If it is a known new-onset A Fib (lets say for argument's sake, less than 1 hour), with unstable presentation (for example, hypotension and s/s of shock), and rate of less than 150 (140, for example), can you cardiovert it?
Bottom line, is 150 a golden rate for cardioversion? or can you cardiovert lower rates given the s/s and presentation???
It's a risk/benefit equation. You can cardiovert as an attempt to convert the rhythm at pretty much any rate. But:-
* As JPINFV very clearly stated, the longer the patient is in a.fib, the greater the likelihood that rhythm conversion may result in embolisation.
* Cardioversion of all but the most unstable patients is going to require procedural sedation, which carries it's own risks.
* True life-threatening unstable a.fib is somewhat rare. You may meet many patients who are both unstable, and in a.fib at a high rate. But in practice, a fair number of these patients are actually compensating for another underlying disease process, e.g. dehydration, sepsis.
In many situations the patient is better served by an attempt to (i) control the rate medically, or a cautious approached where we (ii) monitor and drive to the ER, and let the MDs find the best solution.
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On a physiological note:
There is, and never will be any magical "golden rate". We know that CO = HR * SV, and we know that atrial fibrillation patients lack "atrial kick", the extra preload provided by active filling during atrial systole. At faster heart rates we already have a potential for stroke volume to decrease as filling time (i.e. ventricular diastole) decreases. This is further compounded when we lose atrial contraction. Add to this the potential for other underlying disease processes, e.g. pulmonary disease, ventricular hypertrophy, cardiomyopathy, prior infarction, prescription medication to control the a.fib that may have negative inotropic effects, and we can have further reductions in stroke volume. Individual patients will therefore have different stroke volumes at a given heart rate.
If we consider hypotension, we have the relation BP = CO * SVR. We know that lower cardiac output can be further compensated by increases in systemic vascular resistance. Admittedly this comes at the cost of an increase in afterload, which will decrease the ejection fraction and stroke volume. SVR may be affected by other disease processes, e.g. HTN, peripheral vascular disease, aortic stenosis, etc. It too may be affected by pharmacology, including many prescription antihypertensives, and other medication. It will be affected by the stress response, and by local autoregulation in different vessel beds under conditions of hypoperfusion. This too will vary on a patient by patient basis.
So you have multiple issues. A 30 year old guy, former football player, obese, incipient HTN, goes on a week-long bender on the all-inclusive to mexico and comes back with "Holiday heart" a.fib, is probably going to compensate very well at 150 bpm. The 89 year old urosepsis / early community acquired pneumonia patient with uncontrolled HTN, prior infarction, quad CABG, CHF, renal failure, a resting 6cm aortic aneurysm and a litany of complaints about the youth of today at 150 bpm may be close to death. Treatment for both will differ accordingly.
All the best.
