Nursing 202

Module B
Chapters 37 & 41
CARDIAC
DYRHYTHMIAS

Chapter 37
Properties of Cardiac Cells

 Automaticity
 Excitability
 Conductivity
 contractility
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
 THE SA NODE IS LOCATED IN THE RU ATRIUM, KNOWN AS THE
NATURAL PACER OF THE HEART, NORMALLY SELF-INITIATES
ELECTRICAL ACTIVITY IN THE HEART AT THE RATE OF 60-100/ MINUTE
 THE INTRAATRIAL FIBER IS THE SUBDIVISION OF ANTERIOR
INTERNODAL TRACT, CONDUCTS THE ELECTRICAL ACTIVITY FROM THE
SA TO AV NODE
 THE INTRANODAL TRACTS HAS ANTERIOR MIDDLE AND POSTERIOR
DIVISIONS AND CONDUCT ELECTRICAL ACTIVITY FROM SA TO AV NODE
 AV NODE IS LOCATED ON THE FLOOR OF THE RIGHT ATRIUM ABOVE
THE TRICUSPID VALVE , THE ELECTRICAL ACTIVITY IS DELAYED ABOUT
O.O5 SEC HERE WHICH ALLOWS FOR ATRIAL CONTRACTION AND MORE
COMPLETE FILLING OF VENTRICLES WITH BLOOD, AV JUNCTIONAL
TISSUE CAN SELF INITIATE ELECTRICAL ACTIVITY AT A RATE OF 40-60
/MIN
 BUNDLE OF HIS CONDUCTS ELECTRICAL ACTIVITY FROM AV NODE TO
BUNDLE BRANCHES, PURKINJE FIBERS ARE A FINE NETWORKTHAT
CONDUCT THE ELECTRICAL IMPULSES TO THE VENTRICULAR MUSCLE
Conduction System
 SA Node
 Intra-Atrial pathway
 AV Node
 Bundle of HIS
 Bundle Branches
 Purkinje Fibers
Waveforms
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
Interpretation
P Wave
 Represents atrial depolarization
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
 MEASURED FROM THE BEGINNING OF THE
QRS COMPLEX TO THE END OF THE S WAVE.
 SHOULD MEASURE BETWEEN 0.04-0.10
SECONDS IN DURATION
ST INTERVAL

 An isoelectric line that occurs from the J

point to the beginning of the T wave.
QT 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
EKG Paper
Chest Lead Placement (Telemetry)
12 Lead EKG
Normal Sinus Rhythm
Artifact
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
 PATHOLOGICAL CAUSES INCLUDE INFERIOR
WALL MI, INCREASED ICP, ADDISON’S DISEASE,
MYXEDEMA, HYPOTHERMIA, ANOREXIA
NERVOSA
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 SYMPTOMATIC-
 AIMED 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

 PACS OCCUR EARLIER THAN THE NEXT EXPECTED BEAT,

AND THE P WAVE IS DIFFERENT
 PAT RAPID HR WITH A RATE OF 150-250 MAY BE CALLED
SVT
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
NSR with PAC
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 rapid rate prevents adequate ventricular
filling
PAT
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 DISEASES
 RHEUMATIC

 CORONARY

 HYPERTENSIVE.

 CARDIOMYOPATHY

 HYPOXIA
 HEART FAILURE
 SHOCK

 MAY BE ASYMPTOMATIC OR HAVE PALPITATIONS

 MANAGEMENT- DIGITALIS, BETA BLOCKERS, CALCIUM
CHANNEL BLOCKERS. MAY USE CARDIOVERSION
Atrial Flutter
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

 ANTICOAGULANTS
Atrial Fibrillation
 Common after heart surgery
 Assess for pulse deficit, fatigue, palpitations, weakness,
dyspnea, JVD,dizziness, anxiety, and hypotension.
 Potential for pulmonary emboli
Atrial Fibrillation
 Symptoms of embolic events includes
change in
 mental status
 speech
 Sensory function
 Motor function
Atrial Fibrillation
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
1st Degree AV Heart Block
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
 Treatment

MAYBE NONE
 ATROPINE
 TEMPORARY 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 THAN FIRST DEGREE
 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 ATRIA- PRODUCING 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 HEART FAILURE
 MYOCARDIAL INFARCTION
 CAFFEINE
 ANXIETY
 ALCOHOL, TOBACCO
SYMPTOMS
 FEELINGS OF
 PALPITATIONS
 FLUTTERING
 “SKIPPED BEATS”
MANAGEMENT
 TREAT 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 IF 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
 PALPITATIONS
 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
PVC
Bigeminal PVCs
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

 MAY HAVE DIZZINESS, PALPITATIONS, CHEST PAIN,

SOB, S&S OF DECREASED CARDIAC OUTPUT, LOC
Ventricular Tachycardia
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
Ventricular Fibrillation
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
Ventricular Asystole
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 CONDUCTION
DISTURBANCE THAT CAUSES
SYMPTOMS
 MAY BE USED TO TREAT
TACHYDYSRHYTHMIAS THAT DO NOT
RESPOND TO MEDICATION THERAPY
Pacemaker
Pacemaker Rhythm
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 NO ONE 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
 MIODARONE
 LIDOCAINE
 MAGNESIUM
 PROCAINAMIDE
 GIVEN IF VENTRICULAR DYSRHYTHMIA PERSISTS
Dying Heart/Agonal Rhythm
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
 IC IS THE MOST POWERFUL, BUT ALSO HAS THE HIGHEST
SIDE EFFECTS SUCH AS DEPRESSION OF CARDIAC
CONTRACTILITY
CLASS II
 BETA BLOCKERS – DECREASE
CONDUCTION VELOCITY, AUTOMATICITY
AND RECOVERY TIME ( REFRACTORY
PERIOD)
 PROPRANOLOL
 ACEBUTOLOL
 LEAST TOXIC, MOST POWERFUL
CLASS III
 PROLONG REPOLARIZATION
 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

 ATRIAL FIBRILLATION

 PREVENT RECURRENCE OF PAT

 ATROPINE
 BRADYCARDIA
NUR 202

Module B
Chapter 41
Coronary Artery Disease
CORONARY ARTERY DISEASE

 TYPES:
 ATHEROSCLEROSIS
 ARTERIOSCLEROSIS
ATHEROSCLEROSIS
 AN ABNORMAL ACCUMULATION OF
LIPID, OR FATTY SUBSTANCES AND
FIBROUS TISSUE.
 CREATES 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
 FORMS PLAQUES OR ATHEROMAS WHICH
NARROW THE VESSEL OBSTRUCTING BLOOD
FLOW
Atherosclerosis
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:
 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
 Angina Pectoris
 UNSTABLE
 Variant (Prinzmetal’s Angina)
 INTRACTABLE OR REFRACTORY
 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 SENSATION THAT 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
 C-REACTIVE PROTEIN
 TOTAL CHOLESTEROL – LDL, HDL
 TRIGLYCERIDES
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
MEDICATIONS
 Cardiac glycosides
 Antianginals
 Antidysrhythmics
 Diuretics
 Anticoagulants
 Antiplatelet agents
 Thrombolytic agents
 Analgesics
NURSING PROCESS
 ASSESSMENT –
 FACTORS ABOUT PAIN THAT NEEDS TO BE
ASSESSED
 POSITION/ LOCATION
 PROVOCATION
 QUALITY
 QUANTITY
 RADIATION
 RELIEF
 SEVERITY
 SYMPTOMS
 TIMING
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
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
VARIOUS DESCRIPTIONS
 LOCATION
 LEFT VENTRICLE:
 ANTERIOR, INFERIOR, POSTERIOR, LATERAL WALL
 RIGHT VENTRICLE
 POINT IN TIME
 ACUTE
 EVOLVING
 OLD
MANIFESTATIONS
 CHEST PAIN
 SHORTNESS OF BREATH
 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
 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
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
Before TPA
After TPA
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
 Potential post procedure problems
 acute closure of the vessel

 bleeding from the insertion site

 reaction to the dye used in angiography

 Hypotension

 Hypokalemia

 dysrhythmias
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

NURSING PROCESS
 INTERVENTIONS
 RELIEVE PAIN/ ISCHEMIA
 IMPROVE RESPIRATOY FUNCTION
 PROMOTE TISSUE PERFUSION
 REDUCE ANXIETY
 MONITOR FOR COMPLICATIONS
 TEACH SELF-CARE
CHF Post MI
 Killip Classification
 Class I: Absent crackles and S3
 Class II: Crackles in the lower half of the lung
fields and possible S3
 Class IV: Cardiogenic shock
Class I
 Treatment
 Preload Reduction
 IV Nitrates
 IV Diuretics
 Hourly V/S and I&O
 Monitor serum K+
Class II & III
 More severe than Class I
 Treatment
 Preload and Afterload reduction
 Nitroprusside or nitroglycerin IV drip
 Low dose beta blockers that are titrated for effect.
 Positive inotropes to increase cardiac contractility.
Class IV (Cardiogenic Shock)

 More than 40% of the left ventricle is necrotic.

 Early detection is essential because
established cardiogenic shock has a mortality
rate of 65% to 100%
Cardiogenic Shock
 Manifestations
 Tachycardia
 Hypotension
 BP less than 90 mmhg or 30 mmHg less than the client’s
baseline
 Urine output less than 30 mL/hr
 Cold, clammy skin with poor peripheral pulses
 Agitation, restlessness, or confusion
 Pulmonary congestion
 Tachypnea
 Continuing chest discomfort
Criteria for Bypass Surgery
 Angina with greater than 50% occlusion of the left
main coronary artery
 Unstable angina with severe two vessel or moderate
three vessel disease
 Ischemic heart muscle
 Acute MI
 Complications of PTCA
 Valvular disease
 Cardiogenic
 Coronary vessels unsuitable for PTCA
CABG
Post-OP CABG Management

 Fluid and electrolyte imbalance

 Hypotension
 Hypothermia
 Hypertension
 Bleeding
 Cardiac tamponade
 Pain