November 14, 2021, by Shahriar Lahouti. Last Update 18 July 2026.

CONTENTS

• Introduction with a case
  
• Definition and Diagnosis of AF
  • New onset of AF (NOAF) in critical illness
• Hemodynamic impact of AF
• Etiology of New-onset AF
• Evaluation
• Approach to management of AF in critical illness
  • General principles 
  • Overview of management: Algorithm
    
  • Emergent Cardioversion
  • Common therapeutic measures for AF in unstable patients
    • Hemodynamic optimization
    • Treatment of inciting factors
  • Rate vs. rhythm control strategy
    • Rate control strategy for critically ill patients
      • Amiodarone
      • Beta-blocker
      • Calcium channel blocker
      • Digoxin
    • Rhythm control strategy for critically ill patients
      • Magnesium
      • Amiodarone
      • Ibutilide
      • DC cardioversion
  • Anticoagulation
    • Choice of anticoagulation
• Atrial Flutter 
• Back to drawing case
• RECAP
• AF Tool
• Media
• Further going
• References

Introduction 

Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice 1. In critically ill patients, the incidence of new-onset AF is about 10% (ranging from 5-20% in different studies), but little is known about its treatment. Regrettably, our understanding of AF treatment is based almost exclusively on studies of outpatients with chronic, recurrent AF occurring spontaneously, which is the polar opposite of AF in critically ill patients. This article will focus on the management of AF in critically ill patients and incorporates the 2024 ESC Guidelines for the management of atrial fibrillation.

👩‍⚕️Case scenario: The charge nurse asks you to see a 60-year-old patient in the ED ICU, who she thinks has ST-segment elevation. You walk into the room and see a pale, diaphoretic man with moderate respiratory discomfort. The chart in your hand says that he had severe pancreatitis with acute kidney injury but no prior medical problems. The monitor reveals a heart rate of approximately 143 bpm, but it jumps around a lot from beat to beat. His blood pressure is 85/46 (MAP 59). He is satting 89% on a non-rebreather. The ECG is narrow complex and irregularly irregular. What is the best therapeutic approach for him?

---

---

Definition and Diagnosis

AF may be suspected based on an irregularly irregular heart rate (either on clinical examination or telemetry). However, the diagnosis of AF should always be confirmed with a rhythm documentation with a 12-lead ECG tracing. By convention, an episode lasting at least 30s is diagnostic for clinical AF *.

Diagnostic criteria for AF on ECG  

• Irregularly irregular RR intervals: The RR intervals follow no repetitive pattern (hence labeled as irregularly irregular). There should be no regularity 3. 
  • At very high rates, the heart rate may appear to be regular (“pseudo-regularization”).
  • When in doubt, calipers may help determine whether there is any regularity.
• No discernible P waves: instead, these may be replaced by fibrillation waves. 
  • Fibrillation waves may be best seen in the inferior and right-sided precordial leads.
  • In some patients, fibrillation waves may be small and difficult to distinguish from artifacts.

👉One exception to these criteria is that if AF is combined with heart block, then the ventricular response may be regular (see below)

Classification

AF has been traditionally classified based on the following patterns 4

• Episode persistence: These patterns (paroxysmal, persistent, long-standing, permanent) 5 have been used to characterize the severity of disease, define patient populations in clinical trials, and to form the basis of therapeutic recommendations regarding pharmacological and invasive arrhythmia management. 
• Pathophysiologic pattern of AF: The likelihood of developing AF varies across physiological and pathological states. Within this context, AF may be considered as:
  • Primary: If AF has an established pathophysiologic process. 
  • Triggered-induced AF: New AF episode in close proximity to a precipitating and potentially reversible factor *. Common causes of secondary AF are described below. 

Heart rate among patients with AF

• During AF, electrical activity in the atria can exceed 400 beats/min. The majority of these impulses do not conduct to the ventricles because of the electrical properties of the atrioventricular (AV) node. The ventricular rate is controlled by the conduction properties of the AV node. In the typical patient with untreated AF, the ventricular rate varies between 90 and 170 beats/min (~ 150). 
• 👉Clinical entities that can cause accelerated ventricular response ( HR > ~110) in patients with AF:
  • Catecholamine excess or parasympathetic withdrawal
    • Hyperthyroidism
    • State of shock (e.g. sepsis, hemorrhagic shock etc.)
    • Pulmonary embolism
    • Acute flash pulmonary edema
    • Acute coronary syndrome
    • Alcohol/drug withdrawal
    • Acute exacerbation of COPD
    • Decompensated pulmonary hypertension
    • Worsening valvulopathy (e.g. mitral stenosis, mitral regurgitation)
    • Myocarditis, pericarditis
    • Acute infection: pneumonia, UTI, etc.
  • AF plus Wolf Parkinson White: an accessory pathway as occurs in preexcitation syndrome (If the heart rate is >250, consider the possibility of an accessory tract) 6.
    • Normally, when in AF, the heart rate is limited by the refractory period of the AV node.  Although the AV node may allow for a fast heart rate (e.g. ~120-180), these heart rates are usually tolerated well.
    • When AF occurs in the context of an accessory pathway, both the AV node and the accessory pathway can transmit beats to the ventricles.  Since the accessory pathway often has a shorter refractory period than the AV node, it may drive the ventricle very rapidly (e.g. >250).  This is dangerous because the extremely fast and uncoordinated contractions of the ventricle can promote ventricular tachycardia or cardiovascular collapse.
    • AF with an accessory pathway produces a distinctive pattern of ECG findings:
      • Irregularly irregular heart rate that may be extremely fast (e.g.,>250).
      • Wide-complex beats (resulting from transmission over the accessory pathway).
      • QRS Morphology varies between different beats.

---

• 👉The ventricular rate may be slower (e.g. <60 bpm) in the following settings:
  • Hyperkalemia
  • Increased vagal tone
  • Drugs that affect AV nodal conduction
  • AV nodal disease, which should be suspected if the ventricular rate is below 60 bpm in the absence of a drug that slows AV conduction. Although this relates to AV node dysfunction, AF with slow rates is generally included as a manifestation of sinus node dysfunction.

👉Be careful when cardioverting patients with a heart rate <100, as there may be an increased risk of bradycardia.

---

• 👉Regularized AF:
  • AF is an irregularly irregular rhythm. Remember that a rhythm is irregular if “R-R” variation in a single cardiac cycle > 10%
  • Regularized AF can be caused by 7
    • Digoxin Intoxication
    • Complete Heart Block

---

New onset of AF (NOAF) in critical illness

⭐️Terminology Note: In the 2024 ESC Guidelines, the terms “new-onset AF” (NOAF) and “first-diagnosed AF” are used interchangeably to describe the first detection of the arrhythmia, regardless of its symptoms, duration, or whether a specific trigger is present *. This is distinct from the term “trigger-induced AF,” which describes a specific, potentially reversible cause of that first episode (see Etiology of NOAF section).

◾️NOAF in critical illness is used to refer to patients with no prior history of AF who are admitted in sinus rhythm and subsequently develop new-onset AF while being treated for critical illness 8. A common example is in patients with septic shock, wherein the prevalence of NOAF is ~10% 9. The main differential diagnostic considerations in patients with acute critical illness and AF are:

1. A patient with chronic AF develops critical illness. 
   • Preexisting AF is highly prevalent among older patients with chronic conditions who are at risk for critical illness.
2. A patient who was previously in sinus rhythm develops new-onset AF secondary to the physiologic stress of critical illness (e.g., secondary to sepsis, massive GI bleeding). Features that would support a diagnosis of NOAF rather than chronic, paroxysmal AF may include symptomatic AF or severe physiologic stress triggering transition into AF (e.g., AF immediately following an epinephrine bolus). 

◾️In a recent systematic review and meta-analysis, several risk factors were associated with development of AF in critically ill patients 10:

• Age
• Shock
• Sepsis
• Use of a pulmonary artery catheter 
• Mechanical ventilation
• Increased fluid loading
• Organ failures

◾️Prognosis and follow up

An increased risk of adverse outcomes (increased risk of stroke, ICU length of stay, and mortality) in association with new-onset AF secondary to MI, sepsis, or surgery has been reported 4. However, it remains unclear whether the NOAF causes worse outcomes or the NOAF merely is a marker of sicker patients, or both 11.

• The natural history of NOAF is usually to revert to sinus rhythm on its own, as the underlying critical illness resolves. 
• Irrespective of the cause of secondary AF, long-term recurrence of AF is frequently observed 12 13.

At present, there is limited data to predict which patients will develop recurrent AF beyond an assessment of the traditional risk factors for AF. As such, it is recommended that patients with secondary AF undergo careful reassessment and follow-up.   

---

Hemodynamic impact of AF

This section provides the physiological basis for answering the central question of this article: Is AF an innocent bystander or a criminal? The key issue is whether AF is causing hemodynamic compromise (the “criminal”) or whether it is merely a marker of underlying illness severity (the “innocent bystander”).

AF can lead to a fall in cardiac output with consequent decrease in blood pressure and pulmonary congestion. The following factors may contribute to the adverse hemodynamic changes in AF.

1. Loss of atrial systole (aka. atrial “kick”): Contraction of the left atrium injects a volume of blood under pressure into the left ventricle, leading to increments in ventricular diastolic volume and stroke volume. Loss of atrial kick can therefore diminish the stroke volume. This may be particularly important in the following conditions:

• • Impaired left ventricular compliance: LV compliance is reduced in diastolic dysfunction. In such patients, there is a relative shift of left ventricular filling to the later part of diastole with a greater dependence upon atrial contraction. Clinical examples in which AF can lead to hemodynamic deterioration in patients with diastolic dysfunction include advanced aortic stenosis, which often produces a hypertrophied, poorly compliant left ventricle, and hypertrophic cardiomyopathy.
  • Mitral stenosis: Among such patients, the onset of AF can lead to hemodynamic deterioration. Two factors contribute to this adverse effect: the loss in atrial systole, which plays an important role in the generation of adequate left atrial pressure to maintain blood flow across the stenotic valve and may also reduce effective mitral valve area; and the rapid ventricular response, which, due to the reduction in the duration of diastole, diminishes the time available for filling of the left ventricle
  • Pulmonary hypertension: As left atrial and pulmonary venous pressures increase due to diastolic dysfunction, this increases the pulmonary artery pressure through passive back-transmission of this hydrostatic pressure. With more advanced stages of HFpEF, there may also be changes in pulmonary vascular structure and function leading to a “precapillary” component where pulmonary vascular resistance increases.

   2. Rapid ventricular response 

• While moderate tachycardia often leads to increased cardiac output (CO= HR x SV), severe tachycardia (e.g. HR>150) tends to decrease stroke volume as the LV diastolic filling is reduced.
• The dependence of cardiac output on heart rate is greatest in patients with left ventricular dysfunction, which is often associated with a relatively fixed stroke volume. As an example, the cardiac output is optimal over a narrow range of heart rates in patients with a myocardial infarction, falling significantly with slower or faster heart rates. A rapid ventricular response is also particularly deleterious in patients with mitral stenosis, in whom the reduction in the duration of diastole diminishes the time available for filling of the left ventricle across the stenotic valve. The optimal heart rate for patients in permanent AF is discussed separately.

   3. Other hemodynamic consequences 

• It has been shown in several studies that AF can lead to increased mitral annular dilatation and mitral regurgitation (MR) 14.
  • The presence of AF can create a cycle of worsening AF burden and increasing MR, which can be reversed with a persistent return to normal sinus rhythm.
  • Increased left atrial size in the presence of normal left ventricular function has been associated with increased mitral annular size and more severe MR in some studies, but not in all.

---

Etiology of NOAF 

Understanding the etiology of new-onset AF (NOAF) in critically ill patients is the foundation of the “innocent bystander vs. criminal” framework. If AF is due to a reversible trigger (the “innocent bystander”), treating that trigger is the most important intervention. If AF is the primary driver of instability (the “criminal”), more aggressive rhythm or rate control may be needed.

◾️The “Multi-Hit” Hypothesis

• In most critically ill patients, NOAF is not due to a single cause but rather a combination of factors:
  • Underlying substrate: Many patients have subclinical atrial cardiomyopathy (structural, electrical, or functional changes in the atria) that predisposes them to AF. This may be due to age, hypertension, diabetes, obesity, or other comorbidities.
  • Acute triggers: When a critically ill patient is exposed to one or more acute triggers (sepsis, shock, electrolyte disturbances, etc.), AF is unmasked.
• This “multi-hit” hypothesis explains why some patients develop AF with a given trigger while others don’t, and why AF may recur even after the trigger resolves (the underlying substrate remains).

◾️Common Causes of NOAF in the ICU

• Sepsis and Systemic Inflammation 🦠 🦠
  • Sepsis is one of the most common triggers of NOAF in the ICU, with a prevalence of ~10% in septic shock.
  • The degree of inflammation correlates with the incidence of AF.
  • Mechanisms include:
    • Inflammatory cytokines causing atrial myocyte dysfunction
    • Increased sympathetic tone
    • Endothelial dysfunction
    • Electrolyte disturbances
    • Direct myocardial depression
• Electrolyte Abnormalities 
  • Hypokalemia: Potassium is critical for maintaining normal atrial electrophysiology. Hypokalemia increases the risk of AF and is common in the ICU.
  • Hypomagnesemia: Magnesium acts as a natural calcium channel blocker. Hypomagnesemia increases the risk of AF and may also reduce the efficacy of antiarrhythmic drugs.
  • Other electrolytes: Hypocalcemia, hypophosphatemia, and acid-base disturbances may also contribute.
• Adrenergic Overstimulation 😳
  • Medications:
    • Beta-agonists (norepinephrine, epinephrine, dobutamine)
    • Theophylline
  • Physiologic stress:
    • Pain, anxiety, agitation
    • Shock (septic, hemorrhagic, cardiogenic)
  • Withdrawal states:
    • Alcohol withdrawal
    • Substance withdrawal (opioids, benzodiazepines)
• Respiratory Failure 🫁🫁
  • Hypoxemia: Directly affects atrial myocyte function and can trigger AF.
  • Hypercapnia: Causes acidosis, which affects myocardial contractility and electrophysiology.
  • Specific conditions:
    • Pulmonary embolism (also causes right heart strain and increased sympathetic tone)
    • Pneumonia (also causes systemic inflammation)
    • COPD exacerbation (also causes hyperinflation, which affects intrathoracic pressure and venous return)
• Fluid Status Abnormalities 💦
  • Volume overload: Atrial dilation increases the risk of AF and perpetuates the “AF begets AF” cycle. This is common in heart failure, renal failure, and patients receiving large volume resuscitation 15.
  • Hypovolemia: Can cause compensatory tachycardia and trigger AF, but is less common in the ICU.
• Primary Cardiac Disease ❤️‍🔥❤️‍🔥
  • Myocardial ischemia: AF may be a manifestation of acute coronary syndrome, particularly in patients with significant coronary disease.
  • Pericarditis: Inflammation of the pericardium can irritate the atria and trigger AF.
  • Myocarditis: Direct myocardial inflammation increases the risk of AF.
  • Valvular heart disease: Especially mitral stenosis and mitral regurgitation (see Hemodynamic Impact section).
• Endocrine Disorders 
  • Thyrotoxicosis: Hyperthyroidism is a well-established cause of AF. In the ICU, think of thyroid storm, amiodarone-induced hyperthyroidism, or subclinical hyperthyroidism.
  • Pheochromocytoma: Catecholamine excess can trigger AF.
  • Adrenal insufficiency: May contribute to hemodynamic instability and AF.
• Post-Operative State 🔪🔪
  • Cardiac surgery: The incidence of post-operative AF is 30-50% after cardiac surgery [Echahidi 2008].
  • Non-cardiac surgery: The incidence is 5-30% depending on the procedure.
  • Mechanisms include:
    • Inflammation (surgical trauma)
    • Pericardial irritation
    • Sympathetic stimulation
    • Electrolyte disturbances
    • Fluid shifts
• Neurologic Disorders 🧠🧠
  • Intracranial hemorrhage: Subarachnoid hemorrhage is particularly associated with AF due to sympathetic surge.
  • Ischemic stroke: AF may be a cause or a consequence.
  • Traumatic brain injury: Sympathetic overactivity can trigger AF.
• Medications and Toxins 💊💉
  • Beta-agonists: Norepinephrine, epinephrine, dobutamine, albuterol.
  • Theophylline: Less common now but still used.
  • Cocaine, amphetamines, methamphetamines: Sympathomimetic effects.
  • Alcohol: “Holiday heart syndrome” – binge drinking can trigger AF.
  • Swan-Ganz catheterization: Catheter irritation of the right atrium can trigger AF.

---

Evaluation

◾️Basic evaluation

• ECG
  • Confirm the diagnosis of AF (see Definition and Diagnosis section).
  • Look for signs of ischemia (ST-segment changes, T-wave inversions).
  • Look for signs of structural heart disease (LVH, bundle branch block, prior infarction).
  • Look for conduction abnormalities (prolonged PR, QRS widening).
  • Assess ventricular rate and regularity.
• Blood Tests
  • Electrolytes, including magnesium: Hypokalemia and hypomagnesemia are common triggers of AF.
  • Complete blood count: Look for anemia (reduced oxygen delivery) or infection (elevated WBC).
  • Kidney function: Renal dysfunction affects drug dosing and may indicate organ hypoperfusion.
  • Liver function: Hepatic dysfunction may affect drug metabolism and indicates organ hypoperfusion.
  • Thyroid function tests (TSH, free T4): Should be considered if:
    • There is no obvious cause of AF.
    • Other clinical features suggest thyrotoxicosis.
    • New onset of AF, especially in age >55 yo (since in this population, classic signs and symptoms of hyperthyroidism could be absent).
    • Rapid ventricular response is difficult to control despite appropriate measures.
    • Clinical status of the patient worsens following administration of amiodarone.
  • Troponin: Only if review of ECG and history suggests ischemia. Routine troponin in all patients with AF is not recommended.
• Review of Medication List
  
  • Identify medications that may contribute to AF:
    • Beta-agonists (norepinephrine, epinephrine, dobutamine)
    • Theophylline
    • Alcohol
    • Sympathomimetics (cocaine, amphetamines)
  • Identify medications that may affect AV nodal conduction (beta-blockers, calcium channel blockers, digoxin).
  • Review for drug interactions that may affect rate control or anticoagulation.
• Review of Indwelling Cardiac Devices
  • Pacemakers, ICDs, and implantable loop recorders may detect atrial high-rate episodes (AHREs) that may or may not be true AF.
  • Review device interrogations if available.
  • Determine if device-detected subclinical AF is present

◾️Point of care ultrasound/echo (see media below):

• POCUS is the single most important imaging tool for evaluating AF in the ICU. It provides immediate, bedside information that directly informs the “innocent bystander vs. criminal” question.
  • Assess for Structural Abnormalities that Increase Dependence on Atrial Kick
    • These conditions make patients more vulnerable to hemodynamic compromise from AF (Table below).
    • The TTE may also identify left atrial thrombus, although the sensitivity is low
  • Assess Volume Status
    • IVC assessment: Plethoric IVC suggests volume overload. Collapsed IVC suggests hypovolemia.
    • Lung ultrasound: B-lines suggest pulmonary congestion. Absent B-lines with a collapsed IVC strongly suggest that hemodynamic instability is NOT the result of rapid ventricular response but that the rapid ventricular response is the result of volume depletion.

---

Approach to management of AF in critical illness

General principles

The first priority when evaluating AF in a critically ill patient is assessing hemodynamic status (figure 1). Hemodynamic instability confers an imminent risk of further deterioration, irreversible organ injury, or cardiac arrest and is manifested as 16

• Acute altered mental status
• SBP < 90 mmHg (MAP<65 mmHg)
• Ischemic chest pain
• Dyspnea from pulmonary congestion
• HR in extremis 
• Signs and symptoms of organ hypoperfusion e.g. low urine output, mottled/cold clammy skin.

Circulatory failure (i.e. shock) is often multifactorial in practice, resulting from multiple overlapping derangements in hemodynamic parameters (i.e. Pump failure, tank or pipe problems).

In the context of tachy-or-bradyarrhythmias, the rule of  “Primacy of the Heart Rate” implies that heart rate at extremis should be corrected in the first place even in the presence of multiple overlapping perfusion problems.

• However, this rule often is not true for patients with “AF plus instability”. Therefore, the key question in the approach to unstable patients with AF is: What is driving the instability? (Figure 1 below) 
• Is the AF causing the patient to be unstable? Or is AF merely triggered by underlying instability?
  • Why is it crucial to sort out if the AF is the cause of hemodynamic instability?
    • Because if tachycardia is due to an underlying process, then overly aggressive attempts to reduce the heart rate to a “normal” range may make the condition worse (remember that a mild degree of tachycardia may actually have a compensatory beneficial effect).
  • ⚠️If AF is driven by another underlying process, focusing solely on suppressing the heart rate with medications will fail and may actually make the patient worse.

---

---

Is this AF an innocent bystander or criminal in a patient with hemodynamic instability?

◾️Helpful clues to determine whether atrial fibrillation is driving hemodynamic instability are summarized in the following table. 34

• The “150 bpm Rule of Thumb”: A Practical Bedside Heuristic
  • The HR of 150 bpm threshold is a clinical guideline derived from major resuscitation and cardiology consensus statements *.
  • It indicates that a ventricular rate above this point is more likely to be the primary driver of hemodynamic instability, especially when accompanied by chest pain or signs of shock.
    • However, it is important to remember that this is a rule of thumb. The optimal heart rate varies significantly between patients, with some tolerating rates well above 150 bpm and others becoming unstable at lower rates *. Clinical context, including the presence of structural heart disease, the patient’s baseline status, and the response to initial treatment, remains paramount. 

---

Overview of management: Algorithm

The general outline for management of AF in critical illness is illustrated in the following figure.

---

Emergent cardioversion

1. DC cardioversion will stabilize the patient only if the AF is causing the instability. Therefore, it is only indicated if new-onset AF clearly caused the patient to be severely unstable.
   • 👉This is unusual for most critically ill patients; the AF isn’t the primary driver of instability.
   • Even if cardioversion was successful, most patients with critical illness will revert to AF subsequently 18. 
   • If possible, pretreatment or post-treatment with amiodarone +/- magnesium may enhance the likelihood of achieving and maintaining sinus rhythm.
2. AF with accessory pathway (WPW) should be treated with DC cardioversion.
   • If a patient with AF and an accessory pathway is displaying instability, proceeding directly to DC cardioversion is indicated.
   • AF with an accessory tract shouldn’t be treated with medications that impair the AV node (e.g., beta-blockers, calcium channel blockers, or amiodarone). Blockade of the AV node may merely cause a greater dominance of the accessory pathway, exacerbating matters (to a certain extent, the AV node and the accessory pathway are competing for control of the ventricle). 
     • Antiarrhythmics that may be used are procainamide or ibutilide.

📍Note: Wait-and-See Approach:

• For patients without hemodynamic compromise, a wait-and-see approach for spontaneous conversion to sinus rhythm within 48 hours of AF onset should be considered as an alternative to immediate cardioversion (Class IIa, Level B) *. This avoids the risks of sedation and procedural complications. This is particularly relevant for ICU patients where spontaneous conversion may occur as the underlying critical illness resolves.

---

---

Common therapeutic measures for AF in unstable patients

The most important intervention for critically ill patients with AF is usually treating the causes of AF. There is a risk of getting overly focused on antiarrhythmics and cardioversion, but the most important interventions are often as follows.

Hemodynamic optimization

◾️Optimize volume status

• AF may be caused by volume overload, which causes atrial dilation. If volume overload is present, diuresis may be beneficial.
• If frank hypovolemia is present, then volume administration may be beneficial.  

◾️Protect MAP

• If hypotensive, add vasopressor without beta-adrenergic activity, e.g., vasopressin, phenylephrine.
• Phenylephrine is a good choice, because it will give you alpha-1 vasoconstriction, without stimulating the beta-receptors and raising the rate. More on phenylephrine here.
  
  • Dose (push): 50-200 mcg q1-2 mins PRN (goal DBP ≥ 60)
  • Dose (drip): 40-180 mcg/min, titrated to goal
• Discontinue beta-adrenergic vasopressors; especially epinephrine, dobutamine, and dopamine may increase heart rate and should be weaned if possible 

Treatment of inciting factors

◾️Correct electrolyte abnormalities

• Hypokalemia and hypomagnesemia may trigger AF, so if present these should be treated aggressively.
• The magnesium level should be checked, but administration of magnesium doesn’t need to wait until the level returns. If magnesium hasn’t been checked recently, it is reasonable to empirically give 2-4 grams of magnesium sulfate provided that the patient’s renal function is normal.

◾️Treatment of pain/anxiety/withdrawal

• Untreated distress can drive sympathetic tone and aggravate AF.
• Pain and anxiety should always be treated adequately.
• For uncontrolled anxiety, dexmedetomidine may be considered as an anxiolytic that will reduce sympathetic tone and decrease heart rate.

◾️Respiratory support

• Hypoxemia or respiratory distress may be drivers of AF.
• Respiratory failure should be aggressively treated (e.g., CPAP for heart failure, BiPAP for COPD, HFNC for pneumonia).

◾️Evaluation and treatment of other causes of hemodynamic instability

• Avoid anchoring excessively on AF as the cause of the patient’s hemodynamic instability.
• For ongoing instability, evaluate broadly and treat appropriately. For example, uncontrolled AF could be a manifestation of sepsis, PE, thyrotoxicosis, or any cause of shock.
  • If AF is being driven by another underlying process, focusing solely on suppressing the heart rate with medications will fail and may actually make the patient worse.

---

Rate control vs. rhythm control

No RCTs have been performed comparing rate control vs. rhythm control in a general ICU population. Available studies show no differences in hard endpoints (e.g., mortality or stroke). However, this doesn’t exclude the possibility that some subgroups of patients might benefit more from one strategy.

Generally, both strategies are reasonable, and the choice may depend on patient specifics.

• The decision to provide rate or rhythm control for AF depends on the clinical context, and the risk-benefit balance must take into consideration the underlying medical condition. 

◾️Factors favoring a rate-control strategy

• Chronic AF is perhaps the strongest indicator for a rate-control strategy. AF leads to electrical remodeling, which leaves the atria less able to convert to sinus rhythm.  The longer patients are in AF, the harder it is to convert to sinus rhythm.
• Onset of AF >48 hours previously, in a patient who isn’t anticoagulated:  In this situation, conversion to sinus rhythm may theoretically increase the risk of stroke due to dislodging a clot from the atrial appendage.
• Reduced likelihood of success with rhythm control: ongoing severe physiological stress, uncontrolled thyrotoxicosis, severe left atrial dilation.

◾️Factors favoring rhythm control strategy

• Inability to tolerate AF hemodynamically: AF can cause hemodynamic instability, especially in patients with chronic pulmonary hypertension, mitral stenosis, or diastolic dysfunction (situations where the atrial kick may be especially beneficial).
• New-onset AF: Patients often develop new AF in the context of critical illness. If this occurs while being monitored in the hospital, it may warrant an attempt at rhythm control (explored further below).
• Atrial flutter: This is often a transitional state, as the atria are deciding whether to settle down into sinus rhythm or atrial fibrillation. Atrial flutter is often difficult to treat using rate control, since the rate tends to be stubbornly stuck at around 150.
• Failure of rate control strategy.

◾️Arguments for Attempting Rhythm Control in Critically Ill Patients with New-Onset AF (NOAF)

• In the absence of high-quality evidence regarding the optimal approach to NOAF in the context of critical illness (e.g. sepsis), several considerations should be made here:
  • Most patients with NOAF will eventually revert back into sinus rhythm on their own. However, the risk of stroke may relate to the duration of time that the patient spends in AF (e.g.,>48 hours in NOAF may increase stroke risks). If we can convert patients out of NOAF rapidly, this ought to reduce the risk of stroke.
  • Not all patients with NOAF will spontaneously revert back into sinus rhythm (for example, one series found that 44% of patients were discharged in AF). The longer AF is allowed to continue, the less likely it is to revert to sinus rhythm. Ongoing atrial fibrillation causes electrical remodeling of the atria, which perpetuates the atrial fibrillation (hence the clinical adage, “AF begets AF”). Prompt cardioversion out of NOAF could theoretically increase the likelihood that the patient could successfully revert to sinus rhythm and stay in sinus rhythm on a long-term basis.
  • AF may impair cardiac function in a subset of patients, due to impaired atrial kick. Cardioversion out of NOAF might therefore improve cardiac function in some patients, allowing them to compensate better for their acute critical illness.
  • Even when rhythm control strategies fail to achieve cardioversion, they will generally achieve rate control – so they may remain clinically beneficial.

---

Rate control strategy for critically ill patients

The target heart rate for outpatients is often regarded to be <110 19. However, the optimal HR for critical patients has not been well studied. 

• Keep in mind that at very fast HR, e.g., >150, the diastolic filling impairment may drop the stroke volume and BP.
• However, at heart rates < 150, the diastolic filling is often preserved, so the dominant driver of cardiac output may be the heart rate.  Thus, for example, causing a drop in the heart rate from 130 to 90 may often cause a drop in the cardiac output.
• ⚠️Trying to “normalize” the heart rate (e.g., targeting a rate below 100) may increase the risk of iatrogenic harm in patients with tenuous hemodynamics.
• 🎯For many critically ill patients, a heart rate goal below ~130 might be reasonable.
  • The target may vary depending on patient specifics and clinical response. The optimal target may also vary over time. For example, initially a target of <130 may be reasonable, but as the patient recovers a lower target may become appropriate

◾️Selecting an Agent for Rate Control

• Generally, four medications are commonly used for rate control: amiodarone, beta-blocker, diltiazem, digoxin. Several factors should be considered when selecting a rate-controller among the list (see table below).
  • The most important consideration is how stable the patient is (since most of these agents can cause hypotension).
  • Effect on likelihood of cardioversion
  • Comorbidities

🛠Troubleshooting: If the patient continues to have a fast ventricular response, one should consider the following conditions

• Re-evaluate the patient for possible inappropriate management of underlying problem e.g. hypovolemia, pulmonary edema, sepsis, pulmonary embolism, thyrotoxicosis
• Addition of magnesium.
• Addition of digoxin may be considered in combination with a beta-blocker or diltiazem (AHA/ACC 2023, Class 2A).
• Transition to amiodarone is often useful (amiodarone is more hemodynamically stable and less likely to cause synergistic hypotension in combination with other agents).
• ⚠️ Avoid combining beta-blockers and calcium-channel blockers (overlapping these agents may increase the risk of hypotension).
• Failure of a rate-control strategy is an indication to consider attempting a rhythm-control strategy.
• Atrial flutter: May consider flutter as heart rate control is often difficult. The heart rate has a tendency to get “stuck” at ~150 (2:1 transmission through the AV node) in atrial flutter.

---

Amiodarone

Mechanism of action: broad-spectrum antiarrhythmic action by blockade of certain types of potassium channels, i.e. Ikr (prolongs the action potential duration; QT interval on ECG) and the inactivated sodium channels (depolarized cells). It has weak beta-adrenergic and calcium channel-blocking actions (slowing down the HR and AV conduction).

Indication: May be used for rate control in AF with RVR in patients with potential hemodynamic instability. 

• Achieving rate control may require reloading with 150 mg amiodarone 2-3 times.
• Don’t conclude that amiodarone has failed to work without re-bolusing adequately.

There is a theoretical risk of causing stroke among patients who aren’t anticoagulated and might cardiovert into sinus rhythm. However, for hemodynamically tenuous and critically ill patients, this theoretical risk may often be superseded by the need to achieve hemodynamic stability.

Onset of action (IV route)

• Electrophysiologic effects occur within hours, while antiarrhythmic effects take 3 days to 1-3 weeks.

• Mean onset of effect may be shorter in children vs adults and in patients receiving IV loading doses;

Amiodarone dosing

• Initial IV dosing
  • Load with 150 mg bolus, then infuse at 1 mg/minute.
  • May re-load 1-2 times if inadequate response (for a total of 150-450 mg given in the form of boluses) 20.
• Conversion to oral
  • Infusion may be converted to oral administration after >24 hours.
  • Start at 400 mg PO BID, until the patient has received a total of 10 grams cumulative dose (both IV and PO).  Subsequently, the dose may be decreased to 200 mg daily.
• Eventually transition to another agent
  • Chronic use of amiodarone causes a host of side effects.
  • After patients recover from their critical illness, they should be transitioned to a safer long-term regimen (e.g., a beta-blocker)

---

Beta-blockers

Mechanism of action: Beta-blockade activity slows down atrioventricular conduction with an increased PR interval and AVN conduction velocity, therefore slowing down ventricular response rate in AF. They possess negative inotropic and chronotropic effects. The β-receptor–blocking drugs differ in their relative affinities for β1 and β2 receptors

• Metoprolol, esmolol: β1>>β2 receptor (however, no currently available β1-selective antagonist is sufficiently specific to completely avoid interactions with β2-adrenoceptors).
• Propranolol: β1=β2 receptor

Selection of beta blocker

• IV metoprolol is usually the agent of choice.
• IV esmolol infusion may be used if it’s unclear whether the patient will tolerate a beta-blocker.  This has the advantage that if it causes hypotension, it can be stopped and will wear off fairly rapidly (over ~10 minutes). If the patient responds well to esmolol, they may be transitioned to a longer-acting beta-blocker.
• Blockade of the β2 receptors in bronchial smooth muscle may lead to an increase in airway resistance, particularly in patients with asthma.
  • These drugs should generally be avoided in patients with asthma.
  • However, some patients with chronic obstructive pulmonary disease (COPD) may tolerate β1-selective blockers, and the benefits, for example in patients with concomitant ischemic heart disease, may outweigh the risks.

Metoprolol dosing

• Initial IV loading
  • Usually start with 5 mg IV, which should take effect within ~5 minutes.
  • Additional doses may be given every 5 minutes up to a total of 15 mg as needed. Dosing should be titrated to effect (reduction in heart rate, without causing hypotension).
• Ongoing IV therapy
  • For patients without enteral access, scheduled IV doses may be required.
  • The intravenous form wears off faster than the oral form, so more frequent dosing may be required than is usual with oral metoprolol (e.g. the initial loading dose may be repeated q4hr-q6hr, depending on heart rate and blood pressure).
• Transition to oral administration (PDF)
  • The initial oral dose may be estimated based on the IV dose required, based on a 1 to 2.5 conversion from IV to PO:
    • Response to 5 mg IV → Start metoprolol tartrate 12.5 mg PO q6hr.
    • Response to 10 mg IV → Start metoprolol tartrate 25 mg PO q6hr.
    • Response to 15 mg IV → Start metoprolol tartrate 37.5 mg PO q6hr.
  • The first oral dose can be started 20 minutes after the initial IV dose.
  • Metoprolol tartrate usually isn’t given every six hours.  However, starting with more frequent dosing may allow more flexibility in dose adjustment.

Esmolol dosing

• Starting esmolol: Load with 0.5 mg/kg IV over 1 minute. Then start the infusion at 0.05 mg/kg/min for 4 minutes. 
• Assess the response to this initial infusion rate: it may be a rough indication of the responsiveness of the ventricular rate.
  • If effective, continue with infusion at 50 mcg/kg/minute.
  • If ineffective, the infusion may be up-titrated as follows:
    • Reload with 0.5 mg/kg IV
    • Increase the infusion rate by 0.05 mcg/kg/min
    • Up-titration may be performed about every half hour as needed (up to a maximal infusion rate of 0.2 mg/kg/min).

Propranolol: 1 mg IV over one minute. It may be repeated up to three doses at two-minute intervals.

---

Calcium channel blocker

Diltiazem, verapamil: diltiazem may have less pronounced negative inotropic and hypotensive effects than verapamil. Diltiazem is more frequently used for AF with RVR.

Indication: It may be useful in patients who are hypertensive or more hemodynamically robust, especially patients who have been chronically treated with diltiazem as outpatients.

Diltiazem dosing 21

• Initial loading dose
  • Start with 0.25 mg/kg (max dose 25 mg) IV bolus.
  • if the first dose is tolerated but does not produce the desired response (20% reduction in HR from the baseline) a second bolus of 0.35 mg/kg (max dose dose 25 mg) is given once after 15 minutes
• Maintenance infusion
  • In those who respond to the first or second bolus, a continuous infusion at a rate of 5 to 15 mg/h is initiated.
  • Consider a reduction in the infusion rate after the target heart rate is reached.  Especially with hepatic dysfunction, diltiazem may accumulate.
• Transition to oral
  • Start diltiazem extended release (diltiazem-ER) at a dose roughly equal to 10 [3(infusion rate in mg/hr) +3].  When in doubt, round down. For example:
    • 3 mg/hour →120 mg/day diltiazem-ER
    • 5 mg/hour →180 mg/day diltiazem-ER
    • 7.5 mg/hour → 260 mg/day diltiazem-ER
    • 10 mg/hour → 330 mg/day diltiazem-ER
    • 15 mg/hour →480 mg/day diltiazem-ER
  • Wean off infusion over the next few hours.

---

Digoxin

Mechanism of action

• It inhibits the sodium-potassium pump, increasing the calcium availability to the contractile apparatus.
• Through centrally mediated vagal stimulation (vagotonic effect), it directly controls the ventricular response via action on AV node.

Disadvantages 

• The benefit of digoxin is limited in hyperadrenergic states, limiting its efficacy in critically ill patients.
• Narrow therapeutic index, so a small variation in plasma concentration may rapidly result in toxic or subtherapeutic concentration.

Indications: Potential candidates for digitalization include

• HFrEF
  • Digoxin has positive inotropic effects
  • Uniquely beneficial for patients with heart failure whose hemodynamics are very tenuous, who may have difficulty tolerating a negative inotrope.
• Mild or moderate tachycardia for which immediate control isn’t necessary
  • Digoxin takes several hours to work, and it’s not tremendously potent.
• Chronic AF
  • Digoxin tends to perpetuate AF, rather than favoring cardioversion back to normal sinus rhythm

Loading dose (digitalization): Digoxin takes a little while to work, but if given intravenously it may take effect within several hours.  When initiated for critically ill patients, digoxin will nearly always be started with intravenous loading doses.

👉Total IV loading dose 22

• Normal renal function: 8-12 mcg/kg ideal body weight (usually ~ 600-1,000 mcg).
• Renal insufficiency: 6-10 mcg/kg ideal body weight.
• Err on the lower end in patients with renal dysfunction, hypothyroidism, and/or reduced muscle mass.
• Typically, 50% of the total loading dose is given initially, followed by 25% given twice, every six hours. The first IV dose (typically ~400-600 mcg) takes effect within roughly 1-4 hours.
• Monitor for effect. If an adequate heart rate is achieved, then subsequent doses may be omitted. If bradycardia occurs, further administration should be held.

👉Maintenance doses

• Patients <70 years old with normal renal function:  250 mcg daily.
• Patients over 70 years old or with renal dysfunction:  125 mcg daily.
• Patients who are both >70 yo and have renal dysfunction:  62.5 mcg daily.
• Digoxin has a long half-life (~36-48 hours, or longer in renal insufficiency). Therefore, steady state may not be reached until about a week after a dose adjustment.

Monitoring digoxin levels

• Drug level must be checked several hours after the last digoxin dose, to allow for distribution (e.g. > 8 hours after an oral dose). Ideally this should be a trough level.
• A therapeutic level is ~ 0.5-2 ng/mL
  • 0.5-1 ng/mL might be the optimal concentration for outpatients.
  • 1-2 ng/mL levels may improve contractility, so these aren’t unreasonable levels for closely monitored ICU patients.

If digoxin fails

• Digoxin is not an extremely powerful agent, so it may fail to achieve optimal heart rate control.
• If digoxin does fail, it may be combined with a beta-blocker or diltiazem.
  • The presence of digoxin may reduce the required dose of beta-blocker or diltiazem, thereby improving hemodynamic stability. 
  • In particular, the combination of digoxin plus a beta-blocker may work well for some patients with systolic heart failure.

---

Rhythm control strategy in critically ill patients

For patients who are not crashing, rhythm control may take a stepwise approach:

STEP1: Magnesium

• Among critically ill patients, magnesium seems to have similar efficacy when compared to other antiarrhythmics 23
• It has an excellent safety profile 24 
• Given its efficacy and safety profile, magnesium is the first-line agent among critically ill patients 9.
• Potential benefits of magnesium even if it fails cardioversion:
  • Magnesium augments the efficacy of other antiarrhythmic agents or DC cardioversion 25 26 27
  • It also has some efficacy at reducing the heart rate 28.
• Dosing: For patients with adequate renal function (GFR > 30 ml/min), a protocoled magnesium infusion may be used as shown below 29.  
• For patients with renal insufficiency, intermittent boluses of magnesium may be utilized (targeting a level of 3-4 mg/dL).
• If a recent magnesium level is unavailable, empiric administration of 2-4 g of magnesium sulfate is reasonable in patients with normal renal function *. The magnesium level should be checked promptly, but treatment should not be delayed while awaiting results. This approach is safe, may promote cardioversion, and enhances the efficacy of other antiarrhythmic agents.

STEP 2: Amiodarone or Ibutilide

• Amiodarone is usually the preferred antiarrhythmic for ICU patients due to its ability to both cardiovert patients and subsequently prevent recurrent AF.
• If amiodarone fails to work immediately, continue the infusion. Some patients may have delayed cardioversion (e.g., within the first 24 hours after starting the amiodarone infusion).

• Amiodarone Dosing:
  • For Rhythm Control: Loading dose is 300 mg (or 5-7 mg/kg) 30. Additional boluses may be given as needed up to a total of ~450-600 mg.
  • For Rate Control: Load with 150 mg bolus, then infuse at 1 mg/minute. Achieving rate control may require reloading with 150 mg amiodarone 2-3 times.
  • Follow-up: Infusion at ~1 mg/min. Don’t conclude amiodarone has failed without adequate loading.

Ibutilide

• For patients in whom amiodarone is contraindicated, ibutilide may be considered.
• The main drawback of ibutilide is that, unlike amiodarone, it doesn’t provide ongoing antiarrhythmic support to prevent AF recurrence. 
• The advantage of ibutilide over amiodarone is that it less frequently causes a drop in BP.
• Ibutilide may be superior to procainamide among critically ill patients, because it has greater efficacy and no negative hemodynamic effects 31 32
• Contraindications: QT prolongation, hypokalemia, hypomagnesemia, ejection fraction <30%, or severe LV hypertrophy.
• Dosing: The standard dose is 1 mg infused over 10 minutes (or 0.01 mg/kg for patients <60 kg). This can be repeated once if needed. If cardioversion occurs while ibutilide is being infused, the infusion should be stopped. Patients should be monitored for ~4 hours subsequently (although arrhythmias will generally occur within the first hour after administration). 

---

STEP 3: DC cardioversion

• Most patients with NOAF will cardiovert in response to steps #1-2 above (especially if ~24 hours are allowed for the magnesium and amiodarone infusions to take effect).
• Failure of magnesium and amiodarone to work suggests that the patient’s heart doesn’t want to go into a sinus rhythm (e.g., perhaps due to significant chronic atrial dilation, underlying structural heart disease, or profound systemic inflammation). In this situation, it’s difficult to know whether to accept atrial fibrillation or continue efforts towards conversion to normal sinus rhythm.
• For intubated patients, an attempt at cardioversion may be reasonable (since the risks of sedation are minimal).

◾️Procedural Sedation for Cardioversion:

• For non-intubated patients, two safe and effective options are:

1. 1. Midazolam Monotherapy Protocol *
      • Optimal candidates: no chronic benzodiazepine/alcohol use, no seizure history.
      • Load with midazolam 3-5 mg IV bolus (depending on age, weight).
      • Give 2 mg IV midazolam q2min PRN to target adequate sedation (eyes closed, no response to gentle verbal/tactile stimuli).
      • Reversal with 0.5-1 mg flumazenil IV if adverse effects occur.
   2. MidaKet Strategy (midazolam + ketamine) *
      • Particularly useful for patients resistant to midazolam.
      • Start with midazolam 3-5 mg bolus, then 2 mg q2-4 min PRN.
      • Add ketamine ~50 mg, then 25-50 mg q2 min PRN to deepen sedation.
      • Usual cumulative doses: midazolam 5-10 mg, ketamine 50-100 mg.

• •  

Cardioversion Procedure

◾️Pad Positioning

• Anterior/Lateral Placement is Preferred:
  • The recent EPIC trial demonstrated that anterior/lateral pad placement was more effective than anterior/posterior pad placement for successful cardioversion *.
  • Anterior/Lateral: One pad placed to the right of the sternum (below the clavicle) and the other in the left mid-axillary line (approximately at the V6 position).
  • Anterior/Posterior: One pad placed on the anterior chest (over the precordium) and the other on the back (between the scapulae). This may be considered if anterior/lateral placement fails, but evidence suggests it is inferior.
• Consider Hyperinflation:
  • Hyperinflation (e.g., in COPD, asthma, or high PEEP) may impair conduction of electricity to the heart by increasing the distance between the pads and the heart due to increased intrathoracic air.
  • To counter hyperinflation:
    • Perform cardioversion at end-expiration to minimize lung volume.
    • If cardioversion is failing due to marked hyperinflation and oxygenation allows, it may be reasonable to briefly disconnect the patient from the ventilator to promote chest deflation.
    • Consider reducing PEEP temporarily if clinically safe.

◾️Electricity and Synchronization

• Synchronization:
  • Be sure to synchronize shock delivery to the R wave of the QRS complex.
  • Synchronization prevents delivery of the shock on the T wave, which could precipitate ventricular tachycardia or ventricular fibrillation.
  • If the patient is in AFL with a rapid ventricular rate, synchronization may be challenging; consider using a lower energy setting or alternative pad placement.
• Energy Selection — Use Maximal Energy:
  • Biphasic defibrillators are preferred over monophasic devices.
    • They achieve higher first-shock success rates (RR 1.71 in meta-analyses) with lower energy requirements (e.g., 120 J vs. 200 J), making them the standard of care for electrical cardioversion.
  • Use the maximal energy available on a biphasic defibrillator (e.g., 200-360 J).
  • Rationale:
    1. Safety: There is no evidence that a single high-energy shock is more dangerous than a low-energy shock. On the contrary, a high-energy shock might theoretically be less likely to induce ventricular tachycardia if the shock is not correctly synchronized (e.g., if synchronization is missed and the shock falls on the T wave).
    2. Efficacy: Initial use of the highest energy reduces the likelihood that repeat cardioversion will be needed. This is especially important among non-intubated patients, in whom sedation may wear off over time, necessitating additional sedation for repeat shocks.
  • Note: For monophasic defibrillators (increasingly rare), use 200 J (or 360 J if available).
• Technical Considerations:
  • Ensure good pad-skin contact: If pads are not adherent or there is excessive hair, shave or clip the area before pad placement.
  • Avoid overlapping pads: Ensure pads do not touch or overlap, which can cause arcing.
  • Consider using a conductive gel or paste if pads are not self-adhesive.

◾️Follow-up Care After Cardioversion to Sinus Rhythm:

• If the patient is successfully cardioverted, consider ongoing amiodarone therapy until their critical illness is significantly improved. If amiodarone is stopped while the patient is still critically ill, patients are likely to revert into AF. One multicenter study found that amiodarone had an 87% success rate at achieving cardioversion, but 42% of patients reverted back to AF during their ICU stay.
• For patients who were cardioverted with ibutilide, amiodarone may be started ~6-12 hours afterwards.

---

 

Anticoagulation

Critically ill patients often have systemic inflammation (which may increase their risk for thromboembolic stroke compared to outpatients). On the other hand, they also have numerous risk factors for bleeding (e.g. renal dysfunction, use of antiplatelet medications, invasive procedures).

Risk scores for bleeding and thrombosis haven’t been validated in the ICU (e.g. CHA₂DS₂-VA, HAS-BLED Score for Major Bleeding Risk). This makes it difficult to balance the risks versus benefits of anticoagulation accurately.

• Assessment of Thromboembolic Risk 
  • The 2024 ESC Guidelines have updated the stroke risk score to CHA₂DS₂-VA (removing the sex category). Female sex is an age-dependent stroke risk modifier, not an independent risk factor.

Possible recommendation for anticoagulation among critically ill patients with AF

• New-Onset AF (NOAF) / Trigger-Induced AF:
  • The 2024 ESC Guidelines provide a specific recommendation: “Long-term oral anticoagulation should be considered in suitable patients with trigger-induced AF at elevated thromboembolic risk to prevent ischaemic stroke and systemic thromboembolism.” (Class IIa, Level C) [ESC 2024]
  • However, in the acute phase of critical illness:
    • The risk of bleeding from anticoagulation may outweigh the benefit.
    • Retrospective studies suggest that anticoagulation for AF secondary to critical illness increases bleeding risk without reducing stroke.
    • A survey of UK intensivists found that most (64%) don’t routinely anticoagulate patients with new-onset AF.
    • The Canadian 2020 guidelines state: “In some cases, such as sepsis, the acute administration of intravenous anticoagulation increases the risk of bleeding, but does not appear to reduce the risk of ischemic events.” 

    Key point: If AF persists for weeks (e.g., persists after the acute critical illness resolves), the risk-benefit balance shifts, and long-term OAC should be considered.

• Chronic AF:
  • For patients who appear to have chronic AF, anticoagulation may be considered similarly to that of outpatients (e.g., based on CHA₂DS₂-VA scores).
  • Among patients with long-standing AF who have been previously on anticoagulation, this will often be continued (unless it is necessary to hold it for a procedure or bleeding).

Choice of anticoagulation

◾️DOAC

• Most patients should receive a DOAC (apixaban, dabigatran, edoxaban, or rivaroxaban) in preference to warfarin when OAC therapy is indicated for patients with non-valvular AF.
• DOACs include either direct thrombin inhibitors (dabigatran) or Factor Xa inhibitors (apixaban, edoxaban, rivaroxaban).
• DOACs have largely replaced warfarin due to their ease of use, which includes the elimination of bridging, monitoring, and dietary restrictions. Concerns regarding the current inability to reverse DOACs in case of bleeding have gradually decreased given the continued introduction of reversal agents.
• Dosing is dependent on and may be limited by the patient’s renal and hepatic function (see table 2 below).

◾️Warfarin

• It should be used for patients with a mechanical prosthetic valve and those with AF and moderate to severe mitral stenosis (when indicated).
• Initiate warfarin: 5 mg daily; (1–2 mg daily if frail, low weight, Asian descent).
• Heparin bridging not required unless TEE-guided CV.
• Arrange for INR blood test and review after 3 or 4 doses of warfarin. Subsequent warfarin doses should be communicated to the patient on the day of the INR test.

---

---

Atrial Flutter

Atrial flutter (AFL) is among the most common atrial tachyarrhythmias in the ICU. It often represents a transitional state, as the atria is deciding whether to settle down into sinus rhythm or atrial fibrillation. Over half of all patients with AFL will develop AF *.

◾️Epidemiology and Risk:

• AFL has an overall incidence rate of 88 per 100,000 person-years, rising to 317 per 100,000 person-years in people over 50 years of age *.
• Risk factors for AFL and AF are similar.
• Observational studies suggest that thromboembolic risk is elevated in AFL *.
• In direct comparison of AFL with AF, some studies suggest a similar risk of stroke and others a lower risk in AFL, possibly due to different comorbidity burdens and the impact of confounders such as AFL/AF ablation and anticoagulation *.

◾️Diagnosis:

• ECG Features:
  • Typical AFL (cavo-tricuspid isthmus-dependent): Characteristic “sawtooth” flutter waves (best seen in inferior leads II, III, aVF) at a rate of ~300 bpm with 2:1 AV conduction producing a ventricular rate of ~150 bpm.
  • Atypical AFL: May have variable flutter wave morphology and rates; often occurs after cardiac surgery or catheter ablation.
• Key Point: The heart rate in AFL tends to get “stuck” at ~150 bpm (2:1 conduction through the AV node). This can make rate control challenging.

◾️Thromboembolic Risk and Anticoagulation:

• Oral anticoagulation is recommended in patients with atrial flutter at elevated thromboembolic risk to prevent ischaemic stroke and thromboembolism (Class I, Level B) *.
• Anticoagulation management is modeled off the treatment of atrial fibrillation, although the thromboembolic risk may be lower than with AF *.
• If AFL is a transient episode in the context of critical illness, follow the same principles as for trigger-induced AF (see Anticoagulation section).

Management of Atrial Flutter:

1. Rate Control:

• Rate control in AFL is often difficult because the AV node is bombarded with atrial impulses at ~300 bpm, resulting in a ventricular rate that is stubbornly stuck at ~150 bpm (2:1 conduction).
• Attempts to slow the ventricular rate with AV nodal blockers (beta-blockers, diltiazem, digoxin) may be challenging and often require high doses.
• Key Point: If rate control is proving difficult, consider that the rhythm may be AFL rather than AF. This is a clue to pursue rhythm control.

2. Rhythm Control:

• Rhythm control is more effective than rate control in AFL.
• Electrical Cardioversion: Highly effective. Consider this option if the patient is hemodynamically unstable or if sedation can be safely administered.
• Ibutilide: Generally effective for pharmacological cardioversion of AFL. Aggressive magnesium loading before ibutilide improves its safety and efficacy.
  • Dosing: 1 mg infused over 10 minutes (or 0.01 mg/kg for <60 kg), can be repeated once.
  • Contraindications: QT prolongation, hypokalemia, hypomagnesemia, EF <30%, or severe LV hypertrophy.
• Amiodarone: Less effective than ibutilide for acute cardioversion of AFL, but it does help control the ventricular rate. It may be useful for rhythm control if other agents are contraindicated or if AF is also present.

3. Catheter Ablation:

• Cavo-tricuspid isthmus (CTI) ablation is the definitive treatment for typical AFL.
• Recurrence of AFL is uncommon after achieving and confirming bidirectional block in typical CTI-dependent AFL.
• However, the majority of patients (50-70%) will develop AF during long-term follow-up after AFL ablation *.
• In the ICU, catheter ablation is rarely an acute option but should be considered for patients with recurrent AFL who survive their critical illness.

---

---

Back to drawing case

Immediate trial of DC cardioversion with 200J by biphasic machine followed by second and third shocks was unsuccessful!

POCUS shows bilateral B-profile suggestive of pulmonary edema and moderate pleural effusion as well as massive ascites.

• Further investigation reveals that the patient has received six liters of fluid initially, and has been running net positive 3 liters daily since then (for a total of about 10 liters net positive).

Following administration of PUSH dose phenylephrine, hemodynamically neutral intubation was performed, and the patient was hooked to a mechanical ventilator. After 12 hours of resuscitative measures including ventilation and hemodynamic support, atrial fibrillation converted to sinus rhythm!

⭐️Key Takeaway: AF was an innocent bystander driven by volume overload. Treating the underlying cause (diuresis, respiratory support) was more important than rhythm or rate control.

---

---

RECAP

• Do NOT fall into a trap of AF with RVR in hypotensive patients; assuming that AF is the cause of instability. In some patients, this may be a “sinus tach equivalent” which is due to an underlying problem (e.g. sepsis, PE). Merely trying to slow down the heart rate can be dangerous among these patients, as it may suppress a compensatory tachycardia. 👉Avoid rate control before addressing and treating the underlying etiology. [34]

• In patients with AF and shock, always look for other causes of hemodynamic instability. One helpful clue is that if the HR is <150, the hypotension is likely caused by something other than the arrhythmia. If the HR is >150, the arrhythmia is more likely to be the culprit. Other helpful clues are summarized in Table 1.

• If another cause of shock is identified (e.g., hypovolemia, hemorrhage, sepsis, PE, etc.), treat the underlying cause; treating the compensatory tachycardia may worsen the situation.

• ACLS guidelines typically recommend immediate cardioversion for unstable patients with AF. However, among critically ill patients this has a low success rate. Support the hemodynamic and treat the inciting factors!

• Be aware of AF in WPW. If your patient has HR>250 and irregular (in rate and shape and amplitude) wide complex tachycardia, think WPW and avoid nodal block medication. Immediate DC cardioversion is advised.

• For stable patients, consider a wait-and-see approach for spontaneous conversion within 48 hours. This avoids the risks of sedation and procedural complications.

• Early rhythm control (within 12 months of diagnosis) should be considered in selected patients at risk of thromboembolic events. This is supported by the EAST-AFNET 4 trial and ESC 2024 guidelines.

---

AF Tool

The American College of Emergency Physicians “AF Tool”, exists as a valuable guide for the care of ED patients with AF.

---

Media

Atrial fibrillation on echo

---

10 simple rules of atrial fibrillation on echo

Primary AF causing functional MR

---

Post Peer Reviewed By: Mojtaba Chardoli.

Further going

• Treatment of hemodynamically stable new-onset AF in critical illness (PULMCRIT)
• The Crashing Atrial Fibrillation Patient (EMCrit)
• Approach to shocky patient in AF with RVR (PulmCrit)

References

Expand to view the references list

1. Andrade J, Khairy P, Dobrev D, Nattel S. The clinical profile and pathophysiology of atrial fibrillation: relationships among clinical features, epidemiology, and mechanisms. Circ Res. 2014 Apr 25;114(9):1453-68. doi: 10.1161/CIRCRESAHA.114.303211. PMID: 24763464
2. Hindricks G, Potpara T, Dagres N, Arbelo E, Bax JJ, Blomström-Lundqvist C, Boriani G, Castella M, Dan GA, Dilaveris PE, Fauchier L, Filippatos G, Kalman JM, La Meir M, Lane DA, Lebeau JP, Lettino M, Lip GYH, Pinto FJ, Thomas GN, Valgimigli M, Van Gelder IC, Van Putte BP, Watkins CL; ESC Scientific Document Group. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS): The Task Force for the diagnosis and management of atrial fibrillation of the European Society of Cardiology (ESC) Developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC. Eur Heart J. 2021 Feb 1;42(5):373-498. doi: 10.1093/eurheartj/ehaa612. Erratum in: Eur Heart J. 2021 Feb 1;42(5):507. Erratum in: Eur Heart J. 2021 Feb 1;42(5):546-547. Erratum in: Eur Heart J. 2021 Oct 21;42(40):4194. PMID: 32860505
3. Oishi ML, Xing S. Atrial fibrillation: management strategies in the emergency department. Emerg Med Pract. 2013 Feb;15(2):1-26; quiz 27. Epub 2013 Jan 20. PMID: 23369365
4. Andrade JG, Aguilar M, Atzema C, Bell A, Cairns JA, Cheung CC, Cox JL, Dorian P, Gladstone DJ, Healey JS, Khairy P, Leblanc K, McMurtry MS, Mitchell LB, Nair GM, Nattel S, Parkash R, Pilote L, Sandhu RK, Sarrazin JF, 5. Sharma M, Skanes AC, Talajic M, Tsang TSM, Verma A, Verma S, Whitlock R, Wyse DG, Macle L; Members of the Secondary Panel. The 2020 Canadian Cardiovascular Society/Canadian Heart Rhythm Society Comprehensive Guidelines for the Management of Atrial Fibrillation. Can J Cardiol. 2020 Dec;36(12):1847-1948. doi: 10.1016/j.cjca.2020.09.001. Epub 2020 Oct 22. PMID: 33191198
5. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr, Conti JB, Ellinor PT, Ezekowitz MD, Field ME, Murray KT, Sacco RL, Stevenson WG, Tchou PJ, Tracy CM, Yancy CW; ACC/AHA Task Force Members. 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. Circulation. 2014 Dec 2;130(23):e199-267. doi: 10.1161/CIR.0000000000000041. Epub 2014 Mar 28. Erratum in: Circulation. 2014 Dec 2;130(23):e272-4. PMID: 24682347; PMCID: PMC4676081
6. Silverman A, Taneja S, Benchetrit L, Makusha P, McNamara RL, Pine AB. Atrial Fibrillation in a Patient With an Accessory Pathway. J Investig Med High Impact Case Rep. 2018;6:2324709618802870. Published 2018 Sep 28. doi:10.1177/2324709618802870 
7. Manne JRR. Regularized Atrial Fibrillation. Am J Med. 2018 Sep;131(9):e361-e363. doi: 10.1016/j.amjmed.2018.04.010. Epub 2018 May 1. PMID: 29723516
8. Bosch NA, Cimini J, Walkey AJ. Atrial Fibrillation in the ICU. Chest. 2018 Dec;154(6):1424-1434. doi: 10.1016/j.chest.2018.03.040. Epub 2018 Apr 6. PMID: 29627355; PMCID: PMC6335260
9. Arunachalam K, Kalyan Sundaram A, Jha K, Thakur L, Pond K. Evaluation of Anticoagulation Practice With New-Onset Atrial Fibrillation in Patients with Sepsis and Septic Shock in Medical Intensive Care Unit: A Retrospective Observational Cohort Study. Cureus. 2020 Aug 25;12(8):e10026. doi: 10.7759/cureus.10026. PMID: 32983720; PMCID: PMC7515803
10. Yoshida T, Fujii T, Uchino S, Takinami M. Epidemiology, prevention, and treatment of new-onset atrial fibrillation in critically ill: a systematic review. Journal of Intensive Care. 2015 ;3(1):19. DOI: 10.1186/s40560-015-0085-4. PMID: 25914828; PMCID: PMC4410002. 
11. Wetterslev M, Haase N, Hassager C, Belley-Cote EP, McIntyre WF, An Y, Shen J, Cavalcanti AB, Zampieri FG, Guimaraes HP, Granholm A, Perner A, Møller MH. New-onset atrial fibrillation in adult critically ill patients: a scoping review. Intensive Care Med. 2019 Jul;45(7):928-938. doi: 10.1007/s00134-019-05633-x. Epub 2019 May 14. PMID: 31089761.
12. Walkey AJ, Hammill BG, Curtis LH, Benjamin EJ. Long-term outcomes following development of new-onset atrial fibrillation during sepsis. Chest. 2014 Nov;146(5):1187-1195. doi: 10.1378/chest.14-0003. PMID: 24723004; PMCID: PMC4219336
13. Topaz G, Flint N, Steinvil A, Finkelstein A, Banai S, Keren G, Shacham Y, Yankelson L. Long term prognosis of atrial fibrillation in ST-elevation myocardial infarction patients undergoing percutaneous coronary intervention. Int J Cardiol. 2017 Aug 1;240:228-233. doi: 10.1016/j.ijcard.2017.03.060. Epub 2017 Mar 16. PMID: 28390742
14. Kihara T, Gillinov AM, Takasaki K, Fukuda S, Song JM, Shiota M, Shiota T. Mitral regurgitation associated with mitral annular dilation in patients with lone atrial fibrillation: an echocardiographic study. Echocardiography. 2009 Sep;26(8):885-9. doi: 10.1111/j.1540-8175.2009.00904.x. Epub 2009 Jun 22. PMID: 19552671
15. Arrigo M, Bettex D, Rudiger A. Management of atrial fibrillation in critically ill patients. Crit Care Res Pract. 2014;2014:840615. doi:10.1155/2014/840615
16. Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, Passman RS, White RD, Hess EP, Tang W, Davis D, Sinz E, Morrison LJ. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov 2;122(18 Suppl 3):S729-67. doi: 10.1161/CIRCULATIONAHA.110.970988. Erratum in: Circulation. 2011 Feb 15;123(6):e236. Erratum in: Circulation. 2013 Dec 24;128(25):e480. PMID: 20956224.
17. 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 Jun;27(3):326.e1-8. doi: 10.1016/j.jcrc.2011.10.011. Epub 2012 Jan 4. PMID: 22226423
18. Mayr A, Ritsch N, Knotzer H, Dünser M, Schobersberger W, Ulmer H, Mutz N, Hasibeder W. Effectiveness of direct-current cardioversion for treatment of supraventricular tachyarrhythmias, in particular atrial fibrillation, in surgical intensive care patients. Crit Care Med. 2003 Feb;31(2):401-5. doi: 10.1097/01.CCM.0000048627.39686.79. PMID: 12576943
19. Van Gelder IC, Groenveld HF, Crijns HJ, Tuininga YS, Tijssen JG, Alings AM, Hillege HL, Bergsma-Kadijk JA, Cornel JH, Kamp O, Tukkie R, Bosker HA, Van Veldhuisen DJ, Van den Berg MP; RACE II Investigators. Lenient versus strict rate control in patients with atrial fibrillation. N Engl J Med. 2010 Apr 15;362(15):1363-73. doi: 10.1056/NEJMoa1001337. Epub 2010 Mar 15. PMID: 20231232.
20. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr, Conti JB, Ellinor PT, Ezekowitz MD, Field ME, Murray KT, Sacco RL, Stevenson WG, Tchou PJ, Tracy CM, Yancy CW; ACC/AHA Task Force Members. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society. Circulation. 2014 Dec 2;130(23):2071-104. doi: 10.1161/CIR.0000000000000040. Epub 2014 Mar 28. Erratum in: Circulation. 2014 Dec 2;130(23):e270-1. PMID: 24682348
21. Salerno DM, Dias VC, Kleiger RE, Tschida VH, Sung RJ, Sami M, Giorgi LV. Efficacy and safety of intravenous diltiazem for treatment of atrial fibrillation and atrial flutter. The Diltiazem-Atrial Fibrillation/Flutter Study Group. Am J Cardiol. 1989 May 1;63(15):1046-51. doi: 10.1016/0002-9149(89)90076-3. PMID: 2650517.
22. Pawlosky N, Macdonald E, Patel R, Kanji S. Evaluation of digoxin concentration after loading dose in patients with renal dysfunction. Can J Hosp Pharm. 2013 Mar;66(2):104-9. doi: 10.4212/cjhp.v66i2.1232. PMID: 23616674; PMCID: PMC3633494
23. Moran JL, Gallagher J, Peake SL, Cunningham DN, Salagaras M, Leppard P. Parenteral magnesium sulfate versus amiodarone in the therapy of atrial tachyarrhythmias: a prospective, randomized study. Crit Care Med. 1995 Nov;23(11):1816-24. doi: 10.1097/00003246-199511000-00005. PMID: 7587256
24. O’Bryan LJ, Redfern OC, Bedford J, Petrinic T, Young JD, Watkinson PJ. Managing new-onset atrial fibrillation in critically ill patients: a systematic narrative review. BMJ Open. 2020 Mar 24;10(3):e034774. doi: 10.1136/bmjopen-2019-034774. PMID: 32209631; PMCID: PMC7202704.
25. Malviya A, Kapoor M, Sivam RKN, Khan SA, Pandey R, Kumar U, Ete T, Mishra A. Ibutilide with magnesium for conversion of atrial fibrillation or flutter in rheumatic heart disease patients: Ibutilide with magnesium for chemical cardioversion of atrial fibrillation or flutter. Indian Heart J. 2020 Jul-Aug;72(4):283-288. doi: 10.1016/j.ihj.2020.07.008. Epub 2020 Jul 15. PMID: 32861384; PMCID: PMC7474117
26. Sultan A, Steven D, Rostock T, Hoffmann B, Müllerleile K, Servatius H, Drewitz I, Lüker J, Meyer P, Salukhe T, Willems S. Intravenous administration of magnesium and potassium solution lowers energy levels and increases success rates electrically cardioverting atrial fibrillation. J Cardiovasc Electrophysiol. 2012 Jan;23(1):54-9. doi: 10.1111/j.1540-8167.2011.02146.x. Epub 2011 Aug 4. PMID: 21815963
27. Ganga HV, Noyes A, White CM, Kluger J. Magnesium adjunctive therapy in atrial arrhythmias. Pacing Clin Electrophysiol. 2013 Oct;36(10):1308-18. doi: 10.1111/pace.12189. Epub 2013 Jun 3. PMID: 23731344
28. Davey MJ, Teubner D. A randomized controlled trial of magnesium sulfate, in addition to usual care, for rate control in atrial fibrillation. Ann Emerg Med. 2005 Apr;45(4):347-53. doi: 10.1016/j.annemergmed.2004.09.013. PMID: 15795711.
29. Sleeswijk ME, Tulleken JE, Van Noord T, Meertens JH, Ligtenberg JJ, Zijlstra JG. Efficacy of magnesium-amiodarone step-up scheme in critically ill patients with new-onset atrial fibrillation: a prospective observational study. J Intensive Care Med. 2008 Jan-Feb;23(1):61-6. doi: 10.1177/0885066607310181. PMID: 18320707
30. Slavik RS, Tisdale JE, Borzak S. Pharmacologic conversion of atrial fibrillation: a systematic review of available evidence. Prog Cardiovasc Dis. 2001 Sep-Oct;44(2):121-52. doi: 10.1053/pcad.2001.26966. PMID: 11568824.
31. Stambler BS, Wood MA, Ellenbogen KA. Antiarrhythmic actions of intravenous ibutilide compared with procainamide during human atrial flutter and fibrillation: electrophysiological determinants of enhanced conversion efficacy. Circulation. 1997 Dec 16;96(12):4298-306. doi: 10.1161/01.cir.96.12.4298. PMID: 9416896
32. Volgman AS, Carberry PA, Stambler B, Lewis WR, Dunn GH, Perry KT, Vanderlugt JT, Kowey PR. Conversion efficacy and safety of intravenous ibutilide compared with intravenous procainamide in patients with atrial flutter or fibrillation. J Am Coll Cardiol. 1998 May;31(6):1414-9. doi: 10.1016/s0735-1097(98)00078-3. PMID: 9581743.
33. Kirkland S, Stiell I, AlShawabkeh T, Campbell S, Dickinson G, Rowe BH. The efficacy of pad placement for electrical cardioversion of atrial fibrillation/flutter: a systematic review. Acad Emerg Med. 2014 Jul;21(7):717-26. doi: 10.1111/acem.12407. Epub 2014 Aug 12. PMID: 25117151
34. Stiell IG, de Wit K, Scheuermeyer FX, Vadeboncoeur A, Angaran P, Eagles D, Graham ID, Atzema CL, Archambault PM, Tebbenham T, McRae AD, Cheung WJ, Parkash R, Deyell MW, Baril G, Mann R, Sahsi R, Upadhye S, Brown E, Brinkhurst J, Chabot C, Skanes A. 2021 CAEP Acute Atrial Fibrillation/Flutter Best Practices Checklist. CJEM. 2021 Sep;23(5):604-610. doi: 10.1007/s43678-021-00167-y. Epub 2021 Aug 12. PMID: 34383280; PMCID: PMC8423652
35. PMID: 39210723. Van Gelder IC, Rienstra M, et al; ESC Scientific Document Group. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2024 Sep 29;45(36):3314-3414. doi: 10.1093/eurheartj/ehae176. Erratum in: Eur Heart J. 2025 Nov 3;46(41):4349. doi: 10.1093/eurheartj/ehaf306.