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SUMMARY
The intravenous administration of 50 mgof lidocaine as a single bolus to four
patients with heart disease did not result insignificant change in cardiac output or
a
left ventricular end-diastolic pressure (LVEDP). Two patients had moderate decrease
in systemic arterial pressure which was not accompanied by symptoms, was of short
duration, and did not require therapeutic intervention. Left ventricular function, as
assessed by the relationship of changes in stroke volume index (SVI) and stroke work
index (SWI) to changes in LVEDP, was not significantly affected nor was the maximum
rate of rise of left ventricular pressure (dp/dt).
The intravenous injection of 100 mg of lidocaine into eight additional patients
with heart disease did not produce a statistically significant change in any of these
hemodynamic variables when compared to their respective control values. Examination
of individual responses, however, revealed that some depression of left ventricular func-
tion occurred in at least three and probably four of these patients. Nevertheless, this
depression of myocardial function was not of sufficient magnitude to produce symptoms
or reduce the cardiac output and generally did not result in an inordinate increase in
LVEDP.
It is concluded that 100 mg or less of lidocaine injected intravenously has remarkably
few, if any, adverse hemodynamic effects of clinical significance in man.
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in L/min/m2; LVEDP = left ventricular end-diastolic pressure in mm Hg; SVI = stroke volume
index in mI/M2; SWI = left ventricular stroke work index in g-m/m2; dp/dt = maximum rate
of rise of left ventricular pressure as per cent of control.
Lidocaine, best known as a local anesthetic, Moran17 have demonstrated a negative ino-
has been found to be effective in the treat- tropic effect in dogs.
ment of many tachyarrhythmias,3 13 and The following study was undertaken to
initial studies on the hemodynamic effects of provide information concerning the hemo-
this agent indicated that it had distinct ad- dynamic effects of lidocaine in unanesthetized
vantages over other commonly used anti-ar- humans and in particular to observe its effect
rhythmic drugs when administered intrave- on left ventricular function. Furthermore, it
nously. In animals cardiac output has been was proposed that these effects be examined
found to increase,14 and in man arterial in subjects who would most likely receive this
pressure generally is little affected by the agent therapeutically, for example, patients
administration of therapeutic doses of lido- with heart disease, and that the doses used be
caine.3 9 10 13,15 In addition, Harrison and those which are commonly used in the treat-
associates3 reported that myocardial con- ment of arrhythmias.
tractile force measured directly in patients
at the time of corrective cardiac surgery was Methods
not affected significantly by this agent. How- Twelve male patients, ranging in age from 33
ever, more recently Nelson and Harrison'6 to 73 years (average, 52 years), were the
observed that lidocaine does diminish the subjects of this study. Three patients had hyper-
tensive cardiovascular disease, two had arterio-
force of isometric contraction in the isolated sclerotic heart disease with angina pectoris, and
papillary muscle preparation, and Austen and the remainder were believed to have primary
Circulation, Volume XXXVII, June 1968
HEMODYNAMIC EFFECTS OF LIDOCAINE 967
Table 2
Hemodynamic Effects of 100 mg of Lidocaine (Group 2)
Patient Time Hr Mean art pr CI LVEDP SvI SWI dp/dt
L.H. 0 109 81 1.30 16 12 11.8 100
BSA-1.71 5 107 87 1.37 27 13 12.5 72
Age-58 yr 10 106 83 1.35 19 13 13.5 90
ASHD 15 106 80 1.31 14 12 11.9 92
30 107 77 1.43 7 13 12.0 78
J.B. 0 73 109 2.10 11 29 45.8 100
BSA-1.74 5 84 116 2.10 16 25 37.4 92
Age-49 yr 10 85 118 2.04 16 24 37.7 112
HCVD 15 84 120 1.90 15 23 35.0 108
30 84 115 2.16 13 26 41.6 124
A.B. 0 126 84 3.03 22 24 22.9 100
BSA-1.61 5 134 83 3.12 20 23 21.2 97
Age-40 yr 10 130 80 3.28 17 25 24.7 112
PMD 15 129 80 3.40 20 26 23.0 108
30 124 78 3.25 15 26 24.6 97
W.G. 0 87 85 3.40 6 39 44.0 100
BSA-1.69 5 84 82 3.40 9 41 41.0 77
Age-49 yr 10 81 85 3.60 44
PMD 15 88 87 3.12 9 35 41.0 115
30 92 84 3.13 4 34 35.0 109
D.B. 0 95 80 1.83 30 19 13.9 100
BSA-1.96 5 96 69 1.51 27 16 10.0 86
Age-33 yr 10 89 72 1.27 29 14 10.3 97
PMD 15 93 78 1.95 31 21 15.4 109
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myocardial disease (tables 1 and 2). All patients rhythm, and none had clinical evidence of
but L. L. and G. G. had radiographic evidence congestive heart failure at the time of the study.
of cardiomegaly, a history of congestive heart All studies were performed in the postabsorptive
failure, and were receiving a digitalis glycoside state with the patient in the supine position.
at the time of the study. Patient G. G. (table Secobarbital, 100 mg, was given orally 60 to 90
2) had electrocardiographic evidence of left ven- min before the procedure. Following diagnostic
tricular hypertrophy. All patients were in sinus right and left heart catheterization, catheters
Circulaion, Volume XXXVII, June 1968
968 SCHUMACHER ET AL.
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Figure 1
The effect of lidocaine on hemodynamic variables assessing left ventricular function. For
abbreviations, see text. Values represent mean values + standard error of the mean. Open cir-
cles connected by broken lines indicate values for patients receiving 50 mg of lidocaine; closed
circles connected by solid lines, values for those receiving 100 mg. Abscissa represents control
period (C) and time in minutes after drug injection.
were left in the main pulmonary artery for filter. A standard limb lead of the electrocardio-
purposes of injection and in the left ventricle gram and the brachial arterial pressure were
for the recording of pressure. Cardiac output recorded with the hemodynamic variables on a
was determined by the indicator-dilution method. multi-channel oscillograph. The midthoracic level
Indocyanine-green dye was injected and rapidly was used as the zero reference point for intra-
flushed into the pulmonary artery while blood vascular pressure.
from the brachial artery was withdrawn through After systemic arterial pressure, heart rate, and
a Gilford densitometer. The maximum rate of left ventricular end-diastolic pressure (LVEDP)
rise of left ventricular pressure was measured had remained constant for 15 to 20 min, 50 mg
using an R-C differentiating circuit with a 15-Hz of lidocaine was injected as a single bolus into
Circulation, Volume XXXVII, June 1968
HEMODYNAMIC EFFECTS OF LIDOCAINE 969
the pulmonary artery of four patients (group 1). period and thereafter returned to control
All measurements were then repeated 5, 10, 15, values. In the remaining two patients maxi-
and 30 min after drug injection. Since no adverse mum decreases in SVI of 5 and 8 mI/m2 oc-
effects were noted with this dose of lidocaine,
the next eight patients (group 2) received 100 curred at the 30-min period. SWI also de-
mg of lidocaine injected as a single bolus; mea- creased in each patient at some time after
surements were repeated as above. drug injection with the greatest decrease be-
Stroke work index (SWI) in g-m/m2 was cal- ing 8.7 g-m/m2. In two patients the maximum
culated from the following formula: decrease in SWI occurred at the 5-min period
-;XA7T-SVI X (LVSP - LVEDP) X 1.36
3)vVy whereas in the remaining two this was noted
100 at 30 min. The maximum rate of rise of left
where SVI means the stroke volume index in ventricular pressure fell below the control
milliliters per square meter, LVSP is the mean value in three patients, the greatest decrease
left ventricular pressure during ejection in mm being 13% which occurred at the 30-min pe-
Hg determined planimetrically, and LVEDP is riod. The reduction in dp/dt in the remaining
the left ventricular end-diastolic pressure in mm
Hg. two patients did not exceed 10% and, by the
30-min period, values exceeding the control
Results were observed.
Group 1
Group 2
The individual hemodynamic data before
and after injection of 50 mg of lidocaine are The individual hemodynamic data before
presented in table 1, while the mean values and after 100 mg of lidocaine are given in
are illustrated in figure 1. table 2 and the mean values are illustrated in
In three patients heart rate was essentially figure 1. The mean values for LVEDP, SWI,
unchanged or demonstrated only a slight fall and maximum dp/ dt at the 10-min period
following drug administration, while a fall of include observations on only seven patients.
However, recalculation of mean values for all
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g-m/m2 at rest to 28.9 g-m/m2. This decrease which are reflected only in changes in the
however is somewhat magnified by the failure velocity of myocardial contraction.2'
to obtain measurements at the 10-min period Interpretation of the data from the patients
in one patient. Excluding this patient the given 50 mg of lidocaine is difficult because
average decrease in SWI between the control of the variable results obtained in this small
and 10-min periods was 3.0 g-m/m2. The max- number of patients. However, since it was
imum rate of rise of left ventricular pressure not the purpose of this investigation to study
decreased by more than 5% in five patients. dose response relationships of lidocaine and
In each of these patients the maximum de- since no major untoward hemodynamic ef-
crease occurred at the 5-min period and in
fects occurred in this group of patients, we
four of these patients maximum dp/dt had elected not to include a larger number of
returned toward control values by 30 min.
In the remaining one of these four patients, patients. Two patients given 50 mg of lido-
dp/dt had returned to near control values by caine did develop decreases in mean arterial
the 15-min period but, in association with a pressure of 16 and 11 mm Hg although this
marked fall in LVEDP, decreased again at the was not accompanied by symptoms, was
30-min period. The average decrease in dp/ relatively short-lived, and did not require
dt for the group was small, averaging 4% at therapeutic intervention. A relatively small
the 5-min period and thereafter exceeding decrease in cardiac index was observed in
control values. each patient, the maximum being 0.52 L/min/
m2, whereas a significant rise in LVEDP did
Discussion not occur in any patient. Unequivocal evi-
It was the purpose of the present investiga- dence of a myocardial depressant action with
tion to determine the hemodynamic effects of this dose of the drug was not obtained in
Circulation, Volume XXXVIl, June 1968
HEMODYNAMIC EFFECTS OF LIDOCAINE 971
any patient. Changes in SVI and SWI gen- maximum dp/dt and SWI fell in each and
erally paralleled the changes in LVEDP, and SVI declined in two. In an additional patient
in the two patients in whom changes in these (L. H.), maximum dp/dt fell and SVI and
variables suggested a depression of myo- SWI increased only slightly in spite of an
cardial function, an increase in maximum dp/ increase of 11 mm Hg in LVEDP. Thus the
dt occurred at that time. Furthermore in the effect of 100 mg of lidocaine on myocardial
two patients in whom maximum dp/dt fell function in patients with heart disease is
after lidocaine, the decreases were small, 9 variable. Of equal or greater importance how-
and 7%, and in one this could be attributed to ever is the observation that, even when im-
a simultaneous reduction in heart rate and pairment of left ventricular function did occur,
LVEDP.25, 26 it was not of sufficient magnitude to produce
The administration of 100 mg of lidocaine symptoms or reduce the cardiac output and
to eight patients also resulted in variable but the effect was short-lived.
generally small changes in all hemodynamic It is of interest that the response to lido-
variables, none of which was significantly caine was not influenced by the type of heart
different statistically from its respective con- disease or its severity as judged by the resting
trol at any time period. The maximum CI and LVEDP. However the small number
decrease in mean arterial pressure in any of patients studied would not permit a
individual was 11 mm Hg which occurred in definitive conclusion in this regard. Certainly
one patient at the 5-min period and which it must be appreciated that a more pro-
had returned to control values by the 15-min nounced effect might occur in patients with
period. The maximum decrease in CI in any more advanced heart disease or in those
patient was 0.56 L/min/m2 which occurred receiving larger doses of this drug. Neverthe-
at the 10-min period and which had returned less, it would appear from this study that the
to control values by the 15-min period. In injection of lidocaine in amounts commonly
used in the treatment of arrhythmias exerts
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15. STEINHAUS, J. E., AND HOWLAND, D. E.: Intra- in patients with and without cardiac dysfunc-
venously administered lidocaine as a supple- tion. Circulation 34: 597, 1966.
ment to nitrous oxide-thiobarbiturate anes- 25. GLEASON, W. L., AND BRAUNWALD, E.: Studies
thesia. Anesth Analg (Cleveland) 37: 40, 1958. on the first derivative of the ventricular pres-
16. NELSON, D. H., AND HARRISON, D. C.: Com- sure pulse in man. J Clin Invest 41: 80,
parison of the negative inotropic effects of pro- 1962.
cainamide, lidocaine, and quinidine. Physiol- 26. WALLACE, A. G., SKINNER, N. S., JR., AND
ogist 8: 241, 1965. MITCHELL, J. H.: Hemodynamic determinants
17. AUSTEN, W. G., AND MORAN, J. M.: Cardiac of the maximal rate of rise of left ventricular
and peripheral vascular effects of lidocaine pressure. Amer J Physiol 205: 30, 1963.