Heat Loss Flashcards

1
Q

What is the primary mechanism by which general anesthesia induces hypothermia in the first hour?

A

Redistribution of heat from the core to peripheral compartments due to anesthetic-induced vasodilation.

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2
Q

How does the critical temperature differ between a preterm neonate and an adult?

A

Preterm neonate: 28°C; Adult: 1°C.

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3
Q

Explain why radiation accounts for ~60% of heat loss in the operating room.

A

Radiation transfers heat via infrared waves to cooler surrounding objects, proportional to the fourth power of the temperature difference (e.g., a 2°C drop increases loss by 16x).

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4
Q

Compare non-shivering thermogenesis in neonates vs. adults.

A

Neonates rely on brown adipose tissue for non-shivering thermogenesis due to limited muscle mass. Adults primarily use shivering.

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5
Q

Design a protocol to prevent hypothermia in a preterm neonate during surgery.

A
  1. Warm OR to ≥24°C. 2. Use forced-air warming. 3. Administer warmed IV fluids. 4. Cover with impervious drapes. 5. Use overhead radiant heaters during induction.
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6
Q

Why is pethidine (0.3 mg/kg IV) effective for postanesthetic shivering?

A

Pethidine inhibits shivering centrally without suppressing respiratory drive, but active warming is still required to address hypothermia.

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7
Q

Evaluate the statement: ‘Humidifying inspired gases significantly warms hypothermic patients.’

A

False: Respiratory heat loss accounts for <10% of total loss. Humidification minimizes airway heat loss but does not actively rewarm.

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8
Q

What physiological change explains the 1°C core temperature drop within 30-60 minutes of anesthesia induction?

A

Vasodilation redistributes heat from the core (thoracic/abdominal organs) to cooler peripheral tissues (limbs/skin).

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9
Q

Analyze the clinical impact of a core temperature of 35°C on drug metabolism.

A

Hypothermia slows metabolism: vecuronium duration doubles, propofol plasma concentration increases 30%, and MAC for inhaled anesthetics decreases 5%/°C.

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10
Q

Which temperature measurement site is least reliable for core temperature monitoring?

A

Rectal or bladder temperatures, due to poor perfusion and lag in reflecting rapid core changes.

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11
Q

Propose a treatment plan for intraoperative malignant hyperthermia.

A
  1. Stop triggering agents. 2. Administer dantrolene. 3. Cool with IV fluids, surface cooling, and cold irrigation. 4. Monitor electrolytes/acidosis.
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12
Q

Explain why forced-air warming is more effective than passive insulation.

A

Forced-air actively transfers heat to the periphery, counteracting redistribution. Passive insulation only reduces conductive/convective loss by ~30%.

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13
Q

How does anesthesia alter the inter-threshold range for thermoregulation?

A

General anesthesia increases the inter-threshold range from 0.2–0.5°C to 5°C, delaying vasoconstriction/sweating responses.

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14
Q

Justify the use of warmed IV fluids during major surgery.

A

1 L of room-temperature IV fluid lowers core temperature by ~0.25°C. Warming prevents iatrogenic hypothermia and stabilizes metabolism.

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15
Q

Critique the statement: ‘Shivering increases oxygen consumption but does not cause hypoxemia.’

A

True: Shivering increases O₂ demand, but hypoxemia itself inhibits shivering, preventing a vicious cycle.

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16
Q

Identify three factors that increase evaporative heat loss in neonates.

A
  1. Thin skin. 2. High surface-area-to-volume ratio. 3. Use of skin-preparation solutions in the OR.
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17
Q

Create a differential diagnosis for intraoperative hyperthermia (Temp >38°C).

A
  1. Sepsis. 2. Malignant hyperthermia. 3. Thyroid storm. 4. Transfusion reaction. 5. Drug-induced hyperthermia.
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18
Q

Why is the thermoregulatory range narrower in neonates than adults?

A

Neonates have immature hypothalamic control, limited shivering capacity, and rely on non-shivering thermogenesis, which is easily overwhelmed.

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19
Q

Assess the risk of hypothermia in a patient under spinal anesthesia.

A

Spinal anesthesia blocks vasoconstriction, preventing the plateau phase of hypothermia. Risk is higher due to continuous heat loss without compensation.

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20
Q

What intervention addresses both conductive and convective heat loss?

A

Using forced-air warming blankets, which reduce convective loss by heating ambient air and conductive loss by warming skin contact surfaces.

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21
Q

Front

A

Back

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22
Q

Define normothermia and its clinical significance.

A

Normothermia is a core body temperature of 36.5–37.1°C, maintained within 0.2°C to ensure optimal enzyme function and physiological stability.

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23
Q

How does the peripheral compartment contribute to thermoregulation?

A

It acts as a heat sink, absorbing or releasing thermal energy to maintain the core temperature, with its temperature varying between 36°C and 28°C.

24
Q

What are the physiological mechanisms that regulate body temperature?

A

Behavioral, hormonal, and neuronal responses integrate through hypothalamic control based on afferent thermal inputs from skin, viscera, and spinal cord.

25
What effect does anaesthesia have on behavioral thermoregulation?
It abolishes behavioral responses, increasing reliance on passive or external warming measures during surgery.
26
Explain the role of the hypothalamus in thermoregulation.
The pre-optic nucleus of the anterior hypothalamus integrates thermal information and activates appropriate heat loss or heat conservation responses.
27
Compare and contrast the body's responses when the warm threshold vs. cold threshold is exceeded.
Warm threshold activation leads to vasodilation, sweating, and behavioral cooling, while cold threshold activation triggers vasoconstriction, shivering, and non-shivering thermogenesis.
28
What is the most effective physiological mechanism for heat loss?
Sweating, as it increases evaporative cooling and can account for up to 2 liters per hour in athletes.
29
How does non-shivering thermogenesis generate heat?
Catecholamines (adrenaline and noradrenaline) uncouple oxidative phosphorylation, generating heat instead of ATP; this is prominent in neonates with brown fat.
30
What are the cardiovascular effects of hypothermia?
Bradycardia, vasoconstriction, prolonged conduction intervals, reduced myocardial contractility, and increased risk of ventricular fibrillation below 30°C.
31
How does hypothermia impact oxygen delivery and metabolism?
It reduces oxygen delivery and metabolic rate by 8–10% per 1°C fall in temperature, leading to metabolic acidosis and tissue hypoperfusion.
32
Describe the impact of hypothermia on drug metabolism.
Hypothermia reduces hepatic blood flow and enzymatic activity, slowing drug metabolism and prolonging drug effects.
33
How does the body’s coagulation system respond to hypothermia?
Impaired coagulation due to enzyme dysfunction, thrombocytopenia, and increased blood viscosity by 4–6% per 1°C decrease.
34
Why does hypothermia increase the risk of surgical wound infection?
Immune suppression and impaired neutrophil function reduce the ability to combat infections.
35
At what core temperature do life-threatening arrhythmias become a concern?
Ventricular fibrillation becomes difficult to reverse below 28°C, with cardiac arrest occurring at 24°C.
36
What is the significance of J waves (Osborn waves) on ECG in hypothermia?
J waves are characteristic of hypothermia and appear in 80% of patients below 30°C.
37
How does the oxygen dissociation curve shift in hypothermia?
The curve shifts leftward, increasing hemoglobin's affinity for oxygen and reducing oxygen unloading to tissues.
38
What are the causes of perioperative hypothermia?
Anaesthesia-induced vasodilation, exposure, prolonged surgery, reduced metabolic heat production, and altered thermoregulatory thresholds.
39
List the main mechanisms of intraoperative heat loss.
Radiation, convection, conduction, and evaporation.
40
What anaesthetic agents contribute most to hypothermia?
Volatile anaesthetics, opioids, and propofol lower thermoregulatory thresholds and inhibit shivering.
41
What are the clinical strategies to prevent perioperative hypothermia?
Active warming (forced-air warming, fluid warmers), passive insulation, and maintaining ambient temperature above 21°C.
42
Explain the role of cytokines in fever generation.
Cytokines like interleukins and TNF induce prostaglandin synthesis in the hypothalamus, raising the body's temperature set point.
43
How do NSAIDs reduce fever?
They inhibit cyclooxygenase (COX), preventing prostaglandin synthesis and lowering the hypothalamic temperature set point.
44
Differentiate between hyperthermia and fever.
Fever is a regulated increase in core temperature due to a raised set point, whereas hyperthermia is uncontrolled heat accumulation exceeding heat dissipation.
45
Describe the mechanism of malignant hyperthermia.
A genetic mutation in ryanodine receptors causes excessive calcium release in muscle, leading to sustained contraction, heat production, and metabolic acidosis.
46
What are the triggering agents for malignant hyperthermia?
Volatile anaesthetics (e.g., halothane, sevoflurane) and depolarizing muscle relaxants (e.g., suxamethonium).
47
What is the treatment for malignant hyperthermia?
Immediate administration of **dantrolene**, discontinuation of triggering agents, cooling measures, and metabolic correction.
48
What drugs can cause life-threatening hyperthermia besides anaesthetics?
MDMA (ecstasy) can cause serotonin syndrome, leading to hyperthermia and multi-organ failure.
49
What are the clinical signs of heat stroke?
Core temperature >40°C, confusion, seizures, multi-organ dysfunction, and failure of normal thermoregulatory mechanisms.
50
Explain the mechanism of piloerection and its role in thermoregulation.
Piloerection (goosebumps) occurs via contraction of arrector pili muscles, trapping an insulating layer of air to reduce heat loss.
51
At what core temperature is active rewarming mandatory?
Below 32°C, active rewarming is necessary to prevent cardiovascular collapse.
52
Describe the physiological effects of rewarming shock.
Rapid vasodilation during rewarming can cause hypotension due to vascular volume redistribution.
53
Explain the difference between passive and active rewarming.
Passive rewarming relies on endogenous heat production (e.g., insulation, warm environment), while active rewarming uses external heat sources (e.g., heated IV fluids, forced air warming).
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