Atrial Dysrhythmias

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Atrial Dysrhythmias

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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

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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


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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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• 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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• 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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• 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


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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


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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


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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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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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Atrial Dysrhythmias