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Clinical review: Treatment of new-onset atrial fibrillation in medical intensive care patients: a clinical framework

Critical Care volume 11, Article number: 233 (2007) Cite this article

Abstract

Atrial fibrillation occurs frequently in medical intensive care unit patients. Most intensivists tend to treat this rhythm disorder because they believe it is detrimental. Whether atrial fibrillation contributes to morbidity and/or mortality and whether atrial fibrillation is an epiphenomenon of severe disease, however, are not clear. As a consequence, it is unknown whether treatment of the arrhythmia affects the outcome. Furthermore, if treatment is deemed necessary, it is not known what the best treatment is. We developed a treatment protocol by searching for the best evidence. Because studies in medical intensive care unit patients are scarce, the evidence comes mainly from extrapolation of data derived from other patient groups. We propose a treatment strategy with magnesium infusion followed by amiodarone in case of failure. Although this strategy seems to be effective in both rhythm control and rate control, the mortality remained high. A randomised controlled trial in medical intensive care unit patients with placebo treatment in the control arm is therefore still defendable.

Introduction

Atrial fibrillation (AF) is frequently observed in the medical intensive care unit (MICU) [1], with up to about 15% of MICU patients showing periods of AF [2–4]. AF directly leads to loss of the atrial kick and, as a consequence, reduces ventricular loading. Especially if the ventricular compliance is decreased, as is the case in sepsis and many other medical conditions, this reduction results in decreased cardiac performance. By performance, we mean the capacity to meet pressure and volume requirements. The irregular and mostly rapid ventricular response also shortens the ventricular filling time, and thereby shortens the preload. AF therefore reduces cardiac performance. The reduction is more serious in patients with pre-existing cardiac dysfunction due to decreased ventricular compliance. A persistent high ventricular rate may lead to tachycardia-mediated cardiomyopathy [5]. Conversion to sinus rhythm (SR) improves ventricular function in patients with heart failure [6]. These findings urge most intensivists to treat AF.

Most intensivists may have adopted an AF treatment modality based on their individual experience combined with extrapolation of the treatment of other, mostly unrelated, but well-defined and well-established, patient groups. In most cases this means that, after correction of assumed or perpetuating factors, treatment directly aimed at the rhythm disorder itself will be started. To date, treatment of AF in the MICU cannot be supported by sufficient evidence from the literature. Notwithstanding the large number of patients involved, thorough research in this field is scarce [7]. There are important reasons to believe that MICU patients are different from other patients with AF and therefore require a more tailored therapy. Fundamental questions that remain unanswered for MICU patients are summarised in Table 1.

Table 1 Questions regarding the prevalence and treatment of atrial fibrillation in medical intensive care unit patients
Full size table

To find answers for these questions we searched for direct clinical evidence and – when not available – searched for evidence from related areas. Direct evidence will be considered all results derived from randomised controlled trials or well-conducted epidemiological studies in MICU patients. The aim of the present paper is to improve insight, to explore future research goals and to define an optimal treatment mode based on current knowledge for the population admitted in MICU. We will describe the evidence found per question presented in Table 1 according to the patient group from which it is derived. Each section will start with MICU patients, followed by mixed intensive care unit (ICU) patients, surgical ICU patients and cardiothoracic surgery ICU patients, and will end with the least related patient category – outpatients.

Methodology

We conducted a computer literature search in the databases of MEDLINE, EMBASE and the Cochrane Library, from 1966 to 2007, combining the following key words: 'intensive care' or 'critical care' or 'critically ill' and 'atrial fibrillation' or 'atrial tachyarrhythmia' and 'treatment' or 'aetiology' or 'risk factors'. Reference lists of all selected articles were reviewed to identify other relevant articles. For relevant articles the search was extended in PubMed with the 'related articles' search function. PubMed was checked for other publications by authors of key papers. Web of Science® was checked for papers citing key papers. All selected articles were reviewed by two different reviewers.

Definitions

AF is a supraventricular tachyarrhythmia characterised by uncoordinated atrial activation with subsequent deterioration of atrial mechanical function. On the electrocardiogram, AF is described by the replacement of consistent P waves with rapid oscillations or fibrillatory waves that vary in size, shape and timing, associated with an irregular, frequently rapid, ventricular response when atrioventricular conduction is intact [8]. Recurrent means at least two episodes of AF. Paroxysmal means self-terminating, and persistent means that self-termination is absent and that electrical or pharmacological conversion is necessary to end AF [9]. MICU patients are patients admitted to the ICU not for surgical or cardiological reasons.

What is the pathophysiology of atrial fibrillation?

There are no data on MICU patients specifically, nor data for surgical ICU patients. There are, however, risk factors identified in these patient categories. Risk factors due to causality can in general not be distinguished from epiphenomena. Risk factors can at least suggest a certain pathophysiology, however, and therefore they may help in the identification of a patient population. Independent risk factors for AF are age, disease severity, hypertension, hypoxia, previous AF, congestive heart failure, chronic obstructive pulmonary disease, chest trauma, shock, a pulmonary artery catheter, previous use of calcium-channel blockers, low serum magnesium, withdrawal of β-blocker or angiotensin-converting enzyme-inhibitor and withdrawal of catecholamine use [10–17].

In patients after noncardiac surgery, the right atrial pressure rather than fluid overload or right heart enlargement seems to be correlated with AF [14, 18–20]. Cardiothoracic surgical (CTS) patients with AF, however, tend to have a more positive fluid balance [21, 22]. Interestingly, systemic inflammatory response syndrome and sepsis are also independent risk factors [10, 14]. A proinflammatory state, as measured by leucocytosis or monocyte activation, is associated with AF, although the mechanism is not clear [23–25]. AF is sometimes the first sign of sepsis [4]. A genetic predisposition for an increased inflammatory response is associated with an increased incidence of postoperative AF [26]. Catecholamines influence the susceptibility for AF [10, 27]. Hypovolaemia is also a risk factor [28].

Most knowledge about AF is gained from studies in noncritically ill patients. AF is probably the final common pathway of structural changes in combination with a trigger leading to abnormal activation patterns in the atria [8]. Structural changes can be multiple; for example, fibrosis and amyloidosis. Structural changes increase with age, which might be the explanation for the fact that age is the most important risk factor for AF. There are numerous triggers that can lead to AF when combined with a substrate and a perpetuating factor. Ischaemia, and local (pericarditis or myocarditis) and generalised inflammation can affect the atria [29, 30]. Hypovolaemia and hypervolaemia or a sudden increase in afterload, as in pulmonary embolism, and mitral or tricuspid valve dysfunction are examples of increased atrial workload that can cause AF. Nervous (both sympathic and parasympathic) tone, hormonal changes, electrolyte disturbances and also the preload and the afterload influence excitability and conduction in the atria and atrio–ventricular junction [27]. The cumulative effect of structural changes and one or more of these triggers and perpetuating factors will determine whether AF will occur and will persist [8, 31].

Conclusion on pathophysiology

From human and animal studies it is clear that the cause of AF is multifactorial. There are more or less permanent changes in morphology and more or less temporary changes in haemodynamic balance, electrolyte balance, neural balance and hormonal balance that facilitate an appropriate environment and electrical stage for AF. Given the identified risk factors it is clear that the population admitted to a MICU differs in prevalence of risk factors, and therefore differs in AF mechanism, from other ICU and non-ICU populations. Especially inflammation, haemodynamic changes, increasing age, comorbidity and neuroendocrine disturbances are more frequent in MICU patients. Extrapolation of data from non-MICU patients to MICU patients can only be done with caution.

Does atrial fibrillation attribute to mortality?

AF did not influence mortality significantly in a mixed medical–cardiac ICU [2]. In a general ICU population, however, patients with AF appeared to have a significantly higher mortality compared with patients without AF [3]. Furthermore, surgical patients with new-onset AF have a significantly higher disease severity and higher ICU mortality [4, 11, 32, 33]. A persistent elevated increased heart rate, frequently due to AF, is associated with increased mortality [34]. In a large, retrospective, cohort study in cardiac surgery patients, AF was not an independent predictor for inhospital mortality [35]. Patients outside the ICU setting with AF have increased overall mortality and mortality of cardiovascular causes [36, 37].

Conclusion on mortality

There is an association between AF and mortality in some patient groups. There is, however, no evidence for a causal relationship [38]. Both AF and mortality being a result of disease severity might be one of the explanations for the association [10]. A causal mechanism they have in common (for example, inflammation) might be another explanation.

Does atrial fibrillation attribute to morbidity?

AF did increase the length of stay (LOS) in a mixed medical–cardiac ICU [2]. Onset of AF in a patient in the surgical ICU increases their LOS in the ICU and in the hospital [11, 16, 32, 33, 39, 40]. Onset of AF reduces the systolic blood pressure [41, 42], and also decreases oxygen saturation and increases the pulmonary artery wedge pressure. An increased heart rate is associated with increased morbidity [34].

A number of symptoms in noncritically ill patients have been described [8]. Most relevant for ICU patients is the decreased cardiac output, which is caused by the loss of coordinated atrial contraction, by irregularity of ventricular contraction [43], by inadequate filling time for the left ventricle due to tachycardia, and by tachycardiomyopathy [8, 44]. Tachycardiomyopathy can occur as soon as 24 hours after the start of AF [44].

Conclusion on morbidity

In all patient categories, AF is associated with increased morbidity. This is reflected by the number of reported symptoms and by the days spent in the ICU and in the hospital. Haemodynamic parameters also tend to be worse in patients with AF. As for mortality, the causality of increased morbidity is hard to prove.

Can atrial fibrillation be prevented?

Although advocated in the early days of intensive care, there is no evidence that digoxin or any other antiarrhythmic drug can prevent AF in critically ill patients [41, 45]. There are no trials investigating prevention of AF in MICU patients.

In surgical ICU patients, and especially in CTS patients, there are trials and guidelines evaluating preventive measures [46, 47]. Although prophylactic digoxin, verapamil and β-blockers all decrease the heart rate in cases of postoperative AF, only β-blockers decrease the incidence of postoperative AF as shown in a meta-analysis [48]. In CTS patients, β-blockers can reduce AF by 75% [12].

In randomised controlled trials, amiodarone prevented AF in patients undergoing CTS, and also reduced the hospital LOS and the ICU LOS [49–55]. There is no consensus, however, about the clinical relevance of this finding since data are conflicting [56, 57]. Amiodarone, for example, was found to increase the ICU LOS and the need for vasoactive medication or other haemodynamic support in some studies [13, 58]. More recent meta-analyses show that amiodarone prevents AF but the influence on the LOS or the mortality is not yet unequivocally established [59, 60].

Magnesium and atrial pacing cannot prevent AF in CTS patients, as shown in several randomised controlled trials [13, 52, 61, 62]. In a comparative trial, however, magnesium could prevent AF equally as effectively as sotalol; both drugs combined had a synergistic effect [63]. Amiodarone and magnesium are also synergistic [64], but synergism could not be shown for propranolol and magnesium [65]. Recent meta-analyses show that magnesium can prevent AF but without any effect on the LOS or on the mortality [66, 67]. Cholesterol synthesis inhibitors and corticosteroids also are preventive, perhaps by interaction with inflammatory pathways [68–70].

Studies on prevention have extensively been reviewed recently [15, 59, 60, 71]. Guidelines advise the prophylactic use of β-blocker or amiodarone for elective CTS patients [15, 46, 59, 60]. Generalisation of prevention studies in CTS patients to MICU patients is unproven.

Can atrial fibrillation be treated?

There are no randomised placebo-controlled trials in MICU patients aimed at treating AF once it has occurred. There are, however, comparative trials between drugs that are supposed to be effective. Procainamide and amiodarone are equally effective; after 12 hours, 70% of the patients were in SR [72]. Magnesium, when compared with amiodarone, has been found to be more effective in restoration of SR, while the two treatments are equally effective in rate control [73]. Ibutilide, a relatively new class III agent, can restore SR in 70% of patients that fail rhythm control with amiodarone treatment [74]. Ibutilide can restore SR – with 80% conversion to SR in haemodynamically unstable patients without unmanageable proarrhythmic side effects [75].

In the CTS population, 80% of patients with AF convert to SR within 24 hours. The use of β-blockers before the start of AF and the absence of diabetes and left ventricular hypertrophy were independent predictors of conversion to SR [76]. In a retrospective study of surgical patients with new-onset supraventricular tachycardia (93% with AF), 75% had SR within 48 hours after the start of continuous infusion of amiodarone [77]. In a mixed population with severe left ventricular dysfunction, amiodarone had no apparent negative effect on haemodynamics [78]. When compared with amiodarone, propafenone gives earlier conversion to SR but the ultimate conversion percentage was equal after CTS [79]. Ibutilide showed a dose-dependent conversion rate in a randomised controlled trial [80]. Ibutilide and amiodarone have an equal conversion rate to SR and an equivalent time to conversion, but amiodarone causes more hypotension – probably due to vasodilatation [81, 82]. Direct-current cardioversion has a low rate of conversion to SR in postsurgical new-onset AF [10, 83, 84].

Treatment of AF in CTS patients has been the topic of several reviews and guidelines [85, 86]. The studies in these patients are sufficiently powered to detect effectiveness for their primary end point, prophylaxis or treatment of AF, but are underpowered to detect differences in mortality or adverse effects due to the low incidence of these events.

There are also studies in mixed ICU populations. Diltiazem and amiodarone appeared equally effective in achieving rate control; however, discontinuation of the study drug because of hypotension occurred more often in the diltiazem group [87]. Ibutilide is effective for rapid conversion, but with potentially life-threatening proarrhythmic side effects [88]. Magnesium is more effective in rate control and probably in conversion than diltiazem in a mixed population with longstanding AF paroxysms [52]. With digoxin treatment, no rate control or rhythm control can be reached in a mixed ICU population [28, 41]. The success rate of electric cardioversion is also low in this population [28, 41].

The management of AF in noncritically ill patients has been studied and reviewed extensively [89, 90]. New-onset AF has a high spontaneous conversion rate of 64–90% within 24 hours [91]. Treatment with digoxin has been replaced by treatment with β-blockers and calcium-channel blockers because better rate control can be achieved with these latter drugs. Especially in seriously ill patients, digoxin fails to achieve an adequate reduction of the ventricular rate [92]. Class I and class III antiarrhythmic drugs are effective in conversion of AF in recent-onset AF, especially when combined with verapamil [89, 90, 93]. Amiodarone is also an effective drug because high-dose oral or intravenous amiodarone has a higher conversion ratio to SR than placebo [91, 94–97]. A meta-analysis showed that class IA, class IC and class III antiarrhythmic agents are equally effective in obtaining SR [98]. Meta-analyses comparing amiodarone with class IC antiarrythmic drugs or placebo showed that treatment was equally effective, although conversion was earlier in class IC treatment [96, 99]. None of the drugs was associated with an increased or a decreased mortality [98].

Depending on the AF duration, amiodarone is highly effective in conversion with no more adverse effects than other drugs [100]. In patients with severe congestive heart failure, amiodarone controls the heart rate immediately [101, 102]. Magnesium is safe, reliable and cost-effective compared with diltiazem [52]. Ibutilide is a safe and effective drug in persistent AF [103]. Angiotensin-converting enzyme-inhibitors might be effective in preventing structural changes (for example, fibrosis) and might therefore enhance outcome in AF patients, even in patients with worse underlying heart disease [104]. Glucocorticoid therapy reduces the proinflammatory state as measured by C-reactive protein and probably, as a consequence, the incidence of AF [105].

Electrical cardioversion in noncritically ill patients is effective but has a high relapse rate [8]. The timing of treatment is important because applying electric cardioversion too early leads to an increased recurrence of AF [106]. Whether the findings in noncritically ill patients are relevant for MICU patients is uncertain, but this evidence gives us a direction for research in mechanisms and therapy.

Conclusion on prevention and treatment

The data to support a treatment strategy are insufficient in MICU patients. Patient heterogeneity and spontaneous conversion require randomised controlled trials against a placebo. This trial evidence is not available, so we have to use data from other patient groups. In these patients it appears that electric conversion is not useful because of the high relapse rate. Digoxin is not very effective for SR conversion or rate control. Calcium antagonists are modestly effective but have the serious adverse effect of inducting hypotension. Class IA, class IIC and class III antiarrhythmic drugs are effective but have a significant proarrhythmic effect. The same observation holds true for ibutilide and propafenon. Magnesium is safe and seems effective. Amiodarone is effective but hypotension is seen, although not very frequently. β-Blockers are effective in prevention but data on treatment are less robust. Steroids and statins may prevent AF in patients with a systemic inflammation.

Adverse effects of (preventive) treatment

Pharmacokinetics and pharmacodynamics are changed in ICU patients [107]. Multiple drug use may cause drug interactions [107]. These factors might render ICU patients more prone to side effects [107, 108]. There are limited data, however, for MICU patients. Amiodarone-induced pulmonary toxicity has been described in postmortem MICU patients suffering from acute respiratory distress syndrome [109, 110]. In surgical ICU patients, amiodarone induces hypotension after intravenous loading [81, 82]. Severe hepatoxicity due to amiodarone has been described [111]. Ventricular tachycardia occurred in CTS patients [80].

In non-ICU patients admitted for AF there is a high incidence of adverse events, mainly cardiac, from antiarrhythmic drugs [112]. On the other hand, the incidence of amiodarone-induced proarrhythmic effects is low [113–115]. Nevertheless amiodarone remains a drug with many side effects. Amiodarone pulmonary toxicity, especially in the previously damaged lung, is a hazardous adverse effect [108, 110, 116]. The occurrence is probably cumulative, dose dependent and duration dependent, but adverse pulmonary effects can also be seen within 3 days after the start of administration [110, 114, 115]. Drug interactions might be more frequent for amiodarone but have not extensively been studied [117]. The implications for the ICU patient of the effect of amiodarone on thyroid gland function, which is a major problem in outpatients, are not yet clear [118, 119]. Amiodarone has a complex pharmacokinetic and pharmacodynamic profile [120].

Conclusion on adverse effects

Owing to the multiplicity of symptoms in ICU patients, adverse effects can be easily overlooked or attributed to the underlying disease. Reports on adverse effects of antiarrhythmic drugs have mainly been described in non-ICU patients. The proarrhythmic effect is the most frequent and serious side effect. Hypotension, however, is also an important side effect described in ICU patients. An adverse effect of a specific drug is hard to detect in ICU patients because of the polypharmacy and because of the difficulty to distinguish between adverse effects, underlying disease and other nosocomial complications.

Can treatment of atrial fibrillation improve survival?

There are few data on the effect of treatment of AF on mortality in ICU patients. A meta-analysis in non-ICU patients showed that class IA, class IC and class III antiarrhythmic agents are equally effective in reaching SR. No impact, however, on the quality of life or the mortality could be found [98]. β-Blockers improve survival in patients with heart failure and AF [121]. Amiodarone treatment in patients with AF and congestive heart failure improved conversion to SR and survival [122].

Conclusion on improvement of survival

There are no studies in ICU patients showing a survival advantage in the treatment group; the advantage could either not be shown or was not an endpoint of the study. In non-ICU patients with heart failure and AF there is a survival advantage for β-blockers and amiodarone, which also has β-blocking activity. This might be related to the well-known effect of β-blockers on survival in patients with heart failure and not because of rate control or rhythm control.

Can treatment of atrial fibrillation improve morbidity?

There are no data on MICU patients. In a retrospective study in surgical patients with new-onset supraventricular tachycardia (93% with AF), continuous infusion of amiodarone did not lead to significant differences in haemodynamics in responders compared with nonresponders [77, 123]. Another retrospective study in a selected population of critically ill patients showed that amiodarone improved haemodynamic parameters compared with pretreatment values [42].

In a mixed ICU patient population, conversion to SR did not increase the systolic blood pressure [73]. Most patients are already haemodynamically unstable before AF, and the contribution of AF is uncertain [124].

Conclusion on improvement of morbidity

The best available evidence comes from retrospective studies. The impact of conversion to SR or control of rhythm on haemodynamics is probably limited, although most clinicians intuitively would state that haemodynamics improve with treatment.

Should we aim for rate control or rhythm control?

There are no data in MICU patients. In a pilot trial in CTS patients there was no difference in the LOS or rhythm at discharge between rate control and rhythm control strategies [125, 126]. After cardiac surgery in haemodynamically stable patients, rate control is preferred over rhythm control because almost all patients convert spontaneously within 6 weeks after surgery [12, 86, 125, 127].

Five randomised-controlled trials in non-ICU patients did not show a beneficial effect of rhythm control over rate control in haemodynamically stable patients [128, 129]. These studies have been described in three meta-analyses; rate control showed less adverse events and less hospitalisations [9, 89, 130]. These meta-analyses, however, do not sufficiently cover specific patient groups [124].

Conclusion on rate control or rhythm control

There are insufficient data in ICU patients to justify a choice between therapy directed on rate control or on rhythm control. Rhythm control clearly has no advantage above rate control, as measured both by morbidity or mortality, in non-ICU patients.

Does atrial fibrillation increase stroke incidence in medical ICU patients?

There are no data on stroke incidence in the MICU. Short-term postoperative AF is a risk factor for stroke in CTS patients [131]. Postoperative AF doubles the risk compared with patients without AF, despite the use of aspirin [22, 32, 131, 132].

AF is an independent risk factor for stroke in non-ICU patients [133]. In patients with AF, an inflammatory response is an independent risk for stroke [134]. The prothrombotic state due to inflammation is probably more important than the presence of AF [25]. An increased C-reactive protein level is a risk factor for thromboembolism in patients with AF [135].

Conclusion on stroke incidence

There are insufficient data in medical ICU patients, but in CTS patients it is clear that the stroke incidence is increased in patients with AF. Besides AF, a proinflammatory state is also a risk factor.

Can stroke be prevented?

Since there are no data on stroke incidence in MICU patients, there are also no data on prevention.

In elderly patients undergoing cardiothoracic surgery receiving preventive treatment with amiodarone in addition to β-blocker, the incidence of AF and stroke was significantly reduced but the mortality was not changed [53]. This effect was also shown in a meta-analysis [55].

The stroke incidence in non-ICU patients can be reduced with anticoagulation. The bleeding risk is outweighed by the advantage of a reduced stroke incidence in most patients [8]. There is no difference between rate control and rhythm control in stroke incidence when the patient is on anticoagulation treatment [130]. Treatment of the proinflammatory state can reduce the incidence of stroke.

Conclusion on stroke prevention

The incidence of stroke can probably be reduced in ICU patients with anticoagulation. There are no clear data that this risk reduction outweighs the increased bleeding risk in these patients. The proinflammatory state probably increases the risk for stroke and the risk for AF independently [136].

Discussion

Although AF is a frequent symptom associated with a high mortality in critically ill patients, there are still many lacunae in our knowledge. We evaluated the actual level of knowledge with the purpose to reach a treatment protocol based on best available evidence. There is no literature, however, presenting the criteria of evidence-based medicine. Even the questions of whether AF is the cause of mortality or just an epiphenomenon [3] and of whether treatment improves outcome are still not answered. A treatment protocol therefore has to be based on extrapolation of results from studies performed in other patient groups. But even in these patient groups, there is still a lot of debate about the optimal treatment protocol [137].

Because the beneficial effect of treatment is not certain, any protocol should at least not add serious adverse events; first, do no harm. Doing as little as possible is a defendable credo. This means optimising the fluid balance, correcting electrolyte disturbances, reducing sympaticus tonus and avoiding proarrhythmic drugs. Reduction of the systemic inflammatory state is tempting but is of course always the purpose of ICU treatment. The evidence for the use of steroids for this indication is insufficient. When the ventricular rate is arbitrarily judged acceptable and there is little haemodynamic compromise, no further action is probably required. If this condition is not met, we have to seek the balance between benefit and harm.

Direct-current cardioversion is not useful because of the high relapse rate. In some situations, however, judged to be desperate, direct-current cardioversion will be performed. It has also not been proven that electrical cardioversion does not damage a heart already involved in the multiorgan failure of critical illness. Although the effectiveness of magnesium has been questioned there are no reports on adverse effects. In nonacutely threatened patients, therefore, an attempt to achieve rate control and even rhythm control with intravenous infusion of magnesium is worthwhile. If further treatment is deemed necessary, a choice has to be made between various antiarrhythmic drugs. Class IA, class IC and class III antiarrhythmic drugs all are effective but are also proarrhythmic. Calcium-channel blockers are less effective and have the disadvantage of causing hypotension. Intensivists may have an emotional barrier to using β-blockers in patients also receiving vasopressors and inotropes, but β-blockers could be a rational choice. The choice made by most intensivists, however, is for amiodarone: this drug is effective, although not as fast acting as some other drugs. The acute adverse effects seem to be very limited, but the adverse effects in the long term might be a problem. We therefore advocate short-term use of amiodarone if treatment is deemed necessary.

A protocol concerning AF should also have a statement about stroke prevention. There are, however, no data to support such a statement. We have no data on the stroke incidence of medical ICU patients with AF. Owing to the proinflammatory state, this incidence is probably higher than in other patients with AF. On the other hand, there is also an increased, but unquantified, bleeding risk. Risks and benefits of anticoagulation can therefore not be weighed in general. This balance has to be estimated for individual patients, and an educated guess has to be made [136].

Conclusion

A rational treatment protocol could therefore consist of several steps. First, treatment of predisposing factors is necessary. Second, a short attempt at magnesium supplementation can be done. Third, amiodarone can be administered for a short-term period. Most patients will by then have an acceptable rate or rhythm; however, if the patient does not, ibutilide (a class III drug) can serve as rescue treatment.

We have treated 29 patients in a MICU with this protocol. Ninety per cent of the patients had SR after 24 hours and all patients had an acceptable heart rate. We did not need to use ibutilide treatment, nor direct-current cardioversion. The inhospital mortality in this patient group, however, was still 38% [138].

Having a protocol with a reasonable success rate does not release us from doing further research. The high mortality rate could be caused by the fact that AF is just an epiphenomenon in critically ill patients. The possibility that the mortality is in part caused by insufficient treatment of AF or, on the contrary, is caused by adverse effects of the treatment, however, is too realistic to be ignored. All we have stated about the treatment of AF in MICU patients is based on extrapolation and is therefore just a hypothesis. We should therefore explore the possibility of randomised controlled trials against placebo. These trials should be based on a better understanding of AF in critically ill patients.

Abbreviations

AF:

atrial fibrillation

CTS:

cardiothoracic surgery

ICU:

intensive care unit

LOS:

length of stay

MICU:

medical intensive care unit

SR:

sinus rhythm.

References

  1. Pinski SL: Atrial fibrillation in the surgical intensive care unit: common but understudied. Crit Care Med 2004, 32: 890-891. 10.1097/01.CCM.0000117323.21849.30

    PubMed  Google Scholar 

  2. Reinelt P, Karth GD, Geppert A, Heinz G: Incidence and type of cardiac arrhythmias in critically ill patients: a single center experience in a medical–cardiological ICU. Intensive Care Med 2001, 27: 1466-1473. 10.1007/s001340101043

    CAS  PubMed  Google Scholar 

  3. Artucio H, Pereira M: Cardiac arrhythmias in critically ill patients: epidemiologic study. Crit Care Med 1990, 18: 1383-1388. 10.1097/00003246-199012000-00015

    CAS  PubMed  Google Scholar 

  4. Bender JS: Supraventricular tachyarrhythmias in the surgical intensive care unit: an under-recognized event. Am Surg 1996, 62: 73-75.

    CAS  PubMed  Google Scholar 

  5. Brundel BJ, Shiroshita-Takeshita A, Qi X, Yeh YH, Chartier D, van Gelder I, Henning RH, Kampinga HH, Nattel S: Induction of heat shock response protects the heart against atrial fibrillation. Circ Res 2006, 99: 1394-1402. 10.1161/01.RES.0000252323.83137.fe

    CAS  PubMed  Google Scholar 

  6. Hsu LF, Jais P, Sanders P, Garrigue S, Hocini M, Sacher F, Takahashi Y, Rotter M, Pasquie JL, Scavee C, et al.: Catheter ablation for atrial fibrillation in congestive heart failure. N Engl J Med 2004, 351: 2373-2383. 10.1056/NEJMoa041018

    CAS  PubMed  Google Scholar 

  7. Miller MR, McNamara RL, Segal JB, Kim N, Robinson KA, Goodman SN, Powe NR, Bass EB: Efficacy of agents for pharmacologic conversion of atrial fibrillation and subsequent maintenance of sinus rhythm: a meta-analysis of clinical trials. J Fam Pract 2000, 49: 1033-1046.

    CAS  PubMed  Google Scholar 

  8. Fuster V, Ryden LE, Asinger RW, Cannom DS, Crijns HJ, Frye RL, Halperin JL, Kay GN, Klein WW, Levy S, et al.: ACC/AHA/ESC guidelines 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 European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients with Atrial Fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology. Circulation 2001, 104: 2118-2150.

    CAS  PubMed  Google Scholar 

  9. Lim HS, Hamaad A, Lip GY: Clinical review: clinical management of atrial fibrillation – rate control versus rhythm control. Crit Care 2004, 8: 271-279. 10.1186/cc2827

    PubMed Central  PubMed  Google Scholar 

  10. Seguin P, Laviolle B, Maurice A, Leclercq C, Malledant Y: Atrial fibrillation in trauma patients requiring intensive care. Intensive Care Med 2006, 32: 398-404. 10.1007/s00134-005-0032-2

    PubMed  Google Scholar 

  11. Seguin P, Signouret T, Laviolle B, Branger B, Malledant Y: Incidence and risk factors of atrial fibrillation in a surgical intensive care unit. Crit Care Med 2004, 32: 722-726. 10.1097/01.CCM.0000114579.56430.E0

    PubMed  Google Scholar 

  12. Maisel WH, Rawn JD, Stevenson WG: Atrial fibrillation after cardiac surgery. Ann Intern Med 2001, 135: 1061-1073.

    CAS  PubMed  Google Scholar 

  13. Treggiari-Venzi MM, Waeber JL, Perneger TV, Suter PM, Adamec R, Romand JA: Intravenous amiodarone or magnesium sulphate is not cost-beneficial prophylaxis for atrial fibrillation after coronary artery bypass surgery. Br J Anaesth 2000, 85: 690-695. 10.1093/bja/85.5.690

    CAS  PubMed  Google Scholar 

  14. Knotzer H, Mayr A, Ulmer H, Lederer W, Schobersberger W, Mutz N, Hasibeder W: Tachyarrhythmias in a surgical intensive care unit: a case-controlled epidemiologic study. Intensive Care Med 2000, 26: 908-914. 10.1007/s001340051280

    CAS  PubMed  Google Scholar 

  15. Stricker KH, Rothen HU, Fuhrer J: Atrial tachyarrhythmia after cardiac surgery. Intensive Care Med 1998, 24: 654-662. 10.1007/s001340050641

    CAS  PubMed  Google Scholar 

  16. Nisanoglu V, Erdil N, Aldemir M, Ozgur B, Berat CH, Yologlu S, Battaloglu B: Atrial fibrillation after coronary artery bypass grafting in elderly patients: incidence and risk factor analysis. Thorac Cardiovasc Surg 2007, 55: 32-38. 10.1055/s-2006-924711

    CAS  PubMed  Google Scholar 

  17. Mathew JP, Fontes ML, Tudor IC, Ramsay J, Duke P, Mazer CD, Barash PG, Hsu PH, Mangano DT: A multicenter risk index for atrial fibrillation after cardiac surgery. JAMA 2004, 291: 1720-1729. 10.1001/jama.291.14.1720

    CAS  PubMed  Google Scholar 

  18. Amar D, Roistacher N, Burt M, Reinsel RA, Ginsberg RJ, Wilson RS: Clinical and echocardiographic correlates of symptomatic tachydysrhythmias after noncardiac thoracic surgery. Chest 1995, 108: 349-354.

    CAS  PubMed  Google Scholar 

  19. Sideris DA, Toumanidis ST, Tselepatiotis E, Kostopoulos K, Stringli T, Kitsiou T, Moulopoulos SD: Atrial pressure and experimental atrial fibrillation. Pacing Clin Electrophysiol 1995, 18: 1679-1685. 10.1111/j.1540-8159.1995.tb06989.x

    CAS  PubMed  Google Scholar 

  20. Foroulis CN, Kotoulas C, Lachanas H, Lazopoulos G, Konstantinou M, Lioulias AG: Factors associated with cardiac rhythm disturbances in the early post-pneumonectomy period: a study on 259 pneumonectomies. Eur J Cardiothorac Surg 2003, 23: 384-389. 10.1016/s1010-7940(02)00797-2

    PubMed  Google Scholar 

  21. Kalus JS, Caron MF, White CM, Mather JF, Gallagher R, Boden WE, Kluger J: Impact of fluid balance on incidence of atrial fibrillation after cardiothoracic surgery. Am J Cardiol 2004, 94: 1423-1425. 10.1016/j.amjcard.2004.08.017

    PubMed  Google Scholar 

  22. Hravnak M, Hoffman LA, Saul MI, Zullo TG, Whitman GR, Griffith BP: Predictors and impact of atrial fibrillation after isolated coronary artery bypass grafting. Crit Care Med 2002, 30: 330-337. 10.1097/00003246-200202000-00011

    PubMed Central  PubMed  Google Scholar 

  23. Amar D, Goenka A, Zhang H, Park B, Thaler HT: Leukocytosis and increased risk of atrial fibrillation after general thoracic surgery. Ann Thorac Surg 2006, 82: 1057-1061. 10.1016/j.athoracsur.2006.03.103

    PubMed  Google Scholar 

  24. Fontes ML, Mathew JP, Rinder HM, Zelterman D, Smith BR, Rinder CS: Atrial fibrillation after cardiac surgery/cardiopulmonary bypass is associated with monocyte activation. Anesth Analg 2005, 101: 17-23. table 10.1213/01.ANE.0000155260.93406.29

    PubMed  Google Scholar 

  25. Conway DS, Buggins P, Hughes E, Lip GY: Relationship of interleukin-6 and C-reactive protein to the prothrombotic state in chronic atrial fibrillation. J Am Coll Cardiol 2004, 43: 2075-2082. 10.1016/j.jacc.2003.11.062

    CAS  PubMed  Google Scholar 

  26. Gaudino M, Andreotti F, Zamparelli R, Di Castelnuovo A, Nasso G, Burzotta F, Iacoviello L, Donati MB, Schiavello R, Maseri A, et al.: The -174G/C interleukin-6 polymorphism influences postoperative interleukin-6 levels and postoperative atrial fibrillation. Is atrial fibrillation an inflammatory complication? Circulation 2003,108(Suppl 1):II195-II199.

    PubMed  Google Scholar 

  27. Hashimoto K, Chiba S, Tanaka S, Hirata M, Suzuki Y: Adrenergic mechanism participating in induction of atrial fibrillation by ACh. Am J Physiol 1968, 215: 1183-1191.

    CAS  PubMed  Google Scholar 

  28. Edwards JD, Wilkins RG: Atrial fibrillation precipitated by acute hypovolaemia. Br Med J (Clin Res Ed) 1987, 294: 283-284.

    CAS  Google Scholar 

  29. Aviles RJ, Martin DO, Apperson-Hansen C, Houghtaling PL, Rautaharju P, Kronmal RA, Tracy RP, Van Wagoner DR, Psaty BM, Lauer MS, et al.: Inflammation as a risk factor for atrial fibrillation. Circulation 2003, 108: 3006-3010. 10.1161/01.CIR.0000103131.70301.4F

    PubMed  Google Scholar 

  30. Chung MK, Martin DO, Sprecher D, Wazni O, Kanderian A, Carnes CA, Bauer JA, Tchou PJ, Niebauer MJ, Natale A, et al.: C-reactive protein elevation in patients with atrial arrhythmias: inflammatory mechanisms and persistence of atrial fibrillation. Circulation 2001, 104: 2886-2891. 10.1161/hc4901.101760

    CAS  PubMed  Google Scholar 

  31. Falk RH: Etiology and complications of atrial fibrillation: insights from pathology studies. Am J Cardiol 1998, 82: 10N-17N. 10.1016/S0002-9149(98)00735-8

    CAS  PubMed  Google Scholar 

  32. Creswell LL, Schuessler RB, Rosenbloom M, Cox JL: Hazards of postoperative atrial arrhythmias. Ann Thorac Surg 1993, 56: 539-549.

    CAS  PubMed  Google Scholar 

  33. Brathwaite D, Weissman C: The new onset of atrial arrhythmias following major noncardiothoracic surgery is associated with increased mortality. Chest 1998, 114: 462-468.

    CAS  PubMed  Google Scholar 

  34. Sander O, Welters ID, Foex P, Sear JW: Impact of prolonged elevated heart rate on incidence of major cardiac events in critically ill patients with a high risk of cardiac complications. Crit Care Med 2005, 33: 81-88. 10.1097/01.CCM.0000150028.64264.14

    PubMed  Google Scholar 

  35. Kalavrouziotis D, Buth KJ, Ali IS: The impact of new-onset atrial fibrillation on in-hospital mortality following cardiac surgery. Chest 2007, 131: 833-839. 10.1378/chest.06-0735

    PubMed  Google Scholar 

  36. Benjamin EJ, Wolf PA, D'Agostino RB, Silbershatz H, Kannel WB, Levy D: Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation 1998, 98: 946-952.

    CAS  PubMed  Google Scholar 

  37. Kannel WB, Abbott RD, Savage DD, McNamara PM: Epidemiologic features of chronic atrial fibrillation: the Framingham study. N Engl J Med 1982, 306: 1018-1022.

    CAS  PubMed  Google Scholar 

  38. Heinz G: Atrial fibrillation in the intensive care unit. Intensive Care Med 2006, 32: 1-4. 10.1007/s00134-005-0033-1

    Google Scholar 

  39. Aranki SF, Shaw DP, Adams DH, Rizzo RJ, Couper GS, VanderVliet M, Collins JJ Jr, Cohn LH, Burstin HR: Predictors of atrial fibrillation after coronary artery surgery. Current trends and impact on hospital resources. Circulation 1996, 94: 390-397.

    CAS  PubMed  Google Scholar 

  40. Almassi GH, Schowalter T, Nicolosi AC, Aggarwal A, Moritz TE, Henderson WG, Tarazi R, Shroyer AL, Sethi GK, Grover FL, et al.: Atrial fibrillation after cardiac surgery: a major morbid event? Ann Surg 1997, 226: 501-511. 10.1097/00000658-199710000-00011

    PubMed Central  CAS  PubMed  Google Scholar 

  41. Edwards JD, Kishen R: Significance and management of intractable supraventricular arrhythmias in critically ill patients. Crit Care Med 1986, 14: 280-282. 10.1097/00003246-198604000-00005

    CAS  PubMed  Google Scholar 

  42. Clemo HF, Wood MA, Gilligan DM, Ellenbogen KA: Intravenous amiodarone for acute heart rate control in the critically ill patient with atrial tachyarrhythmias. Am J Cardiol 1998, 81: 594-598. 10.1016/S0002-9149(97)00962-4

    CAS  PubMed  Google Scholar 

  43. Clark DM, Plumb VJ, Epstein AE, Kay GN: Hemodynamic effects of an irregular sequence of ventricular cycle lengths during atrial fibrillation. J Am Coll Cardiol 1997, 30: 1039-1045. 10.1016/S0735-1097(97)00254-4

    CAS  PubMed  Google Scholar 

  44. Shinbane JS, Wood MA, Jensen DN, Ellenbogen KA, Fitzpatrick AP, Scheinman MM: Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies. J Am Coll Cardiol 1997, 29: 709-715. 10.1016/S0735-1097(96)00592-X

    CAS  PubMed  Google Scholar 

  45. Ledingham I, McArdle CS: Septic shock [letter]. Lancet 1978, 2: 470. 10.1016/S0140-6736(78)91463-0

    CAS  PubMed  Google Scholar 

  46. Bradley D, Creswell LL, Hogue CW Jr, Epstein AE, Prystowsky EN, Daoud EG: Pharmacologic prophylaxis: American College of Chest Physicians guidelines for the prevention and management of postoperative atrial fibrillation after cardiac surgery. Chest 2005, 128: 39S-47S. 10.1378/chest.128.2_suppl.39S

    CAS  PubMed  Google Scholar 

  47. Dunning J, Treasure T, Versteegh M, Nashef SA: Guidelines on the prevention and management of de novo atrial fibrillation after cardiac and thoracic surgery. Eur J Cardiothorac Surg 2006, 30: 852-872. 10.1016/j.ejcts.2006.09.003

    PubMed  Google Scholar 

  48. Andrews TC, Reimold SC, Berlin JA, Antman EM: Prevention of supraventricular arrhythmias after coronary artery bypass surgery. A meta-analysis of randomized control trials. Circulation 1991, 84: III236-III244.

    CAS  PubMed  Google Scholar 

  49. Kuralay E, Cingoz F, Kilic S, Bolcal C, Gunay C, Demirkilic U, Tatar H: Supraventricular tachyarrythmia prophylaxis after coronary artery surgery in chronic obstructive pulmonary disease patients (early amiodarone prophylaxis trial). Eur J Cardiothorac Surg 2004, 25: 224-230. 10.1016/j.ejcts.2003.11.006

    PubMed  Google Scholar 

  50. Barnes BJ, Kirkland EA, Howard PA, Grauer DW, Gorton ME, Kramer JB, Muehlebach GF, Reed WA: Risk-stratified evaluation of amiodarone to prevent atrial fibrillation after cardiac surgery. Ann Thorac Surg 2006, 82: 1332-1337. 10.1016/j.athoracsur.2006.04.081

    PubMed  Google Scholar 

  51. Hohnloser SH, Meinertz T, Dammbacher T, Steiert K, Jahnchen E, Zehender M, Fraedrich G, Just H: Electrocardiographic and antiarrhythmic effects of intravenous amiodarone: results of a prospective, placebo-controlled study. Am Heart J 1991, 121: 89-95. 10.1016/0002-8703(91)90960-P

    CAS  PubMed  Google Scholar 

  52. Chiladakis JA, Stathopoulos C, Davlouros P, Manolis AS: Intravenous magnesium sulfate versus diltiazem in paroxysmal atrial fibrillation. Int J Cardiol 2001, 79: 287-291. 10.1016/S0167-5273(01)00450-8

    CAS  PubMed  Google Scholar 

  53. Kluger J, White CM: Amiodarone prevents symptomatic atrial fibrillation and reduces the risk of cerebrovascular accidents and ventricular tachycardia after open heart surgery: results of the Atrial Fibrillation Suppression Trial (AFIST). Card Electrophysiol Rev 2003, 7: 165-167. 10.1023/A:1027471718630

    PubMed  Google Scholar 

  54. Mitchell LB, Exner DV, Wyse DG, Connolly CJ, Prystai GD, Bayes AJ, Kidd WT, Kieser T, Burgess JJ, Ferland A, et al.: Prophylactic Oral Amiodarone for the Prevention of Arrhythmias that Begin Early After Revascularization, Valve Replacement, or Repair: PAPABEAR: a randomized controlled trial. JAMA 2005, 294: 3093-3100. 10.1001/jama.294.24.3093

    CAS  PubMed  Google Scholar 

  55. Aasbo JD, Lawrence AT, Krishnan K, Kim MH, Trohman RG: Amiodarone prophylaxis reduces major cardiovascular morbidity and length of stay after cardiac surgery: a meta-analysis. Ann Intern Med 2005, 143: 327-336.

    CAS  PubMed  Google Scholar 

  56. Balser JR: Pro: all patients should receive pharmacologic prophylaxis for atrial fibrillation after cardiac surgery. J Cardiothorac Vasc Anesth 1999, 13: 98-100. 10.1016/S1053-0770(99)90182-9

    CAS  PubMed  Google Scholar 

  57. Legare JF, Hall RI: Con: atrial arrhythmia prophylaxis is not required for cardiac surgery. J Cardiothorac Vasc Anesth 2002, 16: 118-121. 10.1053/jcan.2002.29696

    PubMed  Google Scholar 

  58. Crystal E, Kahn S, Roberts R, Thorpe K, Gent M, Cairns JA, Dorian P, Connolly SJ: Long-term amiodarone therapy and the risk of complications after cardiac surgery: results from the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT). J Thorac Cardiovasc Surg 2003, 125: 633-637. 10.1067/mtc.2003.9

    CAS  PubMed  Google Scholar 

  59. Crystal E, Garfinkle MS, Connolly SS, Ginger TT, Sleik K, Yusuf SS: Interventions for preventing post-operative atrial fibrillation in patients undergoing heart surgery. Cochrane Database Syst Rev 2004, CD003611.

    Google Scholar 

  60. Bagshaw SM, Galbraith PD, Mitchell LB, Sauve R, Exner DV, Ghali WA: Prophylactic amiodarone for prevention of atrial fibrillation after cardiac surgery: a meta-analysis. Ann Thorac Surg 2006, 82: 1927-1937. 10.1016/j.athoracsur.2006.06.032

    PubMed  Google Scholar 

  61. Hazelrigg SR, Boley TM, Cetindag IB, Moulton KP, Trammell GL, Polancic JE, Shawgo TS, Quin JA, Verhulst S: The efficacy of supplemental magnesium in reducing atrial fibrillation after coronary artery bypass grafting. Ann Thorac Surg 2004, 77: 824-830. 10.1016/j.athoracsur.2003.08.027

    PubMed  Google Scholar 

  62. Kaplan M, Kut MS, Icer UA, Demirtas MM: Intravenous magnesium sulfate prophylaxis for atrial fibrillation after coronary artery bypass surgery. J Thorac Cardiovasc Surg 2003, 125: 344-352. 10.1067/mtc.2003.108

    CAS  PubMed  Google Scholar 

  63. Forlani S, Moscarelli M, Scafuri A, Pellegrino A, Chiariello L: Combination therapy for prevention of atrial fibrillation after coronary artery bypass surgery: a randomized trial of sotalol and magnesium. Card Electrophysiol Rev 2003, 7: 168-171. 10.1023/A:1027423802701

    PubMed  Google Scholar 

  64. Cagli K, Ozeke O, Ergun K, Budak B, Demirtas E, Birincioglu CL, Pac M: Effect of low-dose amiodarone and magnesium combination on atrial fibrillation after coronary artery surgery. J Card Surg 2006, 21: 458-464. 10.1111/j.1540-8191.2006.00277.x

    PubMed  Google Scholar 

  65. Solomon AJ, Berger AK, Trivedi KK, Hannan RL, Katz NM: The combination of propranolol and magnesium does not prevent postoperative atrial fibrillation. Ann Thorac Surg 2000, 69: 126-129. 10.1016/S0003-4975(99)01187-X

    CAS  PubMed  Google Scholar 

  66. Miller S, Crystal E, Garfinkle M, Lau C, Lashevsky I, Connolly SJ: Effects of magnesium on atrial fibrillation after cardiac surgery: a meta-analysis. Heart 2005, 91: 618-623. 10.1136/hrt.2004.033811

    PubMed Central  CAS  PubMed  Google Scholar 

  67. Shiga T, Wajima Z, Inoue T, Ogawa R: Magnesium prophylaxis for arrhythmias after cardiac surgery: a meta-analysis of randomized controlled trials. Am J Med 2004, 117: 325-333. 10.1016/j.amjmed.2004.03.030

    CAS  PubMed  Google Scholar 

  68. Amar D, Zhang H, Heerdt PM, Park B, Fleisher M, Thaler HT: Statin use is associated with a reduction in atrial fibrillation after noncardiac thoracic surgery independent of C-reactive protein. Chest 2005, 128: 3421-3427. 10.1378/chest.128.5.3421

    CAS  PubMed  Google Scholar 

  69. Yared JP, Bakri MH, Erzurum SC, Moravec CS, Laskowski DM, Van Wagoner DR, Mascha E, Thornton J: Effect of dexamethasone on atrial fibrillation after cardiac surgery: prospective, randomized, double-blind, placebo-controlled trial. J Cardiothorac Vasc Anesth 2007, 21: 68-75. 10.1053/j.jvca.2005.10.014

    CAS  PubMed  Google Scholar 

  70. Halonen J, Halonen P, Jarvinen O, Taskinen P, Auvinen T, Tarkka M, Hippelainen M, Juvonen T, Hartikainen J, Hakala T: Corticosteroids for the prevention of atrial fibrillation after cardiac surgery: a randomized controlled trial. JAMA 2007, 297: 1562-1567. 10.1001/jama.297.14.1562

    CAS  PubMed  Google Scholar 

  71. Burgess DC, Kilborn MJ, Keech AC: Interventions for prevention of post-operative atrial fibrillation and its complications after cardiac surgery: a meta-analysis. Eur Heart J 2006, 27: 2846-2857. 10.1093/eurheartj/ehl272

    PubMed  Google Scholar 

  72. Chapman MJ, Moran JL, O'Fathartaigh MS, Peisach AR, Cunningham DN: Management of atrial tachyarrhythmias in the critically ill: a comparison of intravenous procainamide and amiodarone. Intensive Care Med 1993, 19: 48-52. 10.1007/BF01709278

    CAS  PubMed  Google Scholar 

  73. 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, 23: 1816-1824. 10.1097/00003246-199511000-00005

    CAS  PubMed  Google Scholar 

  74. Hennersdorf MG, Perings SM, Zuhlke C, Heidland UE, Perings C, Heintzen MP, Strauer BE: Conversion of recent-onset atrial fibrillation or flutter with ibutilide after amiodarone has failed. Intensive Care Med 2002, 28: 925-929. 10.1007/s00134-002-1317-3

    PubMed  Google Scholar 

  75. Varriale P, Sedighi A: Acute management of atrial fibrillation and atrial flutter in the critical care unit: should it be ibutilide? Clin Cardiol 2000, 23: 265-268.

    CAS  PubMed  Google Scholar 

  76. Soucier RJ, Mirza S, Abordo MG, Berns E, Dalamagas HC, Hanna A, Silverman DI: Predictors of conversion of atrial fibrillation after cardiac operation in the absence of class I or III antiarrhythmic medications. Ann Thorac Surg 2001, 72: 694-697. 10.1016/S0003-4975(01)02817-X

    CAS  PubMed  Google Scholar 

  77. Mayr AJ, Dunser MW, Ritsch N, Pajk W, Friesenecker B, Knotzer H, Ulmer H, Wenzel V, Hasibeder WR: High-dosage continuous amiodarone therapy to treat new-onset supraventricular tachyarrhythmias in surgical intensive care patients: an observational study. Wien Klin Wochenschr 2004, 116: 310-317.

    CAS  PubMed  Google Scholar 

  78. Kumar A: Intravenous amiodarone for therapy of atrial fibrillation and flutter in critically ill patients with severely depressed left ventricular function. South Med J 1996, 89: 779-785.

    CAS  PubMed  Google Scholar 

  79. Larbuisson R, Venneman I, Stiels B: The efficacy and safety of intravenous propafenone versus intravenous amiodarone in the conversion of atrial fibrillation or flutter after cardiac surgery. J Cardiothorac Vasc Anesth 1996, 10: 229-234. 10.1016/S1053-0770(96)80243-6

    CAS  PubMed  Google Scholar 

  80. VanderLugt JT, Mattioni T, Denker S, Torchiana D, Ahern T, Wakefield LK, Perry KT, Kowey PR: Efficacy and safety of ibutilide fumarate for the conversion of atrial arrhythmias after cardiac surgery. Circulation 1999, 100: 369-375.

    CAS  PubMed  Google Scholar 

  81. Cheung AT, Weiss SJ, Savino JS, Levy WJ, Augoustides JG, Harrington A, Gardner TJ: Acute circulatory actions of intravenous amiodarone loading in cardiac surgical patients. Ann Thorac Surg 2003, 76: 535-541. 10.1016/S0003-4975(03)00509-5

    PubMed  Google Scholar 

  82. Bernard EO, Schmid ER, Schmidlin D, Scharf C, Candinas R, Germann R: Ibutilide versus amiodarone in atrial fibrillation: a double-blinded, randomized study. Crit Care Med 2003, 31: 1031-1034. 10.1097/01.CCM.0000053555.78624.0F

    CAS  PubMed  Google Scholar 

  83. Mayr A, Ritsch N, Knotzer H, Dunser 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, 31: 401-405. 10.1097/01.CCM.0000048627.39686.79

    PubMed  Google Scholar 

  84. Donovan KD, Hockings BE: Shocking? Crit Care Med 2003, 31: 639-640. 10.1097/01.CCM.0000048628.73798.E9

    PubMed  Google Scholar 

  85. Dunning J: Are the American College of Chest Physicians guidelines for the prevention and management of atrial fibrillation after cardiac surgery already obsolete? Chest 2006, 129: 1112-1113. 10.1378/chest.129.4.1112

    PubMed  Google Scholar 

  86. Martinez EA, Epstein AE, Bass EB: Pharmacologic control of ventricular rate: American College of Chest Physicians guidelines for the prevention and management of postoperative atrial fibrillation after cardiac surgery. Chest 2005, 128: 56S-60S. 10.1378/chest.128.2_suppl.56S

    CAS  PubMed  Google Scholar 

  87. Delle Karth G, Geppert A, Neunteufl T, Priglinger U, Haumer M, Gschwandtner M, Siostrzonek P, Heinz G, et al.: Amiodarone versus diltiazem for rate control in critically ill patients with atrial tachyarrhythmias. Crit Care Med 2001, 29: 1149-1153. 10.1097/00003246-200106000-00011

    CAS  PubMed  Google Scholar 

  88. Delle Karth G, Schillinger M, Geppert A, Haumer M, Gwechenberger M, Meyer B, Heinz G, Siostrzonek P: Ibutilide for rapid conversion of atrial fibrillation or flutter in a mixed critically ill patient population. Wien Klin Wochenschr 2005, 117: 92-97. 10.1007/s00508-004-0297-4

    CAS  PubMed  Google Scholar 

  89. McNamara RL, Tamariz LJ, Segal JB, Bass EB: Management of atrial fibrillation: review of the evidence for the role of pharmacologic therapy, electrical cardioversion, and echocardiography. Ann Intern Med 2003, 139: 1018-1033.

    PubMed  Google Scholar 

  90. Slavik RS, Tisdale JE, Borzak S: Pharmacologic conversion of atrial fibrillation: a systematic review of available evidence. Prog Cardiovasc Dis 2001, 44: 121-152. 10.1053/pcad.2001.26966

    CAS  PubMed  Google Scholar 

  91. Cotter G, Blatt A, Kaluski E, Metzkor-Cotter E, Koren M, Litinski I, Simantov R, Moshkovitz Y, Zaidenstein R, Peleg E, et al.: Conversion of recent onset paroxysmal atrial fibrillation to normal sinus rhythm: the effect of no treatment and high-dose amiodarone. A randomized, placebo-controlled study. Eur Heart J 1999, 20: 1833-1842. 10.1053/euhj.1999.1747

    CAS  PubMed  Google Scholar 

  92. Goldman S, Probst P, Selzer A, Cohn K: Inefficacy of 'therapeutic' serum levels of digoxin in controlling the ventricular rate in atrial fibrillation. Am J Cardiol 1975, 35: 651-655. 10.1016/0002-9149(75)90051-X

    CAS  PubMed  Google Scholar 

  93. De Simone A, Stabile G, Vitale DF, Turco P, Di Stasio M, Petrazzuoli F, Gasparini M, De Matteis C, Rotunno R, Di Napoli T: Pre-treatment with verapamil in patients with persistent or chronic atrial fibrillation who underwent electrical cardioversion. J Am Coll Cardiol 1999, 34: 810-814. 10.1016/S0735-1097(99)00256-9

    CAS  PubMed  Google Scholar 

  94. Hilleman DE, Spinler SA: Conversion of recent-onset atrial fibrillation with intravenous amiodarone: a meta-analysis of randomized controlled trials. Pharmacotherapy 2002, 22: 66-74. 10.1592/phco.22.1.66.33492

    CAS  PubMed  Google Scholar 

  95. Singh BN: Antiarrhythmic actions of amiodarone: a profile of a paradoxical agent. Am J Cardiol 1996, 78: 41-53. 10.1016/S0002-9149(96)00452-3

    CAS  PubMed  Google Scholar 

  96. Khan IA, Mehta NJ, Gowda RM: Amiodarone for pharmacological cardioversion of recent-onset atrial fibrillation. Int J Cardiol 2003, 89: 239-248.

    PubMed  Google Scholar 

  97. Capucci A, Villani GQ, Aschieri D, Rosi A, Piepoli MF: Oral amiodarone increases the efficacy of direct-current cardioversion in restoration of sinus rhythm in patients with chronic atrial fibrillation. Eur Heart J 2000, 21: 66-73. 10.1053/euhj.1999.1734

    CAS  PubMed  Google Scholar 

  98. Nichol G, McAlister F, Pham B, Laupacis A, Shea B, Green M, Tang A, Wells G: Meta-analysis of randomised controlled trials of the effectiveness of antiarrhythmic agents at promoting sinus rhythm in patients with atrial fibrillation. Heart 2002, 87: 535-543. 10.1136/heart.87.6.535

    PubMed Central  CAS  PubMed  Google Scholar 

  99. Chevalier P, Durand-Dubief A, Burri H, Cucherat M, Kirkorian G, Touboul P: Amiodarone versus placebo and classic drugs for cardioversion of recent-onset atrial fibrillation: a meta-analysis. J Am Coll Cardiol 2003, 41: 255-262. 10.1016/S0735-1097(02)02705-5

    CAS  PubMed  Google Scholar 

  100. Letelier LM, Udol K, Ena J, Weaver B, Guyatt GH: Effectiveness of amiodarone for conversion of atrial fibrillation to sinus rhythm: a meta-analysis. Arch Intern Med 2003, 163: 777-785. 10.1001/archinte.163.7.777

    CAS  PubMed  Google Scholar 

  101. Hofmann R, Wimmer G, Leisch F: Intravenous amiodarone bolus immediately controls heart rate in patients with atrial fibrillation accompanied by severe congestive heart failure [letter]. Heart 2000, 84: 635. 10.1136/heart.84.6.635

    PubMed Central  CAS  PubMed  Google Scholar 

  102. Gullestad L, Birkeland K, Molstad P, Hoyer MM, Vanberg P, Kjekshus J: The effect of magnesium versus verapamil on supraventricular arrhythmias. Clin Cardiol 1993, 16: 429-434.

    CAS  PubMed  Google Scholar 

  103. Ellenbogen KA, Stambler BS, Wood MA, Sager PT, Wesley RC Jr, Meissner MC, Zoble RG, Wakefield LK, Perry KT, VanderLugt JT: Efficacy of intravenous ibutilide for rapid termination of atrial fibrillation and atrial flutter: a dose–response study. J Am Coll Cardiol 1996, 28: 130-136. 10.1016/0735-1097(96)00121-0

    CAS  PubMed  Google Scholar 

  104. Van Noord T, Crijns HJ, Van den Berg MP, Van Veldhuisen DJ, Van Gelder I: Pretreatment with ACE inhibitors improves acute outcome of electrical cardioversion in patients with persistent atrial fibrillation. BMC Cardiovasc Disord 2005, 5: 3. 10.1186/1471-2261-5-3

    PubMed Central  PubMed  Google Scholar 

  105. Dernellis J, Panaretou M: Relationship between C-reactive protein concentrations during glucocorticoid therapy and recurrent atrial fibrillation. Eur Heart J 2004, 25: 1100-1107. 10.1016/j.ehj.2004.04.025

    CAS  PubMed  Google Scholar 

  106. Oral H, Ozaydin M, Sticherling C, Tada H, Scharf C, Chugh A, Lai SW, Pelosi F Jr, Knight BP, Strickberger SA, et al.: Effect of atrial fibrillation duration on probability of immediate recurrence after transthoracic cardioversion. J Cardiovasc Electrophysiol 2003, 14: 182-185.

    PubMed  Google Scholar 

  107. Nolan PE Jr, Raehl CL: Toxic effects of drugs used in the ICU. Antiarrhythmic agents. Crit Care Clin 1991, 7: 507-520.

    PubMed  Google Scholar 

  108. Jessurun GA, Boersma WG, Crijns HJ: Amiodarone-induced pulmonary toxicity. Predisposing factors, clinical symptoms and treatment. Drug Saf 1998, 18: 339-344. 10.2165/00002018-199818050-00003

    CAS  PubMed  Google Scholar 

  109. Donaldson L, Grant IS, Naysmith MR, Thomas JS: Amiodarone pulmonary toxicity. Amiodarone should be used with caution in patients in intensive care [letter]. BMJ 1997, 314: 1832.

    PubMed Central  CAS  PubMed  Google Scholar 

  110. Ashrafian H, Davey P: Is amiodarone an underrecognized cause of acute respiratory failure in the ICU? Chest 2001, 120: 275-282. 10.1378/chest.120.1.275

    CAS  PubMed  Google Scholar 

  111. Bravo AE, Drewe J, Schlienger RG, Krahenbuhl S, Pargger H, Ummenhofer W: Hepatotoxicity during rapid intravenous loading with amiodarone: description of three cases and review of the literature. Crit Care Med 2005, 33: 128-134. 10.1097/01.CCM.0000151048.72393.44

    CAS  Google Scholar 

  112. Maisel WH, Kuntz KM, Reimold SC, Lee TH, Antman EM, Friedman PL, Stevenson WG: Risk of initiating antiarrhythmic drug therapy for atrial fibrillation in patients admitted to a university hospital. Ann Intern Med 1997, 127: 281-284.

    CAS  PubMed  Google Scholar 

  113. Hohnloser SH, Klingenheben T, Singh BN: Amiodarone-associated proarrhythmic effects. A review with special reference to torsade de pointes tachycardia. Ann Intern Med 1994, 121: 529-535.

    CAS  PubMed  Google Scholar 

  114. Connolly SJ: Evidence-based analysis of amiodarone efficacy and safety. Circulation 1999, 100: 2025-2034.

    CAS  PubMed  Google Scholar 

  115. Hughes M, Binning A: Intravenous amiodarone in intensive care. Time for a reappraisal? Intensive Care Med 2000, 26: 1730-1739. 10.1007/s001340000668

    CAS  PubMed  Google Scholar 

  116. Jessurun GA, Crijns HJ: Amiodarone pulmonary toxicity. BMJ 1997, 314: 619-620.

    PubMed Central  CAS  PubMed  Google Scholar 

  117. Gore JM, Haffajee CI, Alpert JS: Interaction of amiodarone and diphenylhydantoin. Am J Cardiol 1984, 54: 1145. 10.1016/S0002-9149(84)80166-6

    CAS  PubMed  Google Scholar 

  118. Ahmed Z, Goldman JM: Reevaluation of amiodarone [letter]. Ann Intern Med 1995, 123: 809.

    CAS  PubMed  Google Scholar 

  119. Podrid PJ: Amiodarone: reevaluation of an old drug. Ann Intern Med 1995, 122: 689-700.

    CAS  PubMed  Google Scholar 

  120. Roden DM: Mechanisms underlying variability in response to drug therapy: implications for amiodarone use. Am J Cardiol 1999, 84: 29R-36R. 10.1016/S0002-9149(99)00699-2

    CAS  PubMed  Google Scholar 

  121. Ramaswamy K: Beta blockers improve outcome in patients with heart failure and atrial fibrillation: U.S. carvedilol study. Card Electrophysiol Rev 2003, 7: 229-232. 10.1023/B:CEPR.0000012388.85901.1c

    PubMed  Google Scholar 

  122. Deedwania PC, Singh BN, Ellenbogen K, Fisher S, Fletcher R, Singh SN: Spontaneous conversion and maintenance of sinus rhythm by amiodarone in patients with heart failure and atrial fibrillation: observations from the veterans affairs congestive heart failure survival trial of antiarrhythmic therapy (CHF-STAT). The Department of Veterans Affairs CHF-STAT Investigators. Circulation 1998, 98: 2574-2579.

    CAS  PubMed  Google Scholar 

  123. Holt AW: Hemodynamic responses to amiodarone in critically ill patients receiving catecholamine infusions. Crit Care Med 1989, 17: 1270-1276.

    CAS  PubMed  Google Scholar 

  124. Slavik RS, Zed PJ: Intravenous amiodarone for conversion of atrial fibrillation: misled by meta-analysis? Pharmacotherapy 2004, 24: 792-798. 10.1592/phco.24.8.792.36065

    CAS  PubMed  Google Scholar 

  125. Lee JK, Klein GJ, Krahn AD, Yee R, Zarnke K, Simpson C, Skanes A: Rate-control versus conversion strategy in postoperative atrial fibrillation: trial design and pilot study results. Card Electrophysiol Rev 2003, 7: 178-184. 10.1023/A:1027428003609

    PubMed  Google Scholar 

  126. Soucier R, Silverman D, Abordo M, Jaagosild P, Abiose A, Madhusoodanan KP, Therrien M, Lippman N, Dalamagas H, Berns E: Propafenone versus ibutilide for post operative atrial fibrillation following cardiac surgery: neither strategy improves outcomes compared to rate control alone (the PIPAF study). Med Sci Monit 2003, 9: I19-I23.

    Google Scholar 

  127. Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, et al.: A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002, 347: 1825-1833.

    CAS  PubMed  Google Scholar 

  128. van Gelder IC, Hagens VE, Bosker HA, Kingma JH, Kamp O, Kingma T, Said SA, Darmanata JI, Timmermans AJ, Tijssen JG, et al.: A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med 2002, 347: 1834-1840. 10.1056/NEJMoa021375

    PubMed  Google Scholar 

  129. Opolski G, Torbicki A, Kosior DA, Szulc M, Wozakowska-Kaplon B, Kolodziej P, Achremczyk P: Rate control vs rhythm control in patients with nonvalvular persistent atrial fibrillation: the results of the Polish How to Treat Chronic Atrial Fibrillation (HOT CAFE) Study. Chest 2004, 126: 476-486. 10.1378/chest.126.2.476

    PubMed  Google Scholar 

  130. de Denus S, Sanoski CA, Carlsson J, Opolski G, Spinler SA: Rate vs rhythm control in patients with atrial fibrillation: a meta-analysis. Arch Intern Med 2005, 165: 258-262. 10.1001/archinte.165.3.258

    PubMed  Google Scholar 

  131. Taylor GJ, Malik SA, Colliver JA, Dove JT, Moses HW, Mikell FL, Batchelder JE, Schneider JA, Wellons HA: Usefulness of atrial fibrillation as a predictor of stroke after isolated coronary artery bypass grafting. Am J Cardiol 1987, 60: 905-907. 10.1016/0002-9149(87)91045-9

    CAS  PubMed  Google Scholar 

  132. Creswell LL: Postoperative atrial arrhythmias: risk factors and associated adverse outcomes. Semin Thorac Cardiovasc Surg 1999, 11: 303-307.

    CAS  PubMed  Google Scholar 

  133. Wolf PA, Abbott RD, Kannel WB: Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke 1991, 22: 983-988.

    CAS  PubMed  Google Scholar 

  134. Conway DS, Buggins P, Hughes E, Lip GY: Prognostic significance of raised plasma levels of interleukin-6 and C-reactive protein in atrial fibrillation. Am Heart J 2004, 148: 462-466. 10.1016/j.ahj.2004.01.026

    CAS  PubMed  Google Scholar 

  135. Thambidorai SK, Parakh K, Martin DO, Shah TK, Wazni O, Jasper SE, Van Wagoner DR, Chung MK, Murray RD, Klein AL: Relation of C-reactive protein correlates with risk of thromboembolism in patients with atrial fibrillation. Am J Cardiol 2004, 94: 805-807. 10.1016/j.amjcard.2004.06.011

    CAS  PubMed  Google Scholar 

  136. Epstein AE, Alexander JC, Gutterman DD, Maisel W, Wharton JM: Anticoagulation: American College of Chest Physicians guidelines for the prevention and management of postoperative atrial fibrillation after cardiac surgery. Chest 2005, 128: 24S-27S. 10.1378/chest.128.2_suppl.24S

    PubMed  Google Scholar 

  137. Nattel S, Opie LH: Controversies in atrial fibrillation. Lancet 2006, 367: 262-272. 10.1016/S0140-6736(06)68037-9

    PubMed  Google Scholar 

  138. Sleeswijk ME, Tulleken JE, van Noord T, Meertens JHJM, Ligtenberg JJM, 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 2007, in press.

    Google Scholar 

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Authors and Affiliations

  1. Flevo Hospital, Almere, Hospitaalweg 1, 1315 RA, Netherlands

    Mengalvio E Sleeswijk

  2. Department of Intensive Care, University Medical Center Groningen, University of Groningen, Groningen, PO 30.001, 9700 RB, Netherlands

    Trudeke Van Noord, Jaap E Tulleken, Jack JM Ligtenberg & Jan G Zijlstra

  3. Department of Intensive Care, University Hospital VU Medical Centre, Amsterdam, Boelelaan 1117, 1081 HV, Netherlands

    Armand RJ Girbes

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  1. Mengalvio E Sleeswijk
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  2. Trudeke Van Noord
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Sleeswijk, M.E., Van Noord, T., Tulleken, J.E. et al. Clinical review: Treatment of new-onset atrial fibrillation in medical intensive care patients: a clinical framework. Crit Care 11, 233 (2007). https://doi.org/10.1186/cc6136

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Critical Care

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