Incidence

It can be as high as 78% in the critically ill population but its hard to nail down an exact number
Having new onset atrial fibrillation in critical illness increases your mortality risk from 22% to 44%. In surgical ICUs that’s a little worse. Mortality rates of 45% vs 16% without a fib.
- Correlation??? afib is unlikely to cause the mortality increase but it is a marker of disease severity

Physiology

Some processes are thought to prime the heart for afib
- chronic processes like: metabolic syndrome, HTN, Mitral valve disease, and age
- acute processes like inflammation and bacterial deposits in the endocardium
- persistent tachycardia of any kind can prime the system for A fib
Then, an arrhythmogenic trigger occurs
- Changes in atrial architecture (stretch, congenital/surgical lesion, myxoma)
- Changes in membrane potentials (drugs, lytes, inflammation - myocarditis)
- Increased sympathetic tone
Why is it more serious than sinus tach?
- Electrical chaos - 700 impulses/min (can’t get through) - leads to loss of coordinated atrial contraction
- Blood pooling - esp left atrial appendage - stasis, incr risk of clot cardioembolic event (small microemboli or larger microemboli - consider when cardioverting)
- Loss of atrial kick - 20 NBD routinely maybe, but shock states - 20% is KBD
- Unlike sinus tach (increased chronotropy WITH a concomitant increase in dromotropy and lusitropy) rapid AF is irregular, uncoordinated, and can quickly reach non-physiologic rates
- Cardiac output eq is CO x HR, but there is an upper limit to HR before you reduce SV from a reduction in filling time

1) Is the patient stable or unstable?
- Unstable (e.g. hemodynamics change)
  - Are the hemodynamics changing because of the critical illness or the afib itself?
  - Synchronized cardioversion
- Stable
2) Can you fix the underlying trigger of afib?
- Can be difficult to determine
3) Rate or rhythm control?
- In the non-ICU population - rate control
- otherwise, it’s the wild wild west

Coming soon