Atrial Fibrillation Flashcards
General findings
La FA può essere valvolare o non valvolare. Cambia la terapia antiaggregante
Attenzione, esiste anche una FA con bradicardia ventricolare, ad esempio nella malattia tachicardia-bradicardia
- Atrial fibrillation (Afib) is a commonly seen type of supraventricular tachyarrhythmia that is characterized by uncoordinated atrial activation resulting in an irregular ventricular response.
- Individuals with Afib are typically asymptomatic. However, when symptoms do occur, these usually include palpitations, lightheadedness, and shortness of breath
- The diagnosis is confirmed by an ECG showing indiscernible P waves and a narrow QRS complex with irregular QRS intervals.
- The diagnosis is confirmed by an ECG showing indiscernible P waves and a narrow QRS complex with irregular QRS intervals.
- Immediate synchronized cardioversion is required in hemodynamically unstable patients. In stable patients, treatment involves the correction of modifiable risk factors, rate or rhythm control strategies, and anticoagulation. Rate control therapy typically involves the use of beta-blockers or nondihydropyridine calcium channel blockers. Rhythm control strategies involve elective synchronized cardioversion and/or the use of antiarrhythmics (e.g., flecainide, propafenone, or amiodarone).
- The need for anticoagulation therapy is determined based on the CHA2DS2-VASc score. Catheter-directed or surgical ablation of the arrhythmogenic tissue is used in refractory or severe Afib.
(In atrial flutter, the atrial rate is slower than in Afib and the ventricular rhythm is usually regular. Treatment is similar to that of Afib, consisting of anticoagulation and strategies to control heart rate and rhythm. Atrial flutter frequently degenerates into atrial fibrillation.)
Epidemiology
- Most common sustained arrhythmia
- prevalenza dell’1%
Risk factors
- Advanced age
- Hypertension
- Diabetes mellitus
- Smoking
- Obesity
- Sleep apnea
Cause intrinseche cardiache
Atrial fibrillation is much more common in patients with mitral stenosis than in those with mitral regurgitation. Approximately two-thirds of patients with mitral stenosis will develop atrial fibrillation at some point.
Coronary artery disease
Valvular heart disease (especially mitral valve disease)
Congestive heart failure (CHF)
Pre-excitation tachycardia. e.g., Wolff-Parkinson-White (WPW) syndrome
Sick sinus syndrome (tachycardia-bradycardia syndrome)
Cardiomyopathies
Pericarditis
Congenital channelopathies
Non-cardiac diseases
👓Pulmonary disease: COPD, pulmonary embolism, pneumonia!!💥
Hyperthyroidism
Catecholamine release and/or increased sympathetic activity
Stress: sepsis, hypovolemia, post-surgical state (especially following cardiac surgery), hypothermia
👓Pheochromocytoma
Cocaine, amphetamines
Electrolyte imbalances (hypomagnesemia, hypokalemia)
Drugs: e.g., adenosine, digoxin
Holiday heart syndrome: irregular heartbeat classically triggered by excessive alcohol consumption, but also sometimes by moderate alcohol consumption, stress, or lack of sleep
Chronic kidney disease
Onset and duration of Afib
- New-onset Af: Af less than 48 hours in duration
- Paroxysmal Af: Af that resolves within 7 days of onset either following treatment or spontaneously
- Persistent Af: continuous Af for > 7 days
- Long-standing persistent Af: continuous Afib for > 1 year
- Permanent Af: long-standing persistent Af that is not treated unless the patient and the treating physician agree to do so
Fisiopatologia
Atrial fibrillation is a supraventricular arrhythmia.
- Volume overload, hemodynamic stress → atrial hypertrophy and/or dilatation
- Atrial ischemia
- Inflammation of the atrial myocardium
- Altered ion conduction by the atrial myocardium
✔Af is triggered by one or both of the following:
- Bursts of electrical activity from automatic foci near the pulmonary veins or in diseased, fibrotic atrial tissue
- Pre-excitation of the atria as a result of aberrant pathways (e.g., WPW syndrome)
✔Af is SUSTAINED by re-entry rhythms and/or rapid focal ectopic firing (The refractory period decreases as the rate of polarization increases, facilitating the conduction of erratic rapid sequence firings. This facilitates the conduction of erratic rapid sequence firings if triggered.)
Re-entry rhythms are more likely to occur with enlarged atria, diseased heart tissue, and/or aberrant pathways (e.g., WPW syndrome).
✔Atrial remodeling
Electrophysiological changes in the atria occur within a few hours of Af onset (electrical modeling).
If Afib persists, atrial fibrosis and dilatation (structural remodeling) occur within a few months. (il rimodellamento cardiaco post infarto compare circa 7 giorni dopo l’evento ischemico)
Electrical and structural remodeling increase susceptibility to Af, resulting in a vicious circle!💥
Effects of Af
The atria contract rapidly but ineffectively and in an uncoordinated fashion → stasis of blood within the atria → risk of thromboembolism and stroke
Irregular activation of the ventricles by conduction through the AV node → tachycardia!
Clinica
Most affected individuals are asymptomatic🧨
Less commonly, affected individuals develop symptoms of arrhythmias such as palpitations, dizziness, syncope, fatigue, and or dyspnea.
- Signs of underlying disease (e.g., murmurs of mitral stenosis)
- Tachycardia with an irregularly irregular pulse
- Apex-pulse deficit: difference between the rate of apex heart beat and that of the peripheral pulse
- Manifests when only some cardiac contractions are strong enough to transmit a pulse wave to the periphery
- Number of cardiac contractions (perceived with stethoscope or palpated on the chest) is higher than the peripheral pulse rate (e.g., radial artery)
Complications of long-standing Afib
- Acute left heart failure → pulmonary edema
- Thromboembolic events: stroke/TIA, renal infarct, splenic infarct , intestinal ischemia , acute limb ischemia
- Life-threatening ventricular tachycardia
NB The brain, kidney, and spleen are the three organs most likely to be damaged by emboli!👓
ECG
💥irregular R-R
1. atrial fibrillation 2. wandering atrial pacemaker 3. multifocal atrial tachycardia (in soggetti con pulmonary embolism o COPD)
1.Irregularly irregular RR intervals (An ECG pattern in which the time interval between two successive QRS complexes varies inconsistently. Can be seen in patients with atrial fibrillation, multifocal atrial tachycardia, and wandering atrial pacemaker)
- P-waves are indiscernible
- Tachycardia
- Narrow QRS complex (< 0.12 seconds) (attenzione: However, atrial fibrillation with wide QRS complexes may occur in individuals with bundle branch blocks or pre-excitation syndromes e.g., WPW syndrome)
👓Holter ECG monitoring should be used in patients with risk factors and symptoms of arrhythmia to rule out paroxysmal Afib.
Echocardiography
NB La transtoracica si fa a prescindere a tutti i pazienti, per la TEE vedi criteri inclusione/esclusione
Transthoracic echocardiogram (TTE)
Indications: all patients with new-onset Af👓
Assesses cardiac function and rule out underlying structural cardiac disease, e.g., mitral valve stenosis
Transesophageal echocardiogram (TEE)
Indicated in patients who meet all of the following criteria:
1.Afib or atrial flutter for > 48 hours or unknown
duration
2.Scheduled electrical or pharmacological
cardioversion
3.No anticoagulation therapy for at least the past 3
weeks
(Questi stessi criteri sono di esclusione per una cardioversione farmacologica previa ecocardiografia tranesofagea, ma il paziente emodinamicamente stabile ne esula, significa cioè che si fa la cardioversione elettrica a prescindere. Se già uno solo di questi criteri è differente, e.g. insorgenza minore delle 48 ore si può procedere con la cardioversione senza effettuare una TEE)
Cosa visualizziamo mediante una TEE?
Visualizes the atria and the left atrial appendage (hotspots for thrombogenesis) to identify thrombi before attempting cardioversion!
Further assesses heart function and rules out underlying structural disease
LAB
Ricorda sempre l’overlapping presente tra patologie differenti. Un soggetto con FA, storia di DVT e segni di PE che presenti D-dimero elevato, va sottoposto a angio-ct!!🧨
- TSH, fT4: to screen for hyperthyroidism
- Serum electrolytes (Na+, K+, Mg2+, and Ca2+): to identify electrolyte imbalances
- Troponin levels: to rule out myocardial infarction
👓D-dimer levels: if risk factors (e.g., DVT) or clinical features of pulmonary embolism are present (If D-dimer test levels are elevated, chest CT is required to rule out pulmonary embolism
- Brain-natriuretic peptide (BNP): to rule out heart failure
- CBC: to identify anemia, infection
- BUN, serum creatinine: to identify chronic kidney disease
- Ethanol levels, digoxin levels, and/or urine toxicology (e.g., cocaine, amphetamines)
DDx
AF should be differentiated from other supraventricular tachyarrhythmias with a narrow QRS complex.
Managment
- Correcting reversible causes and/or treatable conditions (e.g., hyperthyroidism, electrolyte imbalances)
- Controlling heart rate and/or rhythm
- Providing anticoagulation
Controlling heart rate and/or rhythm
ATTENZIONE: i farmaci per il controllo della frequenza riducono i sintomi associati alla FA e sono utili nella gestione di soggetti con concomitante HF, ma non agiscono assolutamente sul rimodellamento cardiaco associato a FA, che si instaura già dopo 6 mesi di permanenza della tachiaritmia. Il controllo sul rimodellamento ventricolare è assicurato invece dai farmaci per il ristoro del ritmo sinusale! (antiaritmici)
- Unstable AF: emergent electrical cardioversion (If AF does not terminate, cardioversion should be repeated with increased shock energy after adjusting the electrodes’ position)
- Stable AF: rate control or rhythm control strategies to control AF and prevent long-term recurrence
Rate control measures are preferred because rhythm control measures are associated with more side effects without being demonstrably superior. The rate control can be used for patients with paroxysmal, persistent, long-standing persistent, and permanent AF. However, since the goal of the rhythm control strategy (amiodarone) is to prevent ventricular remodeling by reverting the patient to sinus rhythm, it cannot be used for patients with long-standing persistent AF because atrial remodeling occurs within about 6 months of onset of AF!💥
Rate control
As symptoms are usually due to an increased ventricular rate, normalizing the rate helps relieve symptoms. The ideal heart rate is < 80 bpm. A less stringent rate control (< 110 bpm) may be permitted if the patient remains asymptomatic.
✔Indications
Elderly individuals, because have decreased clearance of antiarrhythmic drugs and are at increased risk of proarrhythmias (arrhythmias caused by antiarrhythmic therapy).
✔Contraindications
The use of rate control drugs such as digoxin, amiodarone, calcium channel blockers and/or beta blockers depresses AV node conduction. In patients with WPW syndrome, AV blockade can lead to increased conduction through the aberrant pathway and thus precipitate ventricular tachycardia or ventricular fibrillation. In questi casi di scelta diventa il propafenone.
✔Drugs
1st choice: beta blockers (esmolol, propanolol, metoprolol) OR nondihydropyridine calcium channel blockers (diltiazem, verapamil). Beta blockers are the ones most commonly used for rate control followed by nondihydropyridine calcium channel blockers. Beta blockers are preferred when AF is due to hyperthyroidism. Beta blockers should be avoided in a patient with COPD. Nondihydropyridine calcium channel blockers (ndhp CCB) cannot be used among patient with decompensated heart failure (LV systolic dysfunction/low ejection fraction) because they are negatively inotropic and lead to worsening of heart failure. ndhp CCBs may however be used in heart failure with preserved normal LV systolic function🧨
2nd choice: digoxin. Digoxin is preferred as first-line therapy in patients with decompensated HF when beta blockers are contraindicated👓.
3rd choice: dronedarone, amiodarone.Possesses both rate- and rhythm-control mechanisms
✔2nd line (ablative procedures)
AV nodal ablation and implantation of a permanent ventricular pacemaker. The pacemaker should ideally be implanted 4–6 weeks before AV nodal ablation. AV nodal ablation is an irreversible procedure and eliminates the need for rate control drugs. However, it leads to life long dependence on a pacemaker and should therefore not be performed without first attempting rate control with drug therapy. Maximum benefit is seen among elderly patients, patients with tachycardia-induced cardiomyopathy, and those refractory to rate control medications. A biventricular pacing system is recommended for AF patients with decompensated heart failure👓
