Anesthesia for patients with hypertension

INTRODUCTION — Hypertension is a common preexisting diagnosis in surgical patients, reported by nearly one-third of adult patients presenting for noncardiac procedures and two-thirds of those undergoing coronary revascularization [1].

This topic will focus on the anesthetic management of patients with preexisting hypertension. Management of hypertension in the preoperative and postoperative periods and urgent or emergent treatment of severe hypertension are discussed in separate topics:

●(See "Perioperative management of hypertension".)

●(See "Management of severe asymptomatic hypertension (hypertensive urgencies) in adults".)

●(See "Evaluation and treatment of hypertensive emergencies in adults".)

PREANESTHESIA CONSULTATION

Perioperative risk assessment — Chronic hypertension is associated with long-term morbidity (eg, ischemic heart disease, heart failure, cerebrovascular disease, renal insufficiency) and in the 21st century has now surpassed tobacco smoking and household air pollution as the leading modifiable risk factor for global disease burden [2]. Hypertension and associated morbidities increase perioperative risk, as discussed in other topics [3,4]. Perioperative risks of severe, mild-to-moderate, and secondary hypertension are discussed in detail in other topics. (See "Perioperative management of hypertension", section on 'Perioperative risks associated with hypertension' and "Evaluation of cardiac risk prior to noncardiac surgery".)

The consensus among guidelines suggests that elective surgery in a hypertensive patient does not need to be delayed if diastolic blood pressure (BP) is <110 mmHg and systolic BP is <180 mmHg [5]. One study noted that joint guidelines published by the Association of Anaesthetists of Great Britain and Ireland and the British Hypertension Society reduced the number of preoperative cancellations due to hypertension alone [5,6]. Although elective surgery is usually delayed in patients with consistently higher preoperative BP values, the impact of isolated systolic hypertension on operative risk is less clear [7]. (See "Perioperative management of hypertension", section on 'Perioperative risks associated with hypertension'.)

Elevated preoperative BP values are often noted in patients with documented chronic hypertension [8]. However, there is no known benefit, and some potential for harm, when new therapy is initiated in the immediate preoperative period in an attempt to rapidly achieve normal BP values before elective surgery. Many surgical patients with chronic hypertension are older adults with isolated systolic hypertension who may have normal or low diastolic BP. Aggressive attempts to lower systolic BP in such patients may result in diastolic hypotension that compromises mean arterial pressure and thus impairs vital organ perfusion. However, in parallel with perioperative risk assessment, poorly controlled preoperative hypertension should be identified during the preanesthetic consultation so that medical consultation for chronic management can be encouraged. Multiple studies have demonstrated the feasibility and high adherence of anesthesiologists to such initiatives [9-11].

Although rare, acute severe hypertension may indicate malignant underlying conditions such as pheochromocytoma, necessitating medical intervention before elective surgery, or changes in anesthetic management if surgery is emergent. (See "Clinical presentation and diagnosis of pheochromocytoma".)

Determination of target blood pressure values — There is no consensus regarding specific intraoperative BP target values. In most patients, we attempt to maintain BP within 20 percent of the patient's baseline and keep mean arterial pressure (MAP) >65 mmHg, rather than targeting a specific BP value. This approach was examined in a randomized trial in 298 patients undergoing major abdominal surgery (82 percent had chronic hypertension) [12]. The intervention group was treated to maintain systolic BP within 10 percent of the individual's normal resting baseline value, including use of a norepinephrine infusion to increase BP when necessary. The control group was treated to maintain systolic BP ≥80 mmHg or to prevent a 40 percent decrease in BP below baseline. Attempting to maintain systolic BP within 10 percent of baseline led to fewer complications, defined as a composite of systemic inflammatory response syndrome with renal, respiratory, cardiovascular, or neurologic dysfunction (relative risk 0.73, 95% CI 0.56-0.94) [12].

In a study of more than 10,000 noncardiac surgical patients, both absolute decrease and relative maximum decrease in MAP were predictive of perioperative complications of myocardial injury or AKI [13]. A 2018 systematic review of 42 cohorts including various types of noncardiac surgery noted that both duration and degree of intraoperative hypotension (using both absolute and relative definitions) were associated with adverse postoperative outcomes [14]. Even a short duration of MAP <65 mmHg was associated with increased overall mortality, AKI, myocardial injury, and stroke; a MAP <80 mmHg for ≥10 minutes was associated with a small but statistically significant increase in overall mortality. One prospective study found that one-year postoperative mortality increased 4.4 percent for each minute when systolic blood pressure (SBP) fell below 80 mmHg [15]. Others have shown that excess mortality is associated with a drop in SBP below 90 mmHg for even one minute. A retrospective analysis of over 33,000 surgical procedures similarly found that one to five minutes of severe hypotension (MAP <55 mmHg) increased risk of AKI by 18 percent, and MI by 30 percent [16]. Notably, a subsequently published retrospective study of more than 138,000 patients found that the association of intraoperative MAP with postoperative AKI depended on whether preoperative risk factors were present [17].

For chronically hypertensive patients with high baseline blood pressures (eg, MAP >100 mmHg), a MAP target of 65 mmHg may be too low. In a retrospective study of 57,315 patients undergoing noncardiac surgery, low MAP values <65 mmHg or MAP values <20 percent of the individual patient's baseline were associated with myocardial and kidney injury, and such injury was more likely in those with chronic hypertension [18]. In a trial of older adults with chronically elevated MAP (approximately 100 mmHg), maintaining an intraoperative MAP target of 80 to 95 mmHg produced a lower incidence of AKI compared with a lower target of 65 to 79 mmHg or a higher target of 96 to 110 mmHg (6.3 versus 13.5 and 12.9 percent, respectively) [19]. However, intraoperative lability of BP values is common in chronically hypertensive patients, and both severe hypertension and severe hypotension may occur. To avoid undesirable large shifts in BP, short-acting vasoactive medications are selected and are administered in small, carefully titrated doses to treat unacceptably high or low BP values.

Notably, it is unclear which component of BP measurements (eg, systolic BP, diastolic BP, or MAP) should be targeted for monitoring and treatment during the intraoperative period. One retrospective review of more than 18,000 noncardiac surgical patients noted that 30-day mortality was associated with both the degree and the duration of intraoperative hypotension, regardless of whether systolic hypotension <70 mmHg, diastolic hypotension <30 mmHg, or low MAP <50 mmHg was used to define hypotension [20]. Similar findings were noted in a separate retrospective cohort [21].

There are conflicting reports regarding the association of intraoperative hypertension with postoperative morbidity. An analysis of data from 797 subjects undergoing noncardiac surgery found that, among operations lasting longer than 220 minutes in duration, there was an association between adverse outcomes and intraoperative hypertension, while no such association was observed during procedures of shorter duration [22].

Decisions regarding blood pressure monitoring — Continuous invasive BP monitoring with an intra-arterial catheter is often selected for hypertensive patients with coexisting coronary or cerebrovascular ischemic disease and/or if the planned surgical procedure is likely to cause significant bleeding or fluid shifts. (See "Basic patient monitoring during anesthesia", section on 'Invasive blood pressure monitoring'.)

Intermittent oscillometric BP monitoring with noninvasive BP (NIBP) technology (eg, a BP cuff) is most commonly used in routine noncardiac surgical procedures, although limitations to oscillometric technology include a tendency to make high or low extremes in BP appear closer to normal than actual BP [23]. If intermittent NIBP monitoring is selected for a patient with chronic hypertension, the cuff cycling time should be more frequent (eg, every one to two minutes rather than every five minutes) during periods of intense surgical stimulation and during induction and emergence from general anesthesia.

Technologies that enable continuous NIBP monitoring may reduce delays in recognition of hypotension and improve maintenance of BP stability [23-25]. In one randomized trial of 320 patients, those assigned to continuous BP monitoring had less time-weighted average MAP <65 mmHg (ie, less time spent <65 mmHg), compared with those who had intermittent NIBP monitoring [25]. In a retrospective study examining induction-associated hypotension among >300,000 older adults receiving propofol boluses to induce anesthesia, low MAP ≤55 mmHg was observed in 35 percent of patients who had invasive intra-arterial pressure monitoring compared with 20.7 percent of patients who had NIBP monitoring [26]. This finding demonstrates the likelihood that invasive BP monitoring best detects hypotension as well as increased susceptibility to hypotension among patients selected for invasive BP monitoring. (See "Basic patient monitoring during anesthesia", section on 'Noninvasive blood pressure monitoring'.)

Antihypertensive medication management — Generally, oral antihypertensive medications should be continued up to the time of surgery and resumed as soon as possible after completion of surgery with the possible exception of renin-angiotensin-system (RAS) inhibitors [27-34]. Preoperative continuation is particularly important for beta blockers and centrally acting sympatholytic drugs (eg, clonidine, methyldopa) since these agents are associated with acute withdrawal syndromes that may lead to perioperative rebound events. (See "Perioperative management of hypertension", section on 'Management of patients on chronic antihypertensive therapy' and "Perioperative medication management", section on 'Cardiovascular medications'.)

There is an increased risk of intraoperative hypotension in patients taking angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) preoperatively [33-43]. It is reasonable to hold ACE inhibitors and ARBs for a period of 24 hours prior to surgery, or to administer the evening dose on the day before surgery but not on the morning of surgery [4]. In a systematic review that included mostly observational data, withholding these agents prior to noncardiac surgery was associated with a decreased incidence of intraoperative hypotension compared with administration (23 versus 30 percent; odds ratio [OR] 0.63, 95% CI 0.47-0.85) [40]. However, all-cause mortality or major cardiovascular events were similar in both patient groups.

Decisions regarding timing of preoperative ACE inhibitor or ARB dosing are individualized based on the indications for the drug (eg, heart failure), the patient's preoperative BP, and whether significant perioperative fluid shifts are anticipated [39,44]. Importantly, postoperative hypertension is more likely if ACE inhibitors or ARBs are withheld on the day of surgery [45]. Then we carefully reintroduce these agents in the postoperative period since failure to restart them within 48 hours after surgery has been associated with increased 30-day mortality [46,47]. (See "Perioperative medication management", section on 'ACE inhibitors and angiotensin II receptor blockers' and "Perioperative management of heart failure in patients undergoing noncardiac surgery", section on 'Medication management'.)

Perioperative care coordination — In one study, high BP measurements in the preoperative clinic were associated with high BP measurements at home, while self-reported BP control, antihypertensive treatment, availability of primary care, and pain scores demonstrated poor agreement with preoperative elevated BP at home [8]. For patients who likely have chronically elevated BP, efforts aimed at care coordination to promote postoperative medical follow-up may be beneficial [5,48,49].

MANAGEMENT IN THE IMMEDIATE PREOPERATIVE PERIOD

Administration of morning antihypertensive doses — If the patient failed to take a morning dose of a beta-blocker, the missed dose can be administered with a sip of water in the preoperative area when feasible. Clonidine may be administered either orally or transdermally. Decisions to administer other classes of drugs including an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) on the morning of surgery are individualized, as noted above. (See 'Antihypertensive medication management' above.)

Reduction of preoperative anxiety and pain — Pain or anxiety in the immediate preoperative period is common and may result in increased blood pressure (BP). It is reasonable to administer small doses of an intravenous (IV) anxiolytic (eg, midazolam 1 to 2 mg) and/or an IV opioid (eg, fentanyl 25 to 50 mcg) to patients with significant preoperative anxiety or pain. For those who take a benzodiazepine or opioid on a chronic basis, the morning dose should be administered on the day of surgery to prevent withdrawal and assure patient comfort.

PREVENTION AND TREATMENT OF INTRAOPERATIVE HYPERTENSION — Acute intraoperative increases in systemic blood pressure (BP) are more likely to occur in chronically hypertensive patients compared with normotensive patients [33,34,50]. Causes should be anticipated when feasible and immediately treated. (See 'Causes and management of intraoperative hypertension' below.)

Initial treatment — If no reversible or treatable cause of increased BP is identified or if an acute hypertensive episode is severe or persists for longer than several minutes after initial treatment, an intravenous (IV) antihypertensive medication is administered [33,34,50]. Typically, short-acting agents are preferred to avoid overtreatment and consequent hypotension. Examples include bolus doses of a beta blocker (eg, esmolol 10 to 50 mg). Longer-acting drugs such as labetalol 5 to 25 mg or metoprolol 1 to 5 mg can be considered. A vasodilating agent such as the ultra-short-acting calcium channel blocker clevidipine administered as a continuous infusion [51], nicardipine administered in bolus doses (eg, 100 to 500 mcg) or by continuous infusion, or nitroglycerin administered in bolus doses (eg, 10 to 40 mcg) or by continuous infusion may also provide effective and highly titratable blood pressure control in hypertensive surgical patients (table 1).

Causes and management of intraoperative hypertension

Laryngoscopy and endotracheal intubation — Sympathetic responses to laryngoscopy and endotracheal intubation typically increase systemic BP by 20 to 25 mmHg in normotensive patients [50,52]. This increase can be much higher in hypertensive or insufficiently sedated patients. To blunt sympathetic responses and prevent an acute hypertensive episode, an adequate dose of a short-acting hypnotic is administered (eg, propofol 1 mg/kg, with additional boluses of 0.5 mg/kg as needed), in combination with supplemental IV anesthetic agents (eg, fentanyl 1 to 3 mcg/kg, lidocaine 1 to 2 mg/kg) or a potent inhalation anesthetic such as sevoflurane. However, doses of induction agents are administered cautiously (ie, reduced and titrated) in older or frail patients [26], and those who may develop hemodynamic instability due to hypovolemia, vasodilation, or myocardial dysfunction. (See "General anesthesia: Intravenous induction agents", section on 'Dosing considerations' and "Anesthesia for the older adult", section on 'Selection and dosing of anesthetic agents'.)

In addition to hypnotics and analgesics, an antihypertensive agent such as esmolol 10 to 20 mg or clonidine 1 mcg/kg may be preemptively administered to blunt responses to laryngoscopy and intubation [53,54]. Some clinicians also employ topical lidocaine to anesthetize the pharynx and larynx prior to direct laryngoscopy. Although use of a supraglottic airway (SGA) results in less sympathetic stimulation than laryngoscopy and endotracheal intubation, initial anesthetic induction doses may be higher to allow for smooth insertion in the absence of a neuromuscular blocking agent. (See "Induction of general anesthesia: Overview", section on 'Induction with endotracheal intubation' and "Induction of general anesthesia: Overview", section on 'Induction with supraglottic airway placement'.)

If a hypertensive response to laryngoscopy and intubation is severe or persistent, additional antihypertensive agents are administered. (See 'Initial treatment' above.).

Surgical stimulation — Inadequate anesthetic depth during painful surgical stimulation or other interventions often leads to increases in BP, which may be exaggerated in a patient with chronic hypertension. Increased intraoperative BP may be effectively lowered by deepening anesthesia (eg, increasing the concentration of a volatile inhalation anesthetic agent, adding supplemental nitrous oxide [N₂O], or administering doses of an IV sedative agent [eg, opioid agents, dexmedetomidine, lidocaine] or doses of a local anesthetic agent [eg, via a neuraxial or regional catheter or directly at the operative site]). (See "Maintenance of general anesthesia: Overview".)

If the hypertensive response is severe or persistent after treatment of pain and extubation of the trachea, antihypertensive agents are administered. (See 'Initial treatment' above.)

Hypoxemia and/or hypercarbia — Hypoxemia and/or hypercarbia may cause hypertension and tachycardia due to sympathetic stimulation. Typical treatment of hypoxemia includes administering a higher fraction of inspired oxygen (FiO₂), applying recruitment maneuvers, or initiating positive end-expiratory pressure (PEEP). Hypercarbia is typically treated by increasing minute ventilation with assisted or controlled ventilation to reduce arterial carbon dioxide (CO₂). (See "Monitored anesthesia care in adults", section on 'Supplemental oxygen' and "Mechanical ventilation during anesthesia in adults".)

Hypercarbia is particularly common in surgical procedures that require insufflation of CO₂ into the peritoneum or thorax. In some cases, temporary cessation of CO₂ insufflation may be necessary while hypercarbia is treated especially in patients with obstructive pulmonary disease in which the ability to increase minute ventilation is impaired. (See "Anesthesia for laparoscopic and abdominal robotic surgery in adults", section on 'Pulmonary complications'.)

Hypervolemia — Hypervolemia is difficult to assess in patients with longstanding hypertension. Intravascular volume status may be evaluated by respirophasic variations in the arterial pressure waveform if an intra-arterial catheter is present (figure 1), or with qualitative or quantitative assessment of left ventricular end diastolic cavity size via point-of-care ultrasound [55] or transesophageal echocardiography (TEE) (see "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'). Measurement of central venous pressure (CVP) may provide supplemental data but are a poor predictor of fluid responsiveness. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)

Hypervolemia should be suspected in patients with chronic hypertension who take a diuretic and is more likely if a preoperative morning diuretic dose was missed. Hypervolemia can also occur during selected procedures if a large volume of irrigation solution is used (eg, transurethral resection of the prostate, hysteroscopy). In such cases, an intraoperative dose of IV furosemide 5 to 10 mg or bumetanide 0.5 to 1 mg may be administered with careful attention to expected effects on urine output and potassium homeostasis.

Antihypertensive medication withdrawal — If the patient's antihypertensive regimen was interrupted on the day of surgery, persistent intraoperative hypertension can be treated with an IV equivalent of the medication that was missed when feasible. This is particularly important if the missed drug was a beta blocker or clonidine [27-30,33,34]. (See "Perioperative management of hypertension", section on 'Withdrawal syndromes' and "Tapering and discontinuing antihypertensive medications".)

Emergence and tracheal extubation — During emergence, sympathetic stimulation caused by pain and emergence excitement may result in an exaggerated response to stimulation of airway reflexes during suctioning and tracheal extubation, with consequent hypertension as well as tachycardia. These hemodynamic changes are often controlled by ensuring adequate analgesia prior to emergence (eg, by administering a systemic opioid or doses of local anesthetic via a neuraxial or regional catheter). (See "Extubation following anesthesia", section on 'Minimizing physiologic response to extubation'.)

Other causes — Less common causes of persistent or refractory intraoperative hypertension include bladder distention (due to a missing or kinked bladder catheter), elevated intracranial pressure (ICP), alcohol or benzodiazepine withdrawal syndromes, or recent cocaine or amphetamine use. Occasionally, severe persistent hypertension may be caused by serotonin syndrome, thyroid storm, or malignant hyperthermia.

Very rarely, a previously unsuspected pheochromocytoma may cause severe hypertension, typically associated with tachycardia, arrhythmias, and/or cardiovascular collapse [56,57]. Mortality and morbidity are particularly high when pheochromocytoma is previously undiagnosed [58]. (See "Anesthesia for the adult with pheochromocytoma".)

Management of hypertensive emergencies — Most patients with severe asymptomatic hypertension (systolic BP ≥180 mmHg and/or diastolic BP ≥120 mmHg) have no acute end-organ injury. However, patients with significantly elevated BP who have signs or symptoms of acute ongoing target-organ damage are considered to have a hypertensive emergency. (See "Evaluation and treatment of hypertensive emergencies in adults".)

Immediate treatment of severe perioperative hypertension is warranted if there is evidence of an acute cardiovascular emergency (eg, acute coronary syndrome, acute decompensated heart failure), neurologic signs or symptoms (eg, agitation, delirium, stupor, visual disturbances, seizures, stroke), acute renal failure, or a postoperative complication that is exacerbated by the elevated BP (eg, hemorrhage, increased ICP). In these instances, IV antihypertensive agent(s) should be administered immediately while further workup is pursued (table 1). (See 'Initial treatment' above and "Drugs used for the treatment of hypertensive emergencies".)

In a pregnant or postpartum woman, acute perioperative onset of severe hypertension with a systolic BP ≥160 mmHg or a diastolic BP ≥110 mmHg is a hypertensive emergency if these elevated BP values are accurately measured and persist >15 minutes [59]. The National Partnership for Maternal Safety (NPMS) consensus bundle recommends first-line agents for treatment that include IV labetalol 20 mg (followed by 40 mg if not effective within 10 minutes, then 80 mg every 10 minutes to a maximum total dose of 300 mg in the first hour) or hydralazine 5 to 10 mg IV every 20 minutes (to a maximum total dose of 20 mg in the first hour) [60,61]. Oral nifedipine 10 to 20 mg every 30 minutes is an alternative for patients who do not yet have IV access. Second-line antihypertensive agents are administered by infusion (eg, nicardipine, esmolol, labetalol, or, rarely, nitroglycerin if hypertension is associated with pulmonary edema unresponsive to diuretic therapy) (table 1). Providers should be aware of any expected concomitant effects on uterine tone during antihypertensive administration in the parturient. Administration of nitroprusside may result in fetal cyanide poisoning, and is a last resort for urgent control of refractory severe maternal hypertension; its use should be limited to a short period of time. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Acute therapy of severe hypertension' and "Anesthesia for labor and delivery in high-risk heart disease: General considerations", section on 'Effects of drugs commonly used in the labor unit'.)

An intra-arterial catheter for continuous BP monitoring is inserted as soon as feasible in any patient with a hypertensive emergency, particularly if IV antihypertensives are being administered by infusion.

PREVENTION AND TREATMENT OF INTRAOPERATIVE HYPOTENSION — Intraoperative hypotension (defined as systolic blood pressure [BP] <90 mmHg) is associated with an increased risk of mortality and/or myocardial infarction, and the longer the duration of hypotension, the higher the risk [62].

Patients with preexisting hypertension have chronic baroreceptor desensitization, loss of vascular elasticity, or intravascular volume depletion due to diuretic therapy [63]. They may have exaggerated responses to sympathetic inhibition caused by general anesthetic agents, neuraxial blockade, fluid shifts or blood loss occurring during the surgical procedure, or administration of any antihypertensive agent.

Initial treatment — Initial treatment of a hypotensive episode typically includes intravenous (IV) isotonic crystalloid solution administered in 250 to 500 mL increments. If necessary, an IV vasopressor/inotropic agent is administered to increase BP. Typically, small doses of short-acting agents are preferred to avoid overtreatment and consequent hypertension (eg, phenylephrine 40 to 100mcg increments or ephedrine 5 to 10mg increments). For severe or refractory hypotension, infusion of a vasopressor/inotropic agent may be necessary (table 1).

Causes and management of intraoperative hypotension — In the context of acute stabilization of low blood pressure, it is important to rapidly consider common causes. All hypotension is ultimately caused by low cardiac output, low systemic vascular resistance, or a combination of these factors.

Hypovolemia — Relative hypovolemia can result in severe hypotension following induction of anesthesia in a chronically hypertensive patient. If intravascular volume depletion is suspected (eg, due to chronic diuretic therapy or a preoperative bowel prep regimen), modest volume loading of hypertensive patients immediately prior to induction of general anesthesia is reasonable (eg, 250 to 500 mL of IV crystalloid solution).

Like hypervolemia, hypovolemia is difficult to assess in patients with longstanding hypertension (see 'Hypervolemia' above), but may be recognized with assessments of respirophasic variations in the arterial pressure waveform if an intra-arterial catheter is in place (figure 1), or qualitative and quantitative assessment of left ventricular end diastolic volume if transesophageal echocardiography (TEE) monitoring is used. (See "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'.)

Induction of general anesthesia — After the initial sympathetic responses to laryngoscopy and endotracheal intubation that typically increase BP, patients with chronic hypertension often develop marked hypotension, particularly if antihypertensive or supplemental anesthetic agents were administered to blunt these sympathetic responses [50,64].

For this reason, smaller initial doses of a sedative-hypnotic agent are typically used to induce general anesthesia (eg, propofol 1 mg/kg) and additional doses are titrated as necessary, rather than administering a high initial induction dose as a bolus. These precautions are particularly important in older or frail patients [65], and those who may develop hemodynamic instability due to hypovolemia, vasodilation, or myocardial dysfunction. (See "General anesthesia: Intravenous induction agents", section on 'Propofol' and "General anesthesia: Intravenous induction agents", section on 'Dosing considerations' and "Anesthesia for the older adult", section on 'Selection and dosing of anesthetic agents'.)

For selected patients, reasonable alternative anesthetic agents which are unlikely to cause hypotension include etomidate or ketamine. Advantages and disadvantages of these agents are discussed in a separate topic. (See "General anesthesia: Intravenous induction agents", section on 'Etomidate' and "General anesthesia: Intravenous induction agents", section on 'Ketamine'.)

Sympathectomy due to neuraxial block — Sympathectomy due to high neuraxial anesthetic block may result in hypotension, particularly if the sensory block is above the T6 level, and hypotension for this reason may be more likely in a patient with preexisting hypertension [66]. To minimize this risk, initial dosing of the epidural should be gradual, and the use of lower local anesthetic concentrations is reasonable. If hypotension does develop, treatment with IV fluid boluses and a phenylephrine infusion is typically adequate to restore BP to target values. (See 'Determination of target blood pressure values' above and "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Blood pressure'.)

If hypotension does not resolve after administration of fluid, phenylephrine, or other vasopressor/inotropic agents, the neuraxial infusion of local anesthetic is decreased or temporarily discontinued, or may be changed to contain only an opioid without local anesthetic. Also, as with any patient, the location of the epidural catheter is confirmed with aspiration to ensure that the tip has not migrated to enter a blood vessel or the intrathecal space. (See "Continuous epidural analgesia for postoperative pain: Technique and management", section on 'Hypotension'.)

Inhibition of the renin angiotensin system — During general anesthesia, the direct effects of anesthetic agents, inhibition of the sympathetic nervous system, and loss of baroreceptor reflex control of arterial pressure cause reliance on the renin angiotensin system (RAS) to maintain normotension. For this reason, there is an increased risk of intraoperative hypotension in patients taking angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) preoperatively [35,38] (see 'Antihypertensive medication management' above). The probable mechanism for hypotension is inability to activate the sympathetic nervous system when intravascular volume is depleted.

Initial treatment of perioperative hypotension in patients taking ACE inhibitors includes careful volume expansion and/or administration of vasopressor/inotropic agents (table 2). In some cases, administration of vasopressin or alternative agents is necessary to treat vasoplegia that is severe and/or refractory to other medications (table 3). (See "Intraoperative management for noncardiac surgery in patients with heart failure", section on 'Hemodynamic management'.)

Other causes — Similar to normotensive patients, less common causes of severe intraoperative hypotension such as pulmonary embolism, anaphylaxis, sepsis, myocardial infarction, or acute heart failure may also occur in patients with chronic hypertension [67-69]. (See "Intraoperative management of shock in adults" and "Intraoperative management of shock in adults", section on 'Cardiomyopathic shock'.)

MANAGEMENT IN THE IMMEDIATE POSTOPERATIVE PERIOD

Acute postoperative hypertension

Initial assessment and treatment — Patients with chronic hypertension have increased risk of hypertension in the post-anesthesia care unit (PACU) compared with normotensive patients. Hypertension in the PACU is typically treated if systolic blood pressure (BP) is >180 mmHg or diastolic BP is >110 mmHg. In nonemergent situations, the accuracy of BP measurements should be verified (eg, correct BP cuff size and assessment in the contralateral arm). Common postoperative causes should be treated before initiating systemic antihypertensive therapy. If no rapidly reversible or treatable cause of hypertension is identified or if BP remains elevated despite treatment of exacerbating factors, intravenous (IV) antihypertensive agent(s) are administered. (See "Cardiovascular problems in the post-anesthesia care unit (PACU)", section on 'Initial assessment and treatment of hypertension'.)

In the PACU, initial treatment is typically with small bolus doses of rapid-acting IV agents such as labetalol 5 to 25 mg, metoprolol 1 to 5 mg, hydralazine 5 to 10 mg, or nicardipine administered in 100 mcg increments. Agents are titrated to decrease systolic BP to a consistent value <160 mmHg. A beta blocker (eg, metoprolol or labetalol) is preferred for treating hypertension associated with tachycardia [70,71]. In some cases, continuous infusion of an antihypertensive agent is necessary (table 1). Additional treatment of hypertension depends upon the specific etiology.

Treatment of underlying causes — In addition to the initial treatment noted above, specific treatment of the underlying cause of hypertension is necessary. Common causes in the PACU include noxious stimuli (eg, pain, nausea and vomiting, hypoxemia or hypercarbia, delirium with agitation, hypothermia with shivering, bladder distention), hypervolemia, withdrawal from alcohol or opioids, or recent use of cocaine, amphetamine, or phencyclidine. (See "Cardiovascular problems in the post-anesthesia care unit (PACU)", section on 'Treatment of underlying causes of hypertension'.)

Notably, a hypertensive patient may have undiagnosed obstructive sleep apnea (OSA) exacerbated following sedation or general anesthesia. The resulting hypercarbia and hypoxemia worsen preexisting hypertension. Management is described separately. (See "Overview of the management of postoperative pulmonary complications".)

Uncommon causes of hypertension in the PACU include autonomic dysreflexia, intracranial hypertension, thyroid storm, malignant hyperthermia, carcinoid syndrome, or pheochromocytoma.

Reinstitution of antihypertensive medications — Chronically administered oral antihypertensive therapy should be reinstituted as soon as possible in the postoperative period once the patient has recovered from any acute hemodynamic derangements. When available, an IV equivalent may be administered if the patient cannot take oral medications. Any disruption of antihypertensive therapy in otherwise stable postoperative patients may result in perioperative hypertensive episodes. (See "Tapering and discontinuing antihypertensive medications" and "Perioperative management of hypertension", section on 'Withdrawal syndromes'.)

Acute postoperative hypotension

Initial assessment and treatment — Hypotension in the PACU is typically treated when the systolic BP is <90 mmHg, mean BP is <65 mmHg, or the relative decrease in BP is >20 percent below baseline. As with treatment of a hypertensive episode, the accuracy of BP measurements should be assessed before initiating therapy. Support for our approach comes from a post-hoc analysis of a large randomized trial (POISE-2) of interventions to prevent perioperative myocardial infarction [62]. Longer duration of postoperative hypotension on the day of surgery (defined as systolic BP <90 mmHg) was associated with increased risk of death and/or myocardial infarction.

Hypotension may occur due to effects of chronically or recently administered antihypertensive agents, and these effects may be exaggerated in a patient with chronic hypertension. In particular, perioperative administration of longer-acting IV agents (eg, hydralazine, metoprolol, or labetalol) may result in hypotension in the PACU after painful surgical stimulation has ceased.

Initial treatment of hypotension includes IV isotonic crystalloid solution administered in 250- to 500-mL increments. If necessary, IV vasopressor/inotropic agents (eg, phenylephrine 40- to 100-mcg increments or ephedrine 5- to 10-mg increments) are administered to increase BP. For severe or refractory hypotension, infusion of a vasopressor/inotropic agent may be necessary (table 2) (see "Cardiovascular problems in the post-anesthesia care unit (PACU)", section on 'Initial assessment and treatment of hypotension'). It may also be necessary to treat bradycardia (eg, due to the negative chronotropic effects of an antihypertensive drug), if bradycardia is contributing to hypotension. (See "Cardiovascular problems in the post-anesthesia care unit (PACU)", section on 'Bradyarrhythmias'.)

Treatment of underlying causes — In addition to the initial treatment noted above, specific treatment of the underlying cause of hypotension is necessary. As noted above, the sympathectomy produced by neuraxial anesthesia may significantly reduce BP, and this effect may be exaggerated in the hypertensive patient (see 'Sympathectomy due to neuraxial block' above). Thus, initial dosing of an epidural for postoperative analgesia should be gradual, and use of a lower concentration of local anesthetic is reasonable.

Similar to normotensive patients, other common and uncommon causes of hypotension may occur in patients with chronic hypertension (eg, hypovolemia due to inadequate intraoperative fluid replacement or blood loss, residual anesthetic effects, allergic drug reactions, adrenal insufficiency). (See "Cardiovascular problems in the post-anesthesia care unit (PACU)", section on 'Treatment of underlying causes of hypotension'.)

Myocardial ischemia, acute congestive heart failure, or other problems that may result in a hypotensive emergency should also be considered.

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: Hypertension in adults".)

SUMMARY AND RECOMMENDATIONS

●Preanesthesia consultation

•Assessing risk and monitoring decisions – The preanesthesia consultation involves overall risk assessment, blood pressure (BP) measurement, determination of target BP values for the intraoperative period, decisions regarding whether to employ noninvasive BP monitoring or an intra-arterial catheter for direct continuous monitoring, and perioperative care coordination to ensure preoperative medical consultation and postoperative follow-up for patients with poorly controlled hypertension. (See 'Preanesthesia consultation' above.)

•Managing perioperative medications – Generally, oral antihypertensive medications should be continued up to the time of surgery. This is most important for beta blockers and the centrally acting sympatholytic drugs (eg, clonidine, methyldopa), which are associated with acute withdrawal syndromes that may lead to a perioperative hypertensive event. If the patient failed to take a morning dose of an antihypertensive medication, the missed dose is administered with a sip of water in the preoperative area when feasible. Many centers routinely withhold angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) for 24 hours before surgery or administer the evening dose before elective surgery (but not on the morning of surgery), particularly if significant perioperative fluid shifts are anticipated. (See 'Antihypertensive medication management' above and 'Administration of morning antihypertensive doses' above.)

•Determining target BP – For most patients with chronic hypertension, we suggest maintaining BP within 20 percent of resting baseline value and mean arterial pressure (MAP) >65 mmHg (Grade 2C). Some patients may require a higher MAP. Lability of perioperative BP is likely, and we prevent and treat both hypertension and hypotension. (See 'Determination of target blood pressure values' above.)

●Intraoperative hypertension

•Causes – Common causes of acute intraoperative increases in BP include sympathetic stimulation during laryngoscopy and endotracheal intubation, surgical stimulation, emergence and tracheal extubation, hypercarbia or hypoxemia, or withdrawal of antihypertensive medications. (See 'Causes and management of intraoperative hypertension' above.)

•Treatment – Reversible causes of acute intraoperative hypertensive episodes are treated. If an acute hypertensive episode is severe or persists for longer than several minutes, an intravenous (IV) antihypertensive medication is administered. Typically, short-acting agents are preferred to avoid overtreatment and consequent hypotension (eg, a beta blocker such as esmolol 10 to 50 mg, labetalol 5 to 25 mg, or metoprolol 1 to 5 mg and/or a vasodilating agent such as nicardipine 100 to 500 mcg or nitroglycerin 10 to 40 mcg). In some cases, continuous infusion of an antihypertensive agent is necessary (table 1). (See 'Initial treatment' above.)

●Intraoperative hypotension

•Causes – Common causes of intraoperative hypotension include hypovolemia, sympathetic inhibition due to administration of anesthetic agents, neuraxial blockade, inhibition of the renin angiotensin system due to chronic ACE inhibitor or ARB therapy, or recent administration of an IV antihypertensive agent. Perioperative myocardial infarction or acute heart failure is more likely if the patient has coexisting cardiovascular disease. (See 'Causes and management of intraoperative hypotension' above.)

•Treatment – Initial treatment of hypotensive episodes typically includes IV isotonic crystalloid solution administered in 250 to 500 mL increments (figure 1). If necessary, an IV vasopressor/inotropic agent is administered to increase BP. Typically, small doses of short-acting agents are preferred to avoid overtreatment and consequent hypertension (eg, phenylephrine 40 to 100 mcg increments or ephedrine 5 to 10 mg increments). For severe or refractory hypotension, a vasopressor/inotropic infusion may be necessary (table 2). (See 'Initial treatment' above.)

●Postoperative hypertension – Hypertension in the post-anesthesia care unit (PACU) is typically treated if systolic BP is >180 mmHg or diastolic BP is >110 mmHg. Common causes include noxious stimuli (eg, pain, nausea and vomiting, hypoxemia or hypercarbia, delirium with agitation, hypothermia with shivering, bladder distention), hypervolemia, withdrawal from alcohol or opioids, or recent use of cocaine, amphetamine, or phencyclidine. Also, undiagnosed obstructive sleep apnea (OSA) with hypercarbia and hypoxemia may exacerbate preexisting hypertension. (See 'Initial assessment and treatment' above and 'Treatment of underlying causes' above.)

Preoperative oral antihypertensive therapy should be reinstituted in the PACU or as soon as possible, or an IV equivalent may be administered if the patient cannot take oral medications. (See 'Reinstitution of antihypertensive medications' above.)

●Postoperative hypotension – Hypotension in the PACU is typically treated when the systolic BP is <90 mmHg, mean BP is <65 mmHg, or relative BP decrease is >20 percent below baseline. In particular, effects of chronically or recently administered antihypertensive agents or neuraxial blockade due to dosing of an epidural catheter may cause postoperative hypotension once painful surgical stimulation has ceased. Other common causes of postoperative hypotension are similar to those in normotensive patients (eg, hypovolemia due to inadequate intraoperative fluid replacement or blood loss). (See 'Acute postoperative hypotension' above.)