Andrew Stephen, MD
Background
Similar to Type 2 MI and many cases of ARDS, new onset atrial fibrillation(afib) in the SICU is usually not of primary cardiac etiology but usually is marker and a complication of systemic illness. An epidemiologic study from 1990 showed that one in three critically ill patients goes into new onset afib(Artucio CCM). New onset afib can also be a sign that something is amiss postoperatively, e.g. anastomotic leak, obstructed biliary stent, a new infection. Treatment is to find and treat the underlying cause, use medications to control the ventricular rate, and on rare occasion perform DC cardioversion.
Outcomes
There are immediate and longterm issues related to new onset afib in the ICU.
Immediate: Decreased cardiac output, hemodyamic decompensation, organ hypoperfusion, Type 2 MI
Longterm: Associated with increased hospital mortality, higher 5 year risk of ischemic stroke, CHF, mortality. Considered a “sepsis defining organ dysfunction”(Walkey 2017)
Etiologies
A 2018 review from Chest describes a two step process(Bosch).
1. atrial arrhythmogenic substrate
2. a “seed” that initiates afib
Elderly often have the atrial substrate which is a result of comorbidities such as CHF, HTN, valvular disease, prior MI. These lead to some degree of atrial fibrosis creating the sensitive substrate.
In SICU patients there are numerous possible “seeds” and so new onset afib is often multifactorial. Examples of seeds include hypovolemia, hypervolemia, sepsis, vasopressors, hypokalemia, hypomagnesemia, pain, respiratory distress, hypoxia and any condition that stimulates the sympathetic nervous system. Bacteria have even been postulated to embed in the atrial wall and alter calcium ion channel gene expression shortening the atrial refractory period.
Treatment
1. Assess hemodynamics. If unstable can consider electrical cardioversion but it rarely works in SICU patients and almost never maintains the patient in sinus rhythm. Only 23% remain in sinus rhythm at 24 hours(Arrigo CCM 2015)
2. Use primarily a rate control approach with medications. Options:
-IV metoprolol 5-10 mg doses serially or esmolol infusion. Esmolol is short acting and can be titrated rapidly.
-Diltiazem infusion. But calcium channel blockers can cause vasodilation and negative inotropy limiting their utility in the elderly.
-Digoxin load and dosing. Rarely causes hypotension but rarely converts to sinus rhythm.
-Amiodarone load and infusion. Advantage is that it does not cause much negative inotropy, useful then in the elderly or those with low EF.
-Magnesium. Prolongs AV node refractory period, does not cause negative inotropy.
There is a lot of variation in practice. Beta blockers result in higher rates of conversion to sinus rhythm and are less likely to need to be discontinued due to hypotension when compared to calcium channel blockers. In the UK intensivists were surveyed and more than 80% use amiodarone as their first choice.
3. Control the underlying etiology, “the seed”.
Anticoagulation?
Not likely beneficial in most patients. There was a higher rate of clinically significant bleeding in patients with sepsis who were anticoagulated for new onset afib without a difference in rates of in-hospital ischemic CVA. A Chest 2018 review does not recommend starting heparin infusion for ICU patients with new onset afib. We should continue to address it on a case by case basis.
Future questions
In some retrospective studies statins have been shown to reduce risk of developing new onset afib after noncardiothoracic surgery. Should statins be started de novo in patients as a preventive measure? We do know statins reduce certain cytokines after MI, surgery but we do not have enough evidence to start them in patients who are not on them preop.
Glucocorticoids for afib prevention? Also too early to tell. One retrospective trial from 2017 showed lower rates of afib in patients with septic shock in patients on low dose hydrocortisone(Launey JICM).