Class (I/II/III/IV) antiarrhythmics are used as second-line drugs for rate control in atrial fibrillation.
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A 65-year-old woman presents to the emergency department with palpitations, lightheadedness, and shortness of breath. She explains she has experienced these symptoms for the past three days and that her symptoms are not associated with physical exertion. The patient has a history of hypertension, hyperlipidemia, and type 2 diabetes mellitus. The patient denies any loss of consciousness, muscle weakness, sensory deficits, chest pain, vomiting, fever, and chills. Examination shows that her temperature is 37℃ (98.6℉), blood pressure is 150/85 mm Hg, pulse is 160/min, respirations are 17/min, and oxygen saturation is 98% on room air. Cardiac examination reveals an irregularly irregular rhythm and tachycardia, which are both confirmed with an ECG. The patient promptly receives IV metoprolol and is closely monitored. Examination later reveals resolution of her dyspnea and a heart rate of 95 beats per minute. The consulting cardiologist reports that the patient is at moderate-high risk for thromboembolic events and recommends prophylaxis. Which of the following is the most appropriate next step in management?
The heart has four chambers: two upper chambers, the right and left atrium; and two lower chambers, the right and left ventricles. Fibrillation describes when the muscle fibers are all contracting at different times, so the end result is a quivering, or twitching movement.
Normally, an electrical signal is sent out from the sinus node in the right atrium. The signal then propagates out through both atria super fast, which allows them to depolarize at about the same time, so that you end up with a nice, coordinated contraction of the atria. That signal then moves down to the ventricles and causes them to contract shortly after.
With Atrial fibrillation, or A-fib or AF, signals move around the atria in a completely disorganized way that tends to override the sinus node. Instead of one big contraction, you get all these mini contractions that make it look like the atria are just quivering.
On an electrocardiogram, or ECG, normally the “P wave” corresponds to the atrial contraction. The “QRS complex,” which is the ventricular contraction, follows shortly after. During AF, all these small areas contract at different times so that you end up with an electrocardiogram that looks like scribbles, where each little peak corresponds to one spot in the atria twitching. Sometimes, a signal from one of these areas makes it down to the ventricles and cause ventricular contraction; these QRS complexes are interspersed at irregular intervals though, and usually at fairly high rates between 100 and 175 beats per minute.
In the normal heartbeat, a well-coordinated atrial contraction contributes a small amount of blood that’s called the “atrial kick.” People with AF lose this atrial kick; however, this loss isn’t life-threatening.
Okay, but how or why does this happen in the atrium? Why do the cells start depolarizing in a totally uncoordinated way? Well, the answer isn’t super cut-and-dry. There are a ton of risk factors that predispose someone to developing AF, and the exact mechanisms aren’t well understood. AF often happens alongside other cardiovascular diseases, including high blood pressure, coronary artery disease, valvular diseases — essentially anything that can create an inflammatory state or physically stretch out the atria and potentially damage the cells in the atria. Other, non-cardiovascular risk factors include: obesity, diabetes, and excessive alcohol consumption. Additionally, there also seems to be a genetic component.
These factors likely stress the cells in the atria, which can lead to tissue heterogeneity; or in other words, cells start taking on different electrical properties. For example, one cell might start conducting signals faster than its neighbor, and another cell might develop a shorter refractory period — the time following depolarization during which they can’t conduct another signal. These different tissue properties can ultimately cause the conduction in the atria to become unpredictable.
Normally, with tissue that’s the same, you’ll get essentially one wavefront of conduction that moves through the atria. According to the multiple wavelet theory, with different tissue properties, multiple wavelets develop. These wavelets conduct randomly around the atria, sometimes colliding and creating new “daughter wavelets.”
Along with the multiple wavelet theory, there’s also an automatic focus theory. According to the automatic focus theory, there’s a specific origin that is thought to initiate AF by rapid firing of electrical impulses that overtake the sinus node. Combined with risk factors and tissue heterogeneity, this can promote AF. It’s thought that a focused group of cells conduct cells in the cardiac muscle around pulmonary veins — yeah, pulmonary veins! Remember that these veins physically enter the left atrium, and where the pulmonary veins enter there is tissue that has really unique electrical properties.