Environmental: Hyperthermia Flashcards
Fluid loss with sweating
1-3 L/hr
Heat pathophysiology neurological considerations
Decreased Na (sweating) = cerebral edema & seizures -increase temp more
Heat pathophysiology renal considerations
- Na retention attempt trades K = hypokalemia
- Hypoperfusion=pre-renal failure - ATN = kidneys leak fluid rather than retaining.
Heat pathophysiology liver considerations
Hypoperfusion = hypoglycemia, decreased clotting factor production
- increase PT, increase aPTT
- decrease enzymatic activity
- decrease bio transformation.
Heat pathophysiology muscle death
Hypoxia and Hypoperfusion= muscle lysis and death
- myoglobinuria = rhabdomyolysis
- increases CK-MM
Heat pathophysiology and ARDS & DIC
Result from lysosomal enzymes & combination of issues
Heat cramps
Occur in heavily exercised muscles in high heat
-cause is hyponatremia (associated with sweating and only water replacement)
Heat cramps treatment
Cool and rehydrate with salt containing solutions.
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
Heat stroke
Change on LOC
Core temp greater than 42 degrees C
O2 demand exceeds supply
Cause of heat stroke acidosis
Respiratory alkalosis initial attempt to compensate
Metabolic acidosis results from anaerobic metabolism
Heat stroke, airway and ventilator considerations
Aggressive airway management
- high Ve, reduce workload, increase O2 supply
- use of AC ideal or pressure support
Shivering while cooling
NMBA will decrease seizing
Phenothiazine will induce poikilothermia
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
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