Due to the large amount of wavelets occurring in the atria, there is no organized contraction of the atrial tissue. In fact, a visual inspection of a fibrillating atrium resembles a mold made of Jell-O in the shape of the atrium. The atrial myocardium is just simply trembling uncontrollably, or fibrillating, and does not add the atrial kick to superfill the ventricles. Acutely, as mentioned before, many patients cannot compensate for this drop in stroke volume. This alteration in the stroke volume can lead to clinical symptoms and some level of hemodynamic compromise, ranging from mild to severe.
Since cardiac output is equal to stroke volume times the rate, you can imagine what happens when the ventricular rate is also affected. The faster the rate, the less the filling time. The less the filling time, the lower the stroke volume. The lower the stroke volume, the lower the cardiac output.
As you can imagine, the hemodynamic compromise that can be seen in uncontrolled Afib is multifactorial. The rapid ventricular rates, the irregularity of the ventricular response, the loss of the atrial kick, and the presence of significant structural heart disease, either singly or cumulatively, will affect the hemodynamic status of your patient. Uncontrolled rates in Afib can pose a serious, and sometimes deadly, problem for you and your patient. Rate control is essential to clinical management.
We will not be covering treatment in this text in any great detail, but we highly encourage you to study the clinical management of atrial fibrillation, and its inherent complications and implications, quite thoroughly. Management and maintenance of these patients can be quite difficult. If your patient is in life-threatening hemodynamic compromise, electrical cardioversion or defibrillation may need to be attempted. If the patient converts to sinus rhythm, that’s great—just be aware that the patient could revert back into Afib at any time. If your unstable patient does not convert with cardioversion, then pharmacologic means of controlling the rate and blood pressure may be your only option.
If your patient is somewhat hemodynamically competent, converting the patient to sinus rhythm is still an admirable goal; however, unless the patient is definitely in the acute phase, there is a danger of breaking off an atrial clot and causing a catastrophic stroke to develop. It is like jumping from the frying pan into the fire. Slowing or controlling the ventricular response should actually be your primary goal in these cases. If you slow the rate and control the hemodynamic response, you can have some time to thoroughly assess your patient and determine the best course of further action. Chemical or electrical cardioversion can then be approached logically and sequentially, once appropriate anticoagulation has been established and the threat of embolic stroke is reduced.