Shadechapter09.ppt [read only]
- 1. Q I A 9 Fast & Easy ECGs – A Self-Paced Learning Program Atrial Dysrhythmias
- 2. Atrial Dysrhythmias • Originate in the atrial tissue or in the internodal pathways Q
- 3. Atrial Dysrhythmias • Believed to be caused by three mechanisms: – Automaticity – Triggered activity – Reentry I
- 4. Atrial Dysrhythmias • Can affect ventricular filling time and diminish the strength of the atrial contraction • This can lead to decreased cardiac output and ultimately decreased tissue perfusion 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 I
- 6. Wandering Atrial Pacemaker • Pacemaker site shifts between the SA node, atria and/or AV junction – This produces its most characteristic feature – P’ waves that change in appearance I
- 8. Wandering Atrial Pacemaker • Generally caused by the inhibitory vagal effect of respiration on the SA node and AV junction • Normal finding in children, older adults, and well-conditioned athletes • Not usually of any clinical significance • May be related to some types of organic heart disease and drug toxicity, specifically digitalis I
- 9. Premature Atrial Complexes (PACs) • Early ectopic beats that originate outside the SA node
- 10. 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
- 12. Noncompensatory Pause • 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.
- 15. Premature Atrial Complexes • Isolated PACs seen in patients with healthy hearts are considered insignificant • Asymptomatic patients usually only require observation I
- 16. Premature Atrial Complexes • 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
- 18. Premature Atrial Complexes • May have wide QRS complexes when seen with abnormal ventricular conduction – For this reason they can be confused with PVCs I
- 19. Atrial Tachycardia • Rapid dysrhythmia (rate of 150 to 250 BPM) that arises from the atria. • Rate is so fast it overrides the SA node I
- 22. Atrial Tachycardia • May occur in short bursts or may be sustained • Short bursts are well-tolerated in otherwise normally healthy people • With sustained rapid ventricular rates, ventricular filling may not be complete during diastole
- 23. 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 I
- 24. Multifocal Atrial Tachycardia (MAT) • Pathological condition that presents with changing P wave morphology and heart rates of 120 to 150 BPM I
- 25. Supraventricular Tachycardia (SVT) • Arises from above the ventricles but cannot be definitively identified as atrial or junctional tachycardia because the P’ waves cannot be seen sufficiently • Includes paroxysmal supraventricular tachycardia, (PSVT), nonparoxysmal atrial tachycardia, multifocal atrial tachycardia
- 26. Atrial Flutter • Rapid depolarization of a single focus in the atria at a rate of 250 to 350 BPM
- 27. Atrial Flutter • Produces atrial waveforms that have a characteristic saw-tooth appearance – Called flutter waves (F waves)
- 28. Atrial Flutter
- 29. 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 I
- 30. Atrial Fibrillation • Chaotic, asynchronous firing of multiple areas within the atria I A
- 31. Atrial Fibrillation • Totally irregular rhythm with no discernible P waves instead there is a chaotic baseline of fibrillatory waves (f waves) representing atrial activity
- 33. 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)
- 34. Practice Makes Perfect • Determine the type of dysrhythmia I
- 35. Practice Makes Perfect • Determine the type of dysrhythmia I
- 36. Practice Makes Perfect • Determine the type of dysrhythmia I
- 37. Practice Makes Perfect • Determine the type of dysrhythmia I
- 38. Practice Makes Perfect • Determine the type of dysrhythmia I
- 39. Practice Makes Perfect • Determine the type of dysrhythmia I
- 40. Practice Makes Perfect • Determine the type of dysrhythmia I
- 41. Practice Makes Perfect • Determine the type of dysrhythmia I
- 42. Practice Makes Perfect • Determine the type of dysrhythmia I
- 43. Practice Makes Perfect • Determine the type of dysrhythmia I
- 44. 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).
- 45. 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.
- 46. 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.
- 47. 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.