2. Malignant Hyperthermia Flashcards
(101 cards)
MH genetics mutations (2)
mutation in either:
- RyR1
- CaV1.1
RYR1 receptor
Ca2+ release channel
on sarcoplasmic reticulum
RYR1 known mutaions
110
CAV1.1 receptor
DHP receptor
L-type Ca2+ channel
in T-tubule
CAV1.1 known mutations
2
MH chromosome locations
1
15
19
MH genetic pattern
autosomal dominant
w/ variable penetrance
MH genetic prevalance
1:3000
MH genetic concentration
scandinavian descent
higher inicidence of occurrence in wisconsin and upper midwest
_____% of pts who develop MG have have previous uneventful anesthetics with triggering medications
50%
krebs cycle
glucose —>
ATP + CO2 + heat
normal physiology responses
transient hyponatremia
transient hyperkalemia
ATP hydrolysis (incr heat)
SERCA activation (incr heat)
how does MH occur
sustained RyR activation
= sustained Ca2+ release (need more ATP)
Mg2+ inhibition of Ca2+ release is blocked
– Ca2+ release continues
MH most potent trigger
halothane
MH triggers
volatile agents (iso, sevo, des)
sux
MH awake triggers
high intensity exercise
heat
anoxia
apprehension
exercise ____ min prior to trigger _____ severity and _____ onset
exercise <60 min prior to trigger increased severity and hastened onset
MH general clinical signs
incr metabolism
incr sympathetics
muscle damage
hyperthermia
incr metabolism signs 7
incr CO2 production
incr O2 consumption
decr MVO2 tension
metabolic acidosis
respiratory acidosis
cyanosis
mottling
incr sympathetics
tachycardia
hypertension
arrhythmias
MH arrythmia progression
PVCs
bigeminy
VTACH
VFIB
asystole
3 ways to correct hyperkalemia
membrane stabilization
transfer of K+ INTO cells
incr K+ excretion
correct hyperkalemia: membrane stabilization
hyperventilation
give CaCl (500-1000mg) or Ca gluconate (1000mg)
correct hyperkalemia: transfer of extracellular K+ INTO cells
give 5-10 units insulin w/25-50g glucose
(10 units insulin w.50 mL of 50% dextrose)
give beta agonist (albuterol)