYPOTHERMIA
Decrease heat production
• Age extremes
• Inadequate stored fuel (hypoglycemia, malnutrition
• Endocrine or neuromuscular (low thyroid, etc)
Increased heat loss
• Exposure (including poor prep and acclimatization)
• Skin (burns, etc)
Impaired thermoregulation
Cold Water Submersion
COLD DISORDERS
 DEGREES OF HYPOTHERMIA

Mild catecholamine release= peripheral vasoconstriction;

increased ventilatory rate; cold induced dieresis;
(90º - 95ºF)
confusion=faulty judgment, amnesia; ataxia, apathy,
35C – 32C shivering thermogenesis, hyporeflexia.

decreased metabolic rate= decreased oxygen

Moderate consumption, Inability to rewarm spontaneously,
(80º - 90ºF) enzyme suppression, sympathetic nervous reduction,
32C – 28C loss of shivering, hyporeflexia, coagulopathies,
decreased ventilation rate, stupor

Severe/Profo metabolic acidosis= increased cardiac irritability,

und ventricular fibrillation, severe hypotension, decreased
(< 80ºF) or absent ventilation, hyperkalemia, coma.
Profound  asystole, mimic brain death, flat EEG
<28C
Independently, penetrating trauma, GCS <8 or shock
(BP<90mmHg) were all predictive of patients arriving
hypothermic.
TRIAD OF DEATH

Pillars
• Hypothermia (<35C)
• Acidosis (<7.1)
• Coagulopathy (INR > 1.5)

“In the most severely injured casualties, when

the lethal triad are present, death is imminent”
 Bleeding patients with these findings have up
to 90% mortality rate.
ACUTE TRAUMATIC COAGULOPATHY

• Driven by tissue injury and shock (hypoperfusion)

• Associated with increased mortality and worse
outcomes
• Causes Protein C activation which leads to rapid
anticoagulation and fibrinolysis
• Clotting dysfunction begins at the moment of
traumatic impact
• Physiological responses are initiated producing
“acute traumatic coagulopathy (ATC)
PREHOSPITAL PEARLS

• Prevent malignant cardiac dysrhythmias!

• Gentle handling; horizontal position.
• Remove patient to a warm environment.
• Remove wet clothing and replace with dry warm
blankets to also cover head & neck.
• Initiate active gentle external rewarming
• Padded splint to frostbitten extremities to
prevent additional injuries to tissues.
REWARMING
• Passive  prevents further heat loss
• Noninvasive
• Remove wet/cold clothes
• Cover patient in warm environment out of wind
• Healthy patients with mild hypothermia
• Active
• Whenever there is cardiovascular instability (more
susceptible to VF)
• Temp <90ºF
• Age extremes (geriatric and very young)
• Neuro or endocrine insufficiency
ACTIVE CORE REWARMING

Delivers heat directly to the core

• Heated/humidified inhalation
• Heated IV fluids (104-107.6)
• Padded warm packs to major pressure point
areas(neck, axillary, groin)
• Peritoneal lavage (hospital)
• GI/bladder irrigation (hospital)
• Extracorporeal rewarming (hospital)
• Dialysis(hospital)
Best wrap: foil padded space blanket
Advantages of warmed IV Fluids at normal body
temperature is the improved absorption of
administered medications (+/- 10% per degree F
compared to cold IV fluids)
Cold IV fluids may induce hypothermia in
compromised patients and those that are
predisposed to hypothermia, for example:

• further cooling of hypothermic patients

• cooling of traumatized patients (slowed
metabolic heat production)
• cooling of geriatric patients (poor circulation,
slowed metabolism) - diabetic patients
• cooling of pediatric patients (small body
mass)
• cooling of burn victims (replacing plasma loss)
• Holds at a safe temperature indefinitely with
out overheating
HYPOTHERMIA PROTOCOL
COLD WATER SUBMERSION

• E.g : drawning in cold water

• Mammalian Diving Reflex :
• Apnea
• Bradycardia
• Vasoconstriction
• Shunting to inner core of body: pulmonary, coronary, and cerebral circulation.
TREATMENT OF COLD WATER
DROWNING/NEAR DROWNING:

• Remove from water with full spinal precautions preferable.

• Gentle ABC’s of resuscitation asap (pts. respirations and
pulse rate may be difficult to detect; any doubt: start CPR)
• Move to warm environment asap. Forced warm air.
• Gently: remove wet or constricting clothing, dry off, active
rewarming: insulated warm packs to major pressure point
areas & wrap in blankets.
• Warm IV solutions and warm humidified O-2 if possible.
FROSTBITE

• Most common freezing injury of tissues

• Occurs at temp below 32ºF
• Ice crystal formation damages cells
• Stasis progressing to microvascular thrombosis
 FACTORS PREDISPOSING TO FROSTBITE

• Contact with thermal conductors

• Wind-chill quickly freezes acral areas
• Immobility, constrictive clothing
• Atherosclerosis, nicotine, alcohol
SYMPTOMS OF FROSTBITE
• Sensory deficits always present (light-touch, pain,
temperature perception)
• “chunk of wood” sensation and clumsiness
• “frostnip” transient numbness and tingling without
tissue destruction
HOW SHOULD FROZEN TISSUES BE
THAWED?

• May be intensely painful (anticipate analgesics

orders)
• Never use dry heat or allow tissues to refreeze
• Rubbing may be harmful
• Final demarcation may take 60-90 days
CENTRAL
Causes: HYPERTHERMIA
• hypothalamic lesions (infarction, hemorrhage, tumor, trauma,
encephalitis)
• intoxication(anticholinergic and sympatho mimetic drugs,
salicylates, amphetamines, cocaine)
• acute spinal cord transection above T3-4
• delirium, catatonia
• malignant neuroleptic sy.(caused by skeletal muscle rigidity from
treatment with neuroleptic medications (e.g., antipsychotics,
antidepressants, antiemetics).
• malignant hyperhermia (rapid and massive skeletal muscle
contraction from exposure to anesthesia)
• dehydration, heat stroke, generaised tetanus
MECHANISMS IN DAMAGE OF TISSUE IN
HYPETHERMIA
• When blood flow is diverted to the skin, reduced perfusion of
the intestines and other viscera can result in ischemia,
endotoxemia, and oxidative stress
• Excessively high tissue temperatures (heat shock >41° C, 105.8°
F) can produce direct tissue injury
• Heat shock, ischemia, and systemic inflammatory responses can
result in cellular dysfunction, disseminated intravascular
coagulation, and multiorgan dysfunction syndrome
• Reduced cerebral blood flow, combined with abnormal local
metabolism and coagulopathy, can lead to dysfunction of the
central nervous system
Sympoms and signs of heat illness
(hyperthermia)

Minor intensity of heat illness - symptoms and

signs :
• Miliaria rubra (heat rash) - results from occlusion of eccrine
sweat gland ducts
• Heat syncope (fainting) - caused by temporary circulatory
insufficienc as a result of pooling of blood in the peripheral
veins
• Heat cramps (skeletal muscles cramps) - occur during and after
intense exercise and are believed to result from excessive loss of
sodium in sweat
Serious heat illness – sympoms and signs

- Heat exhaustion - a mild to moderate illness characterized

by an inability to sustain cardiac output with moderate
(>38.5° C, 101° F) to high (>40° C, 104° F) body temperatures
(hot skin and dehydration)

- Heat injury - a moderate to severe illness characterized by organ

(e.g. liver, renal) and tissue (e.g. gut, muscle) injury with high
body temperatures, usually but not always greater than 40° C
(104° F)

- Heat stroke - a severe illness characterized by central nervous

system dysfunction with high body temperatures, usually but
not always greater than 40° C (104° F)
REFERENCES

1. Holcomb J et al. The Journal of Trauma, 2007

2. Firth D. et al. Acute Traumatic coagulopathy – 2012
3. Sayad M et al. Emergency medicine International, 2013
4. WMS Practice Guidelines for Hypothermia - Wilderness
and Environmental Medicine, 2015
5. Enviromental Emergencies, chapter 38, 2013