Jan 152019

Jon-Emile S. Kenny MD [@heart_lung] with illustrations by Carla M Canepa MD [@_carlemd_]

“The habit of writing for my eye is good practice. It loosens the ligaments.”

― Virginia Woolf


A 28 year old woman with known severe mitral stenosis from rheumatic heart disease presents with acute onset shortness of breath.  Her acute dyspnea began while walking out of the airport following a 12-hour flight.  She is taking oral contraceptive pills and notes pleuritic chest pain in the emergency department, she also endorses one week of chills with a non-productive cough.  Her heart rate is 145 beats per minute and irregular with a blood pressure of 102/88, an oxygen saturation of 90% and a low-grade fever.  An ECG reveals atrial fibrillation and a CT angiogram is performed to evaluate for pulmonary embolus.  A peripheral wedge-shaped opacity is noted distal to a small, sub-segmental pulmonary embolus.  In the contralateral lung, she is noted to have a dense consolidation as well as bilateral interlobular septal thickening and centrilobular ground-glass.  On the CT scan, her cardiac chambers appear normal in size save for a massively dilated left atrium and enlarged pulmonary veins.  An influenza swab is positive and she is evaluated by both CT surgery and the medical ICU fellow. 


The approach to atrial fibrillation [AF] in the intensive care unit [ICU] or step-down unit can be treacherous.  A few months ago, Josh Farkas provided a really nice overview of the shocked-AF patient.  Further, a recent and excellent review of atrial fibrillation in the ICU was published in Chest; I urge the reader to consider these resources.  While it is common to see atrial fibrillation reflexively treated with rate control and anti-coagulation, both Josh’s podcast and the review in Chest prod the reader to ponder an underlying trigger of atrial fibrillation.  Because treating the heartbreak of sepsis-associated atrial fibrillation only with loads of diltiazem may lead to therapeutic embarrassment.


The mechanisms underpinning the onset and persistence of atrial fibrillation are still not fully realized.  Nevertheless, it may be – like many disease processes – that the heart must harbour a diathesis for dysregulated conduction.  Subsequently, some stress then sparks the persistent and pesky atrial fibrillatory waves with which we are all so familiar.  Indeed, the general prevalence of AF in the critically-ill has been reported to be as high as 78%.

It is thought that two general processes ripen the heart for atrial fibrillation.  The first is atrial fibrosis which is the end-result of both chronic and surprisingly subacute processes – some of which are common in the ICU.  For example, the metabolic syndrome, chronic hypertension, mitral valve disease and age are some of the classically-invoked provocateurs of atrial fibrosis, but so too are acute inflammation and bacterial deposition upon the endocardium.  Secondly, persistent tachycardia of any sort can ‘prime’ the conduction system for atrial fibrillation, partly through variation of ion channel expression.

Figure 1: Consider the many possible triggers for atrial fibrillation in the acute setting before reflexively lowering the heart rate.

With a heart primed for atrial fibrillation, an arryhthmogenic trigger can jolt it into action.  There are many well-known initiators of atrial fibrillation – intrinsic [e.g. shock, pain, anxiety, viscus distension, ventilator dys-synchrony] and extrinsic catecholamines [especially dopamine, epinephrine, other beta-agonists], uremia, hypomagnesemia, hypokalemia, hypercapnia, myocardial ischemia and atrial stretch, etc. can all nudge the atria into fibrillation.

Rate Control and Anticoagulation     

The reflex for rate control in AF likely sprung from two landmark trials published in the same issue of the New England Journal of Medicine in early 2002 – the AFFIRM and RACE trials.  While these were practice-changing investigations that clearly demonstrated rate control to be at least as good as, if not superior to, rhythm control in chronic AF, both studies included stable, outpatients observed cross-sectionally over many years.  The patients of AFFIRM and RACE were not septic patients with AF or AF in acute pancreatitis or GI hemorrhage.  Thus, when encountering rapid AF in the setting of acute and/or critical illness, immediate reduction of the heart rate isn’t necessarily warranted based on the outcomes of AFFIRM and RACE trials.  It, therefore, behooves the clinician to consider underlying, treatable causes for the AF; sometimes treatment of rapid-AF requires not a push of metoprolol but rather the gentle push of a Foley catheter.

Rate control agents include beta-blockers such as the B1 selective esmolol which is rapidly degraded by RBC esterases and is, therefore, largely independent of renal and hepatic function.  Calcium channel blockers [CCB] - which typically have a longer half-life than esmolol - are often used, though these agents have vasodilatory effects in addition to negative inotropic and chronotropic properties.  Digoxin reduces heart rate by increasing vagal tone and may be less effective in critical illness when there exists large amounts of intrinsic and extrinsic sympathetic tone.

In the United States, CCBs are used most frequently, followed by beta-blockers, digoxin and then amiodarone.  In an observational analysis, beta-blockers were associated with lower in-hospital mortality when used for AF in the setting of sepsis; as well, in a controversial randomized controlled trial, beta-blockers resulted in a 30% absolute risk reduction in mortality!  While research is on-going, there is suggestion that beta-blockers are beneficial as compared to other rate-controlling agents.  However, as previously reviewed, advantageous effects upon the microcirculation may be confounded, in my view.

Other agents include intravenous magnesium which is an AV node blocker and may convert the patient to normal sinus rhythm without negative inotropic activity.  Amiodarone has rate and rhythm controlling effects, but can cause acute and chronic lung disease.

In the non-ICU setting, patients with AF and RVR randomized to diltiazem had a higher response rate [i.e. 90%] but also higher rate of discontinuation due to hypotension [i.e. ~30%] as compared to amiodarone and digoxin [i.e. 74% response rate each].  Similarly, in the ICU, diltiazem had a 30% discontinuation rate due to hypotension.

There is relatively scarce data directing the use of anticoagulation in patients with AF in the ICU.  In a retrospective, propensity-score analysis, 35% of patients with sepsis-associated AF received parenteral anticoagulation.  Yet when patients who did and did not receive AC were matched based on propensity score, there was no difference in in-hospital ischemic stroke rates.  Further, there was a 1.4% absolute risk increase in bleeding rates in those who received anticoagulation.  Based on the above, the authors of a recent review on AF in the ICU recommend against AC for AF during acute illness.  Nevertheless, while AF in the acute setting may resolve, long term stroke risk can be high and AC should be considered by the receiving floor team prior to discharge.

In Part 2, nuances of ventricular filling in the setting of AF are considered as physiological rationale for both rate and rhythm control in the acutely-ill.



Dr. Kenny is the cofounder and Chief Medical Officer of Flosonics Medical; he also the creator and author of a free hemodynamic curriculum at heart-lung.org

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Atrial Fibrillation for the Intensivist – part 1