Neuromuscular Blocking Flashcards
Choline Hydrolysis
Acetylcholinesterase (“true” cholinesterase)
VS.
Butyrylcholinesterase (plasma cholinesterase)
PChe - pseudocholinesterase
Synthesized in liver
Succinylcholine hydrolysis in plasma
Muscle Relaxation Onset
Eye muscles > extremities > trunk > abdominal muscles > diaphragm
Neuromuscular Function Clinical Tests
TOF Tetanus Post-tetanic count Single twitch Double-burst suppression
Train of Four
Most widely used
Four separate stimuli every 0.5sec at 2Hz
T1-T4 comparison
Non-depolarizing onset = fade
4 twitches 75-80% receptors can still be blocked
Zero twitches = 100% blocked
Tetany
Continuous electrical stimulation for 5sec at 50-100Hz
Reliable for detecting fade
Sustained contraction w/out fade = paralysis unlikely
Post-Tetanic Count
Tetany followed in 3sec by single twitch stimulations
Higher the count (>8) less intense the block
Single Twitch
Single twitch at 0.1-1Hz for 0.1-0.2sec
Determine when 100% paralysis present
Double-Burst Suppression
Seems to improve ability to detect residual paralysis
Evaluate 2 rather than 4 twitches
Extubation Conditions
5 second head life
Generate peak negative inspiratory pressure 20-30cm H2O
Neuromuscular Blocking Structure
Quaternary ammoniums = ionized
Low Vd - does not cross blood-brain or placenta
Structurally r/t ACh
Primarily synthetic alkaloids
Non-Depolarizing Blockade
Decrease in twitch tension (strength)
Fade during repetitive stimulation
Post-tetanic potentiation
Fade
Concentration
Twitch depression results from blocking post-synaptic nicotinic ACh receptors
Post-tetanic or TOF fade results from blocking PRE-synaptic nAChR ↓ACh released
Depolarizing Blockade
Phase 1 often preceded by muscle fasciculation
Decrease in twitch tension
NO fade during repetitive stimulation
NO post-tetanic potentiation
Phase 2 not commonly seen
Repeated or long-term administration
Doses >6mg/kg
Inhibit pre-synaptic nAChR
Succinylcholine
ONLY depolarizing NMBD
Two ACh molecules linked by acetate methyl groups
Intubating conditions w/in 60sec
Duration 4-5min
Recovery to 90% muscle strength 9-13min (offset)
Short action d/t rapid hydrolysis by butyrylcholinesterase
Butyrylcholinesterase (PChE)
Psuedocholinesterase
Metabolized in liver & found in plasma
Genetic variations prolong effects d/t unable to metabolize succinylcholine
Dibucaine
Local anesthetic than inhibits typical PChE
Number indicates cholinesterase quality NOT quantity
80 = 80% PChE enzyme inhibited
Dibucaine Number
Normal genotype >70 Heterogenous for atypical gene = 40-60 → Prolongs block 1.5-2x longer Homogenous for atypical gene < 30 → Block prolonged 4-8hrs (unable to extubate) → Overnight ICU admission
Succinylcholine SE
Bradycardia, junctional rhythm, sinus arrest
Ventricular dysrhythmias, tachycardia, ↑ BP d/t autonomic ganglia stimulation
Hyperkalemia - severe in burn, abdominal infections, metabolic acidosis, closed head injury, & nAChR upregulation
Myoglobinuria - damage to skeletal muscle (especially in pediatric patients MD or malignant hyperthermia susceptible)
↑ intraocular pressure NOT commonly used in eye surgery
↑ gastric and lower esophageal pressures (↑ gastric contents)
↑ ICP r/t head injury
Masseter spasm (early indicator) - KNOWN TRIGGER for malignant hyperthermia
Myalgias - prominent in neck, back, & abdomen skeletal muscle
Elderly: Slower onset d/t ↓ circulation & reduced PChE levels
Pediatrics: Avoided in patients <5yo, Duchenne muscular dystrophy, cardiac arrest d/t hyperkalemic rhabdomyolysis
Malignant Hyperthermia
Pharmacogenetic disorder triggered by volatile anesthetics, succinylcholine, & stress
Ryanodine receptor gene mutation (chromosome 19)
S/S: ↑ CO2 production (1st sign), muscle rigidity, ↑ peak airway pressure, ↓ TV, metabolic acidosis, ↑ temp (late sign)
Succinylcholine Dose
Intubation 1mg/kg based on ideal body weight