Question 9

College answer

Not available.

Discussion

Cause of AF in ICU is usually non-structural, reversible, and non-cardiac (i.e. related to the cause of the non-cardiac critical illness). Common causes in the ICU include:

• Catecholamine excess, whether exogenous (eg. adrenaline infusion) or endogenous (SAH, stress, pheochromocytoma, thyrotoxicosis)
• Atrial distension (Pulmonary hypertension, OSA, PE, septal defects, valvular disease)
• Abnormality of conducting system: 
  • Congenital cardiac disease, eg. septal defect
  • Infiltrative cardiac disease, eg. amyloidosis
  • Ischaemic heart disease
  • Age-related fibrotic changes
  • Haemochromatosis/iron overload
  • Hypothermia
• Increased atrial automaticity / irritation
  • Drugs: Alcohol, caffeine, catecholamines
  • Electrolyte derangement
  • Myocarditis

Thus:

Assessment of the cause and consequences of AF

• History, looking for features of OSA, ischaemic heart disease, pulmonary hypertension, prior episodes ("paroxysms") of AF, or recently ceased antiarrhythmic medications
• Clinical examination, looking for evidence of heart failure
• 12-lead ECG, looking for ischaemia
• Blood biochemistry, looking for electrolyte derangement
• Troponin, looking for ischaemia or myocarditis
• Thyroid function tests, looking for hyperthyroidism
• Scrutiny of the ICU monitoring equipment, to determine the duration of AF, to see if it coincides with some specific event (eg. the insertion of a line where the guidewire became unusually adventurous)
• CXR, to look for radiological signs of atrial dilatation or cardiomegaly
• TTE, to assess the effect on cardiac function

Assessment of the risk of stroke from AF

• Duration of AF: if it started in the ICU, this should be easy to determine from the monitoring systems.
• Risk stratification tools, such as the  CHA₂DS₂-VASc scoring system, can help determine the risk of stroke (A score of 1 equates to a risk of 1.3%; the maximum score is 9, with an associated stroke risk of 15.2%.)
• TOE, looking for clots in the right atrial appendage, would be helpful if cardioversion is contemplated

Management options

• Addressing the cause:
  • Management of the primary pathology (eg. shock state, sepsis, PE, MI, etc)
  • Correction of correctable predisposing causes (eg. hypoxia, acidosis, electrolyte derangement)
• Cardioversion :
  • best suited to recent-onset AF (with the first 48 hours), or where TOE has demonstrated the absence of clot in the left atrial appendage
  • Should be considered in scenarios where the AF has produced a substantial haemodynamic disadvantage
  • Usually, in the ICU population, this is ineffective in the medium-term, as the pathology which is driving the AF first needs to resolve before sinus rhythm can be sustained.
  • Chemical (eg. amiodarone, IV magnesium, beta-blockers) and electrical cardioversion have a similar risk profile
  • In general, rate control and rhythm control have similar outcome effects, but rate control seems to have some advantage in the outpatient cohort
• Rate control
  • Aim to reduce the rate to 80-100
  • Best suited for patients who are not hemodynamically compromised, and in whom the duration of the AF is unknown
  • Amiodarone or vernakalant are first-line for haemodynamically unstable patients
  • Beta-blockers are the first line for haemodynamically stable patients
  • Cardioselective calcium channel blockers such as verapamil or diltiazem are an alternative for people for whom beta-blockers are not appropriate (eg. asthma, COPD, peripheral vascular disease)
  • Digoxin in the ICU is generally less effective, but might be a better option for patients with poor LV function, as it has a subtle inotropic effect
• Anticoagulation
  • Options include unfractionated heparin infusion, LMWH, warfarin or a DOAC such as dabigatran rivaroxaban or apixaban
  • If you are going to anticoagulate, anticoagulation with something should continue for at least 3 weeks before and 4 weeks after their TOE-cardioversion.