Acute
Thromboembolic events, including stroke
Myocardial infarction
Cardiogenic shock
Acute renal failure
Ventricular tachycardia/fibrillation
Syncope
Subacute
Cognitive dysfunction
Diminished quality of life
Chronic renal failure
Peripheral edema
Tachycardia-mediated cardiomyopathy
Chronic
Stasis ulcers
Shortened life span
Diminished exercise capacity
Depression
Anxiety
Etiologies
There are several conditions associated with both AF [14] and HF [15] such as essential hypertension, diabetes mellitus, coronary heart disease, valvular heart disease, dilated and hypertrophic cardiomyopathies, and bronchopulmonary disease. Most importantly, both AF and HF are risk factors for the development of each other (Table 20.2).
Table 20.2
Common and overlapping conditions associated with AF and HF
Toxins (alcohol, cocaine) Anemia |
Coronary heart disease Chronic kidney disease |
Valvular heart disease |
Cardiomyopathies (dilated, hypertrophic, tachycardia mediated) |
Pericardial disease Constrictive/restrictive myocardial processes Diabetes mellitus |
Essential hypertension |
Bronchopulmonary disease |
Thyroid abnormalities |
Obesity |
Stress/elevated catecholamines |
Metabolic disturbances |
Cardiac and non-cardiac surgeries Congenital heart disease Sleep apnea Smoking Sepsis/systemic infection |
Patient Evaluation
History and Presentation
The presenting symptoms for AF and HF are relatively similar and nonspecific. Typical symptoms of AF include chest pain, light-headedness, fatigue, palpitations, nausea, and dyspnea [16]. The most common symptoms and signs of HF include dyspnea, peripheral edema, cough, orthopnea, chest pain, weakness, nausea/vomiting, and fatigue [17]. The characteristic electrocardiogram (ECG) findings of AF, along with an irregular pulse, are likely to be recognized early on in patients presenting with AF and HF. Once AF is recognized and assuming the patient is not unstable, there are several useful pieces of historical information to obtain. First, it is helpful to ascertain the history of the patient’s current symptoms with a focus on whether or not the AF is a long-standing condition or new in the onset (e.g., <48 h), and whether or not the onset can be accurately identified. In patients with prior episodes of AF, a quick investigation of past ED treatment approaches may also be useful. If HF is suspected clinically, then it is important to gather information regarding prior episodes, potential precipitating factors such as diet, medication omissions/errors, and echocardiogram results (e.g., does the patient have primarily systolic or diastolic dysfunction). Lastly, other comorbidities and current medications the patient is taking, including anticoagulant, antiplatelet, and other cardiovascular (e.g., beta-blockers, digoxin, calcium channel blockers) medications, will help inform subsequent decision-making.
With or without concomitant HF, AF presentations have been categorized in numerous ways such as asymptomatic, paroxysmal, persistent, permanent, perioperative, lone, and recurrent (Table 20.3) [14]. All of these categories refer to the timing of onset and/or duration of AF. For patients not requiring urgent cardioversion due to instability, the duration of AF is the most important factor in determining whether chemical or electrical cardioversion can be safely attempted in the ED.
Table 20.3
Types of AF
AF type | Definition |
---|---|
Asymptomatic | AF without symptoms or patient awareness |
Paroxysmal | A self-limited AF episode lasting <7 days |
Persistent | AF continuing >7 days |
Permanent | AF lasting >1 year or with cardioversion that has failed or not been tried |
Perioperative | AF developing within 48 h after cardiac surgery |
Lone | AF not caused by underlying heart disease |
Recurrent | Having a history of two or more independent episodes of AF |
Exam
For any patient with AF and HF, acquiring vital signs on presentation, setting up critical care monitoring, obtaining IV access, and performing a rapid exam are central to the initial assessment. The focus for patients with AF and HF needs to first be directed at determining if there are signs of instability such as hypotension, respiratory failure, ischemic chest pain, severe HF, or altered mental status. If these, or other signs of instability, are present and the patient is experiencing a rapid heart rate due to AF, then urgent synchronized cardioversion based on advanced cardiac life support [18] (see below) is indicated. At the same time, if HF is felt to be playing a significant role in the patient’s presentation, then respiratory and pharmacologic therapies directed at the HF should be started. If the patient is stable, a thorough exam focusing on mental acuity, neurologic status, heart and lung auscultation, the abdomen, peripheral perfusion, and edema should be undertaken. Paying particular attention to the heart exam may uncover significant valvular disease, which may be contributing to the present symptoms.
Diagnostic Testing
For many patients who meet the clinical criteria for AF and HF, more than one underlying disorder may be contributing to the patients presenting symptoms. Thorough appreciation of all the underlying causes for the patient’s signs and symptoms requires a careful diagnostic workup to achieve the best possible outcomes. In general, the diagnostic testing in patients with AF and HF does not differ significantly from that of patients with HF alone. All patients should receive an electrocardiogram (ECG), cardiopulmonary monitoring, and a chest X-ray on arrival. On the ECG, you would look for the abnormalities such as the characteristic findings of AF, evidence of ischemia, and signs of preexcitation. Laboratory tests may vary with suspicion of certain etiologies for AF and HF but often will include basic hematology tests, serum markers of myocardial injury, a natriuretic peptide, electrolytes, and kidney function. Thyroid function tests, which may often be considered, have been found to be abnormal in many patients with AF but are only rarely (<1 % in a large registry [16]) felt to be the cause of the AF itself. In patients where there are concerns based on history, exam, or ECG for ongoing myocardial ischemia, valvular disease, or pericardial effusion, it may be useful to obtain an urgent echocardiogram in the ED.
Treatment of Symptomatic Patients with Atrial Fibrillation and Heart Failure
Hemodynamically Unstable Patient
The hemodynamically unstable patient with AF and HF needs urgent cardioversion if the instability is felt to be due to AF-mediated tachycardia. Significant acute HF may be a sign of instability in the AF patient regardless of whether the AF caused the HF or vice versa. In either case, converting the AF to sinus rhythm, even transiently, may normalize vital signs and facilitate treatment of the HF.
The preparation for emergent cardioversion includes administering analgesics and sedatives when possible. However, if the patient is suffering a severe decompensation, this step may have to be omitted. In addition for patients whose AF has lasted ≥48 h, intravenous heparin should be administered at the time of cardioversion and continued after the procedure as a bridge to 4 weeks of total anticoagulation [14]. The placement of the defibrillator pads is somewhat controversial but the anterior–posterior position is likely to be the most efficacious in the majority of AF patients [19]. The amount of energy required to convert the patient to sinus rhythm from AF is generally higher than that for atrial flutter [14] and also varies depending on whether the defibrillator is monophasic or biphasic. For monophasic, 200 J is a reasonable starting point, whereas for biphasic, 100 J is likely to be effective [14, 20, 21]. For patients with implanted pacemakers, cardioversion can proceed as usual, but care should be taken to avoid placing the defibrillator pad over the generator [14]. Although therapy with antiarrhythmic agents prior to cardioversion has been shown to increase efficacy of elective cardioversion [22], in the unstable patient, this is generally not an option.
In the setting of concomitant decompensated HF, the rate of recurrence of AF after successful cardioversion is likely to be high [23], so therapies aimed at improving HF should be started immediately once the patient is more stable. The use of antiarrhythmic agents, such as amiodarone, after cardioversion may help to prevent early recurrence, but in the acute setting, the decision to use these agents should be made on a patient-by-patient basis [14] in conjunction with a consultant.
After cardioversion, in addition to treating underlying HF, it is important to obtain another ECG to evaluate for the presence of an acute coronary syndrome (ACS). Furthermore, this reevaluation should maintain a broad differential diagnosis so as not to miss other contributing conditions such as adverse medication reactions, alcohol or drug toxicity (e.g., digoxin), electrolyte disturbances, valvular heart disease, pulmonary emboli, and sepsis/septic shock.
Hemodynamically Stable Patient with Atrial Fibrillation and Heart Failure
Although HF in the setting of AF can be considered a sign of instability, many cases will be of milder severity and not require urgent cardioversion. These patients may fall into various categories such as rapid AF with mild HF, HF with only a history of AF, or HF and AF without tachycardia. In cases where urgent cardioversion is not needed, strategies to control rate, initiate anticoagulation if indicated, potentially convert the rhythm (electrical or chemical), and treat the underlying HF, will all need to be considered and instituted where appropriate.
Rate Control
Due to the risk of thromboembolism, initial heart rate (HR) control, rather than acute rhythm conversion, is likely to be the preferred treatment in the majority of cases. There are several rate-control agents that may be considered and include digoxin, calcium channel blockers, beta-blockers, and amiodarone. In cases where the onset of the AF episode is not clearly within 48 h, then anticoagulation should be initiated early on unless there is a specific contraindication. A reasonable target for rate control is ≤120 beats/min over the first few hours of treatment [24].
Digoxin
When considering rate control for patients with rapid AF and HF, digoxin may be particularly useful agent as it already has an established role in treating HF [25]. In the AF and HF patient, it may be considered a first-line agent [14, 24] and may be most efficacious when used in conjunction with typical AF rate-control agents, such as beta-blockers and diltiazem [14, 26]. The mechanism by which digoxin slows the HR in AF appears to be due to its effect on increasing vagal activity on the AV node [27–29]. In patients who are not on digoxin, it is administered acutely in a series of loading doses over several hours to approximately 1–1.5 g total dose, depending on clinical response [14, 30].
Several trials have examined digoxin use acutely for rapid AF. In the Digitalis in Acute Atrial Fibrillation (DAAF) trial, 239 patients with rapid AF were randomized to receive either digoxin or placebo and then followed over 16 h to determine the effect on HR and conversion to sinus rhythm [31]. In this trial, digoxin was not found to facilitate conversion to sinus rhythm but had a significant effect on rate at 2 h compared to placebo (mean HR 105 vs. 117 bpm). A smaller randomized trial of digoxin versus placebo for rate control found that digoxin’s ability to slow HR was not evident until over 5 h after the first dose was given [29]. Hou et al. compared the ability of digoxin versus amiodarone to slow HR in patients with AF (approximately half of which had NYHA class IV HF) and found that after 1 h, digoxin slowed HRs approximately 10–15 beats/min compared to 30 for amiodarone. There are a number of conditions that either warrant caution or represent contraindications to the use of digoxin. First, AV nodal blocking agents such as digoxin care contraindicated in situations where a preexcitation syndrome such as Wolff–Parkinson–White is known or suspected. Other situations where digoxin should be used cautiously are with renal impairment, with electrolyte disturbances, and with the risk of toxicity when loading patients already on digoxin [30]. Lastly, digoxin may not work as well in the setting of high sympathetic tone [24, 28].
Calcium Channel Blockers
The calcium channel blockers diltiazem and verapamil have both been studied as agents for rate control in rapid AF. Both agents act within 5–10 min to decrease heart rate [28, 32]. In patients with AF and HF (particularly with a low EF), diltiazem is a better choice than verapamil as it has less of a negative inotropic effect and is less likely to lead to worsening HF and hypotension [15, 27, 28, 33]. Goldenberg et al. examined the effectiveness of diltiazem versus placebo to reduce heart rate in the patient with NYHA grade III or IV HF. In this study, 36/37 patients responded to the diltiazem with reduced rates within a median of 15 min compared to 0/15 placebo patients. Furthermore, there were only three adverse events (hypotension) suggesting that in many patients diltiazem may be safe [34]. Theoretically, the negative inotropic effects of calcium channel antagonists may be offset when these agents are used in combination with digoxin [27], but in patients with acute AF and HF, this has not been established. When compared to digoxin, diltiazem is significantly more efficacious in controlling heart rate over the first few hours of acute treatment [35, 36].
Beta-Blockers
Beta-blockers have a well-established role in the treatment of chronic HF [37]. However, in the presence of acute HF and AF, beta-blockers should be used carefully, if at all, with small incremental dosing [24] and close monitoring of the patient’s vital signs. Demerican et al. compared intravenous metoprolol and diltiazem with regard to slowing HR in patients with rapid AF and found that at 20 min, 80 % of the metoprolol patients had significant HR control versus 90 % in the diltiazem group (defined as either HR <100 or a 20 % decrease from the baseline). Furthermore, at all time points, diltiazem resulted in more HR slowing than metoprolol. However, in this trial, patients with class IV HF were excluded, and it is unclear how much HF was present overall. Where there is concern regarding the negative inotropic effects of beta-blockers in patients with HF, the ultrashort-acting beta-blocker esmolol may be a good choice [38]. Esmolol has a 9-min half-life, and therefore, if it needs to be stopped due to worsening HF or hypotension, its effects will rapidly diminish. It has been used in the setting of rapid AF after coronary artery bypass, where some degree of myocardial dysfunction is likely to be present and appears to be more effective than diltiazem and as safe [39, 40]. Esmolol has also been shown to be safe and effective when used in conjunction with digoxin for rapid AF [26].
Amiodarone
Amiodarone may also be considered for rate control in the AF and HF patient unless they are on other antiarrhythmics that should not be combined with amiodarone [24, 41, 42]. The 2006 AHA/ACC guidelines recommend that amiodarone or digoxin be used to acutely control rate in patients with AF and HF (class I recommendation) [14]. However, as it may facilitate conversion to sinus rhythm, it would ideally be used in cases where the patient either meets anticoagulation guidelines for cardioversion or will be given anticoagulants [24]. Amiodarone is also a common choice of agent to be used to maintain sinus rhythm in the AF and HF patient after cardioversion [14]. Dronedarone is a newer antiarrhythmic drug similar in structure to amiodarone. It has been studied in a number of trials looking at its ability to affect rhythm control for AF over the long term [43–45]. It currently has no role for acute rate or rhythm control. In addition, one clinical trial found excess cardiovascular mortality in a dronedarone-treated group of AF patients with poor left ventricular function (EF ≤35 %) [44].
Summary
In summary, HR control for patients with AF and HF can be approached with the usual medications used in patients without HF provided vital signs are monitored closely [14]. The use of digoxin with other rate-control agents may be beneficial, and amiodarone also has a heightened role in these patients [14]. Diltiazem rather than verapamil would be the best choice if calcium channel blockers are used, and incremental beta-blocker dosing or the use of esmolol may help avoid complications with these agents.
Rhythm Control/Conversion
A recent editorial examining rate versus rhythm-control strategies for AF in the ED [46] concluded that there was not enough evidence to support a rhythm-control strategy as opposed to the standard HR control for new-onset AF in the ED. However, Stiell and others have published on the safety and efficacy of acute cardioversion in the ED for patients with rapid AF, but these studies have excluded patients with more significant HF [47, 48]. Their results suggest that cardioversion of AF alone appears to be safe, and it is likely that at least a small percentage of the patients that have undergone cardioversion have had some degree of HF. It is worth noting, however, that in these studies, an antiarrhythmic agent such as procainamide is often given as a first attempt at cardioversion, which may not be feasible in patients with concomitant acute HF or low blood pressure [49]. This “preloading” with an antiarrhythmic may also be influencing their high success rates of electrical cardioversion.Vernakalant is an investigational, relatively atrial selective, antiarrhythmic agent (approved in Europe but not by the FDA) that appears to be successful in converting AF to sinus rhythm. However, one published ED-based study had only a small minority (≤5 %) of patients with HF [50]. It is worth noting that if pharmacologic agents are given, the risk of thromboembolism and stroke appears to be the same as in patients who receive electrical cardioversion [14].
The main concern with acute rhythm conversion is the risk of thromboembolism, which appears to be the same in patients who receive electrical or chemical cardioversion [14]. However, in carefully selected AF patients (e.g., acute onset <48 h of AF), the risk is very low. 357 patients in one study who were admitted with AF ≤48 h who underwent electrical, chemical, or spontaneous cardioversion were found to have a risk of thromboembolism of less than 1 % [51]. This study did not include any patients with reduced EF where the risk of complications may be higher. As one potential treatment option, it seems reasonable to consider acute rhythm conversion in AF patients who have either a history of HF or milder acute HF. This decision will need to be made on a case-by-case basis taking into account each patient’s presentation, history, anticoagulation status, and personal preferences.
Disposition Decisions
Disposition of the AF and HF patient may include any of the following: hospital admission, short-stay unit (SSU) admission, or discharge to home, rehabilitation hospital, or other extended care facilities including hospice. Despite the fact that acute coronary syndromes rarely present as AF alone [52], most patients with AF and HF are likely to require an admission to the hospital as the presence of both entities complicates their evaluation and treatment (see Fig. 20.1). However, the SSU may have a role in these patients as opportunities to reduce cost and improve the quality of care among Medicare recipients are sought as part of current health reform efforts. Among many others, there is likely to be a focus on strategies that can identify patients who can be managed in a SSU and also prevent repeat ED visits and subsequent readmissions.
Fig. 20.1
Clinical management of patients with AF and HF