Atrial Fibrillation and Heart Failure

Today's case featured decompensated heart failure, which had been going on for three days and was thought to be secondary to atrial fibrillation (which was seen on ECG).  The patient was hemodynamically stable.  Intravenous beta blockade was used to control the heart rate, with a resultant increase in blood pressure.  We then discussed the ongoing management which included a discussion of diuresis, atrial fibrillation etiology, and anticoagulation.

There were multiple learning points:

-Rapid atrial fibrillation is probably one of the most common arrhythmia-related referrals you will see.  Atrial fibrillation is also the most common arrhythmia, and has a prevalence nearing 10% in people over the age of 80.  It is challenging to manage these patients when they arrive in the ED.  Always go back to first principles!

-Our ACLS management courses teach us that any arrhythmia needs to first be evaluated in terms of stability.  If the patient has no chest discomfort, dyspnea, altered LOC, or hypotension, they can be considered stable.  The ‘dysnpea’ requirement is somewhat soft in that sometimes patients feel dysnpic but the physician has to make a judgement call regarding management.  Theoretically, unstable atrial fibrillation is a rhythm that should be cardioverted immediately.  That said, if the patient is not hypotensive, beta blockade may slow heart rate, increase diastolic filling time and coronary artery perfusion, leading to improvements in blood pressure and left ventricular end diastolic pressures, alleviating venous congestion.  Sometimes, though, patients will respond poorly to calcium channel or beta blockade by becoming hypotensive (cardiogenic shock) or unstable requiring inotropes and critical care intervention.

-Patients with symptoms of decompensated heart failure are shifted far to the right on their Frank-Starling curve – their venous circulation is therefore overloaded, causing their right ventricles to fill disproportionately to the left, and in some cases cause ventricular interdependence leading to hypotension.  Additionally, their myocytes are stretched far beyond their ideal state due to congestion, leading to ineffective contraction.  This is why reducing preload through intravenous diuresis, nitrates, or other mechanisms leads to improved cardiac output.

-Given the propensity for clot formation after 48 hours of atrial fibrillation, it is ideal to anticoagulate a patient for 3-4 weeks prior to cardioversion and 3-4 weeks following cardioversion.  Alternatively, a left atrial appendage clot can be ruled out with transesophageal echocardiography.

-We talked about possible etiologies of atrial fibrillation.  Always consider ischemic heart disease and hypertensive disease.  Endocrine etiologies like the presence of a pheochromocytoma are also possible.  Consider states of sympathetic overdrive (cocaine use, alcohol withdrawal, hyperthyroidism). Consider valvular etiologies (mitrial stenosis, severe mitral regurgitation) as these can all produce structural changes favouring atrial fibrillation.  Finally, pulmonary embolism can increase right heart pressures and lead to atrial fibrillation.

-The patient in our scenario complained of one year of darkening skin.  This led to a ferritin being ordered, and a transferrin saturation being discovered to be 60%.  This is all consistent with an iron overload syndrome such as hemochromatosis.  In broad strokes, this manifests either with cardiac disease (restrictive cardiomyopathy, arrhythmias), diabetes, or liver disease.

Photo credit for the Frank-Starling curve: edwards.com.  Photo credit for the hemochromatosis picture: meddles.com.

Further Reading:

Borlaug, B. A. (2014). The pathophysiology of heart failure with preserved ejection fraction. Nature Reviews Cardiology.

Siddique, A., & Kowdley, K. V. (2012). Review article: the iron overload syndromes. Alimentary pharmacology & therapeutics, 35(8), 876-893.