for teaching

1. Nursing 202
Module B
Cardiovascular System Alterations

2. CARDIAC
DYRHYTHMIAS

3. REVIEW OF
CONDUCTION

4. ELECTRICAL
CONDUCTION
SINOATRIAL NODE (SA)
INTRAATRIAL FIBER (BACHMAN’S
BUNDLE)
INTRANODAL TRACTS
ATRIOVENTRICULAR (AV) NODE
BUNDLE OF HIS (COMMON BUNDLE)
BUNDLE BRANCHES
PURKINJE FIBERS

5. TERMINOLOGY
WAVE- POSITIVE OR NEGATIVE DEFLECTION
GENERALLY BEGINS AND ENDS AT THE
BASELINE, REPRESENTING DEPOLARIZATION
OR REPOLARIZATION
SEGMENT- LENGTH OF BASELINE BETWEEN
2 WAVES NAMED BY THE WAVE BEFORE AND
AFTER
INTERVAL-LENGTH OF A WAVE OR THE
LENGTH OF A WAVE WITH THE SEGMENT
THAT FOLLOWS
COMPLEX-GROUP OF WAVES THAT FOLLOW
ONE AFTER ANOTHER

7. PR INTERVAL
REPRESENTS TIME FROM THE
BEGINNING OF ATRIAL
DEPOLARIZATION TO THE
BEGINNING OF VENTRICULAR
DEPOLARIZATION, MEASURED
FROM THE BEGINNING OF THE P
WAVE TO THE BEGINNING OF THE
QRS COMPLEX (O.12-O.20)

8. QRS INTERVAL
REPRESENTS THE LENGTH OF TIME
FOR DEPOLARIZATION OF THE
VENTRICULAR MUSCLE AND IS
MEASURED FROM THE BEGINNING
OF THE QRS COMPLEX TO THE END
OF THE S WAVE, SHOULD MEASURE
BETWEEN 0.06-0.10 SECONDS IN
DURATION

9. ST INTERVAL
REPRESENTS THE TOTAL LENGTH OF
TIME FOR VENTRICULAR MUSCLE TO
BE DEPOLARIZED AND
REPOLARIZED, MEASURED FROM
THE BEGINNING OF THE QRS
COMPLEX TO THE END OF THE T
WAVE, NORMAL RANGE IS 0.32-0.42

10. INHERENT RATES
SA 60-100
AV JUNCTION 40-60
VENTRICULAR 20-40

11. SINUS DYSRHYTHMIA
OCCURS IF THE P - P INTERVAL VARY
BY MORE THAN 0.16 . LESS THAN
O.16 IS CONSIDERED NORMAL
BECAUSE OF THE FLUCTUATION OF
THE SYMPATHETIC/
PARASYMPATHETIC STIMULATION
ASSOCIATED WITH RESPIRATION IN
CHILDREN AND ELDERLY

12. SINUS BRADYCARDIA
HR < 60/MIN ARISING FROM THE SA
NODE.
IMPULSES FOLLOW THE NORMAL
PATHWAY THROUGH THE CONDUCTION
SYSTEM
P AND QRS COMPLEXES NORMAL
DURATION AND PATTERN

13. ETIOLOGY
INCREASED VAGAL STIMULATION
MAY BE A NORMAL VARAITION IN ALTHLETES AND
HEALTHY YOUG ADULTS
MEDICAL CONDITIONS:
 ANOREXIA NERVOSA
 ATHEROSCLEROTIC HEART DISEASE
 HYPOENDOCRINE STATES
 HYPOTHERMIA
 INCREASED INTRACRANIAL PRESSURE
 MYOCARDIAL INFARCTION
MEDICATIONS:
 ANTIHYPERTENSIVES
 BETA BLOCKERS
 CALCIUM CHANNEL BLOCKERS
 CNS DEPRESSANTS
 DIGOXIN

14. SYMPTOMS
SYMPTOMS RELATED TO
DECREASE IN CARDIAC OUTPUT
 CHEST PRESSURE AND PAIN
 DYSPNEA
 HYPOTENSION
 DIZZINESS
 SEIZURES
 SYNCOPE

15. TREATMENT
MANAGEMENT -ONLY IF SYMPTOMATIC-
AIMED AT INCREASING THE HEART RATE
MEDICATIONS
 ATROPINE
 ISOPROTERENOL
 PACEMAKER
SUPRESSION OF THE PARASYMPATHETIC
NERVOUS SYSTEM
STIMULATION OF THE SYMPATHETIC NERVOUS
SYSTEM

16. SINUS TACHYCARDIA
HR OF 100-160/ MIN
NORMAL RESPONSE TO
SYMPATHETIC NERVOUS SYSTEM
STIMULATION
ANY CONDITION THAT PRODUCES AN
INCREASE IN METABOLIC RATE

17. ETIOLOGY
DIET – CAFFEINE
LIFE-STYLE – SMOKING / NICOTINE
MEDICAL CONDITIONS – ANEMIA,
HEMORRHAGE, FEVER,
HYPOTENSION, PAIN, SHOCK
MEDICATIONS – CENTRAL NERVOUS
SYSTEM STIMULANTS
MYOCARDIAL DAMAGE

18. SYMPTOMS
PRIMARY SYMPTOMS RELATED TO
DECREASED CARDIAC OUTPUT
 CHEST PRESSURE AND PAIN
 DYSPNEA
 A CHARACTERISTIC “FLUTTERING” IN
THE CHEST
 DIZZINESS
 SYNCOPE

19. TREATMENT
ELIMINATE THE CAUSE OF THE
TACHYCARDIA
MEDICATIONS:
 CALCIUM CHANNEL BLOCKERS
 DIGOXIN
 BETA BLOCKERS
 ANTIANXIETY AGENTS
 ADENOSINE
CAROTID MASSAGE

20. ATRIAL DYSRHYTHMIAS
IMPULSE ARISES OUTSIDE THE SINO
ATRIAL NODE
P WAVES DIFFER IN CONFIGURATION
TYPES
 WANDERING ATRIAL PACEMAKER
 PREMATURE ATRIAL CONTRACTIONS
 PAROXYSMAL ATRIAL TACHYCARDIA
 ATRIAL FLUTTER
 ATRIAL FIBRILLATION

21. ETIOLOGY
CARDIAC DISEASE
 ISCHEMIA
 CORONARY ARTERY DISEASE
 CONGESTIVE HEART FAILURE
 MYOCARDIAL INFARCTION
INCREASED VAGAL STIMULATION
MEDICATIONS

22. PREMATURE ATRIAL
CONTRACTIONS
MOST COMMON ECTOPIC BEAT
OCCURS WHEN IMPULSE IS
GENERATED BY AN IRRITABLE AREA
OF TISSUE IN THE ATRIA
ABNORMALLY SHAPED P WAVE
QRS COMPLEX NOT AFFECTED

23. ETIOLOGY
CARDIAC DISEASE
CHRONIC OBSTRUCTIVE PULMONARY
DISEASE
MEDICATIONS: CENTRAL NERVOUS
SYSTEM STIMULANTS
DIET: CAFFEINE
ELECTROLYTE DISTURBANCES
ANXIETY
LIFE STYLE: EXERCISE, ALCOHOL,
NICOTINE

24. SYMPTOMS
FEELINGS OF PALPITATIONS OR
“SKIPPED BEAT”

25. TREATMENT
TREATMENT DIRECTED TOWARD CAUSE
TREATMENT NOT NECESSARY IF LESS
THAN 6 PER MINUTE
DECREASE CAFFEINE CONSUMPTION
DECREASE STRESS
MEDICATIONS:
 ANTIANXIETY AGENTS
 BETA BLOCKERS
 CALCIUM CHANNEL BLOCKERS

26. PAROXYSMAL ATRIAL
TACHYCARDIA
Caused by an irritable area of tissue in
the atria that dominates the sinoatrial
node and takes over as the pacemaker
Usually preceded by premature atrial
contractions
Begin and end abruptly
The raid rate prevents adequate
ventricular filling

27. ETIOLOGY
SAME AS SEEN WITH PREMATURE
ATRIAL CONTRACTIONS
NOT USUALLY ASSOCIATED WITH
ORGANIC HEART DISEASE

28. SYMPTOMS
CHEST PAIN
DYSPNEA
HYPOTENSION
PALPITATIONS
WEAK RAPID PULSE
DIZZINESS
SYNCOPE

29. TREATMENT
CAROTID SINUS PRESSURE
VAGAL NERVE STIMULATION
MEDICATIONS:
 DILTIAZEM
 VERAPAMIL
 DIGOXIN
 PROPRANOLOL
 PROCAINAMIDE
 QUINIDINE
 VASOPRESSOR

30. ATRIAL FLUTTER
ATRIAL ECTOPIC PACER FIRES AT A RATE OF
250-400/ MIN
OCCURS IN A VARIETY OF HEART DISEASES-
RHEUMATIC, CORONARY, HYPERTENSIVE, ALSO
CARDIOMYOPATHY, HYPOXIA, HEART FAILURE,
MAY BE ASYMPTOMATIC OR HAVE
PALPITATIONS
MANAGEMENT- DIGITALIS, BETA BLOCKERS,
CALCIUM CHANNEL BLOCKERS, MAY USE
CARDIOVERSION

31. ATRIAL FIBRILLATION
SEVERAL ECTOPIC FOCI CAUSING
THE ATRIA TO QUIVER RATHER THAN
CONTRACT.
RATE >400
VENTRICULAR RATE DEPENDS ON
THE NUMBER OF IMPULSES
CONDUCTED THRU THE AV NODE
MANAGEMENT- DIG., BETA
BLOCKERS, CALCIUM CHANNEL
BLOCKERS, COUNTERSHOCK

32. AV HEART BLOCKS
ABNORMAL DELAY IN CONDUCTION
OF IMPULSE FROM THE ATRIUM TO
THE VENTRICLES
USUALLY ASYMPTOMATIC

33. FIRST DEGREE
DELAY OCCURS AT THE AV NODE
PRODUCING A PROLONGED PR
INTERVAL > .20.

34. ETIOLOGY
COMMON OCCURANCE IN NORMAL
HEARTS
CARDIAC DISEASE INCLUDING:
 ARTERIOSCLEROTIC HEART DISEASE,
MYOCARDITIS, ORGANIC HEART DISEASE,
MYOCARDIAL INFARCTION
MEDICATIONS:
 BETA BLOCKERS
 CALCIUM CHANNEL BLOCKERS
 DIGITALIS TOXICITY

35. TREATMENT
USUALLY NOT NECESSARY UNLESS
THE BLOCK THAT IS CAUSED BY
MEDICATION THAT CAN BE
MODIFIED OR WITHHELD

36. SECOND DEGREE
HEART BLOCK
TYPE I- MOBITZ I OR
WENCKEBACH- PROGRESSIVE
LENGTHENING OF THE PR
INTERVAL UNTIL A QRS COMPLEX IS
DROPPED OR NOT CONDUCTED
USUALLY ASYMPTOMATIC
TX- MAYBE NONE, ATROPINE, TEMP.
PACER

37. SECOND DEGREE- TYPE
II
EVERY SECOND THIRD OR FOURTH
SINUS IMPULSE IS BLOCKED MAY HAVE
2,3,4 Ps TO EACH QRS
MORE SERIOUS- AGGRESSIVE
MANAGEMENT TO PREVENT
PROGRESSION TO COMPLETE HEART
BLOCK
TREATMENT:
 PACER
 ATROPINE
 DOPAMINE FOR SEVERE HYPOTENSION

38. THIRD DEGREE HEART
BLOCK
TOTAL DISASSOCIATION OF ATRIA TO VENTRICLES.
VENTRICLES ARE STIMULATED BY A SECONDARY OR
ESCAPE BEAT. THE VENTRICULAR RATE WILL BE 40-60
DEPENDING UPON THE LOCATION OF THE VENTRICULAR
PACEMAKER
BOTH THE SINUS P WAVE AND THE ESCAPE RHYTHM WILL
BE OBVIOUS ON THE ELECTROCARDIOGRAM
ETIOLOGY –
 CARDIAC DISEASE
 MEDICATIONS – BETA BLOCKERS, CALCIUM CHANNEL
BLOCKERS, DIGITALIS TOXICITY
MANIFESTATIONS- FATIGUE, HYPOTENSION, SYNCOPE,
HEART FAILURE
TX.- ATROPINE, ISOPROTERENOL, DOPAMINE, PACER

40. JUNCTIONAL RHYTHMS
RATE 40- 60
THE DOMINANT PACER OF THE HEART
FAILS , RETROGRADE OR BACKWARD
STIMULATION OF THE ATRIA-
PRODUCING A CHARACTERISTIC P WAVE
- MAY BE A NEGATIVE DEFLECTION
BEFORE OR AFTER THE QRS COMPLEX
OR NO P WAVE AT ALL

41. ETIOLOGY
CORONARY ARTERY DISEASE
CONGESTIVE HEARAT FAILURE
MYOCARDIAL INFARCTION
CAFFEINE
ANXIETY
ALCOHOL, TOBACCO

42. SYMPTOMS
FEELINGS OF
 PALPITATIONS
 FLUTTERING
 “SKIPPED BEATS”

43. MANAGEMENT
TX UNDERLYING CAUSE
MODIFY DIET / LIFESTYLE
REDUCE STRESS
MEDICATIONS :
 QUINIDINE

44. PREMATURE JUNCTIONAL
CONTRACTIONS
AN IRRITABLE JUNCTIONAL FOCUS DISCHARGES AN
IMPULSE BEFORE THE SINOATRIAL NODE FIRES
ABNORMAL P WAVES CAN PRECEDE, FOLLOW, OR
OCCUR SIMULTANEOUSLY WITH THE QRS COMPLEX
VENTRICULAR CONTRACTION IS USUALLY NORMAL
MAY BE FOLLOWED BY AN INCOMPLETE OR
COMPENSATORY PAUSE
MAY OCCUR LATE IN THE CYCLE AND IS REFERRED TO
AS JUNCTIONAL ESCAPE BEATS
ETIOLOGY, SYMPTOMS, AND TREATMENT IS THE SAME
AS LISTED UNDER JUNCTIONAL RHYTHMS

45. PAROXYSMAL JUNCTIONAL
TACHCARDIA
A CLUSTER OF THREE OR MORE
PREMATURE JUNCTIONAL
CONTRACTIONS FIRING AT A RATE
OF MORE THAN 150 BEATS/ MINUTE
ETIOLOGY IS THE SAME AS LISTED
UNDER JUNCTIONAL RHYTHMS

46. SYMPTOMS
MAY BE ASYMPTOMATIC IS RATE IS
LESS THAN 150 BEATS/ MINUTE
AT RATES GREATER THAN 150
BEATS/ MINUTE:
 CHEST PAIN, PRESSURE,
PALPITATIONS, DIZZINESS, SYNCOPE

47. TREATMENT
MEDICATIONS:
 CALCIUM CHANNEL BLOCKER
 CENTRAL NERVOUS SYSTEM
 DEPRESSANTS
 DIGOXIN
VAGAL STIMULATION
CARDIOVERSION

48. JUNCTIONAL ESCAPE
BEATS
BEATS THAT OCCUR WHEN THE AV
JUNCTION TAKES OVER THE
PACEMAKER ACTIVITY
OCCUR LATE IN THE CYCLE

49. ETIOLOGY
RHEUMATIC HEART DISEASE
MYOCARDIAL INFARCTION
SINUS ARRHYTHMIAS:
 BRADYCARDIA
 BLOCK
 ARREST
MEDICATIONS
 BETA BLOCKERS
 CALCIUM CHANNEL BLOCKERS
 CENTRAL NERVOUS SYSTEM DEPRESSANTS
 DIGOXIN
 NARCOTICS
 SEDATIVES

50. SYMPTOMS
MOST ARE ASYMPTOMATIC
FEELINGS OF
 PALITATIONS
 FLUTTERING
 “SKIPPED BEATS”

51. TREATMENT
MOST TREATMENT MEASURES ARE
THOSE USED FOR SINUS
BRADYCARDIA

52. VENTRICULAR
DYSRHYTHMIAS
IMPULSE ORIGINATES IN THE
VENTRICLES
CAUSES- DRUG TOXICITY, HYPOXIA,
HYPOTHERMIA, ELECTROLYE
IMBALANCES

53. PREMATURE VENTRICULAR
CONTRACTIONS
OCCUR EARLY- NOTED COMPENSATORY PAUSE, QRS
COMPLEX WIDE
MAY BE MULTIFOCAL OR UNIFOCAL
BIGEMINY, TRIGEMINY OR COUPLETS
THREE OR MORE = VENTRICULAR TACH.
R ON T PHENOMENON
TX- 6 OR > /MIN, COUPLETS , R ON T, OR MULTIFOCAL
ARE NO LONGER CONSIDERED TO BE A WARNING OR
PRECURSOR TO THE DEVELOPMENT OF
VENTRICULAR TACHYCARDIA
LIDOCAINE MOST COMMONLY USED FOR IMMEDIATE
SHORT TERM THERAPY

54. VENTRICULAR TACH
DEFINED AS THREE OR MORE
PREMATURE VENTRICULAR
CONTRACTIONS IN A ROW
RATE OF VENTRICULAR DISCHARGE IS
100-250/MIN
ETIOLOGY- INCREASED MYOCARDIAL
IRRITABILITY ASSOCIATED WITH
CORONARY ARTERY DISEASE,
MYOCARDIAL INFARCTION,
ELECTROLYTE IMBALANCE,
CARDIOMYOPATHY

55. TREATMENT
MANAGEMENT DEPENDS UPON SEVERITY
IF STABLE – CONTINUE MONITORING, OBATIN 12
LEAD ELECTROCARDIOGRAM
 FACTORS DETERMINING MEDICATIONS TO BE
ADMINISTERED:
 MONOMORPHIC OR POLYMORPHIC
 EXISTENCE OF PROLONGED QT INTERVAL PRIOR TO
ONSET
 HEART FUNCTION (NORMAL OR DECREASED)
UNSTABLE- UNCONSCIOUS / WITHOUT A PULSE
– TREAT AS VENTRICULAR FIBRILLATION –
IMMEDIATE DEFIBRILLATION

56. VENTRICULAR
FIBRILLATION
RAPID, DISORGANIZED
VENTRICULAR RHYTHM THAT
RESULTS IN INEFFECTIVE
QUIVERING OF THE VENTRICLES
NO ATRIAL ACTIVITY SEEN ON ECG
ABSENCE OF AUDIBLE HEARTBEAT,
PALPABLE PULSE, AND
RESPIRATION

57. ETIOLOGY
SAME AS VENTRICULAR TACHYCARDIA
UNTREATED VENTRICULAR
TACHYCARDIA
ELECTRICAL SHOCK
BRUGADA SYNDROME

58. TREATMENT
IMMEDIATE DEFIBRILLATION
ACTIVATION OF EMS
CPR
ERADICATING THE CAUSE
VASOACTIVE AND ANTIARRHYTHMIC
MEDICATIONS

59. VENTRICULAR
ASYSTOLE
ABSENCE OF:
 QRS
 HEARTBEAT
 PALPABLE PULSE
 RESPIRATION

60. ETIOLOGY
HYPOXIA
ACIDOSIS
ELECTROLYTE IMBALANCE
DRUG OVERDOSE
HYPOTHERMIA

61. TREATMENT
CARDIOPULMONARY RESUSCITATION
INTUBATION
INTRAVENOUS ACCESS
TRANSCUTANEOUS PACING
EPINEPHRINE
ATROPINE

62. ADJUNCTIVE
MODALITIES AND
MANAGEMENT
TREATMENT DEPENDS UPON
 WHETHER THE DYSRHYTHMIA IS
ACUTE OR CHRONIC
 THE CAUSE OF THE DYSRHYTHMIA
AND ITS POTENTIAL HEMODYNAMIC
EFFECTS

63. PACERS
AN ELECTRICAL IMPULSE THAT
STIMULATES THE MYOCARDIUM TO
DEPOLARIZE, INITIATING A HEARTBEAT
MAY BE DEMAND, FIXED, OR RATE
RESPONSIVE
MAY BE TEMPORARY OR PERMANENT
PACER SPIKE NOTED ON EKG

64. INDICATIONS
A SLOWER THAN NORMAL IMPULSE
FORMATION OR A ACONDUCTION
DISTURBANCE THAT CAUSES
SYMPTOMS
MAY BE USED TO TREAT
TACHYDYSRHYTHMIAS THAT DO
NOT RESPOND TO MEDICATION
THERAPY

65. ASSESSMENT
MONITOR HEART RATE AND RHYTHM BY
ELECTROCARDIOGRAM
ASSESS FOR PACEMAKER SPIKE AND ITS
RELATIONSHIP TO THE SURROUNDING
ELECTROCARDIOGRAM COMPLEXES
ASSESS CARDIAC OUTPUT AND
HEMODYNAMIC STABILITY
INCISION SITE

66. COMPLICATIONS
LOCAL INFECTION AT THE ENTRY SITE
BLEEDING AND HEMATOMA FORMATION
HEMOTHORAX
VENTRICULAR ECTOPY / TACHYCARDIA
DISLOCATION OF THE LEAD
STIMULATION OF THE PHRENIC NERVE
CARDIAC TAMPONADE
MY0CARDIAL WALL PERFORATION

67. PACEMAKER
MALFUNCTION
LOSS OF CAPTURE
UNDERSENSING
OVERSENSING
LOSS OF PACING

69. CLIENT TEACHING
MONITOR PACEMAKER FUNCTION
PROMOTE SAFETY/ PREVENT
INFECTION
ELECTROMAGNETIC
INTERFERENCE

70. CARDIOVERSION AND
DEFIBRILLATION
PADS OR PADDLES ARE USED TO
DELIVER A N ELECTRICAL CURRENT TO
DEPOLARIZE A CRITICAL MASS OF
CARDIAC CELLS IN AN ATTEMPT FOR THE
SINUS NODE TO RECAPTURE THE ROLE
OF THE PACEMAKER
DIFFERENCE BETWEEN CARDIOVERSION
AND DEFIBRILLATION HAS TO DO WITH
THE TIMING OF THE DELIVERY AND THE
CIRCUMSTANCE

71. SAFETY
MAINTAIN GOOD CONTACT
BETWEEN THE PADS OR PADDLES
AND THE SKIN
ENSURE THAT NOONE IS IN
CONTACT WITH THE CLIENT OR
WITH ANYTHING TOUCHING THE
CLIENT

72. CARDIOVERSION
DELIVERY OF A TIMED ELECTRICAL
CURRENT TO TERMINATE A
TACHYDYSRHYTHMIA
THE DEFIBRILLATOR IS SET TO
SYNCHRONIZE WITH THE
ELECTROCARDIOGRAM ON A MONITOR
SO THAT THE ELECTRICAL IMPULSE
DISCHARGES DURING VENTRICULAR
DEPOLARIZATION
VOLTAGE VARIES FROM 25 TO 360
JOULES

73. PREPARATION
ANTICOAGULATION FOR A FEW
WEEKS PRIOR TO PROCEDURE IF
ELECTIVE
DIGOXIN IS WITHHELD FOR 48
HOURS
NPO FOR AT LEAST 8 HOURS
INTRAVENOUS SEDATION
SUPPLEMENTAL OXYGENATION

74. POST PROCEDURE
CARE
MAINTAIN AIRWAY PATENCY
MONITOR VITAL SIGNS AND
OXYGEN SATURATION
ELECTROCARDIOGRAM
MONITORING

75. DEFIBRILLATION
USED IN EMERGENCY SITUATIONS AS THE
TREATMENT OF CHOICE FOR VENTRICULAR
FIBRILLATION AND PULSELESS VENTRICULAR
TACHYCARDIA
ELECTRICAL VOLTAGE IS USUALLY GREATER
THAN WITH CARDIOVERSION
THE USE OF EPINEPHRINE OR VASOPRESSIN
MAY BE HELPFUL
ANTIARRHYTHMIC MEDICATIONS SUCH AS
AMIODARONE, LIDOCAINE, MAGNESIUM,
PROCAINAMIDE ARE GIVEN IF VENTRICULAR
DYSRHYTHMIA PERSISTS

76. ELECTROPHYSIOLOGIC
STUDIES
IDENTIFY IMPULSE FORMATION THROUGH THE
CARDIAC CONDUCTION SYSTEM
ASSESS THE FUNCTION OF THE SA AND AV
NODES
MAP DYSRHYTHMOGENIC FOCI
ASSESS THE EFFECTIVENESS OF
ANTIARRHYTHMIC MEDICATIONS
TREAT CERTAIN DYSRHYTHMIAS THROUGH THE
DESTRUCTION OF CAUSATIVE CELLS
(ABLATION)

77. CARDIAC CONDUCTION
SURGERY
ENDOCARDIAL ISOLATION
ENDOCARDIAL RESECTION
CATHETER ABLATION THERAPY

78. MEDICATIONS
CLASS I – SODIUM CHANNEL BLOCKERS
IA – SLOWS CONDUCTION AND
PROLONGS REPOLARIZATION –
QUINIDINE, PROCAINAMIDE,
DISOPYRAMIDE
IB – SLOWS CONDUCTION AND
SHORTENS REPOLARIZATION –
LIDOCAINE, MEXILETINE HCL
IC- PROLONGS CONDUCTION WITH
LITTLE OR NO EFFECT ON
REPOLARIZATION – ENCAINIDE,
FLECAINIDE

79. CLASS II
BETA BLOCKERS – DECREASE
CONDUCTION VELOCITY,
AUTOMATICITY AND RECOVERY
TIME ( REFRACTORY PERIOD) –
PROPRANOLOL, ACEBUTOLOL

80. CLASS III
PROLONG REPOLARIZATION- ARE
USED IN THE EMERGENCY
TREATMENT OF VENTRICULAR
DYSRHYTHMIAS WHEN OTHER
ANTIDYSRHYTHMICS ARE NOT
EFFECTIVE – BRETYLIUM,
AMIODARONE

81. CLASS IV
CALCIUM CHANNEL BLOCKERS –
BLOCKS CALCIUM INFLUX,
DECREASING THE EXCITABILITY
AND CONTRACTILITY OF THE
MYOCARDIUM – VERAPAMIL,
DILTIAZEM

82. OTHERS
DILANTIN- USED IN THE TX OF
DIGITALIS INDUCED DYSRHYTHMIAS
DIGOXIN- ATRIAL FLUTTER OR
FIBRILLATION, PREVENT
RECURRENCE OF PAT
ATROPINE- BRADYCARDIA

83. NURSING PROCESS -
DYSRHYTHMIA
ASSESSMENT –
 HISTORY
 CAUSES OF DYSRHYTHMIA
 PHYSICAL EXAM
 EFFECT ON CARDIAC OUTPUT

84. NURSING PROCESS
DIAGNOSES:
 DECREASED CARDIAC OUTPUT
 ANXIETY RELATED TO FEAR OF THE
UNKNOWN
 DEFICIENT KNOWLEDGE ABOUT THE
DYSRHYTHMIA AND TREATMENT

85. NURSING PROCESS
PLANNING AND GOALS
 ERADICATING OR DECREASING THE
INCIDENCE OF THE DYSRHYTHMIA
 ACQUIRE KNOWLEDGE ABOUT THE
DYSRHYTHMIA AND TREATMENT

86. NURSING PROCESS
INTERVENTIONS
 MONITOR :
 BLOOD PRESSURE, PULSE RATE AND RHYTHM, RATE
AND RHYTHM OF RESPIRATIONS, BREATH SOUNDS
 EPISODES OF LIGHTHEADEDNESS, DIZZINESS,
FAINTNESS
 RHYTHM STRIPS
 MEDICATION ADMINISTRATION
 ASSIST IN DEVELOPING A PLAN TO MODIFY LIFESTYLE
 MINIMIZE ANXIETY
 TEACH SELF CARE

87. NURSING PROCESS
EVALUATION
 EXPECTED OUCOMES
 MAINTAINS CARDIAC OUTPUT
 EXPERIENCES REDUCED ANXIETY
 EXPRESSES UNDERSTANDING OF THE
DYSRHYTHMIA AND ITS TREATMENT

88. CORONARY ARTERY
DISEASE
TYPES:
 ATHEROSCLEROSIS
 ARTERIOSCLEROSIS

89. ATHEROSCLEROSIS
AN ABNORMAL ACCULULATION OF
LIPID, OR FATTY, SUBSTANCES AND
FIBROUS TISSUE CREATING
BLOCKAGES OR NARROWING OF
THE VESSEL

90. ARTERIOSCLEROSIS
THICKENING OF THE WALLS OF THE
ARTERIOLES, WITH LOSS OF
ELASTICITY AND CONTRACTILITY

91. PATHOPHYSIOLOGY
FATTY STREAKS, LIPIDS THAT ARE
DEPOSITED IN THE INTIMA OF THE
ARTERIAL WALL THAT CONTINUE TO
DEVELOP RELATED TO AN
INFLAMMATORY RESPONSE
FORMING PLAQUES OR
ATHEROMAS WHICH NARROW THE
VESSEL OBSTRUCTING BLOOD
FLOW

92. RISK FACTORS
MODIFIABLE :
 TOBACCO
 HYPERTENSION
 ELEVATED BLOOD LIPID LEVELS
 DIABETES
 OBESITY
 SEDETARY LIFE STYLE
 CHRONIC STRESS
NONMODIFIABLE :
 FAMILY HISTORY
 INCREASING AGE
 GENDER
 RACE

93. CLINICAL
MANIFESTATIONS
MAY BE ASYMPTOMATIC
ANGINA
NAUSEA, VOMITING
DIAPHORESIS
COOL, CLAMMY SKIN
EKG CHANGES

94. MANAGEMENT
LIFESTYLE CHANGES
 DIETARY MEASURES
 Therapeutic Lifestyle Changes diet
 LOW FAT
 LOW CHOLESTEROL
 Increased soluble fiber
 Increased physical activity
 Cessation of tobacco
 Managing hypertension
 Controlling diabetes
 Stress reduction
MEDICATION:
 Lipid lowering agents
 Nitrates
 Antiplatelets
 Beta blockers
 Calcium channel blockers
 Diuretics

95. ANGINA
EPISODES OF PAIN OR PRESSURE IN
THE ANTERIOR CHEST
ETIOLOGY – INSUFFICIENT CORONARY
BLOOD FLOW – RESULTING IN A
DECREASED OXYGEN SUPPLY TO MEET
AN INCREASED MYOCARDIAL DEMAND IN
RESPONSE TO PHYSICAL EXERTION OR
EMOTIONAL STRESS

96. TYPES OF ANGINA
STABLE
UNSTABLE
INTRACTABLE OR REFRACTORY
VARIANT
SILENT

97. FACTORS ASSOCIATED
WITH ANGINA
PHYSICAL EXERTION
EXPOSURE TO COLD
HEAVY MEALS
STRESS

98. MANIFESTATIONS
CHEST PAIN – POORLY LOCALIZED AND MAY RADIATE TO THE
NECK, JAW, SHOULDERS, LEFT ARM
FEELING OF INDIGESTION
CHOKING , TIGHTNESS, HEAVY SENSATIONTHAT HAS A
VISELIKE, INSISTENT QUALITY
FEELING OF WEAKNESS OR NUMBNESS
SHORTNESS OF BREATH
PALLOR
DIAPHORESIS
DIZZINESS
LIGHTHEADEDNESS
NAUSEA
VOMITING
ANXIETY

99. ASSESSMENT/
DIAGNOSTICS
HISTORY
12 LEAD ECG
ECHOCARDIOGRAM
NUCLEAR SCAN
CARDIAC CATHERIZATION
BLOOD LAB VALUES
 C-REACTIVE PROTEIN
 TOTAL CHOLESTEROL – LDL, VLDL, HDL
 TRIGLYCERIDES

100. MEDICAL MANAGEMENT
AIMED AT DECREASING THE OXYGEN DEMAND
OF THE MYOCARDIUM AND TO INCREASE THE
OXYGEN SUPPLY
REVASCULARIZATION PROCEDURES
 CABG
 PERCUTANEOUS TRANSLUMINAL MYOCARDIAL
REVASCULARIZATION
 PERCUTANEOUS CORONARY INTERVENTIONAL
PROCEDURES –
 PERCUTANEOUS TRANSLUMINAL CORONARY
ANGIOPLASTY (PTCA)
 INTRACORONARY STENTS
 ATHERECTOMY

101. MEDICATIONS
NITROGLYCERIN
BETA BLOCKERS
CALCIUM CHANNEL BLOCKERS
ANTIPLATELET / ANTICOAGULANTS

102. NURSING PROCESS
ASSESSMENT –
 FACTORS ABOUT PAIN THAT NEEDS TO BE
ASSESSED
 POSITION/ LOCATION
 PROVOCATION
 WUALITY
 QUANTITY
 RADIATION
 RELIEF
 SEVERITY
 SYMPTOMS
 TIMING

103. NURSING PROCESS
NURSING DIAGNOSES
 INEFFECTIVE MYOCARDIAL TISSUE
PERFUSION SECONDARY TO CORONARY
ARTERY DISEASE
 ANXIETY RELATED TO FEAR OF DEATH
 KNOWLEDGE DEFICIT ABOUT THE
UNDERLYING DISEASE
 NONCOMPLIANCE, INEFFECTIVE
MANAGEMENT OF THERAPEUTIC REGIMEN
RELATED TO FAILURE TO ACCEPT
NECESSARY LIFESTYLE CHANGES

104. NURSING PROCESS
PLANNING AND GOALS
 TREATMENT OF ANGINA
 REDUCTION OF ANXIETY
 AWARENESS OPF DISEASE PROCESS
 UNDERSTANDING OF PRESCRIBED CARE
 ADHERENCE TO SELF-CARE PROGRAM
 ABSENCE OF COMPLICATIONS

105. NURSING PROCESS
INTERVENTIONS
 TREAT ANGINA
 REDUCE ANXIETY
 PREVENT PAIN
 PROMOTE HOME AND COMMUNITY
BASED CARE

106. NURSING PROCESS
EVALUATION
 CLIENT OUTCOMES
 REPORT THAT PAIN IS RELIEVED
PROMPTLY
 REPORTS DECRESED ANXIETY
 UNDERSTANDS WAYS TO AVOID
COMPLICATIONS
 DEMONSTRATES FREEDOM FROM
COMPLICATIONS
 ADHERES TO SELF CARE PROGRAM

107. MYOCARDIAL
INFARCTION
AREAS OF MYOCARDIAL CELLS IN THE
HEART ARE PERMANENTLY DESTROYED
AS CELLS ARE DEPRIVED OF OXYGEN,
ISCHEMIA DEVELOPS, CELLULAR INJURY
OCCURS
OVER TIME, THE LACK OF OXYGEN
RESULTS IN INFARCTION, OR DEATH OF
THE CELLS

108. VARIOUS
DESCRIPTIONS
LOCATION
 LEFT VENTRICLE:
 ANTERIOR, INFERIOR, POSTERIOR, LATERAL WALL
 RIGHT VENTRICLE
POINT IN TIME
 ACUTE
 EVOLVING
 OLD

109. MANIFESTATIONS
CHEST PAIN
SHORTNESS OF BRETH
COOL, PALE, MOIST SKIN
ANXIOUS, RESTLESS INCREASED
HEART AND RESPIRATORY RATE

110. ASSESSMENT AND
DIAGNOSTIC FINDINGS
HISTORY
CHEST XRAY
ECG
ECHOCARDIOGRAM
TRANSESOPHAGEAL ECHOCARDIOGRAM
CARDIAC STRESS TESTING
 EXERCISE
 PHARMACOLOGIC
RADIONUCLIDE IMAGING
COMPUTED TOMOGRAPHY
MAGNETIC RESONANCE IMAGING
CARDIAC CATHERIZATION
LABORATORY TESTS
 CREATINE KINASE AND ISOENZYMES
 MYOGLOBIN
 TROPONIN
 CHOLESTEROL LEVELS
 LIPID PROFILE
 ELECTROLYTES
 BLOOD UREA NITROGEN
 COMPLETE BLOOD COUNT
 PROTHROMBIN TIME/ INTERNATIONAL NORMALIZED RATIO
 PARTIAL THROMBOPLASTIN TIME

111. MANAGEMENT
GOAL – MINIMIZE MYOCARDIAL
DAMAGE, PRESERVE MYOCARDIAL
FUNCTION, PREVENT
COMPLICATIONS
 REPERFUSION
 RESOLUTION OF PAIN AND ECG
CHANGES

112. PHARMACOLOGIC
THERAPY
THROMBOLYTICS
ANALGESICS
ANAGIOTENSIN-CONVERTING
ENZYME INHIBITORS
BETA BLOCKERS

113. INVASIVE CORONARY
ARTERY PROCEDURES
PERCUTANEOUS TRANSLUMINAL
CORONARY ANGIOPLASTY (PTCA)
CORONARY ARTERY STENT
ATHERECTOMY
BRACHYTHERAPY
TRANSMYOCARDIAL
REVASCULARIZATION

114. PERCUTANEOUS CORONARY
INTERVENTION
USED TO OPEN THE OCCLUDED
CORONARY ARTERY AND PROMOTE
REPERFUSION
TREATS THE UNDERLYING
ATHEROSCLEROTIC LESION

115. CARDIAC
REHABILITATION
TARGETS RISK REDUCTION
GOALS
 EXTEND AND IMPROVE QUALITY OF
LIFE
 LIMIT THE EFFECTS AND
PROGRESSION OF ATHEROSCLEROSIS
 RETURN TO PRE-ILLNESS LIFESTYLE
 PREVENT ANOTHER CARDIAC EVENT

116. NURSING PROCESS
ASSESSMENT
 HISTORY
 PHYSICAL ASSESSMENT

117. NURSING PROCESS
NURSING DIAGNOSES
 INEFFECTIVE CARDIOPULMONARY
TISSUE PERFUSION
 POTENTIAL IMPAIRED GAS EXCHANGE
 POTENTIAL ALTERED PERIPHERAL
TISSUE PERFUSION
 ANXIETY
 DEFICIENT KNOWLEDGE ABOUT SELF-
CARE

118. NURSING PROCESS
PLANNING
 RELIEF OF PAIN OR ISCHEMIC SIGNS AND SYMPTOMS
 PREVENTION OF FURTHER MYOCARDIAL DAMAGE
 ABSENCE OF RESPIRATORY DYSFUNCTION
 MAINTENANCE OF ADEQUATE TISSUE PERFUSION
 REDUCE ANXIETY
 ADHERENCE TO SELF-CARE PROGRAM
 ABSENCE OR EARLY RECOGNITION OF
COMPLICATIONS

119. NURSING PROCESS
INTERVENTIONS
RELIEVE PAIN/ ISCHEMIA
IMPROVE RESPIRATOY FUNCTION
PROMOTE TISSUE PERFUSION
REDUCE ANXIETY
MONITOR FOR COMPLICATIONS
TEACH SELF-CARE

120. NURSING PROCESS
EVALUATION
 OUTCOMES
 RELIEF OF ANGINA
 NO SIGNS OF REPIRATORY DIFFICULTIES
 ADEQUATE TISSUE PERFUSION
 DECREASED ANXIETY
 ADHERENCE TO SELF-CARE PROGRAM
 ABSENCE OF COMPLICATIONS

121. ETIOLOGY
REDUCED BLOOD FLOW IN A CORONARY
ARTERY DUE TO ATHEROSCLEROSIS
AND OCCLUSION OF AN ARTERY BY AN
EMBOLUS OR THROMBUS
VASOSPASM OF A CORONARY ARTERY
DECREASED OXYGEN SUPPLY
INCREASED DEMAND FOR OXYGEN