Environmental: Hyperthermia Flashcards Preview

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Flashcards in Environmental: Hyperthermia Deck (21):
1

Fluid loss with sweating

1-3 L/hr

2

Heat pathophysiology neurological considerations

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

3

Heat pathophysiology renal considerations

-Na retention attempt trades K = hypokalemia
-Hypoperfusion=pre-renal failure - ATN = kidneys leak fluid rather than retaining.

4

Heat pathophysiology liver considerations

Hypoperfusion = hypoglycemia, decreased clotting factor production
-increase PT, increase aPTT
-decrease enzymatic activity
-decrease bio transformation.

5

Heat pathophysiology muscle death

Hypoxia and Hypoperfusion= muscle lysis and death
-myoglobinuria = rhabdomyolysis
-increases CK-MM

6

Heat pathophysiology and ARDS & DIC

Result from lysosomal enzymes & combination of issues

7

Heat cramps

Occur in heavily exercised muscles in high heat
-cause is hyponatremia (associated with sweating and only water replacement)

8

Heat cramps treatment

Cool and rehydrate with salt containing solutions.

9

Heat exhaustion

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

Treatment aimed at cooling while replacing water and na and electrolytes

10

Heat stroke

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

11

Cause of heat stroke acidosis

Respiratory alkalosis initial attempt to compensate
Metabolic acidosis results from anaerobic metabolism

12

Heat stroke, airway and ventilator considerations

Aggressive airway management
-high Ve, reduce workload, increase O2 supply
-use of AC ideal or pressure support

13

Shivering while cooling

NMBA will decrease seizing
Phenothiazine will induce poikilothermia

14

Heat stroke treatment cont

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

15

Heat stroke and lab values to monitor

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

16

Rhabdo treatment

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

Two reasons sodium bicarbonate used to treat Rhabdo

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

Sodium replacement

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

central pontine myelinolysis

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

20

Heat stroke and potassium considerations

Initially hypokalemia due to renal wasting / Na retention
Later, acidosis and Rhabdo results in hyperkalemia (late stage)

21

Heat pathophysiology cardiovascular

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