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Cardiovascular System Alterations PowerPoint Presentation

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This medical PowerPoint presentation talks about Cardiovascular System Alterations.

The cardiovascular system is responsible for circulating blood throughout the body, providing oxygen and nutrients to tissues and organs, and removing waste products. Alterations in the cardiovascular system can have a significant impact on overall health and can lead to a variety of diseases and conditions.

The presentation talks about some common cardiovascular system alterations like Hypertension, Coronary artery disease, Heart failure, Arrhythmias, Atherosclerosis, Valve disorders, and Peripheral artery disease.

Tags : Cardiovascular System Alterations, Hypertension, Coronary artery disease, Heart failure, Arrhythmias, Atherosclerosis, Valve disorders, Peripheral artery disease, cardiology, cardiology PowerPoint presentation

Published on : Mar 19, 2023 | Views : 783 | Downloads : 4

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Slide 1-

Nursing 202 Module B Cardiovascular System Alterations
Slide 2-

CARDIAC DYRHYTHMIAS
Slide 3-

REVIEW OF CONDUCTION
Slide 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
Slide 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
Slide 6-

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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)
Slide 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
Slide 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
Slide 10-

INHERENT RATES SA 60-100 AV JUNCTION 40-60 VENTRICULAR 20-40
Slide 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
Slide 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
Slide 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
Slide 14-

SYMPTOMS SYMPTOMS RELATED TO DECREASE IN CARDIAC OUTPUT CHEST PRESSURE AND PAIN DYSPNEA HYPOTENSION DIZZINESS SEIZURES SYNCOPE
Slide 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
Slide 16-

SINUS TACHYCARDIA HR OF 100-160/ MIN NORMAL RESPONSE TO SYMPATHETIC NERVOUS SYSTEM STIMULATION ANY CONDITION THAT PRODUCES AN INCREASE IN METABOLIC RATE
Slide 17-

ETIOLOGY DIET – CAFFEINE LIFE-STYLE – SMOKING / NICOTINE MEDICAL CONDITIONS – ANEMIA, HEMORRHAGE, FEVER, HYPOTENSION, PAIN, SHOCK MEDICATIONS – CENTRAL NERVOUS SYSTEM STIMULANTS MYOCARDIAL DAMAGE
Slide 18-

SYMPTOMS PRIMARY SYMPTOMS RELATED TO DECREASED CARDIAC OUTPUT CHEST PRESSURE AND PAIN DYSPNEA A CHARACTERISTIC “FLUTTERING” IN THE CHEST DIZZINESS SYNCOPE
Slide 19-

TREATMENT ELIMINATE THE CAUSE OF THE TACHYCARDIA MEDICATIONS: CALCIUM CHANNEL BLOCKERS DIGOXIN BETA BLOCKERS ANTIANXIETY AGENTS ADENOSINE CAROTID MASSAGE
Slide 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
Slide 21-

ETIOLOGY CARDIAC DISEASE ISCHEMIA CORONARY ARTERY DISEASE CONGESTIVE HEART FAILURE MYOCARDIAL INFARCTION INCREASED VAGAL STIMULATION MEDICATIONS
Slide 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
Slide 23-

ETIOLOGY CARDIAC DISEASE CHRONIC OBSTRUCTIVE PULMONARY DISEASE MEDICATIONS: CENTRAL NERVOUS SYSTEM STIMULANTS DIET: CAFFEINE ELECTROLYTE DISTURBANCES ANXIETY LIFE STYLE: EXERCISE, ALCOHOL, NICOTINE
Slide 24-

SYMPTOMS FEELINGS OF PALPITATIONS OR “SKIPPED BEAT”
Slide 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
Slide 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
Slide 27-

ETIOLOGY SAME AS SEEN WITH PREMATURE ATRIAL CONTRACTIONS NOT USUALLY ASSOCIATED WITH ORGANIC HEART DISEASE
Slide 28-

SYMPTOMS CHEST PAIN DYSPNEA HYPOTENSION PALPITATIONS WEAK RAPID PULSE DIZZINESS SYNCOPE
Slide 29-

TREATMENT CAROTID SINUS PRESSURE VAGAL NERVE STIMULATION MEDICATIONS: DILTIAZEM VERAPAMIL DIGOXIN PROPRANOLOL PROCAINAMIDE QUINIDINE VASOPRESSOR
Slide 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
Slide 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
Slide 32-

AV HEART BLOCKS ABNORMAL DELAY IN CONDUCTION OF IMPULSE FROM THE ATRIUM TO THE VENTRICLES USUALLY ASYMPTOMATIC
Slide 33-

FIRST DEGREE DELAY OCCURS AT THE AV NODE PRODUCING A PROLONGED PR INTERVAL > .20.
Slide 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
Slide 35-

TREATMENT USUALLY NOT NECESSARY UNLESS THE BLOCK THAT IS CAUSED BY MEDICATION THAT CAN BE MODIFIED OR WITHHELD
Slide 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
Slide 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
Slide 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
Slide 39-

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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
Slide 41-

ETIOLOGY CORONARY ARTERY DISEASE CONGESTIVE HEARAT FAILURE MYOCARDIAL INFARCTION CAFFEINE ANXIETY ALCOHOL, TOBACCO
Slide 42-

SYMPTOMS FEELINGS OF PALPITATIONS FLUTTERING “SKIPPED BEATS”
Slide 43-

MANAGEMENT TX UNDERLYING CAUSE MODIFY DIET / LIFESTYLE REDUCE STRESS MEDICATIONS : QUINIDINE
Slide 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
Slide 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
Slide 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
Slide 47-

TREATMENT MEDICATIONS: CALCIUM CHANNEL BLOCKER CENTRAL NERVOUS SYSTEM DEPRESSANTS DIGOXIN VAGAL STIMULATION CARDIOVERSION
Slide 48-

JUNCTIONAL ESCAPE BEATS BEATS THAT OCCUR WHEN THE AV JUNCTION TAKES OVER THE PACEMAKER ACTIVITY OCCUR LATE IN THE CYCLE
Slide 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
Slide 50-

SYMPTOMS MOST ARE ASYMPTOMATIC FEELINGS OF PALITATIONS FLUTTERING “SKIPPED BEATS”
Slide 51-

TREATMENT MOST TREATMENT MEASURES ARE THOSE USED FOR SINUS BRADYCARDIA
Slide 52-

VENTRICULAR DYSRHYTHMIAS IMPULSE ORIGINATES IN THE VENTRICLES CAUSES- DRUG TOXICITY, HYPOXIA, HYPOTHERMIA, ELECTROLYE IMBALANCES
Slide 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
Slide 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
Slide 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
Slide 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
Slide 57-

ETIOLOGY SAME AS VENTRICULAR TACHYCARDIA UNTREATED VENTRICULAR TACHYCARDIA ELECTRICAL SHOCK BRUGADA SYNDROME
Slide 58-

TREATMENT IMMEDIATE DEFIBRILLATION ACTIVATION OF EMS CPR ERADICATING THE CAUSE VASOACTIVE AND ANTIARRHYTHMIC MEDICATIONS
Slide 59-

VENTRICULAR ASYSTOLE ABSENCE OF: QRS HEARTBEAT PALPABLE PULSE RESPIRATION
Slide 60-

ETIOLOGY HYPOXIA ACIDOSIS ELECTROLYTE IMBALANCE DRUG OVERDOSE HYPOTHERMIA
Slide 61-

TREATMENT CARDIOPULMONARY RESUSCITATION INTUBATION INTRAVENOUS ACCESS TRANSCUTANEOUS PACING EPINEPHRINE ATROPINE
Slide 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
Slide 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
Slide 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
Slide 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
Slide 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
Slide 67-

PACEMAKER MALFUNCTION LOSS OF CAPTURE UNDERSENSING OVERSENSING LOSS OF PACING
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Slide 69-

CLIENT TEACHING MONITOR PACEMAKER FUNCTION PROMOTE SAFETY/ PREVENT INFECTION ELECTROMAGNETIC INTERFERENCE
Slide 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
Slide 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
Slide 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
Slide 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
Slide 74-

POST PROCEDURE CARE MAINTAIN AIRWAY PATENCY MONITOR VITAL SIGNS AND OXYGEN SATURATION ELECTROCARDIOGRAM MONITORING
Slide 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
Slide 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)
Slide 77-

CARDIAC CONDUCTION SURGERY ENDOCARDIAL ISOLATION ENDOCARDIAL RESECTION CATHETER ABLATION THERAPY
Slide 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
Slide 79-

CLASS II BETA BLOCKERS – DECREASE CONDUCTION VELOCITY, AUTOMATICITY AND RECOVERY TIME ( REFRACTORY PERIOD) – PROPRANOLOL, ACEBUTOLOL
Slide 80-

CLASS III PROLONG REPOLARIZATION- ARE USED IN THE EMERGENCY TREATMENT OF VENTRICULAR DYSRHYTHMIAS WHEN OTHER ANTIDYSRHYTHMICS ARE NOT EFFECTIVE – BRETYLIUM, AMIODARONE
Slide 81-

CLASS IV CALCIUM CHANNEL BLOCKERS – BLOCKS CALCIUM INFLUX, DECREASING THE EXCITABILITY AND CONTRACTILITY OF THE MYOCARDIUM – VERAPAMIL, DILTIAZEM
Slide 82-

OTHERS DILANTIN- USED IN THE TX OF DIGITALIS INDUCED DYSRHYTHMIAS DIGOXIN- ATRIAL FLUTTER OR FIBRILLATION, PREVENT RECURRENCE OF PAT ATROPINE- BRADYCARDIA
Slide 83-

NURSING PROCESS - DYSRHYTHMIA ASSESSMENT – HISTORY CAUSES OF DYSRHYTHMIA PHYSICAL EXAM EFFECT ON CARDIAC OUTPUT
Slide 84-

NURSING PROCESS DIAGNOSES: DECREASED CARDIAC OUTPUT ANXIETY RELATED TO FEAR OF THE UNKNOWN DEFICIENT KNOWLEDGE ABOUT THE DYSRHYTHMIA AND TREATMENT
Slide 85-

NURSING PROCESS PLANNING AND GOALS ERADICATING OR DECREASING THE INCIDENCE OF THE DYSRHYTHMIA ACQUIRE KNOWLEDGE ABOUT THE DYSRHYTHMIA AND TREATMENT
Slide 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
Slide 87-

NURSING PROCESS EVALUATION EXPECTED OUCOMES MAINTAINS CARDIAC OUTPUT EXPERIENCES REDUCED ANXIETY EXPRESSES UNDERSTANDING OF THE DYSRHYTHMIA AND ITS TREATMENT
Slide 88-

CORONARY ARTERY DISEASE TYPES: ATHEROSCLEROSIS ARTERIOSCLEROSIS
Slide 89-

ATHEROSCLEROSIS AN ABNORMAL ACCULULATION OF LIPID, OR FATTY, SUBSTANCES AND FIBROUS TISSUE CREATING BLOCKAGES OR NARROWING OF THE VESSEL
Slide 90-

ARTERIOSCLEROSIS THICKENING OF THE WALLS OF THE ARTERIOLES, WITH LOSS OF ELASTICITY AND CONTRACTILITY
Slide 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
Slide 92-

RISK FACTORS MODIFIABLE : TOBACCO HYPERTENSION ELEVATED BLOOD LIPID LEVELS DIABETES OBESITY SEDETARY LIFE STYLE CHRONIC STRESS NONMODIFIABLE : FAMILY HISTORY INCREASING AGE GENDER RACE
Slide 93-

CLINICAL MANIFESTATIONS MAY BE ASYMPTOMATIC ANGINA NAUSEA, VOMITING DIAPHORESIS COOL, CLAMMY SKIN EKG CHANGES
Slide 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
Slide 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
Slide 96-

TYPES OF ANGINA STABLE UNSTABLE INTRACTABLE OR REFRACTORY VARIANT SILENT
Slide 97-

FACTORS ASSOCIATED WITH ANGINA PHYSICAL EXERTION EXPOSURE TO COLD HEAVY MEALS STRESS
Slide 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
Slide 99-

ASSESSMENT/ DIAGNOSTICS HISTORY 12 LEAD ECG ECHOCARDIOGRAM NUCLEAR SCAN CARDIAC CATHERIZATION BLOOD LAB VALUES C-REACTIVE PROTEIN TOTAL CHOLESTEROL – LDL, VLDL, HDL TRIGLYCERIDES
Slide 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
Slide 101-

MEDICATIONS NITROGLYCERIN BETA BLOCKERS CALCIUM CHANNEL BLOCKERS ANTIPLATELET / ANTICOAGULANTS
Slide 102-

NURSING PROCESS ASSESSMENT – FACTORS ABOUT PAIN THAT NEEDS TO BE ASSESSED POSITION/ LOCATION PROVOCATION WUALITY QUANTITY RADIATION RELIEF SEVERITY SYMPTOMS TIMING
Slide 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
Slide 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
Slide 105-

NURSING PROCESS INTERVENTIONS TREAT ANGINA REDUCE ANXIETY PREVENT PAIN PROMOTE HOME AND COMMUNITY BASED CARE
Slide 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
Slide 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
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VARIOUS DESCRIPTIONS LOCATION LEFT VENTRICLE: ANTERIOR, INFERIOR, POSTERIOR, LATERAL WALL RIGHT VENTRICLE POINT IN TIME ACUTE EVOLVING OLD
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MANIFESTATIONS CHEST PAIN SHORTNESS OF BRETH COOL, PALE, MOIST SKIN ANXIOUS, RESTLESS INCREASED HEART AND RESPIRATORY RATE
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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
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MANAGEMENT GOAL – MINIMIZE MYOCARDIAL DAMAGE, PRESERVE MYOCARDIAL FUNCTION, PREVENT COMPLICATIONS REPERFUSION RESOLUTION OF PAIN AND ECG CHANGES
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PHARMACOLOGIC THERAPY THROMBOLYTICS ANALGESICS ANAGIOTENSIN-CONVERTING ENZYME INHIBITORS BETA BLOCKERS
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INVASIVE CORONARY ARTERY PROCEDURES PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY (PTCA) CORONARY ARTERY STENT ATHERECTOMY BRACHYTHERAPY TRANSMYOCARDIAL REVASCULARIZATION
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PERCUTANEOUS CORONARY INTERVENTION USED TO OPEN THE OCCLUDED CORONARY ARTERY AND PROMOTE REPERFUSION TREATS THE UNDERLYING ATHEROSCLEROTIC LESION
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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
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NURSING PROCESS NURSING DIAGNOSES INEFFECTIVE CARDIOPULMONARY TISSUE PERFUSION POTENTIAL IMPAIRED GAS EXCHANGE POTENTIAL ALTERED PERIPHERAL TISSUE PERFUSION ANXIETY DEFICIENT KNOWLEDGE ABOUT SELF-CARE
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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
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NURSING PROCESS INTERVENTIONS RELIEVE PAIN/ ISCHEMIA IMPROVE RESPIRATOY FUNCTION PROMOTE TISSUE PERFUSION REDUCE ANXIETY MONITOR FOR COMPLICATIONS TEACH SELF-CARE
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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
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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