Page 469 - Clinical Application of Mechanical Ventilation

Pharmacotherapy for Mechanical Ventilation 435

A 12 17
11 13 16
1 15
9 14
2
10 8
3 7
5
4 6
B O =
O – C – CH 3
CH 3
N + N
CH 3
H C
3
N + N
H C
3
CH – C – O © Cengage Learning 2014
H
3 =
O
Figure 13-4 (A) Basic steroid structure; (B) A steroidal-based neuromuscular blocking agent,
pipecuronium.

the motor endplate. For example, the release of ACh depends on extracellular calcium
++
c Mg may lead to and magnesium concentrations. Calcium functions to release ACh from the vesicles
T release of ACh and T
muscular contraction. and expose myosin-binding sites on actin. Myosin-binding site exposure is a structural
change that is necessary for the sliding of thin myofilaments past thick myofilaments.
The sliding of these filaments results in muscular contraction (Tortora et al., 2002).
Magnesium works in opposition to calcium. It decreases the release of ACh as well as
the membrane’s sensitivity, thus inhibiting muscle contraction (Ebadi, 1993).
++
++
T Ca or c Mg
enhances neuromuscular Consequently, low calcium and high magnesium levels can enhance the effects
blockade with nondepolarizing of nondepolarizing agents. Increased magnesium levels can magnify the effects of
agents.
depolarizing agents.
Sodium and potassium have a major function in the process of depolarization.
When a muscle cell is at rest, or not depolarized, there is a considerable difference
++
c Mg enhances between the concentration of sodium and potassium outside and inside the plasma
neuromuscular blockade with membrane. At rest, there is an increased concentration of sodium extracellularly and
depolarizing agents.
an increased concentration of potassium intracellularly. The difference in charge on
either side of the membrane of the resting cell is known as the resting potential and
is said to be polarized or charged (Tortora et al., 2002).
An acute decrease in extracellular potassium will result in hyperpolarization and an
Diuretic-induced hypo- increased resistance to depolarization. Hence, hypokalemia augments nondepolarizing
kalemia causes c blockade
with nondepolarizing agents agents and antagonizes depolarizing agents (Ebadi, 1993). Diuretic-induced hypokale-
and T blockade with depo- mia should be corrected to prevent altered effects (potentiation of blockade with non-
larizing agents.
depolarizing agents; reduction of blockade with depolarizing agents) (Halloran, 1991).
Acid-Base Status. Acidemia intensifies neuromuscular blockade, requiring a lower
dosage of paralyzing agent or a higher dosage of reversal agent such as neostigmine
(Kupfer et al., 1987). On the other hand, alkalemia necessitates a higher dosage of

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