Heat Stroke Flashcards

1
Q

what produces most body heat?

A

muscular activity

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2
Q

which structures in the body control body temperature?

A

central and peripheral thermoreceptors

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3
Q

what acts as the thermoregulation centre in the brain?

A

anterior hypothalamus

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4
Q

what is the role of the thermoreceptors?

A

indicate when temperature is above or below the ideal set point

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5
Q

what does the body do if the temperature is above the set point?

A

heat dissipation

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6
Q

what does the body do if the temperature is below the set point?

A

heat conservation and production

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7
Q

what temperature is classed as hyperthermia?

A

> 39.2 C

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8
Q

what are some of the causes of hyperthermia?

A

pyrexia

increased heat production due to increased muscular activity

heat stroke

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9
Q

what are the 2 types of heat stroke?

A

classic heat stroke (reduced heat loss)

exertional heat stroke - overheating due to over-exercise in high temps

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10
Q

what causes heat stroke?

A

failure of heat dissipation

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11
Q

what may lead to failure of heat dissipation?

A

upper respiratory obstruction

increased environmental temperature/humidity

poor environmental ventilation

circulatory compromise

obesity

breed disposition

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12
Q

what body temperature carries risk of organ damage/failure?

A

> 41.6 C

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13
Q

why does a temperature of >41.6 C risk permanent organ damage/failure?

A

caused by cell death due to large increase in oxygen demand and DIC

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14
Q

what are the major clinical signs of heat stroke?

A

stress

hyperthermia

tachycardia

hypovolaemia

hyperdynamic pulses

peripheral vasodilation

collapse

hyperaemic mm (bright red) with rapid CRT

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15
Q

when might heat stroke patients appear normothermic?

A

due to impaired peripheral perfusion - widespread vasodilation

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16
Q

what are the symptoms of advanced stage heat stroke?

A

hypovolaemia

increased intestinal mucosal permeability and impaired GI perfusion

tachypnoea

secondary respiratory complications

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17
Q

why might a patient in advance stage heat stroke be hypovolaemic?

A

GI losses

vasodilation - relative hypovolaemia due to systemic compromise

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18
Q

why are patients in heat stroke at higher risk of sepsis?

A

increase intestinal mucosal permeability and impaired GI perfusion –> endotoxin translocation –> sepsis

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19
Q

how can risk of sepsis due to gut translocation be reduced in the heat stroke patient?

A

patients with severe GI compromise may require mucosal protectants (omeprazole) and IV antibiotics

20
Q

which secondary respiratory complications can occur as a result of heat stroke?

A

aspiration pneumonia
pulmonary oedema
pulmonary haemorrhage (DIC)

21
Q

what are some of the secondary complications of heat stroke?

A

impaired renal perfusion

CNS compromise

disseminated intravascular coagulation

22
Q

why is impaired renal perfusion occur as a secondary complication to heat stroke?

A

due to peripheral shunt of blood - peripheral vasodilation results in reduced blood pressure

23
Q

why does CNS compromise occur as a secondary complication of heat stroke?

A

direct thermal damage
or
secondary effects (hypoglycaemia)

24
Q

what blood abnormalities may be seen as a result of heat stroke?

A

hypoglycaemia

hyperbilirubinaemia

electrolyte derangements

thrombosis

25
Q

what may occur to the muscles as a result of heat stroke?

A

myopathy

26
Q

where is most heat lost in cases of increased body temperature?

A

through the body surface

27
Q

what is the cardiac effect of increased peripheral circulation?

A

increased cardiac output to compensate

28
Q

why do many of the secondary complications of heat stroke occur?

A

due to decreased perfusion of vital organs

29
Q

what is the initial patient response to an increase in environmental temperature?

A

as environmental temperature exceeds body temperature, patient relies on panting to compensate

30
Q

what is involved in emergency management of heat stroke?

A

active cooling

oxygen supplementation and monitoring oxygenation

maintain a patent airway - assess for obstruction

IVFT

bloods

monitor for increased ICP

31
Q

at what body temperature should we start actively cooling a patient?

A

> 41 C

32
Q

why should cold water not be used for active cooling?

A

using water that is too cold will cause peripheral vasoconstriction and impair heat loss further

33
Q

at what body temperature should we stop actively cooling a patient?

A

< 39.4 C to prevent hypothermia

34
Q

how often should we measure a patients temperature during active cooling>

A

every 5 mins minimum

35
Q

why is it important to supplement oxygen in heat stroke patients?

A

will have very elevated RR (fast panting)

36
Q

how can we monitor oxygenation in heat stroke patients?

A

SpO2 or arterial blood gas

37
Q

why is it important to give heat stroke patients IVFT?

A

isotonic crystalloids to support circulation

to replace deficits (requires continuous re-assessment)

38
Q

what blood values are valuable to obtain in a heat stroke patient?

A

PCV

total solids

glucose

electrolytes

coagulation factors

39
Q

why is it important to look for abnormal coagulation factors in heat stroke patients?

A

looking for evidence of coagulopathies - clotting disorders caused by hyperthermia

40
Q

why might patients with heat stroke have increased ICP?

A

cerebral vasodilation due to peripheral vasodilation

41
Q

is pyrexia beneficial to the patient?

A

yes

42
Q

why is pyrexia beneficial to the patient?

A

decreases replication of pathogens and increases function of WBCs

43
Q

should we actively cool patients with pyrexia?

A

no - beneficial to the body

44
Q

when is it appropriate to administer antipyretic drugs?

A

patients with cancer and immune compromise

45
Q

what is an antipyretic drug?

A

a drug used to prevent/reduce fever e.g. paracetamol, NSAIDs

46
Q

what are some of the causes of pyrexia?

A

inflammatory disease - infectious, immune-mediated

neoplastic disease

other causes - opioids, hepatic encephalopathy

blood transfusion (esp xenotransfusion)

47
Q
A