Atrial fibrillation and atrial flutter: Clinical sciences

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Introduction0:00–0:28

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.

Unstable0:28–2:27

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.

Stable2:27–5:08

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.

Treatment5:08–10:11

Next up is stroke prevention. The primary method of stroke prevention in A-fib is using medications to achieve therapeutic anticoagulation with heparin-based medications, warfarin, or direct oral anticoagulants, also known as DOACs.
Keep in mind that therapeutic anticoagulation also increases the risk of undesirable bleeding events, such as intracranial or gastrointestinal bleeding.
Perform risk stratification to determine your patient’s risk of stroke versus bleeding events using validated metrics such as the CHA2DS2-VASc and HAS-BLED tools.
The CHA2DS2-VASc score stands for congestive heart failure; hypertension; age of 75 or more, which if present is worth double points; diabetes; prior stroke or TIA, which is also worth double points; vascular disease; age 65 to 74; and being of the sex of biologic female category.
The total score helps to determine whether an individual’s risk of thromboembolic events is low, moderate, or high. For low-risk individuals, anticoagulation is not necessary.
If there is moderate risk, discuss the risks and benefits of anticoagulation using shared decision-making. Individuals with a high-risk CHA2DS2-VASc score should generally receive therapeutic anticoagulation unless they have a high risk of bleeding.
When it comes to the HAS-BLED score, this one is used to determine bleeding risk from anticoagulation. HAS-BLED stands for hypertension, abnormal kidney or liver function, stroke, bleeding history or predisposition, labile INR, elderly, and drug or alcohol use.
Individuals with low-risk scores can be safely anticoagulated, while in those with higher scores, the risk of bleeding may exceed the risk of stroke.
In high-risk individuals, consider placement of a left atrial appendage occlusion, or LAAO device. This device is placed via catheter into the left atrial appendage, and when deployed, prevents thrombus formation without the need for anticoagulation.
Finally, let’s discuss the options for rate and rhythm control. Rate control aims to reduce symptoms, improve heart function, and reduce the risk of tachycardia-induced cardiomyopathy.
This is especially important for those over the age of 70 with permanent A-Fib and normal left ventricular function. Pharmacotherapy for rate control include beta blockers, like metoprolol; nondihydropyridine calcium channel blockers, like diltiazem; or digoxin if both are contraindicated.
On the other hand, rhythm control focuses on converting and maintaining sinus rhythm. This method is also effective in reducing symptoms, and is preferred in patients with reduced LV function, those less than 70 years of age, and those with A-fib for less than a year.
Pharmacological options for rhythm control include antiarrhythmics like amiodarone, flecainide, or propafenone. Non-pharmacologic options for rhythm control first include electrical cardioversion.
Use synchronized electrical cardioversion as initial therapy for rhythm control or if pharmacological cardioversion is unsuccessful.
This procedure requires sedation but allows for immediate conversion to sinus rhythm. Another option for rhythm control is catheter ablation, which is the first line in symptomatic paroxysmal A-fib and helps prevent progression to persistent A-fib.
Moreover, catheter ablation is superior to pharmacotherapy in patients with heart failure with reduced ejection fraction.
You can offer catheter ablation to those who failed anti-arrhythmic medications or have contraindications to these medications.
Here’s a high-yield fact! For A-flutter, catheter ablation is first line therapy due to its high success rate and low rate of complications.

Review10:11–10:52

Alright, as a quick recap… Unstable A-fib should be recognized immediately and treated with immediate synchronized cardioversion.
On the other hand, stable A-fib is diagnosed with a 12-lead ECG. For treatment, start by addressing underlying causes and risk factors.
Next, focus on preventing stroke and systemic embolization by achieving therapeutic anticoagulation with heparin-based medications, warfarin, or direct oral anticoagulants.
Finally, address rate and rhythm control based on patient factors including age, symptom burden, left atrial size,