Download NUR202-ModuleB

Nursing 202
Module B
Cardiovascular System Alterations
CARDIAC
DYRHYTHMIAS
REVIEW OF
CONDUCTION
ELECTRICAL
CONDUCTION
SINOATRIAL NODE (SA)
INTRAATRIAL FIBER (BACHMAN’S
BUNDLE)
INTRANODAL TRACTS
ATRIOVENTRICULAR (AV) NODE
BUNDLE OF HIS (COMMON BUNDLE)
BUNDLE BRANCHES
PURKINJE FIBERS
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
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)
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
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
INHERENT RATES
SA
60-100
AV JUNCTION
40-60
VENTRICULAR
20-40
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
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
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
SYMPTOMS
SYMPTOMS RELATED TO
DECREASE IN CARDIAC OUTPUT
CHEST PRESSURE AND PAIN
 DYSPNEA
 HYPOTENSION
 DIZZINESS
 SEIZURES
 SYNCOPE

TREATMENT
MANAGEMENT -ONLY IF SYMPTOMATICAIMED AT INCREASING THE HEART RATE
MEDICATIONS



ATROPINE
ISOPROTERENOL
PACEMAKER
SUPRESSION OF THE PARASYMPATHETIC
NERVOUS SYSTEM
STIMULATION OF THE SYMPATHETIC NERVOUS
SYSTEM
SINUS TACHYCARDIA
HR OF 100-160/ MIN
NORMAL RESPONSE TO
SYMPATHETIC NERVOUS SYSTEM
STIMULATION
ANY CONDITION THAT PRODUCES AN
INCREASE IN METABOLIC RATE
ETIOLOGY
DIET – CAFFEINE
LIFE-STYLE – SMOKING / NICOTINE
MEDICAL CONDITIONS – ANEMIA,
HEMORRHAGE, FEVER,
HYPOTENSION, PAIN, SHOCK
MEDICATIONS – CENTRAL NERVOUS
SYSTEM STIMULANTS
MYOCARDIAL DAMAGE
SYMPTOMS
PRIMARY SYMPTOMS RELATED TO
DECREASED CARDIAC OUTPUT
CHEST PRESSURE AND PAIN
 DYSPNEA
 A CHARACTERISTIC “FLUTTERING” IN
THE CHEST
 DIZZINESS
 SYNCOPE

TREATMENT
ELIMINATE THE CAUSE OF THE
TACHYCARDIA
MEDICATIONS:





CALCIUM CHANNEL BLOCKERS
DIGOXIN
BETA BLOCKERS
ANTIANXIETY AGENTS
ADENOSINE
CAROTID MASSAGE
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
ETIOLOGY
CARDIAC DISEASE
ISCHEMIA
 CORONARY ARTERY DISEASE
 CONGESTIVE HEART FAILURE
 MYOCARDIAL INFARCTION

INCREASED VAGAL STIMULATION
MEDICATIONS
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
ETIOLOGY
CARDIAC DISEASE
CHRONIC OBSTRUCTIVE PULMONARY
DISEASE
MEDICATIONS: CENTRAL NERVOUS
SYSTEM STIMULANTS
DIET: CAFFEINE
ELECTROLYTE DISTURBANCES
ANXIETY
LIFE STYLE: EXERCISE, ALCOHOL,
NICOTINE
SYMPTOMS
FEELINGS OF PALPITATIONS OR
“SKIPPED BEAT”
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
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
ETIOLOGY
SAME AS SEEN WITH PREMATURE
ATRIAL CONTRACTIONS
NOT USUALLY ASSOCIATED WITH
ORGANIC HEART DISEASE
SYMPTOMS
CHEST PAIN
DYSPNEA
HYPOTENSION
PALPITATIONS
WEAK RAPID PULSE
DIZZINESS
SYNCOPE
TREATMENT
CAROTID SINUS PRESSURE
VAGAL NERVE STIMULATION
MEDICATIONS:







DILTIAZEM
VERAPAMIL
DIGOXIN
PROPRANOLOL
PROCAINAMIDE
QUINIDINE
VASOPRESSOR
ATRIAL FLUTTER
ATRIAL ECTOPIC PACER FIRES AT A RATE OF
250-400/ MIN
OCCURS IN A VARIETY OF HEART DISEASESRHEUMATIC, CORONARY, HYPERTENSIVE, ALSO
CARDIOMYOPATHY, HYPOXIA, HEART FAILURE,
MAY BE ASYMPTOMATIC OR HAVE
PALPITATIONS
MANAGEMENT- DIGITALIS, BETA BLOCKERS,
CALCIUM CHANNEL BLOCKERS, MAY USE
CARDIOVERSION
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
AV HEART BLOCKS
ABNORMAL DELAY IN CONDUCTION
OF IMPULSE FROM THE ATRIUM TO
THE VENTRICLES
USUALLY ASYMPTOMATIC
FIRST DEGREE
DELAY OCCURS AT THE AV NODE
PRODUCING A PROLONGED PR
INTERVAL > .20.
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
TREATMENT
USUALLY NOT NECESSARY UNLESS
THE BLOCK THAT IS CAUSED BY
MEDICATION THAT CAN BE
MODIFIED OR WITHHELD
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
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
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
JUNCTIONAL RHYTHMS
RATE 40- 60
THE DOMINANT PACER OF THE HEART
FAILS , RETROGRADE OR BACKWARD
STIMULATION OF THE ATRIAPRODUCING A CHARACTERISTIC P WAVE
- MAY BE A NEGATIVE DEFLECTION
BEFORE OR AFTER THE QRS COMPLEX
OR NO P WAVE AT ALL
ETIOLOGY
CORONARY ARTERY DISEASE
CONGESTIVE HEARAT FAILURE
MYOCARDIAL INFARCTION
CAFFEINE
ANXIETY
ALCOHOL, TOBACCO
SYMPTOMS
FEELINGS OF
PALPITATIONS
 FLUTTERING
 “SKIPPED BEATS”

MANAGEMENT
TX UNDERLYING CAUSE
MODIFY DIET / LIFESTYLE
REDUCE STRESS
MEDICATIONS :

QUINIDINE
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
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
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
TREATMENT
MEDICATIONS:
CALCIUM CHANNEL BLOCKER
 CENTRAL NERVOUS SYSTEM
 DEPRESSANTS
 DIGOXIN

VAGAL STIMULATION
CARDIOVERSION
JUNCTIONAL ESCAPE
BEATS
BEATS THAT OCCUR WHEN THE AV
JUNCTION TAKES OVER THE
PACEMAKER ACTIVITY
OCCUR LATE IN THE CYCLE
ETIOLOGY
RHEUMATIC HEART DISEASE
MYOCARDIAL INFARCTION
SINUS ARRHYTHMIAS:



BRADYCARDIA
BLOCK
ARREST
MEDICATIONS






BETA BLOCKERS
CALCIUM CHANNEL BLOCKERS
CENTRAL NERVOUS SYSTEM DEPRESSANTS
DIGOXIN
NARCOTICS
SEDATIVES
SYMPTOMS
MOST ARE ASYMPTOMATIC
FEELINGS OF
PALITATIONS
 FLUTTERING
 “SKIPPED BEATS”

TREATMENT
MOST TREATMENT MEASURES ARE
THOSE USED FOR SINUS
BRADYCARDIA
VENTRICULAR
DYSRHYTHMIAS
IMPULSE ORIGINATES IN THE
VENTRICLES
CAUSES- DRUG TOXICITY, HYPOXIA,
HYPOTHERMIA, ELECTROLYE
IMBALANCES
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
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
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
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
ETIOLOGY
SAME AS VENTRICULAR TACHYCARDIA
UNTREATED VENTRICULAR
TACHYCARDIA
ELECTRICAL SHOCK
BRUGADA SYNDROME
TREATMENT
IMMEDIATE DEFIBRILLATION
ACTIVATION OF EMS
CPR
ERADICATING THE CAUSE
VASOACTIVE AND ANTIARRHYTHMIC
MEDICATIONS
VENTRICULAR
ASYSTOLE
ABSENCE OF:
QRS
 HEARTBEAT
 PALPABLE PULSE
 RESPIRATION

ETIOLOGY
HYPOXIA
ACIDOSIS
ELECTROLYTE IMBALANCE
DRUG OVERDOSE
HYPOTHERMIA
TREATMENT
CARDIOPULMONARY RESUSCITATION
INTUBATION
INTRAVENOUS ACCESS
TRANSCUTANEOUS PACING
EPINEPHRINE
ATROPINE
ADJUNCTIVE
MODALITIES AND
MANAGEMENT
TREATMENT DEPENDS UPON
WHETHER THE DYSRHYTHMIA IS
ACUTE OR CHRONIC
 THE CAUSE OF THE DYSRHYTHMIA
AND ITS POTENTIAL HEMODYNAMIC
EFFECTS

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
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
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
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
PACEMAKER
MALFUNCTION
LOSS OF CAPTURE
UNDERSENSING
OVERSENSING
LOSS OF PACING
CLIENT TEACHING
MONITOR PACEMAKER FUNCTION
PROMOTE SAFETY/ PREVENT
INFECTION
ELECTROMAGNETIC
INTERFERENCE
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
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
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
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
POST PROCEDURE
CARE
MAINTAIN AIRWAY PATENCY
MONITOR VITAL SIGNS AND
OXYGEN SATURATION
ELECTROCARDIOGRAM
MONITORING
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
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)
CARDIAC CONDUCTION
SURGERY
ENDOCARDIAL ISOLATION
ENDOCARDIAL RESECTION
CATHETER ABLATION THERAPY
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
CLASS II
BETA BLOCKERS – DECREASE
CONDUCTION VELOCITY,
AUTOMATICITY AND RECOVERY
TIME ( REFRACTORY PERIOD) –
PROPRANOLOL, ACEBUTOLOL
CLASS III
PROLONG REPOLARIZATION- ARE
USED IN THE EMERGENCY
TREATMENT OF VENTRICULAR
DYSRHYTHMIAS WHEN OTHER
ANTIDYSRHYTHMICS ARE NOT
EFFECTIVE – BRETYLIUM,
AMIODARONE
CLASS IV
CALCIUM CHANNEL BLOCKERS –
BLOCKS CALCIUM INFLUX,
DECREASING THE EXCITABILITY
AND CONTRACTILITY OF THE
MYOCARDIUM – VERAPAMIL,
DILTIAZEM
OTHERS
DILANTIN- USED IN THE TX OF
DIGITALIS INDUCED DYSRHYTHMIAS
DIGOXIN- ATRIAL FLUTTER OR
FIBRILLATION, PREVENT
RECURRENCE OF PAT
ATROPINE- BRADYCARDIA
NURSING PROCESS DYSRHYTHMIA
ASSESSMENT –

HISTORY

CAUSES OF DYSRHYTHMIA
PHYSICAL EXAM
 EFFECT ON CARDIAC OUTPUT

NURSING PROCESS
DIAGNOSES:
DECREASED CARDIAC OUTPUT
 ANXIETY RELATED TO FEAR OF THE
UNKNOWN
 DEFICIENT KNOWLEDGE ABOUT THE
DYSRHYTHMIA AND TREATMENT

NURSING PROCESS
PLANNING AND GOALS
ERADICATING OR DECREASING THE
INCIDENCE OF THE DYSRHYTHMIA
 ACQUIRE KNOWLEDGE ABOUT THE
DYSRHYTHMIA AND TREATMENT

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
NURSING PROCESS
EVALUATION

EXPECTED OUCOMES
MAINTAINS CARDIAC OUTPUT
 EXPERIENCES REDUCED ANXIETY
 EXPRESSES UNDERSTANDING OF THE
DYSRHYTHMIA AND ITS TREATMENT

CORONARY ARTERY
DISEASE
TYPES:
ATHEROSCLEROSIS
 ARTERIOSCLEROSIS

ATHEROSCLEROSIS
AN ABNORMAL ACCULULATION OF
LIPID, OR FATTY, SUBSTANCES AND
FIBROUS TISSUE CREATING
BLOCKAGES OR NARROWING OF
THE VESSEL
ARTERIOSCLEROSIS
THICKENING OF THE WALLS OF THE
ARTERIOLES, WITH LOSS OF
ELASTICITY AND CONTRACTILITY
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
RISK FACTORS
MODIFIABLE :







TOBACCO
HYPERTENSION
ELEVATED BLOOD LIPID LEVELS
DIABETES
OBESITY
SEDETARY LIFE STYLE
CHRONIC STRESS
NONMODIFIABLE :




FAMILY HISTORY
INCREASING AGE
GENDER
RACE
CLINICAL
MANIFESTATIONS
MAY BE ASYMPTOMATIC
ANGINA
NAUSEA, VOMITING
DIAPHORESIS
COOL, CLAMMY SKIN
EKG CHANGES
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:
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Lipid lowering agents
Nitrates
Antiplatelets
Beta blockers
Calcium channel blockers
Diuretics
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
TYPES OF ANGINA
STABLE
UNSTABLE
INTRACTABLE OR REFRACTORY
VARIANT
SILENT
FACTORS ASSOCIATED
WITH ANGINA
PHYSICAL EXERTION
EXPOSURE TO COLD
HEAVY MEALS
STRESS
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
ASSESSMENT/
DIAGNOSTICS
HISTORY
12 LEAD ECG
ECHOCARDIOGRAM
NUCLEAR SCAN
CARDIAC CATHERIZATION
BLOOD LAB VALUES
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C-REACTIVE PROTEIN
TOTAL CHOLESTEROL – LDL, VLDL, HDL
TRIGLYCERIDES
MEDICAL MANAGEMENT
AIMED AT DECREASING THE OXYGEN DEMAND
OF THE MYOCARDIUM AND TO INCREASE THE
OXYGEN SUPPLY
REVASCULARIZATION PROCEDURES
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CABG
PERCUTANEOUS TRANSLUMINAL MYOCARDIAL
REVASCULARIZATION
PERCUTANEOUS CORONARY INTERVENTIONAL
PROCEDURES –
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PERCUTANEOUS TRANSLUMINAL CORONARY
ANGIOPLASTY (PTCA)
INTRACORONARY STENTS
ATHERECTOMY
MEDICATIONS
NITROGLYCERIN
BETA BLOCKERS
CALCIUM CHANNEL BLOCKERS
ANTIPLATELET / ANTICOAGULANTS
NURSING PROCESS
ASSESSMENT –
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FACTORS ABOUT PAIN THAT NEEDS TO BE
ASSESSED
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POSITION/ LOCATION
PROVOCATION
WUALITY
QUANTITY
RADIATION
RELIEF
SEVERITY
SYMPTOMS
TIMING
NURSING PROCESS
NURSING DIAGNOSES
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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
NURSING PROCESS
PLANNING AND GOALS
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TREATMENT OF ANGINA
REDUCTION OF ANXIETY
AWARENESS OPF DISEASE PROCESS
UNDERSTANDING OF PRESCRIBED CARE
ADHERENCE TO SELF-CARE PROGRAM
ABSENCE OF COMPLICATIONS
NURSING PROCESS
INTERVENTIONS
TREAT ANGINA
 REDUCE ANXIETY
 PREVENT PAIN
 PROMOTE HOME AND COMMUNITY
BASED CARE
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NURSING PROCESS
EVALUATION
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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
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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
VARIOUS
DESCRIPTIONS
LOCATION
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LEFT VENTRICLE:
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ANTERIOR, INFERIOR, POSTERIOR, LATERAL WALL
RIGHT VENTRICLE
POINT IN TIME
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ACUTE
EVOLVING
OLD
MANIFESTATIONS
CHEST PAIN
SHORTNESS OF BRETH
COOL, PALE, MOIST SKIN
ANXIOUS, RESTLESS INCREASED
HEART AND RESPIRATORY RATE
ASSESSMENT AND
DIAGNOSTIC FINDINGS
HISTORY
CHEST XRAY
ECG
ECHOCARDIOGRAM
TRANSESOPHAGEAL ECHOCARDIOGRAM
CARDIAC STRESS TESTING
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EXERCISE
PHARMACOLOGIC
RADIONUCLIDE IMAGING
COMPUTED TOMOGRAPHY
MAGNETIC RESONANCE IMAGING
CARDIAC CATHERIZATION
LABORATORY TESTS
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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
MANAGEMENT
GOAL – MINIMIZE MYOCARDIAL
DAMAGE, PRESERVE MYOCARDIAL
FUNCTION, PREVENT
COMPLICATIONS
REPERFUSION
 RESOLUTION OF PAIN AND ECG
CHANGES

PHARMACOLOGIC
THERAPY
THROMBOLYTICS
ANALGESICS
ANAGIOTENSIN-CONVERTING
ENZYME INHIBITORS
BETA BLOCKERS
INVASIVE CORONARY
ARTERY PROCEDURES
PERCUTANEOUS TRANSLUMINAL
CORONARY ANGIOPLASTY (PTCA)
CORONARY ARTERY STENT
ATHERECTOMY
BRACHYTHERAPY
TRANSMYOCARDIAL
REVASCULARIZATION
PERCUTANEOUS CORONARY
INTERVENTION
USED TO OPEN THE OCCLUDED
CORONARY ARTERY AND PROMOTE
REPERFUSION
TREATS THE UNDERLYING
ATHEROSCLEROTIC LESION
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
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NURSING PROCESS
ASSESSMENT
HISTORY
 PHYSICAL ASSESSMENT

NURSING PROCESS
NURSING DIAGNOSES
INEFFECTIVE CARDIOPULMONARY
TISSUE PERFUSION
 POTENTIAL IMPAIRED GAS EXCHANGE
 POTENTIAL ALTERED PERIPHERAL
TISSUE PERFUSION
 ANXIETY
 DEFICIENT KNOWLEDGE ABOUT SELFCARE
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NURSING PROCESS
PLANNING
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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
NURSING PROCESS
INTERVENTIONS
RELIEVE PAIN/ ISCHEMIA
IMPROVE RESPIRATOY FUNCTION
PROMOTE TISSUE PERFUSION
REDUCE ANXIETY
MONITOR FOR COMPLICATIONS
TEACH SELF-CARE
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

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