1. ECG/ DYSRHYTHMIAS
Nancy Lin, RN, MSN

2. Reading Assignment Wong’s Lewis Adams & Urban: Pharmacology
Cardiac dysrhythmias: pp
Lewis
EKG’s: CH 36
Adams & Urban: Pharmacology
Antidysrhythmics CH 40

3. SLO’s Relate electrocardiogram changes to common cardiac problems.
Discuss conduction system and electrocardiographic monitoring in pediatric and adult clients.
Introduction to assessment of normal and abnormal cardiac rhythm and appropriate treatment in pediatric and adult clients.
Compare and contrast nursing and collaborative management of pediatric and adult clients with common dysrhythmias.
Discuss nursing management of pediatric and adult patients with central venous access.

4. Lecture Content EKG’s Cardiac Rhythms Pacemakers
Defibrillation/Cardioversion
Central Venous Access

5. Conduction System of the Heart
Self assessment: E A B

7. Electrocardiogram (ECG)
Detects electrical activity of heart
Components of an ECG waveform
P wave
P-R interval
QRS complex
ST segment
QT interval
T wave

8. P Wave P wave PR interval Begins with firing of SA node
Depolarization of atria
atrial contraction.
PR interval
time period for impulse to spread through atria, AV node, bundle of His & Purkinje fibers.

9. QRS Complex Depolarization from AV node throughout ventricles
ventricular contraction
QRS interval
time it takes for depolarization

10. ST Segment
Time between ventricular depolarization & repolarization

11. T wave Ventricle repolarization U wave
may represent repolarization of Purkinje fibers or assoc. with _____________

13. Principle of ECG Formation

14. Calculating HR From ECG
Count # of QRS complexes in 1 minute.
Count # of R-R intervals in 6 seconds & multiply that # by 10.

15. The ECG Paper

16. Intrinsic Rates of Conduction System
SA node
AV node
Bundle of His, Purkinje fibers

17. Rhythm analysis
Basic rules that can be followed to identify a patient's heart rhythm.
What is the rate?
Is it regular or irregular?
Are P waves present?
Are QRS complexes present?
Is there a 1:1 ratio between P waves and QRS complexes?
Is the PR interval constant?

18. Questions to Consider
1. What is the dominant rhythm and/or dysrhythmia?
2. What is the clinical significance of the findings?
3. What is the treatment for the particular rhythm?

19. Self Assessment A QRS complex represents: a) Atrial depolarization
b) Atrial repolarization
c) Ventricular depolarization
d) Ventricular repolarization

20. Pediatric ECG Normal pediatric ECG:
an ECG that contains a P wave, a QRS complex normal for age and less than or equal to 0.08 second, and a T wave.
Newborn: Resting (awake) ; Resting (sleeping) ; exercise (fever): <220
1wk-3mo: ; ; <220
3mo-2yr: ; ; <200
2yr-10yr: ; ; <180
10yr-adult: 55-90; 50-90; <180

21. Dysrhythmias Caused by disorders of impulse formation
Cause of a dysrhythmia influences treatment of patient.
Common causes:
Cardiac conditions
Other conditions

22. Dysrhythmias In children Occur with CHD Follow surgical repair of CHD
Cardiomyopathy
Cardiac tumors
Metabolic & electrolyte imbalances
Genetic etiology

23. Dysrhythmias
Naming of most cardiac rhythms begin with the site that the impulse originated.

24. Normal Sinus Rhythm Originates in SA node
Follows normal conduction pattern of cardiac cycles
Rhythm: Regular
Rate: bpm
QRS normal
P Wave – visible before each QRS complex
P-R interval: normal (<5 small squares)

25. Normal Sinus Rhythm 1, P wave 2, PR interval 3, QRS complex
4, ST segment
5, T wave
6, QT interval
Isoelectric (flat) line

26. Sinus Bradycardia Conduction pathway same as in NSR
SA node fires at a rate <60 beats/minute
May be normal in Rhythm – Regular
Rate – Less than 60 beats per minute
QRS Duration – Normal
P Wave – visible before each QRS complex
P-R Interval – Normal
Usually benign & often caused by pts on Beta blockers

27. Sinus Tachycardia Rate: >100 beats/minute QRS Duration – Normal
P Wave – Visible before each QRS complex
P-R Interval – Normal
Impulse generating heart beats are nl, but are occurring at faster pace than nl. Seen during exercise.

28. Premature Atrial Contraction
Contraction originating from an ectopic focus
Ectopic signal originates in left or right atrium & travels across atria by an abnormal pathway, creating a distorted P wave.
Clinical Associations
ECG Characteristics
Clinical Significance
Treatment

29. Paroxysmal Supraventricular Tachycardia
Dysrhythmia originating in an ectopic focus anywhere above bifurcation of bundle of His
Paroxysmal: abrupt onset & termination
Some degree of AV block may be present
Can occur in presence of Wolff-Parkingson-White (WPW) syndrome
Rhythm: Regular or sl irregular
Rate – beats per minute
QRS Duration – usually normal
P Wave – often buried in preceding T wave
PR interval – may be shortened or nl

30. Atrial Flutter An atrial tachydysrhythmia
Recurring, regular, sawtooth-shaped flutter waves
Originates from a single ectopic focus in right atrium.
Atrial Rate – about beats per minute
QRS Duration – usually normal
P Wave – Replaced with multiple F (flutter) waves, usually 2:1, but sometimes 3:1
P-R interval: not measurable
Atrial flutter with a 4:1 conduction (four flutter [F] waves to each QRS complex)

31. Atrial Fibrillation
Total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction.
May be chronic or intermittent
Most common dysrhythmia in US
Rhythm – irregularly irregular
Atrial Rate – 350 to 600 beats/min, can be slower
QRS duration – usually normal
P Wave – not distinguishable as atria are firing off all over
P-R interval – not measurable
The atria fire electrical impulses in irregular fashion causing irregular heart rhythm

32. First-Degree AV Block
Every impulse is conducted to ventricles but duration of AV conduction is prolonged.
After impulse moves through AV node, it is usually conducted normally through ventricles.
Rhythm – regular
Rate – normal
QRS Duration – normal
P Wave – Ratio 1:1
P Wave Rate – Normal
P-R interval – prolonged Z(>5 small squares)
First-degree AV heart block with a PR interval of 0.40 seconds.

33. Premature Ventricular Contraction
A contraction originating in an ectopic focus in the ventricles
Premature occurrence of a QRS complex, which is wide & distorted in shape
Multifocal PVCs: PVCs that are initiated from different foci appear different in shape from each other
Unifocal PVCs: PVCs that appear to have same shape
Ventricular bigeminy: when every other beat is a PVC
Ventricular trigeminy: when every 3rd beat is a PVC
Couplet: two consecutive PVCs
Three or more PVCs: Ventricular tachycardia

35. Premature Ventricular Contractions
Clinical Associations
ECG Charcteristics
Clinical Significance
Treatment

36. Ventricular Tachycardia
A run of three or more PVCs occur
Different forms of VT exist, depending on QRS configuration
Monomorphic VT
Polymorphic VT
May be sustained (lasts >30sec) or nonsustained (<30sec)
Development of VT is an ominous sign
A life threatening dysrhythmia

37. Ventricular Tachycardia
Clinical Associations:
ECG Characteristics:
Ventricular rate beats/min.
Rhythm: reg or irregular.
AV dissociation may be present, with P waves occurring independently of QRS complex
P wave usually buried in QRS complex
PR interval: not measurable
QRS: distorted, duration >12 sec
R-R interval: may be irregular or regular
CNS: central nervous system

38. Ventricular Tachycardia
Clinical Significance:
Stable or unstable
Sustained VT will cause severe dec. in CO Results:
Dysrhythmia must be treated quickly
Ventricular fibrillation may develop

39. Ventricular Tachycardia
Treatment:
- Identify & treat precipitating causes

40. Ventricular Tachycardia
VT without a pulse is a life-threatening situation
Treated in same manner as ventricular fibrillation
CPR & defibrillation: 1st line of Rx, followed by administration of epinephrine if defib unsuccessful.

41. Ventricular Fibrillation
A severe derangement of heart rhythm
Irregular undulations of varying shapes & amplitude
Firing of multiple ectopic foci in ventricle
Mechanically ventricle is simple “quivering”, no effective contraction, no CO occurs.
Clinical Associations:
• ECG Characteristics:
HR not measurable
Rhythm irregular & chaotic
P wave: not visible
PR & QRS interval not measurable.

42. Ventricular Fibrillation
Clinical Significance:
results in an unresponsive, pulseless & apneic state
Pt will die if not rapidly treated.
• RX: Immediate CPR & ACLS measures w/use of defib & drug therapy.
• This patient needs to be defibrillated!!! QUICKLY

43. Asystole Total absence of ventricular electrical activity
No ventricular contraction
Pts are unresponsive, pulseless & apneic
Lethal dysrhythmia
Requires immediate treatment
Poor prognosis
Rhythm – flat
Rate – 0 beats per minute
QRS Duration – none
P Wave - none

44. Asystole Clinical Associations: Clinical Significance: Treatment:
Carry out CPR!!!
Intubation
Transcutaneous pacing
IV therapy with epinephrine & atropine

45. Pulseless Electrical Activity
Electrical activity can be observed on ECG, but there is no mechanical activity of ventricles & patient has no pulse.
Poor prognosis
Most frequent causes:
Treatment:
correct underlying cause.

46. Defibrillation
Most effective method of terminating VF & pulseless VT.

47. Defibrillation Monophasic: deliver energy in one direction Biphasic:
deliver energy in two directions
delivers successful shocks at lower energies & w/fewer post shock ECG abnormalities
output measured in joules (watts/sec)

48. Synchronized Cardioversion

49. Implantable Cardioverter-Defibrillator

50. Pacemakers
Indications
Patient monitoring

51. ECG Changes Associated With Acute Coronary Syndrome
ST segment, T wave, and Q wave changes associated with myocardial ischemia (A), injury (B), and infarction (C).

52. Resource
ECG Simulator

53. Antidysrhythmics Used for Classifications
Prevention & Rx of cardiac rhythm disorders
Classifications
Group I drugs
Group II drugs
Group III drugs
Group IV drugs

54. Group I: Fast (Sodium) Channel Blockers
Dec. fast sodium influx to cardiac cells
Drug response
Three groups: IA IB IC

55. Group I-A Drugs Procainamide Most widely used Reduces automaticity
Slows electrical conduction & delays repolarization in atria, ventricles & Purkinje fibers
Indicated for: ____________________________
Given IV or PO
Side effects

56. Group I-B Drugs Lidocaine
Major use in abolishing ventricular dysrhythmias
Administered IV
Contraindicated in _____________
Benefits
Adverse effect

57. Group II: Beta-Blockers
Decrease conduction velocity, automaticity & recovery time.
Slows conduction through AV node
Examples
More frequently prescribed
For vent. Dysrhythmias, Aflutter & afib.

58. Group III: Prolong Repolarization
Used in emergency treatment of ventricular dysrhythmias when other antidysrhythmics are ineffective.
Examples
Increase refractory period & prolong action potential duration (delay repolarization)
Can significantly prolong QT interval & pose risk for ventricular dysrhythmias

59. Group III Drugs Amiodarone Indicated for life-threatening VF & VT
Most frequently used
Dec. automaticity
Prolongs AV conduction
Given IV or PO
Pregnancy safety category: D
Has serious adverse effects
Indicated for life-threatening VF & VT

60. Group IV: Calcium Channel Blockers
Examples
Slow (calcium) channel blocker that blocks calcium influx → ↓ excitability & contractility of myocardium.
↑ refractory period of AV node → ↓ ventricular response.

61. Group IV Drugs
Diltiazem
Indications
Adverse effects

62. References
Hockenberry, M.J. & Wilson, D. (2015). Wong’s Nursing care of infants and children (10th ed.). St. Louis, MO: Mosby.
Lewis, S., Heitkemper, M. & Dirksen, S. (2014). Medical Surgical Nursing: Assessment and Management of Clinical Problems (9th ed.). St. Louis, MO: Mosby