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
what may occur to the muscles as a result of heat stroke?
myopathy
26
where is most heat lost in cases of increased body temperature?
through the body surface
27
what is the cardiac effect of increased peripheral circulation?
increased cardiac output to compensate
28
why do many of the secondary complications of heat stroke occur?
due to decreased perfusion of vital organs
29
what is the initial patient response to an increase in environmental temperature?
as environmental temperature exceeds body temperature, patient relies on panting to compensate
30
what is involved in emergency management of heat stroke?
active cooling oxygen supplementation and monitoring oxygenation maintain a patent airway - assess for obstruction IVFT bloods monitor for increased ICP
31
at what body temperature should we start actively cooling a patient?
>41 C
32
why should cold water not be used for active cooling?
using water that is too cold will cause peripheral vasoconstriction and impair heat loss further
33
at what body temperature should we stop actively cooling a patient?
< 39.4 C to prevent hypothermia
34
how often should we measure a patients temperature during active cooling>
every 5 mins minimum
35
why is it important to supplement oxygen in heat stroke patients?
will have very elevated RR (fast panting)
36
how can we monitor oxygenation in heat stroke patients?
SpO2 or arterial blood gas
37
why is it important to give heat stroke patients IVFT?
isotonic crystalloids to support circulation to replace deficits (requires continuous re-assessment)
38
what blood values are valuable to obtain in a heat stroke patient?
PCV total solids glucose electrolytes coagulation factors
39
why is it important to look for abnormal coagulation factors in heat stroke patients?
looking for evidence of coagulopathies - clotting disorders caused by hyperthermia
40
why might patients with heat stroke have increased ICP?
cerebral vasodilation due to peripheral vasodilation
41
is pyrexia beneficial to the patient?
yes
42
why is pyrexia beneficial to the patient?
decreases replication of pathogens and increases function of WBCs
43
should we actively cool patients with pyrexia?
no - beneficial to the body
44
when is it appropriate to administer antipyretic drugs?
patients with cancer and immune compromise
45
what is an antipyretic drug?
a drug used to prevent/reduce fever e.g. paracetamol, NSAIDs
46
what are some of the causes of pyrexia?
inflammatory disease - infectious, immune-mediated neoplastic disease other causes - opioids, hepatic encephalopathy blood transfusion (esp xenotransfusion)
47