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
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)
Two reasons sodium bicarbonate used to treat Rhabdo
- Decreased blood pH decreases myoglobin binding with other proteins.
- Alkaloid urine - proteins and chemical entering urine become alkalosis as well. Become ionized. Ions cannot cross lipid membranes. Ion trapping.
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
central pontine myelinolysis
Myelin escheat degenerates and falls apart.
Neurological disaster for the rest of their lives,
Comatose, CP, muscular dystrophy
Heat stroke and potassium considerations
Initially hypokalemia due to renal wasting / Na retention
Later, acidosis and Rhabdo results in hyperkalemia (late stage)
Heat pathophysiology cardiovascular
Vasodilation
Requires increase in CO (increases O2 demand)
High output failure may lead to AMI
-prevent shivering on cooling measures.
