Secondary Logo

Journal Logo

Featured Articles

Atrial Fibrillation: Current Evidence and Management Strategies During the Perioperative Period

Karamchandani, Kunal MD, FCCP*; Khanna, Ashish K. MD, FCCP, FCCM†,‡; Bose, Somnath MD§; Fernando, Rohesh J. MD, FASE; Walkey, Allan J. MD, MSc¶,#

Author Information
doi: 10.1213/ANE.0000000000004474
  • Free
  • Take the CME Test
  • Continuing Medical Education

Abstract

Perioperative atrial fibrillation (POAF) is common, with an estimated incidence of 2%–60% depending on the type of surgery.1–4 The reported incidence is lower in noncardiac surgery and ranges from 4.8% following total joint replacements to 12%–19% for esophageal, thoracic, or abdominal surgery.5–13 The true incidence of POAF in patients undergoing noncardiac surgery is likely underestimated because not all patients are monitored continuously in the postoperative period.14 While the risk factors for POAF after cardiac surgery are attributed primarily to underlying cardiac disease and direct manipulation of the heart and pericardium, precipitating factors and mechanisms for POAF after noncardiac surgery are less well defined. Furthermore, no established risk scores predict POAF in patients after noncardiac surgery, and few, evidence-based strategies are available for POAF prevention.15

Although historically considered a self-limiting entity,16 recent evidence suggests that POAF is associated with an increased overall risk of in-hospital morbidity and mortality.2,17 In addition, new-onset POAF is an independent predictor of stroke, which is the primary driver of POAF mortality.18,19 Currently, however, data for outcomes such as acute myocardial infarction (AMI), congestive heart failure, and acute kidney injury are sparse. Although POAF is more common after cardiac than after noncardiac surgery,20 the burden of POAF after noncardiac surgery remains considerable. A retrospective 2014 review found that the most common acute condition predisposing to AF in hospitalized patients was noncardiac surgery.21 AF risk should thus be assessed during perioperative evaluation, with attention to preventable AF triggers and insults during the perioperative period. Preventing AF is ideal because management of perioperative AF can be challenging. A recently conducted international survey, administered to members of the Society of Cardiovascular Anesthesiologists (SCA) and the European Association of Cardiothoracic Anesthesiologists (EACTA), found that, despite existing guidelines from the European Society of Cardiology and American College of Cardiology,22,23 considerable practice variability exists with respect to POAF management in patients after cardiac surgery.24 Because even fewer guidelines exist for patients undergoing noncardiac surgery, it is likely that similar or possibly greater practice variability also extends to this patient population.

With the increase in elderly patients undergoing surgery and the strong correlation between increasing age and likelihood of POAF,25 the incidence of new-onset AF among surgical patients is expected to increase with time. Several clinical challenges thus arise: (1) what is the efficacy of current therapies targeting AF prophylaxis and to what degree does avoiding AF triggers reduce AF incidence; (2) what are the effects of POAF on short- and long-term morbidity and mortality and how aggressively should rapid ventricular rate (RVR), defined as ventricular rate ≥110/min,26 be treated; (3) when and in whom stroke prophylaxis should be initiated; and (4) the optimal duration of rate-control therapy among patients who convert to normal sinus rhythm (NSR) before discharge. This review will briefly describe the pathophysiology of AF, discuss the challenges perioperative physicians face regarding prevention and management of POAF, highlight the short- and long-term outcomes in patients who develop POAF, suggest clinical strategies where appropriate, and suggest future directions for more appropriate perioperative management of POAF.

Pathophysiology of AF

Electrical impulses of the heart normally originate at the sinoatrial (SA) node and are conducted through the atrioventricular (AV) node and down to the bundle of His and Purkinje fibers to depolarize both ventricles. In AF, signals are not initiated at the SA node but, instead, are generated from all over the atria, resulting in uncoordinated atrial activity that is intermittently and irregularly conducted through the AV node. At the atrial level, AF is perpetuated by reentry and/or rapid focal ectopic firing.27 Uncoordinated atrial discharge may result from an irregular atrial response to a rapidly discharging, regularly firing driver or a single localized reentry circuit.

Alternatively, fibrillatory activity may be caused by multiple functional reentry circuits varying in time and space. The Heart Rhythm society defines 3 types of AF: paroxysmal (may occur and terminate spontaneously), persistent (will not terminate without treatment), and permanent (will not terminate even with drug or electrical therapy).28 Paroxysmal AF, the subtype most commonly seen in the perioperative setting, usually results from focal ectopic firing.29 One current hypothesis is that the natural history of AF involves an evolution from paroxysmal to persistent to permanent forms via atrial remodeling caused by the arrhythmia itself and/or progression of underlying heart disease.30–32 Thus, preventing perioperative AF may avoid long-term development of persistent and permanent AF.

Figure 1.
Figure 1.:
The interaction between atrial fibrillation and heart failure. AF indicates atrial fibrillation; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. Reproduced with permission from Iwasaki YK, Nishida K, Kato T, Nattel S, "Atrial Fibrillation Pathophysiology: Implications for Management," Circulation, 2011;124:2264–2274.29

AF may cause left ventricular dysfunction as a result of inappropriately rapid and/or irregular ventricular rhythms and reduced coronary blood flow due to decreased diastolic filling time.33–35 In addition, coordinated atrial contraction, which contributes about 20% of left ventricular stroke volume at rest, is lost in AF and contributes to impaired cardiac output.36 These effects trigger a spiral of adverse cardiac consequences, where AF-induced atrial hypocontractility leads to ventricular dysfunction, which leads to further atrial dilation, stretch, and remodeling that makes AF resistant to therapy (Figure 1).

Causes and Risk Factors

Table 1.
Table 1.:
Patient- and Surgery-Related Risk Factors for Perioperative Atrial Fibrillation

The perioperative period is associated with many factors that predispose to the development of de novo AF, and precipitate RVR in patients with paroxysmal and chronic AF (Table 1). In most cases, many potential mechanisms and factors are involved. One 2012 review examining 139 patients with new-onset POAF found that 73% patients had at least 1 modifiable risk factor and that 45% had 2 or more risk factors.37 Risk factors for POAF can be broadly categorized into patient and surgery related and are summarized in Table 1.

Surgery-Related Risk Factors for POAF

Hypovolemia, intraoperative hypotension, anemia, trauma, and pain increase sympathetic activity, catecholamine release, heart rate, and arrhythmogenicity.14 Operative stress by itself can nonuniformly shorten atrial refractoriness, perpetuating atrial arrhythmias.38 Metabolic disturbances during surgery such as hypoglycemia, hypokalemia, and hypomagnesemia can also lead to development of AF.39–41 In addition, by causing pulmonary arterial vasoconstriction hypoxemia may increase right ventricular pressure and right atrial stretch. Myocardial ischemia itself may alter atrial conduction. Excessive fluid shifts during surgery or afterward may increase intravascular volume and stretch the right atrium, also predisposing to the development of AF.42 The type of surgery may also play a role, with thoracic surgery, abdominal surgery, and major vascular surgery being associated with the highest risk of developing POAF.2,10,43

Patient-Related Risk Factors for POAF

Although multiple patient-related factors predisposing to POAF exist, increased age is the most important25 and the incidence of AF increases with age.44 Atrial fibrosis is more common in the aging heart and forms a substrate for the development of AF.45 Race impacts the development of new-onset POAF, with African Americans having a lower risk.2 As expected, a history of paroxysmal AF increases a patient's risk for development of POAF and conservative estimate suggests that 27%–67% of patients who develop POAF have a preoperative history of paroxysmal AF.2,7

Other patient comorbidities, including preexisting congestive heart failure,2,10,46 ischemic heart disease,2,47 hypertension,2 chronic renal failure,47 sepsis,5,10,43,48–50 shock,49 asthma,10 thyroid disorders,51,52 and valvular disease,10 are all associated with POAF. Obstructive sleep apnea (OSA) is an independent risk factor for AF and the associated nocturnal hypoxemia can precipitate new-onset AF in hospitalized patients.53,54

Impact of POAF

Patients who develop POAF have higher in-hospital mortality, longer hospital lengths of stay, and increased hospitalization costs.2,10 Those with preexisting AF who develop POAF have similar outcomes compared with patients who develop POAF de novo.2 Short-term postoperative morbidity and mortality are similarly worse in patients who develop POAF. Analysis of the 2008 PeriOperative ISchemic Evaluation (POISE) trial suggested that patients who developed new clinically important POAF had a higher risk of stroke within 30 days after surgery (odds ratio [OR], 4.35 [1.87–10.12]).55 A 2012 review of administrative data from nearly 370,000 noncardiac surgical patients across 375 US hospitals determined that those with POAF had higher mortality (OR, 1.72; P < .001), increased length of stay (adjusted relative difference of +24%, P < .001), and a higher cost of hospitalization (adjusted difference of +$4177, P < .001).2 Similarly, in patients undergoing vascular surgery, myocardial ischemia in the first 30 days was more common in the POAF group (53% vs 21%; P = .01) and new-onset POAF was associated with 30-day perioperative cardiovascular events (HR = 6.0; P < .001) and a higher risk of cardiovascular events up to 1 year after surgery (HR = 4.2; P < .001).56 In a 2019 study of patients undergoing noncardiac surgery for malignancy, 30-day complications were higher in the POAF group (OR = 2.84; P < .001).57 Although the most common complications were related to infection and miscellaneous events, outcomes such as AMI, congestive heart failure, and acute kidney injury were also more common in patients with POAF.

The long-term risk of complications is also high in patients who develop POAF. A 2014 study assessing the long-term risk of stroke in patients after cardiac and noncardiac surgery who developed de novo POAF found that the cumulative risk of stroke at 1 year after discharge was 1.47% compared to 0.36% in those with no AF (HR = 2.0; 95% confidence interval [CI], 1.7–2.3).17 Despite a higher incidence of POAF in the cardiac surgery group, the rate of postdischarge encounters for AF and stroke within 1 year were higher in patients who had noncardiac surgery, underscoring the relevance of POAF to long-term outcomes. In addition to stroke, older data suggest that patients with POAF have a higher risk of developing other complications such as congestive heart failure, myocardial infarction, cardiac arrest, bacterial pneumonia, and increased hospital.10 However, these data are almost 20 years old and are unlikely to be accurate in current clinical practice. More research is needed to better characterize the long-term risk of POAF on postoperative complications and resource utilization in today's environment.

Overall, current literature suggests that POAF in noncardiac surgery is associated with increased mortality, increased hospital length of stay, and increased cost of hospitalization. Even though data on specific outcomes are sparse, it is clear that POAF impacts surgical outcomes and that attention to POAF prevention is an important element of perioperative management of high-risk patients.

Prevention

Because POAF is difficult to predict, any of the clinical risk factors for POAF described in Table 1 is a potential target for intervention. Where possible, addressing patient-related factors and averting perioperative triggers of sympathetic stimulation may not only reduce the likelihood of developing de novo AF but also avoid precipitation of RVR in patients with preexisting paroxysmal and chronic AF. Perioperative considerations are summarized in Figure 2.

Figure 2.
Figure 2.:
Perioperative considerations for patients with atrial fibrillation. *β-blockers, Ca2+ channel blockers, amiodarone, digoxin. $Ketamine, adrenergic vasopressors, desflurane, glycopyrrolate, atropine. AF RVR indicates atrial fibrillation with rapid ventricular rate; AV, atrioventricular; CPAP, continuous positive airway pressure; NOAF, new-onset atrial fibrillation; OSA, obstructive sleep apnea; POCUS, point-of-care ultrasound; TEE, transesophageal echocardiography.

Overall, limited data support the routine use of pharmacologic agents for POAF prophylaxis in noncardiac surgery. A 2018 meta-analysis reviewed 21 randomized controlled trials involving medications used for preventing POAF after noncardiac surgery, and concluded that use of amiodarone, β-blockers, and statins was associated with a decrease in incidence of POAF when compared to controls.58 Notably, 19 of the 21 trials included in this analysis involved thoracic surgical patients and thus may not be applicable to patients undergoing noncardiothoracic surgery. In light of potentially undesirable side effects of agents such as amiodarone and β-blockers, at this time, use of pharmacologic prophylaxis should remain case dependent and based on the individual risk to benefit ratio.

Perioperative Interventions

Although little literature exists for specific evidence-based perioperative interventions, general considerations include avoiding sympathetic stimulation, avoiding hyper- or hypovolemia, prompt electrolyte replacement, and avoidance of hypoxia. Intraoperative hypotension may predispose to AF. In a 1998 review of 4181 patients, intraoperative hypotension (>30% decrease in systolic blood pressure or systolic <90 mm Hg) was independently associated with persistent postoperative supraventricular arrhythmias requiring treatment.10 More recently, a 2013 review of 33,000 patients found that duration of mean arterial blood pressure <55 mm Hg correlated with increased myocardial injury.59

Treating hypotension promptly may thus reduce the likelihood of POAF. Although no intraoperative literature informs the choice of vasoactive agent, vasopressin is associated with less AF in the septic surgical and nonsurgical patient when compared with catecholamine-based vasopressors such as norepinephrine.60,61 Earlier use of vasopressin to treat hypotension may thus be preferred in patients with strong risk factors for developing POAF. Phenylephrine causes reflex bradycardia and has been effective in suppressing focal AF.62 However, perioperative studies linking phenylephrine and POAF are lacking.

Although ketamine has not been linked to POAF, it increases sympathetic activity even at subanesthetic doses,63 and its intraoperative use as part of multimodal pain management could potentially predispose patients at risk of developing POAF. It thus may be reasonable to avoid ketamine in elderly patients or those with a history of chronic or paroxysmal AF or AF risk factors. Glycopyrrolate, used in combination with neostigmine for reversal of neuromuscular blockade, is an anticholinergic agent that can cause tachycardia and dysrhythmias.64 The use of sugammadex to reverse neuromuscular blockade may avoid the anticholinergic effects of glycopyrrolate, and its role as an alternative in patients at risk of developing POAF awaits further investigation.

PATIENT-RELATED INTERVENTIONS

Addressing modifiable patient factors can also help prevent the development of POAF. Perioperative β-blockade effectively reduces POAF in patients after cardiac surgery,65 and continuing β-blockers in patients chronically on β-blockers likely has some effect on POAF. β-Blockers have shown mixed results as chemoprophylaxis against perioperative AF. The 2008 POISE trial randomly assigned over 8000 patients undergoing major noncardiac surgery to receive either metoprolol or placebo before surgery.18 Clinically significant new POAF was recorded in 2.2% of patients in the metoprolol group versus 2.9% in the placebo group (hazard ratio [HR], 0.76; 95% CI, 0.58–0.99). In light of an increased risk of mortality and stroke in POISE, and criticisms surrounding the dose of β-blockade in the treatment arm, the clinical relevance of this reduction in POAF with β-blockers is unclear. Early resumption of β-blockers in patients chronically taking these medications remains of critical importance as well. In a 2018 review of >8000 surgical patients receiving β-blockers chronically, the risk of de novo and paroxysmal POAF was reduced if β-blockade was resumed by the end of postoperative day 1 after noncardiothoracic and nonvascular surgery.66 However, resuming β-blockers on postoperative day 0 was not associated with a decreased risk of POAF. This lack of effect with day 0 β-blockade could have been due to the low event rate on postoperative day 0, or an extension of the effects of long-acting preoperative β-blockers. Further study is needed to better understand how the postoperative timing of β-blockade resumption may affect POAF in the postoperative period (Table 2).

Table 2.
Table 2.:
Ideas for Further Research

In patients with OSA, use of continuous positive airway pressure (CPAP) ventilation prevents obstructive respiratory events, reducing sympathovagal activation and reversing atrial remodeling.67,68 Moreover, CPAP decreases the risk of transition from paroxysmal to persistent AF among OSA patients.69 Hence, in patients with OSA, postoperative CPAP may reduce the risk of POAF by addressing mechanistic factors known to play a role.

Management of POAF

Preoperative Period.

Perioperative physicians often wrestle with canceling surgery for additional workup in patients who present for surgery with AF. Because paroxysmal AF is common and often undetected in the general population,70 it is also often unclear if the arrhythmia is new or preexisting. Existing American College of Cardiology/American Heart Association guidelines recommend that new-onset arrhythmias in the preoperative setting should prompt investigation into underlying causes, including cardiopulmonary disease, ongoing myocardial ischemia or myocardial infarction, drug toxicity, and endocrine or metabolic derangements.71 However, they also clarify that the paucity of studies prevents specific evidence-based recommendations. If time and resources permit, cardiology consultation may help identify high-risk patients. Ultimately, the decision to cancel or postpone for workup of AF should be made on a case-by-case basis and include discussions with the surgical team. In patients with preexisting AF and RVR, IV diltiazem or β-blockers are reasonable choices for heart rate control and, if unsuccessful, delaying elective surgery should be considered in patients with other comorbidities such as hemodynamic instability, acute myocardial ischemia/infarction, congestive heart failure, or pulmonary embolism (PE).72 Cardiology consultation may be helpful in identifying underlying pathology and managing these complex patients. Patients with clinically and hemodynamically stable rate controlled AF generally do not require modification of medical management, special evaluation in the perioperative period, or delay of surgery.71 Patients with AF who have been cardioverted in the past may benefit from an electrocardiogram (ECG) before surgery for detection of recurrence, which may be as high as 50%.73

Preoperative medications for rate control should be continued until the day of surgery, while decisions on continuation of anticoagulation are patient- and procedure-dependent. In such cases, the potential for perioperative ischemic stroke needs to be weighed against the risk of perioperative bleeding. A large population-based 2017 study found no difference in 30-day mortality rates in patients with AF who underwent either urgent or elective surgeries with or without preoperative anticoagulation.74 Similarly, 30-day mortality did not differ among patients with AF who were treated with either warfarin or a direct oral anticoagulant (DOAC). Bleeding and thrombotic risks were similar between those treated with either warfarin or DOACs. Perioperative management of anticoagulation in patients with POAF is thus best made on a case-to-case basis with input from surgical and cardiology teams. Evidence-based decision tools may help clinicians with periprocedural management of anticoagulation in patients with nonvalvular AF.75 One approach on withholding versus continuing anticoagulant therapy, for patients on vitamin-K antagonists (VKAs) and DOACs, based on the 2017 ACC expert consensus, is depicted in Figure 3.

Figure 3.
Figure 3.:
Preoperative management of anticoagulation in patients taking VKAs and DOACs. *Bleed risk is considered increased in the presence of any 1 of the following: major bleed or intracranial hemorrhage within 3 mo; quantitative or qualitative platelet abnormality, including aspirin use; supratherapeutic INR; prior bleed during previous bridging or similar procedure. DOAC indicates direct oral anticoagulants; INR, international normalized ratio; VKA, vitamin-K antagonists.

The decision to bridge VKAs and DOACs with unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) is based on the patient's thrombotic risk, bleeding risk, renal function, and the risk of procedural bleeding.75 The timing of either UFH or LMWH is best determined in consultation with the surgeon. The decision to use UFH rather than an LMWH as the bridging agent depends on renal function, the bridging setting (inpatient versus outpatient), and patient comfort with self-injections. Current expert consensus suggests that if creatinine clearance (CrCl) is <30 mL/min, UFH is preferred over LMWH especially in the periprocedural setting.75 UFH may be discontinued 4–6 hours before the procedure or earlier based on the activated partial thromboplastin time. If LMWH is used for bridging, discontinuation is recommended at least 24 hours before the procedure.75 Although perioperative bridging with a parenteral anticoagulant is common, current evidence suggests that such a practice may not decrease the risk of arterial thromboembolism, and may increase the risk of both major adverse cardiovascular events and major bleeding.76 A simple and standardized perioperative DOAC interruption and resumption strategy were recently tested in patients with AF undergoing elective surgery.77 This approach, which avoided heparin bridging and coagulation function testing, showed low rates of bleeding as well as arterial thromboembolism and could be a viable alternative in patients taking DOACs.

Intraoperative Period.

For AF occurring intraoperatively, immediate management depends first on heart rate and blood pressure. RVR combined with hypotension refractory to vasoconstrictor therapy requires emergent electrical cardioversion. For patients with RVR in whom blood pressure remains adequate, rate control (HR < 110/min) can be attempted using β-blockers or Ca2+ channel blockers. Metoprolol is superior to diltiazem in achieving rate control in critically ill patients with RVR and maybe a better perioperative option.78 While targeting rate versus rhythm control does not affect outcomes in ambulatory79 or postcardiac surgery AF,80 no data exist for noncardiac surgical patients. Patients undergoing surgery and anesthesia may be more susceptible than ambulatory patients to hypotension from rate-control agents and rhythm control may be an option if NSR is documented within the last 48 hours. One strategy for rate control is to assess the clinical response to a short-acting β-blocker such as esmolol. If the patient responds with a decrease in heart rate, and no hypotension, either a small dose of metoprolol or an esmolol infusion can be used.

In patients with RVR who cannot tolerate β or Ca2+ channel blockers, amiodarone is a reasonable alternative. An initial 150 mg intravenous bolus, followed by a 1 mg/min infusion, can be started. If the heart rate remains high, an additional 150-mg bolus dose can be given. Phenylephrine is another alternative in patients with RVR and low blood pressures because it reflexively reduces heart rate. No data exist to inform the target heart rate that should be achieved during surgery, but a heart rate <110 bpm is usually acceptable if perfusion is not impaired.28

If possible, causes of AF and modifiable risk factors should be evaluated while stabilizing heart rate and blood pressure. Volatile agents do not differ from total intravenous anesthesia (TIVA) with respect to AF risk but desflurane is associated with increased sympathetic stimulation and potential for arrhythmias.81 Fluid status should be assessed and hypovolemia or hypervolemia, if present, should be addressed. Intraoperative transesophageal echocardiography (TEE) may help rule out AMI and guide fluid management in high-risk patients. If possible, checking electrolytes will permit assessment of metabolic abnormalities such as acidosis, hypomagnesemia, and hypokalemia. Although no clear threshold for replacement exists, a 1999 multicenter review of 2402 patients suggests an increase in arrhythmias with potassium levels <3.5 mg/dL.82 If a central line was recently inserted, the position of the catheter should be confirmed because catheter tip irritation can precipitate AF.

Postoperative Period.

If AF persists after surgery or begins in the postoperative period, the first step would again be the preservation of blood pressure and end-organ perfusion and heart rate control if RVR is present. An effort to identify potentially dangerous causes should proceed concurrently with hemodynamic stabilization. Bedside ultrasound may provide an estimate of the left ventricular function and potentially exclude AMI and/or PE as a cause. A high suspicion of AMI and/or PE might warrant further evaluation by checking serum troponin levels and radiographic evaluation. If the patient was chronically taking a β-blocker or nondihydropyridine Ca2+ channel blocker (NDHP-CCB) preoperatively, restarting the patient's home regimen and/or adjusting the dose may also be appropriate.

As with intraoperative AF, β-blockers, NDHP-CCBs (ie, diltiazem and verapamil), digoxin, and amiodarone can be used to achieve ventricular rate control in the postoperative period. The choice of β-blockers versus diltiazem is frequently debated among clinicians with no clear evidence favoring one over the other. In a substudy of the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial, β-blockers were more efficacious at achieving goal heart rate than Ca2+ channel blockers.83 In addition, because vasodilation with diltiazem may cause hypotension in the perioperative setting and the postsurgical period is already associated with an increased adrenergic tone and catecholamine release, β-blockers may represent a physiologically appropriate first-line therapy in patients who are asymptomatic and have preserved ejection fraction.84–87 Amiodarone is also a viable option for rate control in the postoperative setting, particularly with borderline low blood pressures as the hypotensive effect of amiodarone is less. A loading dose followed by an infusion is usually administered given its long half-life and extensive tissue distribution.85,87 Amiodarone administration can be associated with significant side effects both acutely as well as with chronic use. Acute pulmonary and hepatic toxicity are rare but potentially life-threatening complications and should be considered in patients with acute respiratory compromise and transaminitis after amiodarone administration. The drug should be discontinued if there is more than a 2-fold elevation.88 In the long term, the drug affects the respiratory system, liver, and the thyroid gland predominantly, but photosensitivity, corneal deposits, and neurological side effects are also frequent. Amiodarone-induced pulmonary toxicity (APT), with incidence ranging from 5% to 13%, can manifest acutely as organizing pneumonia or acute respiratory distress syndrome (ARDS) and chronically as interstitial pneumonitis or pulmonary fibrosis.89 Potential risk factors include a high cumulative dose, a daily dose >400 mg/day, duration of therapy exceeding 2 months, increased patient age, preexisting lung disease, and thoracic or nonthoracic surgery.90–93 Hence, it is preferable to avoid amiodarone in patients with preexisting lung disease and/or those undergoing thoracic surgery. While hypo- and hyperthyroidism and hepatic injury are common side effects of chronic amiodarone use, acute exacerbation of thyroid or liver disease with amiodarone administration has not been described. Amiodarone can be administered to patients with preexisting thyroid or liver disease, albeit with caution and close monitoring of thyroid and hepatic function.

Digoxin represents another option for achieving rate control. However, it is less effective in states of elevated sympathetic activity such as the perioperative period,84–87,94 and has a narrow therapeutic/toxic window when compared to β or Ca2+ channel blockers and amiodarone. In addition, because renal function is often compromised in the perioperative setting, digoxin may accumulate as its clearance is predominantly renal.95 Electrolyte imbalances such as hypomagnesemia, hypercalcemia, hypernatremia, and hypokalemia can also alter the effects of digoxin. Hence, digoxin should generally be considered in the perioperative setting only when other pharmacologic options are unsuccessful or contraindicated.

Most patients with new-onset POAF convert to NSR before hospital discharge and >95% of patients remain in NSR 2 months after surgery.96 These patients should be discharged on rate-control agents unless contraindicated and outpatient follow-up is indicated to determine if medication regimens need to be adjusted or discontinued. For patients who develop POAF after thoracic surgery, 2014 American Thoracic Society guidelines recommend that antiarrhythmic therapy be continued for a minimum of 1 week and no longer than 6 weeks beyond the time of discharge.97 However, no data support a specific strategy in patients undergoing noncardiothoracic surgery. In view of the significant side effect profile of amiodarone when used over long term, it may be ideal to either convert to a β-blocker or NDHP-CCB before hospital discharge or schedule a follow-up appointment with a cardiologist to assess discontinuation as soon as possible.

Antithrombotic Management

Antithrombotic therapy should be considered on a case-by-case basis in patients who develop POAF. Patients with paroxysmal AF have a stroke risk similar to those with persistent or permanent AF.85,98 Although current literature suggests no clear association between the duration of AF and stroke,99,100 the risk of stroke for secondary AF such as POAF is similar to traditional AF.101 In patients with an AF burden detectable by clinical examination or 12-lead ECG at multiple time points, anticoagulation therapy reduces stroke risk.102 Similarly, when appropriate surgically, anticoagulation should be restarted in patients with chronic or paroxysmal AF who were receiving anticoagulation before surgery. Perioperative physicians should consider the risk of bleeding associated with the surgical procedure, the patient's general bleeding risk, and the patient's thromboembolic risk on an individual basis when determining the need for starting or reinitiating antithrombotic treatment. Although surgery-specific bleeding risk is difficult to assess, the HAS-BLED (hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile international normalized ratio, elderly, drugs/alcohol concomitantly) score can be used to determine the general bleeding risk of the patient.103 A HAS-BLED score of >3 indicates high bleeding risk and higher scores correlate with higher risk of bleeding.85,104

Clinical scoring systems may help predict the risk of stroke and systemic embolism in patients with AF so that a risk-benefit calculation can be made with respect to bleeding risks associated with anticoagulant therapy. The Congestive heart failure, Hypertension, Age older than 75 years, Diabetes and Stroke (CHADS2) score is the most widely used, with higher scores correlating with higher risk of thromboembolism.84,85,87,96,104–106 The more recent Congestive heart failure, Hypertension, Age older than 75 years, Diabetes, Stroke, Vascular disease, female Sex (CHA2DS2-VASc) score adds an extra point each for female sex and vascular disease (which includes both coronary heart disease and peripheral vascular disease), and divides age into 3 categories (<60 years: 0 point, 60–74 years: 1 point, and ≥75 years: 2 points) instead of the 2 categories in the original CHADS2 score. Oral anticoagulation is indicated in men with CHA2DS2-VASc scores ≥1 and women with scores ≥2.107

Although the CHADS2, CHA2DS2-VASc, and HAS-BLED tools have been validated in general medical patients, they have not been validated in postsurgical patients. Even though the pathophysiology of thrombus development caused by AF is similar in both settings, surgical patients are at a high risk for bleeding. Because the overall rate of thromboembolism is low in both bridged and nonbridged patients in recent studies,76,108 waiting for adequate hemostasis before initiating anticoagulation is reasonable and the decision to restart anticoagulation is best made on a case-by-case basis. Recent studies suggest that real-world application of these risk scores is inconsistent and adequate anticoagulation in at-risk surgical patients is often lacking.109

CONCLUSIONS

AF is the most common perioperative arrhythmia with potentially increasing incidence as progressively older patients present for surgery. POAF can develop both de novo and in patients with a history of AF. Avoiding perioperative triggers and optimizing patient-related factors are currently the mainstay of POAF prevention and further research is needed to better identify the impact of such strategies. Intraoperative prevention follows the same general goals in minimizing potential triggers such as hypotension, sympathetic stimulation, hypoxia/hypercarbia, and metabolic abnormalities. The potential impact of intraoperative anesthetic agents such as ketamine, glycopyrrolate, and desflurane also needs further evaluation. Because the natural history of AF progresses from paroxysmal to persistent to permanent subtypes, preventing paroxysmal AF in the perioperative period may avoid eventual progression to more dangerous forms and have considerable long-term health consequences. Because of surgical stimulation, bleeding, swings in vital signs, and fluctuating volume levels, management of AF can be challenging, and the use of intraoperative TEE and transthoracic ultrasound may rule out dangerous causes such as PE or MI and allow for early, aggressive treatment. Although previously considered a benign and self-limiting entity, POAF worsens postoperative outcomes, can be a harbinger of stroke and severe disability, and increases the risk of postoperative morbidity and mortality. Postoperative continuation of rate-control therapy initiated during the perioperative period is currently recommended even for paroxysmal AF, and further study is needed to validate that approach. Because of the heightened risk of perioperative stroke, prophylaxis should be discussed between anesthesiologist, intensivist, surgeon, and cardiologist with a focus on the risk-benefit profile of such interventions.

DISCLOSURES

Name: Kunal Karamchandani, MD, FCCP.

Contribution: This author helped conceptualize, write and edit the manuscript.

Name: Ashish K. Khanna, MD, FCCP, FCCM.

Contribution: This author helped write and edit the manuscript.

Name: Somnath Bose, MD.

Contribution: This author helped write and edit the manuscript.

Name: Rohesh J. Fernando, MD, FASE.

Contribution: This author helped edit the manuscript and prepare tables and figures.

Name: Allan J. Walkey, MD, MSc.

Contribution: This author helped edit and refine the manuscript.

This manuscript was handled by: Avery Tung, MD, FCCM.

FOOTNOTES

GLOSSARY

AF = = atrial fibrillation;

AFFIRM trial = = Atrial Fibrillation Follow-up Investigation of Rhythm Management trial;

AMI = = acute myocardial infarction;

APT = = amiodarone-induced pulmonary toxicity;

ARDS = = acute respiratory distress syndrome;

ATP = = adenosine triphosphate;

AV = = atrioventricular;

CI = = confidence interval;

CHADS2 score = = Congestive heart failure, Hypertension, Age older than 75 years, Diabetes and Stroke;

CHA2DS2-VASc score = = Congestive heart failure, Hypertension, Age older than 75 years, Diabetes, Stroke, Vascular disease, female Sex;

CPAP = = continuous positive airway pressure;

CrCl = = creatinine clearance;

DOAC = = direct oral anticoagulant;

EACTA = = European Association of Cardiothoracic Anesthesiologists;

ECG = = electrocardiogram;

HAS-BLED score = = Hypertension, Abnormal renal/liver function, Stroke, Bleeding history or predisposition, Labile international normalized ratio, Elderly, Drugs/alcohol concomitantly;

HR = = hazard ratio;

INR = = international normalized ratio

IV = = intravenous;

LA = = left atrium

LMWH = = low-molecular-weight heparin;

LV = = left ventricle;

MINS = = myocardial injury after noncardiac surgery

NDHP-CCB = = nondihydropyridine Ca2+ channel blocker;

NMB = = neuromuscular blockade

NOAF = = new-onset atrial fibrillation

NSR = = normal sinus rhythm;

OR = = odds ratio;

OSA = = obstructive sleep apnea;

PE = = pulmonary embolism;

POAF = = perioperative atrial fibrillation;

POCUS = = point-of-care ultrasound;

POISE trial = = PeriOperative ISchemic Evaluation trial

RA = = right atrium

RV = = right ventricle;

RVR = = rapid ventricular rate;

SA = = sinoatrial;

SCA = = Society of Cardiovascular Anesthesiologists;

TEE = = transesophageal echocardiography;

TIVA = = total intravenous anesthesia;

UFH = = unfractionated heparin;

VKA = = vitamin-K antagonist

REFERENCES

1. Almassi GH, Schowalter T, Nicolosi AC, et al. Atrial fibrillation after cardiac surgery: a major morbid event? Ann Surg. 1997;226:501–511.
2. Bhave PD, Goldman LE, Vittinghoff E, Maselli J, Auerbach A. Incidence, predictors, and outcomes associated with postoperative atrial fibrillation after major noncardiac surgery. Am Heart J. 2012;164:918–924.
3. Echahidi N, Pibarot P, O'Hara G, Mathieu P. Mechanisms, prevention, and treatment of atrial fibrillation after cardiac surgery. J Am Coll Cardiol. 2008;51:793–801.
4. Zaman AG, Archbold RA, Helft G, Paul EA, Curzen NP, Mills PG. Atrial fibrillation after coronary artery bypass surgery: a model for preoperative risk stratification. Circulation. 2000;101:1403–1408.
5. Batra GS, Molyneux J, Scott NA. Colorectal patients and cardiac arrhythmias detected on the surgical high dependency unit. Ann R Coll Surg Engl. 2001;83:174–176.
6. Brathwaite D, Weissman C. The new onset of atrial arrhythmias following major noncardiothoracic surgery is associated with increased mortality. Chest. 1998;114:462–468.
7. Christians KK, Wu B, Quebbeman EJ, Brasel KJ. Postoperative atrial fibrillation in noncardiothoracic surgical patients. Am J Surg. 2001;182:713–715.
8. Curtis JJ, Parker BM, McKenney CA, et al. Incidence and predictors of supraventricular dysrhythmias after pulmonary resection. Ann Thorac Surg. 1998;66:1766–1771.
9. Kahn RL, Hargett MJ, Urquhart B, Sharrock NE, Peterson MG. Supraventricular tachyarrhythmias during total joint arthroplasty. Incidence and risk. Clin Orthop Relat Res. 1993;296:265–269.
10. Polanczyk CA, Goldman L, Marcantonio ER, Orav EJ, Lee TH. Supraventricular arrhythmia in patients having noncardiac surgery: clinical correlates and effect on length of stay. Ann Intern Med. 1998;129:279–285.
11. Sohn GH, Shin DH, Byun KM, et al. The incidence and predictors of postoperative atrial fibrillation after noncardiothoracic surgery. Korean Circ J. 2009;39:100–104.
12. Walsh SR, Tang T, Wijewardena C, Yarham SI, Boyle JR, Gaunt ME. Postoperative arrhythmias in general surgical patients. Ann R Coll Surg Engl. 2007;89:91–95.
13. Schizas D, Kosmopoulos M, Giannopoulos S, et al. Meta-analysis of risk factors and complications associated with atrial fibrillation after oesophagectomy. Br J Surg. 2019;106:534–547.
14. Danelich IM, Lose JM, Wright SS, et al. Practical management of postoperative atrial fibrillation after noncardiac surgery. J Am Coll Surg. 2014;219:831–841.
15. Vallurupalli S, Shanbhag A, Mehta JL. Controversies in postoperative atrial fibrillation after noncardiothoracic surgery: clinical and research implications. Clin Cardiol. 2017;40:329–332.
16. Fuster V, Rydén LE, Cannom DS, et al. 2011 ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 Guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines developed in partnership with the European Society of Cardiology and in collaboration with the European Heart Rhythm Association and the heart rhythm society. J Am Coll Cardiol. 2011;57:e101–e198.
17. Gialdini G, Nearing K, Bhave PD, et al. Perioperative atrial fibrillation and the long-term risk of ischemic stroke. JAMA. 2014;312:616–622.
18. Devereaux PJ, Yang H, Yusuf S, et al. Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial. Lancet (London, England). 2008;371:1839–1847.
19. Royster RL, Deng H, Whalen SP. Postoperative atrial fibrillation. Anesth Analg. 2017;125:10–12.
20. Chelazzi C, Villa G, De Gaudio AR. Postoperative atrial fibrillation. ISRN Cardiol. 2011;2011:203179.
21. Walkey AJ, Benjamin EJ, Lubitz SA. New-onset atrial fibrillation during hospitalization. J Am Coll Cardiol. 2014;64:2432–2433.
22. Hillis LD, Smith PK, Anderson JL, et al.; American College of Cardiology Foundation; American Heart Association Task Force on Practice Guidelines; American Association for Thoracic Surgery; Society of Cardiovascular Anesthesiologists; Society of Thoracic Surgeons. 2011 ACCF/AHA guideline for coronary artery bypass graft surgery. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Developed in collaboration with the American Association for thoracic surgery, society of cardiovascular anesthesiologists, and society of thoracic surgeons. J Am Coll Cardiol. 2011;58:e123–e210.
23. Kirchhof P, Benussi S, Kotecha D, et al. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur J Cardiothorac Surg. 2016;50:e1–e88.
24. Muehlschlegel JD, Burrage PS, Ngai JY, et al. Society of cardiovascular anesthesiologists/European Association of Cardiothoracic Anaesthetists practice advisory for the management of perioperative atrial fibrillation in patients undergoing cardiac surgery. Anesth Analg. 2019;128:33–42.
25. Amar D, Zhang H, Leung DH, Roistacher N, Kadish AH. Older age is the strongest predictor of postoperative atrial fibrillation. Anesthesiology. 2002;96:352–356.
26. Fischer A, Ousdigian KT, Johnson JW, Gillberg JM, Wilkoff BL. The impact of atrial fibrillation with rapid ventricular rates and device programming on shocks in 106,513 ICD and CRT-D patients. Heart Rhythm. 2012;9:24–31.
27. Nattel S. New ideas about atrial fibrillation 50 years on. Nature. 2002;415:219–226.
28. January CT, Wann LS, Alpert JS, et al.; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association task force on practice guidelines and the heart rhythm society. J Am Coll Cardiol. 2014;64:e1–76.
29. Iwasaki YK, Nishida K, Kato T, Nattel S. Atrial fibrillation pathophysiology: implications for management. Circulation. 2011;124:2264–2274.
30. de Vos CB, Pisters R, Nieuwlaat R, et al. Progression from paroxysmal to persistent atrial fibrillation clinical correlates and prognosis. J Am Coll Cardiol. 2010;55:725–731.
31. Nattel S, Burstein B, Dobrev D. Atrial remodeling and atrial fibrillation: mechanisms and implications. Circ Arrhythm Electrophysiol. 2008;1:62–73.
32. Wijffels MC, Kirchhof CJ, Dorland R, Allessie MA. Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. Circulation. 1995;92:1954–1968.
33. Grogan M, Smith HC, Gersh BJ, Wood DL. Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol. 1992;69:1570–1573.
34. Naito M, David D, Michelson EL, Schaffenburg M, Dreifus LS. The hemodynamic consequences of cardiac arrhythmias: evaluation of the relative roles of abnormal atrioventricular sequencing, irregularity of ventricular rhythm and atrial fibrillation in a canine model. Am Heart J. 1983;106:284–291.
35. Kochiadakis GE, Skalidis EI, Kalebubas MD, et al. Effect of acute atrial fibrillation on phasic coronary blood flow pattern and flow reserve in humans. Eur Heart J. 2002;23:734–741.
36. Phan TT, Abozguia K, Shivu GN, et al. Increased atrial contribution to left ventricular filling compensates for impaired early filling during exercise in heart failure with preserved ejection fraction. J Card Fail. 2009;15:890–897.
37. Kanji S, Williamson DR, Yaghchi BM, Albert M, McIntyre L; Canadian Critical Care Trials Group. Epidemiology and management of atrial fibrillation in medical and noncardiac surgical adult intensive care unit patients. J Crit Care. 2012;27:326.e1–326.e8.
38. Waldo AL. Mechanisms of atrial fibrillation, atrial flutter, and ectopic atrial tachycardia–a brief review. Circulation. 1987;75:III37–III40.
39. Khan AM, Lubitz SA, Sullivan LM, et al. Low serum magnesium and the development of atrial fibrillation in the community: the Framingham Heart Study. Circulation. 2013;127:33–38.
40. Krijthe BP, Heeringa J, Kors JA, et al. Serum potassium levels and the risk of atrial fibrillation: the Rotterdam Study. Int J Cardiol. 2013;168:5411–5415.
41. Frier BM, Schernthaner G, Heller SR. Hypoglycemia and cardiovascular risks. Diabetes Care. 2011;34suppl 2S132–S137.
42. Wang TJ, Larson MG, Levy D, et al. Temporal relations of atrial fibrillation and congestive heart failure and their joint influence on mortality: the Framingham Heart Study. Circulation. 2003;107:2920–2925.
43. Goldman L. Supraventricular tachyarrhythmias in hospitalized adults after surgery. Clinical correlates in patients over 40 years of age after major noncardiac surgery. Chest. 1978;73:450–454.
44. Heeringa J, van der Kuip DA, Hofman A, et al. Prevalence, incidence and lifetime risk of atrial fibrillation: the Rotterdam study. Eur Heart J. 2006;27:949–953.
45. Wasmer K, Eckardt L, Breithardt G. Predisposing factors for atrial fibrillation in the elderly. J Geriatr Cardiol. 2017;14:179–184.
46. Burris JM, Subramanian A, Sansgiry S, Palacio CH, Bakaeen FG, Awad SS. Perioperative atrial arrhythmias in noncardiothoracic patients: a review of risk factors and treatment strategies in the veteran population. Am J Surg. 2010;200:601–605.
47. La Manna G, Boriani G, Capelli I, et al. Incidence and predictors of postoperative atrial fibrillation in kidney transplant recipients. Transplantation. 2013;96:981–986.
48. Bender JS. Supraventricular tachyarrhythmias in the surgical intensive care unit: an under-recognized event. Am Surg. 1996;62:73–75.
49. Knotzer H, Mayr A, Ulmer H, et al. Tachyarrhythmias in a surgical intensive care unit: a case-controlled epidemiologic study. Intensive Care Med. 2000;26:908–914.
50. Walsh SR, Oates JE, Anderson JA, Blair SD, Makin CA, Walsh CJ. Postoperative arrhythmias in colorectal surgical patients: incidence and clinical correlates. Colorectal Dis. 2006;8:212–216.
51. Joshi KK, Tiru M, Chin T, Fox MT, Stefan MS. Postoperative atrial fibrillation in patients undergoing non-cardiac non-thoracic surgery: a practical approach for the hospitalist. Hosp Pract (1995). 2015;43:235–244.
52. Park YJ, Yoon JW, Kim KI, et al. Subclinical hypothyroidism might increase the risk of transient atrial fibrillation after coronary artery bypass grafting. Ann Thorac Surg. 2009;87:1846–1852.
53. Gami AS, Pressman G, Caples SM, et al. Association of atrial fibrillation and obstructive sleep apnea. Circulation. 2004;110:364–367.
54. Kendzerska T, Gershon AS, Atzema C, et al. Sleep apnea increases the risk of new hospitalized atrial fibrillation: a Historical Cohort Study. Chest. 2018;154:1330–1339.
55. Alonso-Coello P, Cook D, Xu SC, et al.; POISE Investigators. Predictors, prognosis, and management of new clinically important atrial fibrillation after noncardiac surgery: a Prospective Cohort Study. Anesth Analg. 2017;125:162–169.
56. Winkel TA, Schouten O, Hoeks SE, Verhagen HJ, Bax JJ, Poldermans D. Prognosis of transient new-onset atrial fibrillation during vascular surgery. Eur J Vasc Endovasc Surg. 2009;38:683–688.
57. Higuchi S, Kabeya Y, Matsushita K, et al. Incidence and complications of perioperative atrial fibrillation after non-cardiac surgery for malignancy. PLoS 1. 2019;14:e0216239.
58. Oesterle A, Weber B, Tung R, Choudhry NK, Singh JP, Upadhyay GA. Preventing postoperative atrial fibrillation after noncardiac surgery: a meta-analysis. Am J Med. 2018;131:795.e5–804.e5.
59. Walsh M, Devereaux PJ, Garg AX, et al. Relationship between intraoperative mean arterial pressure and clinical outcomes after noncardiac surgery: toward an empirical definition of hypotension. Anesthesiology. 2013;119:507–515.
60. Hajjar LA, Vincent JL, Barbosa Gomes Galas FR, et al. Vasopressin versus norepinephrine in patients with vasoplegic shock after cardiac surgery: the VANCS randomized controlled trial. Anesthesiology. 2017;126:85–93.
61. McIntyre WF, Um KJ, Alhazzani W, et al. Association of vasopressin plus catecholamine vasopressors vs catecholamines alone with atrial fibrillation in patients with distributive shock: a systematic review and meta-analysis. JAMA. 2018;319:1889–1900.
62. Tai CT, Chiou CW, Wen ZC, et al. Effect of phenylephrine on focal atrial fibrillation originating in the pulmonary veins and superior vena cava. J Am Coll Cardiol. 2000;36:788–793.
63. Liebe T, Li S, Lord A, et al. Factors influencing the cardiovascular response to subanesthetic ketamine: a randomized, placebo-controlled trial. Int J Neuropsychopharmacol. 2017;20:909–918.
64. Mirakhur RK, Dundee JW, Jones CJ, Coppel DL, Clarke RS. Reversal of neuromuscular blockade: dose determination studies with atropine and glycopyrrolate given before or in a mixture with neostigmine. Anesth Analg. 1981;60:557–562.
65. Arsenault KA, Yusuf AM, Crystal E, et al. Interventions for preventing post-operative atrial fibrillation in patients undergoing heart surgery. Cochrane Database Syst Rev. 20131CD003611.
66. Khanna AK, Naylor DF Jr, Naylor AJ, et al. Early resumption of β blockers is Associated with decreased atrial fibrillation after noncardiothoracic and nonvascular surgery: a cohort analysis. Anesthesiology. 2018;129:1101–1110.
67. Bayir PT, Demirkan B, Bayir O, et al. Impact of continuous positive airway pressure therapy on atrial electromechanical delay and P-wave dispersion in patients with obstructive sleep apnea. Ann Noninvasive Electrocardiol. 2014;19:226–233.
68. Mills PJ, Kennedy BP, Loredo JS, Dimsdale JE, Ziegler MG. Effects of nasal continuous positive airway pressure and oxygen supplementation on norepinephrine kinetics and cardiovascular responses in obstructive sleep apnea. J Appl Physiol (1985). 2006;100:343–348.
69. Holmqvist F, Guan N, Zhu Z, et al.; ORBIT-AF Investigators. Impact of obstructive sleep apnea and continuous positive airway pressure therapy on outcomes in patients with atrial fibrillation-results from the Outcomes Registry for Better Informed Treatment of Atrial Fibrillation (ORBIT-AF). Am Heart J. 2015;169:647.e2–654.e2.
70. Potpara TS, Polovina MM, Marinkovic JM, Lip GY. A comparison of clinical characteristics and long-term prognosis in asymptomatic and symptomatic patients with first-diagnosed atrial fibrillation: the Belgrade Atrial Fibrillation Study. Int J Cardiol. 2013;168:4744–4749.
71. Fleisher LA, Fleischmann KE, Auerbach AD, et al.; American College of Cardiology; American Heart Association. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association task force on practice guidelines. J Am Coll Cardiol. 2014;64:e77–137.
72. Amar D. Perioperative atrial tachyarrhythmias. Anesthesiology. 2002;97:1618–1623.
73. Kuppahally SS, Foster E, Shoor S, Steimle AE. Short-term and long-term success of electrical cardioversion in atrial fibrillation in managed care system. Int Arch Med. 2009;2:39.
74. Ge Y, Ha ACT, Atzema CL, et al. Association of atrial fibrillation and oral anticoagulant use with perioperative outcomes after major noncardiac surgery. J Am Heart Assoc. 2017;6:e006022.
75. Doherty JU, Gluckman TJ, Hucker WJ, et al. 2017 ACC expert consensus decision pathway for periprocedural management of anticoagulation in patients with nonvalvular atrial fibrillation: a report of the American College of cardiology clinical expert consensus document task force. J Am Coll Cardiol. 2017;69:871–898.
76. Douketis JD, Spyropoulos AC, Kaatz S, et al.; BRIDGE Investigators. Perioperative bridging anticoagulation in patients with atrial fibrillation. N Engl J Med. 2015;373:823–833.
77. Douketis JD, Spyropoulos AC, Duncan J, et al. Perioperative management of patients with atrial fibrillation receiving a direct oral anticoagulant. JAMA Intern Med. 2019 August 5 [Epub ahead of print].
78. Moskowitz A, Chen KP, Cooper AZ, Chahin A, Ghassemi MM, Celi LA. Management of atrial fibrillation with rapid ventricular response in the intensive care unit: a secondary analysis of electronic health record data. Shock. 2017;48:436–440.
79. Wyse DG, Waldo AL, DiMarco JP, et al.; Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med. 2002;347:1825–1833.
80. Gillinov AM, Bagiella E, Moskowitz AJ, et al.; CTSN. Rate control versus rhythm control for atrial fibrillation after cardiac surgery. N Engl J Med. 2016;374:1911–1921.
81. Kazanci D, Unver S, Karadeniz U, et al. A comparison of the effects of desflurane, sevoflurane and propofol on QT, QTc, and P dispersion on ECG. Ann Card Anaesth. 2009;12:107–112.
82. Wahr JA, Parks R, Boisvert D, et al. Preoperative serum potassium levels and perioperative outcomes in cardiac surgery patients. Multicenter Study of Perioperative Ischemia Research Group. JAMA. 1999;281:2203–2210.
83. Olshansky B, Rosenfeld LE, Warner AL, et al.; AFFIRM Investigators. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study: approaches to control rate in atrial fibrillation. J Am Coll Cardiol. 2004;43:1201–1208.
84. Bekker JG, Macaulay TE. Strategies for the management of postoperative atrial fibrillation. Orthopedics. 2011;34:379.
85. Camm AJ, Kirchhof P, Lip GY, et al.; ESC Committee for Practice Guidelines. Guidelines for the management of atrial fibrillation: the task force for the management of atrial fibrillation of the European Society of Cardiology (ESC). Europace. 2010;12:1360–1420.
86. Fernando HC, Jaklitsch MT, Walsh GL, et al. The society of thoracic surgeons practice guideline on the prophylaxis and management of atrial fibrillation associated with general thoracic surgery: executive summary. Ann Thorac Surg. 2011;92:1144–1152.
87. Fuster V, Rydén LE, Cannom DS, et al.; American College of Cardiology; American Heart Association Task Force; European Society of Cardiology Committee for Practice Guidelines; European Heart Rhythm Association; Heart Rhythm Society. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: full text: a report of the American College of Cardiology/American Heart Association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in collaboration with the European heart rhythm Association and the heart rhythm society. Europace. 2006;8:651–745.
88. Goldschlager N, Epstein AE, Naccarelli G, Olshansky B, Singh B. Practical guidelines for clinicians who treat patients with amiodarone. Practice guidelines subcommittee, North American Society of Pacing and Electrophysiology. Arch Intern Med. 2000;160:1741–1748.
89. Schwaiblmair M, Berghaus T, Haeckel T, Wagner T, von Scheidt W. Amiodarone-induced pulmonary toxicity: an under-recognized and severe adverse effect? Clin Res Cardiol. 2010;99:693–700.
90. Ashrafian H, Davey P. Is amiodarone an underrecognized cause of acute respiratory failure in the ICU? Chest. 2001;120:275–282.
91. Handschin AE, Lardinois D, Schneiter D, Bloch K, Weder W. Acute amiodarone-induced pulmonary toxicity following lung resection. Respiration. 2003;70:310–312.
92. Hughes M, Binning A. Intravenous amiodarone in intensive care. Time for a reappraisal? Intensive Care Med. 2000;26:1730–1739.
93. Ott MC, Khoor A, Leventhal JP, Paterick TE, Burger CD. Pulmonary toxicity in patients receiving low-dose amiodarone. Chest. 2003;123:646–651.
94. Hollenberg SM, Dellinger RP. Noncardiac surgery: postoperative arrhythmias. Crit Care Med. 2000;28:N145–N150.
95. Thakar CV. Perioperative acute kidney injury. Adv Chronic Kidney Dis. 2013;20:67–75.
96. Amar D. Strategies for perioperative arrhythmias. Best Pract Res Clin Anaesthesiol. 2004;18:565–577.
97. Frendl G, Sodickson AC, Chung MK, et al.; American Association for Thoracic Surgery. 2014 AATS guidelines for the prevention and management of perioperative atrial fibrillation and flutter for thoracic surgical procedures. J Thorac Cardiovasc Surg. 2014;148:e153–e193.
98. Hohnloser SH, Pajitnev D, Pogue J, et al.; ACTIVE W Investigators. Incidence of stroke in paroxysmal versus sustained atrial fibrillation in patients taking oral anticoagulation or combined antiplatelet therapy: an ACTIVE W Substudy. J Am Coll Cardiol. 2007;50:2156–2161.
99. Boriani G, Glotzer TV, Santini M, et al. Device-detected atrial fibrillation and risk for stroke: an analysis of >10,000 patients from the SOS AF project (Stroke preventiOn strategies based on atrial fibrillation information from implanted devices). Eur Heart J. 2014;35:508–516.
100. Swiryn S, Orlov MV, Benditt DG, et al.; RATE Registry Investigators. Clinical implications of brief device-detected atrial tachyarrhythmias in a cardiac rhythm management device population: results from the registry of atrial tachycardia and atrial fibrillation episodes. Circulation. 2016;134:1130–1140.
101. Lubitz SA, Yin X, Rienstra M, et al. Long-term outcomes of secondary atrial fibrillation in the community: the Framingham Heart Study. Circulation. 2015;131:1648–1655.
102. Goldstein LB, Bushnell CD, Adams RJ, et al.; American Heart Association Stroke Council; Council on Cardiovascular Nursing; Council on Epidemiology and Prevention; Council for High Blood Pressure Research, Council on Peripheral Vascular Disease, and Interdisciplinary Council on Quality of Care and Outcomes Research. Guidelines for the primary prevention of stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42:517–584.
103. Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ, Lip GY. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro heart survey. Chest. 2010;138:1093–1100.
104. Wann LS, Curtis AB, Ellenbogen KA, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on dabigatran). A report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. Heart Rhythm. 2011;8:e1–e8.
105. Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the national registry of atrial fibrillation. JAMA. 2001;285:2864–2870.
106. Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest. 2010;137:263–272.
107. Lip GYH, Banerjee A, Boriani G, et al. Antithrombotic therapy for atrial fibrillation: CHEST guideline and expert panel report. Chest. 2018;154:1121–1201.
108. Steinberg BA, Peterson ED, Kim S, et al. Use and outcomes associated with bridging during anticoagulation interruptions in patients with atrial fibrillation: findings from the Outcomes Registry for Better Informed Treatment of Atrial Fibrillation (ORBIT-AF). Circulation. 2015;131:488–494.
109. Schoaps RS, Quintili A, Bonavia A, et al. Stroke prophylaxis in critically-ill patients with new-onset atrial fibrillation. J Thromb Thrombolysis. 2019;48:394–399.
Copyright © 2019 International Anesthesia Research Society