This is a sample lesson on atrial fibrillation, which is part of the Mastering Internal Medicine. When you are done learning, feel free to return to the Early Bird page. Enjoy this lesson! If you have any feedback, please reach out to us.
Introduction
- Atrial fibrillation (AF) is the most common type of tachyarrhythmia and a frequent cause of stroke.
- Approximately 3% of the adult population experiences some form of atrial fibrillation, with the risk rising with age.
- Atrial fibrillation presents with a ventricular rate typically between 100-180 beats per minute, irregular in nature, and always lacking a P-wave.
- It is often asymptomatic, leading to detection during screening or due to complications like transient ischemic attack (TIA) or stroke.
- Treatment aims to manage symptoms, prevent complications, achieve frequency control, and restore sinus rhythm, with priority given to frequency control in severe cases.
Definitions
- Atrial fibrillation (AF) – a supraventricular tachyarrhythmia with an atrial rate between 300-600.
- The AV conduction is completely irregular, leading to variable ventricular rates depending on the passage of electrical signals.
- In AF, the ventricular rate typically ranges between 100-180 beats per minute and is irregular, with the absence of a P-wave always noted.
Etiology
More than half of cases can be explained by preexisting cardiovascular disease, such as:
- Hypertension
- Heart failure
- Left ventricular hypertrophy or dilated atria
- Coronary artery disease
- Other atrial arrhythmias such as AVNRT or AVRT
Atrial fibrillation can also be caused secondarily to other conditions (and is in those cases seldom persistent):
- Thyrotoxicosis
- Drug intoxication (adenosine, digoxin, thiazide diuretics, sympaticomimetics)
- Alcohol
- Diabetes
- COPD
- Obesity
- Infection
- Stress
- Surgery
- Obstructive sleep apnea syndrome
In 25% of patients, no underlying cause or risk factor can be identified. These cases are referred to as lone atrial fibrillation.
Classification
- Paroxysmal atrial fibrillation: More than one episode. Duration < 7 days. Automatically converts to sinus rhythm, normally within a few days.
- Persistent atrial fibrillation: >1 week. Does not convert automatically, instead requires pharmacological treatment or cardioversion (discussed more in detail below).
- Long-term persistent atrial fibrillation: Continuous AF for more than one year.
Permanent atrial fibrillation: AF has been accepted and considered chronic. No more attempts to convert to sinus rhythm, instead primary focus is rate control and preventing complications.
Pathophysiology
Triggers and drivers start and maintain atrial fibrillation, respectively. A common trigger is an ectopic focus that fires electrical impulses with a high frequency. To maintain a triggered AF, a driver is needed. A common driver is changes in the heart that cause re-entry waves.
Drivers and triggers are commonly located near where the pulmonary veins enter the left atrium. In some cases, this can motivate surgical treatment with pulmonary vein isolation and catheter ablation (read more here).
In AF, electrical signals circulate in the atria (re-entry waves) which causes contraction of the atria independent of the ventricles. Only some of the circulating signals reach the ventricles. The result is an irregular ventricular frequency and loss of P-wave (since the P-wave represents synchronized atrial depolarization, which is missing in AF).
Fast and irregular ventricular contraction is not physiologically optimal, leading to decreased filling of blood. The result is decreased cardiac output with increased risk of angina or heart failure.
Persistent and paroxysmal AF increases risk of thrombus formation and cerebral emboli by several mechanisms (endothelial damage, stagnant blood in atria, dilation of atria/ventricles). Due to inefficient pumping, blood becomes stagnant in parts of the heart and may form a thrombus which can reach the cerebral circulation. In persistent AF, there is a risk of structural and electrophysiological changes which may make it harder to treat.
Risk factors
Non-modifiable
- Age (degeneration of the myocardium and conduction system, increasing the risk of AF)
- Male sex
- Genetics
Modifiable
- Hypertension
- Heart failure
- Left ventricular hypertrophy
- Cardiomyopathy
- Diabetes
- Thyrotoxicosis
- Sleep apnea
- COPD
- Alcohol consumption
- Smoking
Symptoms
AF is often asymptomatic, and is often diagnosed during screening or due to complications (such as stroke or TIA). Other symptoms include:
- Reduced stamina
- Palpitations and tachycardia
- Fatigue
- Dyspnea
- Angina
- Vertigo
- Increased diuresis
- Due to incomplete emptying of atria → increased atrial pressure → ANP release → increased diuresis
Establishing the diagnosis
History
- Ask patient to describe symptoms
- Exacerbating factors – Physical exercise? Alcohol?
- Past medical history – Cardiovascular disease? TIA/stroke? Diabetes? Hyperthyroidism? COPD?
- Medicines, smoking, alcohol
Information needed in case of cardioversion
- When did the symptoms start? Acute cardioversion can only be done if:
- symptoms debuted <48 hours ago or
- transesophageal echocardiography (TEE) has ruled out thrombi or
- the patient has been on warfarin/NOAC for the last three weeks
- When did the patient last eat or drink? Information needed for sedation. If too short a period there is an increased risk of aspiration.
Physical examination
- Irregular heart sounds on auscultation
- Blood pressure
- Respiratory rate
- Peripheral edema
- Jugular vein stasis (sign of heart failure)
Labs
- Hemoglobin, sodium, potassium, creatinine
- CRP, leukocytes, thrombocytes – infection?
- Glucose
- Thyroid tests (TSH, T3, T4) – thyrotoxicosis?
- proBNP
- INR, APTT
ECG and echocardiography
ECG shows irregular rhythm and absence of P waves. If ECG is normal but strong clinical suspicion remains, a 24-hour ECG may increase the chances of diagnosing paroxysmal AF.
ECG may also show signs of left ventricular hypertrophy and other conduction disorders.
Echocardiography provides information about cardiac function (size, movement and ejection fraction) and may also diagnose valvular disorders.
Transesophageal echocardiography (TEE) should be done before cardioversion if AF has been present for >48 hours to identify possible sources of emboli.
Treatment
The aim of AF treatment is rate control, rhythm control and prevention of complications. In severe cases, rate control is prioritized.
Management of newly diagnosed atrial fibrillation
The first thing to consider is if the patient is hemodynamically stable:
- If hemodynamically unstable, consider acute cardioversion.
- If hemodynamically stable, consider if the goal is sinus rhythm. Permanent AF can be accepted in certain cases:
- Age >80 (high risk of AF relapse)
- Poor compliance
- AF >1 year, often returns to AF after initially successful cardioversion
If sinus rhythm is the goal:
- Did the AF debut during the last 48 hours? If not, has the patient been treated with NOAC or warfarin for the last three weeks?
- The patient does not have mitral stenosis (MS) or a murmur implying MS? If yes, there is an increased risk of thromboembolism from the left atrium due to the backflow of blood.
- Has the patient been fasting for the last 6 hours?
If the answers to these questions are yes:
- Cardioversion followed by four weeks of NOAC treatment
- After four weeks, consider if the patient should be treated with NOAC using CHA2DS2VASc (scoring system used to assess risk of embolic stroke, explained more in detail later)
Rate control
If the goal is rate control, AF has been accepted. The primary goal is to keep the heart rate in an acceptable range and initiate anticoagulation treatment. Ventricular tachycardia increases risk of tachycardiomyopathy, which can lead to heart failure and dilation of the ventricles. Treatment goal is resting heart rate between 80-100 beats per minute.
- Beta blockade: First line. Combined with digoxin and diuretics if concurrent heart failure.
- Calcium blockade: Verapamil or Diltiazem. Negative chronotropic effect (comparable with beta blockers). Contraindicated in patients with heart failure. Mostly used in patients intolerant to beta blockers.
- Digoxin: Decreases heart rate. Does not aid in conversion to sinus rhythm. Mostly used in patients with AF and heart failure. Monitor potassium concentration, even mild hypokalemia increases risk of arrhythmia. Stop treatment in case of bradycardia.
- Amiodarone: Mostly in patients with concurrent heart failure. Prevents relapse of AF. Many side effects and affects organs such as the heart, skin, blood, thyroid, lungs, liver.
Rate controlling medications are combined with anticoagulants in most patients, see more below. Most rate controlling medications can cause bradycardia or sinus node dysfunction.
Rhythm control
In rhythm control, the objective is to maintain sinus rhythm, which can be achieved using medications, cardioversion or catheter ablation/pulmonary vein isolation.
Betablockers have an antiarrhythmic effect but do not aid in the conversion from atrial fibrillation to sinus rhythm. They can be used as symptomatic treatment during AF episodes and as prevention from entering a new AF episode.
Pharmacological conversion
Effective in approximately 80% of cases if treatment is started within a week of debut of symptoms.
- Vernakalant (Brinavess):
- Good effect in AF lasting less than 3-7 days
- Increases the atrial refractory period by blocking several different ion channels in the atria
- Effect normally within 10 minutes
- Caution in patients with heart failure. Contraindicated in hypotension, aortic stenosis or in prolonged QT interval.
- Amiodarone (Cordarone)
- Flecainide
Cardioversion
Cardioversion is the most effective method for conversion from AF to sinus rhythm.
- A synchronized biphasic electrical shock (100-200 J) with the defibrillator pads placed in the anterioposteror or anteriolateral position.
- The patient needs to be fasted for 6 hours and sedated
- Cardioversion improves symptoms but not survival.
- When sinus rhythm is achieved, there is risk of thromboembolism. One of the following conditions needs to be met:
- AF duration max 48 hours
- TEE without thrombi in the atrial auricles
- At least 3 weeks of therapeutic treatment with warfarin or NOAC
Operative measures
- HIS blockade + pacemaker
- Catheter ablation with pulmonary vein isolation, 75% are recurrence-free after 1-2 procedures
Embolism prophylaxis (anticoagulant treatment)
In AF, there is abnormal atrial contraction resulting in increased turbulence, which in turn increases risk of thrombus formation. The risk is greatest when the atria start moving synchronized again.
Anticoagulants are recommended for 4 weeks after cardioversion even for patients who do not meet criteria for anticoagulant treatment according to CHA2DS2-VASc.
Warfarin or NOAC (non-vitamin K dependent oral anticoagulants) can be used, NOAC being the recommended option.
- Warfarin is preferred in patients with mechanical heart valves and significant mitral stenosis. Contraindicated in patients with alcoholism, significant risk of bleeding, uncontrolled hypertension, poor compliance, dementia, impaired balance, pregnancy, malignancy.
- Advantages of NAOC include lower risk of intracranial hemorrhage and no need of INR controls. Consider dose reduction in older patients, in patients with elevated creatinine or if body weight is low.
When starting anticoagulant treatment, assess risk of bleeding – interactions with other medications? HAS-BLED can aid in this assessment (see table below). Liver function testing should also be done.
Finally, use CHAD2DS2-VASc to calculate risk of embolic events. Can be used to support initiation of anticoagulants. (see table below)
0 points = no treatment
Initiate NOAC or warfarin treatment if ≥2 points for men and ≥3 points for women. Consider treatment if 1 point for men and 2 points for women.
Always use the HAS-BLED algorithm to consider risk of bleeding.
≥3 points on HAS-BLED indicates high risk of bleeding in patients with oral anticoagulation treatment.
Complications
- Stroke or thromboembolism (4-5x increased risk)
- Heart failure (2-3x increased risk)
- Mortality (2-3x increased)
- Vascular dementia (40% increased risk)
- Depression
- Impaired quality of life
- Increased hospitalization
Prevention
The risk of AF can be reduced by identifying and treating potential risk factors (such as hypertension, alcohol consumption, structural heart disease etc). ACE inhibitors might offer protection for patients with left-sided ventricular hypertrophy.