610

The administration of a vasoconstrictor in combination

with a local anesthetic has evolved as a method for
decreasing systemic toxicity, increasing the duration of
anesthesia, and providing hemostasis during surgery.
The importance of a vasoconstrictor agent is undis-
puted. Lidocaine with epinephrine has been the most
commonly used throughout the world. However,
epinephrine-containing anesthetics may cause
unwanted side effects in patients with cardiovascular
disease after systemic absorption.
1-3
To avoid any such
adverse cardiovascular effects, especially in high-risk
patients, some authors have recommended the use of
epinephrine-free anesthetics.
4
However, many investi-
gators have reported that plain lidocaine provided
unsatisfactory levels of anesthesia or hemostasis, or
both.
5,6
Inadequate anesthesia results in stressful pain
Cardiovascular response to epinephrine-containing local
anesthesia in patients with cardiovascular disease
Hitoshi Niwa, DDS, PhD,
a
Mitsutaka Sugimura, DDS, PhD,
b
Yuu Satoh, DDS,
c
and Ai Tanimoto,
DDS,
d
Osaka, Japan
OSAKA UNIVERSITY
Objective. The purpose of the present study was to examine the safety of epinephrine-containing local anesthesia for use on
patients with cardiovascular disease.
Study design. Twenty-seven patients with cardiovascular disease were studied. The cardiac functional capacity of 9 patients
was New York Heart Association class I; 11, class II; and 7, class III. Hemodynamic responses to intraoral injection of 1.8 mL
of 2% lidocaine with 1:80,000 epinephrine were measured with impedance cardiography.
Results. Systolic blood pressure and heart rate increased by 4.1% and 5.1%, respectively, immediately after the lidocaine-
epinephrine injection. Consequently, rate pressure product increased by 10.0%. Cardiac index increased by 14.2%, and total
peripheral resistance decreased by approximately 10%. No patient complained of cardiac symptoms. There were no significant
differences in hemodynamic responses related to the extent of the cardiac functional capacity.
Conclusion. We concluded that lidocaine-epinephrine was safe and had few, if any, hemodynamic consequences in patients
with cardiovascular disease.
(Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92:610-6)
a
Professor, Department of Dental Anesthesiology.
b
Associate Professor, Department of Dental Anesthesiology.
c
Assistant Professor, Department of Dental Anesthesiology.
d
Clinical Instructor, Department of Dental Anesthesiology.
Received for publication Apr 16, 2001; returned for revision May 16,
2001; accepted for publication Jul 11, 2001.
Copyright 2001 by Mosby, Inc.
1079-2104/2001/$35.00 + 0 7/13/118903
doi:10.1067/moe.2001.118903
for the patient, whose body releases greater amounts of
endogenous catecholamine. It should be kept in mind
that epinephrine is released endogenously in greater
amounts than that used in dental anesthesia.
7-10
Therefore, a local anesthetic with epinephrine may be
selected to obtain adequate levels of anesthesia and
hemostasiseven in patients with cardiovascular
disease.
There have been many studies of the hemodynamic
effects of dental anesthesia with epinephrine-containing
local anesthetic solutions in young, healthy patients.
11-15
Tolas et al
13
reported no significant cardiovascular
changes after injection of a single cartridge of an anes-
thetic containing 18 g epinephrine, despite a 2-fold
increase in plasma epinephrine. Knoll-Kohler et al
14
and Chernow et al
15
also demonstrated only a small
reduction in mean arterial blood pressure and a slight
increase in heart rate after the injection of low-dose
epinephrine. Consequently, many investigators had
believed that the cardiac effects of epinephrine-
containing local anesthetics were small.
13,15
However,
Dionne et al
16
has shown marked increases in cardiac
output, stroke volume (SV), and heart rate measured by
impedance cardiography after lidocaine with epineph-
rine anesthesia in patients; they found no observable
ORAL MEDICINE Editor: Martin S. Greenberg
ORAL SURGERY
ORAL MEDICINE
ORAL PATHOLOGY
Vol. 92 No. 6 December 2001
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY Niwa et al 611
Volume 92, Number 6
effects on blood pressure. These results show that
commonly used measurements such as heart rate and
blood pressure underestimate the hemodynamic effects
of epinephrine. Therefore, more sensitive tests are neces-
sary. In addition, most previous studies have been on
young, healthy subjects without a history of cardiovas-
cular disease, so the question remains with respect to how
a group of patients with cardiovascular disease would
respond when epinephrine was included in the anesthetic.
Thus, the purpose of the present study was to inves-
tigate the hemodynamic changes produced by infiltra-
tion anesthesia with 1.8 mL of 2% lidocaine with
1:80,000 epinephrine in patients with cardiovascular
disease. To examine the hemodynamic effects of local
anesthesia on such patients, the SV, cardiac index, and
total peripheral resistance were measured by imped-
ance cardiography. In addition, we also explored the
hemodynamic response to low doses of epinephrine
in patients receiving -blocking agents.
METHOD
Characteristics of the patient population
The subjects were 27 patients (16 men and 11 women)
hospitalized in the National Cardiovascular Center
Table I. Clinical characteristics of the studied patients
Cardiovascular Cardiac function/
Sex, age (y) disease fractional shortening (%) Medication
NYHA I
M, 72 HCVD 33 Nifedipine
M, 54 OMI, HCVD 31 Amlodipine, enalapril
M, 47 ARVD 39 (LVEF = 49%) Mexiletine, propranolol
F, 57 HCVD Unknown Nilvadipine
M, 75 OMI 17 Nicorandil, isosorbide, cilazapril, digoxin,
furosemide
F, 66 OMI 41 (LVEF = 65%) Amlodipine, metoprolol, doxazosin, spirono-
lactone
F, 53 HCVD 34 Amlodipine
F, 29 HCM (LVEF = 60%) Verapamil, metoprolol, furosemide
F, 68 AP, OMI, HCVD 35 Nicorandil, diltiazem
NYHA II
M, 76 OMI, unstable AP 24 Isosorbide, spironolactone, furosemide
F, 68 AVR, MVR, CHF 46 Nifedipine, digoxin, isosorbide
F, 58 MSR, AVR, WPW 15 Cibenzoline, spironolactone, furosemide
M, 32 DCM 31 Amiodarone, mexiletine, metoprolol
M, 49 Myocarditis 17 Amlodipine, enalapril, carvedilol
M, 56 AP 43 (LVEF = 61%) Isosorbide, nitroglycerin, nicorandil, meto-
prolol
M, 61 MVR, PH 32 Nitroglycerin, digoxin, spironolactone,
furosemide
M, 48 OMI 24 (LVEF = 37%) Digoxin, amiodarone, isosorbide, propranolol,
mexiletine, spironolactone, furosemide
F, 40 ASD 13 (LVEF = 39%) Digoxin, spironolactone, furosemide
M, 48 Ebsteins anomaly 46 (LVEF = 66%) Bepridil, nisoldipine, atenolol, digoxin
F, 63 HCVD 11 (LVEF = 34%) Enalapril, digoxin
NYHA III
F, 50 Primary PH (LVEF = 56%), (RVEF = 26%) Dobutamine, alprostadil alfadex (PGE1),
spironolactone
M, 30 TOF, PA, AR 20 (LVEF = 35%) Docarpamine, mexiletine, spironolactone
M, 28 DCM 15 (LVEF = 12%) Digoxin, metoprolol, alacepril, isosorbide,
pimobendan, spironolactone, furosemide
M, 67 OMI, unstable AP 23 Nifedipine, isosorbide, metoprolol, diltiazem
M, 70 DCM 12 (LVEF = 28%) Digoxin, enalapril, metoprolol, spironolactone,
furosemide
F, 46 ASD, PH, Eisenmengers syndrome (LVEF = 52%), (RVEF = 30%) Digoxin, furosemide
M, 20 DCM 15 Metoprolol, verapamil, captopril, spironolac-
tone, furosemide
HCVD, Hypertensive cardiovascular disease; OMI, old myocardial infarction; ARVD, arrhythmogenic right ventricular dysplasia; LVEF, left ventricular ejection frac-
tion; HCM, hypertrophic cardiomyopathy; AP, angina pectoris; AVR, aortic valve replacement; MVR, mitral valve replacement; CHF, congestive heart failure; MSR,
mitral stenosis and regurgitation; WPW, Wolff-Parkinson-White syndrome; DCM, dilated cardiomyopathy; PH, pulmonary hypertension; ASD, atrial septal defect;
RVEF, right ventricular ejection fraction; TOF, tetralogy of Fallot; PA, pulmonary atresia; AR, aortic regurgitation.
612 Niwa et al ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY
December 2001
(Suita, Japan) for treatment of heart disease. All patients
required dental treatment, which was performed with
them under local anesthesia. Each patient received a full
explanation of the necessity and risk of the treatment and
gave written informed consent before the study.
Descriptive data for these 27 patients are listed in Table
I. They were suffering from various cardiovascular disor-
ders including ischemic heart disease, cardiomyopathy,
and valve disease. Patients with serious arrhythmia, idio-
pathic hypertrophic subaortic stenosis, and/or pace-
makers were excluded. The patients continued to receive
their prescribed cardiac drugs including calcium channel
antagonists, -blocking agents, and nitrates. Nine
patients were taking
1
selective -blocking agents, and
3 were taking nonselective ones.
Pretreatment cardiac evaluation
Detailed cardiac evaluations are listed in Table I.
Cardiac functional capacity was assessed by cardiolo-
gists according to the criteria of the New York Heart
Association (NYHA
17
; Table II). The functional
capacity of 9 patients was class I; 11, class II; and 7,
class III. Left ventricular function was evaluated with
echocardiography, left ventriculography, and/or radioiso-
tope angiography before the dental treatment.
Study protocol
Arterial blood pressure (systolic blood pressure;
diastolic blood pressure; mean arterial pressure
[MAP]) and heart rate (HR) were monitored by using
an automatic noninvasive pressure device (Life Scope
7; Nihon Kohden Co Ltd, Tokyo, Japan). To evaluate
the left ventricular function during and after infiltration
anesthesia, noninvasive impedance cardiograms (CIC-
1000; Sorba Medical Systems, Inc, Brookfield, Wis)
were recorded throughout the study. SV was measured
every 20 seconds by using a computer-interfaced
impedance device. Cardiac index (CI), total peripheral
resistance (TPR), and rate pressure product were calcu-
lated by the CIC-1000. The patients first rested in the
supine position for 30 minutes, after which baseline
measurements were obtained. The local anesthetic
solution used consisted of 1.8 mL (1 cartridge) of 2%
lidocaine with 1:80,000 epinephrine (L-E; Astra Zeneca,
Osaka, Japan). In total, 22.5 g of epinephrine and 36
mg of lidocaine were used. The L-E was administered
into the operative site over a period of 60 seconds. In all
patients, the aspiration technique was used to prevent
injection of the anesthetic into the vasculature and care
was taken to inject as painlessly as possible. Each hemo-
dynamic parameter was measured at 0, 2, 5, and 10
minutes after the intraoral injection of L-E. Patients
rested for this period, then dental treatment was started.
Statistical analysis
Data were expressed as the percentages of hemody-
namic changes from the baseline value. The results
were statistically analyzed by using repeated measures
1-way analysis of variance, and the Bonferroni correc-
tion was performed for multiple comparisons. A P
value of <.05 was considered statistically significant.
RESULTS
The data from all 3 NYHA groups were initially
analyzed together. Table III shows the hemodynamic
response to L-E injection in all 27 patients. There was
a 4.1% increase in systolic blood pressure and a 5.1%
increase in HR immediately after the injection,
although diastolic blood pressure and MAP remained
unchanged. SV and CI increased significantly from 0
to 10 minutes after the injection; the greatest increases
in SV and in CI, 13.4% and 14.2%, respectively, were
recorded 2 minutes after the injection. A significant
decrease in TPR occurred from 0 to 10 minutes; the
maximal decrease of TPR was approximately 10% at 2
and 5 minutes. Rate pressure product increased by
10.0% to its maximum at 0 minutes. During the study,
no patient complained of any cardiac symptom such as
chest pain, palpitation, or dyspnea. There were no
aggravated arrhythmias or abnormal changes in elec-
trocardiograms in any of the patients.
Table III shows the hemodynamic responses to L-E
compared with the functional classifications of NYHA.
There were no significant differences in blood pressure
Table II. New York Heart Association Functional Classification
17
Class I Patients with cardiac disease but without resulting limitations of physical activity. Ordinary physical activity does not cause undue
fatigue, palpitations, dyspnea, or anginal pain.
Class II Patients with cardiac disease resulting in slight limitations of physical activity. They are comfortable at rest. Ordinary physical
activity results in fatigue, palpitations, dyspnea, or anginal pain.
Class III Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary
physical activity causes fatigue, palpitation, dyspnea, or anginal pain.
Class IV Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of cardiac
insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is
increased.
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY Niwa et al 613
Volume 92, Number 6
response among functional classes I, II, and III at any
time. Although the greatest increase in HR was
recorded immediately after the injection in each class,
there were no significant differences among the 3
groups. Significant changes in SV, CI, and TPR were
seen only in class I and class II patients. However, there
were no significant differences among the 3 groups.
The interaction between L-E and -blocking agents
is depicted in Fig 1. MAP increased by 13.2% in the
patients receiving nonselective -blocking agents.
Consequently, there were significant differences in the
MAP responses among the 3 groups. The increase in
HR was observed only in patients without -blocker
therapy. Although the SV and CI responses seemed to
be smaller in the patients receiving nonselective -
blocking agents than in patients in the other groups,
there were no significant differences among the 3
groups. On the other hand, there were significant
differences in the TPR response among the 3 groups.
DISCUSSION
The use of epinephrine in local anesthetics for
patients with cardiovascular disease has been contro-
versial. There have been many guidelines for the
rational use of vasoconstrictors in patients with cardio-
vascular disease. In 1964, a Working Conference of the
American Dental Association and the American Heart
Association
18
stated that the concentrations of vaso-
constrictors normally used in dental local anesthetic
solutions were not contraindicated in patients with
cardiovascular disease when administered carefully
and with preliminary aspiration. However, they did not
suggest maximal recommended doses of vasoconstric-
tors for cardiac patients, and this lapse proved to be
dangerous.
19
Malamed
7
recommended a much smaller
maximal dose of vasoconstrictor (no more than 40 g
of epinephrine at one appointment) for patients with
severe cardiovascular disease. Little et al
20
recommend
that one, and probably two, cartridges of 2% lidocaine
Table III. Cardiovascular response to L-E injection
NYHA-FC 0 min 2 min 5 min 10 min
SBP (%) I- III +4.1 9.9
*
+2.5 6.1
*
+0.9 6.1 1.2 5.0
I +4.9 12.6 +2.3 9.0 0.5 6.0 2.6 3.5
II +3.3 8.7 +2.9 5.4 +3.1 7.3 +0.6 6.2
III +3.8 9.3 +2.3 2.3 0.5 3.6 1.9 4.0
DBP (%) I-III +2.0 9.2 0.2 10.0 0.3 10.7 2.2 13.6
I +4.9 13.1 2.2 10.7 0.5 16.2 0.6 20.4
II 0.7 6.9 +1.0 11.0 2.3 6.7 3.4 8.9
III +2.3 5.5 +0.3 8.4 +1.7 7.5 2.2 13.6
MAP (%) I-III +2.9 7.6 +1.0 7.1 0.1 6.2 1.9 7.5
I +4.6 10.1 0.0 9.3 1.1 7.2 1.9 10.1
II +1.3 6.7 +1.6 7.0 +0.1 6.5 1.8 6.4
III +3.2 5.6 +1.5 4.5 +0.8 5.0 1.9 6.4
HR (%) I-III +5.1 8.2
*
+1.6 11.4 +0.8 5.9 +1.8 4.3
I +6.0 10.0
*
+1.1 19.7 1.2 8.5 +1.5 4.6
II +5.5 8.1
*
+1.8 4.6 +2.1 4.1 +3.1 4.8
III +3.1 6.5 +1.8 3.2 +1.6 3.8 0.1 2.5
SV (%) I-III +6.9 17.1
*
+13.4 17.3
*
+11.2 11.6
*
+5.3 11.2
*
I +4.2 11.7 +14.8 10.8
*
+11.9 7.2
*
+9.8 10.7
*
II +10.5 24.5 +16.5 24.0
*
+13.7 14.6
*
+1.4 11.3
III +4.7 6.8 +6.9 10.6 +6.6 11.2 +5.6 11.0
CI (%) I-III +12.1 16.9
*
+14.2 18.2
*
+12.4 13.2
*
+7.6 10.5
*
I +10.7 12.5
*
+11.6 14.2
*
+10.4 6.0
*
+12.3 11.6
*
II +15.7 22.6
*
+19.5 23.2
*
+16.2 16.2
*
+4.8 7.0
*
III +8.3 11.8 +9.4 13.3 +9.1 15.1 +6.1 13.0
TPR (%) I-III 6.6 13.6
*
9.8 14.5
*
9.9 12.3
*
8.1 10.9
*
I 5.3 17.5 9.6 14.9 10.6 5.7* 12.7 7.3*
II 9.1 12.2* 12.0 15.9* 11.6 15.2* 5.2 11.6
III 4.3 11.3 6.5 13.1 6.4 14.4 6.7 13.0
RPP (%) I-III +10.0 13.3
*
+3.1 8.2 +2.2 9.2 +1.0 6.8
I +12.1 14.3
*
+0.1 11.8 1.0 10.0 0.1 5.5
II +9.8 13.6 +4.7 6.5 +5.3 10.6 +3.7 8.7
III +7.5 13.2 +4.4 3.5 +1.4 3.1 1.8 3.1
Values are expressed as percentage of hemodynamic change from baseline value (mean SD).
NYHA-FC, New York Heart Association functional capacity; SBP, systolic blood pressure; DBP, diastolic blood pressure; MAP, mean arterial pressure; HR, heart rate;
SV, stroke volume; CI, cardiac index; TPR, total peripheral resistance; RPP, rate pressure product.
*P <.05, versus baseline value.
614 Niwa et al ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY
December 2001
with 1:100,000 epinephrine (18 to 36 g of epineph-
rine) were of little clinical significance to most patients
with hypertension or other cardiovascular diseases.
Kaneko
21
recommended that the total dose of epineph-
rine should be limited to less than 40 g in moderate
cases or 20 g in serious cases, with epinephrine
concentrations of 1:100,000 or less. Current clinical
practice has tacitly accepted the safety of epinephrine
use in patients with cardiovascular disease.
However, there have been some criticisms of these
guidelines. First, previous investigators have not
provided explicit criteria for the categorization of a
patient with severe cardiovascular disease. Second, the
recommendations were made on the basis of the results
from healthy, young volunteers, and these results
should not be extrapolated to patients with cardiovas-
cular disease. Hemodynamic changes due to epineph-
rine in local anesthetic may be well tolerated in
healthy, young subjects; however, it is not clear
whether patients with preexisting cardiovascular
disease would tolerate them as well. Third, most
recommendations have been made on the basis of the
changes in HR and blood pressure produced by
epinephrine. However, it has become evident that the
information obtained by conventional monitoring of
such variables as blood pressure and HR are inadequate
for explaining the pathophysiologic changes that may
occur in the patient.
14,16
Therefore, these recommenda-
tions need to be validated with more sensitive methods
for further examination of patients with cardiovascular
disease.
There have been several reports of the hemodynamic
effects of epinephrine in patients with cardiovascular
disease. Cintron et al
22
reported that dental anesthesia
with 1.0 mL of 2% lidocaine with 1:100,000 epineph-
rine caused no significant changes in HR or blood pres-
sure and was well tolerated by patients with recent
myocardial infarction. Middlehurst and Coulthard
23
reported that approximately 5 mL of 2% lidocaine with
1:50,000 epinephrine and 0.25 IU/mL of vasopressin
did not cause ischemic changes in patients with heart
disease. Davenport et al
6
studied the hemodynamic
effects of moderate doses of epinephrine during peri-
odontal surgery in patients with stable cardiovascular
disease and found no significant changes in HR or
blood pressure, despite the elevation of the plasma
epinephrine concentration. In contrast, Leviner et al
4
reported that local anesthesia without vasoconstrictor
should be preferred for use in severely compromised
patients. However, detailed cardiac functions were not
measured in any of these previous studies.
In the present study, hemodynamic responses to 22.5
g of epinephrine were studied with impedance cardi-
ography. This method is noninvasive and places no
stress on the patients. Its reliability has been estab-
lished in previous studies.
24
The effects of epinephrine may depend on the
specifics of the underlying cardiovascular disease.
Fig 1. Cardiovascular response to L-E injection in patients receiving -blocking agents. (), patients without -
blocker therapy (n = 15); -1 selective, patients taking -1 selective -blocking agents (n = 9); nonselective, patients
taking nonselective -blocking agents (n = 3).
Mean SD;
*
P < .05 versus baseline value;
#
P < .05 () versus nonselective;

P < .05; -1, selective versus non-

selective.
Thus, it was impossible to evaluate the effects of
epinephrine in patients with each type of disease.
Therefore, we divided the patients into 3 groups
according to their cardiac functional capacities (NYHA
class I to III) and assessed the hemodynamic effects in
each group. The criteria of NYHA are simple and
widely used.
When the results of the 3 groups were combined,
MAP remained unchanged by L-E injection, SV and CI
increased by 13%, and TPR decreased by 10%. These
results suggest that the increased cardiac output and
decreased peripheral resistance compensate for each
other to maintain blood pressure within control values.
The transient increases in HR and systolic blood pres-
sure immediately after the injection were likely an
expression of endogenous catecholamine release as a
result of emotional stress or pain and not a pharmaco-
logic effect, because it has been shown that the peak
concentration of exogenous epinephrine occurs 3 to 5
minutes after an injection.
25
The hemodynamic responses in this study were
greater than those in our previous study.
26
Differences
in the emotional conditions and the ages of subjects
may have influenced the results. Subjects were real
dental patients (mean age, 53 years) scheduled for
treatment in the present study, whereas the healthy
young volunteers (mean age, 31 years) underwent only
dental injection in our previous study. However, further
study is necessary to explain this difference, because
there remains a controversy over changing -adren-
ergic responsiveness with aging.
27-29
It is necessary to evaluate whether the hemodynamic
effects of L-E are deleterious to the compromised
heart. During the study, no patient complained of
cardiac symptoms such as chest pain, palpitation, or
dyspnea. Even the class III patients tolerated the hemo-
dynamic changes produced by L-E without any symp-
toms. Therefore, we speculate that the peak increases
in cardiac function produced by L-E are limited and
within normal physiologic variation.
This study failed to disclose any significant differ-
ences in hemodynamic responses among the patients in
classes I, II, and III. However, increases in SV and CI
were observed only in class I and class II patients;
changes in SV and CI were not significant in class III
patients. Likewise, TPR decreased significantly only in
class I and class II patients. These results suggest that
the effects of epinephrine are attenuated in class III
patients with severely failing hearts.
Recent studies have demonstrated that the sympa-
thetic nervous system is unduly activated in patients
with congestive heart failure.
30-32
This augmented
activity is part of a vital compensatory mechanism that
supports cardiac function. The high plasma concentra-
tions of norepinephrine observed in these patients exert
positive inotropic effects from stimulation of myocar-
dial -adrenergic receptors. However, if heart failure
lasts for a long time, this elevated norepinephrine
induces the down-regulation of -adrenergic receptors
and contributes to desensitization.
33
Such alteration of
-adrenergic receptors may provide an explanation for
the attenuation of the effects of epinephrine observed
in class III patients.
In contrast to our results, Hirota et al
34
reported that
greater hemodynamic changes were observed in class
III patients than in patients in other groups. However,
their subjects were so few (n = 2) that their findings
were unreliable.
When excessive concentration or dose of epinephrine
is administered in patients with a normal heart, SV and
cardiac output are further elevated because of the
1
effect of epinephrine, leading to a prominent rise in
blood pressure.
35
Consequently, rate pressure product,
indexes of myocardial oxygen consumption, and left
ventricular stroke work (the product of MAP and SV),
representing the level of work by the left ventricle, also
increase. Although a normal heart can apparently with-
stand these great demands, in failing or ischemic heart,
cardiac functions may be impaired by these changes.
36
The possibility of adverse interactions between
epinephrine and nonselective -blocking agents has
been suggested.
37,38
Epinephrine production may lead
to an exaggerated increase in blood pressure in patients
taking a nonspecific -blocking agent such as propran-
olol. As shown in Fig 1, the response to the low dose of
epinephrine in patients taking nonselective -blocking
agents differed from that in patients not taking such
medication. Little
39
suggested, on the basis of clinical
experience, that 1:100,000 epinephrine (no more than
0.036 mg of epinephrine) in a local anesthetic could
safely be used for patients receiving nonselective -
blocking agents. However, the possibility of a hyper-
tensive interaction occurring with epinephrine should
be considered when epinephrine is used in patients
taking a nonspecific -blocking agent.
This study provides documentation that 1.8 mL of
L-E is safe and has few, if any, hemodynamic conse-
quences in patients with cardiovascular disease. We
concluded that a low dose of epinephrine (22.5 g) in
local dental anesthesia was well tolerated by cardiovas-
cular patients who were in NYHA classes I through III.
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Reprint requests:
Hitoshi Niwa, DDS, PhD
Department of Dental Anesthesiology
Osaka University
Faculty of Dentistry
1-8 Yamadaoka, Suita
Osaka 565-0871
Japan
niwa@dent.osaka-u.ac.jp