Atrial dysrhythmias

djorgenmorris

1. Dysrhythmias Originating in the Atria Wandering Atrial Pacemaker Multifocal Atrial Tachycardia Atrial Tachycardia Premature Atrial Contractions Paroxysmal Supraventricular Tachycardia Atrial Flutter Atrial Fibrillation

2. Dysrhythmias Originating in the Atria Normal QRS Varies PRI Changes from beat to beat P Waves Varies Pacemaker Site Slightly Irregular Rhythm Usually normal Rate Wandering Pacemaker Rules of Interpretation

3. Dysrhythmias Originating in the Atria Wandering Pacemaker Etiology Transfer of pacemaker sites from the sinus node to other latent pacemaker sites in the atria and AV junction A variant of sinus dysrhythmia, a normal phenomenon in the very young or the aged, Ischemic heart disease, atrial dilation Clinical significance Usually has no detrimental effects Precursor of other atrial dysrhythmias such as atrial fibrillation Treatment If the patient is symptomatic, consider adenosine or verapamil

4. Dysrhythmias Originating in the Atria Variable QRS Varies depending on source of impulse PRI Organized, nonsinus P waves; at least 3 forms P Waves Ectopic sites in atria Pacemaker Site Irregular Rhythm More than 100 Rate Multifocal Atrial Tachycardia Rules of Interpretation

5. Dysrhythmias Originating in the Atria Multifocal Atrial Tachycardia Etiology Often seen in acutely ill patients May result from pulmonary disease, metabolic disorders, ischemic heart disease, or recent surgery Clinical Significance Presence of multifocal atrial tachycardia often indicates a serious underlying illness Treatment Treat the underlying illness

6. Dysrhythmias Originating in the Atria Usually normal QRS Varies dependent on foci of impulse PRI Occurs earlier than expected P Waves Ectopic sites in atria Pacemaker Site Usually regular except for the PAC Rhythm Depends on underlying rhythm Rate Premature Atrial Contractions Rules of Interpretation

7. Dysrhythmias Originating in the Atria Premature Atrial Contractions Etiology Single electrical impulse originating outside the SA node May result from use of caffeine, tobacco, or alcohol, sympathomimetic drugs, ischemic heart disease, hypoxia, or digitalis toxicity, or may be idiopathic Clinical Significance None. Presence of PACs may be a precursor to other atrial dysrhythmias. Treatment None if asymptomatic. Treat symptomatic patients by administering high-flow, high-concentration oxygen and establishing IV access.

8. Dysrhythmias Originating in the Atria Usually normal QRS Usually normal PRI Often buried in preceding T wave P Waves Atrial (outside SA Node) Pacemaker Site Regular Rhythm 150–250 Rate Paroxysmal Supraventricular Tachycardia Rules of Interpretation

9. Dysrhythmias Originating in the Atria Paroxysmal Supraventricular Tachycardia Etiology Rapid atrial depolarization overrides the SA node May be precipitated by stress, overexertion, smoking, caffeine Clinical Significance May be tolerated well by healthy patients for short periods Marked reduction in cardiac output can precipitate angina, hypotension, or congestive heart failure

10. Dysrhythmias Originating in the Atria Paroxysmal Supraventricular Tachycardia Treatment Vagal Maneuvers Pharmacological Therapy Adenosine Electrical Therapy Consider if patient symptomatic with HR >150. Synchronized cardioversion starting at 50-100 J (or biphasic equivalent

11. Dysrhythmias Originating in the Atria Normal QRS Usually normal PRI Difficult to see P Waves In the atria Pacemaker Site Regular Rhythm 150-250 bpm Rate Supraventricular Tachycardia Rules of Interpretation

12. Dysrhythmias Originating in the Atria Supraventricular Tachycardia Etiology Refers to tachycardias that originate above the ventricles Use of caffeine, nicotine, or alcohol, cocaine sympathomimetic drugs, ischemic heart disease Clinical Significance Rapid rates can cause a marked reduction in cardiac output because of inadequate ventricular filling time Treatment Manage with tachycardia algorithm

13. Tachycardia Management

14. Dysrhythmias Originating in the Atria Usually normal QRS Usually normal PRI F waves are present P Waves Atrial (outside SA node) Pacemaker Site Usually regular Rhythm Atrial rate 250–350 Ventricular rate varies Rate Atrial Flutter Rules of Interpretation

15. Dysrhythmias Originating in the Atria Atrial Flutter Etiology Results when the AV node cannot conduct all the impulses Impulses may be conducted in fixed or variable ratios Usually associated with organic disease such as congestive heart failure (rarely seen with MI) Clinical Significance Generally well tolerated Rapid ventricular rates may compromise cardiac output and result in symptoms May occur in conjunction with atrial fibrillation

16. Dysrhythmias Originating in the Atria Atrial Flutter Treatment Electrical Therapy Consider if ventricular rate >150 and symptomatic Synchronized cardioversion starting at 100 J Pharmacological Therapy Diltiazem or beta blockers Do not use a calcium channel and beta blockers concomitantly

17. Dysrhythmias Originating in the Atria Normal QRS None PRI None discernible P Waves Atrial (outside SA Node) Pacemaker Site Irregularly irregular Rhythm Atrial rate 350–750 Ventricular rate varies Rate Atrial Fibrillation Rules of Interpretation

18. Dysrhythmias Originating in the Atria Atrial Fibrillation Etiology Results from multiple ectopic foci; AV conduction is random and highly variable Often associated with underlying heart disease Clinical Significance Atria fail to contract effectively, reducing cardiac output Well tolerated with normal ventricular rates High or low ventricular rates can result in cardiac compromise

19. Dysrhythmias Originating in the Atria Atrial Fibrillation Treatment Electrical Therapy Consider if ventricular rate >150 and symptomatic Synchronized cardioversion starting at 100 J Pharmacological Therapy Diltiazem or beta blockers

20. Adenosine Adenocard

21. Class Antidysrhythmic

22. Description A naturally occurring nucleoside that slows AV conduction through the AV node Has an exceptionally short half-life Has a relatively good safety profile

23. Mechanism of Action A naturally occurring substance present in all body cells Decreases conduction of the electrical impulse through the AV node and interrupts AV re-entry pathways in PSVT Can effectively terminate rapid supraventricular arrhythmias

24. Mechanism of Action (cont.) Half-life is approximately 10 seconds Sometimes referred to as chemical cardioversion Effective in 90% of case studies Does not appear to cause hypotension to the same degree as does verapamil

25. Pharmacokinetics Onset 20-30 seconds Peak effects 20-30 seconds Duration 30 seconds Half-life 10 seconds

26. Indications Used in PSVT (including that associated with Wolff-Parkinson-White syndrome) refractory to common vagal maneuvers

27. Contraindications Second heart block Third heart block Sick sinus syndrome Known hypersensitivity

28. Precautions Typically causes dysrhythmias at the time of cardioversion In extreme cases, transient asystole may occur. Should be used cautiously in patients with asthma

29. Side Effects Flushing Headache Shortness of breath Dizziness Nausea

30. Dosage Initial dose is 6 mg rapid IVP over 1-2 sec. Follow the initial dose with a rapid saline flush. Two repeat doses of 12 mg rapid IVP may be administered.

31. Cardizem Diltiazem

32. Class Calcium channel blocker

33. Description A calcium-ion antagonist Causes a relaxation of vascular smooth muscle and slows conduction through the AV node Has a nearly equal effect on vascular smooth muscle and AV conduction

34. Mechanism of Action Causes vascular dilation and slows conduction through the AV node Slows the rapid ventricular rate associated with atrial fibrillation and atrial flutter Also used in the treatment of angina because of its negative inotropic effect and because it dilates the coronary arteries

35. Pharmacokinetics Onset 3 minutes Peak effects 7 minutes Duration 1-3 hours Half-life 2 hours

36. Indications Rapid ventricular rates associated with atrial fibrillation and atrial flutter Angina pectoris PSVT refractory to adenosine

37. Contraindications Severe hypotension or cardiogenic shock Ventricular tachycardia (wide-complex tachycardia) Essential that the paramedic ensures the patient does not have Wolff-Parkinson-White syndrome

38. Precautions Can cause systemic hypotension Calcium chloride can be used in the management of calcium channel blocker overdosage Should be kept refrigerated, but it can be kept at room temperature for 1 month

39. Side Effects Nausea Vomiting Dizziness Headache Bradycardia Heart block Hypotension Asystole

40. Interactions Should not be administered to patients receiving intravenous β -blockers because of an increased risk of congestive heart failure, bradycardia, and asystole

41. Dosage For rapid ventricular rates associated with atrial fibrillation and atrial flutter: 20 mg IVP (0.25 mg/kg) over 2 minutes Maintenance infusion of 5 to 15 mg/hr For PSVT: 0.25 mg/kg IVP over 2 minutes

42. Beta-Blockers Description Beta-Blockers reduce the effects of circulating catecholamines by blocking their ability to bind to beta-adrenergic receptors. Examples: Atenolol, Metoprolol

43. Beta-Blockers Effects Vasodilation Decreased ventricular afterload Decreased heart rate Decreased contractility Decreased ventricular irritability