Hemodynamic Changes During

Laparoscopic Cholecystectomy
Jean L. Joris, MD, Didier P. Noirot, MD, Marc J. Legrand, MD, Nicolas J. Jacquet, MD,
and Maurice L. Lamy, MD,
Departments of Anesthesiology and Abdominal Surgery, CHU of Liege, Domaine du Sart Tilman, B-4000 Liege, Belgium

Hemodynamics during laparoscopic cholecystectomy

under general anesthesia (isofluranein N 2 0 / 0 2 (50%))
were investigated in 15 nonobese ASA Class I patients
by using invasive hernodynamic monitoring including
a flow-directed pulmonary artery catheter. During surgery, intraabdominal pressure was maintained automatically at 14 mm Hg by a C 0 2insufflator,and minute
ventilation was controlled and adjusted to avoid hypercapnia. Hemodynamics were measured before anesthesia, after the induction of anesthesia, after tilting
into 10" head-up position, 5 min, 15 min, and 30 min
after peritoneal insufflation,and 30 min after exsufflation. Induction of anesthesia decreased significantly
mean arterial pressure and cardiac index (CI). Tilting
the patient to the head-up position reduced cardiac pre-

arious pathologic gynecologic conditions have

been diagnosed and treated by using laparoscopy for more than two decades. Endoscopic
surgery has been extended to gastrointestinal surgical
procedures such as appendectomy, peritoneal adhesiolysis, and cholecystectomy (1). The many benefits
reported after laparoscopy (1-3) explain its increasing
success and the efforts to introduce the endoscopic
approach for other surgical procedures. However,
peritoneal insufflation of C 0 2 to create the pneumoperitoneum necessary for laparoscopy induces
intraoperative ventilatory (4-8) and hemodynamic
(4-6,9,10) changes that complicate anesthetic management of laparoscopy. The position of the patient (headdown or head-up) required during these procedures
also contributes to these changes (4,6-7).
The investigation of hemodynamics during gynecologic laparoscopy in the head-down position (6-7,9)
revealed an increase (225%) of mean arterial blood
pressure (MAP), a decrease (%15%)in cardiac output,
and an increase (550%)of systemic vascular resistance
Accepted for publication December 11, 1992.
Address correspondenceand request for reprints to Dr. JeanJoris,
Department of Anesthesiology, CHU of Liege, Domaine du Sart
Tilman, B-4000 Liege, Belgium.
01993 by the International Anesthesia Research Society
0003-2999/93/$5.00

load and caused further reduction of CI. Peritoneal insufflation resulted in a significant increase (235%) of
mean arterial pressure, a significant reduction (220%)
of CI, and a significantincreaseof systemic (265%)and
pulmonary (290%)vascular resistances.The combined
effect of anesthesia, head-up tilt, and peritoneal insufflation produced a 50% decrease in CI. Administration
of increasing concentrations of isoflurane, via its
vasodilatory activity, may have partially blunted
these hemodynamic changes. These results demonstrate that laparoscopy for cholecystectomyin head-up
position results in significanthemodynamicchanges in
healthy patients, particularly at the induction of
pneumoperitoneum.
(Anesth Analg 1993;76:1067-71)

during insufflation. Obese patients with potentially

impaired cardiovascular status explored in one study
(6) and the accuracy of the non-invasive technique
(thoracic electrical bioimpedance) used in the other
studies (9,101 raise questions (11,12). We investigated
the hypothesis that peritoneal insufflation of carbon dioxide for laparoscopic cholecystectomy in the
head-up position would be associated with even
greater decreases in cardiac output than insufflation
for gynecologic laparoscopy in the head-down position. Hemodynamic changes during laparoscopic
cholecystectomy were explored by using invasive
monitoring (e.g., flow-directed pulmonary artery catheter) in non-obese patients without cardiorespiratory
pathology.

Methods
Fifteen fully informed patients scheduled for elective
laparoscopic cholecystectomy gave consent to be included in this study after the approval of the ethics
committee at our institution. Inclusion criteria were
body weight less than 20% more than ideal weight, age
between 18 and 70 yr, no acute cholecystitis, and no
cardiorespiratory disease or medications. All patients
were premedicated with hydroxyzine 50-75 mg by
Anesth Analg 1993;76:1067-71

1067

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ANESTH ANALG
1993;76:1067-71

JORIS ET AL.
HEMODYNAMICS DURING LAPAROSCOPY

mouth 2 h before surgery and an intramuscular (IM)

injection of midazolam, 5 mg, and atropine, 0.25 mg,
just before transfer to the operating theater. General
anesthesia was induced intravenously (IV) with sufentanil, 15-20 pg, thiopental, 5 mg-kg-I, and atracurium,
0.5 mg-kg-I. After tracheal intubation, general anesthesia was maintained with nitrous oxide (50%)in oxygen and isoflurane. Isoflurane concentrations were
adapted to keep the patient hemodynamically stable by
an experienced anesthesiologist: mean arterial pressure
(MAP) was not allowed to increase more than 20%
above preinduction value. In addition to clinical signs,
the anesthesiologist used the usual monitoring for this
surgical procedure (i.e., noninvasive arterial blood
pressure, electrocardiogram (ECG),heart rate, capnography, and pulse oximetry) but was unaware of the
information derived from the invasive monitoring described below. A basal IV infusion (4 mL.kg-'.h-') of
lactated Ringer's solution to compensate for fasting
and intraoperative losses was given. Before the induction of anesthesia, one radial artery was cannulated
and a 7.5 F thermodilution Edwards Swan-Ganz@catheter (Baxter)was introduced via the right internal jugular vein. During surgery, the expired end-tidal Pco2
(PETCO~)
and isoflurane concentrations were monitored
continuously by a Datex Capnomac@sidestream analyzer. Minute ventilation was controlled (Servo 900C;
beSiemens-Elema) and adjusted to keep the PETCO~
tween 30 and 40 mm Hg. During laparoscopy intraabdominal pressure (IAP) was maintained automatically at 14 mm Hg by a C 0 2insufflator (Wolf 2154.201).
The following variables were recorded on a Datex Cardiocap@"monitor: invasive arterial pressure, pulmonary artery pressure, right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP) measured
with a Viggo-Spectramed transducer, and heart rate.
Cardiac output (CO) was calculated by a SAT-1 computer (American Edwards Laboratories), and the average of three measurements made at the end of expiration was considered. Systemic vascular resistance
(SVR) and pulmonary vascular resistance (PVR) were
calculated from the above variables as follows: SVR
= (mean invasive arterial pressure (dynes.~.cm-~)
RAP).8O/CO; PVR (dyne~.s.cm-~)
= (mean pulmonary artery pressure - PCWP).8O/CO. Data were collected before the induction of anesthesia (Tl), 10 min
after the induction of anesthesia (T2), 10 min after tilting into 10" head-up position (T3), 5 min (T4), 15 min
(T5)and 30 min (T6)after the beginning of insufflation,
and finally 30 min after exsufflation (T7). At T7, anesthesia had been terminated for 215 min and the patients, once again in the horizontal position, had been
tracheally extubated and were breathing spontaneously. The pressure transducer was located at the level of
the right atrium and was moved after tilting to remain
at this level. At the same time points, peak and plateau

Table 1. Patient Data

Age, yr
Sex ratio, M / F
Weight, kg
Height, cm
Duration of insufflation, rnin
Results are mean

? \EM

48.9 k 3.7
4/11
66.8 f 3.0
165 ? 1
62.9 ? 4.6

(20-69)
(55-85)
(152-175)
(35-105)

and (range)

airway pressures (Paw) were recorded on the Servo

ventilator 900C (Siemens-Elema) and an arterial blood
sample was drawn to measure arterial Pco2 (Paco2).
Mean intrathoracic pressure was also measured in 12
patients by means of a latex esophageal balloon. The
correct position of the balloon was confirmed by fluoroscopy. Inasmuch as the pressure of the mediastinum
on the balloon changes with patient position, pressures
were recorded only after tilting to the head-up position
(T3 to T6) and expressed as pressure change compared
to T3 value.
Results are reported as mean t standard error (SEM).
Data were analyzed by a one-way analysis of variance
for repeated measures followed by Newman-Keuls test
(13). Results were considered to be statistically significant at the 5% critical level.

Results
Demographic characteristics of the patients are represented in Table 1. After the induction of anesthesia,
MAP and cardiac index (CI) decreased (Table 2). After
tilting to the head-up position, RAP and PCWP decreased and a further reduction of CI and MAP was
observed. From T1 to T3, a linear relationship linked
MAP and CI (MAP = 16.9 CI + 36.7; Y = 0.94, P < 0.05).
After peritoneal insufflation (T4), this relationship
changed. Indeed, whereas MAP increased (35%), CI
significantly decreased (20%). Peritoneal insufflation
also resulted in a significant increase of systemic and
pulmonary vascular resistances (SVR, 65% and PVR,
90%) (Table 2). RAP and PCWP increased significantly
during insufflation and did not change significantly
from T4 to T6. Deepening of anesthesia by the administration of increasing concentrations of isoflurane
(Table3) allowed partial correction of the changes of CI,
SVR, and PVR which, however, remained significantly
different from preoperative values during CO, insufflation (Table 2). No significant changes of heart rate
and Paco2 were noted during surgery (Tables 2 and 3).
The combined effects of anesthesia, the head-up tilt,
and increased intraabdominal pressure produced a significant decrease (50%) of CI (Table 2). After insufflation, peak and plateau Paw as well as intrathoracic
pressure significantly increased (Table 3). Thirty minutes after exsufflation, all hemodynamic variables had
returned to preoperative values.

JORIS ET AL.
HEMODYNAMICS DURING LAPAROSCOPY

ANESTH ANALG
1993;76:3067-71

1069

Table 2. Hemodynamic Changes During Laparoscopic Cholecystectomy

T4
Hemod ynamic
changes*

T1
before
induction

T2
after
induction

T3
head-up

MAP, mm Hg
HR, beats/ min- '
RAP, mm Hg
PCWP, mm Hg
CI, L.rnin-'.rn-,
SVR, dynes.s.cm-'
PVR, dynes.s.cm-'

96 f 13
79 f 4
8f1
9f1
3.6 0.1
1139 f 49
229 f 21

87 f 3
83 + 4
8+1
9f1
2.7 f 0.2t
1389 + 108
292 f 31

71 f 2 t
76 t 4
5+1
7f1
2.2 0.2t
1452 k 111
272 f 28

T5

T6

5 min

15 min

30 min

T7
after
surgery

97 f 5$
79 f 4
11 f 1$
14 f 2t,$
1.8 f O.lt,$
2367 f 251t,$
521 + 55t,$

102 + 5$
81 + 5
10 f 1$
14 f It,$
2.4 t O . l t
1777 f 146t
423 f 36tJ

93 f 5$
81 f 5
10 f 2$
12 f It,$
2.3 f 0.2t
1676 f 120t
397 f 35t,$

105 f 5$
78 f 4
8+1
9+1
3.4 f 0.3
1365 f 96
291 f 3 2

Pneumoperitoneum

Hemodynamic changes were measured or calculated before the induction of anesthesia (Tl), 10 min after the induction of anesthesia (T2), 10 min after tilting
into 10" head-up position (T3), 5 min (T4), 15 min (TS), and 30 min (T6) after the beginning of insufflation, and 30 min after exsufflation (T7).
Results are mean ? SEM.
* Abbreviations used are: MAP, mean arterial pressure; HR, heart rate; RAP, right atrial pressure; PCWP, pulmonary capillary wedge pressure; CI, cardiac index;
SVR, systemic vascular resistance; PVR, pulmonary vascular resistance.
t P < 0.05 as compared with TI; $ P < 0.05 a s compared with T3.

Table 3. Ventilatory Changes During Laparoscopic Cholecystectomy

T4
Ventilatory
changes*
Paco', mm Hg
Pao,, mm Hg
Isoflurane, %
AITP, mm Hg
Peak Paw, cm H 2 0
Plateau Paw, cm H 2 0

T1
before
induction

T2
after
induction

T3
head-up

41.2 f 0.9
84 f 3

36.3 f 1.4t
243 + 12t
0.46 f 0.03

34.1 f 0.7t
216 f 13t
0.38 + 0.04
0
14.9 f 1.3
1.2 t 1.3

14.5 f 1.1
10.6 1.2

T5

T6

Pneumoperitoneum

5 min

15 min

30 min

35.8 t 0.9t
234 f 9 t
0.84 f 0.05$
9.4 f 1.1$
21.8 f 1.9$
17.9 + 1.8$

39.1 f 1.0
230 f l l t
1.02 f 0.084
9.6 f 1.0$
22.6 t 1.2$
18.4 f 1.5$

37.5 f 0.8
222 f 10t
0.90 f 0.8$
8.7 +- 0.8$
22.7 f 1.3$
18.4 + 1.2$

T7
after
surgery
43.2

* 1.2$

82.2k 3.1

'Arterial Pcoz (Pam2)and Poz (Path), expired end-tidal concentration of isoflurane, and peak and plateau airway pressure (Paw) were measured 10 min after
the induction of anesthesia (T2), 10 min after tilting into 10' head-up position (T3), 5 min (T4), 15 min (T5). and 30 min (T6) after the beginning of insufflation.
Pacoz and Pa02 also were measured before the induction of anesthesia (TI) and 30 min after exsufflation (T7). Change in intrathoracic pressure (AITP) as compared
to T3 were calculated during pneumoperitoneum.
Results are mean ? SEM.
t P < 0.05 as compared with T1; $ P < 0.05 as compared with T3.

Discussion
This study demonstrates that peritoneal C 0 2 insufflation to an intraabdominal pressure of 14 mm Hg, necessary for laparoscopic cholecystectomy, induces major
hemodynamic changes in healthy non-obese patients
without cardiac disease. These significant disturbances
are characterized by an increase in MAP, SVR, and PVR,
and a decrease of CI. CI markedly decreased to as much
as 50%of preoperative values 5 min after the beginning
of insufflation. The hemodynamic changes observed in
this study complement the results of recent studies during gynecologic laparoscopy in the head-down position (6,9,10). By using an invasive monitoring in patients in the head-up position, we observed a more
pronounced increase of SVR and PVR.
The pathophysiology of these changes remains unclear. Before insufflation, SVR did not change significantly and a linear relationship linked MAP and CI.
Anesthetic induction drugs depressed the myocardium
and reduced CI and MAP. Tilting the patient to the

head-up position reduced venous return as evidenced

by the fall of RAP and PCWP. Consequently, CI and
MAP further decreased. After peritoneal insufflation,
this relationship changed. Indeed, MAP at T4, although
similar to that at T1, was associated with significantly
lower CI. Only an increase of SVR can explain the increase in MAP pressure observed after insufflation despite the significant reduction of CI. Increased venous
resistance (14) and compression of the abdominal aorta
may coqtribute to the increase in cardiac afterload
(5,9,10). Measurement of the radial-femoral arterial
pressure gradient before and during peritoneal insufflation could help to confirm this hypothesis. It is unlikely that the increases in MAP and SVR are entirely
related to mechanical factors. First, the correction of
these changes was gradual and took several minutes
when the IAP was released suddenly at the end of the
operation (6,10,15). Moreover, since in our study the
IAP was maintained automatically at 14 mm Hg during
laparoscopy, the compression of the abdominal aorta

1070

JORIS ET AL.
HEMODYNAMICS DURING LAPAROSCOPY

did not change and the disturbance of venous return

remained constant, as evidenced by unchanged RAP
and PCWP from T4 to T6. Despite this steady state, SVR
decreased nevertheless. The partial correction of the
hemodynamic variables occurring between T4 and T6
may be attributed to the vasodilating properties of isoflurane (16) and/or to the natural history of the hemodynamic changes. These changes, however, persisted for more than 20 min in other studies (5,17,18).
All these observations suggest the involvement of other
mechanism(s) such as the release of humoral factors.
Potential mediators of the increase in SVR are catecholamines, prostaglandins, the renin-angiotensin system, and vasopressin (10,19,20).Plasma noradrenaline
levels and plasma renin activity did not change during
pneumoperitoneum for diagnostic laparoscopy in patients breathing spontaneously (20).On the other hand,
a fivefold increase of vasopressin was observed in 60%
of patients when IAP was increased to +10 mm Hg (20).
Increases in plasma vasopressin levels were correlated
with changes in IAP, intrathoracic pressure (ITP), and
transmural RAP (20). The increasing pulmonary resistance described in this study is another potential stimulator of vasopressin release (20). Therefore, both mechanical and putative humoral phenomena could
contribute to the increase in SVR.
The mechanism of the decrease of CI may be multifactorial. CO depends on venous return, myocardial
contractility, and cardiac afterload (14). In animal studies, inferior vena caval flow declined with increases of
IAP of 10 mm Hg or more (5,17,18).Femoral vein pressures increased roughly in parallel with the increases of
IAP consequent to pooling of blood in the peripheral
circulation (4,5).The subsequent decline in venous return closely paralleled the decrease in CO (5,171. Paradoxically, we and others (4-6) observed increased cardiac filling pressures (RAP, PCWP) during peritoneal
insufflation. However, consequent to the increase in
IAP, ITP also increased (5,8,20) (Table 3). The increase
of minute ventilation necessary to avoid hypercapnia
(6-8) associated with a decrease of thoracopulmonary
compliance secondary to the elevation of the diaphragm (9) results in an increase of peak and plateau
Paw during mechanical ventilation. This increase in
Paw (Table 3) probably contributes to the increased ITP.
Transmural RAP (i.e., the pressure within the right atria
minus the extracardiac pressure), which should be
used rather than directly measured RAP as an indicator
of venous return to the heart in case of elevated IAP, did
not change very much (5,18). The observation of a significant decrease in stroke volume, despite only a slight
or no decrease of transmural RAP, suggests a shift of the
ventricular function curve (Frank-Starlingslaw) to the
right, perhaps secondary to the increase in afterload
(5,18). The increase in SVR is most likely the cause
of the decreased CO (5,10,18) rather than from an

ANESTH ANALG
1993;761067-71

increased sympathetic activity in response to the decreased CO (9). Indeed, vasodilation by the administration of increasing concentrations of isoflurane improved CO although RAP did not change. Finally, the
concentrations of isoflurane used in this study do not
depress the normal myocardium (16). The effect of increased IAP and ITP on myocardial contractility can
not, however, be determined from this study. Transesophageal echocardiography should be helpful in assessing contractility and venous return. Thus, during
laparoscopy, the decrease in CO can be explained by a
reduction in venous return and/or an increase of SVR.
It seems that the normal heart, which tolerates an increase of afterload very easily in normal conditions,
becomes sensitive to changes in afterload much like a
decompensated heart (21), when this normal heart has
to face the artificial conditions of pneumoperitoneum
under general anesthesia.
These results indicate the need for caution in patients
with impaired cardiac function, anemia, or hypovolemia scheduled for laparoscopy. Such situations may occur during laparoscopy in patients with ruptured ectopic pregnancies, or diagnostic laparoscopy in patients with blunt and penetrating injuries to the abdomen and in patients with peritonitis. These results bear
a particular significance in cases of laparoscopy in older
patients, such as for gastrointestinal surgical procedures; these patients are more likely to have known or
latent cardiac disease. Hemodynamic consequences of
pneumoperitoneum have not been explored in patients
with cardiac disease. However, indirect data suggest
that hemodynamics may be more altered in these patients than in ASA Class I patients (22). In all these
cases, it would seem prudent to reduce the rate of insufflation and limit abdominal inflating pressures to a
minimum. The trend to readily propose the laparoscopic approach for patients with impaired cardiac
function because of easier and smoother postoperative
recovery should be tempered by the risks related to the
intraoperative hemod ynamic changes induced by peritoneal insufflation. The anesthetic management of laparoscopy is beyond the scope of this paper. However,
anesthetics with vasodilating action should be favored,
and anesthetics that directly depress the heart should
be avoided. Pure vasodilator and cardiotonic drugs
may be necessary in patients with compromised cardiac function. Finally, it should be noted that the usual
intraoperative cardiovascular monitoring (blood pressure, heart rate, capnography, pulse oximetry) gives no
accurate information on the increase of SVR and the
reduction of CO.
In conclusion, these results highlight the fact
that laparoscopy induces significant hemod ynamic
changes even in healthy patients and creates increases
of SVR and PVR, an increase of MAP, and a reduction
of CO. These disturbances could be mediated both

ANESTH ANALG
1993;76:1067-71

mechanically and humorally. Whereas these cardiovascular changes should not be hazardous in healthy patients, special care and monitoring are mandatory for
patients with impaired cardiac function. In these patients postoperative benefits of laparoscopy should be
balanced against intraoperative risks.

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