Atrial fibrillation and atrial flutter: Clinical sciences

Atrial fibrillation, also known as A-fib, is the most common atrial cardiac arrhythmia resulting from abnormal electrical impulse generation from multiple sites in the atria. This causes erratic and ineffective atrial contractions that can trigger clot formation and strokes, as well as an increased risk of developing heart failure due to ventricular dysfunction.

Now, if a patient presents with a chief concern suggesting A-fib, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and consider starting your patient on IV fluids. Put your patient on continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry, as well as cardiac rhythm monitoring. Finally, if needed, provide supplemental oxygen.

Next, assess for signs and symptoms of unstable atrial fibrillation, which include hypotension, altered mental status, signs of shock, ischemic chest pain, and acute heart failure. If your patient has these signs and symptoms present, diagnose unstable atrial fibrillation.

Then, you should proceed with immediate synchronized cardioversion. Finally, remember to treat any underlying causes or triggers including myocardial infarction, pulmonary embolism, thyrotoxicosis, or electrolyte abnormalities.

Here’s a clinical pearl! Atrial flutter is another common atrial tachycardia, but unlike A-fib which occurs due to multiple ectopic foci and causes an irregular rhythm, A-flutter is from a single ectopic focus in the atria that causes a reentrant pathway leading to a regular rhythm. They both present with a rapid ventricular rate of greater than 120, however, the atrial rate of A-flutter is around 250-350 beats per minute, displaying a classic sawtooth pattern. While there is predictable and reproducible atrial activity in A-flutter, these waves are not true P waves and are instead called flutter waves.

Okay, now that we’ve discussed unstable patients, let’s return to the ABCDE assessment to look at stable ones. The next step here is to obtain a focused history and physical exam. Your patient might report palpitations, dizziness, shortness of breath, or fatigue. They might have a history of cardiomyopathy, obstructive sleep apnea, diabetes, hypertension, obesity, or hyperthyroidism.

Exam will reveal an irregular pulse and normal blood pressure. The pulse rate, which indicates the ventricular rate, might be normal or high. With these findings, suspect atrial fibrillation. Then, obtain a 12-lead ECG. If the ECG reveals an irregular ventricular response with a variable ventricular rate and an erratic baseline with no distinguishable p waves, diagnose stable A-fib.

Here’s another clinical pearl! Keep in mind that both A-fib and A-flutter predispose to the development of intra-atrial thrombus, most commonly in the left atrial appendage. This thrombus could embolize to the peripheral circulation, especially if normal sinus rhythm is restored. So, always remember to obtain a transesophageal echocardiogram, or TEE, for all patients who present acutely with either A-fib or A-flutter to rule out an intra-atrial thrombus. This is especially important if the arrhythmia is paroxysmal, meaning it alternates with periods of sinus rhythm, or if you’re considering elective cardioversion to restore sinus rhythm. Also, don’t bother getting a transthoracic echocardiogram, or TTE. TEE is much better at visualizing the presence of a left atrial thrombus.

And now another clinical pearl! If your patient has A-fib for less than 48 hours, or TEE excludes a left atrial appendage thrombus, you can perform cardioversion without anticoagulation.

However, for patients with A-fib of at least 48 hours or unknown duration, or if a left atrial appendage thrombus is present, start anticoagulation for at least 3 weeks before elective cardioversion and continue for at least 4 weeks after cardioversion.

Okay, once you’ve diagnosed stable A-fib, move on to treatment. First, identifiable and treatable underlying causes include ischemic heart disease, hyperthyroidism and structural heart disease, while modifiable risk factors include obesity, sleep apnea, diabetes, hypertension, tobacco use, and alcohol consumption.