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Atrial Dysrhythmias
Fast & Easy ECGs, 2nd E – A Self-Paced Learning Program
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Atrial Dysrhythmias
• Originate in the atrial tissue or in the internodal pathways
• Are among the most common types of dysrhythmias, particularly in persons older than 60 years of age Q
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Atrial Dysrhythmias
• Believed to be caused by three mechanisms: – Enhanced automaticity– Circus reentry– Afterdepolarization
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Atrial Dysrhythmias
• Can diminish the strength of the atrial contraction and affect ventricular filling time – This can lead to decreased cardiac output and
ultimately decreased tissue perfusion
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Atrial Dysrhythmias
• Key characteristics include:– P’ waves (if present) that differ in appearance
from normal sinus P waves – Abnormal, shortened, or prolonged P’R intervals – QRS complexes that appear narrow and normal
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Premature Atrial Complexes (PACs)
• Early beats that originate outside the SA node before it has a chance to depolarize
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Premature Atrial Complexes (PACs)
• Produce an irregularity in the rhythm – P’-P and R’-R intervals are shorter than the P-P
and R-R intervals of underlying rhythm
• Have P’ waves that are upright (in lead II) preceding each QRS complex but have a different morphology (appearance) than the P waves of underlying rhythm
• Followed by a noncompensatory pause
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Noncompensatory Pause
• Is a pause where there are less than two full R-R intervals between the R wave of the normal beat which precedes the PAC and the R wave of the first normal beat which follows it
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Causes of PACs
• Most common cause of PACs is enhanced automaticity
• Other causes include:
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Effect of PACs
• Isolated PACs seen in patients with healthy hearts are considered insignificant
• Asymptomatic patients usually only require observation
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Effect of PACs
• May predispose patient with heart disease to more serious atrial dysrhythmias:– atrial tachycardia– atrial flutter– atrial fibrillation
• Can serve as an early indicator of an electrolyte imbalance or congestive heart failure in patients experiencing an acute myocardial infarction
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Grouping of PACs
• PACs can be described by how they are intermingled among normal beats
Q
Bigeminal
Trigeminal
Quadrigeminal
Every other beat is a PAC
Every 3rd beat is a PAC
Every 4th beat is a PAC
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Aberrantly Conducted PAC• Occurs when a
PAC travels through the ventricular conduction pathway abnormally resulting in an abnormal looking QRS complex– For this reason
they can be confused with PVCs
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Blocked PAC• Occurs when an
atrial impulse arrives too early, before the AV node has a chance to repolarize
• As a result, the P’ wave fails to conduct to the ventricles
• Identified by a premature P’ wave that is not followed by a QRS complex
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Treatment of PACs
• Generally do not require treatment • PACs caused by the use of caffeine, tobacco,
or alcohol or by anxiety, fatigue, or fever can be controlled by eliminating the underlying cause
• Frequent PACs may be treated with drugs that increase the atrial refractory time – This includes beta-adrenergic blockers and
calcium channel blockers
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Wandering Atrial Pacemaker• Pacemaker site
shifts between SA node, atria and/or AV junction– This produces its
most characteristic feature – P’ waves that change in appearance
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Causes of Wandering Atrial Pacemaker
• Generally caused by inhibitory vagal effect of respiration on SA node and AV junction
• Other causes include the following:
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Effects of Wandering Atrial Pacemaker
• Wandering atrial pacemaker is rarely serious, having no effect on cardiac output
• Normal finding in children, older adults, and well-conditioned athletes
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Treatment of Wandering Atrial Pacemaker
• No treatment is necessary for patients experiencing wandering atrial pacemaker– However, chronic dysrhythmias are a sign of heart
disease and should be monitored
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Atrial Tachycardia
• Rapid dysrhythmia (rate of 150 to 250 BPM) that arises from the atria
• Rate is so fast it overrides the SA node
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Causes of Atrial Tachycardia• Digitalis toxicity is
the most common cause of atrial tachycardia
• Also, sudden onset atrial tachycardia is common in patients who have Wolff-Parkinson-White syndrome
• Other causes include:
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Effects of Atrial Tachycardia• Symptoms can develop abruptly and may go
away without treatment• Short bursts are well-tolerated in otherwise normally healthy
people• Alternatively, they may last a few minutes or as
long as one to two days, sometimes continuing until treatment is delivered
• With the rapid heartbeat seen with atrial tachycardia, there is less time for the ventricles to fill. – This can reduce stroke volume and lead to decreased
cardiac output
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Effects of Atrial Tachycardia
• Can significantly compromise cardiac output in patients with underlying heart disease
• Fast heart rates increase oxygen requirements – May increase myocardial ischemia and potentially
lead to myocardial infarction
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Atrial Tachycardia with Block
• Due to the rapid atrial rates seen with atrial tachycardia, the AV junction is sometimes unable to carry all the impulses– This is called atrial tachycardia with block
• This then results in more than one P’ wave preceding each QRS complex
• Most commonly, only one of every two beats (a 2 to 1 block) is conducted to the ventricles
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Treatment of Atrial Tachycardia
• Treatment is dependent on the type of tachycardia and symptom severi ty– Directed at eliminating the cause and decreasing
ventricular rate. – Patients who are symptomatic (e.g., chest pain,
hypotension) should receive oxygen, an IV infusion of normal saline administered at a keep-open rate, and prompt delivery of synchronized cardioversion, use of vagal maneuvers or medication administration.
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Treatment of Atrial Tachycardia
• Synchronized cardioversion is indicated if the patient is symptomatic – In the conscious patient, consider sedation before
cardioversion• However, do not delay cardioversion
– If this fails to convert the rhythm, the energy level may be increased
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Treatment of Atrial Tachycardia
• If the patient is stable, vagal maneuvers and drug therapy (adenosine) may be used
• If these treatments fail to resolve the tachycardia, calcium channel blockers (verapamil, diltiazem) and beta-adrenergic blockers (if no contraindications exist) may be considered
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Treatment of Atrial Tachycardia
• Atrial overdrive pacing may be employed to stop this dysrhythmia
• If the dysrhythmia is related to WPW syndrome, catheter ablation may be indicated
• Procainamide, amiodarone, or sotalol may be considered in wide complex tachycardias
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Multifocal Atrial Tachycardia (MAT)• Pathological
condition that presents with changing P wave morphology and heart rates of 120 to 150 BPM
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Appearance of Multifocal Atrial Tachycardia (MAT)
• MAT is often misdiagnosed as atrial fibrillation with rapid ventricular response but can be identified by looking closely for clearly visible but changing P’ waves – P’ waves change in morphology as often as from
beat to beat resulting in three or more different-looking P waves
• Varying PR intervals and narrow QRS complexes also seen
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Causes of Multifocal Atrial Tachycardia (MAT)
• Is more common in the elderly
• It is usually precipitated by acute exacerbation (with resultant hypoxia) of COPD, elevated atrial pressures, or heart failure
• Other causes include:
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Effects of Multifocal Atrial Tachycardia (MAT)
• Patient may complain of palpitations • Signs and symptoms of decreased cardiac
output, such as hypotension, syncope, and blurred vision, may be seen
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Treatment of Multifocal Atrial Tachycardia (MAT)
• Appropriate therapy is treatment of the underlying condition
• In symptomatic patients treatment may include administering calcium channel blockers (verapamil, diltiazem)– Beta-adrenergic blockers are typically
contraindicated because of the presence of severe underlying pulmonary disease
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Supraventricular Tachycardia (SVT)• Arises from
above the ventricles but cannot be definitively identified as atrial or junctional tachycardia because the P’ waves cannot be sufficiently seen
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Supraventricular Tachycardia (SVT)
• This group of tachycardias includes paroxysmal SVT (PSVT), nonparoxysmal atrial tachycardia, MAT, AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia, and junctional tachycardia
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Supraventricular Tachycardia (SVT)
• Sometimes wide QRS complexes are seen– Due to an intraventricular conduction defect or
other condition such as aberrant conduction – Makes assessment of SVT difficult as it appears to
be ventricular tachycardia• Called wide complex tachycardia of unknown origin
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Atrial Flutter• Results from
circus reentry– Impulse from
SA node circles back through atria, returning to the SA node region and repeatedly restimulating the AV node over and over at a rate of 250 to 350 BPM
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Appearance of Atrial Flutter
• On the ECG, the P waves lose their distinction due to the rapid atrial rate
• Waves blend together in a saw-tooth or picket fence pattern called flutter waves, or F waves– Produces atrial waveforms that have a
characteristic saw-tooth appearance called flutter waves (F waves)
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Causes of Atrial Flutter
• Usually caused by conditions that elevate atrial pressures and enlarge the atria
• Another cause is increased automaticity
• Other causes include:
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Effects of Atrial Flutter
• Often well-tolerated• The number of impulses conducted through
the AV node determines the ventricular rate (i.e. 3:1 conduction ratio) – Slower ventricular rates (< 40 BPM) or faster
ventricular rates (> 150 BPM) can seriously compromise cardiac output
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Treatment of Atrial Flutter
• Vagal maneuvers may make flutter waves more visible by transiently increasing the degree of the block
• In patients experiencing an associated rapid ventricular rate who are symptomatic but stable, treatment is directed at controlling the rate or converting the rhythm to sinus rhythm
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Treatment of Atrial Flutter
• Symptomatic patients (e.g., hypotension, signs of shock, or heart failure) should receive oxygen, an IV infusion of normal saline administered at a keep-open (TKO) rate, and prompt treatment
• Synchronized cardioversion should be considered in unstable patients– If necessary, the energy may be increased with
subsequent shocks
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Atrial Fibrillation• Results for
chaotic, asynchronous firing of multiple areas within the atria
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Appearance of Atrial Fibrillation
• Totally irregular rhythm with no discernible P waves– Instead there is a chaotic baseline of fibrillatory
waves (f waves) representing atrial activity
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Causes of Atrial Fibrillation• Atrial fibrillation is
more common than atrial tachycardia or atrial flutter
• It can occur in healthy persons after excessive caffeine, alcohol, or tobacco ingestion or because of fatigue and acute stress
• Other causes include:
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Effects of Atrial Fibrillation
• Leads to loss of atrial kick decreasing cardiac output by up to 25%
• Patients may develop intra-atrial emboli as the atria are not contracting and blood stagnates in the atrial chambers forming a thrombus (clot) – Predisposes patient to systemic emboli (stroke)
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Treatment of Atrial Fibrillation
• If the rate of ventricular response is normal, the dysrhythmia is usually well tolerated and requires no immediate intervention
• Patients experiencing atrial fibrillation and an associated rapid ventricular rate who are symptomatic but stable, treatment is directed at controlling the rate or converting the rhythm to sinus rhythm
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Treatment of Atrial Fibrillation
• Symptomatic patients (e.g., hypotension, signs of shock, or heart failure) should receive oxygen, an IV infusion of normal saline administered at a TKO rate, and prompt synchronized cardioversion – If necessary, the energy level may be increased
with subsequent shocks
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Practice Makes Perfect
• Determine the type of dysrhythmia
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Practice Makes Perfect
• Determine the type of dysrhythmia
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Practice Makes Perfect
• Determine the type of dysrhythmia
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Practice Makes Perfect
• Determine the type of dysrhythmia
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Practice Makes Perfect
• Determine the type of dysrhythmia
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Practice Makes Perfect
• Determine the type of dysrhythmia
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Practice Makes Perfect
• Determine the type of dysrhythmia
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Practice Makes Perfect
• Determine the type of dysrhythmia
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Practice Makes Perfect
• Determine the type of dysrhythmia
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Practice Makes Perfect
• Determine the type of dysrhythmia
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Summary• Atrial dysrhythmias originate outside the SA node
in the atrial tissue or in the internodal pathways• Three mechanisms responsible for atrial
dysrhythmias are increased automaticity, triggered activity and reentry
• Key characteristics for atrial dysrhythmias: – P’ waves (if present) that differ from sinus P waves– Abnormal, shortened, or prolonged P’R intervals– QRS complexes that appear narrow and normal
(unless there is an intraventricular conduction defect, aberrancy or preexcitation)
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Summary• With wandering atrial pacemaker the pacemaker
site shifts between the SA node, atria and/or AV junction– Produces its most characteristic feature, P’ waves that
change in appearance• Premature atrial complexes (PACs) are early
ectopic beats that originate outside the SA node – Produce an irregularity in the rhythm – P’ waves should be an upright (in lead II) preceding
the QRS complex but has a different morphology than the P waves in the underlying rhythm
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Summary
• Atrial tachycardia is a rapid dysrhythmia (rate of 150 to 250 beats per minute) that arises from the atria
• Multifocal atrial tachycardia (MAT) is a pathological condition that presents with the same characteristics as wandering atrial pacemaker but has heart rates of 120 to 150 beats per minute
• Supraventricular tachycardia arises from above the ventricles but cannot be definitively identified as atrial or junctional because the P’ waves cannot be seen with any real degree of certainty
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Summary
• Atrial flutter is a rapid depolarization of a single focus in the atria at a rate of 250 to 350 beats per minute – Produces atrial waveforms that have a characteristic
saw-tooth or picket fence appearance • Atrial fibrillation occurs when there is chaotic,
asynchronous firing of multiple areas within atria at a rate greater than 350 beats per minute– Produces a totally irregular rhythm with no
discernible P waves
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