Anesthesia For Endos
Anesthesia For Endos
Anesthesia For Endos
KEYWORDS
Pneumoperitoneum Gas embolism One-lung ventilation V/Q mismatch
Capnothorax CO2
KEY POINTS
Anesthetists should focus on only anesthetic management and not be distracted by
setting up the endoscopic equipment.
No single anesthetic protocol has proved superior to other protocols for endoscopic
surgery.
Insufflation induces significant cardiovascular and respiratory changes.
One-lung ventilation devices should be placed with a bronchoscope.
INTRODUCTION
compared with healthy patients, and the rate of complications might be higher than in
healthy patients. In addition to these concerns associated with endoscopic surgery,
patients’ comorbidities affect anesthetic management adversely.11
Anesthetists must understand the possible systemic changes and complications
that are associated with endoscopic surgery before anesthetizing any patient, even
a healthy one. Although it is important to know how comorbidities affect anesthetic
management, this article focuses only on anesthetic management of patients under-
going endoscopic surgery and specifically on the systemic changes and complica-
tions that can occur.
EFFECT OF PNEUMOPERITONEUM
increases, so too does ICP. PaCO2 is one of the major factors influencing CBF, and an
increase of PaCO2 increases CBF because of cerebral vascular vasodilation, resulting in
increase of ICP.20 In patients with an intracranial space-occupying mass, increase of
ICP caused by high PaCO2 associated with CO2-induced pneumoperitoneum can cause
the patient’s condition to deteriorate. Despite maintaining PaCO2 within the normal
range, pneumoperitoneum can increase blood flow in the brain independently and in-
crease ICP.21,22 For these reasons, if a patient is known to have or is suspected of hav-
ing an intracranial space-occupying mass, inducing pneumoperitoneum should be
avoided.
Renal function can also be affected by pneumoperitoneum. In people, high IAP de-
creases renal blood flow and glomerular filtration rate.9 Urine output significantly de-
creases during insufflation but returns to normal once abdominal pressure returns to
normal.23
Pneumoperitoneum-induced increases in IAP significantly affect cardiovascular,
respiratory, and renal function and can also increase ICP.8,9,22 Because of these ef-
fects, pneumoperitoneum should not be induced in patients with the following condi-
tions: ventricular peritoneal shunts for treating hydrocephalus; hypovolemia; high ICP;
renal failure; and tissue or organ damage within the abdominal cavity. For these pa-
tients, laparotomy or gasless laparoscopy may be safer than laparoscopy with
pneumoperitoneum.
PREOPERATIVE PREPARATION
The choice of drugs to use for premedication and anesthetic induction of patients un-
dergoing laparoscopic surgery is complicated by 2 important issues: (1) pain, espe-
cially in the postoperative period; and (2) potential drug effects on splenic size,
specifically splenomegaly. In terms of pain, the type of endoscopic surgery the patient
4 Asakawa
is having influences the pain that is experienced. Endoscopic surgery has been clas-
sified as complete or assisted surgery. Complete endoscopic surgery is performed
only through instrument ports, but assisted endoscopic surgery requires an additional
incision or an extended incision at a port site, the latter often involving extensive
stretching of the incision by instruments. Although endoscopic surgery is considered
to be less invasive than open surgery, it still causes tissue trauma that stimulates noci-
ceptive receptors and induces the stress response, so patients should receive analge-
sics perioperatively. The benefits of providing analgesia are many, including smoother
anesthetic induction, stabilized anesthetic maintenance, reduction of minimum alve-
olar concentration of the inhalant anesthetic, and potentially less postoperative
pain.24,25 Opioids, classified as pure mu agonists, partial mu agonists, and agonist-
antagonists, have analgesic as well as sedative properties, and they are often used
alone or in combination with other drugs for premedication as well as intraoperative
and postoperative analgesia.
If the patient is undergoing complete endoscopic surgery, a partial mu agonist such
as buprenorphine should provide sufficient analgesia during surgery. However, if the
patient is undergoing assisted endoscopic surgery that involves an additional incision
or stretching of a port site, and a partial mu agonist may not provide enough analgesia
during surgery, and a pure mu agonist, such as hydromorphone, oxymorphone, meth-
adone, or morphine, is preferred for perioperative analgesia. Some pure mu agonists
induce nausea and vomiting, which is uncomfortable for the patient and may lead to
perioperative aspiration of gastric contents. Fentanyl does not induce nausea, but
its half-life is short and its analgesic effect lasts less than 30 minutes after a single
bolus. A technique for overcoming the short duration of effect when using fentanyl
as a premedicant is to give the drug intravenously (IV) before induction. If the patient
has an intravenous catheter or tolerates insertion of an intravenous catheter without
sedation, small amounts of fentanyl (3–5 mg/kg) can be given as a premedicant fol-
lowed by propofol for induction. To ensure adequate analgesia during surgery, a local
anesthetic can be infiltrated at the site of port insertion or a fentanyl constant-rate infu-
sion (CRI) (0.2–0.4 mg/kg/min IV) can be administered.
Drug-induced splenomegaly may increase the risk of injury to the enlarged spleen
when the Veress needle or port is inserted into the abdomen. Selecting drugs that
cause minimal or no splenic enlargement is important and several studies have
addressed this issue.26–28 In one study, significant splenic enlargement was seen after
administering acepromazine or thiopental, but not after administering propofol.26
Another study found that a combination of acepromazine and butorphanol followed
by induction with propofol had minimal effect on splenic volume, whereas medetomi-
dine and butorphanol as premedicants followed by ketamine and diazepam for induc-
tion were associated with a significant increase in splenic volume.27 In a more recent
study, acepromazine, propofol, and thiopental treatments caused the greatest in-
crease in splenic volume, whereas hydromorphone and dexmedetomidine used in
combination as premedicants did not cause a significant change in splenic volume.28
Taken together, these studies suggest that, for premedication, combinations of ace-
promazine plus butorphanol, or hydromorphone plus dexmedetomidine followed by
induction with propofol are more likely to have little effect on splenic volume. Other
concerns may favor some drugs more than others. Thiopental for induction is not
appropriate, because it causes significant splenic engorgement.26,28
Alpha-2 agonists, such as dexmedetomidine, can be used for endoscopic anes-
thesia and might help attenuate cardiovascular effects associated with pneumoperito-
neum.29 However, doses typically used for premedication induce significant
hemodynamic changes that may not be desirable in patients with cardiac diseases.
Anesthesia for Endoscopy 5
Most induction agents, such as propofol, etomidate, and alfaxalone, can be used
without problems. However, in addition to its effects on splenic volume, ketamine
stimulates the sympathetic nervous system and increases the release of cate-
cholamines.30,31 Because pneumoperitoneum also increases the release of cate-
cholamines, ketamine may not be the best choice, especially in patients with
cardiovascular disease.9
High IAP can increase vagal tone; therefore, giving anticholinergics such as glyco-
pyrrolate, or atropine as a part of premedication is appropriate. In addition to IAP, us-
ing opioids also increases vagal tone, which makes patients more prone to develop
bradycardia during surgery.
Isoflurane and sevoflurane are appropriate to use for a maintenance agent. Howev-
er, halothane increases the sensitivity of the heart to catecholamines, so should be
avoided.32 Propofol CRI (0.2–0.5 mg/kg/min IV) can be used safely for a maintenance
agent in dogs but not in cats.33
N2O is not an ideal anesthetic gas during endoscopic surgery because it diffuses
into gas-filled spaces such as the abdominal cavity and thoracic cavity and increases
pressure over time. Also, if a gas embolus occurs during surgery, the volume of the
embolus is increased dramatically, and N2O worsens the situation.
Neuromuscular paralytic drugs, such as atracurium (0.1–0.2 mg/kg IV), can be used
during surgery to improve relaxation of the abdominal wall. As a result, less IAP is
required to achieve adequate visualization of the surgical field and hemodynamic
and ventilatory changes associated with pneumoperitoneum may be minimized.34
Use of neuromuscular paralytics requires the use of a mechanical ventilator and moni-
toring of cardiopulmonary variables; at the end of surgery the neuromuscular blockade
must be reversed.
MONITORING
helpful for detecting gas embolism and monitoring hemodynamic changes. However,
it is not necessary in routine endoscopic anesthesia unless the patient has severe car-
diac or respiratory disease.
Core body temperature is affected by endoscopic procedures because the gas
used for insufflation is at room temperature or cools the patient during insufflation,
thus directly cooling abdominal organs; monitoring and supporting body temperature
is crucial. Although thoracoscopy does not require insufflation of gas into the thoracic
cavity, ambient air does enter the thoracic cavity and reduces esophageal tempera-
ture. Therefore, to accurately monitor body temperature the monitor probe should
be in the rectum during thoracoscopy and inserted into the esophagus during laparos-
copy to obtain accurate core temperature measurements.
Pulse oximetry provides continuous information concerning hemoglobin saturation
with oxygen. Because endoscopic procedures depress ventilation, early detection of
hypoxemia is important to avoid complications.
ETCO2 measures partial pressure of CO2 (PCO2) at the end of expiration, which rep-
resents PCO2 in the alveoli. Because alveolar PCO2 is supposed to be the same as
PaCO2, ETCO2 can be used for estimating PaCO2 and ventilatory function. Laparoscopy
increases PaCO2 because of insufflation of CO2 and ventilatory depression associated
with high IAP.9 Thoracoscopy also induces pneumothorax, which depresses ventila-
tion. Therefore, monitoring ETCO2 to detect hypoventilation is important. In addition,
ETCO2 guides adjustment of ventilator settings to effectively treat hypoventilation dur-
ing general anesthesia.
ANESTHETIC MANAGEMENT
LAPAROSCOPIC SURGERY
than 12 mm Hg, these hemodynamic changes are not significant.9 If insufflation is too
rapid, significant hemodynamic changes can occur but can be counteracted by mak-
ing sure the patient is adequately hydrated before inducing the pneumoperitoneum.
Giving a bolus of crystalloids (10–20 mL/kg) over 10 to 15 minutes before starting
insufflation can minimize these hemodynamic changes, especially if the patient has
cardiac disease or is hypovolemic.9 Induction of pneumoperitoneum should be per-
formed smoothly and slowly.
Insufflation of CO2 increases PaCO2 because of absorption through the abdominal
peritoneum.8 This increase in PaCO2 can be normalized by adjusting ventilator settings
to increase minute ventilation. However, if the ventilator setting adversely affects car-
diovascular function and does not normalize PaCO2, maintaining PaCO2 around 50 mm
Hg is acceptable in most patients as long as blood pH is higher than 7.3. An exception
is patients with intracranial disease, because hypercapnia increases CBF and, as a
result, increases ICP. In patients with intracranial disease, normocapnia must be main-
tained throughout the anesthetic period to prevent brain injury.
Increased IAP shifts the diaphragm cranially and decreases FRC and compliance of
the lung.8,9 Because these changes adversely affect ventilatory function, patients
should be mechanically ventilated. Adjusting ventilator settings to normalize PaCO2
can be challenging with these respiratory changes, especially the reduced lung
compliance. Usually a larger tidal volume setting and a slower than normal respiratory
frequency provide better ventilation with these pulmonary changes than do small tidal
volumes and a fast rate.9 In some patients, it is necessary to apply a small amount of
positive end-expiratory pressure (PEEP), such as 5 cm H2O, to prevent atelectasis.40
Although rare, gas embolism can occur during pneumoperitoneum.9 Usually gas
absorption from the abdominal cavity through the peritoneum is minimal. However,
if the peritoneum is damaged because of surgical manipulation or the patient develops
subcutaneous emphysema caused by gas insufflation, the amount of gas absorbed
can become significant and may induce gas embolism.10 If a gas embolus develops,
ETCO2 decreases suddenly because of high V/Q ratio even though the ventilator setting
has not been changed.31 In addition to ETCO2 changes, blood pressure and SpO2 may
decrease at the same time, but depend on the size of the embolus.
Making a diagnosis of gas embolism is not easy and requires chest radiographs, CT
examination with angiography, or the use of a transesophageal echocardiography;
however, these modalities may not be available or may take time to acquire. Gas em-
bolism can be fatal. In the absence of a clear diagnosis, anesthetists must start appro-
priate treatments or prevent worsening of the situation if any of the signs discussed
earlier are seen. Gas insufflation must be promptly discontinued, and the abdomen
deflated as soon as possible. The patient should be positioned in the Trendelenburg
position (tilt head down with patient in dorsal recumbency) to prevent further gas
movement toward the heart.9 If the symptoms are severe, such as adversely affecting
cardiac output, inserting a central venous catheter to the level of the right heart and
aspirating the gas may remove the embolus.41 If the patient is in an emergency con-
dition and has minimal cardiac output, shaking the patient’s body may decrease the
size of the gas embolus and may help to reestablish blood flow through the heart
and pulmonary artery.42 Once the major gas embolus is cleared, small gas emboli
dissolve into the blood quickly, especially if the gas used for insufflation was CO2.
Another complication that may occur during pneumoperitoneum is pneumothorax,
which is often caused by accidental diaphragmatic injury. If CO2 was used for insuf-
flation and the patient developed pneumothorax, it is called capnothorax, which in-
creases ETCO2 and inspiratory airway pressure. Subcutaneous emphysema also
increases ETCO2; an easy means for distinguishing between capnothorax and
8 Asakawa
THORACOSCOPIC SURGERY
After placing the introducer, a small amount of gas is insufflated into the thoracic cavity
or room air is used to create pneumothorax before placing the next port. Pneumo-
thorax reduces the size of the lung on the surgical side and creates a space between
chest wall and lung, which reduces the risk of lung puncture or laceration associated
with inserting an additional port. This pneumothorax also improves visualization of the
intrathoracic structures during the surgical procedure. Unlike laparoscopy, thoraco-
scopic procedures are performed without pressurized insufflation because the chest
cavity is less compliant than the abdominal cavity and because of the severe effects
that increased intrathoracic pressure would have on both ventilation and circulation.
In addition to purposely inducing pneumothorax, 1-lung ventilation (OLV) is often
performed to obtain maximum visibility during surgery. OLV is induced by using a spe-
cial endotracheal tube or a bronchial blocker. These devices occlude 1 bronchus,
which results in cessation of ventilation of the occluded lung while the other lung
Anesthesia for Endoscopy 9
remains normally ventilated. Although the blocked side of the lung has no ventilation, it
is still perfused by the pulmonary circulation, which carries away gas from alveoli in the
occluded lung. As a result, the occluded lung collapses within a few minutes because
of gas absorption by pulmonary circulation, especially when greater than 95% oxygen
is used as the carrier gas for the inhalant anesthetic agent. Collapsing the lung on the
operative side provides a much better surgical field than that provided by a
pneumothorax.
The special endotracheal tube, a double-lumen endobronchial tube (Fig. 1), has 1
short tube and 1 longer tube and 2 cuffs. The end of the longer tube fits into the left
bronchus and the shorter tube is in the trachea. Inflating the cuffs allows positive pres-
sure ventilation of both the right and left lungs. The cuff on the longer end seals only
the left bronchus, which isolates the left lung from the right lung. If the shorter tube is
occluded, the right lung will not be ventilated, whereas the left lung is ventilated. In
contrast, if the longer tube is occluded and not the shorter tube, the right lung is
ventilated.
Double-lumen endotracheal tubes are made for human patients, and people have
shorter tracheas compared with dogs. If the veterinary patient weighs more than
20 kg, even the longer of the two tubes may not extend to the bronchus. Also, a
small-diameter tube is not available, so these tubes are too big for use in small patients
such as shih tzu dogs. Use of this endotracheal tube is limited by its circumference
and length. If a double-lumen endobronchial tube is appropriate for a given patient,
it is important to choose a double-lumen tube with a longer tube that fits into the
left bronchus. Longer tubes that fit into the right bronchus of humans do not fit in
dogs because of anatomic differences.
An endobronchial blocker (also called bronchial blocker) is also used for OLV during
thoracoscopy. The endobronchial blocker (Fig. 2) is inserted through an endotracheal
tube to either the right or left bronchus; once in position, the cuff on the blocker is
inflated, thus occluding the selected bronchus. This device has been used in veteri-
nary medicine more commonly than double-lumen endotracheal tubes because
they are not limited by size or length. Correct positioning of either device can be ascer-
tained by auscultation (blind technique); however, the malpositioning rate is high; us-
ing a bronchoscope to confirm correct placement is highly recommended.46
OLV decreases V/Q ratio (only 1 side of the lung ventilated and blood flow perfuses
both side) and worsens pulmonary gas exchange. Although OLV has adequate gas
Fig. 1. Double-lumen endobronchial tube is connected to the rebreathing circuit (left). The
blue tube is marked with the word “Bronchial”, indicating that it is the longer side.
10 Asakawa
Fig. 2. Endobronchial blocker has a cuff at the near end of the blocker to occlude the bron-
chus (top right).
RECOVERY
Despite better pulmonary function following endoscopic surgery than following lapa-
rotomy, before extubating a patient its pulmonary function must be evaluated to
ascertain that it is adequate. Evaluation of pulmonary function includes oxygenation
and ventilatory function. Testing oxygenation can be done with an oxygen challenge
test using either a pulse oximeter or blood gas analysis. This test evaluates the pa-
tient’s arterial oxygen saturation level while it is breathing room air (fraction of inspired
oxygen [FiO2], 21%) during anesthetic recovery; this gives an indication as to what the
patient’s oxygenation will be after recovery. Reducing FiO2 from greater than 95% can
be achieved either by disconnecting the endotracheal tube from the breathing circuit
or by decreasing FiO2 using air and oxygen blender on the anesthesia machine, if avail-
able. While the patient is breathing room air, SpO2 is monitored with the pulse oxime-
ter; if SpO2 decreases to less than 92%, the test must be stopped and the patient
allowed to breathe gas with an FiO2 greater than 50%. If the patient can maintain
SpO2 more than 93% while breathing room air for 3 to 5 minutes, most likely the patient
can be recovered without oxygen support. However, if the patient cannot maintain
oxygenation, it should be evaluated to determine what factors may be decreasing
oxygenation, such as pain, pneumothorax(capnothorax), pneumoperitoneum, dislo-
cation of endotracheal tube, pulmonary embolism, atelectasis, or respiratory depres-
sion. If necessary, providing oxygen supplementation after recovery should be
considered.
ETCO2 should be monitored to check that the patient is adequately ventilating. If the
patient cannot maintain ETCO2 less than 50 mm Hg, it must be evaluated for factors
that can cause hypoventilation or airway obstruction. During anesthetic recovery, res-
piratory depression often occurs because of too much analgesic or sedative drugs. If a
drug is suspected of causing respiratory depression, it should be reversed if possible,
and reversal must be done carefully so as not to reverse the salutary effects (eg, anal-
gesia) of the drug.
SpO2 and ETCO2 should be measured early in the recovery period so that the anes-
thetist is aware of what these variables are after extubation. Once the patient becomes
too awake to keep it intubated, these variables often are difficult to monitor and may
not be reliable. Knowing how these variables are trending before extubation gives the
anesthetist confidence in assessing and managing the patient’s recovery. The cardio-
vascular system must be monitored during recovery, including ECG, heart rate, and
blood pressure. Again, these variables help the anesthetist assess the patient’s
recovery.
If the patient has cardiac disease, monitoring should extend for at least 24 hours af-
ter surgery. After general anesthesia, crackles or increased lung sounds are usually
auscultated because of intubation and dry air stimulating mucus production in the air-
ways. If the anesthetist has any concern regarding pulmonary edema, auscultation
should not be the single diagnostic tool and a chest radiograph should be taken.
SUMMARY
positive pressure ventilation, which requires intubation, are crucial during endo-
scopic surgery. Any sudden change of ETCO2 should be monitored closely because
this could indicate development of complications. Endoscopic surgery should be a
less invasive procedure; however, providing appropriate analgesia remains
necessary.
ACKNOWLEDGMENTS
John W. Ludders.
REFERENCES
1. Haque Z, Rahman M, Siddique MA, et al. Metabolic and stress responses of the
body to trauma: produced by the laparoscopic and open cholecystectomy.
Mymensingh Med J 2004;13:48–52.
2. Lee JY, Kim MC. Comparison of oxidative stress status in dogs undergoing lapa-
roscopic and open ovariectomy. J Vet Med Sci 2014;76:273–6.
3. Ravimohan SM, Kaman L, Jindal R, et al. Postoperative pulmonary function in
laparoscopic versus open cholecystectomy: prospective, comparative study. In-
dian J Gastroenterol 2005;24:6–8.
4. Joris JL, Hinque VL, Laurent PE, et al. Pulmonary function and pain after gastro-
plasty performed via laparotomy or laparoscopy in morbidly obese patients. Br J
Anaesth 1998;80:283–8.
5. Stevens HP, van de Berg M, Ruseler CH, et al. Clinical and financial aspects of
cholecystectomy: laparoscopic versus open technique. World J Surg 1997;21:
91–6.
6. Ros A, Gustafsson L, Krook H, et al. Laparoscopic cholecystectomy versus mini-
laparotomy cholecystectomy: a prospective, randomized, single-blind study. Ann
Surg 2001;234:741–9.
7. Arulpragasam SP, Case JB, Ellison GW. Evaluation of costs and time required for
laparoscopic-assisted versus open cystotomy for urinary cystolith removal in
dogs: 43 cases (2009-2012). J Am Vet Med Assoc 2013;243:703–8.
8. Safran DB, Orlando R 3rd. Physiologic effects of pneumoperitoneum. Am J Surg
1994;167:281–6.
9. Gutt CN, Oniu T, Mehrabi A, et al. Circulatory and respiratory complications of
carbon dioxide insufflation. Dig Surg 2004;21:95–105.
10. Fors D, Eiriksson K, Arvidsson D, et al. Gas embolism during laparoscopic
liver resection in a pig model: frequency and severity. Br J Anaesth 2010;
105:282–8.
11. Bille C, Auvigne V, Libermann S, et al. Risk of anaesthetic mortality in dogs and cats:
an observational cohort study of 3546 cases. Vet Anaesth Analg 2012;39:59–68.
12. Gupta A, Watson DI, Ellis T, et al. Tumour implantation following laparoscopy us-
ing different insufflation gases. ANZ J Surg 2002;72:254–7.
13. Wong YT, Shah PC, Birkett DH, et al. Peritoneal pH during laparoscopy is depen-
dent on ambient gas environment: helium and nitrous oxide do not cause perito-
neal acidosis. Surg Endosc 2005;19:60–4.
14. Richter S, Hückstädt T, Aksakal D, et al. Embolism risk analysis–helium versus
carbon dioxide. J Laparoendosc Adv Surg Tech A 2012;22:824–9.
15. Wahba RW, Béı̈que F, Kleiman SJ. Cardiopulmonary function and laparoscopic
cholecystectomy. Can J Anaesth 1995;42:51–63.
Anesthesia for Endoscopy 13
34. Madsen MV, Staehr-Rye AK, Gätke MR, et al. Neuromuscular blockade for opti-
mising surgical conditions during abdominal and gynaecological surgery: a sys-
tematic review. Acta Anaesthesiol Scand 2015;59:1–16.
35. Staffieri F, Lacitignola L, De Siena R, et al. A case of spontaneous venous embo-
lism with carbon dioxide during laparoscopic surgery in a pig. Vet Anaesth Analg
2007;34:63–6.
36. Feldman HS, Arthur GR, Covino BG. Comparative systemic toxicity of convulsant
and supraconvulsant doses of intravenous ropivacaine, bupivacaine, and lido-
caine in the conscious dog. Anesth Analg 1989;69:794–801.
37. Skarda RT, Tranquilli WJ. Local anesthetics. In: Tranquilli WJ, Thurmon JC,
Grimm KA, editors. Lumb & Jones veterinary anesthesia and analgesia. 4th edi-
tion. Ames (IA): Blackwell Publishing; 2007. p. 395–418.
38. Feierman DE, Kronenfeld M, Gupta PM, et al. Liposomal bupivacaine infiltration
into the transversus abdominis plane for postsurgical analgesia in open abdom-
inal umbilical hernia repair: results from a cohort of 13 patients. J Pain Res 2014;
16:477–82.
39. Owen RT. Bupivacaine liposome injectable suspension: a new approach to post-
surgical pain. Drugs Today (Barc) 2013;49:475–82.
40. Russo A, Di Stasio E, Scagliusi A, et al. Positive end-expiratory pressure during
laparoscopy: cardiac and respiratory effects. J Clin Anesth 2013;25:314–20.
41. Burcharth J, Burgdorf S, Lolle I, et al. Successful resuscitation after carbon diox-
ide embolism during laparoscopy. Surg Laparosc Endosc Percutan Tech 2012;
22:164–7.
42. Liska WD, Poteet BA. Pulmonary embolism associated with canine total hip
replacement. Vet Surg 2003;32:178–86.
43. Joris JL. Anesthesia for laparoscopic surgery. In: Miller RD, editor. Miller’s anes-
thesia. 6th edition. Philadelphia: Elsevier; 2005. p. 2285–306.
44. Myles PS. Bradyarrhythmias and laparoscopy: a prospective study of heart rate
changes with laparoscopy. Aust N Z J Obstet Gynaecol 1991;31:171–3.
45. Rist M, Hemmerling TM, Rauh R, et al. Influence of pneumoperitoneum and pa-
tient positioning on preload and splanchnic blood volume in laparoscopic sur-
gery of the lower abdomen. J Clin Anesth 2001;13:244–9.
46. Benumof JL. The position of a double-lumen tube should be routinely determined
by fiberoptic bronchoscopy. J Cardiothorac Vasc Anesth 1993;7:513–4.