PEDIATRIC ANESTHESIA
SECTION EDITOR
WILLIAM J. GREELEY
The Hemodynamic Effects of Propofol in Children with
Congenital Heart Disease
Glyn D. Williams, FFA(SA)*, Thomas K. Jones,
Jeffrey P. Morray, MD*
Departments of *Anesthesiology and †Pediatrics, University of Washington School of Medicine and Children’s Hospital
and Regional Medical Center, Seattle, Washington
We studied the hemodynamic effects of propofol dur-
ing elective cardiac catheterization in 30 children with
congenital heart disease. Sixteen patients were without
cardiac shunt (Group I), six had left-to-right cardiac
shunt (Group II), and eight had right-to-left cardiac
shunt (Group III). The mean (6sd) ages were 3.8 6
3.1 yr (Group I), 3.2 6 3.7 yr (Group II), and 1.0 6 0.6 yr
(Group III). After sedation and cardiac catheter inser-
tion, hemodynamic data and oxygen consumption
were measured before and after the administration of
propofol (2-mg/kg bolus, 50- to 200-mg z kg21 z min21
infusion), and values were compared by using a paired
t-test (significance: P , 0.05). After the propofol admin-
istration, systemic mean arterial pressure and systemic
vascular resistance decreased significantly and sys-
temic blood flow increased significantly in all patient
groups; heart rate, pulmonary mean arterial pressure,
and pulmonary vascular resistance were unchanged.
T
he goals for anesthetic management of children
undergoing cardiac catheterization include ade-
quate analgesia, sedation, and immobility, with
minimal depression of cardiac function and respira-
tory drive. Propofol has become increasingly popular
as an anesthetic for cardiac catheterization in children
(1,2), primarily because it is an IV anesthetic with
favorable pharmacokinetic and pharmacodynamic
characteristics. It has rapid clearance and redistribu-
tion, which result in prompt, clear-headed return of
orientation with a low incidence of nausea and vom-
iting (3,4). Although propofol’s safety and efficacy in
pediatric patients have been well demonstrated (5–9),
there has been little published about its use in children
with congenital heart disease (10 –12). Propofol de-
creases systemic blood pressure (6 –9), and the hemo-
dynamic changes induced by propofol may alter the
information obtained during cardiac catheterization.
Accepted for publication August 27, 1999.
Address correspondence to Glyn D. Williams, Department of
Anesthesia and Critical Care, Children’s Hospital and Medical Cen-
ter, 4800 Sand Point Way NE, P.O. Box C5371, Seattle, WA 98105.
©1999 by the International Anesthesia Research Society
0003-2999/99
SOCIETY FOR PEDIATRIC ANESTHESIA
MD†, Kimberly A. Hanson, MD, PhD*, and
Pulmonary to systemic resistance ratio increased
(Group I, P 5 0.005; Group II, P 5 0.03; Group III, P 5
0.10). In patients with cardiac shunt, propofol resulted
in decreased left-to-right flow and increased right-to-
left flow; the pulmonary to systemic flow ratio de-
creased significantly (Group II, P 5 0.005; Group III,
P 5 0.01). Clinically relevant decreases in Pao2
(P 5 0.008) and Sao2 (P 5 0.01) occurred in Group III
patients. We conclude that propofol can result in clini-
cally important changes in cardiac shunt direction and
flow. Implications: The principal hemodynamic effect
of propofol in children with congenital heart defects is a
decrease in systemic vascular resistance. In children
with cardiac shunt, this results in a decrease in the ratio
of pulmonary to systemic blood flow, and it can lead to
arterial desaturation in patients with cyanotic heart
disease.
(Anesth Analg 1999;89:1411–6)
In particular, the effects on the magnitude and direc-
tion of intracardiac shunt have not been reported in
this population. We designed our study to investigate
the hemodynamic consequences of propofol adminis-
tered during diagnostic cardiac catheterization to chil-
dren with congenital heart disease.
Methods
After institutional review board approval and in-
formed parental consent, 31 children, ASA physical
status II or III, aged 3 mo to 12 yr, who were scheduled
for elective cardiac catheterization were enrolled. Pa-
tients requiring mechanical ventilation or IV inotropic
support, patients with hepatic or renal dysfunction,
and patients with suspected allergy to propofol were
excluded.
All patients were monitored with a precordial
stethoscope, electrocardiograph (lead II), a noninva-
sive blood pressure device (Dynamap; Critikon Inc.,
Tampa, FL), pulse oximeter (Nellcor Inc., Hayward,
CA), and skin temperature probe. Depending on the
Anesth Analg 1999;89:1411–6 1411
1412 PEDIATRIC ANESTHESIA WILLIAMS ET AL.
PROPOFOL IN CHILDREN WITH HEART DISEASE
anesthesiologist’s preference, children either were not
premedicated or received oral midazolam (0.5 mg/kg)
or rectal methohexital (30 mg/kg). An IV catheter was
placed in a peripheral vein, and lactated Ringer’s so-
lution was infused at maintenance rates. During the
period before propofol administration, incremental IV
boluses (2–5 mg/kg) of thiopental were administered
to keep the patient appropriately sedated for the car-
diac catheterization procedure. Care was taken to limit
the total thiopental dose to the minimum necessary. In
an attempt to reduce the influence of thiopental on
hemodynamic measurements, data were not recorded
within 10 min of a thiopental bolus, and thiopental
was discontinued at least 15 min before propofol ad-
ministration. All patients breathed spontaneously, and
airway support was not provided. Supplemental oxy-
gen was not provided until completion of the study.
Catheters were inserted under local anesthesia by the
cardiologist for pressure and oxygen saturation (So2)
measurements from the vena cavae, left and right
atria, left and right ventricles, pulmonary artery, and
aorta. Blood for analysis of oxygen tension (Po2), car-
bon dioxide tension (Pco2), and pH was obtained from
the femoral artery and from the site judged optimal for
obtaining mixed venous samples (pulmonary artery
for patients without cardiac shunt and superior vena
cava for patients with shunt). Oxygen consumption
(V̇o2) was noted every minute and averaged over the
period of hemodynamic measurements. After baseline
measurements had been taken, propofol was admin-
istered in 0.5-mg/kg increments to a total dose of
2 mg/kg over a 5-min period. A propofol infusion
(100 mg z kg21 z min21) was also initiated. The infu-
sion was maintained for the duration of the catheter-
ization procedure and adjusted (50–200 mg z kg21 z min21)
depending on the patient’s clinical response. Approx-
imately 3 min after the propofol loading dose, all
pressure and oxygen saturation measurements were
repeated, as were pulmonary artery/superior vena
cava and femoral artery blood gas analyses.
Pulmonary blood flow (Qp) and systemic blood
flow (Qs) were calculated by using the Fick equation;
pulmonary vascular resistance (PVR) and systemic
vascular resistance (SVR) were calculated using stan-
dard formulae (13).
Data are reported as mean 6 sd. Based on the
calculated ratio of Qp:Qs, children were separated into
three groups: patients without cardiac shunt (Group
I); patients with Qp:Qs $1 both before and after
propofol administration (Group II); and patients with
Qp:Qs ,1 either before or after propofol administra-
tion (Group III). Demographic and selected pre-
propofol baseline values were compared among the
three groups of children by using the Kruskal-Wallis
test. Within each group, values before and after the
propofol administration were compared by using a
ANESTH ANALG
1999;89:1411–6
paired Student’s t-test. Statistical significance was set
at P ,0.05.
Results
Thirty-one children were enrolled. One patient be-
came apneic after propofol administration and was
excluded because the study protocol was not com-
pleted. Patient demographics for the 30 children (14
female, 16 male) who completed the study are shown
in Table 1. Two Group I and three Group III patients
were taking chronic medication for congestive heart
failure. Children in Group III were significantly
younger and smaller than children in the other groups
(Table 1); consequently, fewer of these patients re-
ceived premedication (proportion premedicated in
Group I 16 of 16, Group II 5 of 6, Group III 4 of 8).
Group III patients suffered from cyanotic heart disease
and had significantly lower baseline Sao2 values than
patients in Groups I and II (Table 2). Baseline hemo-
globin values were also significantly higher for Group
III patients (Group I 10.5 6 1.1 g/dL, Group II 12.0 6
1.9 g/dL, Group III 13.5 6 2.0 g/dL; P 5 0.003). The
total thiopental dose was 13.1 6 7.6 mg/kg for Group
I (administered over 65 6 18 min) 10.0 6 3.7 mg/kg
(over 60 6 11 min) for Group II, and 12.8 6 8.5 mg/kg
(over 55 6 9 min) for Group III. There was no differ-
ence among the three groups in the total doses (per
kilogram body weight) of thiopental or propofol.
In all three patient groups, propofol administration
was associated with significant decreases in mean sys-
temic arterial pressure (SAP) and SVR and with a
significant increase in Qs, whereas mean pulmonary
artery pressure (PAP), PVR, and Qp did not change
significantly (Table 3). These changes resulted in a
significant increase in the pulmonary to systemic re-
sistance ratio (Rp:Rs) in Groups I and II. Propofol
administration did not alter heart rate or V̇o2 in any of
the three patient groups (Table 3).
Fourteen children had some form of cardiac
shunt(s). All six patients in Group II were calculated to
have Qp:Qs $1 (left-to-right shunt) both before and
after the administration of propofol. Six of the eight
patients in Group III were calculated to have Qp:Qs
,1 (right-to-left shunt) both before and after propofol
administration. For the remaining two patients in
Group III (both with unrepaired tetralogy of Fallot),
the baseline shunt was left-to-right (Qp:Qs ratios of
1.03 and 1.39) but became right-to-left (Qp:Qs ratios of
0.54 and 0.83, respectively) after propofol administra-
tion. Therefore, propofol was associated with reversal
of shunt flow in these children.
The effects of propofol on shunt direction and flow
for Groups II and III are illustrated in Figure 1. Re-
gardless of the direction of shunt at baseline, the drug
ANESTH ANALG PEDIATRIC ANESTHESIA WILLIAMS ET AL. 1413
1999;89:1411–6 PROPOFOL IN CHILDREN WITH HEART DISEASE

Table 1. Demographics of All Patients

Cardiac diagnosis Age (yr) Weight (kg)
Group I (n 5 16)
Tetralogy of Fallot (repaired) 1.4 12.7
Truncus arteriosus (repaired) 2.5 12.4
Coarctation of the aorta 1.3 13.8
Left coronary artery anomaly 0.9 8.6
Tetralogy of Fallot with absent pulmonary valve (repaired) 4.8 18.0
Coarctation of the aorta 0.5 5.6
Pulmonary valve stenosis 0.8 9.0
Pulmonary valve stenosis 2.9 15.7
Tetralogy of Fallot (repaired) 2.6 18.3
Double outlet right ventricle, pulmonary artery stenosis (repaired) 6.6 18.3
Pulmonary valve stenosis 3.9 19.3
Atrioventricular canal (repaired) 4.3 14.3
Tetralogy of Fallot (repaired) 3.8 12.6
Aortic valve stenosis 9.3 30.4
Coarctation of the aorta 3.1 16.2
Tetralogy of Fallot, pulmonary artery stenosis (repaired) 11.7 35.5
Mean 6 sd 3.8 6 3.1 16.3 6 7.6
Group II (n 5 6)
Partial anomalous pulmonary venous return, atrial septal defect 8.1 38.9
Tetralogy of Fallot (repaired), residual ventricular septal defect 7.8 22.5
Atrial and multiple ventricular septal defects 0.8 7.6
Pulmonary atresia (modified BTS) 0.6 7.1
Tetralogy of Fallot (repaired), APC 1.1 9.4
Double inlet left ventricle, L-TGA, pulmonary stenosis, APC 0.6 7.2
Mean 6 sd 3.2 6 3.7 15.5 6 12.9
Group III (n 5 8)
Pulmonary atresia (RV-PA conduit and modified BTS) 0.8 8.2
Tetralogy of Fallot (repaired), residual ventricular septal defect 2.1 12.7
Hypoplastic left heart syndrome (bidirectional Glenn procedure) 1.5 11.3
Tricuspid atresia, pulmonic stenosis, atrial septal defect, APC 0.6 7.0
Tetralogy of Fallot 0.5 7.6
Tetralogy of Fallot, pulmonary atresia (RV-PA conduit) 0.6 6.8
Tetralogy of Fallot 0.4 6.0
Tetralogy of Fallot, pulmonary atresia, APC (RV-PA conduit) 1.1 8.6
Mean 6 sd 1.0 6 0.6 8.5 6 2.3
APC 5 aortopulmonary collaterals, BTS 5 Blalock-Taussig shunt, RV-PA 5 right ventricle to pulmonary artery, TGA 5 transposition of the great arteries.
Group III patients weighed less (P 5 0.02) and were shorter (P 5 0.02) and younger (P 5 0.02) than patients in Groups I and II (Kruskal-Wallis test).

decreased left-to-right shunt and increased right-to-
left shunt. Left-to-right flow decreased significantly
(P 5 0.045) in Group II, and right-to-left increased
significantly (P 5 0.006) in Group III. Consequently,
Qp:Qs decreased significantly in both Group II (P 5
0.005) and Group III (P 5 0.01).
In children with cyanotic heart disease (Group III),
this decrease in Qp:Qs with propofol administration
was associated with statistically significant decreases
in Pao2 and Sao2. Sao2 decreased by .10 percentage
points in two patients.
Although mean values remained within normal
limits, all patient groups experienced a small decrease
in arterial blood pH and a small increase in Paco2.
Changes in values attained statistical significance in
Groups I and III (Table 2). The respiratory depressant
effects of propofol became important in one patient, a
10-yr-old with dilated cardiomyopathy (without car-
diac shunt) and pulmonary hypertension. A loading
dose of propofol resulted in hypoventilation (arterial
pH decreased from 7.37 to 7.26, and Paco2 increased
from 45 to 60 mm Hg) and a marked increase in PVR
(from 640 to 1040 dynes z s21 z cm25). The patient was
withdrawn from the study, and after tracheal intuba-
tion and assisted ventilation, PVR was restored to
baseline values. The catheterization continued with-
out further incident, and the patient’s recovery was
uneventful.
Discussion
In this study of sedated children with congenital heart
defects undergoing cardiac catheterization, propofol’s
principal effect was a substantial reduction in SVR.
Because PVR remained constant, the ratio between
pulmonary and systemic resistance was increased. In
1414 PEDIATRIC ANESTHESIA WILLIAMS ET AL. ANESTH ANALG
PROPOFOL IN CHILDREN WITH HEART DISEASE 1999;89:1411–6

Table 2. Arterial Blood Gas Analysis Data for All Patients

Group I Group II Group III
Before After P Before After P Before After P
Variable propofol propofol value* propofol propofol value* propofol propofol value*
Arterial pH 7.36 6 0.02 7.32 6 0.03 ,0.001 7.37 6 0.03 7.33 6 0.04 0.07 7.37 6 0.02 7.32 6 0.04 0.009
Paco2 42 6 5 46 6 6 0.005 40 6 7 44 6 11 0.23 34 6 7 39 6 7 0.002
(mm Hg)
Pao2 98 6 10 93 6 14 0.06 78 6 31 63 6 9 0.15 52 6 10† 46 6 11 0.008
(mm Hg)
Sao2 (%) 96 6 1 95 6 2 0.01 93 6 3 89 6 5 0.04 83 6 7† 76 6 10 0.01
Data are mean 6 sd.
* Data before and after propofol administration were compared (paired Student’s t-test, significance set at P ,0.05).
† Pre-propofol values differed significantly among groups (Kruskal-Wallis test, significance set at P ,0.05).

Table 3. Hemodynamic and Oxygen Consumption Data for All Patients

Group I Group II Group III
Before After P Before After P Before After P
Variable propofol propofol value* propofol propofol value* propofol propofol value*
Oxygen consumption 140 6 32 136 6 32 0.37 139 6 35 136 6 44 0.76 171 6 33 183 6 46 0.43
(mL z min21 z m22)
Heart rate (bpm) 105 6 20 108 6 15 0.29 106 6 23 106 6 21 1.0 128 6 11 127 6 11 0.27
Systemic mean arterial 86 6 11 75 6 9 ,0.001 74 6 11 66 6 6 0.009 75 6 4 69 6 6 0.006
pressure (mm Hg)
Systemic vascular 1635 6 492 1285 6 298 ,0.001 1880 6 504 1134 6 384 0.001 1300 6 448 860 6 302 0.003
resistance
(dynes z s21 z cm25)
Systemic blood flow 4.0 6 0.8 4.4 6 0.9 0.005 3.12 6 0.93 4.76 6 2.01 0.04 5.10 6 2.02 6.96 6 2.56 0.005
(L z min21 z m22)
Pulmonary mean arterial 23 6 8 24 6 8 0.18 18 6 4 20 6 6 0.08 14 6 3 16 6 5 0.10
pressure (mm Hg)
Pulmonary vascular 225 6 144 210 6 142 0.38 94 6 32 146 6 80 0.10 130 6 59 180 6 140 0.22
resistance (PVR)
(dynes z s21 z cm25)
Pulmonary blood flow 4.0 6 0.8 4.4 6 0.9 0.005 6.01 6 1.8 6.17 6 2.17 0.87 3.64 6 1.02 3.41 6 1.17 0.93
(L z min21 z m22)
Pulmonary to systemic 0.14 6 0.1 0.17 6 0.1 0.005 0.06 6 0.03 0.13 6 0.07 0.03 0.10 6 0.05 0.24 6 0.23 0.10
resistance ratio
* Data before and after propofol administration were compared (paired Student’s t-test, significance set at P ,0.05).

children with cardiac shunt, the increased Rp:Rs led to
diminished left-to-right shunt, increased right-to-left
shunt, and a decrease in Qp:Qs. For patients with
acyanotic heart defects, the propofol-induced reduc-
tion in Qp:Qs seemed well tolerated and could have
been advantageous by diminishing pulmonary con-
gestion. In contrast, some patients with cyanotic heart
defects experienced reduced pulmonary blood flow,
thereby increasing the risk of arterial oxygen desatu-
ration. This is the first study to document the effects of
propofol on the amount and direction of shunt flow in
children with congenital heart disease.
In all patient groups, Qs increased after propofol
administration. The 21% reduction in SVR in children
without shunt lesions (Group I) was associated with a
9% increase in cardiac output, presumably due to an
increase in stroke volume (as heart rate did not
change).
The observation that propofol did not influence nor-
mal baseline PVR is consistent with data from a per-
fused lung model—propofol administration did not
change pulmonary resistance when baseline PVR val-
ues were normal, but it reduced PVR when baseline
values were increased (14). In our patients with in-
creased baseline PVR, the effect of propofol was in-
consistent. Further studies of the effect of propofol
(with Paco2 held constant) are required in children
with pulmonary hypertension.
Propofol (in combination with fentanyl) has been
compared with ketamine anesthesia in 20 unpremedi-
cated children with congenital heart disease undergo-
ing cardiac catheterization (1). Patients in that study
had a broad spectrum of anatomic defects, including
cardiac shunts. Those in the propofol group were
more likely to experience a decrease in SAP of .20%
(compared with baseline) during anesthetic induction.
ANESTH ANALG
1999;89:1411–6
Figure 1. Calculated left-to-right and right-to-left cardiac shunt and calculated ratio of pulmonary to systemic blood flow for patients with
cardiac shunt (Groups II and III).
Heart rate was not significantly altered. These obser-
vations are consistent with our study. Of the 10 pa-
tients who received propofol, 4 developed arterial
desaturations of .5 percentage points by pulse oxim-
etry. All periods of desaturation occurred on induc-
tion, concomitant with a transient decrease in systemic
blood pressure. However, the explanation for these
desaturation episodes remains unclear, because SAP
and heart rate were the only hemodynamic variables
measured. In our study, small but statistically signifi-
cant decreases in Sao2 where observed in patients
without shunt or with increased pulmonary flow
(Groups I and II), which suggests that respiratory
depression probably contributed to changes in oxy-
genation in some patients.
The cardiovascular effects of IV propofol induction
in premedicated children without congenital heart
disease have been reported (9). Propofol induction
resulted in approximately a 30% reduction in SAP and
a 15% reduction in SVR. Heart rate decreased 10%–
20%, and stroke volume index increased by 12%.
These changes are similar to those noted in our pa-
tients with congenital heart disease. Propofol had no
effect on sinoatrial or atrioventricular node function in
pediatric patients undergoing radiofrequency catheter
ablation (12). Likewise, in our study, no alteration of
heart rate or cardiac rhythm was noted.
Propofol’s cardiovascular effects have also been
evaluated in adults undergoing cardiac surgery. Most
such studies involved patients with ischemic heart
disease and normal left ventricular function (15–19).
Propofol caused a 20%– 40% decrease in blood pres-
sure (16,20), primarily via systemic vasodilation (16,
17,19). Heart rate was usually unchanged or decreased
(21). Our study data are consistent with these observa-
tions. Propofol can produce rate- and dose-dependent
myocardial depression (22). The increase in cardiac in-
dex noted in our Group I patients suggests that children
with congenital heart defects without baseline myocar-
dial depression tolerate propofol’s effects well in the
doses administered.
PEDIATRIC ANESTHESIA WILLIAMS ET AL. 1415
PROPOFOL IN CHILDREN WITH HEART DISEASE
Propofol is likely to be used increasingly in children
with congenital heart disease. It may become a pre-
ferred option for pediatric cardiac patients with good
ventricular function in whom rapid recovery from
anesthesia is desirable. Current practice at our institu-
tion is similar to that described by Reich (2), in that
propofol is used as the primary anesthetic for most
children undergoing cardiac catheterization. Like oth-
ers (1,23,24), we emphasize that propofol should only
be administered to pediatric cardiac patients when the
drug’s properties are appropriate for the child’s clin-
ical situation. Propofol’s hemodynamic profile sug-
gests caution in patients for whom systemic afterload
reduction may be harmful (e.g., patients with severe
aortic stenosis, hypertrophic obstructive cardiomyop-
athy) and in cyanotic patients whose pulmonary blood
flow depends on the balance between systemic and
pulmonary vascular resistance (e.g., patients with te-
tralogy of Fallot, hypoplastic left heart syndrome after
the Norwood palliation). The potential for respiratory
depression should be considered and precautions
taken to avoid deleterious consequences, particularly
in patients who may have pulmonary hypertension.
Propofol can alter the patient’s hemodynamic pro-
file. Interpretation of hemodynamic data obtained
during cardiac catheterization of children requires an
awareness of the hemodynamic consequences of the
anesthetic techniques used.
Midazolam and/or barbiturates were given before
propofol because it was considered unethical (and
technically difficult) to initiate a cardiac catheteriza-
tion in awake young children. The duration of thio-
pental administration was approximately one hour,
and the range in total dose (expressed as a rate) was
moderate (0.17– 0.23 mg z kg21 z min21). By studying
each patient before and after propofol administration,
we attempted to minimize the hemodynamic effects of
sedatives. Nevertheless, prior administration of mida-
zolam or thiopental may have influenced baseline he-
modynamic variables and the response to propofol
(25). In addition, these drugs may have accentuated
the respiratory depressant effects of propofol (26).
1416 PEDIATRIC ANESTHESIA WILLIAMS ET AL.
PROPOFOL IN CHILDREN WITH HEART DISEASE
In summary, we studied the hemodynamic effects
of propofol in sedated children with congenital heart
defects undergoing cardiac catheterization. Propofol
resulted in a significant decrease in SAP and SVR and
increase in Qs in all patients, whereas heart rate, PAP,
PVR, and Qp remained unchanged. Qp:Qs decreased
in patients with cardiac shunt, leading to further de-
saturation in patients with cyanotic heart disease
(Qp:Qs ,1). Awareness of propofol’s significant car-
diorespiratory effects can facilitate the appropriate se-
lection of anesthetics for children with congenital
heart disease and can also aid in the interpretation of
cardiac catheterization data obtained during propofol
anesthesia.
We thank the cardiac catheterization laboratory staff for their cheerful
support and Donald Baptiste for his expert and willing assistance.
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