Hemodynamic and cardiovascular complications occur in approximately 5% of PACU admissions, with hypotension, arrhythmias, myocardial ischemia, and pulmonary edema being the most common complications recorded. Of interest, postoperative hypertension and tachycardia are associated with an increased risk of unplanned critical care admission and a higher mortality than hypotension and bradycardia.

1. Hypotension should prompt a review of the patient’s history and the intraoperative management to generate a differential diagnosis. The anesthetist who performed the case can be contacted to help interpret the current events. Hemorrhage must remain a primary consideration in the evaluation of hypotension in the postoperative patient.
   1. Hypovolemia is the most common cause of hypotension in the PACU, and administration of a fluid bolus during the initial assessment is generally appropriate. Ongoing hemorrhage, inadequate fluid replacement, osmotic polyuria, and fluid sequestration (eg, intestinal obstruction and ascites) are among the causes of hypovolemia in the PACU. Nonspecific signs include tachycardia, dry mucous membranes, oliguria, and thirst. A meaningful volume challenge (250-1000 mL of crystalloid or an equivalent volume of synthetic colloid, blood products, or both) should be considered for specific indications. Persistent hypotension after a seemingly adequate volume replacement mandates further assessment, starting with placement of a urinary catheter and consideration of ongoing surgical bleeding. Additional diagnostics may include transthoracic echocardiogram, a pulmonary artery catheter, or noninvasive cardiac output monitoring.
   2. Impaired venous return occurs when mechanical forces decrease the venous return to the heart in the absence of a reduction of circulating blood volume. Common causes include positive-pressure ventilation, dynamic hyperinflation of the lungs resulting in autopositive end-expiratory pressure, pneumothorax, and pericardial tamponade. Signs of obstruction to venous return are similar to those of true hypovolemia except for the presence of jugular vein distention, an elevated central venous pressure, and possibly decreased breath sounds and heart tones. Volume administration is the mainstay of symptomatic therapy, but treatment of the underlying cause is the definitive intervention.
   3. Vasodilation leading to hypotension can be caused by neuraxial anesthesia, residual inhalation agents, rewarming after hypothermia, transfusion reactions, adrenal insufficiency, anaphylaxis, systemic inflammation, sepsis, recent use of pharmacologic renin-angiotensin-aldosterone pathway modifiers, and the administration of vasodilating drugs. Hypovolemia accentuates the hypotension due to vasodilatation, but volume replacement alone cannot fully restore the blood pressure. Pharmacologic treatment includes α–adrenergic receptor agonists such as phenylephrine, norepinephrine, and even epinephrine. Diagnosis and treatment of the specific etiology should be concurrent with symptomatic treatment.
   4. Decreased cardiac output can be caused by myocardial ischemia and infarction, dysrhythmias, congestive heart failure, administration of negative inotropic drugs (anesthetics, β-adrenergic blockers, calcium channel blockers, and antidysrhythmics), sepsis, and hypothyroidism (see Chapters 3, 7, and 17). Symptoms include dyspnea, diaphoresis, cyanosis, jugular vein distention, oliguria, rhythm disturbances, wheezing, dependent crackles, and an S₃ gallop on auscultation. A CXR, 12-lead ECG, and basic laboratory tests may help with diagnosis. Invasive monitoring may be necessary to guide pharmacologic therapies, including:
      1. Inotropic agents such as dopamine, dobutamine, epinephrine, norepinephrine, and milrinone.
      2. Afterload reduction with nitrates and calcium channel blockers.
      3. Diuresis with loop diuretics for fluid overload.
      4. Antiarrhythmics or electrical cardioversion for arrhythmias.
2. Hypertension is most commonly observed in patients with preexisting hypertensive disease, particularly if antihypertensive medications were held preoperatively. Certain types of surgery such as carotid, vascular, endocrine, and intrathoracic procedures are more likely to be followed by hypertensive events. Other postoperative etiologies for hypertension may include pain, bladder distention, fluid overload, hypoxemia, hypercarbia, hypothermia, increased intracranial pressure (ICP), and administration of vasoconstrictive agents. Hypertension is usually asymptomatic, but patients with malignant hypertension may have headache, visual disturbances, dyspnea, restlessness, and even chest pain. In the initial assessment, one should verify the accuracy of blood pressure measurement by checking cuff size and placement, review the patient’s history and operative course, and rule out correctable etiologies. The management of hypertension is aimed at restoring blood pressure close to the patient’s baseline. Tight blood pressure control is extremely important after surgery for intracranial aneurysm, creation of vascularized muscular flaps, microvascular surgery, and in patients with severe vascular disease. If possible, resumption of chronic antihypertensive oral therapy is ideal. If needed, this can be supplemented or substituted with a fast-onset, short-acting IV medication.
   1. β-Adrenergic blockers:labetalol (an α-blocker and a β-blocker), 5 to 20-mg IV bolus or up to 2-mg/min IV infusion, and esmolol (β₁-blocker), 20- to 100-mg IV bolus or 25- to 300-μg/kg/min IV infusion, are first-line agents.
   2. Calcium channel blockers:nicardipine initiated at 5 to 15 mg/h or clevidipine 2 to 20 mg/h. Sublingual nifedipine is not recommended because it may cause an unpredictable, and at times severe, drop in blood pressure that may induce myocardial ischemia.
   3. Hydralazine: 5- to 20-mg IV bolus, vasodilator, and may induce reflex tachycardia.
   4. Nitrates: nitroglycerin, starting at 25 μg/min IV infusion, is preferentially a venodilator and useful for coexisting myocardial ischemia. Sodium nitroprusside, starting at 0.5 μg/kg/min IV infusion, is a potent arterial and venodilator and requires invasive blood pressure monitoring.
3. Dysrhythmias in the perioperative period can be caused by increased sympathetic outflow, hypoxemia, hypercarbia, electrolyte and acid-base imbalance, myocardial ischemia, increased ICP, drug toxicity, thyrotoxicosis, and malignant hyperthermia. Premature atrial contractions and unifocal premature ventricular contractions (PVCs) generally do not require treatment. In the presence of more worrisome rhythm disturbances, supplemental O₂ and supportive management should be administered while the etiology is investigated.
   1. Common supraventricular dysrhythmias
      1. Sinus tachycardia may be secondary to pain, agitation, hypovolemia, fever, hyperthermia, hypoxemia, hypercarbia, congestive heart failure, and pulmonary embolism. Symptomatic treatment with β-blockers should be instituted only after its etiology is addressed, unless the patient is at risk of myocardial ischemia.
      2. Sinus bradycardia may result from a high neuraxial anesthetic block, opioid administration (with the exception of meperidine), vagal stimulation, β-adrenergic blockade, and increased ICP. Symptomatic treatment with anticholinergic muscarinic agents, atropine, 0.4 mg IV, or glycopyrrolate, 0.2 mg IV, is indicated when hypotension is present or for severe bradycardia (see Chapter 39).
      3. Paroxysmal supraventricular tachydysrhythmias occur with a higher incidence in patients over 70 years of age; after abdominal, thoracic, or major vascular procedures; and in patients with preoperative premature atrial contractions. They include paroxysmal atrial tachycardia, multifocal atrial tachycardia, junctional tachycardia, atrial fibrillation, and flutter. These rhythms may cause significant hypotension, and treatment may include the following:
         1. Synchronized cardioversion should be used if the patient is hemodynamically unstable, as per the ACLS protocol (see Chapter 39).
         2. Adenosine: 6 mg followed by 12 mg IV, administered rapidly, has a high success rate in converting paroxysmal atrial tachycardia to sinus rhythm.
         3. Verapamil (2.5- to 5-mg IV bolus) or diltiazem (5- to 20-mg IV bolus, or as an infusion with an initial 0.25- to 0.35-mg/kg IV bolus followed by an infusion rate of 5-15 mg/h IV) will slow the ventricular response.
         4. Amiodarone is the antiarrhythmic of choice for rate control of atrial dysrhythmias in the setting of a decreased myocardial function.
         5. β-Blockers (metoprolol, esmolol, and atenolol) also decrease the ventricular response to supraventricular tachydysrhythmias.
   2. Stable ventricular dysrhythmias such as PVCs and stable nonsustained ventricular tachycardia generally do not require treatment; however, a search for reversible causes (hypoxemia, myocardial ischemia, acidosis, hypokalemia, hypomagnesemia, and irritation due to a central venous catheter) should be conducted. Stable sustained ventricular tachycardia can be treated with synchronized cardioversion or pharmacologic modalities. PVCs that are multifocal and occur in runs, or are close to the preceding T wave, should be treated, especially in patients with structural heart disease, owing to the risk of developing an unstable ventricular rhythm.
      1. β-Blockers: esmolol, 20- to 100-mg IV bolus, or 25- to 300-μg/kg/min IV infusion, metoprolol, 2.5 to 10 mg IV, and propranolol, 0.5- to 2.0-mg IV increments, may be used.
      2. Amiodarone: 150-mg IV bolus over 10 minutes followed by 1-mg/min IV infusion for 6 hours and then 0.5-mg/min IV infusion is indicated in patients with a decreased myocardial function.
   3. Management for unstable ventricular tachycardia and ventricular fibrillation are described in the ACLS protocol (see Chapter 39).
4. Myocardial ischemia and infarction
   1. T-wave changes (inversion, flattening, and pseudonormalization) may be associated with myocardial ischemia and infarction, electrolyte changes, hypothermia, surgical manipulation of the mediastinum, or incorrect lead placement. Isolated T-wave changes must be considered within the clinical context because they are common postoperatively and do not always indicate myocardial ischemia.
   2. ST segment changes including depressions and elevations are generally indicative of myocardial ischemia and infarction, respectively. ST segment elevation can be a normal variant or can occur in other conditions such as left ventricular hypertrophy, left bundle branch block, and hyperkalemia. Unlike myocardial infarctions in the nonsurgical setting, in the postoperative period, most myocardial infarctions are associated with ST depression and have a non–Q-wave pattern. As supplemental O₂ is administered and a 12-lead ECG and cardiac enzymes are obtained, possible precipitating factors for the ST segment changes must be reviewed and corrected. Common etiologies include hypoxemia, anemia, tachycardia, hypotension, and hypertension. If ischemia is present, patients should be rate controlled with a β-blocker. Aspirin and statins may decrease the mortality of patients with acute coronary syndrome in the perioperative period. IV nitroglycerin is a good option for cases with ST segment elevations. Cardiology consultation and transfer to an ICU should be considered.
   3. In patients at high risk for cardiac events (patients with a history of ischemic heart disease, congestive heart disease, cerebrovascular disease, renal insufficiency, and diabetes mellitus and patients undergoing intrathoracic, intraperitoneal, or suprainguinal vascular procedures), continuation, and in some settings initiation, of β-blockade may decrease the risk of adverse cardiac events perioperatively.
5. The patient with a permanent pacemaker (PPM) or an intracardiac defibrillator (ICD) requires special care in the PACU. Information about the patient’s pacemaker dependency state and the features of the device must be obtained from the OR team. Continuous ECG monitoring with special attention to the patient’s rhythm, rate, and hemodynamic status is indicated. Electrocautery used during the surgery can potentially trigger arrhythmia responses in PPM and ICD. Modern devices are less likely to be affected by intraoperative electromagnetic interference. Placing a magnet over the PPM or ICD should not be standard practice without precise knowledge of its effects. Communication with the electrophysiology service before and after surgery is highly recommended for interrogation of the device. Interrogation and reprogramming of the device to the original parameters may be required in the PACU after the operation.