{
Metabolism and
Thermoregulation
ISHAK LEWI NDAUMANU
SURTI WULAN KHARISMA
YULIUS HERMANTO
FINI MEIRISA ALNAZ
M. RAZAK SUDARMAN
YUDI PURNAMA NUGRAHA
ANDREA NISTIANA
ERA YULIAN INEKA
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
Thermoregulation
 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
Homeothermic
 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
BT measurement
Human
Thermoregulation
Control Mechanism
 Hypothalamus
 Peripheral thermoreceptors
Thermoregulation
Thermosensitive neurons
in hypothalamus balance
heat production and
dissipation
Mechanisms of Heat Loss
 Activated by cold exposure
 Reflex vasoconstriction
 Stimulation of the hypothalamic nuclei
 Heat preservation mechanism
 Shivering
 Autonomic and endocrine responses
 Adaptive behaviors
Body Temperature Regulation
Thermoregulation of human body
Heat regulation in humans
nerves
Less heat generated
More water covers the
skin.
More evaporation
Skin arteries dilate
More blood to the
skin.
More radiation &
conduction of heat
Muscles of
skin arteriole
walls relax
Sweat
glands
increase
secretion
Muscles
reduce
activity
Core body
temperature
>37°C
Hypothalamus
Thermoreceptors
Increase Body Temperature
nerves
More heat
generated
Less water covers the
skin.
Less evaporation
Skin arteries
constrict
Less blood to the
skin.
Less radiation &
conduction of heat
Muscles of
skin arteriole
walls
constrict
Sweat
glands
decrease
secretion
Muscles
shivering
nerves
Core body
temperature
<37°C
Thermoreceptors Hypothalamus
Decrease Body Temperature
Increase Body Temperature Decrease 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.
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.
Central
Trauma or Neoplastic lesions,
degenerative processes, congenital
Peripheral
Acute spinal cord transection (loss of
peripheral vasoconstriction)
Metabolic
DKA, uremia, hypoglycemia, sepsis,
pancreatitis
Medications
Narcotics (stops shivering response)
barbituarates, benzodiazepines, anti-
seizure meds, anti-psychotics and
sedative, NSAIDS
Impaired Thermoregulation
{
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.
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
Factors Predisposing to Hypothermia
Cold Disorders
Mild
(90º - 95ºF)
35C – 32C
catecholamine release= peripheral
vasoconstriction; increased ventilatory rate; cold
induced dieresis; confusion=faulty judgment,
amnesia; ataxia, apathy, shivering thermogenesis,
hyporeflexia.
Moderate
(80º - 90ºF)
32C – 28C
decreased metabolic rate= decreased oxygen
consumption, Inability to rewarm spontaneously,
enzyme suppression, sympathetic nervous
reduction, loss of shivering, hyporeflexia,
coagulopathies, decreased ventilation rate, stupor
Severe/Prof
ound
(< 80ºF)
<28C
metabolic acidosis= increased cardiac irritability,
ventricular fibrillation, severe hypotension,
decreased or absent ventilation, hyperkalemia,
coma.
Profound  asystole, mimic brain death, flat
EEG
Degrees of Hypothermia
Independently, penetrating trauma, GCS <8 or shock
(BP<90mmHg) were all predictive of patients arriving
hypothermic.
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.
Triad Of Death
 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)
Acute Traumatic Coagulopathy
 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.
Prehospital Pearls
 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
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)
Active Core Rewarming
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
 E.g : drawning in cold water
 Mammalian Diving Reflex :
 Apnea
 Bradycardia
 Vasoconstriction
 Shunting to inner core of body: pulmonary, coronary, and
cerebral circulation.
Cold Water Submersion
 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.
Treatment of cold water drowning/near drowning:
“Patient is not dead until rewarmed.”
 Most common freezing injury of tissues
 Occurs at temp below 32ºF
 Ice crystal formation damages cells
 Stasis progressing to microvascular thrombosis
Frostbite
 Contact with thermal conductors
 Wind-chill quickly freezes acral areas
 Immobility, constrictive clothing
 Atherosclerosis, nicotine, alcohol
Factors Predisposing to Frostbite
 Sensory deficits always present (light-touch, pain, temperature
perception)
 “chunk of wood” sensation and clumsiness
 “frostnip” transient numbness and tingling without tissue
destruction
Symptoms of Frostbite
 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
How should frozen tissues be
thawed?
Causes:
 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
Central hyperthermia
 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
Mechanisms in damage of tissue in
hypethermia
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
Sympoms and signs of heat illness
(hyperthermia)
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)
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
References
Thank You

Metabolism and thermoregulation

  • 1.
    { Metabolism and Thermoregulation ISHAK LEWINDAUMANU SURTI WULAN KHARISMA YULIUS HERMANTO FINI MEIRISA ALNAZ M. RAZAK SUDARMAN YUDI PURNAMA NUGRAHA ANDREA NISTIANA ERA YULIAN INEKA
  • 2.
    Process of transferand transformation of Heat Energy To maintain balance between Heat Production & Heat Loss Homeostasis requires stable temperature of 98.6°F  37 degree Celsius Thermoregulation
  • 3.
     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 Homeothermic
  • 4.
     Orally (0.3to 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 BT measurement
  • 5.
  • 6.
    Control Mechanism  Hypothalamus Peripheral thermoreceptors Thermoregulation Thermosensitive neurons in hypothalamus balance heat production and dissipation
  • 7.
  • 8.
     Activated bycold exposure  Reflex vasoconstriction  Stimulation of the hypothalamic nuclei  Heat preservation mechanism  Shivering  Autonomic and endocrine responses  Adaptive behaviors Body Temperature Regulation
  • 9.
  • 10.
  • 11.
    nerves Less heat generated Morewater covers the skin. More evaporation Skin arteries dilate More blood to the skin. More radiation & conduction of heat Muscles of skin arteriole walls relax Sweat glands increase secretion Muscles reduce activity Core body temperature >37°C Hypothalamus Thermoreceptors Increase Body Temperature
  • 12.
    nerves More heat generated Less watercovers the skin. Less evaporation Skin arteries constrict Less blood to the skin. Less radiation & conduction of heat Muscles of skin arteriole walls constrict Sweat glands decrease secretion Muscles shivering nerves Core body temperature <37°C Thermoreceptors Hypothalamus Decrease Body Temperature
  • 13.
    Increase Body TemperatureDecrease 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. 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.
  • 14.
    Central Trauma or Neoplasticlesions, degenerative processes, congenital Peripheral Acute spinal cord transection (loss of peripheral vasoconstriction) Metabolic DKA, uremia, hypoglycemia, sepsis, pancreatitis Medications Narcotics (stops shivering response) barbituarates, benzodiazepines, anti- seizure meds, anti-psychotics and sedative, NSAIDS Impaired Thermoregulation
  • 15.
  • 16.
    Accidental Hypothermia  Body’score 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.
  • 17.
    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 Factors Predisposing to Hypothermia
  • 18.
  • 19.
    Mild (90º - 95ºF) 35C– 32C catecholamine release= peripheral vasoconstriction; increased ventilatory rate; cold induced dieresis; confusion=faulty judgment, amnesia; ataxia, apathy, shivering thermogenesis, hyporeflexia. Moderate (80º - 90ºF) 32C – 28C decreased metabolic rate= decreased oxygen consumption, Inability to rewarm spontaneously, enzyme suppression, sympathetic nervous reduction, loss of shivering, hyporeflexia, coagulopathies, decreased ventilation rate, stupor Severe/Prof ound (< 80ºF) <28C metabolic acidosis= increased cardiac irritability, ventricular fibrillation, severe hypotension, decreased or absent ventilation, hyperkalemia, coma. Profound  asystole, mimic brain death, flat EEG Degrees of Hypothermia
  • 20.
    Independently, penetrating trauma,GCS <8 or shock (BP<90mmHg) were all predictive of patients arriving hypothermic.
  • 21.
    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. Triad Of Death
  • 22.
     Driven bytissue 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) Acute Traumatic Coagulopathy
  • 23.
     Prevent malignantcardiac 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. Prehospital Pearls
  • 24.
     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 Rewarming
  • 25.
    Delivers heat directlyto 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) Active Core Rewarming
  • 27.
    Best wrap: foilpadded space blanket
  • 29.
    Advantages of warmedIV 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
  • 31.
  • 32.
     E.g :drawning in cold water  Mammalian Diving Reflex :  Apnea  Bradycardia  Vasoconstriction  Shunting to inner core of body: pulmonary, coronary, and cerebral circulation. Cold Water Submersion
  • 33.
     Remove fromwater 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. Treatment of cold water drowning/near drowning:
  • 34.
    “Patient is notdead until rewarmed.”
  • 35.
     Most commonfreezing injury of tissues  Occurs at temp below 32ºF  Ice crystal formation damages cells  Stasis progressing to microvascular thrombosis Frostbite
  • 36.
     Contact withthermal conductors  Wind-chill quickly freezes acral areas  Immobility, constrictive clothing  Atherosclerosis, nicotine, alcohol Factors Predisposing to Frostbite
  • 37.
     Sensory deficitsalways present (light-touch, pain, temperature perception)  “chunk of wood” sensation and clumsiness  “frostnip” transient numbness and tingling without tissue destruction Symptoms of Frostbite
  • 38.
     May beintensely painful (anticipate analgesics orders)  Never use dry heat or allow tissues to refreeze  Rubbing may be harmful  Final demarcation may take 60-90 days How should frozen tissues be thawed?
  • 39.
    Causes:  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 Central hyperthermia
  • 40.
     When bloodflow 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 Mechanisms in damage of tissue in hypethermia
  • 41.
    Minor intensity ofheat 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 Sympoms and signs of heat illness (hyperthermia)
  • 42.
    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)
  • 43.
    1. Holcomb Jet 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 References
  • 44.