Digoxin
Digoxin is a medication that is commonly used for congestive heart failure (CHF) and arrhythmias like atrial fibrillation or flutter with rapid ventricular rates (RVR). It has largely been replaced by medications that have a safe side-effect panel like beta-blockers and calcium channel blocks, but you will still see patients on this medication every now and then. Even though prescribing this medication is reserved for cardiology, it is still important for perioperative providers to understand how this medication works and why it is used. This video will focus on the indications and mechanism of action - the next video will focus on the toxicity associated with it.
There are two main mechanisms of action that make Digoxin suitable for both CHF and Afib/flutter with RV. It all starts with Digoxin binding to the potassium-binding site on the sodium-potassium (Na-K) ATPase channel found on myocardiocytes. By blocking this channel, it functionally reduces the amount of Na that is being released from the cell and causes a rise in intracellular Na. This not only changes in the intra/extracellular concentration gradient of Na, it causes an influx of calcium (Ca2+) into the myocardiocytes. This is where the magic happens.
An increase of calcium within heart cells leads to increase contractility - or positive inotropy. This is useful for CHF patients who may have reduced ventricular function and reduced contractility.
You will also see AV node inhibition from the rise of intracellular Ca2+. This leads to a prolonged phase 4 and phase 0 of the cardiac action potential and an increase in parasympathetic tone. This is useful for patients who don’t respond to beta-blockers or calcium channel blockers in the setting of afib/flutter with RVR. Slowing this conduction (negative dromotrophy) leads to a slowed ventricular rate.
Some of the hesitation from using Digoxin is its narrow therapeutic index and risk of side effects from toxicity.
Patient-specific risk factors for Digoxin toxicity include advanced age, worsening renal function, low body weight, and medication noncompliance (ie. taking more than what is prescribed). There are also electrolyte imbalances that lead to toxic levels. The major one is HYPOkalemia (low potassium). Other electrolyte abnormalities that make toxicity more likely include hypercalcemia and hypomagnesemia.
There are a variety of signs and symptoms to look out for with Digoxin toxicity. The mild ones include: nausea, vomiting, diarrhea, and abdominal pain. The visual changes are quite specific, or pathognomonic, for digoxin toxicity - yellow to green tint in vision, blurry vision, flashes of light. The severe symptoms involving arrhythmias occurs when digoxin blood levels are supratherapeutic (0.8-2 ng/mL): ventricular tachycardias and atrial tachycardias with AV blocking.
There are normal EKG changes that are associate with Digoxin use. The most common rhythms changes are bradycardia and PVCs. There are other changes that can be worrisome for things like myocardial ischemia, but are normal in this setting. These changes include:
Down-sloping ST-segment depressions (“scooped appearance”)
Decreased QT interval
Increased PR interval
T-wave inversion/flattening
Lastly, if you patient is having life-threatening Digoxin toxicity (ie. Ventricular tachycardias), there is an antidote available known as Digibind or DigiFab. This is a digoxin-specific antibody (Fab) fragments. When they bind Digoxin, there form complexes that are removed from the circulating blood volume and excreted in the urine.
