1. Focus on Dysrhythmias
(Relates to Chapter 36, “Nursing Management: Dysrhythmias,” in the textbook)

2. Dysrhythmias Abnormal cardiac rhythms are termed dysrhythmias
Prompt assessment of dysrhythmias and the patient’s response to the rhythm is critical

3. Properties of Cardiac Cells
Automaticity
Excitability
Conductivity
Contractility

4. Rhythm Strips 5 things to interpret Rate Rhythm P Waves
PR Interval ≤0.2 seconds
QRS Complex ≤0.12 seconds

5. Rate Most common method is the “6 second strip”
Print off a six second strip
Count the QRS complexes
Multiply by 10 = Rate

6. Normal Sinus Rhythm Sinus node fires 60 to 100 times per minute
Follows normal conduction pattern
Fig. 36-8

7. Sinus Bradycardia Sinus node fires <60 times per minute
Normal rhythm is aerobically trained athletes and during sleep
Fig A

8. Sinus Bradycardia (Cont’d)
Clinical associations
Occurs in response to
Carotid sinus massage
Hypothermia
Increased vagal tone
Administration of parasympathomimetic drugs

9. Sinus Bradycardia (Cont’d)
Clinical associations
Occurs in disease states
Hypothyroidism
Increased intracranial pressure
Obstructive jaundice
Inferior wall MI

10. Sinus Bradycardia (Cont’d)
Clinical significance
Dependent on symptoms
Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
Shortness of breath

11. Sinus Bradycardia (Cont’d)
Treatment
Atropine
Pacemaker may be required

12. Sinus Tachycardia
Discharge rate from the sinus node is increased as a result of vagal inhibition and is >100 beats/min
Fig B

13. Sinus Tachycardia (Cont’d)
Clinical associations
Associated with physiologic stressors
Exercise
Pain
Hypovolemia
Myocardial ischemia
Heart failure (HF)
Fever

14. Sinus Tachycardia (Cont’d)
Clinical significance
Dizziness and hypotension due to decreased CO
Increased myocardial oxygen consumption may lead to angina

15. Sinus Tachycardia (Cont’d)
Treatment
Determined by underlying cause
-Adrenergic blockers to reduce HR and myocardial oxygen consumption
Antipyretics to treat fever
Analgesics to treat pain

16. Paroxysmal Supraventricular Tachycardia (PSVT)
Originates in ectopic focus anywhere above bifurcation of bundle of His
Run of repeated premature beats is initiated and is usually a PAC
Paroxysmal refers to an abrupt onset and termination

17. Paroxysmal Supraventricular Tachycardia (PSVT) (Cont’d)
Fig

18. Paroxysmal Supraventricular Tachycardia (PSVT) (Cont’d)
Clinical significance
Prolonged episode and HR >180 beats/min may precipitate ↓ CO
Palpitations
Hypotension
Dyspnea
Angina

19. Paroxysmal Supraventricular Tachycardia (PSVT) (Cont’d)
Treatment
Vagal maneuvers: Valsalva, coughing
IV adenosine
If vagal maneuvers and/or drug therapy is ineffective and/or patient becomes hemodynamically unstable, DC cardioversion should be used

20. Atrial Fibrillation
Total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction
Most common dysrhythmia
Prevalence increases with age

21. Atrial Fibrillation
Fig B

22. Atrial Fibrillation (Cont’d)
Clinical associations
Usually occurs with
Underlying heart disease, such as rheumatic heart disease, CAD
Cardiomyopathy HF
Pericarditis

23. Atrial Fibrillation (Cont’d)
Clinical associations
Often acutely caused by
Thyrotoxicosis
Alcohol intoxication
Caffeine use
Electrolyte disturbance
Cardiac surgery

24. Atrial Fibrillation (Cont’d)
Clinical significance
Can result in decrease in CO due to ineffective atrial contractions (loss of atrial kick) and rapid ventricular response
Thrombi may form in the atria as a result of blood stasis
Embolus may develop and travel to the brain, causing a stroke

25. Atrial Fibrillation (Cont’d)
Treatment
Goals
Decrease ventricular response
Prevent embolic stroke
Drugs for rate control: digoxin, -adrenergic blockers, calcium channel blockers
Long-term anticoagulation: Coumadin

26. Atrial Fibrillation (Cont’d)
Treatment
For some patients, conversion to sinus rhythm may be considered
Antidysrhythmic drugs used for conversion: Amiodarone, propafenone
DC cardioversion may be used to convert atrial fibrillation to normal sinus rhythm

27. Atrial Fibrillation (Cont’d)
Treatment
If patient has been in atrial fibrillation for >48 hours, anticoagulation therapy with warfarin is recommended for 3 to 4 weeks before cardioversion and for 4 to 6 weeks after successful cardioversion

28. Atrial Fibrillation (Cont’d)
Treatment
Radiofrequency catheter ablation
Maze procedure
Modifications to the Maze procedure
Use of cold (cryoablation)
Use of heat (high-intensity ultrasound)

29. Junctional Dysrhythmias
Dysrhythmia that originates in area of AV node
SA node has failed to fire or impulse has been blocked at the AV node

30. Junctional Dysrhythmias (Cont’d)
Fig

31. Junctional Dysrhythmias (Cont’d)
Clinical associations
CAD HF
Cardiomyopathy
Electrolyte imbalances
Inferior MI
Rheumatic heart disease
Drugs: Digoxin, amphetamines, caffeine, nicotine

32. Junctional Dysrhythmia (Cont’d)
Clinical significance
Serves as safety mechanism when SA node has not been effective
Escape rhythms should not be suppressed
If rhythms are rapid, may result in reduction of CO and HF

33. Junctional Dysrhythmias (Cont’d)
Treatment
If symptomatic, atropine
If accelerated junctional rhythm and junctional tachycardia caused by digoxin toxicity, digoxin is held
-Adrenergic blockers, calcium channel blockers, and amiodarone used for rate control for junctional tachycardia not caused by digoxin toxicity
DC cardioversion is contraindicated

34. First-Degree AV Block
Every impulse is conducted to the ventricles, but duration of AV conduction is prolonged
Fig A

35. First-Degree AV Block (Cont’d)
Clinical associations
Usually occurs with MI
CAD
Rheumatic fever
Hyperthyroidism
Vagal stimulation
Drugs: Digoxin, -adrenergic blockers, calcium channel blockers, flecainide

36. First-Degree AV Block (Cont’d)
Clinical significance
Usually asymptomatic
May be a precursor to higher degrees of AV block
Treatment
Check medications
Continue to monitor

37. Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)
Gradual lengthening of the PR interval due to prolonged AV conduction time
Atrial impulse is nonconducted, and a QRS complex is blocked (missing)
Usually block occurs at AV node, but can occur in His-Purkinje system

38. Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach) (Cont’d)
Fig B

39. Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach) (Cont’d)
Clinical associations
Drugs: digoxin, -adrenergic blockers
May be associated with CAD and other diseases that can slow AV conduction

40. Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach) (Cont’d)
Clinical significance
Usually a result of myocardial ischemia or infarction
Almost always transient and well tolerated
May be a warning signal of a more serious AV conduction disturbance

41. Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach) (Cont’d)
Treatment
If symptomatic, atropine or a temporary pacemaker
If asymptomatic, monitor with a transcutaneous pacemaker on standby
Symptomatic bradycardia is more likely with one or more of the following: hypotension, HF, shock

42. Second-Degree AV Block, Type 2 (Mobitz II)
P wave is nonconducted without progressive antecedent PR lengthening
Usually occurs when a block in one of the bundle branches is present

43. Second-Degree AV Block, Type 2 (Mobitz II) (Cont’d)
Fig C

44. Second-Degree AV Block, Type 2 (Mobitz II) (Cont’d)
Clinical associations
Rheumatic heart disease
CAD
Anterior MI
Digitalis toxicity

45. Second-Degree AV Block, Type 2 (Mobitz II) (Cont’d)
Clinical significance
Often progresses to third-degree AV block and is associated with a poor prognosis
Reduced HR often results in decreased CO with subsequent hypotension and myocardial ischemia

46. Second-Degree AV Block, Type 2 (Mobitz II) (Cont’d)
Treatment
If symptomatic (e.g., hypotension, angina) before permanent pacemaker can be inserted, temporary transvenous or transcutaneous pacemaker
Permanent pacemaker

47. Third-Degree AV Heart Block (Complete Heart Block)
Form of AV dissociation in which no impulses from the atria are conducted to the ventricles
Atria are stimulated and contract independently of the ventricles
Ventricular rhythm is an escape rhythm
Ectopic pacemaker may be above or below the bifurcation of the bundle of His

48. Third-Degree AV Heart Block (Complete Heart Block) (Cont’d)
Fig D

49. Third-Degree AV Heart Block (Complete Heart Block) (Cont’d)
Clinical associations
Severe heart disease: CAD, MI, myocarditis, cardiomyopathy
Systemic diseases: Amyloidosis, scleroderma
Drugs: Digoxin, -adrenergic blockers, calcium channel blockers

50. Third-Degree AV Heart Block (Complete Heart Block) (Cont’d)
Clinical significance
Decreased CO with subsequent ischemia, HF, and shock
Syncope may result from severe bradycardia or even periods of asystole

51. Third-Degree AV Heart Block (Complete Heart Block) (Cont’d)
Treatment
If symptomatic, transcutaneous pacemaker until a temporary transvenous pacemaker can be inserted
Drugs (e.g., atropine, epinephrine): Temporary measure to increase HR and support BP until temporary pacing is initiated
Permanent pacemaker as soon as possible

52. Premature Ventricular Contractions
Contraction originating in ectopic focus of the ventricles
Premature occurrence of a wide and distorted QRS complex
Multifocal, unifocal, ventricular bigeminy, ventricular trigeminy, couples, triplets, R on T phenomena

53. Premature Ventricular Contractions (Cont’d)
Fig

54. Premature Ventricular Contractions (Cont’d)
Clinical associations
Stimulants: Caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol
Digoxin
Electrolyte imbalances
Hypoxia
Fever
Disease states: MI, mitral valve prolapse, HF, CAD

55. Premature Ventricular Contractions (Cont’d)
Clinical significance
In normal heart, usually benign
In heart disease, PVCs may decrease CO and precipitate angina and HF
Patient’s response to PVCs must be monitored
PVCs often do not generate a sufficient ventricular contraction to result in a peripheral pulse
Apical-radial pulse rate should be assessed to determine if pulse deficit exists

56. Premature Ventricular Contractions (Cont’d)
Clinical significance
Represents ventricular irritability
May occur
After lysis of a coronary artery clot with thrombolytic therapy in acute MI—reperfusion dysrhythmias
Following plaque reduction after percutaneous coronary intervention

57. Premature Ventricular Contractions (Cont’d)
Treatment
Based on cause of PVCs
Oxygen therapy for hypoxia
Electrolyte replacement
Drugs: -Adrenergic blockers, procainamide, amiodarone, lidocaine

58. Ventricular Tachycardia
Run of three or more PVCs
Monomorphic, polymorphic, sustained, and nonsustained
Considered life-threatening because of decreased CO and the possibility of deterioration ventricular fibrillation

59. Ventricular Tachycardia (Cont’d)
Fig A

60. Ventricular Tachycardia (Cont’d)
Fig B

61. Ventricular Tachycardia (Cont’d)
Clinical associations MI
CAD
Electrolyte imbalances
Cardiomyopathy
Mitral valve prolapse
Long QT syndrome
Digitalis toxicity
Central nervous system disorders

62. Ventricular Tachycardia (Cont’d)
Clinical significance
VT can be stable (patient has a pulse) or unstable (patient is pulseless)
Sustained VT: Severe decrease in CO
Hypotension
Pulmonary edema
Decreased cerebral blood flow
Cardiopulmonary arrest

63. Ventricular Tachycardia (Cont’d)
Clinical significance
Treatment for VT must be rapid
May recur if prophylactic treatment is not initiated
Ventricular fibrillation may develop

64. Ventricular Tachycardia (Cont’d)
Treatment
Precipitating causes must be identified and treated (e.g., hypoxia)
VT without a pulse is a life-threatening situation
Cardiopulmonary resuscitation (CPR) and rapid defibrillation
Epinephrine if defibrillation is unsuccessful

65. Ventricular Fibrillation
Severe derangement of the heart rhythm characterized on ECG by irregular undulations of varying contour and amplitude
No effective contraction or CO occurs

66. Ventricular Fibrillation (Cont’d)
Fig

67. Ventricular Fibrillation (Cont’d)
Clinical associations
Acute MI, CAD, cardiomyopathy
VF may occur during cardiac pacing or cardiac catheterization
VF may occur with coronary reperfusion after fibrinolytic therapy
Accidental electrical shock
Hyperkalemia
Hypoxia
Acidosis
Drug toxicity

68. Ventricular Fibrillation (Cont’d)
Clinical significance
Unresponsive, pulseless, and apneic state
If not treated rapidly, death will result

69. Ventricular Fibrillation (Cont’d)
Treatment
Immediate initiation of CPR and advanced cardiac life support (ACLS) measures with the use of defibrillation and definitive drug therapy

70. Asystole Represents total absence of ventricular electrical activity
No ventricular contraction (CO) occurs because depolarization does not occur

71. Asystole (Cont’d) Clinical associations Advanced cardiac disease
Severe cardiac conduction system disturbance
End-stage HF

72. Asystole (Cont’d) Clinical significance
Unresponsive, pulseless, and apneic state
Prognosis for asystole is extremely poor

73. Asystole (Cont’d) Treatment
CPR with initiation of ACLS measures (e.g., intubation, transcutaneous pacing, and IV therapy with epinephrine and atropine)

74. Defibrillation
Most effective method of terminating VF and pulseless VT
Passage of DC electrical shock through the heart to depolarize the cells of the myocardium to allow the SA node to resume the role of pacemaker

75. Synchronized Cardioversion
Choice of therapy for hemodynamically unstable ventricular or supraventricular tachydysrhythmias
Synchronized circuit delivers a countershock on the R wave of the QRS complex of the ECG
Synchronizer switch must be turned on

76. Implantable Cardioverter- Defibrillator (ICD)
Appropriate for patients who
Have survived SCD
Have spontaneous sustained VT
Have syncope with inducible ventricular tachycardia/fibrillation during EPS
Are at high risk for future life-threatening dysrhythmias

77. Implantable Cardioverter- Defibrillator (ICD) (Cont’d)
ICD sensing system monitors the HR and rhythm and identifies VT or VF
Approximately 25 seconds after detecting VT or VF, ICD delivers <25 joules
If first shock is unsuccessful, ICD recycles and delivers successive shocks

78. Implantable Cardioverter- Defibrillator (ICD) (Cont’d)
ICDs are equipped with antitachycardia and antibradycardia pacemakers
Initiates overdrive pacing of supraventricular and ventricular tachycardias
Provides backup pacing for bradydysrhythmias that may occur after defibrillation discharges

79. Implantable Cardioverter- Defibrillator (ICD) (Cont’d)
Fig
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80. Implantable Cardioverter- Defibrillator (ICD) (Cont’d)
Education is extremely important
Variety of emotions are possible
Fear of body image change
Fear of recurrent dysrhythmias
Expectation of pain with ICD discharge
Anxiety about going home

81. Pacemakers
Used to pace the heart when the normal conduction pathway is damaged or diseased
Electrical signal (stimulus) travels from the pacemaker, through the leads, to the wall of the myocardium
Myocardium is “captured” and stimulated to contract

82. Pacemakers (Cont’d)
Fig

83. Pacemakers (Cont’d)
Initially indicated for symptomatic bradydysrhythmias
Antitachycardia and overdrive pacing
Antitachycardia pacing: Delivery of a stimulus to the ventricle to terminate tachydysrhythmias
Overdrive pacing: Pacing the atrium at rates of 200 to 500 impulses per minute to terminate atrial tachycardias

84. Pacemakers (Cont’d) Temporary pacemaker: Power source outside the body
Transvenous
Epicardial
Transcutaneous

85. Pacemakers (Cont’d) Fig. 36-26 Fig. 36-25
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86. Pacemakers (Cont’d) Fig. 36-27
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87. Pacemakers (Cont’d)
Permanent pacemaker: Implanted totally within the body
Cardiac resynchronization therapy (CRT): Pacing technique that resynchronizes the cardiac cycle by pacing both ventricles
Combined CRT with an ICD for maximum therapy

88. Pacemakers (Cont’d) Fig. 36-24 A
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89. Pacemakers (Cont’d) Pacemaker malfunction
Failure to sense: Failure to recognize spontaneous atrial or ventricular activity, and pacemaker fires inappropriately
Lead damage, battery failure, dislodgement of the electrode

90. Pacemakers (Cont’d) Pacemaker malfunction Patient education
Failure to capture: Electrical charge to myocardium is insufficient to produce atrial or ventricular contraction
Lead damage, battery failure, dislodgement of the electrode, fibrosis at the electrode tip
Patient education