CARDIAC Rhythms Arrhythmias Dysrhythmias Oh, my!

# CARDIAC Rhythms Arrhythmias Dysrhythmias Oh, my!

## CARDIAC Rhythms Arrhythmias Dysrhythmias Oh, my!

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1. CARDIACRhythmsArrhythmiasDysrhythmiasOh, my! Lecture 3 NUR240 JB 9/10

2. Arrhythmia ARRHYTHMIA – VARIATION IN NORMAL RHYTHM DYSRHYTHMIA – ABNORMAL, DISTURBED RHYTHM RESULTS FROM IMPULSE FORMATION DISTURBANCE OR CONDUCTION DISTURBANCE

3. AXIOM ALL RHYTHM INTERPERTATION MUST BE CORRELATED WITH SIGNS & SYMPTOMS AND PATIENT CONDITION… “TREAT THE PATIENT, NOT THE MONITOR”

4. Dysrhythmia Impulse formation (site of impulse origin) SA Node AV Node Ventricle Ectopic Premature Beat

5. Dysrhythmia Altered conduction • Bradycardia / Tachycardia • Flutter / Fibrillation • Heart blocks

6. Basic Rhythm Strip Interpretation • Determine the rate. Does the atrial rate equal the ventricular rate. • Is the rhythm regular/irregular? • Find the P wave. Is there a P wave for every QRS? • Determine the PRI (Normal 0.12-0.20 sec) • Find the QRS (Normal <0.12seconds) • Any ectopic beats? • Find the T wave. http:www.rnceus.com EKG strip identification and evaluation

7. Determine heart rate REGULAR RHYTHM – count boxes between 2 “R” waves and divide into 300 5 300 / 5 = 60 1 small box = .04 second 30 large boxes = 6 seconds 1 large box = .20 second 300 large boxes = 1 minute 15 large boxes = 3 seconds 1 mm = 0.1 millivolt (mV)

8. Determine heart rate • Irregular rhythm – count R - R intervals on a 6 sec. strip and multiply by 10

9. Normal Sinus Rhythm • NORMAL SINUS RHYTHM IS PRODUCED BY THE SA NODE • P – WAVE FOLLOWS QRS COMPLEX IN A PREDICTABLE RELATIONSHIP • ALL “P” WAVES LOOK ALIKE, ALL QRS COMPLEXES ARE NARROW • R – R INTERVAL IS REGULAR • RATE: 60 – 100 bpm

10. Normal Sinus Rhythm

11. Normal Sinus Rhythm

12. Sinus / Atrial dysrhythmia • ORIGINATE FROM SA NODE OR ATRIA (ABOVE VENTRICLES) • CONDUCTION WITH VENTRICLE IS UNDISTURBED • USUALLY BENIGN & SYMPTOMATIC • RHYTHM MAY BE IRREGULAR

13. Sinus / Atrial dysrhythmias • SINUS TACHYCARDIA • SINUS BRADYCARDIA • ATRIAL FIBRILLATION • ATRIAL FLUTTER • Premature atrial contractions • Paroxysmal atrial tachycardia • Supraventricular Tachycardia

14. Sinus Tachycardia • VENTRICULAR RATE  100 bpm ETIOLOGY: • MAY REFLECT PHYSIOLOGIC DEMAND FOR  O2 • SYMPATHOMIMETIC DRUGS • FEVER • PAIN

15. Sinus Tachycardia • CLINICAL SIGNS: •  HR  MYOCARDIAL DEMAND FOR O2

16. Treatment • MAY RESOLVE WITH TREATMENT OF UNDERLYING CAUSE • DRUGS WITH RATE SLOWING EFFECT: DIGOXIN, β-BLOCKERS • CAROTID MASSAGE • VAGAL MANEUVER

17. Sinus Bradycardia • VENTRICULAR RATE =  60 ETIOLOGY: RESPONSE TO MYOCARDIAL ISCHEMIA VAGAL STIMULATION ELECTROLYTE IMBALANCE DRUGS  I.C.P. HIGHLY TRAINED ATHLETE

18. CLINICAL SIGNS •  C.O. IF BODY CAN’T COMPENSATE OR IMPROVED C.O. DUE TO  DIASTOLIC FILLING TIME MAY LEAD TO ARRHYTHMIA • TREATMENT – DEPENDS ON CAUSE: • ATROPINE • AVOID VALSALVA • HOLD RATE SLOWING DRUGS I.E.: DIGOXIN, blockers

19. Atrial Flutter • ATRIAL RATE = 250 – 400 IMPULSES/ MINUTE • ETIOLOGY: • OCCURS /W HEART DISEASE • CAD • VALVE DISORDERS • CLINICAL SIGNS • “SAW TOOTH” P-WAVES, CALLED F-WAVES • ATRIAL RATE = 250 – 400/ MIN • AV NODE BLOCKS SOME IMPULSES • INCOMPLETE EMPTYING OF ATRIA CAUSE RISK FOR THROMBUS GIVE ANTICOAGULANTS

20. Atrial Flutter • TREATMENT • TREAT UNDERLYING CAUSE •  IRRITABILITY,  RAPID VENTRICULAR RESPONSE • DIGOXIN SLOWS RATE BY ENHANCING AV BLOCK • QUINIDINE SUPRESSES ATRIAL ECTOPIC BEATS • AMIODARONE • CALCIUM CHANNEL & β-BLOCKERS • CONSIDER CARDIOVERSION

21. Atrial Fibrillation • CHAOTIC ELECTRICAL ACTIVITY IN ATRIA • ATRIA QUIVER (>500 beats/minute) INSTEAD OF CONTRACTING AS A UNIT • ETIOLOGY: ADVANCED AGE VALVE DISORDERS CARDIOMYOPATHY

22. Atrial Fibrillation “F” FIBRILLATORY WAVES ø P-WAVES, ø P-R INTERVAL QRS normal VENTRICULAR RATE IS IRREGULAR RAPID VENTRICULAR RESPONSE  PULSE DEFICIT

23. Atrial Fibrillation TREATMENT • Amiodarone-may cause liver, lung damage and worsening of arrhythmias. Pt to report SOB, wheezing, jaundice, palpitations, lightheadedness • Pronestyl, Ca channel blockers, beta blockers, digoxin • Synchronized cardioversion if unstable • Radio frequency catheter ablation • Anticoagulation therapy

24. Atrial Rhythms

25. Synchronized Electrical Cardioversion

26. Cardioversion Synchronized shock with the QRS complex

27. JUNCTIONAL DYSRHYTHMIAS • IMPULSE BEGINS IN AV NODE • VENTRICULAR RATE IS EXTREMELY SLOW • MONITOR FOR SYMPTOMS OF REDUCED CARDIAC OUTPUT AND HEMODYNAMIC INSTABILITY

28. Paroxysmal Supraventricular Tachycardia • ABRUPT ONSET OF  HR • ETIOLOGY: SNS STIMULATION CARDIOMYOPATHY • CLINICAL SIGNS: ABRUPT ONSET/ CESSATION S/S ARE RELATED TO  C.O. RATE = 150 – 250 bpm

29. PSVT • TREAT UNDERLYING CAUSE • DRUGS: ADENOSINE, β-BLOCKERS, DIGOXIN, MS, QUINIDINE • CAROTID / VAGAL MANEUVERS • SYNCHRONIZED CARDIOVERSION IF UNSTABLE

30. Ventricular Arrhythmias • ORIGINATES IN VENTRICLES • PATIENT MAY BE SYMPTOMATIC, REQUIRES IMMEDIATE ATTENTION • PVC, couplet, bigeminy, trigeminy • V-TACH (ventricular tachycardia) • V-Fib (Ventricular fibrillation)

31. PREMATURE VENTRICULAR CONTRACTION (PVC) • EARLY IRREGULAR VENTRICULAR BEATS • QRS IS WIDE /BIZZARE • CAN BE CHRONIC ASYMPTOMATIC ABNORMALITY OR WARNING OF SERIOUS DYSRHYTHMIA

32. PREMATURE VENTRICULAR CONTRACTION (PVC) • ETIOLOGY: HYPOXIA DIGOXIN TOXICITY MECHANICAL STIMULATION ELECTROLYTE (K) IMBALANCE MI

33. PVCs

34. PREMATURE VENTRICULAR CONTRACTION (PVC) • CLINICAL SIGNS: • DEPEND ON FREQUENCY • PVC  SHORT DIASTOLIC FILLING TIME  C.O. • FREQUENT PVC – SENSATION OF PALPATIONS, SKIPPED BEATS • BIGEMINY – PVC EVERY OTHER BEAT • TRIGEMINY – PVC EVERY 3RD BEAT

35. PREMATURE VENTRICULAR CONTRACTION (PVC) • TREATMENT: • TREAT IMPAIRED HEMODYNAMICS • ANTIARRHYTHMICS • OXYGEN • MONITOR FOR PVC LANDING ON T-WAVE • OBSERVE FOR UNIFOCAL (VS) MULTIFOCAL

36. Ventricular Arrhythmias • VENTRICULAR TACHYCARDIA • 3 OR MORE PVC’s • QRS IS WIDE/ BIZARRE EXTREMELY SERIOUS MAY LEAD TO LETHAL RHYTHMS • ETIOLOGY: SAME CAUSES AS PVC, ALSO CARDIOMYOPATHY, MYOCARDIAL IRRITABILITY

37. Ventricular Tachycardia

38. Treatment • VT /W PULSE - CARDIOVERT • MONITOR MORE CLOSELY • PREPARE FOR CARDIOVERSION (O2, LIDOCAINE, TREAT CAUSE) • VT W/O PULSE - DEFIBRILLATE

39. VENTRICULAR FIBRILLATION TOTAL UNORGANIZED MULTIFOCAL RHYTHM, VENTRICLES QUIVER, NO CARDIAC OUTPUT

40. V-fib • ETIOLOGY: SAME AS VT, PVC SURGICAL MANIPULATION OF HEART FAILED CARDIOVERSION • CLINICAL SIGNS: SAME AS CARDIAC ARREST EKG SHOWS DISORGANIZED RHYTHM

41. V-fib • TREATMENT IMMEDIATE DEFIBRILLATION X3 CPR SURVIVAL IS < 10% FOR EVERY MINUTE THE PATIENT REMAINS IN V-fib

42. SCREAM for Vfib and Pulseless VTach 1.Shock360J* monophasic, 1st and subsequent shocks.(Shock every 2 minutes if indicated) 2.CPR After shock, immediately begin chest compressions followed by respirations (30:2 ratio) for 2 minutes. 3.Rhythm check after 2 minutes of CPR (and after every 2 minutes of CPR thereafter) and shock again if indicated. Check pulse only if an organized or non-shockable rhythm is present.

43. SCREAM

44. CARDIAC ARREST • VENTRICULAR ASYSTOLE • 80 – 90% DUE TO V-fib • TOTAL ABSENCE OF ELECTRICAL AND MECHANICAL ACTIVITY • ETIOLOGY TRAUMA OVERDOSE MI • CLINICAL SIGNS • ASYSTOLE or V-fib • NO DEFINABLE WAVE FORMS • ABSENCE OF VITAL SIGNS

45. Ventricular Asystole

46. PEA- Pulseless Electrical Activity • Asystole Algorithm • P E A • Problem search • Epinephrine – 1mg IV/IO q3-5min • Atropine- with a slow HR, I mg IV/IO q3-5min • Consider termination of efforts if asystole persists despite appropriate interventions.

47. CARDIAC ARRESTReview ACLS Guidelines 2005 TREATMENT: IMMEDIATE CPR • AIRWAY/ ADVANCED AIRWAY CONTROL • BREATHING/ POSITIVE PRESSURE VENTILATION • CIRCULATION/ CPR, START IV • DEFIBRILLATE (V-fib, V-tach ONLY) E. DRUGS-Antidysrhythmic tx

48. CARDIAC ARREST • EPINEPHRINE 1:10,000 IV PUSH REPEAT Q 5 MIN. • AMIODORONE: • ATROPINE: • VASOPRESSIN: • CONSIDER ANTIARRHYTHMICS • USE ACLS ALGORITHMS

49. CARDIAC ARREST • TREATMENT: POST CARDIAC ARREST MONITOR - CARDIAC STATUS RESPIRATORY STATUS TREAT UNDERLYING CAUSE EMOTIONAL SUPPORT SAFE ENVIRONMENT

50. DEFBRILLATION (vs) CARDIOVERSION • DEFIBRILLATION ASYNCHRONOUS ELECTRICAL DISCHARGE THAT CAUSES DEPOLARIZATION OF ALL MYOCARDIAL CELLS AT ONCE. THIS ALLOWS (HOPEFULLY) THE SA NODE TO RESTORE ITS PACEMAKER FUNCTION AND DICTATE A REGULAR SINUS RHYTHM. USED FOR PULSELESS V-tach AND V-fib VOLTAGE: 200 – 360 joules (“stacked shock”) or AED