Hemodynamic management during anesthesia in adults

INTRODUCTION — Intraoperative hemodynamic perturbations are common due to the effects of anesthetic agents and techniques, surgical manipulations, and the patient's medical comorbidities. This topic reviews prevention, evaluation of causes, and appropriate treatment of clinically significant hypotension, hypertension, tachycardia, or bradycardia in this setting.

Use of vasoactive agents (eg, vasopressors, inotropes, or antihypertensive agents) to treat episodes of hypotension or hypertension in intraoperative and other settings is discussed in separate topics. (See "Intraoperative use of vasoactive agents" and "Use of vasopressors and inotropes" and "Drugs used for the treatment of hypertensive emergencies", section on 'Parenteral drugs'.)

Management of intraoperative arrhythmias is discussed separately. (See "Arrhythmias during anesthesia".)

Hemodynamic management in specific intraoperative settings is reviewed in individual topics:

●(See "Anesthesia for craniotomy in adults", section on 'Hemodynamic management'.)

●(See "Anesthesia for cesarean delivery", section on 'Hemodynamic management'.)

●(See "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Hypotension'.)

●(See "Anesthesia for adult trauma patients", section on 'Hemodynamic management'.)

●(See "Intraoperative management of shock in adults", section on 'Initial resuscitation'.)

BLOOD PRESSURE MANAGEMENT: GENERAL CONSIDERATIONS

Blood pressure measurement — Standard measurements of blood pressure (BP) during anesthesia are made intermittently, at least every five minutes, using an automated noninvasive oscillometric BP cuff. In select patients, particularly those for whom continuous monitoring is indicated, an intra-arterial catheter is used. In addition, other non-invasive modalities are used less commonly and include noninvasive continuous finger cuff measurements [1-3]. These methods are discussed separately. (See "Basic patient monitoring during anesthesia", section on 'Blood pressure' and "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation", section on 'Monitoring blood pressure'.)

Blood pressure targets — In general, we maintain BP within 20 percent of the patient's baseline and keep mean arterial pressure (MAP) ≥65 mmHg (and systolic BP ≥100 mmHg) to avoid myocardial infarction (MI) or myocardial injury after noncardiac surgery (MINS), acute kidney injury (AKI), stroke, delirium, or mortality [1,4-14]. However, it is not known which specific component of BP (eg, systolic, diastolic, or MAP) is the most appropriate target for treatment. The average lower limit of cerebral blood flow autoregulation in normotensive adults is a MAP of 70 mmHg or greater, although there is considerable individual variability in this lower limit and in blood flow reserve that can temporarily buffer the CNS against hypotension [8]. Although some studies suggest that patients with chronic hypertension may require an intraoperative MAP target higher than 65 mmHg to avoid adverse cardiovascular events or organ dysfunction [15,16], data are not consistent [17]. (See "Anesthesia for patients with hypertension", section on 'Determination of target blood pressure values'.)

Notably, the definition of an individual patient's "baseline" BP is not standardized, and the MAP measured shortly before induction of general anesthesia is a poor surrogate for an individual patient's normal average MAP. A prospective observational study of automated BP measurements obtained in 370 healthy ambulatory patients before noncardiac surgery demonstrated wide variations for the first preinduction MAP that were both above and below the average daytime ambulatory MAP (figure 1) [18]. Furthermore, 71 percent of the patients in this study had lower intraoperative MAPs during general anesthesia than the lowest nighttime MAP measured during the preoperative period (a value considered by the investigators to be an individual's safe minimum target).

Although the optimum intraoperative BP target is unclear, episodes of either hypotension or hypertension should be avoided or promptly treated to minimize the potential for adverse cardiovascular and cerebrovascular outcomes (see 'Adverse effects of hypotension' below and 'Adverse effects of hypertension' below). In a multicenter randomized trial comparing a hypotension-avoidance strategy (mean arterial pressure (MAP) target ≥80 mmHg) versus a hypertension-avoidance strategy (MAP target ≥60 mmHg) in nearly 7500 noncardiac surgery patients receiving long-term antihypertensive medications, the incidence of a composite of cardiovascular morbidity and mortality within 30 days was 14 percent, with no difference between strategies [19]. Specific management of intraoperative hypotensive or hypertensive episodes depends on the presumed cause, timing of the occurrence, and the patient's preexisting comorbidities. Notably, perioperative management of BP and heart rate (HR) are interrelated. (See 'Hypotension: Prevention and treatment' below and 'Hypertension: Prevention and treatment' below.)

Some centers have employed modeling or machine learning (the process by which computers use algorithms and statistical models to predict outcomes based on previously analyzed training datasets), to predict episodes of intraoperative hypotension. Approaches have used preoperative patient variables [20], multiple characteristics of the arterial pressure waveform (requiring invasive intra-arterial monitoring), or evaluation of several preinduction and early postinduction clinical and hemodynamic variables [21-25]. Although it is hoped that such individualized intraoperative hemodynamic management may reduce postoperative complications, challenges include the need for frequent manual adjustments of infusions of vasopressors and fluids throughout major surgical procedures [1,26,27].

Adverse effects of hypotension

●Adverse cardiovascular and cerebrovascular outcomes – In a multicenter case-control study, 326 noncardiac surgical patients with MI within 30 postoperative days (59 with type 1 MI due to coronary occlusion, plaque rupture, or thrombosis; 267 with type 2 MI due to supply-demand imbalance causing ischemia) were matched with 326 controls who did not develop MI after surgery [11]. In this study, intraoperative hypotension increased odds for postoperative MI more than threefold if systolic BP decreased from the patient’s preoperative resting baseline by 41 to 50 mmHg for at least five minutes (odds ratio [OR] 3.42, 95% CI 1.13-10.3), and more than 20-fold if the decrease from baseline was >50 mmHg for at least five minutes (OR 22.6, 95% CI 7.7-66.2). Similarly, a multicenter retrospective study in 368,222 noncardiac surgical patients noted that the adjusted odds ratio (aOR) for a composite outcome (acute MI, acute ischemic stroke, or mortality) increased with severity of hypotension measured with MAP (aOR 1.12 for MAP ≤75 mmHg [95% CI 1.11-1.14]; aOR 1.17 for MAP ≤65 mmHg [95% CI 1.15-1.19]; aOR 1.26 for MAP ≤55 mmHg [95% CI 1.22-1.29]) [12]. However, data are not consistent. In another retrospective study of 358,391 noncardiac surgical patients at two institutions, MAP <55 mmHg for a short duration (<15 minutes) or for a prolonged duration (≥15 minutes) was not associated with postoperative stroke [28].

●Delirium – In a retrospective multicenter study that included 316,717 patients, development of postoperative delirium within 30 days of surgery in 2183 patients (0.7 percent) within 30 days of surgery was associated with a long duration of MAP lasting ≥15 minutes (adjusted OR 1.57, 95% CI 1.27-1.94), or even a short duration of MAP <55 mmHg lasting <15 minutes (adjusted OR 1.22, 95% CI 1.11-1.33) [13].

●Acute kidney injury – A 2019 meta-analysis noted that MAP <60 mmHg for more than one minute was associated with risk for acute kidney injury (AKI) in noncardiac surgical patients [14]. However, data are not consistent, as other studies have not noted an association between duration of intraoperative hypotension and AKI [29].

It is likely that the adverse impact (eg, disruption of cerebral autoregulation, MINS) resulting from hypotension less than a specific BP cutoff depends on both the duration and magnitude of hypotension [1,30-32]. However, the minimal duration of hypotension resulting in perioperative complications has not been established. There is increasing evidence that even brief durations of systolic arterial pressure <100 mmHg or MAP <60 to 70 mmHg are harmful during non-cardiac surgery [1,33]. In a 2018 systematic review of various types of noncardiac surgery, adverse postoperative outcomes were associated with both duration and degree of intraoperative hypotension (using both absolute and relative definitions) in various types of noncardiac surgery (42 studies; median of 1523 patients per study) [7]. In a subsequently published retrospective study of nearly 1000 noncardiac surgical patients, perioperative hypotension (defined as systolic BP <90 mmHg for ≥10 minutes during surgery or for any duration after surgery if intervention was required) was associated with MI or cardiovascular death within 30 days of surgery, regardless of the degree of coronary artery disease documented on preoperative coronary computed tomographic angiography (hazard ratio 3.17, 95% CI 1.99-5.06) [34]. Similarly, a large multicenter observational study of more than 16,000 noncardiac surgical patients noted that a minimum intraoperative systolic BP <100 mmHg was associated with MINS (OR 1.21, 95% CI 1.05-1.39) and mortality (OR 1.81, 95% CI 1.39-2.37) [35]. In this study, 2.8 percent had an MI, 7 percent sustained MINS, while 2 percent died within 30 days of surgery. MINS was most likely if low systolic BP <100 mmHg occurred when heart rate was >100 beats per minute (bpm; OR 1.42, 1.15-1.76). However, high systolic BP values exceeding 160 mmHg have also been associated with MINS (OR 1.16, 95% CI 1.01-1.34) and MI (OR 1.34, 95% CI 1.09-1.64), suggesting that both low and high BP extremes should be avoided [35]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia'.)

Postoperative control of BP may be equally important in reducing perioperative adverse events [1,36-38]. In a study of 502 patients undergoing abdominal surgery, hypotension (defined as MAP <70 mmHg lasting at least 30 minutes) occurred in 24 percent in the first 48 postoperative hours [38]. In another study of 1710 patients undergoing major noncardiac surgery, postoperative hypotension <60 mmHg lasting at least two hours occurred in 8 percent, while postoperative hypotension <75 mmHg lasting at least four hours occurred in 48 percent [39]. The aOR for MINS (defined as elevated peak troponin T) ranged from 2.18 to 3.26 in this study, depending on the assessed threshold and duration of hypotension.

Adverse effects of hypertension

●Adverse cardiovascular and cerebrovascular outcomes – In a large retrospective study that included 55,563 surgical patients with normal BP at rest, 4.1 percent developed postoperative major adverse cardiac events (MACE) defined as acute MI, heart failure, or nonfatal cardiac arrest within seven postoperative days [40]. In this study, an increase ≥50 mmHg between their baseline systolic BP and the first systolic BP recorded in the operating room was associated with MACE (OR 1.35. 95% CI 1.11-1.59). Other factors associated with MACE were older age, extreme body mass index (BMI), cancer-related or other major surgical procedure, and intraoperative hypotension or blood transfusion [40].

●Delirium – In a study in cardiac surgical patients, the product of the magnitude and duration of MAP above an upper limit of autoregulation OR, 1.09; 95% CI, 1.03-1.15) [41]. However, data are not consistent, and other studies in cardiac and noncardiac surgical patients have not found an association between intraoperative hypotension and postoperative delirium [42-44].

Notably, postoperative hypertension is common. In the study noted above that included 502 patients undergoing abdominal surgery [38], hypertension (defined as MAP >110 mmHg lasting at least 30 minutes) was observed in 42 percent in the first 48 postoperative hours.

HYPOTENSION: PREVENTION AND TREATMENT — Hypotension is the most common hemodynamic perturbation requiring intraoperative treatment [35].

Selection and dosing of anesthetic agents — Selection of anesthetic agents and techniques, as well as dosing adjustments, may be employed to prevent or treat episodes of hypotension.

General anesthesia — Either intravenous (IV) or inhalation anesthetic agents or their combination may cause or exacerbate hypotension.

●Induction – Hypotension is particularly likely during induction of general anesthesia. Selection of specific IV anesthetic induction agents, speed of induction with inhalation anesthetics, and dosing of all anesthetic and adjunct agents are factors affecting the likelihood of development of hypotension.

These factors can be manipulated by selection and dosing of anesthetic agents and techniques, as discussed in separate topics:

•(See "General anesthesia: Intravenous induction agents".)

•(See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Cardiovascular effects'.)

•(See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Induction of general anesthesia'.)

●Maintenance – Both inhalation and IV anesthetic agents are titrated and adjusted as necessary throughout a surgical procedure in order to maintain an adequate level of anesthesia and stable hemodynamics, as described in detail in separate topics:

•(See "Maintenance of general anesthesia: Overview", section on 'Inhalation anesthetic agents and techniques' and "Inhalation anesthetic agents: Clinical effects and uses", section on 'Maintenance of general anesthesia (all inhalation agents)'.)

•(See "Maintenance of general anesthesia: Overview", section on 'Total intravenous anesthesia' and "Maintenance of general anesthesia: Overview", section on 'Adjuvant agents'.)

•(See "Accidental awareness during general anesthesia", section on 'Risk factors'.)

Neuraxial or regional anesthesia — Hypotension commonly occurs shortly after administration of a neuraxial anesthetic, as described in other topics:

●(See "Spinal anesthesia: Technique", section on 'Hemodynamic management'.)

●(See "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Hemodynamic management'.)

●(See "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Hypotension'.)

Also, hypotension may be a sign of local anesthetic toxicity, which can occur during any regional anesthetic technique. (See "Local anesthetic systemic toxicity", section on 'Clinical presentation of toxicity'.)

Monitored anesthetic care with sedation — Hypotension can occur during monitored anesthesia care due to the cardiovascular effects of sedative and analgesic agents. (See "Monitored anesthesia care in adults", section on 'Complications during monitored anesthesia care'.)

Fluid administration — Hypotension is more likely to occur if hypovolemia is present. Administering IV fluid boluses in fluid-responsive patients increases stroke volume and cardiac output (CO), with resultant increases in BP in patients with fluid responsiveness (defined as an increase in CO of >15 percent after a fluid bolus) (figure 2). In a retrospective multicenter study that included 32,250 patients undergoing surgery between 2015 and 2019, the investigators noted that the total volume of administered crystalloid and the proportion of patients receiving >10 mL/kg per hour decreased, while the amount of norepinephrine equivalents increased during that time period [45]. These investigators reported a lower risk of acute kidney injury (AKI) for patients receiving a total crystalloid volume >10 mL/kg per hour (risk ratio [RR] 0.42, 95% CI 0.4230-0.4232) compared with lower total volumes. However, risk of AKI started to increase for total crystalloid volumes >20 mL/kg per hour.

In one randomized study, fluid administration in the preoperative period decreased the incidence of a significant decrease blood pressure after induction of general anesthesia [46]. A prospective multicenter study of 330 patients undergoing high-risk noncardiac surgery noted that desired increases in stroke volume were achieved more often with computer-assisted assessment of fluid responsiveness and initiation of fluid boluses compared with clinician-initiated fluid boluses (66 versus 30 percent) [47].

Typically, a balanced electrolyte crystalloid solution is selected, and administered in 250 mL increments; colloid solution or red blood cells may be administered in specific circumstances. However, fluid optimization before induction of general anesthesia does not always prevent hemodynamic instability in patients with a preexisting fluid deficit [48]. Further discussion of monitoring intravascular volume status and selection and administration of intraoperative fluids is available separately. (See "Intraoperative fluid management".)

Intravascular volume status has been assessed with ultrasound of the inferior vena cava (IVC). In spontaneously breathing patients in the preoperative period, the collapsibility index of the IVC diameter reliably predicted development of significant hypotension during anesthetic induction, particularly when the index was ≥43 percent [49]. Similarly, in mechanically ventilated critically ill patients, respiratory changes in IVC diameter of 12 to 18 percent have been associated with fluid responsiveness. (See "Novel tools for hemodynamic monitoring in critically ill patients with shock", section on 'Vena cava assessment'.)

Trendelenburg positioning — In selected cases, placing the patient in the head down position (or passive leg raising) can be a simple maneuver to temporarily increase BP in a volume-responsive patient [50]. Passive leg raising or changing to a head down position mobilizes blood volume from the lower extremities into the central circulation, and may temporarily improve hemodynamic stability, presumably by increasing venous return to improve CO and BP. Some clinicians use such maneuvers for a brief period while they establish additional IV access to begin more rapid administration of fluids. However, passive leg raising is not usually feasible without interrupting the surgical procedure, and the Trendelenburg position cannot be maintained for prolonged periods due to concerns regarding development of upper body (eg, airway and ophthalmologic) edema. (See "Novel tools for hemodynamic monitoring in critically ill patients with shock", section on 'Passive leg raising or fluid bolus challenge' and "Patient positioning for surgery and anesthesia in adults", section on 'Physiologic effects of Trendelenburg positioning'.)

Furthermore, the Trendelenburg position should be avoided in patients with:

●Elevated intracranial pressure (ICP). Cerebral perfusion is not improved and may be worsened due to simultaneous increases in central venous pressure and ICP.

●Bleeding from areas that will become dependent in the head down position

●An unprotected airway in a patient at risk for aspiration

Reassessment of underlying causes — For persistent, severe, or refractory hypotension, the clinician should reassess the patient for less common underlying causes. Examples include hypovolemic shock due to occult bleeding, distributive shock due to anaphylaxis, or obstructive shock due to pneumothorax, pulmonary embolus, or unrecognized clinical entities, such as aortic stenosis or hypertrophic obstructive cardiomyopathy. (See "Intraoperative management of shock in adults".)

The clinician should also consider adrenal insufficiency in selected patients who seem unresponsive to standard vasopressor or catecholamine therapy (eg, recent use of steroid supplementation, septic shock) [51,52]. Treatment is administration of a "stress dose" of steroids (eg, IV hydrocortisone 100 mg). (See "Treatment of adrenal insufficiency in adults", section on 'Adrenal crisis'.)

Administration of vasopressor or inotropic agents — Intraoperative use of vasopressor and positive inotropic agents is discussed in a separate topic. (See "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'.)

HYPERTENSION: PREVENTION AND TREATMENT — Although there is no consensus regarding specific intraoperative blood pressure (BP) target values, high BP increases blood loss from wounds and surgical incisions, particularly arterial sites. In patients with ischemic heart disease, elevated BP increases afterload stress on the heart, which may cause myocardial injury after noncardiac surgery (MINS) (table 1) (see "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia'). In patients with aortic dissection or aneurysm, elevated BP increases risk for extension of arterial dissection or rupture. (See "Anesthesia for open abdominal aortic surgery", section on 'Hemodynamic management' and "Anesthesia for open descending thoracic aortic surgery", section on 'Hemodynamic management'.)

Intraoperative hypertension occurs due to increased systemic vascular resistance (SVR), or increased cardiac output (CO) when stroke volume, heart rate (HR), or both increase. Determining whether the primary cause is increased SVR, CO, or a combination of these factors can be difficult if only noninvasive monitoring techniques are available. Generally, elevations in SVR are more common in older adult patients and those with chronic hypertension, while tachycardia leading to increased CO is more commonly associated with hypertension in younger patients.

Adjustment of anesthetic depth — Selection of anesthetic agents and techniques, as well as dosing adjustments, may be employed to prevent or treat episodes of hypertension.

An inadequate depth of anesthesia for any given magnitude of intraoperative stimulus is a common cause of intraoperative hypertension. Examples include sympathetic responses to pain, laryngoscopy with insertion of an endotracheal tube (ETT) or other airway device shortly after induction of anesthesia, or responses to incision and surgical manipulations during the maintenance phase of anesthesia, as well as excitement and further stimulation of airway reflexes during emergence and extubation. Hypertension due to sympathetic stimulation is often associated with tachycardia. This cause of hypertension is treated by temporarily increasing the doses of intravenous (IV) and inhalation anesthetic agents to deepen anesthesia, or administering vasoactive agents to lower BP in patients who are adequately anesthetized [53]. Further discussion of hypertensive responses to nociceptive stimuli is available in another topic:

●(See "Anesthesia for patients with hypertension", section on 'Laryngoscopy and endotracheal intubation'.)

●(See "Anesthesia for patients with hypertension", section on 'Surgical stimulation'.)

●(See "Anesthesia for patients with hypertension", section on 'Emergence and tracheal extubation'.)

Reassessment of underlying causes — For persistent or refractory hypertension, the clinician should reassess the patient for unusual or unexpected underlying causes. Examples include sympathetic stimulation due to hypoxemia, hypercarbia, bladder distention, or elevated ICP. The clinician should also consider hypervolemia, particularly if a morning dose of a chronically administered diuretic was missed, or if large volumes of intraoperative fluid were administered. (See "Anesthesia for patients with hypertension", section on 'Hypoxemia and/or hypercarbia' and "Anesthesia for patients with hypertension", section on 'Hypervolemia'.)

Less common causes of hypertension include recent cocaine or amphetamine use, serotonin syndrome, thyroid storm, malignant hyperthermia, or pheochromocytoma. (See "Anesthesia for patients with hypertension", section on 'Other causes'.)

Administration of antihypertensive agents — Intraoperative use of antihypertensive agents is discussed in a separate topic. (See "Intraoperative use of vasoactive agents", section on 'Antihypertensive agents'.)

HEART RATE MANAGEMENT

Heart rate targets — In general, we attempt to avoid tachycardia and maintain a heart rate (HR) <100 bpm. In patients with ischemic heart disease, we maintain a lower HR (eg, 50 to 80 bpm) since tachycardia compromises both myocardial oxygen supply and demand (table 1). Similar to management of intraoperative blood pressure (BP), prevention and treatment of tachycardia or bradycardia depend on the likely cause, timing of intraoperative occurrence, and the patient's baseline condition. (See "Arrhythmias during anesthesia", section on 'Causes of sinus tachycardia' and "Arrhythmias during anesthesia", section on 'Causes of sinus bradycardia'.)

Adverse effects of tachycardia — In a large multicenter observational study that included more than 16,000 noncardiac surgical patients, intraoperative tachycardia with a HR >100 bpm was associated with myocardial injury after noncardiac surgery (MINS; OR 1.27, 95% CI 1.07-1.50) and myocardia infarction4 (OR 1.34, 95% CI 1.05-1.70), as well as mortality (OR 2.65, 95% CI 2.06-3.41). An even higher risk of MINS was noted if the duration of tachycardia exceeded 30 minutes (OR 2.22, 95% CI 1.71-2.88). Conversely, a slow intraoperative HR <55 bpm was associated with reduced risk for MINS (OR 0.70, 95% CI 0.59-0.82), or MI (OR 0.75, 95% CI 0.58-0.97), as well as mortality (OR 0.58, 95% CI 0.41-0.81), with a trend toward decreasing likelihood of MINS with increasing duration of slow recorded HR <55 bpm [35]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia'.)

Adverse effects of bradycardia — Severe bradycardia decreases cardiac output and can result in inadequate perfusion or myocardial ischemia [54].

Management of atrial tacharrrhythmias — Sinus tachycardia and other atrial arrhythmias Intraoperative tachycardia with a heart rate (HR) >100 beats per minute (bpm) is usually sinus tachycardia (waveform 1). Causes and management of this and other intraoperative atrial tachyarrhythmias are discussed separately:

●(See "Arrhythmias during anesthesia", section on 'Sinus tachycardia'.)

●(See "Arrhythmias during anesthesia", section on 'Other narrow QRS complex atrial tachyarrhythmias'.)

●(See "Arrhythmias during anesthesia", section on 'Wide QRS complex atrial tachyarrhythmias'.)

Managemenf of atrial bradyarrhythmias — Notably, mean intraoperative HR is lower than mean nighttime HR in most patients [54]. Bradycardia with a heart rate (HR) <60 beats per minute (bpm) is usually sinus bradycardia. Severe bradycardia is typically treated if HR is <40 bpm, associated with transient episodes of asystole, or is hemodynamically significant with signs of inadequate perfusion (eg, hypotension, electrocardiographic evidence of ischemia). (See "Arrhythmias during anesthesia", section on 'Bradyarrhythmias'.)

Causes and management of this and other intraoperative bradyarrhythmias are discussed separately:

●(See "Arrhythmias during anesthesia", section on 'Sinus bradycardia'.)

●(See "Arrhythmias during anesthesia", section on 'Other bradyarrhythmias'.)

●(See "Arrhythmias during anesthesia", section on 'Asystole'.)

SUMMARY AND RECOMMENDATIONS

●Blood pressure targets – We suggest maintaining blood pressure (BP) within 20 percent of the patient's baseline and keeping systolic BP >100 mmHg and mean arterial pressure (MAP) >65 mmHg in most patients (Grade 2C). Higher thresholds may be reasonable in chronically hypertensive patients with high baseline BP values. We promptly treat episodes of intraoperative hypotension since the likelihood of adverse impact depends on its duration and severity. (See 'Blood pressure management: General considerations' above.)

•Adverse effects of hypotension – These include increased risk for adverse cardiovascular and cerebrovascular outcomes (eg, acute myocardial infarction [MI], stroke), delirium, and acute kidney injury. (See 'Adverse effects of hypotension' above.)

•Adverse effects of hypertension – These include increased risk for acute MI, heart failure, or nonfatal cardiac arrest, as well as delirium. (See 'Adverse effects of hypertension' above.)

●Prevention and treatment of hypotension – Management of intraoperative hypotension depends on the presumed causes (see 'Hypotension: Prevention and treatment' above):

•(See 'Selection and dosing of anesthetic agents' above.)

•(See 'Fluid administration' above.) (figure 2)

•(See 'Trendelenburg positioning' above.)

•(See 'Reassessment of underlying causes' above.)

•(See "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'.)

●Prevention and treatment of hypertension – Management of intraoperative hypertension depend on the presumed causes (see 'Hypertension: Prevention and treatment' above):

•(See 'Adjustment of anesthetic depth' above.)

•(See 'Reassessment of underlying causes' above.)

•(See "Intraoperative use of vasoactive agents", section on 'Antihypertensive agents'.)

●Heart rate targets – In general, we attempt to avoid tachycardia and maintain a heart rate (HR) <100 beats per minute (bpm). In patients with ischemic heart disease, we maintain a lower HR (eg, 50 to 80 bpm) since tachycardia compromises both myocardial oxygen supply and demand (table 1). (See 'Heart rate targets' above.)

•Adverse effects of tachyarrhythmias – Tachycardia with a HR >100 bpm is associated with myocardial injury after noncardiac surgery (MINS). (See 'Adverse effects of tachycardia' above.)

•Adverse effects of bradyarrhythmias – Severe bradycardia decreases cardiac output and can result in inadequate perfusion or myocardial ischemia. (See 'Adverse effects of bradycardia' above.)

●Causes and management of atrial tachyarrhythmias – Causes and management of sinus tachycardia and other atrial tachyarrhythmias are discussed in a separate topic. (See "Arrhythmias during anesthesia", section on 'Atrial tachyarrhythmias'.)

●Causes and management of atrial bradyarrhythmias – Sinus bradycardia is typically treated pharmacologically if it is more severe (HR <40 bpm) or associated with signs of inadequate perfusion. (See "Arrhythmias during anesthesia", section on 'Bradyarrhythmias'.)