Cardiovascular problems in the post-anesthesia care unit (PACU)

INTRODUCTION — Hemodynamic aberrations in the post-anesthesia care unit (PACU) include hypotension, hypertension, and/or cardiac arrhythmias, and may be caused by or result in cardiovascular complications (eg, myocardial ischemia, decompensated heart failure). Although nausea and vomiting or respiratory problems occur more frequently, cardiovascular events are the third most common problem requiring treatment in the immediate postoperative period [1-3]. In this topic, we review the diagnosis and treatment of causes of hemodynamic instability and cardiovascular complications in the immediate postoperative period. Complications that occur after cardiac surgery are discussed separately. (See "Postoperative complications among patients undergoing cardiac surgery" and "Early cardiac complications of coronary artery bypass graft surgery".)

RISK FACTORS — The likelihood of cardiovascular instability due to hypotension, hypertension, or cardiac arrhythmias after noncardiac surgery is associated with various patient-associated and procedure associated factors, as noted in the tables (algorithm 1 and table 1 and table 2 and table 3):

●Preoperative factors:

•Severity of preexisting cardiovascular comorbidities (eg, ischemic heart disease, chronic hypertension, congestive heart failure, renal insufficiency, valvular heart disease, atrial and ventricular arrhythmias, peripheral vascular disease)

•Recent stroke

•Recent placement of coronary artery stents

•Acute trauma (eg, hip fracture)

•Urgent or emergency surgery

●Intraoperative factors:

•Invasiveness of the surgical procedure (table 3) [4]

•Severity of perioperative stresses (eg, blood loss, fluid shifts, sepsis, pain, hypothermia, hypotension)

•Effects of anesthetic agents and techniques

●Postoperative factors:

•Bleeding and/or hypovolemia

•Hypoxemia

•Pain

HYPOTENSION

Initial assessment and treatment of hypotension

●Determining target values – Hypotension may be absolute (eg, systolic blood pressure [BP] <90 mmHg or mean arterial pressure [MAP] <65 mmHg) or relative (eg, systolic BP decrease >20 percent of baseline). These values serve as a guide for treatment, although there is no widely accepted definition of perioperative hypotension [5]. In general, rather than targeting a specific BP value, we attempt to maintain systolic BP values within 20 percent of the patient's baseline and MAP >65 mmHg while the patient is in the PACU. Furthermore, low BP is treated if there is evidence of hypoperfusion (eg, change in mental status associated with lower blood pressure). (See "Anesthesia for patients with hypertension", section on 'Determination of target blood pressure values'.)

Also, diastolic "hypotension" is common in older patients since vascular aging leads to arterial rigidity causing isolated systolic hypertension with associated lowering of diastolic BP and widened pulse pressure. While clinical definitions of hypotension and management are typically based on systolic BP, it is prudent to also note the diastolic BP since organ perfusion occurs primarily during diastole.

●Initial treatment – Initial treatment of hypotension in the PACU should be based on the etiology. Prior to initiating treatment, the accuracy of monitors should be assessed (see "Basic patient monitoring during anesthesia", section on 'Invasive blood pressure monitoring'). When hypovolemia (the most common cause) is suspected, management includes administration of intravenous (IV) isotonic crystalloid solution 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 also administered to rapidly increase BP.

●Treatment of severe or refractory hypotension – Small bolus doses of diluted IV epinephrine 10 to 50 mcg, norepinephrine 4 to 8 mcg, or vasopressin 1 to 2 units may be administered while a vasopressor/inotropic infusion is prepared (table 4).

●Discharge disposition – Patients with refractory hypotension requiring continued treatment with vasopressors/inotropic therapy should be admitted to an inpatient setting for further observation, rather than discharged home. Diagnoses of myocardial infarction, decompensated heart failure, or other causes of potentially worsening hypotension should be ruled out. (See 'Postoperative cardiovascular complications' below and 'Hypotensive emergencies' below.)

Treatment of underlying causes of hypotension

Hypovolemia — Patients undergoing major surgical procedures may develop intraoperative hypovolemia due to large fluid shifts or significant bleeding that has not been adequately corrected when the patient is admitted to the PACU. Other factors that may contribute to hypovolemia in the postoperative period include prolonged preoperative fasting, postoperative diuresis, ongoing postoperative fluid losses from the gastrointestinal tract, skin, or due to persistent unrecognized bleeding (eg, swallowed blood after tonsillectomy).

●Assessment – The intraoperative records are reviewed to assess estimated blood loss and other perioperative fluid deficits and losses (eg, preoperative dehydration, intraoperative urine output) (see "Intraoperative fluid management", section on 'Causes and consequences of intravascular volume derangements'). Also the amount and type of intraoperative fluid replacement therapy is noted. If available, central venous pressure (CVP) is measured to provide supplemental information regarding adequacy of intravascular volume, although CVP is poorly predictive of fluid responsiveness in most patients. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)

Since intraoperative blood loss is commonly underestimated, hemoglobin (Hgb) is measured if significant bleeding may have occurred. However, an individual Hgb value may not accurately reflect blood loss during or immediately after an acute bleeding episode. Also, bleeding may continue into the postoperative period due to circumstances that are case-specific (eg, delayed blood loss after knee surgery with intraoperative use of a tourniquet) or patient-specific (eg, preexisting coagulation disorders) [6]. For these reasons, serial Hgb measurements are more useful than a single value.

●Treatment – If there is evidence of inadequate fluid replacement, a balanced electrolyte crystalloid solution is administered in 250- to 500-mL IV boluses, with reassessment of intravascular volume status and BP after each bolus. (See "Intraoperative fluid management", section on 'Choosing a fluid management strategy'.)

Red blood cells (RBCs) are reserved until a transfusion threshold is met (typically when Hgb is <7 to 8 g/dL or hematocrit is <21 to 24 percent), similar to the intraoperative setting. However, patients with significant ongoing bleeding, known acute coronary syndrome, or signs of myocardial or other organ ischemia should receive RBC transfusion at a higher Hgb threshold (eg, <9 g/dL or hematocrit <27 percent). (See "Intraoperative transfusion and administration of clotting factors", section on 'Red blood cells' and "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Thresholds for specific patient populations'.)

In rare cases, significant hypotension may occur during transfusion of blood products due to an acute transfusion reaction (algorithm 2 and table 5). If this is suspected, the transfusion is stopped, IV fluids and vasopressor/inotropic agents are administered, and other standard treatments for such allergic reactions are initiated as appropriate (table 6). The blood bank should be notified if a transfusion reaction is suspected. (See "Approach to the patient with a suspected acute transfusion reaction".)

Drug effects — Review of preoperative medications, anesthetic techniques, and intraoperative drugs that were administered may suggest likely causes of postoperative hypotension.

Antihypertensive agents — Intraoperative or postoperative administration of longer-acting IV agents such as hydralazine, metoprolol, or labetalol may result in postoperative hypotension once painful surgical stimulation has ceased.

Effects of chronically administered antihypertensive agents may cause hypotension during the intraoperative and/or postoperative periods. In particular, there is an increased risk of perioperative hypotension in patients taking angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) preoperatively. The probable mechanism is inability to activate the sympathetic nervous system when intravascular volume is depleted. (See "Anesthesia for patients with hypertension", section on 'Antihypertensive medication management' and "Anesthesia for patients with hypertension", section on 'Inhibition of the renin angiotensin system'.)

As noted above, treatment includes careful volume expansion and/or administration of vasopressor/inotropic agents (see 'Initial assessment and treatment of hypotension' above). In some patients taking ACE inhibitors or ARBs, administration of vasopressin may be necessary to treat severe vasoplegia refractory to other medications (table 4). An alternative treatment is administration of methylene blue 1 to 2 mg/kg IV over 20 minutes to reduce resistance vessel responsiveness to nitric oxide.

If a slow HR is contributing to hypotension due to the negative chronotropic effects of an antihypertensive agent, then it is also necessary to treat bradycardia. (See 'Bradyarrhythmias' below.)

Anesthetic agents — Residual effects of anesthetic agents or excessive opioid doses may result in hypotension, particularly in patients who have little pain after surgery. Such patients are typically somnolent or obtunded, and may exhibit respiratory depression as well as hypotension. (See "Overview of the management of postoperative pulmonary complications".)

●Opioids – If excessive opioid dosing is suspected, small IV doses of naloxone 40 to 80 mcg may be administered until opioid-related sedative and respiratory depressant effects are reversed (table 7). When opioids are the cause of persistent hypotension, the blood pressure should increase as the patient becomes more alert and has normal respiration.

In most patients, titration of low doses of naloxone safely reverses opioid effects. However, sudden reversal of analgesic effects may cause extreme discomfort and a sympathetic surge resulting in hypertension, tachycardia, and myocardial ischemia in susceptible patients (see 'Myocardial injury' below). Also, flash pulmonary edema has been reported after a large dose of naloxone in rare cases [7].

The half-life of naloxone is 1 to 1.5 hours, which may be shorter than the half-life of the opioid being reversed. In these cases, postoperative monitoring should continue because additional doses of naloxone may be required. (See "Acute opioid intoxication in adults", section on 'Management'.)

●Benzodiazepines – Oversedation with hypotension caused by benzodiazepines is uncommon in the postoperative setting. When this is suspected, IV flumazenil may be administered to reverse this effect (table 7). (See "Benzodiazepine poisoning", section on 'Role of antidote (flumazenil)'.)

●Other agents – Intraoperative administration of propofol and/or inhalational anesthetic agents are unlikely to cause postoperative hypotension because of their brief duration of action. In contrast, intraoperative dexmedetomidine infusion, particularly at high doses, may cause hypotension in the postoperative period [8,9]. (See "Maintenance of general anesthesia: Overview", section on 'Dexmedetomidine'.)

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. Patients with preexisting hypertension may be at higher risk [10]. (See "Overview of neuraxial anesthesia", section on 'Cardiovascular'.)

If the neuraxial anesthetic includes a continuous infusion, this should be discontinued. In addition, hypotension is treated with vasopressor/inotropic agents (see 'Initial assessment and treatment of hypotension' above), and if hypovolemia is suspected, IV fluids are also administered. Also, the epidural catheter is aspirated to confirm that the catheter tip has not migrated into a blood vessel or the intrathecal space. If correct positioning of the catheter is confirmed, the neuraxial anesthetic infusion may be reinstituted using an opioid without local anesthetic in some patients. (See "Continuous epidural analgesia for postoperative pain: Technique and management", section on 'Hypotension'.)

Adrenal insufficiency — Acute adrenal insufficiency uncommonly occurs in a patient receiving chronic glucocorticoid therapy, but if corticosteroid replacement therapy is inadequate, this may be a cause of postoperative hypotension. This unusual cause of hypotension should be considered when hypotension is refractory to standard treatment with fluids and vasopressors in a patient with a history of chronic steroid therapy. Treatment includes IV hydrocortisone 100 mg or dexamethasone 4 mg. (See "Treatment of adrenal insufficiency in adults", section on 'Adrenal crisis'.)

Hypotensive emergencies — Certain conditions can cause profound hypotension and/or hemodynamic collapse requiring immediate lifesaving interventions. In the PACU setting, such conditions may include:

●Hemorrhagic or nonhemorrhagic hypovolemic shock — Treatment is discussed separately. (See "Intraoperative management of shock in adults", section on 'Hypovolemic shock management'.)

Hemorrhage is the most common cause of hypovolemic shock in surgical patients. Nonhemorrhagic causes of severe hypovolemia in surgical patients include gastrointestinal losses (eg, vomiting, diarrhea, bowel preparation), skin losses (eg, burns), ascites, and prolonged surgery with an open abdominal cavity that may eventually lead to increased bowel edema and sequestration of fluid. (See "Intraoperative fluid management", section on 'Causes and consequences of intravascular volume derangements'.)

●Septic shock — Treatment is discussed separately. (See "Intraoperative management of shock in adults", section on 'Septic shock'.)

Sepsis is the most common cause of distributive shock in surgical patients, and may be preexisting before surgery, or may develop during or after surgery in patients with active infection. Sepsis should be suspected in susceptible patients with profound hypotension due to vasodilation (with high cardiac output if intravascular volume is adequate). After emergency management is initiated in the PACU, the surgeon and an infectious disease specialist are consulted to ensure that surgical causes have been addressed and that antibiotic coverage is appropriate and cultures have been sent. (See "Evaluation and management of suspected sepsis and septic shock in adults".)

●Anaphylactic shock — Treatment is based on prompt administration of IV epinephrine and fluid resuscitation, as well as other therapies, such as inhaled bronchodilators, IV steroids, and H1 and H2 antihistamines if symptoms persist. Treatment is discussed in detail in a separate topic (table 6) (see "Perioperative anaphylaxis: Clinical manifestations, etiology, and management", section on 'Initial management'). Steroids and H2 blockers should be included in the initial management of anaphylactic shock.

Severe postoperative hypotension may occur due to exposure to latex or a medication administered during or after surgery (eg, antibiotics, protamine) (table 8). Accompanying respiratory symptoms may include bronchospasm, inspiratory stridor, or oral edema. Allergic reactions typically present as itching, rash, or hives, but minor symptoms may not be noticed by a patient with residual postoperative sedation. (See "Perioperative anaphylaxis: Clinical manifestations, etiology, and management", section on 'Etiologies' and "Perioperative anaphylaxis: Clinical manifestations, etiology, and management", section on 'Clinical manifestations and diagnosis'.)

●Cardiogenic shock — Treatment of cardiogenic shock complicating acute myocardial infarction (MI) is discussed separately (table 9). (See "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction".)

MI is the most common perioperative cause of severe myocardial dysfunction, and cardiogenic shock may occur if >40 percent of the myocardium is involved. Patients with ischemic heart disease are at risk, particularly if they had preoperative unstable angina, recent percutaneous coronary intervention, or emergency or high-risk surgery (table 10). (See 'Myocardial injury' below.)

●Arrhythmogenic shock — Management of arrhythmogenic causes of shock is described in advanced cardiac life support protocols. (See "Advanced cardiac life support (ACLS) in adults", section on 'Management of specific arrhythmias'.)

●Local anesthetic systemic toxicity — Treatment is outlined in the table and discussed separately (table 11). (See "Local anesthetic systemic toxicity", section on 'Management of LAST' and "Local anesthetic systemic toxicity", section on 'Lipid rescue'.)

Local anesthetic systemic toxicity (LAST) causing profound hypotension and arrhythmias (eg, tachycardia, bradycardia, ventricular arrhythmias, asystole) may occur in the postoperative period after dosing a catheter that is misplaced in an intravascular location. Rarely, accidental IV administration of a local anesthetic infusion intended for epidural or perineural administration may occur. (See "Prevention of perioperative medication errors", section on 'Wrong route errors' and "Local anesthetic systemic toxicity", section on 'Risk factors for LAST'.)

Although the clinical presentation of LAST is highly variable, central nervous system symptoms (eg, perioral numbness, metallic taste, ringing in the ears, agitation, visual changes, muscle twitching, and ultimately, seizures) commonly precede signs of cardiovascular toxicity. (See "Local anesthetic systemic toxicity", section on 'Clinical presentation of toxicity'.)

●Tension pneumothorax — Treatment of suspected life-threatening tension pneumothorax does not require a chest radiograph before emergent needle decompression (using a 14 to 16 gauge IV catheter inserted in the second or third intercostal space in the midclavicular line) or emergent tube thoracostomy (using a 24 or 28 Fr tube inserted in the fifth intercostal space in the midaxillary line). (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Tension pneumothorax' and "Thoracostomy tubes and catheters: Indications and tube selection in adults and children", section on 'Tension pneumothorax'.)

Tension pneumothorax should be suspected in patients with risk factors such as perioperative attempted or actual central line insertion, a surgical procedure that involved the neck or thorax, or chronic lung disease. In addition to hypotension, signs and symptoms include worsening oxygenation, dyspnea, tachypnea, unilateral diminished breath sounds and pleuritic chest pain, distended neck veins, and tracheal deviation away from the affected side.

●Pulmonary embolus — Pulmonary embolism is suspected in a hypotensive patient with acute onset of shortness of breath, tachycardia, and hypoxia. Treatment of patients who are hemodynamically unstable is discussed separately (algorithm 3). (See "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults", section on 'Hemodynamically unstable'.)

●Left ventricular outflow tract obstruction — Immediate treatment of left ventricular outflow tract (LVOT) obstruction causing severe hypotension includes (see "Hypertrophic cardiomyopathy: Management of patients with outflow tract obstruction", section on 'Acute shock'):

•Increasing left ventricular volume with fluid administration

•Increasing systemic vascular resistance with vasoconstrictors that do not have inotropic properties (eg, phenylephrine or vasopressin)

•Decreasing inotropy and heart rate (HR) with beta blockers

In a susceptible patient with hypertrophic cardiomyopathy, dynamic LVOT obstruction can be precipitated by hypovolemia, vasodilation, tachycardia, and/or a high catecholamine state (eg, due to postoperative pain). Rapid diagnosis is possible with echocardiography. (See "Intraoperative rescue transesophageal echocardiography (TEE)", section on 'Left ventricular outflow tract obstruction'.)

HYPERTENSION

Initial assessment and treatment of hypertension

●Determining target values – Hypertension in the PACU is typically treated if systolic blood pressure (BP) is >180 mmHg or diastolic BP is >110 mmHg, particularly if hypertension persists after treatment of presumed etiologies. For patients who had severe preoperative hypertension (ie, ≥180/≥120 mmHg), treatment thresholds may differ. We review the patient's preoperative and baseline BP, as well as the home medication list and timing of last doses of antihypertensive medications. There is no known benefit from initiation of new therapy in the perioperative period to achieve normal BP values or goals appropriate for chronic control [11]. Further management is discussed separately. (See "Anesthesia for patients with hypertension", section on 'Determination of target blood pressure values' and "Anesthesia for patients with hypertension", section on 'Acute postoperative hypertension'.)

●Initial treatment – Prior to initiating treatment, the accuracy of monitors should be assessed (see "Basic patient monitoring during anesthesia", section on 'Invasive blood pressure monitoring'). Immediate treatment of the primary problem is necessary (see 'Noxious stimuli' below). In addition, small bolus doses of rapid-acting intravenous (IV) agents such as labetalol 5 to 25 mg, metoprolol 1 to 5 mg, hydralazine 5 to 10 mg, or nicardipine 0.2-mg increments may be titrated to decrease systolic BP to target values. Since metoprolol and labetalol have beta-blocking properties, these agents are preferred if hypertension is associated with tachycardia [12,13].

●Treatment of severe or refractory hypertension – In some cases, continuous infusion of an antihypertensive agent may be necessary as the specific etiology is being treated (table 12). (See 'Treatment of underlying causes of hypertension' below.)

●Discharge disposition – Patients with severe, refractory, or worsening hypertension should be admitted to an inpatient setting for further observation, rather than discharged home. Most patients who achieve hemodynamic stability after initial treatment, with stable BP within 20 percent of baseline values (typically <160 systolic and <100 diastolic) can be discharged home if this is otherwise appropriate. (See 'Postoperative cardiovascular complications' below and 'Hypotensive emergencies' above.)

Hypertensive emergencies — Emergency treatment of severe hypertension is warranted if there is evidence of acute neurologic signs or symptoms (eg, agitation, delirium, stupor, visual disturbances, seizures, stroke) or a cardiovascular emergency (eg, acute coronary syndrome, acute decompensated heart failure, aortic dissection). In these instances, an IV antihypertensive agent(s) is immediately initiated while further workup is pursued (table 12). (See "Evaluation and treatment of hypertensive emergencies in adults" and "Drugs used for the treatment of hypertensive emergencies".)

Rarely, a pheochromocytoma may cause severe hypertension in the PACU, typically associated with tachycardia, arrhythmias, and/or cardiovascular collapse [14-16]. Mortality risk is high. Treatment in the perioperative setting is described separately. (See "Anesthesia for the adult with pheochromocytoma", section on 'Treatment of hypertension and arrhythmias'.)

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 [17]. Treatment in the perioperative setting for these patients is described separately. (See "Anesthesia for patients with hypertension", section on 'Management of hypertensive emergencies' and "Treatment of hypertension in pregnant and postpartum patients", section on 'Acute therapy of severe hypertension'.)

Treatment of underlying causes of hypertension

Preexisting hypertension — Undiagnosed or poorly controlled preexisting hypertension is the most common cause of perioperative hypertension, particularly in patients receiving chronically administered antihypertensive medications that were not continued up until the time of surgery. Beta blockers and centrally acting sympatholytic drugs (eg, clonidine, methyldopa) have been associated with severe acute withdrawal syndromes and perioperative hypertensive events. Postoperative hypertension is also more likely if an angiotensin converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) is withheld on the day of surgery [18]. (See "Tapering and discontinuing antihypertensive medications" and "Perioperative management of hypertension", section on 'Withdrawal syndromes'.)

Chronically administered oral antihypertensive therapy should be reinstituted as soon as possible in the postoperative period, or an IV equivalent may be administered if the patient cannot take oral medications. (See "Tapering and discontinuing antihypertensive medications" and "Perioperative management of hypertension", section on 'Withdrawal syndromes'.)

Noxious stimuli — Noxious stimuli may cause marked sympathetic stimulation resulting in hypertension and tachycardia in the PACU. Hypertension and associated tachycardia typically resolve with appropriate treatment of the primary problem.

●Pain – (See "Approach to the management of acute pain in adults".)

●Nausea and/or vomiting – (See "Postoperative nausea and vomiting", section on 'Rescue therapy'.)

●Hypoxia and/or hypercarbia – (See "Respiratory problems in the post-anesthesia care unit (PACU)".)

●Emergence delirium and agitation – (See "Delayed emergence and emergence delirium in adults", section on 'Emergence delirium'.)

●Hypothermia with shivering – Hypothermia results in sympathetic stimulation with hypertension and/or tachycardia causing increased myocardial oxygen consumption, particularly if shivering occurs [19-21]. In a patient with ischemic heart disease, these effects can lead to myocardial ischemia and arrhythmias [22]. (See 'Myocardial injury' below and "Perioperative temperature management", section on 'Postoperative temperature derangements'.)

●Bladder distention – A distended bladder is a common and often overlooked cause of sympathetic stimulation causing hypertension in the PACU, particularly in patients with preexisting urinary retention, and in those who had a neuraxial block, excessive fluid administration, or certain types of surgery (eg, gynecologic, anorectal, hernia repair) [23,24]. Management is described separately. (See "Overview of post-anesthetic care for adult patients", section on 'Inability to void'.)

Bladder or bowel distention in a patient with a high spinal cord injury (SCI) may cause autonomic dysreflexia, an exaggerated sympathetic response manifested by diffuse vasoconstriction below the level of SCI causing hypertension with bradycardia or tachycardia, and other symptoms. Management includes alleviation of the inciting cause, administration of oxygen, treatment of hypertension and arrhythmias, and assessment for myocardial ischemia. (See "Anesthesia for adults with chronic spinal cord injury", section on 'Autonomic dysreflexia' and "Anesthesia for adults with chronic spinal cord injury", section on 'Management of intraoperative autonomic dysreflexia'.)

Hypervolemia — Hypervolemia is suspected in patients who did not receive a dose of a chronically administered diuretic on the morning of surgery, if a large volume of irrigation solution was given into an organ cavity (eg, transurethral resection of the prostate, hysteroscopy), or if intraoperative fluid therapy was excessive. Intravascular volume status is best evaluated with dynamic hemodynamic parameters, as described separately. (See "Intraoperative fluid management", section on 'Monitoring intravascular volume status'.)

Initial therapy is administration of an IV diuretic (typically furosemide 20 to 40 mg), with vasodilator therapy (typically an infusion of IV nitroglycerin or nitroprusside (table 12)) as second-line treatment if hypervolemic hypertension is severe or associated with acute decompensated heart failure. (See 'Decompensated heart failure' below.)

Drug effects

Alcohol or opioid withdrawal — Patients chronically using alcohol or opioids may develop hypertension and/or tachycardia in the PACU due to sympathetic stimulation associated with withdrawal.

●Alcohol withdrawal – Symptoms of alcohol withdrawal (eg, hypertension, tachycardia, tremulousness, sweating, nausea, anxiety) may manifest as early as 6 to 24 hours after the last drink, and can progress to delirium tremens with worsening hypertension in 48 to 96 hours. Benzodiazepines (eg, IV lorazepam) are administered to treat withdrawal symptoms. Other aspects of management of alcohol withdrawal are discussed separately. (See "Management of moderate and severe alcohol withdrawal syndromes".)

●Opioid withdrawal – Symptoms of opioid withdrawal include hypertension, as well as tachycardia, mydriasis, piloerection, nausea, and dysphoria (table 13). In chronic opioid users, postoperative hypertension may be exacerbated by inadequately treated pain due to opioid tolerance and/or opioid-induced hyperalgesia [25,26]. (See "Management of acute pain in the patient chronically using opioids for non-cancer pain".)

Recent use of cocaine, amphetamine, phencyclidine, or MDMA — Recent use of drugs that produce a hyperadrenergic state (eg, cocaine, amphetamine, phencyclidine, 3,4-methylenedioxymethamphetamine [MDMA], lysergic acid diethylamide [LSD], or monoamine oxidase inhibitors) can cause sympathetic overactivity and hypertension, tachycardia, and cardiac arrhythmias [27]. Vasodilators such as hydralazine 5 to 10 mg bolus doses or a continuous infusion of nitroglycerin, nicardipine, or clevidipine may be used to control hypertension in an acutely intoxicated patient (table 12). Beta-blockers (eg, metoprolol, propranolol, esmolol) are relatively contraindicated in the treatment of hypertension in a patient who has recently used cocaine due to risk of inducing unopposed alpha-adrenergic stimulation [27,28].

An exaggerated severe hypertensive response or life-threatening dysrhythmias may occur after administration of any sympathomimetic agent (eg, ephedrine) to a patient who has recently used any of these drugs. (See 'Hypertensive emergencies' above and "Cocaine: Acute intoxication", section on 'Cardiovascular complications'.)

Further details regarding management of hypertension and hemodynamic instability in patients intoxicated with substances of abuse are available in individual topics:

●(See "Acute amphetamine and synthetic cathinone ("bath salt") intoxication", section on 'Hypertension'.)

●(See "Phencyclidine (PCP) intoxication in adults", section on 'Treatment of complications'.)

●(See "MDMA (ecstasy) intoxication", section on 'Cardiovascular stimulation' and "MDMA (ecstasy) intoxication", section on 'Cardiac effects'.):

●(See "Intoxication from LSD and other common hallucinogens".)

CARDIAC ARRHYTHMIAS — Etiologies and acute management of postoperative cardiac arrhythmias are similar to the intraoperative setting, as discussed in detail separately. (See "Arrhythmias during anesthesia".)

Most arrhythmias noted in the PACU are transient and clinically insignificant. If an arrhythmia persists in the PACU, proper lead placement for the electrocardiogram (ECG) should be confirmed and a 12-lead ECG should be obtained as soon as feasible. Stable waveforms from the pulse oximeter, intra-arterial catheter, and/or central venous catheter may be helpful to distinguish artifact from a true arrhythmia. (See "Basic patient monitoring during anesthesia", section on 'Sources of ECG artifact'.)

Causes of an arrhythmia should be identified and treated (eg, hypoxemia, hypoventilation, acidemia, anemia, electrolyte abnormalities) (table 14). In a patient with preexisting cardiovascular disease, the appearance of a new arrhythmia may indicate myocardial ischemia [29]. (See 'Myocardial injury' below.)

Atrial tachycardias

●Sinus tachycardia – Sinus tachycardia is a narrow complex regular tachycardia with heart rate (HR) >100 beats per minute (bpm), and is relatively common in the PACU. The most likely potential causes include (see "Arrhythmias during anesthesia", section on 'Causes of sinus tachycardia'):

•Pain – Hypertension is typically also present (see 'Noxious stimuli' above).

•Hypovolemia – Hypotension is typically also present (see 'Hypovolemia' above).

•Anemia – Hypotension is typically also present (see 'Hypovolemia' above).

Other possible causes include hypoxemia, hypercarbia, sepsis, fever, myocardial ischemia, pulmonary embolism, hyperthyroidism, and malignant hyperthermia.

Treatment of the underlying problem typically restores a normal HR. (See "Arrhythmias during anesthesia", section on 'Sinus tachycardia' and "Sinus tachycardia: Evaluation and management".)

●Atrial fibrillation – Atrial fibrillation (AF) is a narrow complex irregular arrhythmia that may be chronic or occur with sudden onset during or shortly after surgery (waveform 1) [30,31]. Common risk factors include preexisting AF or ischemic heart disease, while specific factors in the PACU include increased sympathetic activity due to stress of surgery, hypoxia, pain, acute anemia, or myocardial irritability caused by procedures performed near the heart (eg, pulmonary or esophageal surgery) [30,31]. (See "The electrocardiogram in atrial fibrillation".)

Treatment of AF depends upon hemodynamic stability, as described separately (algorithm 4). (See "Arrhythmias during anesthesia", section on 'Atrial fibrillation' and "Advanced cardiac life support (ACLS) in adults", section on 'Tachycardia'.)

Notably, patients with a preoperative history of atrial fibrillation have a higher risk of developing postoperative cardiovascular complications compared with those without [32]. (See 'Postoperative cardiovascular complications' below.)

●Other atrial tachycardias – Treatment of other narrow QRS complex tachycardias that may occur in the PACU (eg, atrial flutter, atrioventricular [AV] node reentrant tachycardia, multifocal atrial tachycardia) or wide QRS complex tachycardias (eg, supraventricular tachycardia [SVT] with aberrant conduction, Wolff-Parkinson-White [WPW] syndrome) is similar to treatment in the intraoperative setting. (See "Arrhythmias during anesthesia", section on 'Wide QRS complex atrial tachyarrhythmias' and "Arrhythmias during anesthesia", section on 'Other narrow QRS complex atrial tachyarrhythmias'.)

Ventricular arrhythmias

●Premature ventricular contractions – Occasional, isolated premature ventricular contractions (PVCs) are relatively common in the PACU due to increased sympathetic stimulation (waveform 2); they typically resolve without treatment. Frequent new onset PVCs, however, warrant further observation since they can degenerate into dangerous arrhythmias. (See "Arrhythmias during anesthesia", section on 'Premature ventricular contractions' and "Premature ventricular complexes: Clinical presentation and diagnostic evaluation".)

Three or more consecutive ventricular beats at a rate >120 bpm and lasting less than 30 seconds are considered to be nonsustained ventricular tachycardia (NSVT) (waveform 3). In some patients, frequent PVCs or NSVT may be evidence of myocardial ischemia. (See 'Myocardial injury' below.)

For hemodynamically stable patients with nonsustained VT who have a heart rate (HR) >100 bpm a beta blocker or calcium channel blocker may be administered to reduce the ventricular rate while the patient is in the PACU (table 15). Amiodarone or class IB agents (eg, lidocaine) may also be effective to maintain sinus rhythm. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management".)

●Ventricular fibrillation and pulseless ventricular tachycardia – Ventricular fibrillation (waveform 4) should be treated immediately with defibrillation and advanced cardiac life support (ACLS) (algorithm 5). A regular rhythm with a widened QRS complex (ie, monomorphic ventricular tachycardia [VT] (waveform 5)) should also be treated immediately with defibrillation if there is no pulse, whereas VT with a pulse may be treated with synchronized cardioversion (algorithm 4). (See "Advanced cardiac life support (ACLS) in adults", section on 'Pulseless ventricular tachycardia and ventricular fibrillation' and "Arrhythmias during anesthesia", section on 'Ventricular arrhythmias'.)

●Polymorphic ventricular tachycardia (torsades de pointes) – Torsades de pointes (TdP) is an irregular polymorphic ventricular tachycardia (waveform 6 and waveform 7). Management includes prompt defibrillation in a hemodynamically unstable patient, as in the intraoperative setting. (See "Overview of the acute management of tachyarrhythmias", section on 'Polymorphic ventricular tachycardia' and "Arrhythmias during anesthesia", section on 'Polymorphic ventricular tachycardia (torsades de pointes)'.)

Certain agents that are commonly administered in the PACU and perioperative period (eg, methadone, droperidol, ondansetron) may prolong the QT interval and increase risk for TdP and malignant ventricular arrhythmias (table 16). These agents are avoided in patients with known prolonged QT interval. (See "Arrhythmias during anesthesia", section on 'Medications that may prolong the QT interval'.)

•Methadone – Methadone administered in large doses prolongs the QT interval and has been linked with TdP [33,34]. Patients receiving chronic methadone therapy should have a preoperative baseline ECG before receiving any other perioperative medications that may further prolong the QT interval.

•Droperidol and haloperidol – Low doses of the butyrophenone antiemetic agents haloperidol and droperidol are used for prophylaxis or management of postoperative nausea and vomiting (PONV); however, these agents are associated with an increase in the QT interval and should be avoided in patients with preexisting QT prolongation [35,36]. The US Food and Drug Administration (FDA) issued a boxed warning for droperidol regarding the potential for sudden cardiac death with its use. (See "Postoperative nausea and vomiting", section on 'Antidopaminergics'.)

•Ondansetron – The serotonin antagonists (ondansetron, granisetron, and, outside the United States, dolasetron, ramosetron, and tropisetron) may prolong the QT interval and should be avoided in a patient with preexisting QT prolongation. (See "Postoperative nausea and vomiting", section on 'Serotonin (5-hydroxytryptamine) receptor antagonists'.)

Other causes and potentiators of long QT syndrome are listed in the table (table 17).

Bradyarrhythmias

●Initial assessment and treatment – Mild sinus bradycardia (ie, HR 40 to 60 bpm) that remains stable in an asymptomatic patient and is not associated with major alterations in blood pressure [BP]) does not require treatment, and is relatively common in the PACU setting. Comparison with the patient's preoperative HR is necessary prior to initiating treatment. (See "Sinus bradycardia".)

Moderate bradycardia in a patient with mild symptoms may be initially treated with intravenous (IV) glycopyrrolate in 0.2 mg increments up to 1 mg and/or ephedrine in 5 to 10 mg increments.

Severe bradycardia (HR <40 bpm) in a patient who is symptomatic (eg, altered mental status) or unstable (eg, hypotension) is treated with IV atropine 0.5 mg, and this dose may be repeated every three to five minutes up to a total of 3 mg (algorithm 6).

Further management of severe sinus bradycardia, sinus node dysfunction, bundle branch blocks, or conduction defects may include positive chronotropic agents and/or temporary pacing, as discussed separately. (See "Advanced cardiac life support (ACLS) in adults", section on 'Bradycardia' and "Arrhythmias during anesthesia", section on 'Sinus bradycardia'.)

●Assessment and treatment of underlying causes – Assessment for the possibility of the following potential causes of bradyarrhythmias is necessary in the PACU setting:

•Medications – Negative chronotropic agents administered in the perioperative period (eg, beta blockers, calcium channel blockers, digoxin, amiodarone), anticholinesterase agents used to reverse the effects of a nondepolarizing neuromuscular blocking agent (NMBA) near the end of a surgical procedure, large bolus doses of an opioid, or a reflex response to hypertension caused by administration of a large dose of a vasoconstrictor agent (eg, phenylephrine) may all cause bradycardia. (See "Arrhythmias during anesthesia", section on 'Sinus bradycardia'.)

•Neuraxial anesthesia – Neuraxial anesthesia with a T1 to T4 anesthetic level may cause sinus bradycardia as well as associated hypotension. If an epidural infusion is being administered, it should be temporarily discontinued. Although atropine may be effective, bradycardia caused by neuraxial anesthetic blockade of the cardiac accelerator fibers responds best to beta-adrenergic agonists (eg, ephedrine 5 to 10 mg or, if severe or persistent, epinephrine 10 to 20 mcg, titrated to effect, then followed by an epinephrine infusion (table 4)). (See "Arrhythmias during anesthesia", section on 'Sinus bradycardia'.)

•Bowel or bladder distention – Visceral distention of the bowel or bladder may initiate a vagal reflex, causing sinus bradycardia. (See "Overview of post-anesthetic care for adult patients", section on 'Inability to void'.)

In a patient with a high spinal cord injury (SCI), bowel or bladder distention may cause autonomic dysreflexia, an exaggerated sympathetic response manifested by diffuse vasoconstriction below the level of SCI causing hypertension with bradycardia (or tachycardia). (See 'Noxious stimuli' above and "Anesthesia for adults with chronic spinal cord injury", section on 'Management of intraoperative autonomic dysreflexia'.)

•Respiratory problems – Hypoxemia may cause bradycardia. (See "Respiratory problems in the post-anesthesia care unit (PACU)".)

•Myocardial ischemia – Sinus bradycardia occurs in 15 to 25 percent of patients having an acute myocardial infarction, particularly if ischemia involves the right coronary artery. (See 'Myocardial injury' below and "Supraventricular arrhythmias after myocardial infarction", section on 'Sinus bradycardia'.)

POSTOPERATIVE CARDIOVASCULAR COMPLICATIONS — Surgery may precipitate complications such as myocardial infarction or injury, cardiac arrest, congestive heart failure, or death from cardiac causes [37,38].

Myocardial injury — Prevention, early recognition, and prompt treatment of myocardial injury after noncardiac surgery (MINS) are critically important [38-40]. Continuous electrocardiography (ECG) monitoring is employed for all patients in the PACU. If available, multiple leads (eg, II and V₅) and computerized ST-segment analysis are employed in patients with risk factors for myocardial ischemia after noncardiac surgery (table 10 and table 2 and table 3) [41]. MINS is usually asymptomatic, but is a leading cause of postoperative death [37,38,40,42]. Approximately 40 percent of MINS occurs on the day of surgery [40]. Thus, a 12-lead ECG and, most importantly, troponin measurements are obtained for patients at high risk [38-40,43]. A cardiologist is consulted for any patient with symptoms or signs suggestive of myocardial ischemia since urgent subspecialist interventions may be necessary if an acute coronary syndrome is developing (table 18). Recommendations for postoperative management of MINS are discussed in detail separately. (See "Perioperative myocardial infarction or injury after noncardiac surgery", section on 'Acute treatment'.)

Postoperative hypotension is strongly associated with MINS, particularly if prolonged or severe, and should be detected and promptly treated [40,44]. Acute postoperative pain and tachycardia have also been associated with MINS [45,46]. Furthermore, hypothermia results in sympathetic stimulation with hypertension and/or tachycardia causing increased myocardial oxygen consumption, particularly with shivering [19,21,22] (see "Perioperative temperature management", section on 'Postoperative temperature derangements' and "Perioperative temperature management", section on 'Shivering'). Optimal myocardial oxygen (O₂) supply and minimal O₂ demand are achieved by maintaining normal to high blood pressure (BP), low to normal heart rate (HR), euvolemia, and normothermia (table 19) [19,21,22,40,44,45]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Postoperative management'.)

Decompensated heart failure — Patients at increased risk for development of acute decompensated heart failure (HF) in the immediate postoperative period include those with a history of HF (with reduced or preserved ejection fraction). Perioperative exacerbation of chronic HF may occur due to excessive intraoperative fluid administration, prolonged unfavorable surgical positioning (eg, supine positioning of a patient who cannot tolerate this position while awake), myocardial ischemia, or stress-induced (Takotsubo) cardiomyopathy. (See "Intraoperative management for noncardiac surgery in patients with heart failure".)

Acute postoperative decompensated HF typically manifests as respiratory distress with or without pulmonary edema, and may be accompanied by hypertension due to hypervolemia or hypotension in a patient with cardiogenic shock. Any patient with evidence of pulmonary edema should be evaluated for new or unstable myocardial ischemia including cardiac monitoring, ECG, and serial cardiac enzyme measurements. Other treatment of acute decompensated HF in the PACU setting includes (table 20) (see "Perioperative management of heart failure in patients undergoing noncardiac surgery", section on 'Postoperative management'):

●Administration of supplemental O₂. Persistent respiratory distress and/or hypoxemia despite oxygen therapy is treated with either a trial of noninvasive ventilation (NIV) or endotracheal intubation and mechanical ventilation as appropriate in this clinical setting. (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Supplemental oxygen and assisted ventilation' and "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications", section on 'Acute cardiogenic pulmonary edema (ACPE)'.)

●For pulmonary edema or fluid overload, intravenous (IV) diuretics are administered. (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Diuretics'.)

●Initiation of vasodilator therapy in the following settings: early IV nitroglycerin as a component of therapy in patients with refractory HF (eg, inadequate response to diuretics and/or low cardiac output), or IV arterial vasodilator therapy to reduce afterload in patients with severe hypertension (table 12). (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Vasodilator therapy'.)

●For patients with known HF with reduced ejection fraction and developing signs of cardiogenic shock, management includes infusion of an inotrope (eg, milrinone or dobutamine), in combination with a vasopressor if necessary to maintain systemic BP (eg, norepinephrine (table 4)). Inotropes are not indicated for treatment of HF with preserved ejection fraction. (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Inotropic agents'.)

●Consultation with a cardiologist or other specialist (eg, an intensivist) to arrange transfer to an intensive care unit and further management. (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Approach to long-term therapy in hospitalized patients'.)

SUMMARY AND RECOMMENDATIONS

●Risk factors – The likelihood of cardiovascular instability due to hypotension, hypertension, or cardiac arrhythmias after noncardiac surgery is associated with various patient-associated and procedure associated factors, as noted in the tables (algorithm 1 and table 1 and table 2 and table 3). (See 'Risk factors' above.)

●Hypotension

•Definition and initial treatment – Hypotension in the post-anesthesia care unit (PACU) is typically treated if systolic blood pressure (BP) <90 mmHg, mean arterial pressure (MAP) <65 mmHg, or relative changes are significant (eg, systolic BP decrease >20 percent of baseline). Accuracy of measured BP values is ensured before initial treatment with intravenous (IV) isotonic crystalloid solution administered in 250- to 500-mL increments, and IV vasopressor/inotropic agents as needed (eg, phenylephrine 40- to 100-mcg increments or ephedrine 5- to 10-mg increments). For severe or refractory hypotension, small bolus doses of diluted IV epinephrine 10 to 50 mcg, norepinephrine 4 to 8 mcg, or vasopressin 1 to 2 units may be administered while a vasopressor/inotropic infusion is prepared (table 4). (See 'Initial assessment and treatment of hypotension' above.)

•Treat causes – Underlying causes of hypotension include hypovolemia, drug effects (eg, antihypertensive agents, anesthetic agents), sympathectomy due to neuraxial blockade, or adrenal insufficiency. (See 'Treatment of underlying causes of hypotension' above.)

•Treatment of severe hypotension – Severe hypotension or hemodynamic collapse requiring immediate lifesaving intervention may occur due to hemorrhagic or nonhemorrhagic shock, septic shock, anaphylactic shock, cardiogenic shock, arrhythmogenic shock, local anesthetic systemic toxicity, tension pneumothorax, pulmonary embolus, or dynamic left ventricular outflow tract obstruction. (See 'Hypotensive emergencies' above.)

●Hypertension

•Definition and initial treatment – Hypertension in the PACU is typically treated if systolic BP is >180 mmHg or diastolic BP is >110 mmHg; thresholds for patients who had severe preoperative hypertension (ie, ≥180/≥120 mmHg) may differ. (See 'Initial assessment and treatment of hypertension' above.)

•Treat causes – Underlying causes of hypertension include missed doses of chronically administered antihypertensive medications, noxious stimuli (eg, pain, nausea and/or vomiting, hypoxia and/or hypercarbia, agitation, hypothermia with shivering, bladder distention), hypervolemia, alcohol or opioid withdrawal, or recent use of drugs that produce a hyperadrenergic state such as cocaine, amphetamine, phencyclidine, lysergic acid diethylamide (LSD), 3,4-methylenedioxymethamphetamine (MDMA), or monoamine oxidase inhibitors. (See 'Treatment of underlying causes of hypertension' above.)

•Treatment of severe hypertension – Emergency treatment of severe hypertension is warranted if there is evidence of acute neurologic signs or symptoms (eg, agitation, delirium, stupor, visual disturbances, seizures, stroke) or cardiovascular emergency (eg, acute coronary syndrome, acute decompensated heart failure, aortic dissection). In these instances, an IV antihypertensive agent(s) is immediately initiated while further workup is pursued (table 12). (See 'Hypertensive emergencies' above.)

●Arrhythmias – Most arrhythmias noted in the PACU are transient and clinically insignificant. For persistent arrhythmias, proper lead placement for the electrocardiogram (ECG) should be confirmed, a 12-lead ECG should be obtained, and causes contributing to persistence of an arrhythmia should be identified and treated (eg, hypoxemia, hypoventilation, acidemia, anemia, electrolyte abnormalities) (table 14). Acute management of postoperative cardiac arrhythmias is similar to that in the intraoperative setting. (See 'Cardiac arrhythmias' above and "Arrhythmias during anesthesia".)

●Postoperative cardiovascular complications

•Myocardial injury – Myocardial injury after noncardiac surgery (MINS) is a leading cause of postoperative death. Thus, a 12-lead ECG and troponin measurements are obtained for patients at high risk (table 10 and table 2 and table 3). Optimal myocardial oxygen (O₂) supply and minimal O₂ demand are achieved by maintaining normal to high BP, low to normal heart rate (HR), normothermia, and euvolemia, as well as avoiding or treating postoperative pain (table 19). (See 'Myocardial injury' above and "Perioperative myocardial infarction or injury after noncardiac surgery".)

•Decompensated heart failure – Acute postoperative decompensated heart failure (HF) typically manifests as respiratory distress with or without pulmonary edema, and may be accompanied by hypertension due to hypervolemia or hypotension in a patient with cardiogenic shock. Any patient with evidence of pulmonary edema should be evaluated for new or unstable myocardial ischemia including cardiac monitoring, ECG, and serial cardiac enzyme measurements. Diagnosis and treatment of acute decompensated HF are noted in the table and discussed separately (table 20). (See 'Decompensated heart failure' above and "Perioperative management of heart failure in patients undergoing noncardiac surgery", section on 'Postoperative management'.)