Pharm: NMBD drugs Flashcards
Rocuronium (Zemuron) drug class
Aminosteriod
Rocuronium (Zemuron) concentrations
10mg/mL
Rocuronium (Zemuron) standard induction dose
0.6mg/kg
Rocuronium (Zemuron) RSI dose
1.2mg/kg
Rocuronium (Zemuron) maintenance dose
5-10mg (frequently 10mg)
Rocuronium (Zemuron) onset and duration for standard and RSI doses
standard:
Onset: 1.5-3 m
Duration: 15-30 m
RSI
Onset: 30-45 sec
Duration: 45-150 m
Rocuronium (Zemuron) elimination
10-25% renal
10-20% hepatic
50-70% biliary
Vecuronium (Norcuron) drug class
Aminosteriod
Vecuronium (Norcuron) concentration
1mg/mL
Vecuronium (Norcuron) induction dose
0.1mg/kg
Vecuronium (Norcuron) maintenance dose
1-2mg
Vecuronium (Norcuron) onset and duration
onset: 3-5m
duration 25-40m
Vecuronium (Norcuron) elimination
15-25% renal
20-30% hepatic
40-75% biliary
Pancuronium (Pavulon) drug class
aminosteriod
Pancuronium (Pavulon) concentration
1mg/mL
Pancuronium (Pavulon) induction dose
0.1mg/kg
Pancuronium (Pavulon) infusion dose
1-15mcg/kg/min
Pancuronium (Pavulon) onset and duration
Onset: 4 m
Duration: 100 m
Pancuronium (Pavulon) elimination
80% renal
10% hepatic
10% biliary
(prolong duration
with disease)
Pancuronium (Pavulon) PSNS effects
blocks M2 receptors causing increased HR, MAP, CO
Atracurium (Tracrium) drug class
benzylisoquinolinium
Atracurium (Tracrium) concentration
10mg/mL
Atracurium (Tracrium) induction dose
0.5mg/kg
Atracurium (Tracrium) onset and duration
Onset: 2-2.5 m
Duration: 20-35 m
Atracurium (Tracrium) elimination
90% Hoffman
10% renal
Hoffman elimination
Hoffman
elimination is
dependent on
normal body temp
and pH (acidosis
and hypothermia
decrease)
Cisatracurium (Nimbex) drug class
benzylisoquinolinium
Cisatracurium (Nimbex) concentration
2mg/mL
Cisatracurium (Nimbex) induction dose
0.1mg/kg -0.2mg/kg (4x ED95)
Cisatracurium (Nimbex) onset and duration
Onset: 2.5 min
Duration: 40-60 sec
Cisatracurium (Nimbex) elimination
Hoffman elimination
Cisatracurium (Nimbex) potency and histamine response
3x more potent than atracurium w/ decreased release of histamine
Mivacurium (Mivacron) drug class
benzylisoquinolinium
Mivacurium (Mivacron) concentration
2mg/mL
Mivacurium (Mivacron) induction dose
0.15mg/kg over 30-60 seconds
Mivacurium (Mivacron) onset and duration
onset 3-5min
duration 20 min
Mivacurium (Mivacron) metabolism
metabolized by plasma cholinesterase
Non-depolarizing NMBD
compete with ACh for active binding sites; competitive antagonist
Depolarizing NMBD
similar structure to ACh, acts as partial agonist at postsynaptic Nm junction causing prolonged depolarization
Factors influencing choice of NMBDs
- potency, dose-response relationship (inversely related to onset of block)
- onset time, relationship b/t twitch depression and dose (ED 95 causes 95% suppression, 2 x ED 95 used for intubating)
-increasing dose will increase onset of block
-duration of action = administration time to 90% recovery of twitch response
-lipophilicity, drugs ability to move toward the neuromuscular junction
Impact of low potency
require high dosing for diffusion gradient (i.e. Rocuronium)
Defasciculating dose goal and administration procedure
Goal: decrease intensity of fasciculations and myalgia
Admin 1/10 of non-depolarizing blockade 3-4 minutes prior to succ.
Admin 50-70% more succ (1.5 mg/kg)
Aminosteriod Compouds
- Rocuronium (Zemuron)
- Vecuronium (Nocuron)
- Pancuronium (Pavulon)
Benzylisoquinolinium compound
- Atracurium (Tracrium)
- Cisatracurium (Nimbex)
- Mivacurium (Mivacron)
**more likely to release histamines
short acting NMBD
Mivacurium
10-20m
Intermediate NMBD
(20-50 m)
- Rocuronium
- Vecuronium
- Atracurium
- Cistracurium
Long acting NMBD
> 50min Pancuronium
Effect of NMBD: increased potency
- inhalation agents
- des> sevo> iso> halo
- antibiotics (aminoglycosides)
- hypothermia
- antiarrhythmic (quinidine)
- magnesium sulfate
- large dose of LA
Effects of NMBD: decrease potency
- chronic anticonvulsant
- hypercalcemia
- up-regulation of receptors (burns, atrophy, denervation)
Adverse outcomes of residual blockade
1.Increased risk of aspiration
-Impairment of pharyngeal coordination and force of contraction
-Swallowing dysfunction/delayed initiation of swallowing reflex
-Reductions in upper esophageal sphincter tone
2.Upper airway obstruction
-Reduction in airway volumes and inspiratory flow
-Impairment of upper airway dilator muscle function
-Impaired hypoxic ventilatory drive
3.Symptoms of muscle weakness (visual disturbances, severe facial weakness, difficulty speaking)
4.Increased risk of postop hypoxemia
5.Interop awareness
Clinical signs of recovery
- Adequate tidal volume and respiratory rate
- Respirations smooth and unlabored
- Effective swallowing and sustained bite
- Effective cough
- Sustain head or leg lift for at least 5 sec
- Strong, constant hand grip
-TOF >0.9, no fade - Sustained tetanic response to 50Hz for 5 sec