1 / 70

CARDIAC Rhythms Arrhythmias Dysrhythmias Oh, my!

CARDIAC Rhythms Arrhythmias Dysrhythmias Oh, my!. Lecture 3. NUR240. Arrhythmia. ARRHYTHMIA – VARIATION IN NORMAL RHYTHM DYSRHYTHMIA – ABNORMAL, DISTURBED RHYTHM RESULTS FROM IMPULSE FORMATION DISTURBANCE OR CONDUCTION DISTURBANCE. AXIOM.

Télécharger la présentation

CARDIAC Rhythms Arrhythmias Dysrhythmias Oh, my!

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  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

More Related