(1)
Division of Pulmonary and Critical Care Medicine, Eastern Virginia Medical School, Norfolk, VA, USA
Keywords
Atrial fibrillationArrhythmiasVentricular tachycardiaVentricular fibrillationMagnesiumDiltiazemCardioversionSupraventricular tachycardiaRate controlSustained arrhythmias occur in approximately 10–15 % of general ICU patients [1, 2]. As a general rule the development of arrhythmias is a reflection of the severity of the underlying disease and they do not appear to be independent predictors of death, although they increase the risk of neurological sequela. Atrial arrhythmias (atrial fibrillation/flutter) are the most common arrhythmia. AF/Aflutter are usually secondary to the underlying disease process (respiratory failure), while ventricular arrhythmias are usually due to preexistent cardiac disease or acute ischemia. Atrial arrhythmias are usually the consequence of acute respiratory failure (acute cor pulmonale-pulmonary hypertension, right ventricular failure and atrial distension) [3]. Left ventricular systolic and diastolic dysfunction (sepsis, ARDS, etc.) as well as abnormalities in fluid balance and electrolytes may contribute to the development of sustained arrhythmias in critically ill ICU patients. The management of arrhythmias in acutely ill ICU patients differs from that of patients with primary cardiac disease. Unfortunately, there is little (if any) evidence based literature to guide the management of these arrhythmias in the ICU.
Arrhythmias and Electrolyte Disturbances
Intravenous magnesium has been used to prevent and treat many different types of cardiac arrhythmia. It has diverse electrophysiological actions on the conduction system of the heart; including prolonging sinus node recovery time, and reducing automaticity, atrioventricular nodal conduction, antegrade and retrograde conduction over an accessory pathway, and His-ventricular conduction. Intravenous magnesium can also homogenize transmural ventricular repolarization. Because of its unique and diverse electrophysiological actions, intravenous magnesium has been reported to be useful in preventing atrial fibrillation and ventricular arrhythmias after cardiac and thoracic surgery; in reducing the ventricular response in acute onset atrial fibrillation, including patients with Wolff-Parkinson-White syndrome; in the treatment of digoxin induced supraventricular and ventricular arrhythmias, multifocal atrial tachycardia, and polymorphic ventricular tachycardia or ventricular fibrillation from drug overdoses [4]. In addition magnesium has synergistic activity when combined with other rate and rhythm controlling drugs [5]. Magnesium sulfate, when used to supplement other standard rate-reduction therapies, enhances rate reduction and conversion to sinus rhythm in patients with rapid atrial fibrillation [6]. Magnesium has a relatively wide toxic/therapeutic window; the most common reported side effects are a transient sensation of warmth and flushing. Magnesium should be considered the “first line” agent for control of arrhythmias in the ICU even in patients with normal serum magnesium (1.6–2.5 mg/dL)… aim to achieve a serum magnesium level of about 2.8–3.0 mg/dL.
Magnesium is the Intensivists anti-arrhythmic agent of first choice!
Hypokalemia causes cellular hyperpolarity, increases resting potential, hastens depolarization, and increases automaticity and excitability. Hypokalemia appears to be a risk factor for the development of both atrial and ventricular arrhythmias. In the Study of Prevention of Postoperative Atrial Fibrillation (SPPAF), the rate of postoperative AF was 51 % in patients with a serum potassium <3.9 mmol/L compared to 33 % in patients with a serum potassium >4.3 mmol/L (p < 0.05) [7].
Acute Atrial Fibrillation/Flutter
Atrial tachyarrhythmias are the commonest arrhythmias occurring in ICU patients, with a reported prevalence of between 6 and 28 % [1, 2, 8, 9]. Atrial fibrillation is the commonest atrial arrhythmia, followed by atrial flutter and multifocal atrial tachycardia (MAT). Since the etiology and management strategies of atrial fibrillation and atrial flutter overlap, for the purposes of this discussion they will be considered one entity (AF). Patients who develop AF have a worse prognosis than those who remain in sinus rhythm (SR); however, the attributable mortality of AF is unclear [8]. Loss of atrioventricular synchrony will compromise stroke volume and cardiac output to a variable degree depend upon ventricular compliance, venous filling pressure, ventricular rate, and other hemodynamic factors. In the study by Annane and colleagues the presence of a supraventricular arrhythmia doubled the risk of a neurological sequelae (OR 2.64; 95 % CI 1.19–5.84) [1].
AF is particularly common in ICU patients with cardiovascular disorders, respiratory failure and sepsis. The etiology is largely multifactorial with hypoxia, electrolyte disturbance, myocardial ischemia, increased sympathetic tone and atrial distention being implicated. Pulmonary hypertension with right atrial distension may be an important precipitant in patients with respiratory failure and sepsis.
The components of the acute management of AF include;
assessment of the need for urgent cardioversion
correct treatable precipitating factors
control the ventricular response rate
prophylaxis against thromboembolic events in those patients who remain in AF
Drugs such as dopamine should be stopped. Pain and anxiety, which increases sympathetic activity, should be treated. New onset atrial fibrillation may occur in patients with pulmonary embolism; this diagnosis should be considered.
Urgent Cardioversion
Electrical cardioversion is a time-honored highly effective method for converting AF to sinus rhythm. Urgent cardioversion is indicated when the ventricular response is greater than 130/beats/min in association with:
angina/myocardial ischemia on ECG
acute cardiac failure
hypotension (MAP < 70 mmHg or fall in MAP > 15 mmHg)
indices of inadequate tissue perfusion
Rate Control
Rate control can improve hemodynamics even if the patient remains in AF. Digoxin is commonly used in the treatment of AF in ICU patients. Yet, in the critically ill ICU patient digoxin is probably the least effective drug in controlling the ventricular response in AF. Digoxin decreases ventricular response in AF by vagotonic mechanisms. In critically ill patients, AF occurs in the setting of high sympathetic tone and frequently with the use of vasopressors and inotropic agents, a situation in which digoxin is likely to be ineffective. In addition, this drug has a very narrow therapeutic index and should be avoided except in patients with poor LV function.
Diltiazem is an effective agent for rate control in most patients with a response rate of between 93 and 97 %. Diltiazem is given as a 5 mg bolus every 5 min until rate control is achieved or a maximal dose of 15 mg is administered, followed by an infusion of up to 15 mg/h. Esmolol, an ultrashort acting selective beta-blocker has been demonstrated to be effective in controlling the ventricular response in AF. Similarly, IV metoprolol (5 mg boluses) may used for rate control. However, beta-blockers may cause hypotension particularly in patients with poor LV function. Amiodarone (or digoxin) may be used for rate control in patients with poor LV function. Magnesium has been shown to reduce the ventricular response in AF, with a greater effect when combined with digoxin. Magnesium may act by increasing the atrio-His interval and atrioventricular nodal refractoriness.
Digoxin and calcium channel blockers should not be given to patients who have atrial fibrillation with an anterogradely conducting accessory pathway, because blocking atrioventricular nodal conduction may provoke conduction down the accessory pathway, leading to an increase rather than decrease in the ventricular rate and hemodynamic collapse.
Pharmacologic Cardioversion
A number of randomized controlled studies (RCT’s) have evaluated procainamide, amiodarone, flecainide, sotalol, propafenone and ibutilide in patients presenting to hospital with acute atrial fibrillation (non-ICU setting). In general these studies have found the rate of conversion to be similar with the antiarrhythmic drug as with placebo, with approximately 60 % of patients spontaneously converting to sinus rhythm within 24 h [10]. The natural history of AF in acutely ill ICU patients has not been studied. However, it is likely that untreated the arrhythmia will persist until the underlying medical condition which precipitated the arrhythmia has improved or resolved. The role of anti-arrhythmic agents in facilitating pharmacological cardioversion is unclear; however it would appear that these agents have a limited role in the critically ill patient. Amiodarone is the agent most commonly used to facilitate cardioversion in the ICU. Amiodarone is not without risks, with hypotension and bradycardia being the most common adverse events, usually occurring during the loading infusion. Acute hepatotoxicity with liver function test abnormalities has been reported in 9–17 % of patients Amiodarone has also been associated with acute pulmonary toxicity presenting as ARDS. High inspired oxygen concentration and pre-existing ARDS may be risk factors for acute amiodarone pulmonary toxicity. Sleeswijk et al. reported the efficacy of a magnesium-amiodarone step-up scheme in critically ill patients with new-onset atrial fibrillation [11]. A MgSO4 bolus (0.037 g/kg body weight in 15 min) was followed by continuous infusion (0.025 g/kg body weight/h) [bolus of 2–3 g followed by infusion at 2 g/h in 70 kg patient]. Intravenous amiodarone (loading dose 300 mg, followed by continuous infusion of 1,200 mg/24 h) was given to those not responding to MgSO4 within 1 h. Clinical response was defined as conversion to sinus rhythm or decrease in heart rate <110 beats/min. Sixteen of the 29 patients responded to MgSO4 monotherapy, whereas the addition of amiodarone was required in 13 patients. Median time until conversion to sinus rhythm after MgSO4 was 2 h while the median conversion time in patients requiring amiodarone was 4 h. The 24-h conversion rate was 90 %. As this approach obviates the need for anticoagulation, it may be the preferable approach to AF in ICU patients. Kanji et al. determined the outcome of patients in a mixed ICU who had preexistent AF (186 pts) or developed new onset AF (139 pts) in the ICU (10.5 % of all patients) [9]. Hemodynamic instability developed in 37 % of patients with new-onset AF with pharmacologic rhythm conversion was attempted in 76 % those with new-onset AF. Although initially successful in 87 % of new-onset cases, 42 % reverted back to AF. Only 18 % of patients with new-onset AF who survived to ICU discharge left the ICU in AF.