1. CARDIAC Rhythms Arrhythmias Dysrhythmias Oh, my!
NUR240
Lecture 3
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 SA Node AV Node Ventricle Ectopic Premature Beat
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 sec)
Find the QRS (Normal <0.12seconds)
Any ectopic beats?
Find the T wave.
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 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 MAY REFLECT PHYSIOLOGIC
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 CardioversionOh
O2 Saturation Monitoring
Say
Suction Equipment It
IV Line
Isn’t
Intubation equipment So
Sedation and possibly analgesics

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 CLINICAL SIGNS 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 Acronym Comments T Transcutaneous Pacemaker
Only effective with early implementaion
E Epinephrine
1 mg IV q3-5 min
A Atropine

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 ARREST Review 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

51. CARDIOVERSION (aka) SYNCHRONIZED CONVERSION
ELECTRICAL IMPULSE IS DISCHARGED DURING QRS (VENTRICULAR DEPOLARIZATION)
USUALLY TIMED /W CARDIAC MONITOR TO PREVENT SHOCK ON
T-WAVE
USED FOR RAPID A-fib, V-tach /W PULSE AND PERSISTENT PAT / PSVT
VOLTAGE: 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 BLOCK CAUSES: ORGANIC HEART DISEASE
MI, Dig toxicity, B and Ca Channel Blockers
DIGOXIN TOXICITY
SYMPTOMS
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 3RD 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 Pacemakers
Use a 5 letter code system, first 3 used more often:
Chamber being paced: A, V, D
Chamber being sensed: A, V, D, O
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