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NUR202-ModuleB
NUR202-ModuleB
NUR202-ModuleB
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 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
MYOCARDIAL INFARCTION
USUALLY ASYMPTOMATIC
FIRST DEGREE
“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
PREVENT PAIN
DECREASED ANXIETY
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