Page 468 - Clinical Application of Mechanical Ventilation

434 Chapter 13

TABLE 13-9 Depolarizing and Nondepolarizing Agents

Initial Dose Onset
Agents (mg/kg) (min) Duration Drug Clearance

Depolarizing
Succinylcholine (Anectine, 0.3 to 1.1 1 Short Metabolized by plasma
Quelicin) cholinesterase

Nondepolarizing
Pancuronium bromide 0.07 5 to 7 Long Metabolized by liver,
(Pavulon) excreted in urine
Atracurium (Tracrium) 0.4 to 0.5 4 to 5 Intermediate Self-destroying

Vecuronium bromide 0.05 4 to 6 Intermediate Metabolized by liver,
(Norcuron) excreted in urine

Rocuronium (Zemuron) 0.3 3 to 4 Short Metabolized by liver
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been implicated in drug accumulation in patients with renal insufficiency. Ve-
Organ failure may curonium is also poorly eliminated in patients with hepatic failure. Atracurium is
decrease drug clearance,
increase drug accumulation, preferred in the presence of organ failure because it is self-destroying and does not
and prolong neuromuscular rely on organ metabolism and excretion (Halloran, 1991).
blockade.
Drug Interaction. Some cardiovascular and antiarrhythmic agents may interact and
potentiate the effects of nondepolarizing agents. They include beta blockers, pro-
cainamide, quinidine, calcium channel blockers, and nitroglycerin. High con-
centrations of antibiotics may also potentiate the effects of competitive agents by
Beta blockers,
procainamide, quinidine, decreasing the release of ACh. These antibiotics include the aminoglycosides and
calcium channel blockers, and polymyxins as well as tetracycline, erythromycin, and vancomycin (Halloran, 1991).
nitroglycerin may potentiate
the effects of nondepolarizing Steroidal-based vecuronium bromide and pancuronium bromide may be particu-
agents. larly dangerous if administered along with systemic corticosteroids (Watling et al.,
1994). A significant number of asthmatics receiving these neuromuscular blocking
agents in combination with steroid therapy have experienced prolonged blockade
for several days following discontinuation of the paralyzing agent (Kupfer et al.,
1987). This prolonged blockade is possibly related to the comparable chemical struc-
ture of steroid and steroidal-based agents; however, the mechanism is unknown.
Figure 13-4 shows the basic steroid structure and pipecuronium, a steroidal-based
paralyzing agent. Until studies become conclusive, use of corticosteroids should
be avoided during prolonged muscle blockade with any neuromuscular blocking
agent (Hansen-Flaschen et al., 1993).
c Ca may lead to Electrolyte Imbalance. The normal physiology of muscle contraction depends on the regu-
++
c release of ACh and c
muscular contraction. lation of electrolytes. Abnormal levels of calcium and magnesium affect the quality of
contraction, while imbalances in potassium and sodium levels alter the excitability at

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