Environmental: Hyperthermia Flashcards

1
Q

Fluid loss with sweating

A

1-3 L/hr

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2
Q

Heat pathophysiology neurological considerations

A
Decreased Na (sweating) = cerebral edema & seizures
-increase temp more
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3
Q

Heat pathophysiology renal considerations

A
  • Na retention attempt trades K = hypokalemia

- Hypoperfusion=pre-renal failure - ATN = kidneys leak fluid rather than retaining.

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4
Q

Heat pathophysiology liver considerations

A

Hypoperfusion = hypoglycemia, decreased clotting factor production

  • increase PT, increase aPTT
  • decrease enzymatic activity
  • decrease bio transformation.
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5
Q

Heat pathophysiology muscle death

A

Hypoxia and Hypoperfusion= muscle lysis and death

  • myoglobinuria = rhabdomyolysis
  • increases CK-MM
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6
Q

Heat pathophysiology and ARDS & DIC

A

Result from lysosomal enzymes & combination of issues

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7
Q

Heat cramps

A

Occur in heavily exercised muscles in high heat

-cause is hyponatremia (associated with sweating and only water replacement)

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8
Q

Heat cramps treatment

A

Cool and rehydrate with salt containing solutions.

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9
Q

Heat exhaustion

A

Increase core temp without neurological impairment
-patient is still able to sweat

Treatment aimed at cooling while replacing water and na and electrolytes

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10
Q

Heat stroke

A

Change on LOC
Core temp greater than 42 degrees C
O2 demand exceeds supply

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11
Q

Cause of heat stroke acidosis

A

Respiratory alkalosis initial attempt to compensate

Metabolic acidosis results from anaerobic metabolism

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12
Q

Heat stroke, airway and ventilator considerations

A

Aggressive airway management

  • high Ve, reduce workload, increase O2 supply
  • use of AC ideal or pressure support
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13
Q

Shivering while cooling

A

NMBA will decrease seizing

Phenothiazine will induce poikilothermia

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14
Q

Heat stroke treatment cont

A

Cooing measures, NG/OG, expose, fluids, foley (monitor for UO and Rhabdo), H2 blockers (cimetidine - acidosis can lead to gastric ulcers and bleeding), monitor labs

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15
Q

Heat stroke and lab values to monitor

A

ABGs (correction of acidosis is #1 priority)
Clotting factors PT, PTT, INR (Watch for DIC)
Monitor liver enzymes
Na levels

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16
Q

Rhabdo treatment

A

Increase urinary output to 2 ml/kg/hr
Sodium bicarbonate to alkaline urine
Assist diuresis with mannitol and / or Lasix
(Mannitol: osmotic diuretic; Lasix: Loop diuretic)

17
Q

Two reasons sodium bicarbonate used to treat Rhabdo

A
  1. Decreased blood pH decreases myoglobin binding with other proteins.
  2. Alkaloid urine - proteins and chemical entering urine become alkalosis as well. Become ionized. Ions cannot cross lipid membranes. Ion trapping.
18
Q

Sodium replacement

A

Can be replaced with slow 3% saline administration

  • consult with receiving on rate and amount
  • can result in central pontine myelinolysis if given too quickly
19
Q

central pontine myelinolysis

A

Myelin escheat degenerates and falls apart.
Neurological disaster for the rest of their lives,
Comatose, CP, muscular dystrophy

20
Q

Heat stroke and potassium considerations

A

Initially hypokalemia due to renal wasting / Na retention

Later, acidosis and Rhabdo results in hyperkalemia (late stage)

21
Q

Heat pathophysiology cardiovascular

A

Vasodilation
Requires increase in CO (increases O2 demand)
High output failure may lead to AMI
-prevent shivering on cooling measures.