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# Lecture 3 cardiac rhythms

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• 1. CARDIAC RhythmsArrhythmiasDysrhythmias Oh, my! NUR240 Lecture 3 JB 9/10
• 2. ArrhythmiaARRHYTHMIA – VARIATION INNORMAL RHYTHMDYSRHYTHMIA – ABNORMAL,DISTURBED RHYTHM RESULTS FROM IMPULSEFORMATION DISTURBANCE ORCONDUCTION DISTURBANCE
• 3. AXIOMALL RHYTHM INTERPERTATION MUSTBE CORRELATED WITH SIGNS &SYMPTOMS AND PATIENTCONDITION… “TREAT THE PATIENT, NOT THE MONITOR”
• 4. DysrhythmiaImpulse formation (site of impulse origin) SA Node Ectopic AV Node Premature Beat Ventricle
• 5. DysrhythmiaAltered conduction • Bradycardia / Tachycardia • Flutter / Fibrillation • Heart blocks
• 6. Basic Rhythm Strip Interpretation1. Determine the rate. Does the atrial rate equal the ventricular rate.2. Is the rhythm regular/irregular?3. Find the P wave. Is there a P wave for every QRS?4. Determine the PRI (Normal 0.12-0.20 sec)5. Find the QRS (Normal <0.12seconds)6. Any ectopic beats?7. Find the T wave.http:www.rnceus.comEKG strip identification and evaluation
• 7. Determine heart rateREGULAR 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 WAVESø P-WAVES,ø P-R INTERVALQRS normalVENTRICULAR RATE IS IRREGULARRAPID VENTRICULAR RESPONSE PULSE DEFICIT
• 23. Atrial FibrillationTREATMENT1. Amiodarone-may cause liver, lung damage and worsening of arrhythmias. Pt to report SOB, wheezing, jaundice, palpitations, lightheadedness2. Pronestyl, Ca channel blockers, beta blockers, digoxin3. Synchronized cardioversion if unstable4. Radio frequency catheter ablation5. Anticoagulation therapy
• 24. Atrial Rhythms
• 25. Synchronized Electrical CardioversionOh O2 Saturation MonitoringSay Suction EquipmentIt IV LineIsn’t Intubation equipmentSo Sedation and possibly analgesics
• 26. CardioversionSynchronized 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 VTach1.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 AsystoleAcronym CommentsT Transcutaneous Only effective with early Pacemaker implementaionE Epinephrine 1 mg IV q3-5 minA Atropine 1 mg IV q3-5 min
• 46. PEA- Pulseless Electrical Activity• Asystole Algorithm• PEA• 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 2005TREATMENT: IMMEDIATE CPRA. AIRWAY/ ADVANCED AIRWAY CONTROLB. BREATHING/ POSITIVE PRESSURE VENTILATIONC. CIRCULATION/ CPR, START IVD. 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
• 51. CARDIOVERSION (aka)SYNCHRONIZED CONVERSIONELECTRICAL IMPULSE IS DISCHARGEDDURING QRS (VENTRICULARDEPOLARIZATION)USUALLY TIMED /W CARDIAC MONITOR TOPREVENT SHOCK ONT-WAVEUSED FOR RAPID A-fib, V-tach /W PULSE ANDPERSISTENT PAT / PSVTVOLTAGE: 50 – 100 joules
• 52. EQUIPMENT REVIEW• DEFIBRILLATOR SELECT ENERGY LEVEL, THEN CHARGE• PADDLES USE 25 POUNDS OF PRESSURE WHEN APPLIED TO CHEST, Placed 2nd RICS and 5th LAAS• CONDUCTING AGENT GEL OR PAD WHICH ESTABLISHES SKIN CONTACT, REDUCES SKIN BURNS• JOULES MEASUREMENT OF ELECTRICAL ENERGY• DISCHARGES NO ONE SHOULD COME IN CONTACT WITH PATIENT OR BED DURING DISCHARGE
• 53. HEART BLOCK• DEPRESSED CONDUCTION OF IMPULSE FROM ATRIA TO VENTRICLES• AV NODE BECOMES DEFECTIVE AND IMPULSES (P-WAVES) ARE BLOCKED FROM BEING TRANSMITTED TO VENTRICLES FIRST DEGREE SECOND DEGREE TYPE I TYPE II THIRD DEGREE
• 54. 1° HEART BLOCK• PR INTERVAL > 0.20 SECONDS• CAUSES: MAY BE NORMAL VARIANT INFERIOR WALL MI DRUGS: DIGOXIN VERAPAMIL• TREATMENT: MONITOR OBSERVE FOR SYMPTOMS
• 55. FIRST DEGREE HEART BLOCK
• 56. 2° HEART BLOCK• ONE OR MORE P-WAVES ARE NOT CONDUCTED THROUGH THE VENTRICLE• HEART RATE - VENTRICULAR RATE SLOW TO NORMAL ATRIAL RATE MAY BE 2 – 4 X’s FASTER THAN VENTRICULAR
• 57. 2° HEART BLOCKCAUSES: ORGANIC HEART DISEASE MI, Dig toxicity, B and Ca Channel Blockers DIGOXIN TOXICITYSYMPTOMS• Tx: Monitor HR Atropine Temporary pacemaker Avoid meds that decrease conductivity 2 TYPES OF 2° HEART BLOCK MOBITZ TYPE I- Wenkeback MOBITZ TYPE II
• 58. Second Degree Heart Block Mobitz I• PRI becomes progressively longer until drops QRS
• 59. Second Degree Heart Block Mobitz Type II• PRI constant and regular, but in a 2:1 , 3:1 pattern
• 60. 3° HEART BLOCK (COMPLETE HEART BLOCK)• ATRIAL IMPULSES & VENTRICULAR RESPONSE ARE IN TOTAL DISASSOCIATION• P-WAVES ARE SEEN & ARE IRREGULAR• QRS COMPLEX ARE SEEN & ARE IRREGULAR (ESCAPE RHYTHM)• NO CORRELATION BETWEEN P-WAVES & QRS (RATE IS SLOW) – independent rhythms
• 61. 3° HEART BLOCK(COMPLETE HEART BLOCK)• CAUSES ORGANIC HEART DISEASE MI DRUGS ELECTROLYTE IMBALANCE EXCESS VAGAL TONE• SIGNS & SYMPTOMS EXTREME DIZZINESS HYPOTENSION SYNCOPE S/S OF  C.O. ALTERED MENTAL STATUS
• 62. NSR vs 3 RD Degree Block
• 63. 3° HEART BLOCK (COMPLETE HEART BLOCK)• TREATMENT PACEMAKER TEMPORARY OR PERMANENT
• 64. PACEMAKER• Indications: Speed up a slow HR or Slow down a rapid HR• ELECTRICAL DEVICE THAT DELIVERS CONTROLLED ELECTRICAL STIMULUS THROUGH ELECTRODES PLACED IN CONTACT WITH HEART MUSCLE• 2 PIECES PULSE GENERATOR IMPLANTED IN CHEST WALL UNDER R CLAVICLE PACEMAKER ELECTRODES IMPLANTED IN MYOCARDIAL TISSUE
• 65. Paced Rhythm• Pacemaker spike
• 66. PACEMAKER• TEMPORARY PACEMAKER – USED IN EMERGENCY SITUATION – FIXED (COMPETITIVE) PACEMAKER SENDS STIMULUS TO VENTRICLE AT A FIXED RATE, REGARDLESS OF VENTRICULAR ACTIVITY
• 67. Types of PacemakersUse a 5 letter code system, first 3 used more often:1. Chamber being paced: A, V, D2. Chamber being sensed: A, V, D, O3. Type of response by the PM to the sensing: I, T, D, O
• 68. PATIENT TEACHING• Carry PM ID card• MEDI ALERT BRACELET• Avoid swimming, golf and weight lifting• AVOID MRI• Check PM q3-6 mos.• PACEMAKER SURVEILANCE• Monitor pulse rates• Don’t hold cell phones over generators
• 69. AUTOMATIC IMPLANTABLE CARDIOVERSION DEFIBRILLATOR (AICD)• PROVIDES INTERNAL SHOCKS WHEN SERIOUS ARRHYTHMIA IS DETECTED (V-tach OR V-fib)• Has a pulse generator and a sensor that monitors the heart• If pt has dysrhythmia it delivers a shock which the pt will feel• USEFUL WHEN ARRHYTHMIA IS UNRESPONSIVE TO MEDS OR SURGICAL ABLATION OR IRRITABLE MYOCARDIAL TISSUE
• 70. References• http://www.rnceus.com/ekg/ekgsecond2.html• ACLS Guidelines 2005• www.EMS-ED.net• http://www.doctorshangout.com/forum/topi cs/acls-algorithms-1