Atrial Arrhythmia EKG Recognition Etiology Evaluation Therapy

Premature Atrial P w/ early Normal variant None necessary if No therapy indicated unless significantly
Contractions occurring QRS Stimulants (Caffeine, EtOH, asymptomatic symptomatic
identical to sinus Cocaine, Catecholamines) Consider beta blocker, rarely antiarrhythmic
beats preceded by a Atrial enlargement
P wave HTN
May occur in runs Valvular disease (Mitral or
Tricuspid regurge, Aortic
Stenosis)
Ischemia
Irritants (pneumonia, surgery,
mediastinitis)
Paroxysmal Atrial Regular tachycardia HYPERthyroidism EKG Immediate intervention to ablate
Tachycardia rate 150-250 bpm Toxins, especially EtOH and TSH, Digoxin level DC cardioversion if hypotensive or in CHF
P waves evident sympathetic amines (if appropriate) Adenosine 6mg IV via proximal vein,
before each QRS HTN Echocardiogram repeated with 12mg if unsuccessful
Usually narrow Rarely ischemia Consider exercise Diltiazem 20mg IV or Verapamil 5mg IV,
complex QRS Digoxin toxicity stress testing repeated x2 if unsuccessful
Sudden onset and Metoprolol or Atenolol 5mg IV, repeated x3
cessation if unsuccessful
Long term therapy
Metoprolol 50mg bid or Atenolol 50mg qd
Verapamil or Diltiazem 240mg daily
Consider antiarrhythmic if above
unsuccessful
Atrial Flutter regular atrial waves Irritants Drug screen Acute intervention for tachycardic response
at rate 250-350/min Toxins Echocardiogram Beta Blocker, Calcium Blocker, digoxin
QRS rate generally Stimulants Consider stress Vagal maneuver
regular, but may be Atrial enlargement testing Adenosine occasionally helpful
irregular Valvular disease DC Cardioversion if in extremis
Atrial waves often Long term management
have biphasic Beta Blocker, Digoxin, Calcium Blocker
configuration Consider antiarrhythmic
Consider anticoagulation
Ablation/pacemaker
Multifocal Atrial Irregular rhythm Most commonly assoc. w/ Anticoagulation now indicated to prevent
Rhythm with P waves before decompensated pulmonary embolus
each QRS, but at disease (COPD) Poorly responsive to medications which slow
least three different Occasionally assoc. w/ AV conduction
morphologies valvular disease 25-35% response to antiarrhythmics
Often difficult to Maintenance depends on therapy of
distinguish from pulmonary condition
atrial fibrillation

1
Atrial Arrhythmia EKG Recognition Etiology Evaluation Therapy
Atrial Fibrillation Irregular rhythm with no reproducable P waves See below Echocardiogram Control ventricular response
May have coarse or fine baseline deflections Labs for TSH, toxins Convert to sinus rhythm
Rate widely variable Stress testing Prevent thrombosis/embolism
Invasive therapies

Atrial Fibrillation
An irregularly irregular rhythm with no discernable P waves
Small irregular deviations of the baseline are called f waves (may be coarse or fine)
Conduction to ventricle may range from bradycardic to severe tachycardia
Epidemiology
Found in 1% of population over 60, and 6% in population over 70 somewhat more common in men than women
With coronary disease in age group>70, incidence is 10%
Extended List of Etiologies
Ischemic Heart Disease
Acute inflammation
pericarditis
pneumonia/pleuritis
Chronic inflammation
connective tissue disorder
chronic pericardial effusion
Valvular heart disease
Chronic and acute hypertension
Cardiotoxins chemotherapeutics, EtOH, stimulant drugs
Thyrotoxicosis and hyperthyroidism
Cardiomyopathy
Lone no discernable etiology; us. seen in younger age group
Physical findings
irregularly irregular rhythm
varying intensity of first heart sound; occasional pulse deficit compared to auscultated rate
other findings associated with etiology
Screen for etiology
echocardiogram for valve disorder, cardiomyopathy, and pericardial effusion
stress testing for ischemia
laboratory evaluation for thyroid function, glucose, and inflammatory markers if indicated
cardiac catheterization may be indicated if ischemia suspected

2
Methods to identify the occurrence of fibrillation if not present at time of examination
24 hour Holter monitoring
30 day Event recorder
Continuous loop recorder
Implanted continuous recorder
Therapy
Control Ventricular Response any agent that reduces AV node conduction will slow ventricular response
Digoxin effectiveness limited to resting HR; poor control of exercise response; little effect on arrhythmia prevention;
allows for rapid return to sinus rhythm; relatively safe
Verapamil/Diltiazem similar to digoxin in mechanism of effect; better rate control w/ exercise; excellent indication w/
HTN
Beta Blocker
Adenosine NOT indicated (short acting AV node blocker of little use)
Therapeutic options: acute
IV beta blocker propranol, metoprolol, atenolol
IV diltiazem
IV verapamil
IV digoxin
Therapeutic options: chronic
Oral beta blocker. NOT carvedolol
Oral digoxin
Oral diltiazem
Oral verapamil
Conversion to sinus rhythm
Often occurs spontaneously in acute setting when ventricular rate is controlled with medications
Digoxin: effective for low risk patients only
Verapamil/diltiazem: low and moderate risk patients
Amiodarone: statistically best for maintenance in all risk groups
Sotolol: nearly as effective as amiodarone, but cannot be used in patients with heart failure
Cardioversion with Type Ia (Quinidine) or Type Ic (Ibutilide) 50-60% successful
DC Cardioversion acutely if in extremis (pt. hemodynamically unstable)
Bipolar countershock most effective at lower energy
Sedation required
Rare serious complications ventricular fibrillation, cardiac standstill, embolization
85% successful initially

3
 Reversion to fibrillation most frequent within 24 hours
Elective cardioversion 85% successful initially. Problem is maintenance.
Address and stabilize causative factors
Success less with significant enlargement of LV, LA or RA, or with significant valve disease
Long term success of conversion varies depending on etiology and duration of fibrillation
Low risk patients require no antiarrhythmic for maintenance
Higher risk patients require antiarrhythmics, and still the recurrence rate is 50% at three years
Maintenance of sinus rhythm
Dependent on cause of fib; acute stress inducing illness or respiratory compromise failure rate; unrepaired
valvular disease failure
Large atria ( 5cm) assoc. w/ 75% reversion rate; severe LV dysfunction (LVEF less than 40%) assoc. w/ 50%
reversion rate
Quinidine/ Procainamide/ Disopyramide 40-50% effective in direct arrhythmia prevention; risk of sudden cardiac
death (Quinidine); significant drug specific side effects
Amiodarone 70% effective in direct arrhythmia prevention; rare but highly morbid side effects (thyroid, lungs, liver)
Sotolol 65% effective in direct arrhythmia prevention; high risk of proarrhythmia
Prevention of thrombosis/embolism heparin acutely, Warfarin, Aspirin
Clinically most important risk of atrial fibrillation is thrombosis and embolus, especially cerebral
Highest risk rheumatic or other significant valvular disease; dilated LA or LV with Cardiomyopathy; prior embolic
event
Risk of embolus 14% annual risk in highest group; 7% annual risk in general group; <1% risk in Lone A-Fib
Multiple randomized trials over the past ten years clearly indicate the benefit of anticoagulation risk reduction by
60%
Requires warfarin anticoagulation to an INR level of 2.0 to attain best reduction
Risk of bleed when carefully monitored is less than 3% per year in patients under 70years of age
Anticoagulation not indicated for pts. w/ bleeding disorders, history of hemorrhage, compliance problems, CNS tumor
Alternative in these cases is Aspirin therapy at 325-650mg daily. Risk reduction 30%
Invasive Therapies Indicated for refractory arrhythmia & for high risk patients unable to tolerate medical therapy
Maze procedure open heart surgery to incise atrium and create electrical channel from sinus to AV node; 80%
successful; does not guarantee atrial function; may still require anticoagulation
Catheter AV node ablation w/ pacemaker insertion; disallows AV synchrony; requires anticoagulation