AF is very common in the ICU, reflecting in the increasing number of past paper SAQs which discuss the fibrillating atrium, and what precisely you ought to do about it.
Chapter 22 of Oh's Manual (Management of cardiac arrhythmias by Andrew Holt) was my first instinctive reference for this topic. The chapter is a marvellous resource, consisting of highly concentrated information compacted in layers upon layers into a dense sedimentary deposit. Nuggets of gold are embedded within. Most of the end section (pages 216 to 224) deals almost exclusively with atrial fibrillation, and this summary chapter uses it and its references ad libitum to answer the SAQs. As far as useful information goes, the AHA's 2014 guidelines statement can be viewed as the definitive document for management and investiations, in spite of the fact that its intended audience is largely ward-based and outpatient physicians. As is pointed out below, AF in the ICU is a completely different animal to "outpatient AF".
Oh's Manual pays a little token attention to flutter before engaging in a detailed discussion of AF. Yes, both are atrial arrhythmias, but totally different pathology is involved in each. Flutter is an intra-atrial re-entrant circuit which just goes around and around (usually, counter-clockwise and in the right atrium). It is apparently notoriously drug-resistant and Holt recommends ibutilide as the drug most likely to cardiovert this rhythm. Judging by the tone of Holt's chapter, there is nothing to recommend any specific agent to the task of controlling ventricular rate in flutter. A group is listed in a nonchalant manner ("Drugs such as digoxin, diltiazem, beta-adrenergic blockers, sotalol and amiodarone may be tried; the choice depends on LV function"). We are warned against the use of Class 1A and 1C agents, as they may result in 1:1 conduction (and a ventricular rate in excess of 200). By comparison, the more recent article by Herzog et al (2017) is much more firmly prescriptive. It separates the management of flutter into four main areas, described by the RACE acronym: Rate control, Anticoagulation, Cardioversion and Electrophysiology. The article summarises the recommendations from the most recent guidelines from the AHA/ACC:
Generally, rate control is more difficult to achieve than with AF. UpToDate authors suggest calcium channel blockers (diltiazem or verapamil) but the level of evidence is somewhat sub-standard ("we prefer", the authors say). The problem with ICU patients is that frequently, the (higher) dose required to slow AV nodal conduction would produce an intolerable level of toxicity (i.e. the LV would not be grateful for the decreased contractility). Ergo, amiodarone becomes the natural choice in the ICU, because it covers both the "R" and the "C" of the RACE algorithm.
Why do we even try to control AF?
Question 14 from the first paper of 2012 asked the candidates to list several non-cardiac causes of AF. The list of causes could be long, and it is possible to organise it in several ways. One way is the familiar VINDICATE framework which should theoretically make it easier to memorise the causes. A strategy which might be more useful (actually enhancing one's practice) would be to organise the causes according to their pathophysiology. Both are made available below.
Abnormality of conducting system
Increased atrial automaticity / irritation
"Outline your initial management of the tachycardia", asks Question 14 from the first paper of 2012. Treatment for AF is a pursuit of several goals: control of ventricular rate, protection from systemic emboli and restoration of sinus rhythm.
Holt's chapter for Oh's Manual mentions four studies (AFFIRM, RACE, STAF and PIAF) in support of rate control instead of rhythm control. They were published between 2000 and 2003. A more recent meta-analysis (Caldeira et al, 2012) identified four more (a total of eight) suitably high-quality studies, featuring data from 7499 patients. The mortality data from these was underwhelming. "No clear survival benefit is apparent", laments Holt. Rate control was found to be superior only in terms of the composite endpoint (death, stroke and recurrent hospitalisation). Theoretically, rhythm control should actually be better (particularly in the absence of significant structural heart disease) because it may prevent myocardial remodelling due to AF.
Multiple methods are available. Oh's Manual lists essentially the entire antiarrhythmic arsenal, cautioning against the use of digoxin in patients with enhanced sympathetic tone (useless, apparently). Single-dose flecainide is apparently also good, but in patients with structural heart disease it tends to cause sudden cardiac death.
The 2014 AHA statement gives the following recommendations:
They recommend a rate of 80 or so as the endpoint to aim for, but give a slightly weaker recommendation in favour of a more "lenient" rate (~110) provided the LV function is well-preserved.
For the haemodynamically unstable patient, DC cardioversion is the gold standard. The arrhythmia management algorithm in the pre-arrest management section of the ARC ALS Handbook (based on ILCOR Guidelines) recommends this approach. For the haemodynamically stable patient, there are a variety of chemical cardioversion options, among which amiodarone and vernakalant (the latter being a novel drug with rapid activity against AF and a reasonably benign side-effect profile). Electrical cardioversion may still be an option, within 48 hours of onset or later following adequate anticoagulation and TOE.
The options are:
The 2014 AHA statement recommends:
The CHA2DS2-VASc scoring system is the recommended method of determining the risk of stroke. In essence it comes down to three main categories: score 0, score 1 and any score of 2 or more.
|C||Congestive heart failure (or Left ventricular systolic dysfunction)||
|H||Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)||
|A2||Age ≥75 years||
|S2||Prior Stroke or TIA or thromboembolism||
|V||Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)||
|A||Age 65–74 years||
|Sc||Sex category (i.e. female sex)||
A score of 0 is hard to get, but confers a virtually negligible risk of stroke (~ 0%). A score of 1 equates to a risk of 1.3% and a score of 2 puts you in a high risk category (2.2%). The maximum score is 9, with an associated stroke risk of 15.2%. Mind you, these are annual risks. What's the daily risk in ICU patients? Nobody knows. Sibley et al (2015) mulls the problem over and concludes that whatever that risk is, it surely mist be higher in the ICU population, particularly among patients with sepsis. At present there does not appear to be either any sort of scoring system or any sort of guidelines statement to help direct the intensivist here, apart from generic guidelines like the 2014 AHA statement.
There are several important differences between "free-range" AF in the movie-going public and "ICU AF " in the critically ill patient.