Atrial fibrillation in the ICU

Atrial fibrillation in the ICU

Atrial fibrillation Preexisting or incident (new onset) among nearly one in three critically ill patients Formation of arrhythogenic substrate usually fibrosis (CHF, hypertension, valve disease, MI) (Also through electoral remodeling by persistent tachycardia + Arrhythmogenic trigger Hypokalemia Hypomagnesemia Hypovolemia Changes in parasympathetic and sympathetic activity

Pre-Critical Illness Age Diabetes CHF CKD Tachycardia Structural remodeling Altered ion channel activity Electrical remodeling Normal Atria TGF-B1 Renin-angiotensin Inflammation/ROS Critical Illness Arrhythmogenic Atria Normal Atria Surgery Bacterial Infection Volume overload Glucocorticoids? Statins? Inflammation Accelerated fibrosis Atrial Stretch Structural remodeling Electrical remodeling Arrhythmogenic Atria Altered ion channel expression Altered intracellular ion handling Sustained tachycardia Bacterial Toxins Thyroid Storm Antiarrhythmics Vasopressors Sepsis Betaagonists Beta-blockers? Excessive adrenergic stimulation Trigger Myocyte trauma/injury Altered intracellular ion handling Uremic Toxins Myocardial ischemia Right heart catheterization Ventilator dyssynchrony Atrial Fibrillation Electrolyte derangements

Prediction of AF in septic patients in the ICU https://safescore.shinyapps.io/safe

Clinical consequences of new onset AF Decompensation due to loss of atrial kick especially in patients with diastolic dysfunction (e.g. sepsis) and rapid ventricular response 40 30 Consequences of new onset AF in ICU 37 % 20 25 10 0 11 Immediate instability Heart rate > 150 Cardiac ischemia / CHF

Consequences New onset AF Increased direct mortality Increased risk for AF < 5 y % 60 45 30 15 0 Sepsis No AF Sepsis AF 2 Incidence AF < 5 Y

Acute management Assess the effect on hemodynamics and the underlying mechanism Removal of arrhythmogenic trigger Treatment strategy that maximizes potential benefit and minimizes risk Rate control if high heart rate is main problem Rhythm control if atrial kick is main problem or rate control ineffective Assessment for thromboprophylaxis

New AF Discontinue betaagonists and antiarrhythmics if possible Change vasopressors if using dopamine or epinephrine Rapid Clinical Assessment 1. Hemodynamic compromise? 2. Offending agent present? 3. Reversible inciting factors? 4. Is AF still present and causing adverse effects despite above measures? DCCV High rate of recurrence 70-80% Correct electrolytes Correct ventilator dyssynchrony Treat myocardial ischemia Optimize volume status Treat underlying infection Adverse effects of AF are due primarily to elevated HR or of unknown cause Adverse effects of AF are due primarily to loss of atrial systole First line Beta-blocker (esmolol) Second line Nondihydropyridine calcium channel blocker Digoxin Rate control ineffective First line Magnesium infusion Second line Amiodarone

Intervention and Dose Class and Mechanism Expected Efficacy a Onset of Effect Contraindications Potential Adverse Effects Esmolol: Load 500 mg/kg IV (may repeat); followed by 50-300 mg/kg/min 56 Beta-blocker: blocks binding of catecholamines to beta 1 - receptors, decreases AV node conduction, reduces arrhythmia induction and inotropy Noncritical illness SVT with RVR: mean decrease in heart rate of 39 beats/min 57 Metoprolol tartrate: 2.5- Same as above Noncritical illness SVT: mean 5 mg IV every 2 to 5 min 58 decrease in heart rate of 28 beats/min 59 Diltiazem: Load 0.25 mg/kg IV, followed by 5-15 mg/h 60 Verapamil: Load 0.075-0.15 mg/kg IV, followed by 0.005 mg/kg/min 61 Digoxin: Load 0.25 mg IV, followed by repeat dosing (maximum 1.5 mg/24 h). 62 Dose lower in renal failure Amiodarone: Load 150 mg IV over 10 min, followed by 1 mg/min for 6 h, followed by 0.5 mg/min for 18 h 63 Nondihydropyridine calcium channel blocker: inhibits L-type voltage-gated calcium channels, decreases AV node conduction, reduces inotropy Same as above Cardiac glycoside: inhibits Na-K ATPase increasing intracellular sodium and calcium, vagomimetic Class 3 antiarrhythmic: blocks adrenergic signaling and ion flow, extends refractory period, decreases AV node conduction, reduces membrane excitability Critical illness SVT with RVR: mean decrease in heart rate of 44 beats/min after 4 h 46 Noncritical illness AF or atrial flutter with RVR: mean decrease in heart rate of 45 beats/min 57 Noncritical illness AF with RVR: mean decrease in heart rate of approximately 30 beats/min within 6 h of administration 54 Critical illness AF or atrial flutter with RVR: mean decrease in heart rate of 37 beats/min 64 Noncritical illness AF: restoration of SR in 83% 20 h after administration 65 5 min 56 Bradycardia; decompensated heart failure; 2nd or 3rd degree heart block; sick sinus syndrome; AF with an accessory pathway 56,58 Bradyarrhythmia hypotension; heart block; hyperkalemia; hypoglycemia; bronchospasm (rare with beta 1 - antagonist) 56,58 20 min 58 Same as above Same as above 3 min 60 Bradycardia; decompensated heart failure; 2nd or 3rd degree heart block; sick sinus syndrome; AF with an accessory pathway 60,61 Bradyarrhythmia peripheral edema; hypotension; constipation 60,61 10 min 61 Same as above Same as above 5-30 min 62 Ventricular fibrillation 62 Digoxin toxicity (monitor levels); dysrhythmias; increased myocardial oxygen demand 62 8 h (mean time to SR) 65 Bradycardia; Cardiogenic shock, 2nd or 3rd degree heart block; severe sinus node disorders 63 Bradyarrhythmia ventricular arrhythmias; hypotension (IV formulation); organ toxicity (liver, thyroid, skin, and lung) 63 Intervention and Dose Class and Mechanism Expected Efficacy a Onset of Effect Contraindications Potential Adverse Effects (Continued) Magnesium sulfate: 1-3 g over 10 min; repeat if no response in 15 min 66 Within 30 min 66 2nd or 3rd degree heart block 67 Direct current cardioversion: QRS synchronized 120-200 J biphasic or 200 J monophasic Electrolyte: blocks calcium channels and activates Na-K ATPase promoting resting polarization 67 Electrical shock: electrical energy depolarizes all excitable membranes Combined critical and noncritical illness AF with RVR: 21.4% have resolution of RVR 66 Postoperative AF: 71% initial conversion to SR, 23% in SR after 24 h 39 Heart block; hypotension; CNS depression; hyporeflexia; respiratory depression 67 Instant Digitalis toxicity Embolic stroke, pain, skin burns, arrhythmias 68

Thromboprophylaxis Patients with critical illness and new onset AF have a 2 fold higher in-hospital risk of ischemic stroke. However, bleeding risk is also increased No current guidelines - routine thromboprophylaxis not indicated - individualize AF resolves in approximately 85% before hospital discharge