1. Cardiac Dysrhythmias
Nuro 438
February 2015

2. Learning Objectives At the completion of this presentation, the nursing student will be able to successfully
Describe cardiac anatomy and physiology
Describe the function of the heart, including circulation and automaticity
Describe and define the major cardiac waves in an EKG
Define normal sinus rhythm
Differentiate between rate, conduction, atrial, and ventricular arrhythmias
Recognize life-threatening dysrhythmias
Identify nursing considerations related to various cardiac dysrhythmias
Differentiate types of medications to treat arrhythmias
Identify risks for cardiac arrhythmias
Identify adverse effects associated with cardiac dysrhythmias
Analyze EKG Rhythm strips

3. Cardiac Anatomy

4. Cardiac Anatomy 4 Chambers, 2 Atria, 2 Ventricles 4 Valves
Acts as a PUMP
Receives deoxygenated blood from body, pumps to lungs
Receives oxygenated blood from lungs, pumps to body

5. Cardiac Circulation

6. Cardiac Function
Heart functions a pump to deliver blood to the body

7. Automaticity

8. Impulse Generation Under Usual circumstances
Impulse generated from pacemaker cells in SA node
Impulse then travels to AV node
Impulse then travels to Bundle of His
Impulse then travels to Right and Left Bundle Branches
Impulse travels to Perkinje Cells that innervate ventricles

9. Components of an EKG

10. EKG Graph Displays electrical activity of heart
X Axis = time
Y Axis = amplitude
Displays electrical activity of heart
Electrical impulse precedes contraction
Depolarization and repolarization are depicted as waves
Atrial Depolarization = P wave
Atrial repolarization occurs during ventricular depolarization
Ventricular depolarization = QRS complex
Ventricular repolarization = T wave

11. EKG Basics
Bipolar lead: positive and negative electrode. Measures electrical potential between the electrodes
AKA ‘Standard Limb Leads’
Leads I,II,III
Used to monitor only for dysrhythmias
Lead II most commonly used

12. Telemetry Placement Red = Brake (right), Green = Gas (left)
Smoke (black) over Fire (red), Snow (white) on the Trees (green)
Stars and Stripes

13. Lead II

14. 12 Lead EKG 3 Standard (bipolar) Limb Leads
3 Augmented (unipolar) Leads (aVR, aVL, aVF)
Triaxial reference- measures the difference in electrical potential between one of three extremity electrodes and the central terminal
6 Precordial (unipolar) Leads (V1, V2, V3, V4, V5, V6)

15. aVR, aVL, aVF

16. The V Leads

17. Cardiac Waves

18. The P wave Pacemaker is SA node, rate 60 - 100
Correlates with atrial depolarization (begins in SA node moves R-> L and down)
PR interval
Determine atrial rate
Compare atrial rate to ventricular rate

19. The QRS Complex Represents normal depolarization of the ventricles
Normal duration
Measured from Q wave (first deviation from isoelectric line) to S wave (the return to isoelectric line)
Abnormal QRS is abnormal depolarization
BBB
Ventricular pre-excitation
Cardiac pacemaker

20. The T Wave Represents Ventricular repolarization
Occurs during end of ventricular systole
Typically in same direction as QRS complex
Lasts 0.10 – 0.25

21. U Wave
Final stage of repolarization, thought to be repolarization of Perkinje Fibers
Not usually seen
May indicate
Hypokalemia
Cardiomyopathy
LVH
Dig toxicity

22. EKG Paper At the 25 mm speed, Each mark at top is 3 seconds
There are three large boxes between each mark
Each large box is 1 second or 25 mm
Each large box has 5 medium boxes in it
Each medium box is 0.2 seconds or 5 mm
Each medium box is made up of 5 small boxes (or dots)
Each small box (dot) = 0.04 seconds or 1 mm

23. EKG Paper

24. Steps to Interpreting Cardiac Rhythms
Determine the Heart Rate
Determine the Regularity
Identify and analyze P waves or flutter
Determine PR interval and AV conduction
Identify and analyze QRS complex
Determine site of origin of dysrhythmia
Identify dysrhythmia
Evaluate significance of dysrhythmia

25. Determine the Heart Rate
The Six-second Method
Most common/least accurate
Simplest, quickest
Heart Rate Calculator
The Rule of 300
Must be regular
R-R Interval Method
Rhythm must be regular
Distance between peaks of 2 R waves and /60

26. Describe the Rate & Rhythm
Normal =
Tacchycardia >100
Bradycardia <60
Regular
Irregular
Regularly-irregular

27. Sinus Arrhythmias
ST = HR >100
SB = HR ,60

28. Steps to Interpreting Cardiac Rhythms
Determine the Heart Rate
Determine the Regularity
Identify and analyze P waves or flutter
Determine PR interval and AV conduction
Identify and analyze QRS complex
Determine site of origin of dysrhythmia
Identify dysrhythmia
Evaluate significance of dysrhythmia

29. Measuring the Waves

30. PR Interval
Represents progression of electrical impulse from the SA node or an ectopic pacemaker (in atria or AV junction) through entire conduction system of the heart to the ventricular myocardium
Normal duration 0.12 – 0.20
PR >0.20 represents delayed conduction of impulse

31. Irregular P Wave Remember P wave represents atrial depolarization
Irregular P represents altered, damaged, or abnormal atria
Increased Right Atrial Pressure or hypertrophy as seen in COPD and CHF = tall peaked P wave
Increased left atrial pressure or hypertrophy = wide notched P wave

32. Ectopic P Wave
Electrical impulse for ectopic P wave originated outside SA node or in AV junction
Occur in
PAC’s
Atrial tacchycardia
SVT

33. PAC’s Premature Atrial Contraction P wave followed by normal QRS
Generally followed by noncompensatory pause
P waves vary, PR intervals normal
AV Ratio 1:1 Conduction

34. Causes of PAC’s Increased sympathetic tone Infection Emotional Stress
Stimulants
Medications; epinephrine
Hypoxia
Digitalis toxicity
ACS or CHF

35. QRS Complex Represents normal depolarization of the ventricles
Onset is point where first wave (Q) deviates from isoelectric line
End is where last wave (S) returns to isoelectric line
Duration 0.06 – 0.12

36. Irregular QRS Represents abnormal depolarization of ventricles
Irregular QRS present in
Bundle Branch Block
Ventricular preexcitation
Cardiac pacemaker

37. QT Interval
Represents time it takes for ventricles to depolarize and repolarize
Prolonged QT associated with pericarditis, myocarditis, MI, LVH, hypothermia, CVA, increased IC trauma or hemorrhage, medication SE, electrolyte imbalances (K, Ca), or liquid protein diets

38. ST Segment
Represents early part of repolarization of right and left ventricles
Duration < 0.20
Normally ST segment is flat
Elevation can be evidence of myocardial ischemia or infarction, coronary vasospasm, pericarditis, LBBB, LVH, raised ICP

39. Steps to Interpreting Cardiac Rhythms
Determine the Heart Rate
Determine the Regularity
Identify and analyze P waves or flutter
Determine PR interval and AV conduction
Identify and analyze QRS complex
Determine site of origin of dysrhythmia
Identify dysrhythmia
Evaluate significance of dysrhythmia

40. Arrhythmias Rate Arrhythmias Atrial Arrhythmias Conduction Arrhythmias
Tachycardia
Bradycardia
Atrial Arrhythmias
Afib/Aflutter
WPW
SVT
Conduction Arrhythmias
Bundle Branch Blocks
AV Conduction Block (1st, 2nd, 3rd Degree)
Life Threatening Arrhythmias
V Fib
Complete Heart Block
Asystole

41. Living Arrhythmias M

42. Atrial Arrhythmias Atrial Tacchycardia Atrial fibrilation
Atrial flutter
Supra Ventricular Tacchycardia
Wolf-Parkinson-White
8 Steps
ID P or F waves
Conduction ratio, is every P followed by QRS

43. Atrial Tachycardia Rate is usually 160-240 beats
Type of SVT, where generation for impulse is outside SA node
A Fib and Aflutter are most common forms
P waves are uniform
PR intervals are normal
AV conduction is 1:1

44. Atrial Tachycardia Clinical significance Nursing Assessment
Dependent on presence and extent of heart disease
Palpitations, nervousness, anxiety
Perfusion
Syncope
Workload of heart
Nursing Assessment

45. Atrial Tachycardia

46. A Flutter Causes Cardiomyopathy Atrial dilation Valve Disease
Thyrotoxicities
Hypoxia
CHF
ETOH Abuse

47. A Flutter Risks; Incomplete emptying of ventricles Treatments
Thrombi formation
Loss of atrial kick
Syncope, hypotension
CHF
Treatments
Beta Blockers
CCB
Digoxin
Warfarin
Cardioversion if uncontrolled
Ablation

48. Atrial Flutter
Impulse generated by ectopic pacemaker or reentry pathway
F waves have a saw-tooth appearance
Rate; Atrial , Ventricular half the atrial rate
Rate is regular
Normal P waves absent
Unable to measure PR intervals
Expressed as ratio 4: 1 Flutter

49. Atrial Fibrillation Atrial Rate 350-600
Ventricular rate < 100 = controlled, >100 = uncontrolled
Irregularly irregular rate
P waves absent, F waves absent

50. Atrial Fib
Causes and treatments similar to A Flutter

51. SVT Rapid rhythm (>100) that generated outside the ventricles
AKA Paroxysmal Atrial Tach (PAT)
Symptoms
Palpitations
Lightheadedness
Dizziness
Maybe symptomless, self limiting
Treatments
Beta Blockers, CCB,antiarrhythmics

52. SVT

53. WPW
Ventricular pre-excitation; early activation of ventricles by impulse that bypasses the AV node
Impulse can be generated in accessory pathway or bypass tract that abnormally
Most frequent AV bypass tract in WPW is Bundle of Kent
Presence of Delta wave

54. Wandering Atrial Pacemaker
Dysrhythmia originating in multiple pacemaker sites that shift between SA node and AV junction
Rate 60 – 100
Irregular
P waves vary in size and shape
PR intervals are normal to very short
AV Conduction ratio 1:1

55. Wandering Atrial Pacemaker

56. Conduction Arrhythmias
Conduction Block/ AV Block
Bundle Branch Block

57. AV Blocks First Degree AV Block Second Degree Type I AV Block
Second Degree Type II AV Block
Third Degree AV Block

58. First Degree AV Block
Delay in conduction of electrical impulse, usually through the AV node
Most common Heart Block
Prolonged PR (> 0.20)
Rate and Rhythm Regular
AV Conduction 1:1
Causes 1* AV Block
Acute Inferior Wall MI
Ischemic Heart Disease
Digitalis Toxicity
Medications (B Blockers, CCB)
Hyperkalemia

59. First Degree AV Block

60. Second Degree Type I AV Block
AKA Wenckebach
Usually temporary condition, and asymptomatic
Prolonging PR form one QRS to the next until one QRS is not conducted or “dropped” then pattern starts over again
P to P intervals are regular
R to R intervals are irregular
More P waves than QRS complexes
Causes; Acute inerior wall MI, Ischemic heart disease, Dig Toxicity, BB, CCB, Hyperkalemia

61. Second Degree AVB, Type I

62. Second Degree Type II AV Block
Dysrhythmia with constant P-R interval with missing QRS complexes
Complete block of conduction in one bundle branch and an intermittent block in the other bundle branch
Can present as pattern, ie 2:1 block or 3: 1 block OR without pattern of QRS/ unstable QRS
Causes; Damage to Bundle Branches p MI,
Very high potential to convert to Third Degree (Complete) Heart Block
Excessively slows HRMay require pacemaker, Atropine not effective

63. Second Degree AVB

64. Third Degree COMPLETE HB
Complete absence of conduction of electrical impulse through AV node, Bundle of His, and BB
Atria rhythm independent from Ventricular rhythm; Regular P-P and regular R-R
LIFETHREATENING Rhythm, will lead to asystole
Requires Pacing
Causes; Inferior wall MI, Ischemic Heart Disease, Medications (Dig, BB, CCB), hyperkalemia

65. Complete Heart Block

66. Treatment of CHB Cardioversion or Defibrillation
Transcutaneous pacing for symptomatic bradycardia
Medications
Atropine
Vasopressors
CCB BB
Nursing Assessment

67. Bundle Branch Block
Irregular conduction or block of electrical pathway through bundle branches
Ventricles do not contract simultaneously
QRS > 0.12, appears “notched”

68. Ventricular Arrhythmias
PVC’s
Ventricular Tachycardia
Ventricular Fibrillation

69. Premature Ventricular Contraction, PVC’S
Abnormally wide, bizarre QRS complex, not associated with P wave
Electrical impulse generated in ventricle, Bundle Branch, or Perkinje Fibers
Does not lead to contraction of ventricles, therefor not “perfused”
Usually followed by compensatory pause
Can be observed with or without a pattern

70. Causes of PVCs Increased Catecholamine and increased sympathetic tone
Stimulants
Amphetamine and cocaine
Myocardial ischemia or infarction
CHF
Hypoxemia
Acidosis
Dig Toxicity
Hypokalemia
Hypomagnesemia

71. Significance of PVCs
Isolated PVC without hx heart disease are usually insignificant, and require no treatment
May indicate presence of ventricular abnormality
Can lead to V tach or V fib

72. Single PVC

73. Ventricular Bigeminy

74. Ventricular Trigeminy

75. Couplet

76. Run PVC

77. Ventricular Tachycardia
AKA V Tach
Dysrhythmia originating in an ectopic pacemaker in the bundle branches, perkinje fibers, or ventricular myocardium
Rate 100 – 250 bpm
P wave absent
QRS abnormally wide and bizarre

78. V Tach

79. Causes of V Tach Significant Cardiac Disease Dig Toxicity
CAD
ACS
Cardiomyopathy
LVH
Dig Toxicity
QT interval Prolongation
Electrolyte disturbances
Liquid protein diets

80. Clinical Significance of V Tach
Determine inset and termination
More than 3 PVCs is sustained V Tach
Can be short, nonsustained and asymptomatic
Increased frequency can lead to Ventricular Fibrillation which is LIFETHREATENING
PULSELESS V TACH IS TREATED THE SAME AS V FIB!

81. Ventricular Fibrillation
No coordinated ventricular beats are present
No P wave or QRS complexes noted
Electrical Chaos in Heart
Ventricles ‘contract’ at rate of 300 – 500 bpm
EMERGENCY
Cardiac output CEASES
Nursing Considerations

82. V FIB

83. Asystole Total Absence of electrical activity in heart
Pt is clinically dead
Absence of P wave and QRS complex
Flat line
Remember, if your patient is speaking to you then they are NOT in a systole

84. Treatments Cardioversion and Defibrillation Medical Management
Atropine
Vasopressors
Calcium Channel Blockers
Beta Blockers
Nursing Considerations
Oxygen, Pain management

85. Atropine Blocks parasympathetic nervous system influence on the heart
Accelerates SA node firing rate
Increases HR
Increases conduction velocity
Administered by IV bolus
Used in
Symptomatic Bradycardia
Second Degree Type I AVB
Second Degree 2:1 AVB
Third Degree AVB with narrow QRS complexes

86. Atropine Ineffective in Second Degree Type II AVB Use with Caution
Advanced AVB with wide QRS complexes
Third Degree AVB with wide QRS Complexes
Use with Caution
Acute MI
Worsening myocardial ischemia
Heart Transplant patient

87. Vasopressors
Cause vasoconstriction on arterioles and venous circulation
Improves blood pressure
Increases HR and Strength of Contraction
Epinephrine
Vasopressin (DOC in asystole)
Dopamine
Norepinephrine
Dobutamine
Isopreterenol

88. Antidysrhythmics Adenosine; depress AV node and Sinus node activity
SVT, Tachycardia
Will not terminate Afib/flutter but will slow rate
Amiodarone; Affects NA, K, and Ca channels
SVT
VT Vfib
Lidocaine; Widely used, ? Effectiveness in VT
SE; altered consciousness, seizures, bradycardia
Procainamide; supresses atrial and ventricular dysrhythmias by slowing conduction
VT, control of rate in AF/AF, PVST

89. Calcium Channel Blockers
Diltiazem and Verapamil
Slow conduction and increase conduction time through AV node
Used in
Afib and A flutter with rapid ventricular response
Contraindicated in
2nd and 3rd Degree AVB
With Beta Blocker Therapy
Use with caution on CHF and hypotension

90. Beta Blockers Decrease HR and BP Used in SVT
To control rate in Afib Aflutter

91. Time for a Game EKG Jeopardy!
jeopardylabs.com/play/ekg- jeopardy#.VOLPYmdso-w.gmail
Fifteen Question EKG Rhythm Strip Analysis m

92. Wave Matching Ventricular Depolarization Sets Normal Heart Rate
Irregular Ventricular Beat
A. AV Node
Atrial Depolarization
B. T wave
C. PAC
Ventricular Repolarization
D. SA Node
Backup pacemaker Rate
E. PVC
F. P wave
Early atrial beat
G. QRS Complex
Pacemaker site

93. Take Home Points EKG is measurement of ELECTRICAL activity
Look at the patient
Irregular activity can progress from asymptomatic to life threatening
Causes are similar (electrolytes, hypoxia, ischemia…)
Treatments also very similar (BB, CCB, antiarrhythmic)

94. References http://lifeinthefastlane.com/ecg-library/
ekg.aspx?seq=11&courseid=315
ent-education