PRIMER

Cardiovascular and Ventilatory Consequences

of Laparoscopic Surgery

ABSRACT: Although laparoscopic surgery accounts for >2 million surgical Tamara M. Atkinson, MD
procedures every year, the current preoperative risk scores and guidelines George D. Giraud, MD,
do not adequately assess the risks of laparoscopy. In general, laparoscopic PhD
procedures have a lower risk of morbidity and mortality compared with Brandon M. Togioka, MD
operations requiring a midline laparotomy. During laparoscopic surgery, Daniel B. Jones, MD
carbon dioxide insufflation may produce significant hemodynamic and Joaquin E. Cigarroa, MD
ventilatory consequences such as increased intraabdominal pressure and
hypercarbia. Hemodynamic insults secondary to increased intraabdominal
pressure include increased afterload and preload and decreased
cardiac output, whereas ventilatory consequences include increased
airway pressures, hypercarbia, and decreased pulmonary compliance.
Hemodynamic effects are accentuated in patients with cardiovascular
disease such as congestive heart failure, ischemic heart disease, valvular
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heart disease, pulmonary hypertension, and congenital heart disease.

Prevention of cardiovascular complications may be accomplished
through a sound understanding of the hemodynamic and physiological
consequences of laparoscopic surgery as well as a defined operative plan
generated by a multidisciplinary team involving the preoperative consultant,
anesthesiologist, and surgeon.

L
aparoscopic surgery accounts for >2 million surgical procedures per year in the
United States with cholecystectomy, appendectomy, colectomy, Roux-en-Y gas-
tric bypass, sleeve gastrectomy, and hysterectomy among the most performed.1
Although the overall mortality of laparoscopic surgery is low, ranging from 0.3% to
1.8%, preoperative consultation to estimate the risk of perioperative cardiovascu-
lar events is common.2,3 Laparoscopic surgery is frequently utilized in higher risk
patient groups, including the elderly, obese patients, and in those with preexisting
conditions, including cardiovascular and pulmonary diseases. Frequently used risk Correspondence to: Joaquin
assessment tools, such as the Revised Cardiac Risk Index, have not been validated E. Cigarroa, MD, Knight
Cardiovascular Institute,
in patients undergoing laparoscopic surgery.4 Newer scores have been studied in Cardiovascular Division, UHN-
patients undergoing open or laparoscopic surgery, such as the American College of 62, Oregon Health & Science
Surgeons’ National Surgical Quality Improvement Program Myocardial Infarction or University, 3181 SW Sam Jackson
Cardiac Arrest score, which accounts for differences in surgical procedures based Park Rd, Portland, OR 97239.
on organ system; analyses restricted to risk prediction in laparoscopic patients have Email Cigarroa@ohsu.edu
not been published.5 Furthermore, established cardiovascular risk calculators and Key Words: cardiovascular
American Heart Association/American College of Cardiology perioperative guidelines complications ◼ surgery
do not incorporate laparoscopic approach when characterizing operative risk.2 Al- © 2017 American Heart
though laparoscopic surgery has a lower risk of cardiovascular mortality compared Association, Inc.

700 February 14, 2017 Circulation. 2017;135:700–710. DOI: 10.1161/CIRCULATIONAHA.116.023262


with open surgery, one must understand the unique he-
modynamic and ventilatory effects that may increase the
risk of cardiovascular complications in high-risk popula-
tions, including congestive heart failure, ischemic heart
disease, valvular heart disease, congenital heart disease,
and pulmonary hypertension.6 By understanding the ef-
fects of abdominal insufflation during the different phases
of laparoscopic surgery, identification of patients at in-
creased risk is possible and discussion of approaches to
mitigate the risk may be entertained (Figure 1).
ABDOMINAL INSUFFLATION
(PNEUMOPERITONEUM)
Laparoscopic surgery begins with intraabdominal place-
ment of the insufflation needle or trochar, followed by
carbon dioxide (CO2) insufflation of the abdominal cavity
to an intraabdominal pressure (IAP) of 12 to 15 mm Hg.7,8
CO2 is an ideal gas for pneumoperitoneum secondary to
its low combustibility and high blood solubility, which de-
creases the risk of gas embolism (0.0014%–0.6%).9–13
Inadvertent placement of the trochar into a major ves-
sel or vessel injury can lead to blood loss and CO2 gas
embolism, which can result in cardiovascular collapse.
Transesophageal echocardiography (TEE) can be used
to assess the stage of gas embolism based on filling of
the right-sided heart chambers.14 Management of CO2,
embolism includes cessation of CO2, placement of the
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patient in the left lateral decubitus position, and adminis-
tration of 100% FiO2.15,16
The 2 main components of CO2 insufflation, which im-
pact the cardiovascular, respiratory, and renal systems,
Figure 1. Phases of laparoscopic surgery.
Laparoscopic surgery consists of 4 phases: induction of anesthesia, abdominal insufflation, abdominal desufflation, and recovery
from anesthesia. Each phase has unique hemodynamic and ventilatory changes. CI indicates cardiac index; CO, cardiac output;
HR, heart rate; MAP, mean arterial pressure; PCWP, pulmonary capillary wedge pressure; RAP, right atrial pressure; and SVR,
systemic vascular resistance.
Circulation. 2017;135:700–710. DOI: 10.1161/CIRCULATIONAHA.116.023262
Cardiovascular Effects of Laparoscopic Surgery
are increased IAP and hypercarbia (Figure 2).17,18 Human
and animal studies have demonstrated that hemodynam-
ic consequences of increased IAP are secondary to me-
chanical and neurohormonal responses.19 Elevated IAP
can lead to (1) inferior vena cava compression, (2) aortic
compression, (3) decreased splanchnic blood flow, (4)
decreased renal blood flow, and (5) diaphragmatic dis-
placement.20
Inferior vena cava compression from increased IAP
leads to complex changes in venous return and venous
resistance.17 In an experimental swine model, inferior
vena cava pressure parallels the increase in IAP, which
results in an initial rise in right atrial pressure (RAP),
which plateaus at an IAP of 15 mm Hg.21 The initial in-
crease in venous return results in an early rise in cardiac
output (CO) at an IAP of 5 mm Hg in normovolemic ani-
mals, but as IAP rises, venous return and CO levels de-
crease.17 The initial rise in venous return is secondary to
compression of the splanchnic vasculature, which shifts
blood volume into the central venous system.21 As IAP
STATE OF THE ART
further increases, venous return to the heart decreases
secondary to inferior vena cava compression and pool-
ing of venous blood in the lower extremities. In addition,
hepatic arterial and portal venous blood flow also de-
crease, which further reduces splanchnic blood flow and
redistributes blood volume into the central venous sys-
tem, contributing to the sustained elevation in RAP.22,23
Pneumoperitoneum increases mean arterial pressure
(MAP) and systemic vascular resistance (SVR) and may
decrease CO.24 Studies in healthy individuals have dem-
onstrated an abrupt rise in SVR and MAP within the first
5 minutes of abdominal insufflation caused by abdominal
aortic compression and neuroendocrine effects.20,24–27
February 14, 2017 701
 Atkinson et al
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Figure 2. Two components of laparoscopic surgery.
Detrimental effects of increased IAP and hypercarbia are listed. CO indicates cardiac output; GFR, glomerular filtration rate; IAP,
intraabdominal pressure; MAP, mean arterial pressure; PAP, pulmonary artery pressures; RAP, right atrial pressure; and SVR,
systemic vascular resistance.
Studies have demonstrated elevations in plasma nor-
epinephrine, epinephrine, cortisol, vasopressin, atrial
naturetic peptide, renin, and aldosterone levels.27 A re-
duction in renal blood flow, secondary to mechanical
compression of the renal arteries from increased IAP and
a decrease in cardiac output, stimulates renin release.24
Elevations in renin and aldosterone temporally correlate
with an increase in MAP.24 CO changes as IAP increases
during abdominal insufflation. Although the overall trend
is a reduction in CO when IAP is >15-20 mm Hg, a bipha-
sic response occurs with an early rise in CO secondary to
an increase in preload, followed by a reduction in CO as
a consequence of subsequent decreased venous return
and increased afterload.10,21,26,28 At an IAP of 7.5 mm Hg,
RAP, left atrial pressure (LAP), and CO all increase.21 As
IAP further increases to 15 mm Hg and 30 mm Hg, RAP
remains elevated, whereas LAP declines but remains
above baseline, and CO drops below baseline (Figure 3).21
702 February 14, 2017
This result defines the critical IAP threshold of 15 mm Hg
where further increases in IAP decrease CO.
TEE has provided additional insight into the cardio-
vascular consequences of increased IAP during laparo-
scopic surgery. TEE demonstrated within 3 minutes of
abdominal insufflation a significant rise in left ventricular
preload (left ventricular end diastolic diameter), afterload
(left ventricular end systolic wall stress), and a decrease
in cardiac function (fractional area shortening).29,30 These
changes, however, returned to baseline after 30 minutes
of insufflation in healthy individuals.25
Pneumoperitoneum has important effects on renal
physiology. Direct compression of the renal vasculature,
ureters, and kidneys can lead to a reduction in renal
blood flow, glomerular filtration rate, and oliguria.16,31,32
Although uncommon, laparoscopy poses an increased
risk of acute kidney injury in patients with chronic kidney
disease.31,33
Circulation. 2017;135:700–710. DOI: 10.1161/CIRCULATIONAHA.116.023262

Figure 3. Hemodynamic effects of IAP.
In an animal model, IAP was increased from 7.5 mm Hg to
15 mm Hg and 30 mm Hg, which was plotted on the X-axis.
As IAP increases, initial rises in RAP, LAP, and CO are seen at
an IAP of 7.5 mm Hg. As IAP increases, RAP elevation is sus-
tained and LAP declines but remains above baseline, whereas
CO declines and drops below baseline. The critical threshold
for the decline in LAP and CO occurs at 15 mm Hg, which is
represented by the dashed vertical line. The Y-axis on the left
defines the left and right atrial pressure in mm Hg. The Y-axis
on the right defines the CO in mL/min. CO indicates cardiac
output; IAP, intraabdominal pressure; LAP, left atrial pressure;
and RAP, right atrial pressure. Adapted from Kitano et al.21
©1999 The American Physiological Society (APS). All rights
reserved.
Abdominal insufflation impacts pulmonary function.
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As IAP increases, the diaphragm is displaced cephalad,
which is exacerbated in the Trendelenburg position.10
The upward diaphragmatic displacement along with in-
creased minute ventilation increase airway pressures.
Studies have demonstrated a reduction in pulmonary
compliance with a rise in peak and plateau airway pres-
sures along with reduction in functional residual capacity,
which can predispose to ventilation-perfusion mismatch,
leading to hypoxemia.8,10,12,29 The insufflation gas, CO2,
partitions into the blood, increasing circulating partial
pressure of CO2, which can be seen within 5 minutes
after abdominal insufflation in healthy individuals.10 In-
creased ventilatory rate is required to promote CO2 ex-
halation and maintain partial pressure of CO2 in or near
the normal range.12,34 If end-tidal CO2 (ETCO2) continues
to rise after 30 minutes, then subcutaneous emphysema
should be suspected.12,16,35 Subcutaneous emphysema
occurs in 0.43% to 2.3% secondary to gas extravasa-
tion into the subcutaneous tissue, which can lead to hy-
percarbia and acidosis.36 Risk factors for development
of subcutaneous emphysema include prolonged surgery
>3.5 hours, IAP >15 mm Hg, placement of cannulas out-
side the peritoneal cavity, disruption of fascial planes,
ETCO2 >50 mm Hg, use of >5 cannulas, and high gas
flow rates.36 Procedural surgical techniques to minimize
CO2 extravasation include securing the Hasson ports
and minimizing the number of tissue extractions through
Circulation. 2017;135:700–710. DOI: 10.1161/CIRCULATIONAHA.116.023262
Cardiovascular Effects of Laparoscopic Surgery
port sites. Management includes hyperventilation and, if
inadequate, abdominal deflation.
The 4 major pulmonary complications that can occur
with abdominal insufflation include hypercarbia, hypox-
emia, reduction in pulmonary compliance, and subcuta-
neous emphysema.37 Hypercarbia can cause systemic
vasodilatation, arrhythmias, myocardial depression, and
exacerbation of pulmonary hypertension.38 Therefore,
acceptable partial pressure of CO2 concentrations must
be maintained by increased minute ventilation to pro-
mote increased ventilatory CO2 exhalation.9,35
Abdominal insufflation stretches the peritoneum,
which increases vagal tone and can lead to bradyar-
rhythmias and asystole.16,39 In a young healthy popu-
lation, the incidence of bradyarrhythmias is 14%
to 27%.12 Many cardiac patients are prescribed β-
blockers, which increase the risk for bradyarrhyth-
mias.2,40 Slower insufflations, lower IAP, and premedi-
cation with glycopyrrolate can attenuate the vagal
response and prevent cardiovascular collapse.16,41,42 If
STATE OF THE ART
bradycardia occurs, then the surgeon must open the
ports to decrease IAP. After a fluid bolus and discus-
sion between the surgeon and anesthesiologist, a sec-
ond attempt at insufflation with a lower IAP is usually
safe. The inability to tolerate pneumoperitoneum may
require conversion to open laparotomy. Bradycardia
must be recognized and treated promptly because this
condition can be an early predictor of cardiac arrest,
which occurs infrequently.43
Abdominal Desufflation and Recovery
Desufflation, removal of CO2 from the abdomen, and re-
covery are the final phases of anesthesia. Despite desuf-
flation, minute ventilation requirements remain elevated,
as <120 L of CO2 can remain stored in the body. CO2
is eliminated by the lungs and renal proton excretion.44
In the presence of significant hypercarbia, the anesthe-
siologist should determine the optimal timing of extu-
bation to ensure adequate removal of CO2. Incomplete
CO2 removal can lead to significant postoperative pain,
which is sometimes referred to the left shoulder, mim-
icking cardiac chest pain.45,46 In healthy individuals, he-
modynamics return to baseline immediately after desuf-
flation, whereas in patients with cardiovascular disease,
they may persist for ≥65 minutes.29,47 In elderly patients
with cardiovascular disease, desufflation has been as-
sociated with an increase in heart rate (HR), cardiac in-
dex, left ventricular stroke work index, ejection fraction,
and decrease in SVR.47,48 In patients with cardiovascular
disease undergoing laparoscopic surgery, 2 in 10 pa-
tients developed heart failure within 3 hours after the
procedure.47 Those patients who developed heart failure
had a significant reduction in cardiac index (to 65% of
baseline), left ventricular stroke work, and stroke vol-
ume. Therefore, it is essential to monitor for symptoms
February 14, 2017 703
 Atkinson et al
of myocardial ischemia and heart failure in the period
immediately after surgery.
HEMODYNAMIC EFFECTS OF PROCEDURAL
AND PATIENT CHARACTERISTICS
Patient Positioning
Trendelenburg (head down) or reverse Trendelenburg
(head up) position provides optimal visualization of the
surgical field. The Trendelenburg position is necessary
for visualization of the lower abdomen and pelvis dur-
ing gynecological or urological procedures, whereas re-
verse Trendelenburg position is used for upper abdomi-
nal surgeries (Table 1).
In the Trendelenburg position, the diaphragm and
abdominal contents move cephalad, which reduce
pulmonary compliance and increase peak airway pres-
sures. While pulmonary compliance is compromised,
the Trendelenburg position increases venous return
and pulmonary capillary wedge pressure (PCWP),
which prevents the decline in CO after abdominal in-
sufflation.7,8,26,27 The neuroendocrine response to the
Trendelenburg position is notable for an increase in
noradrenaline levels and an increase in plasma NT-
proANP (N-terminal proatrial natriuretic peptide), which
suggests increased atrial stretch caused by increased
venous return.27
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The reverse Trendelenburg position produces favor-
able ventilatory changes yet unfavorable cardiovascular
changes.7 Along with increased IAP for insufflation, the
head-up position decreases venous return, which reduc-
es RAP, PCWP, and CO.8,26,27,30 Plasma noradrenaline lev-
els are elevated by the reverse Trendelenburg position,
which increases SVR and further reduces CO.27
With the hemodynamic changes seen during laparo-
scopic surgery, it is important to assess the patient’s
intravascular fluid volume status during preoperative
Table 1. Hemodynamic Effects of Patient Positioning
and Intravascular Fluid Volume Status
Variable RAP PCWP CO/CI SVR PC PAP
Patient position
Trendelenburg ↑ ↑ ↑ ↑
Reverse Trendelenburg ↓ ↓ ↓ ↑↑
Intravascular fluid volume
status
Hypovolemia ↓ ↓ ↓ ↑
Hypervolemia ↑ ↑ ↑ ↑
CO/CI indicates cardiac output/cardiac index; NH, neurohormones; PAP,
pulmonary artery pressure; PC, pulmonary compliance; PCWP, pulmonary
capillary wedge pressure; RAP, right atrial pressure; and SVR, systemic
vascular resistance.
704 February 14, 2017
evaluation (Table 1). Intravascular fluid volume status can
attenuate or accentuate the hemodynamic consequenc-
es of laparoscopic surgery. Venous return and ventricu-
lar preload are key determinants of CO.21 Studies show
that after the initial increase in CO as IAP increases, CO
decreases. The decrease in CO is accentuated by hypo-
volemia and attenuated by hypervolemia.17,49 Minimizing
the duration of fasting, adequate preoperative hydration,
and the use of IAP <15 mm Hg may reduce the decrease
in CO.
Special Patient Populations
It is critical to identify patients who are vulnerable to ad-
verse hemodynamic and ventilatory changes to create
a comprehensive operative plan with the preoperative
consultant, anesthesiologist, and surgeon. Laparoscopic
surgery increases preload and afterload and decreases
CO. These changes are accentuated or attenuated by
intraoperative patient positioning, intravascular fluid vol-
ume status, and underlying cardiovascular conditions
such as congestive heart failure, ischemic heart dis-
ease, valvular heart disease, congenital heart disease,
pulmonary disease, and obesity (Table 2).50 In patients
with cardiovascular disease, laparoscopic surgery can
cause substantially higher elevations in RAP and PCWP
and a decrease in CO.47 Mechanisms to counterbalance
these changes should be identified preoperatively, in-
cluding adequate hydration, positioning, use of lowest
IAP feasible, and hemodynamic monitoring.16
Congestive Heart Failure
In patients with decreased contractile reserve, conges-
tive heart failure can be precipitated by increases in
IAP, which increase preload (RAP, PCWP) and afterload
(SVR).8,25,26,30 Patients with heart failure may be unable
to compensate, leading to further reductions in CO, hy-
potension, and cardiogenic shock.19 This outcome can
be mitigated with preoperative intravascular fluid vol-
ume status optimization, appropriate heart failure medi-
cations, and limiting IAP to <15 mm Hg. Hypertension
must be managed perioperatively with vasodilators to
optimize left ventricular workload during pneumoperito-
neum.42 Desufflation of the abdomen does not lead to
↓ ↑ immediate recovery of baseline hemodynamics.47 There-
↑ ↓ fore, it is critical to monitor for cardiovascular decom-
pensation in the immediate postoperative period, with
close attention to blood pressure, HR, intravascular fluid
volume status, and urine output, with early intervention
↓
provided when necessary.
↑
Ischemic Heart Disease
Surgery, including laparoscopy, causes inflammation,
hypercoagulability, and pain, which increase the risk for
Circulation. 2017;135:700–710. DOI: 10.1161/CIRCULATIONAHA.116.023262
 Cardiovascular Effects of Laparoscopic Surgery

Table 2. Special Cardiovascular Disease Populations

Hemodynamic Changes
With Laparoscopic Potential Pre-Op Peri-op Post-op
Patient Population Surgery Complications Management Management Management
Congestive heart ↑ RAP, ↑ SVR, ↑ PCWP, ↓ CO Pulmonary Diuresis to euvolemia, ↓ afterload, Monitor volume status,
failure edema, optimization of CHF IAP <15 mm Hg early diuresis
cardiogenic medications
shock
Valvular heart disease
Aortic ↑ SVR, ↓ CO Increased valvular Goal SBP <140 ↓ afterload Goal SBP <140
regurgitation regurgitation, monitor volume status
↓ CO
Aortic stenosis ↑ RAP, ↑ SVR, ↑ PCWP, ↓ CO Myocardial Avoid hypovolemia Avoid vasodilators, Monitor volume status
ischemia, HR 60–90,
cardiovascular phenylephrine prn
collapse hypotension
Mitral ↑ SVR,↑ PCWP, ↓ CO Increased valvular Goal SBP <140 ↓ afterload Goal SBP <140,
regurgitation regurgitation, ↓ monitor volume status
CO, pulmonary

STATE OF THE ART

edema
Mitral stenosis ↑ SVR, ↑ PAP, ↑ PCWP, ↑ HR Pulmonary HR<70, NSR HR<70, NSR, HR<70, NSR, monitor
edema and heart adequate preload, volume status
failure, ↓ CO avoid N2O
Tricuspid ↑ RAP, ↑ PVR Increased valvular Monitor volume status
regurgitation regurgitation,
↓ CO
Ischemic heart disease
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Acute coronary ↑ inflammation & Peri/postoperative Continue aspirin if Continue β-blockers Continue aspirin
thrombosis hypercoagulable state myocardial previous coronary
infarction stent
Myocardial ↑ SVR, ↑ LVEDP, HR Peri/postoperative Continue β-blockers Humidified Double product control
supply-demand variability myocardial peritoneal gas to (HR/BP),
ischemia infarction reduce postop pain pain management
Bradyarrhythmias ↑ IAP, ↑ CO2 Asystole Slow insufflation;
consider atropine
or glycopyrrolate
preinsufflation if
resting bradycardia
Congenital heart disease
Cyanotic heart ↑ RAP, ↑ PVR, ↓ CO ↓ CO, R→L Measure arterial CO2 Measure arterial CO2
disease shunt, hypoxemia
Fontan/surgical ↑ RAP, ↑ PVR, ↓ CO Shunt thrombosis Minimize PEEP
shunts
ASD/PFO ↑ RAP, ↑ PVR, ↓ CO Hypoxemia, Consider TEE for
R→L shunt, shunt monitoring
paradoxical
embolism
Other conditions
COPD ↑ peak and plateau airway Acidosis, Avoid steep
pressures, ↑ CO2 bullae rupture, Trendelenburg
subcutaneous angles
emphysema,
pneumothorax
(Continued )

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 Atkinson et al

Table 2. Continued
Hemodynamic Changes
With Laparoscopic Potential Pre-Op Peri-op Post-op
Patient Population Surgery Complications Management Management Management
Pulmonary ↑ CO2 → pulmonary Right ventricular Pulmonary
hypertension vasoconstriction failure vasodilators*,
avoid acidosis, avoid
N2O
Chronic kidney ↓ GFR, ↓ RBF Oliguria, acute Avoid hypolemia IAP <15 mm Hg Monitor UOP
disease renal failure
Morbid obesity Diaphragmatic displacement, Acidosis, higher Avoid steep Avoid early extubation,
high baseline IAP, increased ventilation Trendelenburg extubate to CPAP/
airway pressures, ↑ CO2, ↓ requirements angles. BiPAP
pulmonary compliance sequential
compression devices
ASD indicates atrial septal defect; CHF, congestive heart failure; CO, cardiac output; CO2, carbon dioxide; COPD, chronic obstructive pulmonary disease;
GFR, glomerular filtration rate; HR, heart rate; IAP, intraabdominal pressure; LVEDP, left ventricular end diastolic pressure; N2O, nitrous oxide; NSR,
normal sinus rhythm; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PEEP, positive end expiratory pressure; PFO, patent
foramen ovale; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RBF, renal blood flow; SBP, systolic blood pressure; SVR, systemic vascular
resistance; TEE, transesophageal echocardiogram; and UOP, urine output.
*Milrinone, nitric oxide, iloprost.

myocardial ischemia.51 Although the overall incidence of
myocardial ischemia and infarction during laparoscopic
surgery is low, it is not well defined in the literature, with
limited studies in the elderly reporting myocardial infarc-
tion in 0.3% to 0.6% of patients.52,53 Myocardial isch-
emia is precipitated by increases in myocardial oxygen
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verity of regurgitation in 93% secondary to changes
in both preload and afterload.56 Left-sided regurgitant
lesions may lead to decreased CO and pulmonary
edema, which can precipitate myocardial ischemia in
patients with ischemic heart disease.56 In patients with
left-sided regurgitant valve lesions, preoperative anti-

demand, which can be amplified during laparoscopic
surgery secondary to increases in HR, MAP, SVR, and
left ventricular end systolic wall stress.29 Hypercarbia
impairs hemoglobin affinity and oxygen transport, which
may contribute to myocardial ischemia.45,54 The exist-
ing literature does not provide specific data on whether
ischemic events are lower in patients treated with lapa-
roscopic procedures.
Optimal β-blockade before surgery and during the
perioperative period can prevent myocardial ischemia
in patients with ischemic heart disease who are chroni-
cally on β-blockers. It may be reasonable to start β-
blockers preoperatively in patients with intermediate- to
high-risk ischemia on stress test or an Revised Cardiac
Risk Index score of >3, but they should not be started
the day of surgery because of increased risk of stroke,
hypotension, bradycardia, and death.2,16,40 Peri- and
postoperative pain predispose patients to myocardial
ischemia and should be mitigated with adequate anal-
gesia.2,55
Valvular Heart Disease
Regurgitant valve lesions lead to volume overload,
whereas stenotic valve lesions lead to pressure over-
load. In patients with trace-mild tricuspid or mitral
regurgitation, abdominal insufflation increases the se-
hypertensive medication titration is essential to avoid
systolic hypertension, whereas perioperative care fo-
cuses on afterload optimization and maintenance of
adequate preload to maintain forward CO.2 Stenotic
valve lesions such as aortic stenosis (AS) and mitral
stenosis can substantially impact the hemodynamic
changes as IAP increases. Left ventricular hypertro-
phy, decreased ventricular compliance, and suben-
docardial myocardial ischemia associated with AS
make the left ventricle more sensitive to changes in
afterload and preload.57 Induction of anesthesia is a
critical time point for AS secondary to the vasodilatory
effects of anesthesia. In patients with AS, hypoten-
sion and subsequent reduction in coronary perfusion
pressure should be avoided. Perioperative vulnerability
secondary to hypotension and tachycardia can lead to
cardiovascular collapse. Intraoperative hemodynamic
monitoring with arterial line placement and TEE is pre-
ferred, but pulmonary artery catheter placement may
be considered in selective high-risk patients.2 Obstruc-
tion to blood flow makes patients with mitral stenosis
sensitive to changes in HR, LAP, and pulmonary artery
pressures during laparoscopic surgery. Perioperative
management of HR with β-blockers is essential to
maintain optimal diastolic filling time preventing further
elevations in LAP, which in turn can cause pulmonary
edema in patients with mitral stenosis. Pre-operative

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evaluation should identify patients with valvular heart
disease and optimize intravascular fluid volume status,
HR, and systemic arterial pressure. Perioperative man-
agement must avoid hypotension in AS, tachycardia in
mitral stenosis, and increased afterload in left-sided
regurgitant valve lesions.
Congenital Heart Disease
Adults with previous heart surgery from congenital or
early acquired heart disease undergoing noncardiac
surgery have a higher morbidity and mortality com-
pared with age-matched controls.58 Patients with con-
genital heart disease, especially those with cyanotic
heart disease and Fontan, are vulnerable to hemody-
namic changes during abdominal insufflation second-
ary to decreased venous return, hypercarbia, which
can increase pulmonary vascular resistance, and in-
creased airway pressures, which decrease pulmonary
blood flow.59 The cumulative effect of increased IAP,
positive pressure ventilation, and reverse Trendelen-
burg position in patients with Fontan or surgical shunts,
can be devastating secondary to decreased CO and
an increased risk of shunt thrombosis.59,60 Elevations
in pulmonary vascular resistance can have significant
consequences with decreased pulmonary blood flow
and increased right-to-left shunting.61 Perioperative
management of patients with Fontan includes less
steep Trendelenburg position angles, lower abdomi-
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nal insufflation pressures <12 mm Hg, and minimized
intrathoracic pressure through intermittent positive
pressure ventilation.62 Because of the critical nature of
patients with Fontan and cyanotic hearts, a multidisci-
plinary approach involving a congenital heart special-
ist, anesthesiologist, and surgeon should outline crite-
ria for termination of procedure, conversion to open
surgery, and management of cardiovascular collapse.
ETCO2 monitoring is not accurate in patients with cya-
notic heart disease, and therefore arterial blood gas
monitoring of CO2 with an arterial line rather than
ETCO2 is essential.60 Another vulnerable population
includes patients with an atrial septal defect, patent
foramen ovale or fenestrated Fontans, which predis-
poses to right-to-left shunting causing hypoxemia or
paradoxical CO2 gas embolism.63 Subclinical CO2 gas
embolism was seen in 17.1% of patients without an
atrial septal defect or patent foramen ovale because
of placement of the insufflation needle into the venous
system or injured vessels within the peritoneum.11 El-
evations in RAP greater than PCWP lead to right-to-left
shunting during all phases of laparoscopy, especially
in the Trendelenburg position.64 Minimizing positive end
expiratory pressure and administering inhaled nitric ox-
ide to lower pulmonary vascular resistance and RAP
reduces the RAP-LAP gradient decreasing right-to-left
shunt.65 CO2 gas embolism can be avoided by careful
Circulation. 2017;135:700–710. DOI: 10.1161/CIRCULATIONAHA.116.023262
Cardiovascular Effects of Laparoscopic Surgery
insertion of the needle into the peritoneum and slower
abdominal insufflation. In the period after surgery, un-
explained hypoxemia not reversible with 100% oxygen
should trigger an evaluation for atrial septal defect/
patent foramen ovale. TEE can be performed intraop-
eratively to monitor for shunts in patients at risk.
Chronic Obstructive Pulmonary Disease
and Pulmonary Hypertension
Respiratory compromise can occur during laparoscopic
surgery in patients with chronic obstructive pulmonary
disease and pulmonary hypertension. Pneumoperito-
neum further exacerbates pulmonary hypertension by
increases in pulmonary vascular resistance, which can
be attenuated with perioperative pulmonary vasodila-
tors such as inhaled nitric oxide, iloprost, or milrinone.
Patients with chronic obstructive pulmonary disease
can have significant ventilation-perfusion mismatch,
which leads to abnormal gas exchange and consequent
STATE OF THE ART
hypoxemia and hypercarbia, especially in those with
baseline hypercarbia.12 The inability to compensate for
arterial CO2 elevation can precipitate significant acido-
sis, which can lead to cardiovascular and respiratory
collapse; therefore, hyperventilation after intubation is
required.35 If acidosis develops and cannot be reversed,
then the procedure may need to be converted to open
laparotomy. Special care must be given to patients with
severe chronic obstructive pulmonary disease because
higher airway pressures are required to ventilate pa-
tients during laparoscopy, predisposing patients to bul-
lae rupture.
Morbid Obesity
Given the obesity epidemic, the number of laparoscop-
ic bariatric surgeries has increased.66 Morbid obesity
is associated with comorbidities, including restrictive
lung disease, diabetes mellitus, obesity hypoventila-
tion syndrome, obstructive sleep apnea, and chroni-
cally elevated IAP. Studies have demonstrated similar
cardiovascular and respiratory perturbations in mor-
bidly obese patients undergoing laparoscopic surgery
compared with nonobese patients.66 However, morbid-
ly obese patients have lower respiratory compliance
and higher peak airway pressures requiring higher
minute ventilation to maintain normocarbia compared
with nonobese individuals, with further reduction in re-
spiratory compliance with pneumoperitoneum.67 Simi-
lar cardiovascular effects of pneumoperitoneum are
seen but are less pronounced because of the chroni-
cally elevated IAP of 9 to 10 mm Hg in morbidly obese
patients.66,68 Venous stasis and risk of thrombosis are
higher in morbidly obese patients and are exacerbated
because of decreased femoral venous blood flow from
increased IAP.66
February 14, 2017 707
 Atkinson et al
CONCLUSIONS
Preoperative consultation to determine perioperative
cardiovascular risk remains an integral component
of consultative cardiovascular medicine. Current risk
scores have not been validated in patients undergoing
laparoscopic surgery. Newer indications and procedures
have increased the number of patients treated laparo-
scopically while maintaining an overall lower risk profile
than open surgery. Despite the lower risk, understanding
the unique hemodynamic and ventilatory consequences
of laparoscopic surgery is essential to identify vulner-
able populations at risk of cardiovascular complications.
Increased IAP and hypercarbia are the main components
leading to hemodynamic changes during laparoscopic
surgery. Prevention of cardiovascular catastrophes can
be accomplished by:
1. Understanding the hemodynamic and physiologi-
cal consequences of laparoscopic surgery.
2. Optimizing preoperative intravascular fluid volume
status to avoid hypovolemia.
3. Utilizing slow abdominal insufflation with maximum
IAP of <15 mm Hg coupled with minimized dura-
tion of extreme patient positioning.16
4. Hemodynamic monitoring with direct arterial line
and TEE placement in selected high-risk individuals.
5. Placing an arterial line for monitoring of partial
pressure of CO2 in patients whom ETCO2 may be
unreliable.
Downloaded from http://ahajournals.org by on August 4, 2023
6. Applying a team-based approach among the preop-
erative consultant, anesthesiologist, and surgeon
to determine the intraoperative plan to mitigate
cardiovascular risk.
DISCLOSURES
None.
AFFILIATIONS
From Knight Cardiovascular Institute (T.M.A., G.D.G.), Depart-
ment of Anesthesiology and Perioperative Medicine (B.M.T.),
Oregon Health and Science University, Portland; Division
of Cardiology, Portland VA Medical Center, Oregon (T.M.A.,
G.D.G.); and Beth Israel Deaconess Medical Center, Harvard
University, Boston, MA (D.B.J.).
FOOTNOTES
Circulation is available at http://circ.ahajournals.org.
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