Intraoperative Management of Shock in Adults

20/6/23, 19:30 Intraoperative management of shock in adults - UpToDate
Intraoperative management of shock in adults

AUTHORS: Carmen Hrymak, MD, Duane J Funk, MD, FRCP(C), Michael F O'Connor, MD, FCCM, Eric Jacobsohn, MBChB, MHPE,
FRCPC
SECTION EDITOR: Roberta Hines, MD
DEPUTY EDITOR: Nancy A Nussmeier, MD, FAHA
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2023.

This topic last updated: Sep 16, 2022.
INTRODUCTION
Shock is a condition of circulatory failure with decreased oxygen delivery to body tissues that
results in cellular hypoxia and life-threatening end-organ dysfunction.
This topic reviews intraoperative resuscitation and anesthetic management for patients with
reversible causes of shock. Management of shock in other settings (eg, emergency
department, intensive care unit) may overlap with the perioperative period, as discussed in
separate topics:
● (See "Evaluation of and initial approach to the adult patient with undifferentiated
hypotension and shock", section on 'Clinical manifestations'.)
● (See "Approach to shock in the adult trauma patient".)
● (See "Evaluation and management of suspected sepsis and septic shock in adults".)
● (See "Prognosis and treatment of cardiogenic shock complicating acute myocardial
infarction".)
RAPID PREOPERATIVE EVALUATION
Intraoperative shock is generally attributable to hypovolemic, cardiogenic, distributive, or

obstructive causes, similar to other settings ( table 1). Each of these categories has several
potential etiologies that may be diagnosed by point-of-care ultrasound examination
( table 2) or the hemodynamic profile of pulmonary artery catheter (PAC) values ( table 3)
[1,2]. (See "Definition, classification, etiology, and pathophysiology of shock in adults".)
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Multiple shock categories are often present during surgery. For example, a trauma patient
with hemorrhage (hypovolemic shock) may also have a tension pneumothorax (obstructive
shock) or spinal cord injury (neurogenic shock). Another example is severe ischemic
myocardial dysfunction (cardiogenic shock) caused by hypotension due to sepsis (distributive
shock). (See "Evaluation of and initial approach to the adult patient with undifferentiated
hypotension and shock", section on 'Clinical manifestations'.)
Simultaneous evaluation and resuscitation may be necessary before and during emergency
surgery in a shock patient (see 'Initial resuscitation' below). In some cases, life-saving
treatment must be initiated without a complete history, laboratory results, or diagnostic
images ( algorithm 1 and algorithm 2).
General assessment
● Vital signs – Clinical features of shock typically include tachycardia, tachypnea, and
hypotension. Hypotension may be absolute (systolic blood pressure [BP] <90 mmHg,
mean arterial pressure <65 mmHg) or relative (eg, a decrease that is ≥40 mmHg below
the patient's baseline).
Hypotension may not be evident in the earliest stages of shock because of

cardiovascular homeostatic mechanisms. Since systemic BP is dependent upon both
cardiac output (CO) and systemic vascular resistance (SVR), BP may be temporarily
maintained by vasoconstriction in a patient with reduced CO, or by increasing the CO in a
patient with reduced SVR.
Pulse pressure (PP) is the difference between systolic and diastolic BP (Psystolic - Pdiastolic),
as measured by invasive or noninvasive methods. The PP represents the dynamic
between CO and SVR ( figure 1 and figure 2). Assessment of PP may be helpful for
categorizing shock into a high or low CO state, but should be considered in the context
of the diastolic BP (rather than as an absolute value):
• Reduced PP – Reduced PP may be due to a low CO with vasoconstriction, which

occurs in most types of shock. For example, a vasoconstricted shock patient with BP
90/60 mmHg has a small PP of only 30 mmHg, which is less than the diastolic BP.
• Increased PP – Increased PP may be due to a high CO with vasodilation, which occurs

in distributive shock. For example, a vasodilated patient with BP 90/35 has a large PP
of 55 mmHg, which is higher than the diastolic BP.

● Available preoperative tests – The electrocardiogram and results of laboratory tests

are examined. These may include arterial blood gases, serum lactate, renal and liver
function tests, cardiac biomarkers, and complete blood count, as well as imaging studies
(eg, portable chest radiograph, computed tomography [CT] of the head, spine, chest,
abdomen, pelvis, or pulmonary artery).
Point-of-care ultrasonography — Point-of-care ultrasonography may be useful to diagnose

or confirm the cause(s) of shock in the preoperative area or after arrival in the operating room
( algorithm 2). Ultrasonography is typically performed if shock etiology is uncertain,
equipment and expertise are available, and if the examination will not unduly delay
emergency surgical intervention. (See "Indications for bedside ultrasonography in the
critically ill adult patient", section on 'Training and competence'.)
In this setting, a systematic approach such as rapid ultrasound in shock (RUSH) is used to
examine the heart first, followed by brief imaging of the chest, abdomen, and major arteries
and veins to assess "the pump, the tank, and the pipes" ( table 2) [3-6]. (See "Evaluation of
and initial approach to the adult patient with undifferentiated hypotension and shock",
section on 'Point-of-care ultrasonography'.)
● The pump – Assessment of the left ventricle (LV), right ventricle (RV), and pericardium
can rapidly diagnose the etiology of shock.
• Cardiogenic shock – Severely decreased contractility of the LV, RV, or both.

• Hypovolemic shock – Small LV and RV.
• Distributive shock – Small LV with hyperdynamic contractility.
• Obstructive shock – Pericardial effusion, pneumothorax (suggested by absence of
lung sliding) or pulmonary embolus (suggested by RV enlargement and dysfunction).
● The tank – Assessment of the inferior vena cava (IVC), internal jugular (IJ) vein, lungs,
pleural space, and peritoneal cavity can determine volume status.
• Empty tank – Small IVC size, IJ vein collapse at the end of expiration [7,8].
• Leaking tank – Pleural effusion, peritoneal fluid accumulation, leaking aortic
aneurysm.
• Overloaded tank – Pulmonary edema due to volume overload (suggested by presence
of B lines [narrow vertical hyperechoic reflections that arise at the pleural line and
extend to the bottom of the ultrasound screen]).
● The pipes – Assessment of the abdominal and thoracic aorta and the femoral and
popliteal veins can detect vascular problems.
• Aortic dissection or aneurysm

• Deep vein thrombosis in the lower extremities
Further details regarding advantages and limitations of urgent and emergency

ultrasonography are available in other topics:
● (See "Indications for bedside ultrasonography in the critically ill adult patient".)
● (See "Bedside pleural ultrasonography: Equipment, technique, and the identification of
pleural effusion and pneumothorax".)
● (See "Emergency ultrasound in adults with abdominal and thoracic trauma".)
Urgency of the planned procedure — Decisions regarding urgency of the surgical

intervention depend on the cause(s) of shock, as in the following examples:
● Hypovolemic hemorrhagic shock due to trauma – Immediate damage control surgery is

necessary to treat life-threatening conditions. (See "Overview of damage control surgery
and resuscitation in patients sustaining severe injury".)
● Obstructive shock – Immediate intervention is typically necessary to rapidly decompress

the compartment causing intrathoracic or intra-abdominal obstruction of blood flow or
compression or vital organs.
● Septic shock – Urgent surgery is often the most effective treatment to control the
infection source. Examples include debridement of necrotizing fasciitis, resection of
perforated viscus, removal of an infected foreign body, or drainage of an abscess. (See
"Evaluation and management of suspected sepsis and septic shock in adults", section on
'Septic focus identification and source control'.)
● Cardiogenic shock – For patients with cardiogenic shock due to a recent myocardial
infarction (MI), unstable angina, decompensated heart failure (HF), high-grade
arrhythmias, or hemodynamically important valvular heart disease such as aortic
stenosis, surgery is delayed if possible, because of a high risk for postoperative
complications (eg, worsening of the MI and/or HF, ventricular fibrillation, complete heart
block, cardiac arrest, cardiac death). If urgent or emergency surgery is necessary,
benefits and risks of timing strategies are discussed among the cardiologist, surgeon,
and anesthesiologist. (See "Management of cardiac risk for noncardiac surgery", section
on 'For urgent or emergency surgery'.)
INTRAOPERATIVE MONITORING

Standard monitors — Standard monitors are attached prior to induction of anesthesia

( table 4) [9]. (See "Basic patient monitoring during anesthesia", section on 'Standards for
monitoring during anesthesia'.)
Standard intraoperative electrocardiography (ECG) may be useful for diagnosis of arrhythmias

or abnormalities suggestive of ischemia or pericarditis (ST segment changes), pericardial
effusion (low voltage of the QRS complex or electrical alternans), or pulmonary embolism
(S1Q3T3 pattern, new right bundle branch block, or anterior T-wave inversion).
Invasive cardiovascular monitors — Advanced cardiovascular system monitoring may be

helpful to provide real-time information for management of resuscitation in a patient with
shock. In an emergency, insertion of invasive monitors is delayed until after surgery has
commenced. (See "Basic patient monitoring during anesthesia", section on 'Circulatory system
monitoring'.)
Intra-arterial catheter — An intra-arterial catheter is inserted if not already present.

Although insertion is ideally accomplished before anesthetic induction, this should not unduly
delay emergency surgical intervention.
The intra-arterial catheter is used for the following purposes:
● Continuous monitoring of arterial blood pressure (BP) for immediate detection of

hypotension [10,11]. Pulse pressure (PP) is also monitored to provide supplemental
information that distinguishes a vasoconstricted state with low cardiac output (CO)
versus a vasodilated state with high CO ( figure 1 and figure 2). Accuracy of
measurements depends upon having an arterial pressure waveform that is not
underdamped or overdamped.
● Monitoring of respirophasic variation in the arterial pressure waveform during positive

pressure ventilation as a primary or supplementary dynamic parameter to determine
fluid responsiveness ( figure 3) [12,13]. Newer monitors have automated algorithms
derived from the arterial waveform that enable beat-to-beat calculation of specific
dynamic parameters such as pulse pressure variation (PPV) ( figure 4 and figure 5),
systolic pressure variation (SPV) ( figure 6), and stroke volume variation (SVV). Each of
these dynamic parameters has advantages and disadvantages ( table 5). Also, systolic
pressure variation (SPV) is readily appreciated by observing the arterial waveform [14].
Fluid responsiveness (ie, improvement in cardiac index with administration of
intravenous [IV] fluids) is suggested by respirophasic SPV >15 percent. (See
"Intraoperative fluid management", section on 'Dynamic parameters to assess volume

responsiveness' and "Novel tools for hemodynamic monitoring in critically ill patients
with shock", section on 'Volume tolerance and fluid responsiveness'.)
● Intermittent blood sampling to measure arterial blood gases, pH, base deficit, serum
lactate, hemoglobin, electrolytes, glucose, and activated clotting time (ACT). Additional
tests of hemostasis are obtained if there is evidence of coagulopathy or significant
bleeding [15]. (See "Clinical use of coagulation tests", section on 'Point-of-care testing'.)
Central venous catheter — If not already present, a central venous catheter (CVC) is usually
inserted. However, placement should not unduly delay urgent or emergency surgical
intervention. As an alternative, two large-bore peripheral IV catheters (eg, 16 G or larger) can
be inserted for initial rapid administration of medications and fluid or blood transfusions.
A CVC is used for the following purposes:
● Infusion of vasoactive drugs.
● Venous access for fluid and blood administration. If this is the primary purpose of the
CVC, a large bore catheter such as an 8.5 F introducer is preferred.
● Measurement of central mixed venous oxygen saturation (ScvO2) in blood drawn from
the distal port of a CVC to serve as a surrogate for adequacy of CO if a pulmonary artery
catheter (PAC) is not available (see "Oxygen delivery and consumption", section on
'Oxygen content'). SCVO2 >70 percent is considered to be a good target during
resuscitation efforts. Notably, the value for ScvO2 drawn from a CVC is typically 3 to 5
percent higher than that of a mixed venous saturation [SvO2] value obtained from the
pulmonary arterial port of a PAC. The SvO2 reflects the true mixing of venous return, and
thus the balance between oxygen delivery and utilization [16].
● Measurement of central venous pressure (CVP) to provide supplemental data regarding

intravascular volume status [12], although CVP is a poor predictor of fluid
responsiveness. (See "Intraoperative fluid management", section on 'Traditional static
parameters'.)
Pulmonary artery catheter — A PAC is not routinely inserted because its use has not been
shown to improve survival or other outcomes in critically ill patients [17-19]. However, many
clinicians insert a PAC for patients with severe right ventricular (RV) dysfunction, pulmonary
hypertension, or cardiogenic shock due to acute valvular disease.
Measurements obtained with a PAC include (see "Pulmonary artery catheterization:

Interpretation of hemodynamic values and waveforms in adults"):
● Hemodynamic measurements such as CO (and cardiac index), systemic vascular

resistance (SVR), pulmonary artery pressures, pulmonary artery occlusion pressure
(PAOP), CVP, and pulmonary vascular resistance (PVR) ( table 6).
● Mixed venous oxygen saturation values in blood drawn from the pulmonary arterial port
(SvO2). This blood includes drainage from the coronary sinus which has a low saturation;
thus, SvO2 will be slightly lower than ScvO2. (See 'Central venous catheter' above.)
These measurements may be helpful to diagnose the cause of hypotension, particularly in the
postoperative period when ultrasonography may not be readily available.
Values obtained with a PAC that are consistent with each cause of shock are listed in the table
( table 3). These measurements also may be useful to guide therapy, including fluid
resuscitation, titration of vasopressors, and assessment of the hemodynamic effects of
changes in mechanical ventilator settings ( table 7). (See "Pulmonary artery catheterization:
Indications, contraindications, and complications in adults".)
Transesophageal echocardiography — During the intraoperative period, transesophageal

echocardiography (TEE) monitoring is frequently employed in unstable patients to confirm the
cause(s) of shock as well as for continuous monitoring of cardiac function and intravascular
volume status. Specifically, intraoperative TEE monitoring is used for the following purposes:
● Left ventricular end-diastolic volume (LVEDV) is assessed to determine intravascular

volume status. Treatment of hypovolemia is assessed by monitoring changes in left
ventricular (LV) cavity size. Hypovolemia with likely fluid responsiveness (ie, improvement
in cardiac index with administration of IV fluids) is suggested by decreased LV cavity size
( table 8 and movie 1). Hypervolemia may also be detected. (See "Intraoperative
transesophageal echocardiography for noncardiac surgery", section on 'Assessment of
left ventricular volume'.)
● SVR is assessed. It is often difficult to establish whether a hypotensive patient is

hypovolemic, has a low SVR, or both. With either condition, TEE views show a low LVEDV
and hyperdynamic global ventricular systolic function ( movie 2). If LV cavity size is
normal or increased, vasodilation with low SVR is more likely than hypovolemia
( table 8). Also, if administration of fluids does not result in increased cavity size and
increased BP, it is likely that vasodilation is the cause of hypotension. (See
"Intraoperative transesophageal echocardiography for noncardiac surgery", section on
'Systemic vascular resistance'.)

● Regional and global left ventricular dysfunction can be detected. New regional wall
motion abnormalities (RWMAs; eg, hypokinesis or akinesis) indicating myocardial
ischemia may appear before ischemic changes are noted with ECG or PAC monitors
( figure 7 and figure 8). (See "Intraoperative transesophageal echocardiography for
noncardiac surgery", section on 'Ventricular function'.)
● Global RV systolic function is assessed. Myocardial ischemia, exacerbation of pulmonary

hypertension, or acute pulmonary embolus may each cause severe RV dysfunction
( movie 3). (See "Intraoperative transesophageal echocardiography for noncardiac
surgery", section on 'Global RV systolic function'.)
● Valvular structure and function are assessed. (See "Intraoperative transesophageal

echocardiography for noncardiac surgery", section on 'Valvular structure and function'.)
Clinical information provided by TEE [20,21] (or transthoracic echocardiography [TTE] [22])
often complements data provided by other advanced cardiovascular monitoring methods, as
discussed further in a separate topic. (See "Intraoperative transesophageal echocardiography
for noncardiac surgery".)
Even if a TEE probe is not inserted initially, rapid deployment may be urgently needed to
diagnose the cause of worsening or refractory hypotension (ie, "rescue" TEE). (See
"Intraoperative rescue transesophageal echocardiography (TEE)".)
Cardiac output monitors — Determining whether a patient has a low or high CO state is
helpful to guide intraoperative resuscitative efforts. Several invasive and noninvasive
technologies have been developed to measure CO, including arterial pulse waveform analysis,
thoracic electrical bioimpedance, aortic Doppler, point-of-care echocardiography, and carbon
dioxide rebreathing [23]. Each of these technologies has advantages and limitations with
respect to accuracy of CO measurements, compared with the known limitations of
measurements obtained from a PAC. Details are available in a separate topic. (See "Novel tools
for hemodynamic monitoring in critically ill patients with shock", section on 'Cardiac output'
and "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms
in adults", section on 'Calculation of cardiac output'.)
Bladder catheter — A bladder catheter with a temperature probe is inserted to measure

urine output and core temperature.
INITIAL RESUSCITATION

Initial interventions — Supplemental oxygen (O2) and resuscitative therapies are provided
during the initial preoperative assessment (see 'Rapid preoperative evaluation' above). Specific
interventions depend on the cause of shock, although etiology may be complex or uncertain
in patients presenting to the operating room for emergency surgery ( table 1).
For most surgical patients in shock, initiation or continuation of the following therapies is
immediately necessary:
● Administration of intravenous (IV) crystalloid fluid boluses (typically 500 mL per bolus)
for initial management of most shock etiologies [24]. Exceptions to this approach include
conditions in which excess fluid will worsen cardiac function (eg, cardiogenic shock with
evidence of pulmonary edema, obstructive shock due to pulmonary embolism). For
patients with severe or ongoing hemorrhage, blood products are ordered and
transfused as soon as available, in preference to other fluid therapy (eg, colloids or
crystalloids). (See "Evaluation of and initial approach to the adult patient with
undifferentiated hypotension and shock", section on 'Intravenous fluids'.)
● Hemodynamic support with continuous infusion of a vasopressor agent if administration

of IV fluids does not rapidly restore adequate blood pressure and/or tissue perfusion. We
typically select a continuous infusion of norepinephrine at 0.01 to 0.3 mcg/kg/min as the
first-line vasopressor in undifferentiated shock, although the optimal initial vasopressor
is unknown ( table 9) [24,25] One randomized trial in 310 patients with hypotension
due to sepsis noted that control of shock (defined as mean arterial pressure [MAP] ≥65
mmHg plus either urine output greater than 0.5 mL/kg per hour or a 10 percent decline
in lactate from baseline) within six hours was more likely to be achieved with early
administration of norepinephrine compared with standard care (76 versus 48 percent;
odds ratio [OR] 3.4, 2.1-5.5) [26]. Another randomized trial in 57 patients with
hypotension due to cardiogenic shock noted that a lower incidence of refractory shock in
patients receiving norepinephrine compared with epinephrine [27]. (See "Evaluation of
and initial approach to the adult patient with undifferentiated hypotension and shock",
section on 'Vasopressors'.)
While the optimal end-organ perfusion pressure is unclear, we suggest a target MAP of
approximately 65 mmHg (ie, 65 to 70 mmHg) for most patients rather than employing a
higher target (eg, ≥75 mmHg) in agreement with the CCCS-SSAI WikiRecs clinical practice
guideline [28]. In a systematic review of two randomized trials that included 894 critically
ill adults requiring vasopressor support for treatment of hypotension, a higher target
MAP had no mortality benefit but conferred a higher risk of supraventricular
arrhythmias, compared with a lower target MAP (risk ratio [RR] 2.1, 95% CI 1.3-3.4;
98/100 versus 47/1000) [29]. Most patients included in these trials had a primary
diagnosis of septic shock. The high and low MAP targets in one trial were 80 to 85 versus
65 to 70, and were 75 to 80 versus 60 to 65 in the other [30,31]. In both trials, actual MAP
values in the lower target groups were higher than the target MAP specified in the
protocol, possibly due to challenges in precise titration of vasopressor therapy.
● Bicarbonate therapy may be necessary if the patient has severe metabolic acidosis
limiting the effectiveness of vasopressor and inotropic support [32]. If arterial blood
gases reveal metabolic acidosis with pH <7.1 and serum bicarbonate ≤6 mEq/L, sodium
bicarbonate 1 to 2 mEq/kg is administered as an IV bolus. The dose is repeated if pH
remains <7.1 after 30 minutes. (See "Bicarbonate therapy in lactic acidosis".)
Target values for resuscitation — The goals for initial and ongoing shock resuscitation are to
restore tissue perfusion pressure, return oxygen delivery to normal levels, and prevent organ
damage. Target values for initial and continuing resuscitation in the operating room include:
● MAP 65 to 70 mmHg [28]

● Urine output ≥0.5 mL/kg per hour
● Decreasing serum lactate levels on sequential arterial blood gases [33]
Monitoring cardiac output (CO), mixed venous oxygen saturation, arterial blood gases, and/or
intravascular volume status (ie, fluid responsiveness) may also be helpful to assess efficacy of
initial and ongoing therapy. (See 'Intraoperative monitoring' above.)
HYPOVOLEMIC SHOCK MANAGEMENT
Patients with hemorrhagic or other causes of hypovolemic shock have hypotension with
reduced cardiac output (CO) due to reduced intravascular volume (ie, reduced preload). The
primary intervention is fluid and/or blood administration; vasopressors are added only if
necessary to maintain blood pressure (BP). (See "Definition, classification, etiology, and
pathophysiology of shock in adults", section on 'Hypovolemic'.)
Hemorrhagic or nonhemorrhagic etiology — Hemorrhage is the most common cause of

hypovolemic shock in surgical patients.
Nonhemorrhagic causes of severe hypovolemia in surgical patients include gastrointestinal

losses (eg, vomiting, diarrhea, bowel preparation), skin losses (eg, burns, Stevens-Johnson
syndrome, heat illness), pancreatitis, ascites, and losses into the interstitial space (eg, trauma).
Intraoperative management
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● Fluid administration – Initial management of hypovolemic shock is rapid administration

of intravenous (IV) crystalloid fluid in 500 mL boluses. Typically, 1 to 2 L is administered
initially, but additional fluid may be necessary if losses are continuing.
• Type of fluid – A balanced electrolyte crystalloid solution (eg, Ringer's lactate) is

widely used in preference to conventional saline solutions for initial fluid resuscitation
and replacement of ongoing intraoperative losses, since large volumes of normal (0.9
percent) saline can lead to hyperchloremic metabolic acidosis. (See "Treatment of
severe hypovolemia or hypovolemic shock in adults", section on 'Buffered crystalloid'
and "Intraoperative fluid management", section on 'Crystalloid solutions'.)
Large volumes of IV fluid may lead to development of tissue edema and resultant
complications. An approach that combines crystalloids and colloids may limit the total
amount of administered fluid [34-37]. We typically use this approach to replace blood
loss until blood is available for transfusion, with selection of albumin as the colloid
solution. Hyperoncotic starch colloid solutions (eg, hydroxyethyl starch, pentastarch)
are not used in shock resuscitation [38,39]. In patients with acute traumatic brain
injury, we usually avoid albumin and other colloids and administer only crystalloid
solution [40]. (See "Treatment of severe hypovolemia or hypovolemic shock in adults",
section on 'Normal saline (crystalloid)' and "Anesthesia for patients with acute
traumatic brain injury", section on 'Intraoperative fluid management'.)
• Amount of fluid – Although initial fluid resuscitation may be necessarily rapid, it is

important to decide when to reduce the rate of fluid administration. Resuscitation
endpoints include clinical evidence of normovolemia determined by monitoring
available static and dynamic parameters of intravascular volume status, as well as
achieving target values for resuscitation such as an adequate BP and decreasing
serum lactate levels [33]. Dynamic parameters are preferred to assess intravascular
volume status and guide fluid administration in the operating room (eg,
transesophageal echocardiography [TEE] changes in left ventricular cavity size
( movie 1) or respirophasic variation in the intra-arterial pressure waveform during
positive pressure ventilation ( table 5 and figure 3 and figure 6)) [12,41,42].
Fluid responsiveness (ie, improvement in cardiac index with administration of IV
fluids) is suggested by decreased left ventricular (LV) cavity size on TEE or by
respirophasic systolic pressure variations in the arterial waveform that exceed 15
percent. (See 'Target values for resuscitation' above and "Intraoperative fluid
management", section on 'Monitoring intravascular volume status'.)

If there is evidence of pulmonary edema or high filling pressures, fluids are

administered with caution (ie, in small volume increments of approximately 250 mL)
even if dynamic parameters indicate fluid responsiveness, with close monitoring of
the clinical response to fluid increments (ie, improvement or worsening) [43]. (See
"Intraoperative fluid management", section on 'Dynamic parameters to assess
volume responsiveness' and "Novel tools for hemodynamic monitoring in critically ill
patients with shock", section on 'Volume tolerance and fluid responsiveness'.)
Static physiological parameters such as heart rate, BP, peripheral oxygen saturation,
urine output, central venous pressure (CVP), and pulmonary capillary wedge pressure
(PCWP) provide supplemental data. However, these are suboptimal surrogates to
determine fluid responsiveness, and do not detect or predict impending pulmonary
edema due to hypervolemia [41,44,45]. (See "Intraoperative fluid management",
section on 'Traditional static parameters'.)
● Blood administration – For patients with severe or ongoing hemorrhage, red blood
cells (RBCs) and other appropriate blood products are transfused as soon as they are
available, rather than crystalloid or colloid. (See "Massive blood transfusion" and "Initial
management of moderate to severe hemorrhage in the adult trauma patient".)
● Vasopressors – In addition to fluid administration, vasopressors may be necessary to

restore adequate tissue perfusion ( table 9). In one study of trauma patients with
hemorrhagic shock, survival was not adversely affected by early use of norepinephrine
after failure to restore systemic BP to target values with initial crystalloid fluid challenges
of 1000 to 1500 mL [46]. Although vasopressors may be temporarily necessary to
maintain adequate systemic BP, they are not used as a substitute for fluid administration
and are discontinued as soon as possible [47,48]. (See "Initial management of moderate
to severe hemorrhage in the adult trauma patient", section on 'Vasopressors'.)
● Other considerations
• Calcium administration – Calcium may be depleted due to hemodilution after

administration of large volumes of crystalloid, or due to binding by the citrate in
blood products during massive transfusion. Replacement of calcium by continuous
infusion is often the most convenient way to correct hypocalcemia in this setting.
Administration of either 10 percent calcium gluconate (eg, 10 to 20 mL for each 500
mL of blood) or 10 percent calcium chloride (eg, 2 to 5 mL per 500 mL of blood) is
appropriate. (See "Massive blood transfusion", section on 'Hypocalcemia from citrate
toxicity'.)

• Mechanical ventilation – During general anesthesia with mechanical ventilation, it is

important to avoid high levels of positive end-expiratory pressure (PEEP) and dynamic
hyperinflation with development of auto-PEEP secondary to incomplete expiration.
PEEP and auto-PEEP can increase intrathoracic pressure, decrease venous return, and
further reduce CO. (See "Clinical and physiologic complications of mechanical
ventilation: Overview", section on 'Hypotension'.)
DISTRIBUTIVE SHOCK MANAGEMENT
Patients with distributive shock have hypotension with reduced systemic vascular resistance
(SVR) due to severe peripheral vasodilation. The initial intervention is fluid administration
and/or vasopressors to maintain blood pressure (BP). (See "Definition, classification, etiology,
and pathophysiology of shock in adults", section on 'Distributive'.)
Septic shock — Sepsis is the most common cause of distributive shock in surgical patients.
Initial treatment is with fluid therapy to treat intravascular hypovolemia (which may be severe)
and/or vasopressor therapy (typically norepinephrine) if necessary to restore MAP to ≥65 to 70
mmHg. Other vasopressor agents, inotropic therapy, or blood transfusion are additional
therapies that may be added. Ensuring adequate organ perfusion is emphasized, rather than
achieving a higher MAP target (eg, ≥75 mmHg) which may be associated with harm [28-30].
Patients with chronic hypertension may require a higher MAP. Ideally, urine output will be
restored to ≥0.5 mL/kg per hour. (See "Evaluation and management of suspected sepsis and
septic shock in adults".)
● Fluid administration – Similar to hypovolemic shock, a balanced electrolyte crystalloid

solution (eg, Ringer's lactate) is administered in 500 mL boluses. Approximately 2 to 5 L
of fluid may be necessary to restore MAP to ≥65 to 70 mmHg [49,50]. (See "Evaluation
and management of suspected sepsis and septic shock in adults", section on 'Volume'.)
If larger volumes of intraoperative crystalloid are required, albumin may be substituted

for crystalloid solution. However, there are no outcome differences for septic shock
patients treated with human albumin compared with normal saline. Hyperoncotic starch
solutions (eg, hydroxyethyl starch or pentastarch) are avoided due to concerns regarding
increased renal injury and mortality. (See "Evaluation and management of suspected
sepsis and septic shock in adults", section on 'Choice of fluid'.)
Hemodilution may result in anemia, particularly if surgical bleeding is occurring. We

typically reserve red blood cell (RBC) transfusion for patients with a hemoglobin (Hgb)

level ≤7 g/dL. (See "Evaluation and management of suspected sepsis and septic shock in
adults", section on 'Red blood cell transfusions'.)
● Vasopressors – If fluid administration does not restore MAP to 65 to 70 mmHg, a

vasopressor infusion, typically norepinephrine, is administered ( table 10 and
table 9) [24,49,51-53]. Phenylephrine may be substituted if tachycardia or arrhythmias
are evident during norepinephrine infusion.
If fluids and norepinephrine infusion are ineffective, a vasopressin infusion is initiated

and titrated as necessary ( table 10), since acquired vasopressin deficiency may occur
after protracted hypoperfusion due to septic shock [54,55]. If cardiac function is
adequate, administration of vasopressin typically results in normalization of MAP and
may decrease risk of atrial fibrillation and possibly mortality in patients with distributive
shock and hypotension that is refractory to administration of fluids and other
vasopressors [56-59]. Administration of vasopressin or a combination of vasopressin
with norepinephrine may be associated with lower rates of atrial fibrillation compared
with administration of norepinephrine alone [58,59]. If there is evidence of low cardiac
output (CO) in a septic patient with refractory shock, additional inotropic therapy may be
warranted. (See "Evaluation and management of suspected sepsis and septic shock in
adults", section on 'Vasopressors' and "Evaluation and management of suspected sepsis
and septic shock in adults", section on 'Inotropic therapy'.)
Methylene blue has been used in patients with refractory hypotension due to vasoplegia
caused by sepsis or other etiologies (eg, anaphylaxis, vasoplegia following
cardiopulmonary bypass) ( table 10) [53,60-65]. Production of nitric oxide (NO) is
increased in many types of vasodilatory shock. Methylene blue administered as a dose of
1 to 2 mg/kg over 20 minutes inhibits guanylyl cyclase and NO synthase activity, which
reduces resistance vessel responsiveness to nitric oxide, and thereby increases SVR.
Methylene blue may interfere with measurements of oxygen saturation using oximetry
technology and may cause serotonin syndrome in patients taking other serotonergic
agents. (See "Serotonin syndrome (serotonin toxicity)" and "Methemoglobinemia",
section on 'Methylene blue (MB)'.)
Angiotensin II, a component of the renin-angiotensin-aldosterone system, is a potent

vasoconstrictor approved for treatment of vasodilatory shock ( table 10) [66-70].
Angiotensin II increases blood pressure and reduces catecholamine doses in patients
unresponsive to conventional vasopressors (eg, norepinephrine, vasopressin) [71,72].
(See "Use of vasopressors and inotropes", section on 'Angiotensin II'.)

Adjunctive agents that are used more rarely and with limited evidence include vitamin C
and hydroxycobalamin ( table 10) [64,65,70,73,74]. In some cases, combinations of
vasopressors, inotropes, and other pharmacologic agents and therapies may be
necessary for effective treatment, and may limit potential toxicities of any one agent
[59,64-66]. Further details regarding management of vasoplegia due to septic shock are
available in a separate topic. (See "Evaluation and management of suspected sepsis and
septic shock in adults".)
● Other considerations
• Antibiotics – Broad spectrum intravenous (IV) antibiotic therapy should be

administered as quickly as possible, and definitely within three hours of presentation
to hospital, since delay is associated with increased mortality. Ideally, blood cultures
should be drawn before antibiotics are administered so that subsequent
antimicrobial therapy can be targeted against specific organisms based on blood
culture results and bacterial sensitivities. (See "Evaluation and management of
suspected sepsis and septic shock in adults", section on 'Choosing a regimen'.)
• Hyperglycemia – Most patients with septic shock have hyperglycemia and insulin
resistance. IV insulin therapy is typically required to achieve a target blood glucose
level between 140 and 180 mg/dL (7.7 to 10 mmol/L). (See "Glycemic control in
critically ill adult and pediatric patients".)
• Relative adrenal insufficiency – For patients with severe septic shock refractory to
adequate fluid and vasopressor therapy, IV corticosteroid therapy is administered,
typically hydrocortisone 50 mg every six to eight hours. Details regarding
glucocorticoid therapy in septic shock patients are discussed elsewhere. (See
"Glucocorticoid therapy in septic shock in adults".)
For new onset of refractory hypotension, a stress dose of a glucocorticoid is

administered (eg, an IV bolus of hydrocortisone 100 mg or dexamethasone 4 mg),
particularly in a patient who received etomidate for induction of anesthesia. (See
'Endocrine shock' below and "General anesthesia: Intravenous induction agents",
section on 'Disadvantages and adverse effects'.)
Anaphylactic shock — Agents commonly used in the operating room may cause anaphylaxis
(eg, antibiotics, neuromuscular blocking agents, latex ( table 11)). Also, immunologic
anaphylactic reactions may occur due to transfusion of a blood product. (See "Approach to the
patient with a suspected acute transfusion reaction", section on 'Anaphylactic transfusion
reaction'.)
Treatment is based upon prompt administration of IV epinephrine and fluid resuscitation

( table 12). Details are available in a separate topic. (See "Perioperative anaphylaxis: Clinical
manifestations, etiology, and management".)
Neurogenic shock — Spinal cord injury with neurogenic shock may be present in a surgical
trauma patient. Neurogenic shock is typically associated with tachycardia in a paraplegic
patient, or bradycardia in a quadriplegic patient. Management is described separately. (See
"Anesthesia for adults with acute spinal cord injury".)
Severe hypotension after a neuraxial anesthetic is another potential cause of neurogenic

shock in the operating room. (See "Overview of neuraxial anesthesia", section on
'Cardiovascular'.)
Endocrine shock
● Addisonian crisis – During surgery, an Addisonian crisis due to adrenal insufficiency

may occur in a patient with longstanding corticosteroid use due to inability to mount a
stress response to surgical trauma. Stress-induced adrenal insufficiency can also occur in
certain patients who are not taking steroids chronically (eg, trauma patients with adrenal
hemorrhage or septic patients with adrenal infarcts). Primary or secondary adrenal
insufficiency should be suspected in a patient with shock who is not responding to initial
resuscitation efforts. In such cases, administration of an IV bolus of hydrocortisone 100
mg or dexamethasone 4 mg is critical, since failure to administer a therapeutic dose of
glucocorticoid may result in unsuccessful resuscitation and death. (See "Treatment of
adrenal insufficiency in adults", section on 'Adrenal crisis'.)
Hypoglycemia in a hypotensive shock patient may occur due to Addisonian crisis. Other
signs include electrolyte and acid base disturbances, although intraoperative fluid
resuscitation and preexisting comorbidities such as renal failure may mask classic
findings of hyponatremia and hyperkalemia. Addisonian crisis may also mimic septic
shock, since a low-grade fever is typically present. Preemptive prevention of Addisonian
crisis with specific perioperative glucocorticoid regimens is based on the type and
anticipated duration of the surgical procedure ( table 13). Details are available
elsewhere. (See "The management of the surgical patient taking glucocorticoids".)
● Myxedema coma or thyrotoxicosis – Rarely, severe hypothyroidism (ie, myxedema

coma) or severe hyperthyroidism (ie, thyrotoxicosis) can mimic shock in an anesthetized
patient; treatment is discussed in other topics. (See "Nonthyroid surgery in the patient
with thyroid disease" and "Anesthesia for patients with thyroid disease and for patients
who undergo thyroid or parathyroid surgery", section on 'Preanesthesia evaluation'.)
Drug and toxin-induced shock — Vasoplegia may occur in the perioperative period in
patients receiving preoperative angiotensin-converting enzyme (ACE) inhibitors or calcium
channel blockers. This occurs most commonly during cardiac surgery with cardiopulmonary
bypass (CPB), possibly due to exacerbating effects of the systemic inflammatory response
syndrome (SIRS) induced by CPB. (See "Postoperative complications among patients
undergoing cardiac surgery", section on 'Vasodilatory shock'.)
Certain infections in surgical patients are associated with toxic shock syndrome (eg,
Streptococcus, Staphylococcus aureus, and Clostridium sordelli). Treatment is described
separately. (See "Invasive group A streptococcal infection and toxic shock syndrome:
Treatment and prevention" and "Staphylococcal toxic shock syndrome" and "Toxic shock
syndrome due to Clostridium sordellii".)
In burn patients, carbon monoxide or cyanide poisoning may cause mitochondrial

dysfunction resulting in perioperative shock. (See "Carbon monoxide poisoning" and "Cyanide
poisoning" and "Inhalation injury from heat, smoke, or chemical irritants", section on
'Systemic toxicity'.)
CARDIOGENIC SHOCK MANAGEMENT
Patients with cardiogenic shock have hypotension with reduced cardiac output (CO) due to an
intracardiac cause of cardiac pump failure. Initial treatment is inotropic support to improve
myocardial contractility and treatment of arrhythmias. In contrast to hypovolemic or
distributive shock, administration of intravenous (IV) fluid boluses is contraindicated as first
line therapy in cardiogenic shock, particularly if there is evidence of pulmonary edema or
elevated atrial pressure. A summary of appropriate hemodynamic goals in left ventricular (LV)
cardiogenic shock due to various causes is presented in the table ( table 14). (See
"Definition, classification, etiology, and pathophysiology of shock in adults", section on
'Cardiogenic'.)
Patients with cardiogenic shock do not undergo surgery unless they have a life-threatening
surgical condition (see "Management of cardiac risk for noncardiac surgery", section on 'For
urgent or emergency surgery'). However, severe secondary myocardial dysfunction may
complicate management of other types of shock (eg, septic or neurogenic shock); this
possibility should be considered and treated in a hypotensive patient who is not responding
to resuscitation efforts.
Cardiomyopathic shock

● Myocardial infarction – Myocardial infarction (MI) is the most common intraoperative

cause of severe myocardial dysfunction; shock is more likely if >40 percent of the
myocardium is involved. Even if a smaller portion of myocardial tissue is infarcted,
extensive ischemia, stunned myocardium, or the systemic inflammatory response
syndrome (SIRS) response that occurs after cardiac arrest may result in severe
ventricular dysfunction [75]. (See "Clinical manifestations and diagnosis of cardiogenic
shock in acute myocardial infarction".)
Primary treatment is with infusion of a sympathomimetic agent with inotropic and

vasopressor properties, typically, norepinephrine ( table 9) [24,27,76]. In a randomized
trial comparing administration of norepinephrine versus epinephrine to treat
cardiogenic shock after acute MI, effects of these agents on blood pressure (BP) and
cardiac index were similar; however, patients receiving epinephrine had a higher
incidence of refractory shock (37 versus 7 percent; 57 patients) [27]. (See "Prognosis and
treatment of cardiogenic shock complicating acute myocardial infarction", section on
'Vasopressors and inotropes'.)
Intraoperative volume administration is guided by dynamic parameters to assess

intravascular volume status (eg, transesophageal echocardiography [TEE] changes in LV
cavity size ( movie 1) or respirophasic variation in the intra-arterial pressure waveform
during positive pressure ventilation ( table 5 and figure 3 and figure 6)) [41,42].
If there is evidence of volume overload with high filling pressures, acute decompensated
right ventricular (RV) failure, and/or cardiogenic pulmonary edema, fluids are
administered with caution (ie, in increments of approximately 100 mL), even if dynamic
parameters indicate fluid responsiveness [43]. (See "Intraoperative management for
noncardiac surgery in patients with heart failure", section on 'Management of fluids and
blood products' and "Intraoperative fluid management", section on 'Dynamic
parameters to assess volume responsiveness' and "Novel tools for hemodynamic
monitoring in critically ill patients with shock", section on 'Volume tolerance and fluid
responsiveness'.)
● Acute decompensated heart failure – Left, right, or biventricular heart failure may
cause cardiogenic shock. The algorithms describe intraoperative management of
presumed LV failure ( algorithm 3) and RV failure ( algorithm 4).
• Left-sided heart failure – In general, goals during the intraoperative period are to
reduce preload and afterload, maintain sinus rhythm and a normal to high heart rate

(HR) of 80 to 100 beats per minute, and improve contractility. (See "Intraoperative
management for noncardiac surgery in patients with heart failure".)
Because decompensated left-sided heart failure is often associated with pulmonary

edema, appropriate levels of positive end-expiratory pressure (PEEP; eg, 5 to 10 cm
H2O) are employed to improve oxygenation. However, high PEEP >10 cm H2O is
generally avoided, as this may deleteriously reduce venous return and CO. (See
"Positive end-expiratory pressure (PEEP)", section on 'Potential sequelae'.)
• Right-sided heart failure – Perioperative right-sided cardiogenic shock is

aggressively treated since it rapidly leads to multiorgan system failure ( figure 9
and figure 10). Infusion of an inodilator agent such as milrinone or dobutamine is
usually indicated ( table 9). However, inodilator administration may reduce systemic
vascular resistance (SVR) and BP, with adverse consequences for RV function. Thus,
concomitant use of a vasopressor infusion such as norepinephrine or vasopressin is
typically required to maintain adequate coronary perfusion. Specific effects of
vasoactive agents in patients with right-sided cardiogenic shock are noted in the
table ( table 15). (See "Treatment of acute decompensated heart failure: Specific
therapies", section on 'Management of hypotensive patients'.)
Pulmonary vascular resistance (PVR) should be minimized by maintaining normal

PaCO2, PaO2, and pH levels. Excessive tidal volumes, excessive PEEP, and atelectasis
should be avoided (see "Clinical and physiologic complications of mechanical
ventilation: Overview", section on 'Hypotension'). It is also important to maintain
normothermia (see 'Temperature management' below). If necessary, inhaled nitric
oxide or prostanoids (eg, epoprostenol) may be administered to reduce PVR. (See
"Treatment of pulmonary arterial hypertension (group 1) in adults: Pulmonary
hypertension-specific therapy" and "Inhaled nitric oxide in adults: Biology and
indications for use".)
Rarely, mechanical ventricular support or extracorporeal membrane oxygenator (ECMO)

support through venoarterial ECMO is used to manage profound cardiogenic shock that
is unresponsive to conventional therapy. (See "Short-term mechanical circulatory assist
devices" and "Extracorporeal life support in adults in the intensive care unit: Overview".)
● Other causes of cardiomyopathic shock – Intraoperative management of other causes

of cardiogenic shock (eg, hemodynamic instability after cardiac arrest, traumatic
myocardial contusion, myocarditis, drug-induced causes [eg, beta blockers]) is similar to
that for shock due to decompensated heart failure. Details are available elsewhere:

• (See "Anesthesia for emergency surgery after cardiac arrest".)

• (See "Anesthesia for thoracic trauma in adults", section on 'Blunt cardiac injury'.)
• (See "Treatment and prognosis of myocarditis in adults", section on 'Heart failure
therapy'.)
• (See "Beta blocker poisoning", section on 'Management'.)
Arrhythmogenic shock — Management of arrhythmogenic causes of shock is described in

advanced cardiac life support protocols. (See "Advanced cardiac life support (ACLS) in adults",
section on 'Management of specific arrhythmias'.)
Of note, surgical patients in shock who have a fixed-rate pacemaker occasionally require an
increase in the underlying rate to restore adequate perfusion. This is accomplished by the
cardiology or institutional cardiac implantable electronic device (CIED) care team. (See
"Perioperative management of patients with a pacemaker or implantable cardioverter-
defibrillator".)
Mechanical shock
● Left ventricular outflow tract (LVOT) obstruction – Dynamic left ventricular outflow
tract (LVOT) obstruction with mitral regurgitation and severe hypotension can be
precipitated in a susceptible surgical patient with hypertrophic cardiomyopathy if
hypovolemia, vasodilation, tachycardia, and/or a high catecholamine state develop [77].
Since these conditions occur in hypovolemic shock and distributive shock, LVOT
obstruction should be suspected in a patient who is not responding to resuscitation
efforts during surgery.
Rapid diagnosis is possible with TEE. (See "Intraoperative rescue transesophageal

echocardiography (TEE)", section on 'Left ventricular outflow tract obstruction'.)
Immediate treatment of hemodynamically significant LVOT obstruction includes (see

"Hypertrophic cardiomyopathy: Management of patients with outflow obstruction",
section on 'Acute shock'):
• Increasing LV volume with fluid administration.

• Increasing SVR with vasoconstrictors that do not have inotropic properties (eg,
phenylephrine 50 to 100 mcg boluses followed by initiation of an infusion, or
initiation and titration of a vasopressin infusion) ( table 9).
• Decreasing inotropy and HR with anesthetic agents or beta blockers.

● Acute valvular or ventricular structural pathology – Other mechanical causes of

suddenly developing cardiogenic shock may occur after an acute intraoperative MI (eg,
severe mitral regurgitation due to rupture of the papillary muscles or chordae tendineae,
or ventricular septal defect or free wall rupture) (see "Acute myocardial infarction:
Mechanical complications"). Patients undergoing thoracic surgery after blunt chest
trauma may develop acute aortic regurgitation due to aortic dissection extending into
the aortic valve (see "Acute aortic regurgitation in adults"). In such cases, survival
typically depends on prompt diagnosis with intraoperative TEE and emergency cardiac
surgical intervention. (See "Intraoperative rescue transesophageal echocardiography
(TEE)".)
OBSTRUCTIVE SHOCK MANAGEMENT
Patients with obstructive shock have hypotension with reduced CO due to an extracardiac
cause of pump failure, and often associated with poor right ventricular output. Treatment is
decompression or specific surgical intervention to relieve the obstruction. Administration of
fluids and/or vasopressors does not correct the cause of obstructive shock, but may provide
temporary hemodynamic stability to allow definitive surgical treatment. (See 'Initial
resuscitation' above and "Definition, classification, etiology, and pathophysiology of shock in
adults", section on 'Obstructive'.)
Pericardial tamponade — Obstructive shock may be caused by cardiac tamponade due to

trauma or other etiologies. Anesthetic management is discussed separately. (See "Anesthesia
for thoracic trauma in adults", section on 'Cardiac tamponade' and "Anesthesia for thoracic
trauma in adults", section on 'Anesthetic considerations for specific procedures'.)
Tension pneumothorax or hemothorax — Intraoperative tension pneumothorax most

commonly occurs after attempted or actual central venous catheter (CVC) insertion, and in
patients undergoing surgery in the neck or thorax, or after blunt thoracic trauma.
Hypotension is typically accompanied by worsening oxygenation. Emergency needle
decompression is followed by chest tube placement by the surgeon. (See "Thoracostomy
tubes and catheters: Indications and tube selection in adults and children", section on
'Tension pneumothorax'.)
Auto-PEEP — Auto-positive end-expiratory pressure (auto-PEEP, also called intrinsic PEEP)

exists when there is positive airway pressure at the end of expiration due to incomplete
exhalation. This phenomenon can cause shock by reducing the amount of venous return, as
determined by the pressure gradient from the extrathoracic systemic veins to the right

atrium. Auto-PEEP improves when the breathing circuit is transiently disconnected. (See
"Clinical and physiologic complications of mechanical ventilation: Overview", section on
'Hypotension' and "Clinical and physiologic complications of mechanical ventilation:
Overview", section on 'Auto-PEEP'.)
Air embolism — Intraoperative venous air embolism may occur as a complication of CVC
insertion, after blunt trauma to the chest, or during neurosurgical, otolaryngological, and
other surgical procedures. (See "Air embolism", section on 'Intravascular catheters' and "Air
embolism", section on 'Surgery and trauma'.)
The anesthesiologist immediately places the patient in a left lateral decubitus or

Trendelenburg position, or both (ie, left lateral decubitus head down position). Thus, the right
ventricular outflow tract will be inferior to the right ventricular cavity, causing air to migrate
superiorly into a position within the right ventricle from which it is less likely to embolize. (See
"Air embolism", section on 'Positioning the patient'.)
Crystalloid fluid boluses (eg, 500 mL per bolus) are administered to increase venous pressure
to avoid further entry of gas into the venous system, and a vasopressor is administered to
restore blood pressure (BP). (See 'Initial resuscitation' above.)
Other specific interventions may be employed by the surgeon (eg, withdrawal of air from the
right atrium, cardiac massage) or the patient may be transferred to a hyperbaric oxygen
facility, if available. (See "Air embolism", section on 'Supportive therapy' and "Air embolism",
section on 'Definitive therapy'.)
Pulmonary embolism — Patients with massive pulmonary embolus (PE) may undergo
emergency surgical embolectomy, typically performed by a cardiac surgeon with the aid of
cardiopulmonary bypass (CPB). Severe RV dysfunction is typically present; thus, anesthetic
management is similar to that for right-sided cardiogenic shock ( table 9 and table 15).
(See 'Cardiomyopathic shock' above and "Treatment, prognosis, and follow-up of acute
pulmonary embolism in adults", section on 'Surgical embolectomy'.)
Increased intra-abdominal pressure — Abdominal compartment syndrome may necessitate

urgent or emergency surgery to decompress the abdomen. Similar to management of shock
from other causes, crystalloid fluid boluses (eg, 500 mL per bolus) and vasopressor agents are
administered as necessary to restore BP until decompression is achieved. (See 'Initial
resuscitation' above and "Abdominal compartment syndrome in adults".)
ANESTHETIC MANAGEMENT
General anesthesia — Anesthetic induction and maintenance agents with minimal

hemodynamic effects are administered to surgical patients in shock. Doses are usually
reduced to avoid exacerbation of hypotension.
Induction — The goal of induction of general anesthesia is to produce an unconscious state

while maintaining adequate organ perfusion. Either etomidate or ketamine is typically
selected as the primary induction agent in a hemodynamically unstable patient ( table 16).
Adjuvant agents (eg, opioids, lidocaine, midazolam) are usually eliminated, or at least
reduced. (See "General anesthesia: Intravenous induction agents".)
Induction agents and techniques include:
● Etomidate – Etomidate has rapid onset without changes in blood pressure (BP), cardiac
output (CO), or heart rate (HR). Although etomidate is often selected for shock patients,
it causes transient acute adrenal insufficiency. The preponderance of evidence suggests
that etomidate is not associated with increased mortality in critically ill patients
compared with other induction agents [78]. In an individual patient, the risk of transient
cortisol suppression is weighed against adverse hemodynamic effects that may be
caused by alternative induction agents. We usually select an alternative agent for
patients with known septic shock, although there is no evidence that a single dose of
etomidate increases mortality in these patients [79].
If refractory hypotension develops after use of etomidate, an intravenous (IV) stress dose
of a glucocorticoid should be administered (eg, hydrocortisone 100 mg or
dexamethasone 4 mg). (See "General anesthesia: Intravenous induction agents", section
on 'Etomidate' and 'Septic shock' above.)
● Ketamine – Ketamine has rapid onset and typically increases BP, HR, and CO by
increasing sympathetic tone ( table 16). We typically avoid ketamine in patients with
cardiogenic shock caused by myocardial ischemia because the increases in HR and BP
may detrimentally unbalance myocardial oxygen supply versus demand. Also, the
sympathomimetic effects of ketamine may detrimentally increase pulmonary artery
pressure (PAP) in patients with pulmonary hypertension or right-sided heart failure.
Ketamine has mild intrinsic dose-related myocardial depressant properties that are
normally overcome by increased sympathetic tone, but may become apparent in a
patient with profound shock and depleted catecholamine reserves. The induction dose
of ketamine is reduced in such patients. (See "General anesthesia: Intravenous induction
agents", section on 'Ketamine'.)

● Opioids – A high-dose opioid technique with a synthetic opioid (eg, fentanyl or

sufentanil) is employed for induction of anesthesia in selected patients with severe
cardiovascular disease because these agents have minimal myocardial depressant
effects. However, we avoid high opioid doses in patients with hypovolemic, distributive,
or obstructive shock, since this technique may cause hypotension in a patient who is
dependent on high catecholamine levels. (See "Anesthesia for cardiac surgery: General
principles", section on 'Higher-dose opioid technique'.)
● Propofol – A typical bolus induction dose of propofol is avoided since this may
exacerbate hypotension by causing dose-dependent venous and arterial dilation and
decreased contractility. However, small titrated doses of propofol combined with other
intravenous or inhalation anesthetic agent(s) is a reasonable choice for induction. (See
"General anesthesia: Intravenous induction agents", section on 'Propofol'.)
Management of dose-related potential adverse effects of any selected agent is critically

important. Potential cardiovascular effects of induction agent(s) may be exacerbated in a
patient with shock (eg, due to a smaller volume of the central compartment). Therefore, dose
reduction is usually prudent. (See "General anesthesia: Intravenous induction agents", section
on 'Dosing considerations'.)
Before beginning induction, a vasopressor infusion should be connected "in line" in the
intravenous (IV) tubing so that it is ready for immediate administration ( table 9). In some
cases, a bolus dose of a vasopressor is administered concurrently with the induction agent to
prevent exacerbation of hypotension (eg, phenylephrine 100 to 200 mcg, norepinephrine 4 to
8 mcg, vasopressin 0.2 to 0.4 units). (See "Induction of general anesthesia: Overview", section
on 'Vasopressor agents'.)
Maintenance — Anesthetic agents for maintenance of anesthesia are selected with

consideration of dose-dependent cardiovascular effects. In most cases, a volatile inhalation
anesthetic agent is initiated at a lower concentration than in healthy patients, with titration to
maintain anesthesia while avoiding a further decrease in end-organ perfusion. (See
"Maintenance of general anesthesia: Overview", section on 'Inhalation anesthetic agents and
techniques'.)
The use of unprocessed or processed electroencephalography (EEG) provides information

regarding anesthetic depth but cannot reliably confirm that a patient is unaware. Anesthetic
underdosing and awareness with recall occur more commonly in patients with shock
compared with healthy patients. (See "Accidental awareness during general anesthesia",

section on 'Brain monitoring' and "Accidental awareness during general anesthesia", section
on 'Risk factors'.)
Regional anesthesia — Neuraxial anesthetic techniques are avoided in patients with shock
because of the potential for hypotension due to vasodilation and/or bradycardia. (See
"Overview of neuraxial anesthesia", section on 'Cardiovascular' and "Adverse effects of
neuraxial analgesia and anesthesia for obstetrics", section on 'Hypotension'.)
The use of peripheral nerve blocks for selected procedures is an attractive option because of
minimal effects on hemodynamics. However, most patients with shock have hemodynamic
and/or respiratory instability, requiring endotracheal intubation and controlled ventilation
under general anesthesia for a surgical intervention.
Temperature management — Warming devices are employed to maintain normothermia

(temperature ≥35.5°C) throughout the intraoperative period. These include upper- and lower-
body forced-air warming devices and blankets, insulation water mattresses, and devices for
warming all IV fluids. (See "Perioperative temperature management", section on 'Prevention
and management'.)
Hypothermia results in sympathetic stimulation with increased myocardial oxygen

consumption, particularly if shivering occurs, which may lead to myocardial ischemia. Other
adverse consequences of hypothermia include sepsis, coagulopathy, decreased platelet
function, and increased mortality. A decrease in body temperature as little as 2°C also slows
drug metabolism (particularly degradation of neuromuscular blocking agents). (See
"Perioperative temperature management", section on 'Consequences'.)
POSTOPERATIVE TRANSPORT AND HANDOFF IN THE ICU
Transport to the intensive care unit — Most patients with intraoperative shock remain
intubated and sedated with controlled ventilation in the immediate postoperative period.
Details regarding safe transport of critically ill patients are discussed separately. (See
"Transport of surgical patients" and "Transport of surgical patients", section on
'Considerations for critically ill patients'.)
Handoff in the intensive care unit — Upon arrival in the ICU, patient information is
communicated from the surgical team to the ICU team using a formal process termed a
"handoff" or "handover" ( table 17) [80-83]. In all cases, the anesthesiologist should remain
with the patient until hemodynamic and overall stability are ensured. (See "Handoffs of
surgical patients".)
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: Use of point-of-care
echocardiography and ultrasonography as a monitor for therapeutic intervention in critically
ill patients".)
SUMMARY AND RECOMMENDATIONS
● Rapid preoperative evaluation
• General assessment – Intraoperative shock, as in other settings, is generally

attributable to hypovolemic, cardiogenic, distributive, or obstructive causes
( table 1). Simultaneous evaluation and resuscitation may be necessary for urgent
or emergency surgery ( algorithm 1 and algorithm 2). (See 'Rapid preoperative
evaluation' above.)
• Point-of-care ultrasonography – Rapid examination of the heart, chest, abdomen,

major arteries and veins using point-of-care ultrasonography in the preoperative area
or operating room may confirm the cause(s) of shock ( table 2). Typical
hemodynamic profiles noted on a pulmonary artery catheter (PAC) may also be
helpful ( table 3). (See 'Point-of-care ultrasonography' above and 'Pulmonary artery
catheter' above.)
• Assessing urgency – Decisions regarding urgency of the procedure are

individualized depending on the specific etiology (eg, hypovolemic [hemorrhagic or
nonhemorrhagic], distributive, cardiogenic, obstructive) and severity of the cause of
shock. (See 'Urgency of the planned procedure' above.)
● Intraoperative monitoring
• Intra-arterial catheter – An intra-arterial catheter is inserted for continuous

monitoring of arterial blood pressure (BP), pulse pressure (PP) ( figure 1), and
respirophasic variation in the pressure waveform as a dynamic parameter to
determine fluid responsiveness ( figure 3 and figure 6). (See 'Intra-arterial
catheter' above.)
• Central venous catheter (CVC) – A CVC is inserted for infusion of vasoactive drugs,
venous access for fluid and blood administration, measurements of central mixed
venous oxygen saturation (ScvO2), and supplemental data regarding intravascular

volume status. (See 'Central venous catheter' above.)
• Transesophageal echocardiography (TEE) – TEE can be employed to confirm

cause(s) of shock and continuously monitor cardiac function and intravascular
volume status. (See 'Transesophageal echocardiography' above.)
• Other invasive cardiovascular monitors – In selected patients, a PAC ( table 3) or

novel cardiac output (CO) monitor may be employed. (See 'Pulmonary artery catheter'
above and 'Cardiac output monitors' above.)
● Initial resuscitation – Intraoperative resuscitation target values include a mean arterial

pressure (MAP) value of 65 to 70 mmHg, urine output ≥0.5 mL/kg per hour, and
decreasing serum lactate levels. Specific therapies depend on the underlying shock
etiology ( table 1). (See 'Target values for resuscitation' above.)
● Hypovolemic shock – Etiologies in surgical patients include hemorrhagic or

nonhemorrhagic hypovolemia with reduced CO. (See 'Hypovolemic shock management'
above.)
• Initial treatment is intravenous (IV) fluid administered as 500 mL boluses of a

balanced electrolyte crystalloid solution rather than normal saline. For patients with
severe or ongoing hemorrhage, blood products are transfused as soon as available.
An approach that combines crystalloids and colloids (typically albumin) may limit the
total administered volume. Dynamic parameters are employed to assess intravascular
volume status to guide volume administration (eg, respirophasic variation in the
intra-arterial pressure waveform or TEE changes in left ventricular [LV] diameter).
• Vasopressor infusion (typically norepinephrine) is necessary if fluid administration

does not restore MAP to 65 to 70 mmHg ( table 9). Replacement of depleted
calcium or inotrope administration may also be necessary.
● Distributive shock – Etiologies in surgical patients include anaphylactic ( table 12),

septic, neurogenic, endocrine (eg, Addisonian crisis), or drug-induced vasodilation. (See
'Distributive shock management' above.)
Sepsis is the most common cause of distributive shock in surgical patients. Initial
treatment is with fluid therapy to treat intravascular hypovolemia due to vasodilation
(approximately 2 to 5 L) and/or vasopressor therapy (typically norepinephrine
( table 9)) to ensure adequate tissue perfusion. Red blood cells (RBCs) are transfused if

hemoglobin level is ≤7 g/dL. Other vasopressor agents such as vasopressin or methylene

blue may be selected for refractory hypotension ( table 10). IV insulin therapy to
maintain blood glucose level between 140 and 180 mg/dL (7.7 to 10 mmol/L), stress
doses of an IV glucocorticoid agent, and broad spectrum IV antibiotics are typically
necessary as well. (See 'Septic shock' above.)
● Cardiogenic shock – Etiologies include intracardiac causes of cardiac pump failure that
reduce CO. (See 'Cardiogenic shock management' above.)
• Cardiomyopathic shock may be due to left-sided or right-sided heart failure

( algorithm 3 and algorithm 4), myocardial ischemia or infarction, hemodynamic
instability after cardiac arrest, traumatic myocardial contusion, myocarditis, or drug-
induced causes (eg, beta blockers). Initial treatment is with inotropic agents
( table 9). In contrast to hypovolemic or distributive shock, administration of IV fluid
boluses is contraindicated as first line therapy, particularly if there is evidence of
cardiogenic pulmonary edema. (See 'Cardiomyopathic shock' above.)
• Arrhythmogenic shock management is described in advanced cardiac life support

protocols. (See 'Arrhythmogenic shock' above and "Advanced cardiac life support
(ACLS) in adults".)
• Mechanical causes of cardiogenic shock include left ventricular outflow tract (LVOT)
obstruction, which is treated by volume administration, increasing SVR, and
decreasing inotropy. (See 'Mechanical shock' above.)
● Obstructive shock – Etiologies in surgical patients include extracardiac causes of

cardiac pump failure that reduce CO (eg, pericardial tamponade, tension pneumothorax,
air embolism, pulmonary embolism). (See 'Obstructive shock management' above.)
• Treatment is decompression to relieve the obstruction.
• Administration of fluids and vasopressors does not correct the cause, but may
provide temporary hemodynamic stability to allow definitive surgical treatment.
● Anesthetic management – Induction and maintenance agents with minimal

hemodynamic effects are selected, doses are reduced, and vasopressor agents are
administered if necessary to prevent or treat hypotension. Warming devices are
employed to maintain normothermia. (See 'Anesthetic management' above.)
● Postoperative transport and handoff – The anesthesiologist should continuously

monitor the patient throughout transport to the intensive care unit (ICU) after surgery.
Upon arrival, patient information is communicated to the ICU team using a formal
process termed a "handoff" or "handover" ( table 17). (See 'Postoperative transport
and handoff in the ICU' above.)
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20/6/23, 19:30 Intraoperative management of shock in adults - UpToDate

Literature review current through: May 2023.

RAPID PREOPERATIVE EVALUATION

Intraoperative shock is generally attributable to hypovolemic, cardiogenic, distributive, or

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Hypotension may not be evident in the earliest stages of shock because of

• Reduced PP – Reduced PP may be due to a low CO with vasoconstriction, which

• Increased PP – Increased PP may be due to a high CO with vasodilation, which occurs

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● Available preoperative tests – The electrocardiogram and results of laboratory tests

Point-of-care ultrasonography — Point-of-care ultrasonography may be useful to diagnose

• Cardiogenic shock – Severely decreased contractility of the LV, RV, or both.

• Aortic dissection or aneurysm

Further details regarding advantages and limitations of urgent and emergency

Urgency of the planned procedure — Decisions regarding urgency of the surgical

● Hypovolemic hemorrhagic shock due to trauma – Immediate damage control surgery is

● Obstructive shock – Immediate intervention is typically necessary to rapidly decompress

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Standard monitors — Standard monitors are attached prior to induction of anesthesia

Standard intraoperative electrocardiography (ECG) may be useful for diagnosis of arrhythmias

Invasive cardiovascular monitors — Advanced cardiovascular system monitoring may be

Intra-arterial catheter — An intra-arterial catheter is inserted if not already present.

The intra-arterial catheter is used for the following purposes:

● Continuous monitoring of arterial blood pressure (BP) for immediate detection of

● Monitoring of respirophasic variation in the arterial pressure waveform during positive

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A CVC is used for the following purposes:

● Infusion of vasoactive drugs.

● Measurement of central venous pressure (CVP) to provide supplemental data regarding

Measurements obtained with a PAC include (see "Pulmonary artery catheterization:

● Hemodynamic measurements such as CO (and cardiac index), systemic vascular

Transesophageal echocardiography — During the intraoperative period, transesophageal

● Left ventricular end-diastolic volume (LVEDV) is assessed to determine intravascular

● SVR is assessed. It is often difficult to establish whether a hypotensive patient is

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● Global RV systolic function is assessed. Myocardial ischemia, exacerbation of pulmonary

● Valvular structure and function are assessed. (See "Intraoperative transesophageal

Bladder catheter — A bladder catheter with a temperature probe is inserted to measure

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● Hemodynamic support with continuous infusion of a vasopressor agent if administration

● MAP 65 to 70 mmHg [28]

HYPOVOLEMIC SHOCK MANAGEMENT

Hemorrhagic or nonhemorrhagic etiology — Hemorrhage is the most common cause of

Nonhemorrhagic causes of severe hypovolemia in surgical patients include gastrointestinal

● Fluid administration – Initial management of hypovolemic shock is rapid administration

• Type of fluid – A balanced electrolyte crystalloid solution (eg, Ringer's lactate) is

• Amount of fluid – Although initial fluid resuscitation may be necessarily rapid, it is

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If there is evidence of pulmonary edema or high filling pressures, fluids are

● Vasopressors – In addition to fluid administration, vasopressors may be necessary to

• Calcium administration – Calcium may be depleted due to hemodilution after

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• Mechanical ventilation – During general anesthesia with mechanical ventilation, it is

DISTRIBUTIVE SHOCK MANAGEMENT

● Fluid administration – Similar to hypovolemic shock, a balanced electrolyte crystalloid

If larger volumes of intraoperative crystalloid are required, albumin may be substituted

Hemodilution may result in anemia, particularly if surgical bleeding is occurring. We

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