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Anesthesia for coronary artery bypass grafting surgery - UpToDate
Official reprint from UpToDate®
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Anesthesia for coronary artery bypass grafting surgery
AUTHOR: Atilio Barbeito, MD, MPH
SECTION EDITOR: Jonathan B Mark, MD
DEPUTY EDITOR: Nancy A Nussmeier, MD, FAHA
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jun 2023.
This topic last updated: Jun 30, 2022.
INTRODUCTION
Coronary artery bypass grafting (CABG) is the most commonly performed cardiac surgical
procedure in the United States [1]. Anesthetic planning depends partially on the expected
surgical approach to revascularization. CABG is typically performed via a midline sternotomy
incision with the aid of cardiopulmonary bypass (CPB). In selected patients, off-pump coronary
artery bypass (OPCAB) without CPB may be accomplished via either a full sternotomy or a small
anterior left thoracotomy incision, termed a minimally invasive direct coronary artery bypass
(MIDCAB) approach.
This topic will discuss anesthetic management of patients undergoing on-pump or off-pump
CABG surgery.
General considerations during the perioperative period for patients undergoing cardiac surgical
procedures and cardiopulmonary bypass are also reviewed separately:
● Preoperative considerations (See "Preoperative evaluation for anesthesia for cardiac
surgery".)
● Prebypass considerations
• (See "Anesthesia for cardiac surgery: General principles", section on 'Monitoring'.)
• (See "Anesthesia for cardiac surgery: General principles", section on 'Induction of
general anesthesia'.)
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• (See "Anesthesia for cardiac surgery: General principles", section on 'Maintenance of
general anesthesia'.)
• (See "Anesthesia for cardiac surgery: General principles", section on 'Preparations for
cardiopulmonary bypass'.)
● Cardiopulmonary bypass
• (See "Initiation of cardiopulmonary bypass".)
• (See "Management of cardiopulmonary bypass".)
• (See "Weaning from cardiopulmonary bypass".)
● Postbypass considerations
• (See "Anesthesia for cardiac surgery: General principles", section on 'Management
during the postbypass period'.)
• (See "Intraoperative problems after cardiopulmonary bypass".)
PREBYPASS PERIOD
The key steps that must be completed in the prebypass period are listed in the table and are
discussed in a separate topic (
table 1). (See "Anesthesia for cardiac surgery: General
principles".)
The following sections note specific management considerations during the prebypass period
for patients undergoing coronary revascularization.
Avoidance and treatment of ischemia — It is particularly important to detect, prevent, and
treat myocardial ischemia throughout the prebypass period.
Monitoring for ischemia — We simultaneously and continuously monitor the
electrocardiogram (ECG) to detect ST-segment depression or elevation and the transesophageal
echocardiogram (TEE) to detect new regional wall motion abnormalities (RWMAs) (eg,
hypokinesis or akinesis). Also, elevations in right or left ventricular (LV) filling pressures (eg, the
central venous pressure [CVP] or the pulmonary artery wedge pressure [PAWP]) may indicate
ischemia. These commonly employed monitoring modalities to detect ischemia have varying
degrees of sensitivity and specificity [2]. (See "Anesthesia for cardiac surgery: General principles",
section on 'Monitoring'.)
We conduct an initial comprehensive prebypass TEE examination , followed by continuous use of
the TEE to monitor for ischemia, as well as monitoring ventricular function and volume [3-5].
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Regional wall motion abnormalities indicating ischemia (
figure 1 and
figure 2), as well as
global left and right ventricular function are assessed. Details are described in a separate topic.
(See "Anesthesia for cardiac surgery: General principles", section on 'Monitoring with
transesophageal echocardiography' and "Anesthesia for cardiac surgery: General principles",
section on 'Initial transesophageal echocardiography examination'.)
Maintaining hemodynamic goals — Myocardial oxygen (O2) supply is determined by the
oxygen content in the blood (hemoglobin level and saturation) and by coronary blood flow.
Myocardial O2 demand is determined by factors that influence myocardial work (heart rate,
myocardial wall stress, and contractility). (See "Angina pectoris: Chest pain caused by fixed
epicardial coronary artery obstruction", section on 'Pathophysiology of myocardial ischemia'.)
Hemodynamic and physiologic goals are prevention of ischemia by providing optimal myocardial
O2 supply and minimizing demand (
table 2). (See "Anesthesia for noncardiac surgery in
patients with ischemic heart disease", section on 'Prevention of ischemia' and "Anesthesia for
noncardiac surgery in patients with ischemic heart disease", section on 'Treatment of ischemia'.)
Specific hemodynamic goals include:
● Blood pressure (BP) is maintained within 20 percent of baseline (typically, a mean arterial
BP 75 to 95 mmHg and/or diastolic BP 65 to 85 mmHg).
● A low to normal heart rate (HR) (eg, 50 to 80 beats per minute [bpm]) is maintained.
Tachycardia compromises both oxygen supply and demand (
figure 3).
● Tachycardia with hypotension is typically treated by administering bolus doses of a pure
alpha-1 agonist agent (eg, phenylephrine 50 to 100 mcg boluses or a phenylephrine
infusion (
table 3)) to restore normal blood pressure.
● Tachycardia with hypertension is treated by increasing anesthetic depth (eg, administering
a bolus dose of a rapid-acting opioid such as fentanyl 50 to 250 mcg or propofol 10 to 50
mg, or increasing the concentration of a volatile anesthetic agent) if the likely cause is pain
or inadequate anesthesia. If anesthetic agents are not effective, small boluses of a beta
blocker (eg, esmolol, metoprolol, or labetalol) or an infusion of nitroglycerin are typically
administered (
table 4).
● Fluid administration is restricted, which helps to avoid fluid overload with resultant LV
distention and increased wall stress. (See "Anesthesia for cardiac surgery: General
principles", section on 'Prebypass fluid management'.)
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Induction and maintenance of general anesthesia — The goals of general anesthetic
induction and maintenance are to produce and maintain unconsciousness, attenuate the
hemodynamic responses to endotracheal intubation and surgical stimulation, and prevent or
treat hemodynamic changes that lead to myocardial oxygen imbalance and ischemia.
Hemodynamic manipulation is typically required in patients with ischemic heart disease to
achieve a simultaneous state of unconsciousness while maintaining a favorable myocardial
oxygen balance. Severe pain and endogenous catecholamine release during initial incision and
subsequent sternotomy necessitate adequate depth of general anesthesia to prevent
tachycardia and hypertension. Subsequently, it is appropriate to reduce anesthetic doses to
avoid hypotension during the periods of reduced surgical stimulation that typically follow
sternotomy. (See "Anesthesia for cardiac surgery: General principles", section on 'Induction of
general anesthesia' and "Anesthesia for cardiac surgery: General principles", section on
'Maintenance techniques'.)
Positioning — After sternotomy, placement of a sternal retractor is necessary for harvesting the
internal thoracic or internal mammary artery (IMA) (see 'Incision, sternotomy, and harvesting of
venous and arterial grafts' below). Retractor positioning is closely observed since the steel post
attaching it to the operating table may compress the upper arm causing radial nerve injury, and
may also be associated with brachial plexus injury [6-8]. In addition, when the retractor lifts the
sternum, the patient's head may be lifted off the supporting head cushion, particularly in an
older patient who has cervical spine arthritis. If this occurs, the retractor should be adjusted or
the patient's head should be repositioned with additional pillow support.
Other positioning considerations are discussed in a separate topic. (See "Anesthesia for cardiac
surgery: General principles", section on 'Patient positioning'.)
Incision, sternotomy, and harvesting of venous and arterial grafts — Incision, sternotomy,
harvesting of peripheral vein(s) and/or a peripheral artery, dissection to free the IMA from the
chest wall, and exposure of the heart and great vessels are the fundamental surgical steps that
precede aortic and venous cannulation.
CARDIOPULMONARY BYPASS
Initiation, management, and weaning from cardiopulmonary bypass (CPB) are discussed in
separate topics:
● (See "Initiation of cardiopulmonary bypass".)
● (See "Management of cardiopulmonary bypass".)
● (See "Weaning from cardiopulmonary bypass".)
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POSTBYPASS PERIOD
Key steps for any cardiac surgical procedure in the period immediately after cardiopulmonary
bypass (CPB) include venous and arterial decannulation, reversal of anticoagulation with
protamine administration, insertion of temporary or backup epicardial pacing wires, and
reinfusion of pump blood (
table 1).
Hemodynamic stability must be maintained after weaning from CPB. Cardiovascular problems
that result in hypotension are identified and treated (
table 5 and
table 3). (See
"Intraoperative problems after cardiopulmonary bypass", section on 'Cardiovascular problems'.)
Recognition and management of other intraoperative problems that may occur during the
postbypass period are discussed separately. (See "Intraoperative problems after
cardiopulmonary bypass".)
Postbypass transesophageal echocardiography — Transesophageal echocardiography (TEE)
examination immediately after coronary artery bypass grafting (CABG) surgery emphasizes the
following aspects [3,4,9]:
● Global left ventricular (LV) and right ventricular (RV) function are evaluated.
● LV regional wall motion abnormalities (RWMAs) are documented as part of the overall
assessment of the adequacy of revascularization in territories of myocardium perfused by
each of the major coronary arteries supplying the LV (
figure 1 and
figure 2).
Previously ischemic or hibernating myocardium may show improved function in the early
postbypass period. However, myocardial stunning is common and consequently,
myocardial segments that had abnormal contraction in the prebypass period may remain
impaired even after adequate coronary blood flow has been restored.
Significant deterioration of regional wall motion in previously normal myocardial segments
may indicate a technical problem with a coronary graft (eg, poor quality of a bypass graft
anastomosis, kinking, vasospasm, or embolization of air or microparticulate debris into the
graft) (
movie 1). Poor graft flow can be confirmed by a Doppler flow probe applied to the
graft. ST-segment changes on the electrocardiogram (ECG) or hypotension with low cardiac
output may also be noted. Detection of such problems allows surgical correction prior to
leaving the operating room. (See "Intraoperative problems after cardiopulmonary bypass",
section on 'Surgical or technical problems'.)
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In patients who require ventricular pacing after CPB, a distinct septal motion abnormality
termed "septal bounce" is often observed; this occurs due to the abnormal pattern of
ventricular depolarization that accompanies RV epicardial pacing (
movie 2). Septal
bounce can be distinguished from a true RWMA because septal thickening persists during
ventricular pacing but is absent when the septum is ischemic. If this is difficult to discern
visually, a brief pause in ventricular pacing may be helpful.
New or worsening mitral regurgitation (MR) in the postbypass period should prompt a
thorough evaluation for LV RWMAs indicating an ischemic cause of the MR.
● LV and RV chamber sizes are assessed to determine intravascular volume status
(
movie 3). This is important because CVP and PAP measurements are poor predictors of
intravascular volume and fluid responsiveness [10]. (See "Intraoperative transesophageal
echocardiography for noncardiac surgery", section on 'Volume status'.)
● Hypotension after myocardial revascularization may occasionally be caused by dynamic left
ventricular outflow tract (LVOT) obstruction with systolic anterior motion (SAM) of the mitral
valve anterior leaflet [11].
● If aortic dissection is suspected following decannulation (eg, in a patient with a calcific or
diffusely atheromatous ascending aorta, or one who develops postbypass hypotension that
is unresponsive to treatment), the ascending aorta is evaluated to identify this potentially
fatal complication (
image 1).
● Adequacy of any additional surgical repair (eg, repair or replacement of a cardiac valve) is
assessed.
Additional considerations for the postbypass TEE examination are discussed separately. (See
"Anesthesia for cardiac surgery: General principles", section on 'Postbypass transesophageal
echocardiography'.)
TEE is also used for continuous monitoring throughout the postbypass period to assess
ventricular volume and function, and to detect development of hypovolemia, hypervolemia, or
low systemic vascular resistance [4]. (See "Anesthesia for cardiac surgery: General principles",
section on 'Monitoring with transesophageal echocardiography'.)
Transport and handoff in the intensive care unit — Preparations, transport, and handoff in
the intensive care unit are addressed separately. (See "Handoffs of surgical patients", section on
'Operating room to intensive care unit' and "Anesthesia for cardiac surgery: General principles",
section on 'Transport and handoff in the intensive care unit'.)
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Further details regarding postoperative complications after on-pump or off-pump CABG surgery
are addressed in the following topics [12]:
● (See "Early cardiac complications of coronary artery bypass graft surgery".)
● (See "Early noncardiac complications of coronary artery bypass graft surgery".)
● (See "Off-pump and minimally invasive direct coronary artery bypass graft surgery: Clinical
use".)
OFF-PUMP CORONARY ARTERY BYPASS SURGERY
General considerations — Off-pump coronary artery bypass graft surgery (OPCAB) refers to
coronary artery bypass grafting (CABG) without the use of cardiopulmonary bypass (CPB). This
technique avoids potential morbidity associated with aortic cannulation and cross-clamping (eg,
embolism of aortic plaque with consequent stroke), and with use of CPB (eg, systemic
inflammatory response, platelet activation, fibrinolysis, bleeding, vasodilatory shock). (See
"Intraoperative problems after cardiopulmonary bypass".)
Outcomes such as death, cardiovascular events, and need for revascularization are no better and
may be worse in many patients undergoing OPCAB compared to on-pump CABG [13-15] (see
"Off-pump and minimally invasive direct coronary artery bypass graft surgery: Clinical use",
section on 'Outcomes'). However, OPCAB is often selected for patients at high risk for stroke due
to extensive atheromatous involvement of the ascending aorta. (See "Off-pump and minimally
invasive direct coronary artery bypass graft surgery: Clinical use", section on 'Patient selection'.)
OPCAB is usually accomplished via a standard midline sternotomy incision. In some cases, a
small left anterior thoracotomy incision (termed minimally invasive direct coronary artery bypass
[MIDCAB]) is suitable to approach an anterior coronary vessel, typically the left anterior
descending artery [16]. (See "Minimally invasive coronary artery bypass graft surgery: Definitions
and technical issues".)
Details regarding patient selection, surgical techniques, advantages, disadvantages, and
outcomes for OPCAB and MIDCAB are available in other topics. (See "Minimally invasive coronary
artery bypass graft surgery: Definitions and technical issues" and "Off-pump and minimally
invasive direct coronary artery bypass graft surgery: Clinical use".)
Anesthetic management — Anesthetic management for OPCAB differs from management for
on-pump CABG in the following ways:
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● Less systemic anticoagulation is required (typically 100 to 200 units/kg of intravenous [IV]
heparin, approximately one-third of the dose employed for CPB). Activated whole blood
clotting time (ACT) is checked before partial clamping of the aorta or other vessels (eg, the
internal mammary artery [IMA]). An ACT value of 250 to 300 seconds is targeted in most
institutions, although evidence defining optimal ACT for OPCAB is lacking. This level of
anticoagulation balances ischemic and hemorrhagic complications, particularly in patients
recently receiving antiplatelet agents.
● We do not routinely administer an antifibrinolytic agent (eg, epsilon-aminocaproic acid
[EACA] or tranexamic acid [TXA]) after systemic heparinization for OPCAB surgery. TXA
reduces exposure to allogeneic RBC in OPCAB, but an optimal dosing regimen has not been
established. In addition, its impact on clinically relevant outcomes in this setting is
unknown [17,18].
● Fluid loading (typically 15 to 20 mL/kg) to provide optimal preload is employed to maintain
hemodynamic stability during coronary artery grafting and manipulation, rotation, and
lifting of the heart required during OPCAB [19]. This is in contrast to the fluid restriction
employed during the prebypass period for patients undergoing CABG surgery with CPB.
(See "Anesthesia for cardiac surgery: General principles", section on 'Prebypass fluid
management'.)
The Trendelenburg (head down tilt) position is also frequently used to improve preload
during off-pump manipulation of the heart [20]. (See "Patient positioning for surgery and
anesthesia in adults", section on 'Trendelenburg'.)
● Vasoactive infusions (eg, phenylephrine and/or norepinephrine (
table 3)) are typically
necessary to maintain hemodynamic stability during off-pump periods of manipulation of
the heart [19]. In particular, marked hemodynamic instability is noted with displacement of
the heart during mobilization for posterior coronary targets [19,21]. Constant
communication between the surgical and anesthesiology teams is necessary to recognize
and aggressively treat instability (eg, with adjustments in the positioning of the heart and
vasoactive infusion management) [19].
● Atrial pacing is used as a means of enhancing arterial blood pressure and cardiac output,
especially when preoperative beta blockade-induced bradycardia is present [22].
● Transesophageal echocardiography is particularly helpful to differentiate between
hemodynamic instability due to myocardial ischemia (presenting as regional wall motion
abnormalities [RWMAs] in the distribution of the coronary artery undergoing
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revascularization) compared with restricted chamber filling resulting from external
compression of the heart [19,23].
● There may be increased risk for myocardial ischemia after revascularization during the
intraoperative and early postoperative periods since the heart was not protected from
ischemia with CPB and administration of cardioplegia. Thus, close continuous monitoring
of the electrocardiogram (ECG) and TEE images (while the TEE probe remains in place) for
ischemic changes is necessary [19].
● Normothermia should be maintained during the intraoperative period. In one study of
1714 patients undergoing OPCAB, moderate-to severe hypothermia (<35.5°C) at the time of
admission to the postoperative intensive care unit was associated with a higher mortality
risk compared with those who were normothermic (adjusted hazard ratio [HR] 2.03, 95% CI
1.41-2.93) [24].
● In some patients, it may be necessary to convert an OPCAB procedure to on-pump CABG
with CPB due to intractable hemodynamic instability, malignant arrhythmias, global
ventricular ischemia, and/or technical difficulty with adequate exposure and mobilization of
target coronary vessels [19,25].
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Coronary artery bypass
graft surgery".)
SUMMARY AND RECOMMENDATIONS
● Induction and maintenance of anesthesia – Goals of general anesthetic induction and
maintenance during coronary artery bypass grafting (CABG) surgery are to produce and
maintain unconsciousness, attenuate the hemodynamic responses to endotracheal
intubation and surgical stimulation, and prevent or treat hemodynamic changes that lead
to myocardial oxygen imbalance and ischemia. Severe pain and endogenous catecholamine
release during initial incision and subsequent sternotomy necessitate adequate depth of
general anesthesia to prevent tachycardia. Subsequently, it is appropriate to reduce
anesthetic doses to avoid hypotension during the periods of reduced surgical stimulation
that typically follow sternotomy. (See 'Induction and maintenance of general anesthesia'
above.)
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● Avoidance and treatment of ischemia – It is particularly important to detect, prevent, and
treat myocardial ischemia throughout the prebypass period. Specific hemodynamic and
physiologic goals maintain optimal myocardial oxygen supply and minimize demand
during induction and the prebypass periods (
table 2). (See 'Avoidance and treatment of
ischemia' above.)
● Use of transesophageal echocardiography (TEE) – TEE is typically used for patients
undergoing CABG to:
• Conduct an initial comprehensive prebypass TEE examination, and a focused postbypass
examination. (See 'Postbypass transesophageal echocardiography' above and
"Anesthesia for cardiac surgery: General principles", section on 'Initial transesophageal
echocardiography examination'.)
• Continuously monitor for regional wall motion abnormalities (RWMAs) that may indicate
ischemia (
figure 1 and
figure 2 and
movie 1), as well as for monitoring global
ventricular function and volume status throughout the prebypass and postbypass
periods. (See "Anesthesia for cardiac surgery: General principles", section on 'Monitoring
with transesophageal echocardiography'.)
● Off-pump coronary artery bypass graft (OPCAB) surgery – Off-pump coronary artery
bypass graft surgery (OPCAB) refers to CABG without the use of CPB. Anesthetic
management differs from management for on-pump CABG in the following ways (see 'Offpump coronary artery bypass surgery' above):
• Less systemic anticoagulation is required.
• Antifibrinolytics are not administered.
• Fluid loading (typically 15 to 20 mL/kg), Trendelenburg positioning, and vasoactive
infusions (eg, phenylephrine and/or norepinephrine (
table 3)) are typically employed
to maintain hemodynamic stability during surgical manipulation of the heart.
ACKNOWLEDGMENT
The editorial staff at UpToDate acknowledge Ryan Konoske, MD, who contributed to an earlier
version of this topic review.
Use of UpToDate is subject to the Terms of Use.
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Topic 90607 Version 31.0
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GRAPHICS
Key periods during cardiac surgery
Period
Prebypass period
Anesthetic goals
Induction and
maintenance of
anesthesia
Maintain optimal myocardial O2 supply and minimize
demand to prevent or treat ischemia
Antibiotic
prophylaxis
Timely administration of selected antibiotics
Positioning
Careful arm, hand, and head positioning to avoid injuries
Fluid
management
Restrict fluid administration since initiation of CPB causes
significant hemodilution
Prebypass TEE
examination
Assess regional LV wall motion abnormalities
Assess global LV function
Assess global RV function
Assess structure and function of cardiac valves
Evaluate thoracic aorta, interatrial septum, and left
atrium with left atrial appendage
Detect development of ischemia, hypovolemia,
hypervolemia, or low SVR
Incision and
sternotomy
Treat hypertension and tachycardia due to painful stimuli
Harvesting of the
Reduce tidal volume
internal
mammary artery
Briefly interrupt ventilation during sternotomy to avoid
lung injury
Anticoagulation
for CPB
Administer heparin and ensure adequate anticoagulation
Antifibrinolytic
administration
Administer antifibrinolytic agent to minimize
Perfusionist
Confer with perfusionist if indicated
completes CPB
circuit setup,
(confirm with ACT)
microvascular bleeding
priming, testing
of alarms and
circuit, adherence
to checklist
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Initiation of CPB
Anesthesia for coronary artery bypass grafting surgery - UpToDate
Aortic cannulation
Reduce systolic BP to <100 mmHg to reduce risk of aortic
dissection
Venous
cannulation
Treat hypotension or initiate CPB for malignant
arrhythmias
Retrograde
autologous
priming
Gradual onset of CPB to reduce hemodilution from
crystalloid prime
Control of O2
delivery, CO2
removal, and
pump flow
assumed by
perfusionist
Discontinue controlled ventilation and anesthetic
administration via the anesthesia machine
Anesthetic
administration
Initiate volatile anesthetic administration via vaporizer
attached to CPB circuit, or use TIVA technique
Discontinue cardiac support (eg, inotropic agents, IABP)
Monitor raw and/or processed EEG and expired
anesthetic gas from the oxygenator to prevent
awareness
Monitor neuromuscular function; administer NMBAs to
prevent movement or shivering
Placement of
aortic crossclamp
and
administration of
cardioplegia
Ensure complete myocardial arrest (absence of ECG
electrical activity)
Placement and
monitoring of
TEE assessment of coronary sinus catheter placement for
retrograde cardioplegia delivery
coronary sinus
catheter and LV
vent
Maintenance of
Cooling
CPB
TEE monitoring for aortic insufficiency and LV distension
during antegrade cardioplegia delivery
Monitor coronary sinus pressure
TEE assessment of correct LV vent placement and
effective LV decompression
Maintain temperature gradient between venous inflow
and arterial outlet <10°C
Maintenance
Maintain MAP ≥65 mmHg (or ≥75 mmHg for patients
with cerebrovascular disease or severe aortic
atherosclerosis)
Monitor temperature at oxygenator arterial outlet
temperature (surrogate for cerebral temperature) and
other sites (eg, nasopharyngeal, bladder, blood)
Maintain Hgb ≥7.5 g/dL (Hct ≥22%); suggest
hemoconcentration if Hgb <7.5 g/dL, then transfuse
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PRBC if necessary
Maintain SvO2 ≥75%; suggest increase in pump flow if
SvO2 <75%
Rewarming
Slow rewarming ≤0.5°C/minute, with temperature
gradient between venous inflow and arterial outlet ≤4°C
Avoid hyperthermia; target temperature is 37°C at
nasopharyngeal site and 35.5°C at bladder site
Monitor for awareness or return of neuromuscular
function
Removal of aortic
crossclamp
Weaning from
Refer to UpToDate topic on weaning from
cardiopulmonary bypass (CPB)
CPB
Post-bypass
Defibrillate and administer antiarrhythmic agents if
necessary to treat ventricular fibrillation
Venous
decannulation
Ensure initial reinfusion of blood drained from the
venous tubing into the pump reservoir in 50- to 100-mL
aliquots
TEE assessment for adequate ventricular filling
Anticoagulation
reversal, pump
suckers turned
off, intravascular
vents removed
Administer protamine slowly, treat protamine reactions
Aortic
decannulation
Reduce systolic BP to <100 mmHg to reduce risk of aortic
dissection
Pacemaker
management
Ensure optimal pacemaker settings
Postbypass TEE
examination
Assess regional LV wall motion abnormalities
Ensure complete reversal of anticoagulation
Assess global LV function
Assess global RV function
Monitor LV and RV chamber sizes to assess intravascular
volume status
Evaluate the ascending aorta to rule out dissection
Hemostasis
Ensure absence of residual heparin
Check point-of-care and laboratory tests of coagulation if
bleeding persists
Manage anemia, thrombocytopenia, and coagulopathy if
necessary
Chest closure
Observe for RV compression and dysfunction, coronary
graft compromise, pacing wire displacement, or lung
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compression
Transport to ICU
and handover
Ensure optimal patient condition prior to transport
Immediate availability of airway equipment, emergency
drugs, and defibrillator on the transport bed
Continuous monitoring of ECG, SpO2, and intraarterial BP
during transport
Use of a formal protocol for communication and transfer
of technology during handover to the ICU team
O2: oxygen; CPB: cardiopulmonary bypass; TEE: transesophageal echocardiography; LV: left
ventricular; RV: right ventricular; SVR: systemic vascular resistance; ACT: activated clotting time; BP:
blood pressure; CO2: carbon dioxide; IABP: intraaortic balloon pump; TIVA: total intravenous
anesthesia; EEG: electroencephalography; MAP: mean arterial pressure; Hgb: hemoglobin; Hct:
hematocrit; SVO2: mixed venous oxygen saturation; ECG: electrocardiogram; SpO2: peripheral oxygen
saturation; ICU: intensive care unit.
Graphic 108173 Version 2.0
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LV perfusion territories
The regional distribution of LV segmental wall motion abnormalities detected
by TEE can be used to help determine the location of disease within the
coronary arteries. The diagram displays the typical territories of myocardium
perfused by each of the major coronary arteries supplying the LV in the TEE
mid-esophageal four-chamber view, TEE mid-esophageal two-chamber view,
TEE mid-esophageal long-axis view, and TEE transgastric LV short-axis view.
Anatomic variations and coronary collateral flow may produce different
patterns of coronary perfusion in individual patients.
LV: left ventricle/left ventricular; TEE: transesophageal echocardiography; LAD:
left anterior descending; Cx: circumflex; RCA: right coronary artery.
Modified from: Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines for performing a
comprehensive intraoperative multiplane transesophageal echocardiography examination:
recommendations of the American Society of Echocardiography Council for Intraoperative
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Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification
in Perioperative Transesophageal Echocardiography. J Am Soc Echocardiogr 1999; 12:884.
Graphic 104112 Version 2.0
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LV segmental anatomy
The regional distribution of myocardial ischemia can be detected as
segmental LV wall motion abnormalities by TEE. The entire LV in the 17segment model can be imaged in long-axis using a combination of the TEE
mid-esophageal four-chamber view (a), TEE mid-esophageal two-chamber
view (b), and TEE mid-esophageal long-axis view (c). Alternatively, all 17 LV wall
segments can be imaged using the TEE transgastric LV short-axis views at the
levels of the LV base (d), papillary muscles (e), and apex (not shown).
Alternatively, an earlier version of a 16-segment LV model that excludes the
apical cap is often used for TEE studies.
LV: left ventricle/left ventricular; TEE: transesophageal echocardiography.
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Modified from: Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines for performing a
comprehensive intraoperative multiplane transesophageal echocardiography examination:
recommendations of the American Society of Echocardiography Council for Intraoperative
Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for
Certification in Perioperative Transesophageal Echocardiography. J Am Soc Echocardiogr 1999;
12:884.
Graphic 104113 Version 2.0
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Myocardial ischemia: Factors governing O2 supply and demand
Factors that ↓ O2 supply
Factors that ↑ O2 demand
↑ Heart rate*
↑ Heart rate*
↓ Arterial O2 content
↑ LV systolic wall stress (LV afterload)
↓ Hemoglobin
↑ Systolic blood pressure (SBP)
↓ SaO2
↑ LV chamber size (↑ LV end-diastolic
↓ Coronary blood flow
↓ Coronary perfusion pressure (CPP) =
diastolic blood pressure (DBP) – LV enddiastolic pressure (LVEDP)
volume [LVEDV])
↓ LV wall thickness
↑ Contractility
↓ DBP
↑ LVEDP
↑ Coronary vascular resistance
A number of clinical conclusions should be drawn from this table. First, increased heart rate
(tachycardia) is harmful because it both decreases oxygen supply and increases oxygen demand.
Second, severe anemia or severe hypoxemia is harmful because of reduced supply. Third,
increases in LVEDV and LVEDP, which often (but not always) occur together, are harmful because
of both decreased supply (decreased CPP) and increased demand (afterload). Fourth, the ideal
blood pressure is patient-dependent, but severe hypotension is likely to reduce supply (DBP) more
than its beneficial effect on demand (SBP). But, conversely, severe hypertension typically increases
demand (afterload) more than it improves supply (DBP).
Left ventricular (LV) afterload is best defined as LV systolic wall stress. Based on Laplace's law, LV
systolic wall stress = (LV systolic pressure × LV end-diastolic radius) / 2 × LV wall thickness.
Therefore, factors that increase LV afterload include increased SBP and/or increased LV radius or
LVEDV. Note that the normal (chronic) compensatory response to these hemodynamic changes is
for the LV walls to thicken or hypertrophy, which works to normalize systolic wall stress, but
requires months or years for change to occur. Therefore, of the hemodynamic variables that often
change during the perioperative period, increases in SBP or LVEDV are harmful, owing to their
deleterious effects on LV afterload.
O2: oxygen; SaO2: oxygen saturation of arterial blood; LV: left ventricular; SBP: systolic blood
pressure.
* Affects both supply and demand.
Original figure modified for this publication. Royster RL, Butterworth JF IV, Groban L, et al. Cardiovascular Pharmacology. In:
Essentials of Cardiac Anesthesia. Kaplan JA (Ed), Saunders Elsevier, Philadelphia 2008. Illustration used with the permission of
Elsevier Inc. All rights reserved.
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Graphic 91907 Version 8.0
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Total time spent in diastole
Total time spent in diastole each minute plotted as a function of heart
rate in beats per minute. The reduction in diastolic interval leads to
diminished time for diastolic coronary artery blood flow.
Reproduced with permission from: Green MS, Okum GS, Horrow JC. Anesthetic
Management of Myocardial Revascularization In: A Practical Approach to Cardiac
Anesthesia, 5th ed, Hensley FA, Martin DE, Gravlee GP (Eds), Lippincott Williams &
Wilkins, Philadelphia 2013. Copyright © 2013 Lippincott Williams & Wilkins.
Graphic 94174 Version 9.0
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Vasopressors and inotropic agents used in the operating room: Adult
dosing* ¶
Drug
Ephedrine
Functional class
(predominant receptor or
mechanism of action)
Inotrope/chronotrope/vasopressor
(alpha1-adrenergic receptor
agonist; beta1- and beta2adrenergic receptor agonist)
Bolus
dose
5 to 10 mg
boluses
Infusion dose
N/A
Comm
Tachyphyl
occur with
repeated d
to indirect
postsynap
release of
norepinep
Cardiovas
effects att
by drugs t
ephedrine
into adren
nerves (eg
or those th
deplete
norepinep
reserves (e
reserpine)
Administe
extreme c
(eg, in sma
increment
of 2.5 mg)
patients u
monoamin
oxidase (M
inhibitors
methamp
since exag
hypertens
responses
threatenin
dysrhythm
occur
Phenylephrine
Vasopressor (alpha1-adrenergic
receptor agonist)
50 to 100
10 to 100
mcg
boluses
mcg/minute
Often sele
treat hypo
or
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Norepinephrine
Anesthesia for coronary artery bypass grafting surgery - UpToDate
Inotrope/vasopressor (alpha1- and
beta1-adrenergic receptor agonist)
(may begin
infusion if
repeated
bolus
doses are
necessary)
0.1 to 1
mcg/kg/minute
4 to 8 mcg
(may begin
infusion if
repeated
bolus
doses are
necessary)
1 to 20 mcg/minute
normal or
HR is pres
Genetic
polymorp
lead to va
individual
responses
or
0.01 to 0.3
mcg/kg/minute
Often sele
first-line a
during no
surgery, p
for treatm
most type
Norepinep
mcg is
approxima
equivalent
potency to
phenyleph
mcg
Periphera
extravasat
high conce
may cause
damage
Epinephrine
Inotrope/chronotrope/vasopressor
(alpha1-adrenergic receptor
agonist; beta1- and beta2adrenergic receptor agonist)
4 to 10
mcg
initially; up
to 100 mcg
boluses
may be
1 to 100
mcg/minute
or
0.01 to 1
mcg/kg/minute
used when
initial
response is
inadequate
Note changing
effects across dose
range:
Low doses
have primarily
beta2adrenergic
effects at 1 to 2
mcg/minute or
0.01 to 0.02
mcg/kg/minute
First-line t
for cardiac
and for an
May be
administe
or via an
endotrach
in emerge
Low doses
bronchodi
effects an
cause arte
vasodilatio
decreased
Intermedi
cause incr
HR and BP
High dose
vasoconst
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Intermediate
doses have
primarily
beta1- and
beta2adrenergic
effects at 2 to
10 mcg/minute
or 0.02 to 0.1
mcg/kg/minute
with possi
hypertens
adverse m
effects
Individual
responses
related eff
variable
High doses
have primarily
alpha1adrenergic
effects at 10 to
100
mcg/minute or
0.1 to 1
mcg/kg/minute
Vasopressin
Vasopressor (vasopressin1 and
vasopressin2 receptor agonist)
1 to 4 units
0.01 to 0.04
units/minute
Doses >0.04
units/minute up to
0.1 units/minute are
reserved for salvage
therapy (ie, failure to
achieve adequate BP
goals with other
vasopressor
agents) ¶
Effective f
treatment
hypotensi
refractory
administra
catecholam
sympatho
such as ep
phenyleph
norepinep
No direct e
HR
Little effec
can cause
splanchnic
vasoconst
Individual
responses
related eff
variable
Periphera
extravasat
cause skin
Dopamine
Inotrope/vasopressor/dosedependent chronotropy
(dopaminergic, beta1-, beta2-, and
N/A
2 to 20
mcg/kg/minute
Low doses
exacerbat
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alpha1-adrenergic receptor
agonist)
Note changing
effects across dose
range:
Low doses
have primarily
dopaminergic
effects at <3
mcg/kg/minute
hypotensi
beta2 stim
High dose
cause
vasoconst
adverse m
effects, an
arrhythmi
Intermediate
doses have
primarily
beta1- and
beta2adrenergic
effects at 3 to
10
mcg/kg/minute
High doses
have primarily
alpha1adrenergic
effects >10
mcg/kg/minute
Dobutamine
Inotrope/vasodilator/dosedependent chronotropy (beta1and beta2-adrenergic receptor
agonist)
N/A
1 to 20
mcg/kg/minute
Exacerbat
hypotensi
possible d
dose-depe
vasodilatio
beta2 stim
concurren
administra
potent
vasoconst
such as
norepinep
vasopress
necessary
Milrinone
Inotrope/vasodilator
(phosphodiesterase inhibitor)
N/A
0.375 to 0.75
mcg/kg/minute (a
(decreases rate of cyclic adenosine
monophosphate [cAMP]
loading dose of 50
mcg/kg over ≥10
degradation)
minutes may be
administered, but
Exacerbat
hypotensi
due to vas
(via
phosphod
inhibition)
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Isoproterenol
Anesthesia for coronary artery bypass grafting surgery - UpToDate
Inotrope/chronotrope/vasodilator
(beta1- and beta2-adrenergic
receptor agonist)
N/A
may be omitted to
avoid hypotension)
concurren
administra
potent
vasoconst
such as
norepinep
vasopress
necessary
5 to 20 mcg/minute
Exacerbat
hypotensi
due to dos
dependen
vasodilatio
beta2 stim
or
0.05 to 0.2
mcg/kg/minute
May cause
arrhythmi
Not availa
most setti
N/A: not applicable; HR: heart rate; IV: intravenous; IM: intramuscular; BP: blood pressure; PVR:
pulmonary vascular resistance.
* Dose ranges are based on adult patients of average size.
¶ Refer to related UpToDate content on hemodynamic management during anesthesia and surgery.
Graphic 119747 Version 4.0
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Drugs used to lower blood pressure in the operating room: Adult dosing* ¶
Functional
Drug
class
(predominant
receptor or
mechanism)
Bolus dose
Infusion
dose
Comments
Beta blocking agents – Generally avoided in patients with acute decompensated heart
failure
Esmolol
Beta1-selective
adrenergic
10 to 50 mg,
which may be
receptor
blockade
repeated (every 5
to 15 minutes
depending upon
the initial dose
used, the desired
effect, and the
patient's risk for
hemodynamic
decompensation)
Metoprolol
Beta1-selective
adrenergic
receptor
blockade
1 to 5 mg,
followed by 2.5 to
15 mg every 3 to
6 hours
N/A
Commonly used
agent to treat
suspected
myocardial ischemia
due to tachycardia
with normal or
elevated blood
pressure
Labetalol
Blockade of
Initial bolus of 5
0.5 to 2
postsynaptic
alpha1-
to 25 mg, which
may be followed
mg/minute up
to a maximum
Often selected as a
first-line agent to
adrenergic
receptors and
by repeated
boluses every 10
of 10
mg/minute
non-selective
beta blockade
minutes (up to
300 mg)
(generally
reserved for
for beta1- and
beta2-adrenergic
receptors
50 to 300
mcg/kg/minute
Rapid onset and very
short duration of
action
Clearance is not
dependent on renal
or hepatic function
due to rapid
metabolism by
plasma esterases
hypertensive
emergencies)
treat concomitant
hypertension and
tachycardia
Use cautiously in
patients with
obstructive or
reactive airway
disease
Avoid in
hyperadrenergic
states (eg,
pheochromocytoma
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or cocaine or
methamphetamine
overdose) since beta
blockade and loss of
beta2-mediated
vasodilation induced
by labetalol can lead
to severe
hypertension when
prior alpha1adrenergic blockade
is incomplete
Calcium channel blocking agents – Use cautiously in patients with increased ICP
Nicardipine*
Clevidipine
Selective
dihydropyridinetype calcium
channel blocker;
selective
arteriolar
smooth muscle
relaxation
100 to 500 mcg
Selective
dihydropyridinetype calcium
channel blocker;
selective
arteriolar
smooth muscle
relaxation
N/A
5 to 15
mg/hour
Predominantly
arteriolar vasodilator
Commonly used for
neurosurgical
patients
Initial dose 1 to
2 mg/hour, with
rapid titration
up to 16
mg/hour
Rapid onset and
short duration of
action
Clearance is not
dependent on renal
or hepatic function
due to rapid
metabolism by
plasma esterases
Direct vasodilators (direct relaxation of vascular smooth muscle) – Generally avoided in
patients with increased ICP
Hydralazine
Highly selective
Initial bolus of
vasodilation of
arterial
2.5 mg followed
by repeated
resistance
vessels
boluses every 5
minutes to a
N/A
Minimal or no effect
on the venous
circulation
Relatively slow onset
compared with other
antihypertensive
maximum 20 mg
agents
Nitroglycerin
(glyceryl
Nitrodilator that
causes increased
10 to 40 mcg,
which may be
trinitrate)
release of NO,
resulting in
repeated and/or
10 to 200
mcg/minute
or
Continuous
monitoring using an
intra-arterial
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smooth muscle
relaxation
followed by
infusion
0.1 to 3
mcg/kg/minute
catheter is
warranted as soon
as feasible,
particularly if higher
doses are used
SL or paste forms of
nitroglycerin paste (1
to 2 inches)
formulations also
available
Nitroprusside
Nitrodilator that
directly releases
NO, resulting in
smooth muscle
relaxation
N/A
10 to 200
mcg/minute
or
0.1 to 3
mcg/kg/minute
Continuous
monitoring using an
intra-arterial
catheter is necessary
Cyanide
accumulation may
occur
Other antihypertensive agents
Fenoldopam
Selective agonist
for D1 dopamine
receptors; binds
with moderate
affinity to alpha2adrenoceptors
N/A
Initial dose at
0.1
mcg/kg/minute
titrated up to a
maximum of
1.6
mcg/kg/minute
Rarely used in
perioperative
settings
Generally avoided in
patients with
glaucoma or
increased ICP
N/A: not applicable; ICP: intracranial pressure; NO: nitric oxide; SL: sublingual.
* Dose ranges are based on adult patients of average size.
¶ Refer to related UpToDate content on hemodynamic management during anesthesia.
Graphic 119750 Version 2.0
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Hemodynamic management of hypotension during and after weaning from
CPB
CVP
PAP
PADP
or
PAWP*
Cardiac
output
Blood
pressure
LV function
by TEE
RV function
by TEE
Diagnosi
Low
Low
Low
Low
Low
Normal or
hyperdynamic
Normal or
hyperdynamic
Hypovolem
Low or
normal
Low or
normal
Low or
normal
High
Low
Normal or
hyperdynamic
Normal or
hyperdynamic
Vasoplegia
High or
High
Low or
High
Low
Normal
Normal or
Pulmonary
hypocontractile
hypertensio
normal ¶
normal
High
Normal
or low
Normal
or high ¶
Low
Low
Normal
Hypocontractile,
often dilated
Right
ventricular
dysfunction
Normal
or high
Normal
or high
High
Low
Low
Hypocontractile,
often dilated
Normal
Left
ventricular
dysfunction
CPB: cardiopulmonary bypass; CVP: central venous pressure; PAP: pulmonary artery pressure; PADP:
pulmonary artery diastolic pressure; PAWP: pulmonary artery wedge pressure; LV: left ventricular;
TEE: transesophageal echocardiography; RV: right ventricular.
* PAWP should not be measured prior to neutralizing heparin following CPB. Initially, PADP is
measured, the PADP may overestimate PAWP when patients have elevated pulmonary vascular
resistance (eg, pulmonary hypertension).
¶ PADP or PAWP are indirect measures of LV filling pressure. With RV dysfunction and dilation,
ventricular septal shift may increase LV filling pressure despite low or normal LV filling volume.
Graphic 93595 Version 8.0
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Type A aortic dissection with aortic insufficiency
Intraoperative TEE image of the aortic valve, aortic root, and proximal ascending aorta in a long-axis view,
with color-flow Doppler imaging in diastole demonstrating severe aortic regurgitation with an acute aortic
dissection. The presence of an intimal flap in the aortic root (arrowheads) is diagnostic for Stanford type A
aortic dissection. Severe aortic regurgitation is present as a mosaic regurgitant jet in the LVOT caused by
acute enlargement of the aortic root due to the dissection.
LVOT: left ventricular outflow tract; Ao: ascending aorta; TEE: transesophageal echocardiography.
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Contributor Disclosures
Atilio Barbeito, MD, MPH No relevant financial relationship(s) with ineligible companies to
disclose. Jonathan B Mark, MD No relevant financial relationship(s) with ineligible companies to
disclose. Nancy A Nussmeier, MD, FAHA No relevant financial relationship(s) with ineligible companies to
disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy
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