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 "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".)
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 "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
●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 "Physiologic and pathophysiologic consequences of mechanical ventilation", section on 'Hemodynamics'.)
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 or 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 "Physiologic and pathophysiologic consequences of mechanical ventilation", section on 'Hemodynamics'). 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 membrane oxygenation (ECMO) in adults".)
●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: Medical management for non-heart failure symptoms", section on 'Acute hemodynamic collapse in the setting of LVOT obstruction'):
•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 "Physiologic and pathophysiologic consequences of mechanical ventilation", section on 'Hemodynamics' and "Physiologic and pathophysiologic consequences of mechanical ventilation".)
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.)
