Nursing 202

Module B Cardiovascular System Alterations

CARDIAC DYRHYTHMIAS

REVIEW OF CONDUCTION

ELECTRICAL CONDUCTION
SINOATRIAL NODE (SA) INTRAATRIAL FIBER (BACHMANS 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
AV JUNCTION VENTRICULAR

60-100
40-60 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 ANTIHYPERTENSIVES BETA BLOCKERS CALCIUM CHANNEL BLOCKERS CNS DEPRESSANTS DIGOXIN

MEDICATIONS:

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 BETA BLOCKERS CALCIUM CHANNEL BLOCKERS CENTRAL NERVOUS SYSTEM DEPRESSANTS DIGOXIN NARCOTICS SEDATIVES

MEDICATIONS

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 FAMILY HISTORY INCREASING AGE GENDER RACE

NONMODIFIABLE :

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 Lipid lowering agents Nitrates Antiplatelets Beta blockers Calcium channel blockers Diuretics

MEDICATION:

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

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

CABG PERCUTANEOUS TRANSLUMINAL MYOCARDIAL REVASCULARIZATION PERCUTANEOUS CORONARY INTERVENTIONAL PROCEDURES

PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY (PTCA) INTRACORONARY STENTS ATHERECTOMY

MEDICATIONS
NITROGLYCERIN BETA BLOCKERS CALCIUM CHANNEL BLOCKERS ANTIPLATELET / ANTICOAGULANTS

NURSING PROCESS
ASSESSMENT

FACTORS ABOUT PAIN THAT NEEDS TO BE ASSESSED

POSITION/ LOCATION PROVOCATION WUALITY QUANTITY RADIATION RELIEF SEVERITY SYMPTOMS TIMING

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

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

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

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

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

LEFT VENTRICLE:

ANTERIOR, INFERIOR, POSTERIOR, LATERAL WALL

RIGHT VENTRICLE ACUTE EVOLVING OLD

POINT IN TIME

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

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

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

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

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

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