1. Fast & Easy ECGs, 2nd E – A Self-Paced Learning Program12
Atrial Dysrhythmias
Fast & Easy ECGs, 2nd E – A Self-Paced Learning Program

2. 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
Question to ask “What is the normal pacemaker site which initiates the heartbeat?”
Instructional Point:
Most atrial dysrhythmias are benign, but tachycardias that originate from the atria can be dangerous. Q I

3. Atrial Dysrhythmias Believed to be caused by three mechanisms:
Enhanced automaticity
Circus reentry
Afterdepolarization
Instructional point:
Increased automaticity and triggered activity are disorders of impulse formation. Reentry is a problem with impulse conduction. In increased automaticity, the atrial cells spontaneously depolarize and initiate impulses before the SA node has a chance to generate a normal impulse. Injured cells sometimes only partially repolarize. Partial repolarization can lead to a repetitive ectopic firing called triggered activity. Reentry occurs when an impulse is delayed along a slow conduction pathway and the impulse is able to remain active long enough to produce another impulse in the atria while the ventricles are repolarizing. I

4. 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
Instructional point:
The atrial contraction is called the atrial “kick” and normally supplies the ventricles with about 30% of their blood. I

5. 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
Instructional point:
With atrial dysrhythmias, the appearance of the P’ waves will depend on the site where the atrial impulses originate. Typically, the closer the site of origin is to the SA node, the more it looks like a normal P wave.
Also, the QRS complexes may be wider than normal if there is intraventricular conduction defect, aberrancy or preexcitation. I

6. Premature Atrial Complexes (PACs)
Early beats that originate outside the SA node before it has a chance to depolarize

7. 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

8. 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
Instructional point:
The reason a noncompensatory pause occurs is that the electrical activity of the premature atrial beat can enter the sinus node and reset its timing, thus allowing it to fire before its next scheduled beat. This creates an irregularity in the R-R pattern. I

9. Causes of PACs Most common cause of PACs is enhanced automaticity
Other causes include:
Instructional point:
In some cases there is no apparent cause. I

10. Effect of PACs
Isolated PACs seen in patients with healthy hearts are considered insignificant
Asymptomatic patients usually only require observation
Instructional points:
PACs commonly cause no symptoms and can go unrecognized for years.
The patient may perceive PACs as “palpitations” or skipped beats. I

11. 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

12. Grouping of PACs
Bigeminal
PACs can be described by how they are intermingled among normal beats
Every other beat is a PAC
Trigeminal
Every 3rd beat is a PAC
Ask question – “What do bigeminal, trigeminal and quadrigeminal mean?”
Quadrigeminal
Every 4th beat is a PAC Q

13. 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
Instructional point:
To tell the difference between PACs and PVCs look for either a compensatory or non-compensatory pause and the presence or absence of P waves. I

14. 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
Instructional Point:
Also referred to as nonconducted PACs

15. 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

16. 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
Instructional point:
With wandering atrial pacemaker the regularity of the rhythm also varies slightly. I

17. Causes of Wandering Atrial Pacemaker
Generally caused by inhibitory vagal effect of respiration on SA node and AV junction
Other causes include the following:

18. 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

19. 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

20. Atrial Tachycardia
Rapid dysrhythmia (rate of 150 to 250 BPM) that arises from the atria
Rate is so fast it overrides the SA node
Instructional point:
When the onset of the atrial tachycardia is sudden (and typically witnessed) it is called paroxysmal. I

21. 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:

22. 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

23. 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
Instructional point:
Atrial tachycardia can cause vertigo (dizziness), lightheadedness, syncope, hypotension and congestive heart failure. I

24. 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
Instructional point:
If the block is constant, it will have the same number of P’ waves preceding each QRS complex, but, if the block is variable, the number of P’ waves will change. I

25. Treatment of Atrial Tachycardia
Treatment is dependent on the type of tachycardia and symptom severi­ty
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.

26. 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
Instructional point:
When atrial tachycardia is due to some underlying abnormality (e.g., electrolyte imbalance, drug toxicity), the conversion to a normal rhythm with cardioversion may be temporary because the causative factor has not been eliminated. In such cases, a recurrence of atrial tachycardia soon after successful electrical cardioversion does not warrant additional electrical cardioversion attempts until the underlying problem has been resolved. In the patient with COPD, correction of hypoxia and electrolyte imbal­ances is indicated I

27. 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
Instructional point:
Adenosine can be used in aberrancy. If the ectopy turns out to be PVCs, adenosine will not cause any harm. I

28. 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

29. Multifocal Atrial Tachycardia (MAT)
Pathological condition that presents with changing P wave morphology and heart rates of 120 to 150 BPM
Instructional point:
Multifocal atrial tachycardia has the same characteristics (changing P wave morphology) as wandering atrial pacemaker. I

30. 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

31. 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:

32. 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

33. 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

34. 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

35. 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

36. 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

37. 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

38. 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)

39. Causes of Atrial Flutter
Usually caused by conditions that elevate atrial pressures and enlarge the atria
Another cause is increased automaticity
Other causes include:

40. 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
Instructional point:
Rapid ventricular rates can produce a loss of “atrial kick,” decreased ventricular filling time and decreased coronary artery perfusion. This can lead to angina, heart failure, pulmonary edema, hypotension and syncope. I

41. 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

42. 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

43. Atrial Fibrillation
Results for chaotic, asynchronous firing of multiple areas within the atria
Instructional point:
it is believed that atrial fibrillation stems from the rapid firing of ectopic impulses (greater than 350 beats per minute) in circus reentry pathways. I

44. 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

45. 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:

46. 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)

47. 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

48. 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

49. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 375 BPM, Ventricular rate 100 BPM, regular rhythm, atrial waveforms have saw-tooth pattern F waves are present, , QRS (more accurately described as RS) complexes at 0.08 seconds, PRI immeasurable, QT immeasurable. Atrial flutter with a 4 to 1 conduction ratio. I

50. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate is greater than 350 BPM, Ventricular rate 100 BPM, totally irregular, P waves are indiscernible f waves are present, QRS (more accurately described as QS) complexes at 0.12 seconds, PRI is immeasurable, QT is immeasurable. Atrial fibrillation. I

51. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 65 BPM, Ventricular rate 65 BPM, occasionally irregular (due to the premature beat), normal and upright P waves in the underlying rhythm, P′ wave of premature beat differs from P waves of underlying rhythm, notched QRS complexes at 0.10 seconds,
PRI 0.16 seconds, QT 0.38 seconds. Normal sinus rhythm with a premature atrial complex (PAC)
(2nd beat). I

52. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 300 BPM, Ventricular rate 70 BPM, variably irregular rhythm, atrial waveforms have sawtooth pattern F waves are present, normal QRS complexes at 0.08 seconds, PRI immeasurable, QT immeasurable. Atrial flutter with a variable conduction ratio. I

53. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 80 BPM, Ventricular rate 80 BPM, regular rhythm, varying P waves, normal QRS complexes at 0.08 seconds, PRI varies, QT seconds, normal. Wandering atrial pacemaker. I

54. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 60 BPM, Ventricular rate 60 BPM, occasionally irregular (due to the premature beat), normal and upright P waves in the underlying rhythm, P′ wave of premature beat differs from P waves of underlying rhythm, normal QRS complexes at 0.10 seconds, PRI 0.16 seconds, QT 0.48 seconds. Normal sinus rhythm with a premature atrial complex (PAC) (2nd beat). I

55. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 214 BPM, Ventricular rate 214 BPM, regular rhythm, P is absent, normal QRS complexes at 0.08 seconds, PRI is immeasurable, QT seconds. Supraventricular tachycardia. I

56. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 58 BPM, Ventricular rate 58 BPM, frequently irregular (for what you see on the tracing), normal and upright P waves (P′ waves of premature beat differ from the P waves of the underlying rhythm, and one is buried in T wave of the preceding beat), QRS (more accurately described as RS) complexes at 0.10 seconds, PRI 0.24 seconds, QT 0.48 seconds. Sinus bradycardia with 2 premature atrial complexes (PACs) (4th and 6th beats). There is also a 1st-degree AV heart block. I

57. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 120 BPM, Ventricular rate 120 BPM, irregular, varying P waves, normal QRS complexes at 0.06 seconds, PRI immeasurable, QT seconds. Multifocal atrial tachycardia. I

58. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 60 BPM at first then immeasurable, Ventricular rate 60 BPM accelerating to 167 BPM, regular then sudden acceleration in heart rate, normal P waves then absent, normal QRS complexes at 0.10 seconds, PRI seconds, QT seconds. Paroxysmal supraventricular tachycardia. I

59. 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)

60. 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

61. 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

62. 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