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. Intraoperative management of common and uncommon intraoperative arrhythmias is discussed separately. (See "Arrhythmias during anesthesia".)
Hemodynamic management in special settings, such as neurosurgery, labor and delivery, shock, or trauma is reviewed separately.
●(See "Anesthesia for craniotomy", 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 'Management of hemodynamic instability'.)
●(See "Intraoperative management of shock in adults".)
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 [1,2]. 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 [1,3-13]. 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 [7]. Many patients may require an intraoperative MAP target higher than 65 mmHg to avoid adverse cardiovascular events or organ dysfunction, particularly those with chronic hypertension [14,15]. (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) [16]. 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).
Hypotension and hypertension should be avoided or promptly treated during the perioperative period to avoid potential adverse outcomes (see 'Adverse effects of hypotension' below and 'Adverse effects of hypertension' below). Specific management of hypotensive (or hypertensive) episodes depends on the presumed cause, timing of intraoperative 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 and 'Heart rate management' below.)
Some centers have employed 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 utilize either multiple characteristics of the arterial pressure waveform (requiring invasive intra-arterial monitoring) or evaluation of several preinduction and early postinduction clinical and hemodynamic variables [17-21]. Although 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 [1,22,23].
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 [10]. 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]) [11].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 [24].
●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) [12].
●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 [13]. However, data are not consistent, as other studies have not noted an association between duration of intraoperative hypotension and AKI [25].
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 [1,26-28]. 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 [1,29]. 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) [6]. 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) [30]. 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) [31]. 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 [31]. (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 [1,32-34]. 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 [34]. 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 [35]. 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 [36]. 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 [36].
●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) [37]. 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 [38-40].
Notably, postoperative hypertension is common. In the study noted above that included 502 patients undergoing abdominal surgery [34], 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 [31].
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'.)
●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 one randomized study, preoperative fluid administration decreased the incidence of a significant decrease blood pressure after induction of general anesthesia [41]. 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) [42].
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 [43]. 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 [44]. 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'.)
Vasopressor and positive inotropic agents — Vasopressor bolus doses and/or continuous infusions are administered to treat hypotension that does not immediately respond to decreasing anesthetic depth and/or fluid administration (table 1 and table 2) [45]. Vasopressors raise BP by increasing systemic vascular resistance (SVR), whereas inotropic (and positive chronotropic) agents typically increase CO through effects on contractility and heart rate (HR). However, the anesthesiologist will not be aware of changes in CO unless this is being directly monitored during the surgical procedure using a pulmonary artery catheter or other CO monitoring device. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults", section on 'Calculation of cardiac output' and "Novel tools for hemodynamic monitoring in critically ill patients with shock", section on 'Cardiac output'.)
Both inotropes and vasodilators may alter venous return through effects on splanchnic blood flow and venous return to the heart. Drugs that increase HR and CO as well as BP (eg, ephedrine, epinephrine) may be detrimental in selected patients with ischemic heart disease (table 3) or left ventricular (LV) outflow tract obstruction. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia' and "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery".)
Thus, although vasopressors may be necessary to adequately treat hypotension, potentially remediable causes should be identified and treated to minimize duration of vasopressor infusion [46,47].
Specific vasopressor agents include:
●Ephedrine – Ephedrine is often selected to treat acute decreases in BP, particularly in patients with bradycardia since this agent stimulates alpha, beta1, and beta2 receptors. It is administered as 5 to 10 mg bolus doses. Ephedrine has predominantly indirect effects on adrenergic receptors; it causes presynaptic release of norepinephrine and may have additional effects on postsynaptic release and inhibition of norepinephrine uptake [48,49]. Beta effects of ephedrine result in increased HR via sinoatrial node stimulation and increased inotropy, while its alpha effects cause peripheral vasoconstriction [50].
•Advantages
-Increases BP and CO and HR with beneficial hemodynamic effects in most patients, particularly if bradycardia originates within or above the atrioventricular node (eg, due to beta blocking agents).
-Ephedrine has bronchodilating beta2 effects, which can be of benefit in the setting of perioperative bronchospasm [51-53].
-Duration of action of ephedrine is typically longer than equipotent small bolus doses of epinephrine.
-Ephedrine may better preserve cerebral blood flow and cerebral oxygenation compared with phenylephrine [54-57].
•Disadvantages
-Tachyphylaxis may occur in patients with depleted stores of endogenous norepinephrine (eg, those with hemorrhagic shock) and may occur with repeated doses. Typically, another agent is added or substituted for ephedrine after 50 to 60 mg have been administered [3].
-Drugs that block ephedrine uptake into adrenergic nerves (eg, cocaine) and those that deplete norepinephrine reserves (eg, reserpine) attenuate the cardiovascular effects of ephedrine.
-In patients using monoamine oxidase inhibitors or certain drugs of abuse, such as methamphetamines, ephedrine should be avoided or administered with extreme caution (eg, in small incremental doses of 2.5 mg), due to the potential for an exaggerated hypertensive response or life-threatening dysrhythmias. (See "Perioperative medication management", section on 'Monoamine oxidase inhibitors' and "Anesthesia for patients with substance use disorder or acute intoxication", section on 'Amphetamines and similar agents' and "Anesthesia for patients with substance use disorder or acute intoxication", section on 'Hallucinogens and dissociative drugs'.)
-In obstetrical anesthesia, use of ephedrine may be associated with increased risk of fetal acidosis. (See "Anesthesia for cesarean delivery", section on 'Vasopressors'.)
-Either ephedrine or phenylephrine, by virtue of their synthetic origin, may rarely cause allergic reactions, such as contact allergic responses with topical use (eg, during ophthalmologic surgery), and delayed severe dermatitis following IV injection has been reported [58,59].
-Ephedrine cannot be administered as a continuous infusion.
●Phenylephrine – Phenylephrine is often selected to treat hypotension if normal or elevated HR is present, and is the most commonly selected intraoperative vasopressor in the United States. Phenylephrine exclusively stimulates alpha1 adrenergic receptors, and is usually associated with baroreceptor reflex-mediated decreases in HR. Phenylephrine may be administered either as bolus doses (eg, 50 to 100 mcg) or as a continuous infusion at 10 to 100 mcg/min.
•Advantages
-A decreased or stable HR is desirable in patients with ischemic heart disease (table 3) [60-62]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia'.)
-Agents with primarily alpha agonist properties, such as phenylephrine, are best initial treatment options for hypotension in patients with LV outflow tract obstruction, aortic stenosis, or tetralogy of Fallot. (See "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery" and "Anesthesia for noncardiac surgery in patients with aortic or mitral valve disease", section on 'Hemodynamic management' and "Anesthesia for adults with congenital heart disease undergoing noncardiac surgery", section on 'Right-to-left shunt with cyanosis'.)
-Phenylephrine may be administered as a bolus or as a continuous infusion.
•Disadvantages
-Individual responses may be variable, and there are ethnic variations in vascular responsiveness to phenylephrine [63-65]. Genomic studies of polymorphisms of the beta-2 adrenergic receptor suggest that Gly16 carriers may require larger doses of intraoperative vasopressor (ephedrine or phenylephrine) likely due to association of the Gly16 allele with vasodilation and higher CO than other genotypes [66].
-Alpha1 receptor-mediated vasoconstriction caused by phenylephrine may reduce CO due to decreased stroke volume and arterial compliance [67-69]. Although ephedrine and norepinephrine also cause arterial vasoconstriction, both are more likely to increase CO compared with phenylephrine, due to positive inotropic effects (as well as increased HR when ephedrine is selected) [60-62,67,70-73]. However, the CO responses to either phenylephrine or norepinephrine have been shown to depend on baseline intravascular volume status and evidence of fluid responsiveness (based on dynamic hemodynamic parameters) [74-76]. (See "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'.)
-The effects of alpha-mediated vasoconstriction on splanchnic blood volumes and venous return are unclear [68,69].
-Patients with impaired ventricular function and chronic heart failure may have decreased alpha1 receptor responsiveness limiting the effectiveness of phenylephrine.
-For patients with aortic or mitral regurgitation, vasoconstriction and decreases in HR are detrimental. (See "Anesthesia for noncardiac surgery in patients with aortic or mitral valve disease", section on 'Aortic regurgitation' and "Anesthesia for noncardiac surgery in patients with aortic or mitral valve disease", section on 'Mitral regurgitation'.)
-As with ephedrine, rare localized allergic reaction may occur.
●Vasopressin and terlipressin – Vasopressin is typically used for treatment of hypotension that is refractory to administration of catecholamines or sympathomimetics, particularly for patients with vasodilatory shock (eg, septic shock). It is often added as a supplementary agent to treat hypotension after an inadequate response to other vasopressors.
Vasopressin is a naturally-occurring nonapeptide essential for maintenance of plasma osmolality due to its antidiuretic actions. It also acts as a vasoconstrictor by stimulating the nonadrenergic V1 receptor if administered in supraphysiologic concentrations (eg, bolus doses of 1 to 4 units or as a continuous infusion at 0.01 to 0.04 units/minute). Higher vasopressin doses up to 0.1 units/minute are reserved for instances when a MAP goal cannot be achieved with lower vasopressin doses in combination with other vasopressor agents [77]. Although efficacy of vasopressin is relatively equivalent to equipotent doses of epinephrine in producing profound arterial vasoconstriction during resuscitation, high bolus doses (ie, 40 units) are no longer recommended as an alternative to epinephrine in the American Heart Association (AHA) advanced cardiovascular life support algorithm for cardiac arrest due to efforts by the AHA to simplify this algorithm (algorithm 1). (See "Use of vasopressors and inotropes", section on 'Vasopressin and analogs' and "Intraoperative management of shock in adults", section on 'Distributive shock management'.)
Terlipressin is a synthetic prodrug analog of vasopressin that is not available in the United States. Compared with vasopressin, terlipressin has a considerably longer half-life (six hours) and greater selectivity for the V1 receptor [77]. Due to its selective splanchnic arteriolar vasoconstrictive effects, terlipressin is typically used to decrease esophageal variceal bleeding, or to treat portal hypertension and hepatorenal syndrome. (See "Methods to achieve hemostasis in patients with acute variceal hemorrhage", section on 'Terlipressin' and "Hepatorenal syndrome", section on 'Terlipressin plus albumin where available'.)
•Advantages
-Vasopressin is effective for treatment of hypotension refractory to administration of catecholamines or sympathomimetics (eg, ephedrine, phenylephrine, norepinephrine). Examples include vasoplegia due to chronic administration of angiotensin-converting enzyme inhibitors, prolonged cardiopulmonary bypass, or sepsis [77,78].
-Vasopressin has no direct effects on HR; a slower HR is desirable in patients with ischemic heart disease (table 3). (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia'.)
-Vasopressin has no vasoconstrictive effect on pulmonary arteries; thus, it is the preferred agent in patients with pulmonary hypertension [79-81]. (See "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'Vasopressors and inotropes'.)
-An agent with pure vasoconstrictor activity such as vasopressin is the best option for patients with LV outflow tract obstruction, aortic stenosis, or tetralogy of Fallot when treatment with a vasopressor is necessary. (See "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery" and "Anesthesia for noncardiac surgery in patients with aortic or mitral valve disease", section on 'Hemodynamic management' and "Anesthesia for adults with congenital heart disease undergoing noncardiac surgery", section on 'Right-to-left shunt with cyanosis'.)
-Vasopressin may be administered either as a bolus or as a continuous infusion.
•Disadvantages
-Peripheral extravasation of vasopressin can cause skin necrosis [82].
-The half-life of vasopressin is longer than that of phenylephrine or catecholamine agents (ie, norepinephrine, epinephrine). Thus, vasopressin is more difficult to titrate.
-Vasopressin is usually avoided in patients with neurologic injury and in those undergoing craniotomy because it can cause cerebral vasoconstriction [83]. However, it may be used if hypotension is refractory to adrenergic agents. (See "Anesthesia for craniotomy", section on 'Vasoactive drugs'.)
-Since vasopressin and particularly terlipressin cause selective splanchnic arteriolar vasoconstriction, these agents are used cautiously in patients at risk for splanchnic hypoperfusion [77].
●Norepinephrine – Norepinephrine (and epinephrine, which is converted from norepinephrine by phenylethanolamine-N-methyltransferase in the adrenal medulla) is an endogenous catecholamine. It may be administered as bolus doses of 4 to 8 mcg, or as a continuous infusion at 1 to 20 mcg/min. Norepinephrine is commonly used in patients undergoing cardiac surgery, and its use is increasing in those undergoing noncardiac surgery, including titrated infusion via a peripheral IV catheter [3,84-88].
•Advantages
-Owing to its positive inotropic effects, norepinephrine will maintain or increase CO in most patients, while simultaneously causing arterial vasoconstriction and increasing blood pressure [73,85].
-Compared with phenylephrine, 8 mcg norepinephrine is approximately equal to 100 mcg of phenylephrine [89]. At comparable doses, norepinephrine is more likely to increase BP without significantly decreasing stroke volume or arterial compliance [67,73,90].
-Often selected as a first-line agent during noncardiac surgery, particularly for treatment of most types of shock. (See "Intraoperative management of shock in adults".)
-Limited data also support the safety and efficacy of norepinephrine in obstetrical anesthesia [91]. (See "Anesthesia for cesarean delivery", section on 'Vasopressors'.)
-Norepinephrine may be administered either as a bolus or as a continuous infusion.
•Disadvantages
-Like phenylephrine, norepinephrine-induced alpha1 receptor-mediated vasoconstriction may reduce CO in some patients. However, in patients who demonstrate fluid responsiveness (see "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'), administration of norepinephrine can increase CO due to greater venous return and consequently increased preload [73], as well as its positive inotropic effects.
-A central venous catheter or peripherally inserted central catheter is usually employed for prolonged administration of norepinephrine due to concern regarding tissue damage if peripheral extravasation occurs. However, since small doses of norepinephrine (approximately 10 mcg total) may be effective for initial treatment of hypotension, dilute solutions containing norepinephrine 4 to 8 mcg/mL may be administered as a bolus when necessary [89]. Furthermore, in a retrospective study that included 14,385 patients who received an infusion of diluted norepinephrine (20 mcg/mL) via a peripheral IV catheter, a low incidence of extravasation was observed in five patients (0.035 percent, 95% CI 0/011-0.081 percent), with zero complications requiring surgical or medical intervention [92]. Other reviews have also noted that dilute solutions of norepinephrine and other vasopressors rarely cause tissue damage when administered through a free-flowing large-bore peripheral IV catheter [93,94].
The optimal position in the arm for a peripheral IV catheter is the basilic or cephalic vein. In a systematic review of 325 extravasation and local tissue injury events occurring during vasopressor infusions in critically ill patients, more than 85 percent occurred at an infusion site located distal to the antecubital fossa in the upper extremity, or distal to the popliteal fossa in the lower extremity [93]. Although catheterization of a vein directly in the antecubital fossa may be used, this position has the potential for penetration of the vein with arm flexion and is avoided if possible [94].
●Epinephrine – Epinephrine administration as a first-line agent to treat intraoperative hypotension is typically reserved for treatment of anaphylaxis or cardiac arrest (table 4 and algorithm 1) (see "Perioperative anaphylaxis: Clinical manifestations, etiology, and management" and "Advanced cardiac life support (ACLS) in adults"). However, it may be used safely as a low dose bolus drug to treat hypotension, typically with doses of 8 to 16 mcg.
At low-dose infusions of approximately 1 to 2 mcg/minute (ie, 0.01 to 0.02 mcg/kg per minute in a 100 kg patient), epinephrine has primarily beta2 adrenergic effects; at these doses, epinephrine infusion has beneficial bronchodilatory effects and may cause arterial vasodilation with decreased BP. At high doses of approximately 10 to 100 mcg/minute (ie, 0.1 to 1 mcg/kg per minute), epinephrine has primarily alpha adrenergic effects resulting in vasoconstriction with possible hypertension and adverse metabolic effects. Intermediate dose ranges of approximately 2 to 10 mcg/minute (ie, 0.02 to 0.1 mcg/kg per minute) primarily cause both beta1 and beta2 adrenergic effects, resulting in increased BP and HR, as well bronchodilation. However, individual responses to dose-related effect are variable.
•Advantages
-Epinephrine is the first-line therapy for cardiac arrest and for anaphylaxis, and may be administered via an intramuscular route or through an endotracheal tube if IV access is lost during such emergencies. (See "Anaphylaxis: Emergency treatment", section on 'Epinephrine'.)
-Epinephrine may be administered either as a bolus or as a continuous infusion.
•Disadvantages
-Titrating the balance between the alpha and beta receptor effects of epinephrine can be challenging because individual responses to dose-related effects are variable.
-Large bolus doses of epinephrine can cause profound hypertension due to its alpha effects, particularly if a rapidly reversible cause of hypotension is treated shortly after epinephrine administration.
-Adverse metabolic effects of excessive beta2 stimulation include hyperglycemia, lipolysis, and metabolic acidosis (due to type B lactic acidosis) [95,96].
●Other vasopressor agents – Administration of other vasopressors may be initiated for vasoplegia that is unresponsive to high doses of norepinephrine and/or vasopressin [97]. Agents include methylene blue [98-100], angiotensin II [98,101-103], vitamin C [98,104,105], and hydroxycobalamin (table 5) [98-100], but none of these are the first line of treatment. (See "Intraoperative management of shock in adults", section on 'Distributive shock management'.)
●Other inotropic agents – Infusions of other inotropic drugs may have been initiated to support the circulation and maintain or increase the blood pressure in critically ill patients before their arrival in the operating room. Examples include dopamine, dobutamine, and milrinone (table 1). Such infusions may be continued, but these agents are not used as first-line vasoactive choices to treat new intraoperative hypotension. (See "Intraoperative management of shock in adults".)
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 [106]. 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) [107,108]. 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'.)
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 3) (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 aortic surgery requiring deep hypothermia", 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 [109]. 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'.)
Antihypertensive agents — Bolus doses and/or continuous infusions of antihypertensive agents may be administered to treat hypertension that does not immediately respond to increasing anesthetic depth, administration of analgesic agents, or removal of a noxious stimulus, such as the ETT (table 6). If increases in BP are thought to be due to interruption of the patient's chronic antihypertensive regimen on the day of surgery, treatment with an IV equivalent of the missed medication is ideal, particularly if that medication was a beta blocker or clonidine. (See "Anesthesia for patients with hypertension", section on 'Antihypertensive medication withdrawal' and "Perioperative management of hypertension", section on 'Withdrawal syndromes'.)
In the setting of untreated hypovolemia, any antihypertensive agent is likely to result in precipitous hypotension, particularly those that reduce preload (eg, nitroglycerin, nitroprusside). For this reason, intravascular volume status should be assessed before administration of an antihypertensive agent.
Vasodilating agents (ie, nitroprusside, nitroglycerin, hydralazine, and the calcium channel blockers) dilate the cerebral circulation and can increase cerebral flow; thus, these agents are used with caution in patients with increased intracranial pressure (ICP). (See "Anesthesia for craniotomy", section on 'Vasoactive drugs'.)
Specific antihypertensive agents include:
●Beta blocking agents – Hypertension associated with increased HR and/or CO is typically treated with bolus doses of a beta blocker (eg, labetalol 5 to 25 mg, esmolol 10 to 50 mg, metoprolol 1 to 5 mg), which may be repeated. Beta blockers are avoided in patients with significant hypovolemia or acute hemorrhage causing anemia [110,111], and in those with decompensated heart failure. Also, patients with acute or severe bronchospastic lung disease and those with severe sinus bradycardia or a markedly impaired cardiac conduction system (eg, sinus node dysfunction) should not receive beta blockers. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Adrenergic-blocking agents' and "Treatment of acute decompensated heart failure: Specific therapies", section on 'Approach to long-term therapy in hospitalized patients' and "Management of the patient with COPD and cardiovascular disease", section on 'Effects of beta-blockers on mortality and COPD exacerbations'.)
Furthermore, beta blockers are relatively contraindicated in patients with cocaine intoxication due to risk of inducing unopposed alpha-adrenergic stimulation, which may lead to hypertension and myocardial ischemia from coronary vasoconstriction. (See "Cocaine: Acute intoxication", section on 'Use of beta adrenergic antagonists (beta blockers)'.)
Labetalol, which has both non-selective blockade for beta-adrenergic receptors and selective blockade of postsynaptic alpha1-adrenergic receptors, is a particularly good choice in patients with concomitant tachycardia and hypertension [112]. It is often selected to treat suspected myocardial ischemia due to tachycardia in patients with normal or elevated blood pressure. However, labetalol is a nonselective beta blocker that is not typically used in patients with severe asthma or chronic obstructive lung disease, heart failure, or bradycardia. Furthermore, labetalol is avoided in hyperadrenergic states, such as pheochromocytoma or cocaine or methamphetamine overdose, since paradoxical episodes of severe hypertension can occur if alpha blockade is incomplete.
Continuous infusions of labetalol are generally reserved for hypertensive emergencies. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Labetalol'.)
Esmolol is a very cardioselective beta1 blocker that has a rapid onset and a short duration of action (with a clinical effect lasting approximately 10 to 15 minutes) [113]. Clearance is not dependent on renal or hepatic function due to rapid metabolism by plasma esterases. For persistent hypertension with elevated HR, appropriate choices include an infusion of esmolol (eg, 50 to 300 mcg/minute), or boluses of the longer-acting cardioselective beta1 blocker metoprolol.
Landiolol is a short-acting IV beta blocker with similar kinetics but greater negative chronotropic effects than esmolol due to more selective beta1 effects; however, landiolol is not available in the United States [113,114]. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Esmolol'.)
For patients chronically receiving a beta blocker as part of an antihypertensive or antianginal regimen, a missed dose on the day of surgery may result in a rebound hypertensive response. If this is suspected, administration of IV dose(s) of a beta blocker is prudent. (See "Withdrawal syndromes with antihypertensive drug therapy" and "Perioperative management of hypertension", section on 'Withdrawal syndromes'.)
●Calcium channel blocking agents – Selective dihydropyridine-type calcium channel blockers inhibit calcium influx to provide selective arteriolar smooth muscles relaxation. These agents (eg, nicardipine, clevidipine) have no atrioventricular nodal blocking properties. They are commonly used to treat increased BP due to increased SVR. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Calcium channel blockers'.)
•Nicardipine – Nicardipine has been widely used in a variety of surgical settings, including neurosurgical and cardiac surgical settings [112]. Studies suggest that nicardipine has no major impact on preload or CO, and only minor negative inotropic action [115]. It can be administered by either IV bolus (eg, 100 to 500 mcg increments) or by continuous infusion at 5 to 15 mg/hour. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Nicardipine'.)
A study comparing nicardipine with esmolol for control of post-craniotomy emergence hypertension noted similar efficacy, but a greater need for a second "rescue" agent in patients receiving esmolol [116]. A study comparing continuous infusions of nicardipine or labetalol to manage hypertension after acute stroke noted similar safety and efficacy for both agents [117].
•Clevidipine – Clevidipine is a newer short-acting IV calcium channel blocker with rapid metabolism by plasma esterases that may confer an advantage over either nicardipine or nitroglycerin in patients requiring tight BP control within a narrow range [118,119]. Clearance is not dependent on renal or hepatic function. Clevidipine is only administered by continuous infusion (eg, beginning at 1 to 2 mg/hour with titration up to 16 mg/hour). Efficacy in controlling BP in stroke patients is similar to nicardipine [120-122]. However, costs are higher with clevidipine compared with nicardipine administration, and data regarding bolus dosing are lacking. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Clevidipine'.)
●Direct vasodilators – These agents directly relax vascular smooth muscle. Although the precise mechanisms causing vasodilation are not well established, these probably include opening of K+ channels, inhibition of inositol 1,4,5 triphosphate-induced release of calcium from smooth muscle sarcoplasmic reticulum, and stimulation of nitric oxide formation by the vascular endothelium.
•Hydralazine – Hydralazine is a direct-acting vasodilator that may be selected to treat increased BP, particularly for a patient with bradycardia. Hydralazine is highly selective for arterial resistance vessels, and has minimal or no effect on the venous circulation [123]. Administration may result in some increase in HR due to activation of the baroreceptor reflex. Hydralazine is administered as bolus doses (eg, 2.5 mg), which may be repeated every 5 minutes up to 20 mg. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Hydralazine'.)
Disadvantages include relatively slow onset compared with other IV antihypertensive agents, with a less predictable antihypertensive response.
•Nitroglycerin – Nitroglycerin is also commonly selected for treatment of intraoperative hypertension in patients with increased preload or increased SVR, particularly those with known or suspected ischemic heart disease. Nitroglycerin is an organic nitrovasodilator that causes increased release of nitric oxide (NO) via an enzymatic process. NO then activates smooth muscle guanylyl cyclase (GC) thereby increasing formation of cyclic guanosine monophosphate (cGMP) and inhibiting calcium entry into the cell, with consequent smooth muscle relaxation [124].
Nitroglycerin may be administered as IV bolus doses, a continuous infusion, as a sublingual dose, or by application of a paste. Low bolus doses (eg, 10 to 40 mcg) or the paste formulation of nitroglycerin primarily cause venodilation, thereby reducing preload. Higher doses administered as repeated boluses or by continuous carefully titrated infusion at 10 to 200 mcg/min (approximately 0.1 to 3 mcg/kg per minute) result in arteriolar dilation, thereby reducing SVR. Nitroglycerin is not appropriate for patients with hypovolemia. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Nitroglycerin'.)
Disadvantages include a propensity to cause a reflex increase in HR, and increased intrapulmonary shunt has also been reported [125]. Although nitroglycerin is rapidly titratable, continuous monitoring using an intra-arterial catheter is warranted when a continuous infusion is administered.
•Nitroprusside – Nitroprusside is occasionally selected to treat severe hypertension in the intraoperative setting to be administered as a continuous carefully titrated infusion at 10 to 200 mcg/minute or 0.1 to 3 mcg/kg per minute. Nitroprusside is a nitrovasodilator that directly releases NO with consequent arteriolar dilation as described above. Advantages include its potency, balanced venous and arteriolar effects, and the ability to rapidly titrate its effects.
However, nitroprusside has several disadvantages that have greatly decreased its use in most institutions. These include concerns regarding requirements for invasive BP monitoring since it is usually administered by continuous infusion, reflex tachycardia, prohibitive cost, poor control with attempts to use even small bolus doses, cyanide accumulation, and development of safer alternative agents suitable for continuous infusion. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Nitroprusside'.)
●Other antihypertensive agents – Other agents that may be available are rarely used to lower BP in the intraoperative setting:
•Fenoldopam – Fenoldopam is a selective dopamine receptor agonist that produces systemic vasodilation. It is administered by continuous infusion initially at 0.1 mcg/kg per minute and may be increased up to a maximum dose of 1.6 mcg/kg per minute. Fenoldopam is avoided in patients with increased ICP or glaucoma. Although it has potentially beneficial effects on renal function, there are no outcome data proving efficacy for renal protection. Thus, use of fenoldopam is generally restricted to treatment of hypertensive emergencies or high-risk vascular surgery in some centers [126,127]. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Fenoldopam'.)
•Enalaprilat – Enalaprilat is the only available IV angiotensin-converting enzyme inhibitor. The hypotensive response to enalaprilat is unpredictable, and it may cause precipitous hypotension in hypovolemic patients with a high plasma renin activity. Also, this agent has a slow onset over 15 to 30 minutes and a long duration of effect. For these reasons, enalaprilat is rarely used in the perioperative setting, but may be used in addition to other agents for hypertensive emergencies [128]. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Enalaprilat'.)
•Clonidine and dexmedetomidine – Clonidine and dexmedetomidine are alpha2-adrenoreceptor agonists.
Dexmedetomidine is occasionally administered as an anesthetic adjunct agent (eg, as a continuous infusion at 0.1 to 0.7 mcg/kg/hour as part of a total intravenous anesthesia technique). Due to its sympatholytic effects, dexmedetomidine typically decreases both BP and HR, so it may be selected to adjust anesthetic depth in a patient with hypertension and tachycardia [129,130] (see 'Adjustment of anesthetic depth' above). Also, if it is prudent to avoid beta blocking agents, then dexmedetomidine is a good choice.
Due to its potent bradycardic effects, dexmedetomidine should be used with caution during a high spinal or epidural block and in beta blocked patients. Also, decreases in HR and BP resolve slowly and may persist even after emergence from general anesthesia [129]. (See "Maintenance of general anesthesia: Overview", section on 'Dexmedetomidine' and "Emergence from general anesthesia", section on 'Intravenous agents'.)
For patients chronically receiving clonidine as part of an antihypertensive regimen, a missed dose on the day of surgery may result in a rebound hypertensive response. This can be avoided by application of a transdermal patch of clonidine during the preoperative period. If intraoperative clonidine withdrawal is suspected, a dexmedetomidine infusion could be initiated as noted above, or clonidine 0.1 mg could be administered via an orogastric tube (with repeat dosing as necessary). (See "Withdrawal syndromes with antihypertensive drug therapy" and "Perioperative management of hypertension", section on 'Withdrawal syndromes'.)
•Diuretics – Hypertensive patients who are hypervolemic or show signs of pulmonary edema may benefit from diuresis (eg, with administration of IV furosemide 10 to 20 mg), particularly if the morning dose of a chronically administered diuretic was missed. However, since most vasodilating agents administered in the perioperative setting will temporarily reduce preload, administration of a diuretic is not typically necessary.
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'.)
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 3). 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 [31]. (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 [131].
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 [131]. 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 'Vasopressor and positive inotropic agents' above.) (table 1 and table 5 and table 2)
•(See 'Trendelenburg positioning' above.)
•(See 'Reassessment of underlying causes' above.)
●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 'Antihypertensive agents' above.) and (table 6)
•(See 'Reassessment of underlying causes' above.)
●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 3). (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'.)
