British Journal of Anaesthesia 1996; 76: 278–283
Electromyographic and mechanomyographic characteristics of
neuromuscular block by magnesium sulphate in the pig†
C. LEE, X. ZHANG AND W.-F. KWAN
Summary
In spite of its well known propensity to cause
accidental paralysis by a specific mechanism of
;
action, Mg2 -induced neuromuscular block has not
been examined systematically for its characteristics
of muscle response to nerve stimulation. We
examined in seven anaesthetized domestic pigs the
mechanomyographic (MMG) and neurally evoked
compound electromyographic (ncEMG, EMG) responses of the tibialis anterior muscle to stimulation
of its motor nerve, at baseline and during three
levels of neuromuscular block induced by infusion
of MgSO4 (at approximately 25 %, 50 % and 75 %
depression of the 0.1-Hz EMG). We observed that:
at 0.1 Hz, the MMG tended to be more depressed
than the EMG; the train-of-four (2 Hz) was essentially non-fading; the tetanic force (50 Hz)
showed tetanic ascent instead of tetanic fade and
reached its baseline control value at 5 s in spite of
depression of the twitch; the EMG counterpart of
the tetanus showed escalation of the train of
ncEMG, so that the fourth ncEMG was much
greater than the first; and the post-tetanic twitch
;
was also relatively spared from Mg2 -induced
neuromuscular block. Sparing of the tetanus and
post-tetanic twitch resulted in large gains in the
tetanus : twitch ratio and the post- : pre-tetanic
twitch ratio, which increased at the 75 % level of
depression from 2.8 (SD 0.7) to 11.5 (4.0), and
from 1.5 (0.3) to 4.6 (1.4) (P : 0.01), respectively. These characteristics of neuromuscular block
;
by Mg2 reflect its prejunctional mechanism of
action by depression of transmitter release. (Br. J.
Anaesth. 1996; 76: 278–283)
Key words
Ions, magnesium. Neuromuscular block, measurement of response. Measurement technique, mechanomyography. Measure
ment technique, electromyography. Pig.
The non-depolarizing neuromuscular block produced by blockers of the curare-type (“curariform”)
is recognized by train-of-four (TOF) fade, tetanic
fade and post-tetanic enhancement of twitch response (‘post-tetanic potentiation’). In comparison,
depolarizing neuromuscular block does not manifest
fade or post-tetanic potentiation, but the changing
nature of its block from phase I to phase II is
recognized by these signs [1, 2]. Between the nondepolarizing and depolarizing blocks, mechano-
myographic (MMG) and electromyographic (EMG)
responses to motor nerve stimulation differ in
relative sensitivity [1]. Fade observed during curariform neuromuscular block in vivo is generally
attributed to diminution of successive end-plate
potentials (EPP) observed in vitro, which in turn is
attributed to depression of acetylcholine mobilization prejunctionally [3]. TOF fade [4] has yielded
the “TOF count” [5], a method which is now used
as a routine to estimate curariform neuromuscular
block clinically. The diminishing TOF ratio during
continuous administration of suxamethonium is also
useful in defining phase II vs phase I neuromuscular
block [2, 6]. At the end of surgery, these monitoring
techniques also guide dosing and reversal of neuromuscular block in anaesthetic practice.
In contrast with the extensive literature on
curariform and depolarizing neuromuscular blocks,
there is a remarkable paucity of literature on the
features of magnesium-induced neuromuscular
block in vivo. Many reports have documented
accidental paralysis as a side effect of magnesium
sulphate (MgSO4) therapy [7]. Magnesium (Mg2;)
blocks prejunctionally, with a different mechanism
of action from the curariform and depolarizing
blockers.
As indications for MgSO4 therapy have increased
rapidly [8, 9], we feel that Mg2; deserves an
independent study of its neuromuscular blocking
characteristics. We have recently quantified the
dose–response relationship of Mg2;-induced neuromuscular block in an animal model while studying
the effect of Mg2; on the refractoriness of neuromuscular transmission [10]. The present study
describes in qualitative and quantitative terms the
MMG and EMG responses to motor nerve stimulation during three levels of Mg2;-induced neuromuscular block.
Materials and methods
With institutional approval, seven male Duroc
brown pigs, 9–12 kg, were anaesthetized with pentobarbitone 50 mg kg91 i.p., supplemented with
CHINGMUH LEE, MD, XIAOYAN ZHANG, MD, WING-FAI KWAN, MD,
Department of Anesthesiology, Harbor-UCLA Medical Center,
Torrance, CA 90509-2910, USA. Accepted for publication:
September 5, 1995.
† Presented in part at the Annual Meeting of the American
Society of Anesthesiologists, October 24, 1995, Atlanta, Georgia,
USA.
Mg 2+-induced neuromuscular block
Figure 1 Differential depression by Mg2; of the neurally
evoked 0.1-Hz MMG ( ) and EMG ( ) responses from their
respective baselines at approximately 25 % (level I), 50 % (level
II) and 75 % (level III) depression of the ncEMG.
2–5 mg kg91 i.v. as required during the study. A
cuffed tracheal tube of 6-mm internal diameter was
inserted and ventilation of the lungs was controlled
with a Harvard respirator pump at a rate of 15 times
per minute. Tidal volume of air was adjusted to
maintain an end-expiratory carbon dioxide concentration of 4–4.5 %. A cannula was inserted into a
carotid artery for continuous monitoring of arterial
pressure. A peripheral venous cannula was inserted
for hydration and infusion of MgSO4. Each pig
received approximately 120–180 ml of 5 % glucose in
normal saline during the entire experiment. The
oesophageal temperature was maintained at 36–38 ⬚C
by a heating lamp. A pair of fine Grass EEC
platinum solid needle electrodes (type E2) were
inserted s.c., slightly posterior and distal to the
proximal head of the fibula. Several attempts were
made to position these electrodes close together
(1–2 mm at the tips) and as close to the common
peroneal nerve as possible, so that the electrical
stimulus required for supramaximal stimulation and
the stimulus artefact were as small as possible.
279
Three other identical electrodes were used for
detection of the neurally evoked compound electromyogram (ncEMG), as described previously [11].
Guided by palpation of the twitch, the sensing
electrode was inserted s.c. along the frontal aspect of
the tibialis anterior muscle, crosswise to the muscle
at its belly. A reference electrode was inserted s.c.
near the insertion of this muscle, away from all
muscles. A reference electrode was inserted s.c.
between the stimulating and sensing pairs of electrodes. The EMG sensing electrode was repositioned
several times to assure an optimal waveform, without
double peaking or excessive stimulus artefact. Each
preparation must produce a stable unipolar waveform typical of the ncEMG, as described previously
[11], before the experiment can begin. The electric
stimuli were generated by a Grass S88 stimulator
and passed through a Grass SIU5 stimulus isolation
unit. The supramaximal stimulus was determined,
and 20–50 % of the voltage added. The stimulus was
rectangular and of 0.1 ms duration. The ncEMG
response was digitized, processed and reconverted to
analogue waveforms for immediate online recording,
as described previously [12]. Side by side with the
ncEMG, the MMG response of the same tibialis
anterior muscle was recorded simultaneously. The
tendon was detached from its insertion with a chip of
bone, freed from constraints and connected to a
Grass force displacement transducer (FT10C). The
motor nerve was stimulated at 0.1 Hz. Periodically
(see below) the 0.1-Hz stimulation was interrupted
for TOF (2 Hz) and tetanic (50 Hz, 5 s) stimulations.
The first post-tetanic 0.1-Hz stimulation was delivered 5 s after the tetanus. Of the 250 ncEMG
responses corresponding to a 50-Hz, 5-s tetanus, the
first four could be processed and recorded in time
before the first post-tetanic twitch was evoked. These
four were recorded online for analysis.
After the preparation had stabilized for 30–45 min,
Figure 2 Neurally evoked MMG twitch (0.1 Hz), TOF (2 Hz), tetanus (50 Hz, 5 s) and post-tetanic twitches at
baseline (upper panel) and during Mg2;-induced neuromuscular block (lower panel). Note the increasing tetanus
(“tetanic ascent”) during neuromuscular block. In this experiment, the 0.1-Hz twitch was depressed by 45 %.
TOF responses neither clearly faded nor escalated at baseline or during block. The tetanus was sustained at
baseline. It was depressed by 32 % during block, but increased steadily so that at 5 s it was depressed by only
11 % from baseline. The post-tetanic twitch was potentiated at baseline. The potentiation was augmented during
block, so that the post-tetanic twitch was depressed by only 16 % from baseline.
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British Journal of Anaesthesia
baseline values of a series of EMG and MMG
responses were obtained. The series consisted of
0.1 Hz (“twitch”), TOF, tetanic and post-tetanic
responses. MgSO4 was then infused to establish
three levels of neuromuscular block in succession, at
approximately 25 %, 50 % and 75 % depression of
the 0.1-Hz EMG. Each level, when established, was
maintained 5–10 min at the end of which a series of
twitch, TOF, tetanic and post-tetanic responses
were again obtained. Because various EMG and
MMG variables of response were expected to differ,
the three levels of neuromuscular block were established according to the amplitude of the 0.1-Hz
EMG, irrespective of other variables. Levels I, II
and III therefore refer to approximately 25 %, 50 %
and 75 % depression of the amplitude of the 0.1-Hz
ncEMG, respectively. Data are expressed as mean
(SD), and paired data sets were compared with repeat
measures ANOVA or Student’s paired t test (twotailed). P : 0.05 was considered statistically significant.
Results
The three levels of neuromuscular block actually
established were 25 (3)%, 51 (3)% and 74 (2)%
depression of the ncEMG, respectively (fig. 1). The
MMG twitch response tended to be more depressed
than the EMG counterpart. Figure 2 illustrates the
MMG twitch, TOF, tetanic and post-tetanic twitch
responses at baseline and during Mg2;-induced
neuromuscular block. Figure 3 illustrates the EMG
counterparts. The TOF ratio at control was 1 with
every experiment. The TOF responses remained
non-fading in character during all levels of Mg2;induced neuromuscular block, although the EMG
and MMG TOF ratios were both slightly but consistently diminished from 1 (P : 0.05) to approximately 0.9.
Mg2;-induced neuromuscular block did not cause
tetanic fade. Instead, it caused a tetanic increase so
that the tetanic contractile force was greater at 5 s
(fig. 2, T50b) than at the beginning of tetanus (fig. 2,
Figure 4 Tetanic ascent observed during Mg2;-induced
neuromuscular block. The thick line : the 5-s tetanus; the
vertical error bars : SD. T50a and T50b : tetanic force at the
beginning and end of the 5-s, 50-Hz tetanus, respectively. The
thin numbered horizontal or slanting lines : individual pigs.
Level tetanus at baseline (pigs 1, 2) ascended with any
neuromuscular block, while fading tetanus at baseline (pigs 5,
6, 7) reversed at deeper levels of block to show an ascent.
T50a). Figure 4 shows the varied behaviour of the
tetanus among pigs. Some pigs showed mild tetanic
fade at baseline, which reversed at various levels of
neuromuscular block to become a tetanic increase.
At deeper levels of block, all pigs showed marked
tetanic increase. Corresponding with the tetanic
ascent, the fourth ncEMG of the tetanus was much
greater in amplitude than the first during neuromuscular block (fig. 3, 50 Hz; fig. 5).
The tetanus was spared from Mg2;-induced
neuromuscular block (fig. 6). Comparing the contractile forces at 5 s (T50b), the tetanus elicited during
MgSO4 infusion did not show a statistically significant difference from the tetanus elicited at baseline
(P 9 0.5 for all three levels). The post-tetanic twitch
was also spared markedly, although not completely.
Figure 3 Neurally evoked compound EMG responses at baseline (upper panel) and during Mg2;-induced
neuromuscular block (lower panel). The TOF responses (2 Hz) did not fade at baseline but faded slightly during
block. The next four ncEMG responses, marked “50 Hz, 5 s”, represent the first 80 ms of the 5-s tetanus. They
showed marked escalation during neuromuscular block. This escalation is the EMG counterpart of the increasing
tetanic force. As is in the case of the MMG, the 5-s post-tetanic twitch was less depressed than the pre-tetanic
twitch. The 50 Hz and 2 Hz EMG were displaced with the same spacing for clarity [11, 12].
Mg 2+-induced neuromuscular block
Figure 5 The first ( ) and fourth (■) of the train of ncEMG
of a tetanus (50 Hz) evoked at baseline and at three levels of
Mg2;-induced neuromuscular block. At each level, the first
ncEMG corresponds to the singly evoked ncEMG (0.1 Hz) and
shows the degree of neuromuscular block. The fourth ncEMG
was relatively spared from the block. The fourth : first ratio
increased from 1.1 (0.2) to 1.3 (0.1), 1.5 (0.1) and 2.0 (0.2) at
the three levels of block, respectively (P : 0.05). The discrete
EMG escalated as the fused tetanic contraction ascended.
Figure 6 Sparing of tetanus ( ) and post-tetanic twitch (■)
from Mg2;-induced neuromuscular block. Tetanic force
(50 Hz, 5 s) was measured at 5 s, as the T50b. The post-tetanic
twitch was evoked 5 s after the end of the tetanus. Note that
the tetanic force measured at 5 s did not diminish from baseline
(P 9 0.5, all three levels) in spite of depression of the twitch
( ). The post-tetanic twitch was slightly depressed from
baseline (P : 0.05), but less so than the twitch at any level
(P : 0.01).
As a result of tetanic and post-tetanic sparing, the
tetanus : twitch ratio and post-:pre-tetanic twitch
ratio were increased markedly (table 1).
Discussion
There is a clear distinction between prejunctional
and postjunctional sites of action and between
mobilization and release mechanisms of the prejunctional actions of neuromuscular blocking agents. For
decades, Mg2; has been recognized as the prototype
of the latter mechanism of prejunctional neuromuscular block in vitro [13]. It causes accidental
paralysis by itself or in interaction with other
neuromuscular blockers in vivo. In addition to
obstetric use, Mg2; is being used increasingly by
paediatricians [14], endocrinologists [15], cardiologists [16–19], cardiac surgeons [20] and emergency
[21, 22] and other specialists [8, 23]. Examples of
new indications for MgSO4 which are of interest to
anaesthetists are phaeochromocytoma [24–26], re-
281
fractory cardiac arrhythmia [16] and resuscitation
[21, 22]. A method of diagnosis of Mg2;-induced
neuromuscular block by nerve stimulation therefore
deserves exploration.
According to our results, Mg2;-induced neuromuscular block may be characterized as follows: the
MMG response tends to be more depressed than the
EMG response; TOF responses do not fade; tetanus
does not fade, instead its contractile force increases;
the train of successive EMG responses during tetanic
stimulation escalate; the peak tetanic force does not
diminish although the tetanus starts at a lower point;
and the physiological potentiation of the post-tetanic
twitch is augmented so that the post-tetanic twitch is
relatively spared. As a result of tetanic and posttetanic sparing, the tetanus:twitch ratio and the
post- : pre-tetanic twitch ratio increase markedly.
This set of characteristics clearly distinguish Mg2;induced neuromuscular block from curariform,
phase I (depolarizing), phase II (post-depolarizing,
desensitization) and post-junctional irreversible nondepolarizing (␣-bungarotoxin) types of neuromuscular block [27] (table 2).
TOF fade is explained by diminution in successive
EPP, which result from depressed mobilization of
the transmitter, which in turn is caused by occupation of the prejunctional “mobilization
receptors”, according to Bowman [3]. This theory
requires that neuromuscular block achieved by
occupation of postjunctional receptors alone, such as
by ␣-bungarotoxin, does not manifest tetanic or
TOF fade. This, indeed, is the case [27]. In the case
of Mg2;, our observations are explicable by the
generally accepted main mechanism of neuromuscular action of Mg2;, which is depression of prejunctional release of acetylcholine. As successive
motor impulses lead to accumulation of Ca2; in the
motor nerve terminal, successive EPP become less
depressed by Mg2;. This escalation of the train of
EPP results in “tetanic escalation” of the ncEMG
responses. It also causes the increasing tetanic force
(“tetanic ascent”) which spares the tetanus from
depression. The enhanced post-tetanic potentiation
can similarly be explained by accumulation of Ca2;
during tetanic stimulation. The MMG twitch tends
to be more depressed than its corresponding EMG
because Mg2; is also thought to directly depress the
contractility of the muscle [13]. The reason for the
slight TOF fade is unclear. Ramanathan and colleagues [28] reported TOF escalation in preeclamptic patients. Toxaemia of pregnancy may
account for the difference. In any case, the TOF
ratio did not change by more than 10 % from
baseline.
From the above, it becomes obvious that the word
“non-depolarizing” is generic and fails to distinguish prejunctional (mobilization, release) and postjunctional (competitive, non-competitive) nondepolarizing neuromuscular blocks from curariform
(mobilization and competitive) block (table 2).
Because of this, we prefer to call neuromuscular
block of the curare type “curariform” block, to
facilitate its distinction from other types of nondepolarizing neuromuscular block, including the
“release block” by Mg2;.
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British Journal of Anaesthesia
Table 1 Tetanus and Post-tetanic twitch, as multiples of the pre-tetanic twitch, during 25 % (level I), 50 % (level
II) and 75 % (level III) Mg2+-induced depression of the 0.1-Hz ncEMG. *P : 0.05: level I, II or III vs baseline
values, both rows
Tetanus : twitch ratio*
Post- : pre-tetanic twitch ratio
Baseline
Level I
Level II
Level III
2.7 (0.7)
1.5 (0.3)
4.6 (1.7)
2.2 (0.6)
6.7 (2.7)
3.0 (0.9)
11.5 (4.3)
4.6 (1.4)
Table 2 Patterns of mechanomyographic neuromuscular responses to nerver stimulation distinguishing various
mechanisms of neuromuscular block in vivo
MMG vs EMG
TOF fade
Tetanus
Tetanus sparing
Post-tetanic twitch
potentiation
MgSo4
Phase I
Phase II
Curariform
␣-Bungarotoxin
More sensitive
Negligible
Increases
Marked
Marked
Less sensitive
Negligible
Level
?
Minimal
?
Emerges
Fade emerges
?
Emerges
More senstive
Marked
Fades
Clear
Marked
?
Negligible
Level
?
Clear
The clinical implications of our observations can
only be speculative at present, and only a few
obvious possibilities are examined below. First,
neuromuscular block by the same mechanism of
action should exhibit similar or the same patterns of
response to nerve stimulation. Aminoglycoside antibiotics block neuromuscular transmission mainly by
competition with Ca2;, as is the case with Mg2; [29,
30]. In agreement with this, we have previously
observed that streptomycin and neomycin also block
neuromuscular transmission with tetanus and posttetanic sparing [31]. We surmise that the extremely
high mortality associated with antibiotic-induced
neuromuscular block in the 1970s might be partially
attributable to failure to differentially diagnose
aminoglycoside-induce neuromuscular block from
curariform or depolarizing neuromuscular block
[32].
Second, humans usually exhibit similar qualitative
patterns of neuromuscular block as do most laboratory animals. Quantitatively, domestic pigs are
useful for predicting human responses to neuromuscular blocking agents [33, 34]. As escalation of
the train of ncEMG responses in the beginning of
tetanus is a consistent and clear-cut finding, a very
brief burst of nerve stimuli delivered rapidly might
be the best candidate for clinical development as a
diagnostic tool of Mg2;-induced neuromuscular
block. Such a brief single burst of stimulation should
cause no greater pain than the double-burst stimulation. Similar to the TOF [4] or count [5], the
escalation ratio and the tetanus : twitch ratio require
no historical control for quantitative assessment of
neuromuscular block.
Third, tetanic sparing should imply that in spite of
depression of the twitch, physiological muscle functions, all of which are tetanic in nature, may be well
preserved. The fact that the tetanic force takes a few
seconds to reach maximum may imply that sustained
motions such as headlift or breathing may be less
depressed than brisk motions such as knee jerk or
cough. Indeed, toxaemic patients are often given
MgSO4 until the knee jerk disappears, without
obvious loss of ability to lift the head and to breathe.
On the one hand, therefore, tetanic sparing repre-
sents a margin of safety of physiological functions.
On the other hand, however, this pattern of paresis
may lead to failure to observe Mg2;-induced neuromuscular block clinically, which is a danger. Finally,
in a patient who has previously received both MgSO4
and a curariform blocker, detection of TOF and
tetanic fades should reveal the continuous presence
of the curariform block while demonstration of a
tetanic ascent should imply dominance of Mg2;induced neuromuscular block. A level tetanus may
imply absence of any neuromuscular block or a
balance of tetanic fade and tetanic ascent.
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