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Atrial Fibrillation
Atrial fibrillation occurs when the normal electrical signal generated by the sinoatrial
(SA) node is overwhelemed by disorganized signals originating in other areas. When this
happens, the myocytes contract at different times and the atrium “quivers” instead of
beating in a coordinated manner. Atrial fibrillation may be paroxysmal or permanent.
Atrial fibrillation is the most common cardiac arrhythmia.
The single most important risk factor for atrial fibrillation is mitral valve stenosis.
Incidence of atrial fibrillation increases with age – 8% of patients over age 80 have atrial
fibrillation.
The AV node only conducts some of the atrial impulses through to the ventricles. The
atrial rate may exceed 500 bpm, but the ventricular rate is typically 120-180 bpm
Atrial fibrillation leads to a rapid and irregular heartbeat, which in turn causes
palpitations and exercise tolerance. Since the “quivering” atria are unable to pump
blood effectively, venous stasis may lead to congestive symptoms such as shortness of
breath and edema. This rhythm (and its symptoms) may occur intermittently.
Physical exam findings include an irregular heart rate >100 beats per minute EKG will
show disorganized baseline electrical activity in the absence of p-waves., a heart rate
>100bpm, and narrow QRS complexes (since the signal originates upstream of the AV
node).
Because blood pressure varies beat to beat, digital blood pressure machines often have
trouble getting accurate measurements in patients with atrial fibrillation.
Laboratory workup should include, at a minimum, testing for renal function,
electrolytes, TSH, and CBC.
Complications of atrial fibrillation arise from reduced cardiac output, increased cardiac
oxygen demand, or thromboembolism.
Because the atria quiver instead of contracting, blood remains in the atrium and may
clot, leading to embolic events such as stroke. The risk of stroke may be increased even
further if the patient has other risk factors (hypertension, etc).
Myocardial infarction may arise secondary to increased cardiac oxygen demand.
Reduced cardiac output may lead to symptoms of congestive heart failure, such as
pulmonary or lower etremity edema.
Treatment of atrial fibrillation may include rate control and/or rhythm control.
Anticoagulation is added to prevent stroke and thromboembolism.
Warfarin is the medication of choice to prevent stroke in atrial fibrillation, but other
anticoagulants such as dabigatran (Pradaxa) may be used. Note: Remember that
anticoagulants are not the same as antiplatelet medications such as aspirin and
clopidogrel (Plavix).
Note that coagulation studies (aPTT/INR) should be ordered before beginning
anticoagulant therapy.
Rate control is achieved using beta blockers or calcium channel blockers.
Rhythm control is achieved using synchronized cardioversion or antiarrhythmic agents
such as procainamide, amiodarone and ibutilide. Long-term oral medications may be
necessary for maintenance.

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Atrial fibrillation

  • 1. Atrial Fibrillation Atrial fibrillation occurs when the normal electrical signal generated by the sinoatrial (SA) node is overwhelemed by disorganized signals originating in other areas. When this happens, the myocytes contract at different times and the atrium “quivers” instead of beating in a coordinated manner. Atrial fibrillation may be paroxysmal or permanent. Atrial fibrillation is the most common cardiac arrhythmia. The single most important risk factor for atrial fibrillation is mitral valve stenosis. Incidence of atrial fibrillation increases with age – 8% of patients over age 80 have atrial fibrillation. The AV node only conducts some of the atrial impulses through to the ventricles. The atrial rate may exceed 500 bpm, but the ventricular rate is typically 120-180 bpm Atrial fibrillation leads to a rapid and irregular heartbeat, which in turn causes palpitations and exercise tolerance. Since the “quivering” atria are unable to pump blood effectively, venous stasis may lead to congestive symptoms such as shortness of breath and edema. This rhythm (and its symptoms) may occur intermittently. Physical exam findings include an irregular heart rate >100 beats per minute EKG will show disorganized baseline electrical activity in the absence of p-waves., a heart rate >100bpm, and narrow QRS complexes (since the signal originates upstream of the AV node). Because blood pressure varies beat to beat, digital blood pressure machines often have trouble getting accurate measurements in patients with atrial fibrillation. Laboratory workup should include, at a minimum, testing for renal function, electrolytes, TSH, and CBC. Complications of atrial fibrillation arise from reduced cardiac output, increased cardiac oxygen demand, or thromboembolism. Because the atria quiver instead of contracting, blood remains in the atrium and may clot, leading to embolic events such as stroke. The risk of stroke may be increased even further if the patient has other risk factors (hypertension, etc). Myocardial infarction may arise secondary to increased cardiac oxygen demand.
  • 2. Reduced cardiac output may lead to symptoms of congestive heart failure, such as pulmonary or lower etremity edema. Treatment of atrial fibrillation may include rate control and/or rhythm control. Anticoagulation is added to prevent stroke and thromboembolism. Warfarin is the medication of choice to prevent stroke in atrial fibrillation, but other anticoagulants such as dabigatran (Pradaxa) may be used. Note: Remember that anticoagulants are not the same as antiplatelet medications such as aspirin and clopidogrel (Plavix). Note that coagulation studies (aPTT/INR) should be ordered before beginning anticoagulant therapy. Rate control is achieved using beta blockers or calcium channel blockers. Rhythm control is achieved using synchronized cardioversion or antiarrhythmic agents such as procainamide, amiodarone and ibutilide. Long-term oral medications may be necessary for maintenance.