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 Coronary artery disease And nursing implications  Coronary artery disease And nursing implications

Coronary artery disease And nursing implications - PowerPoint Presentation

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Coronary artery disease And nursing implications - PPT Presentation

Most common form of heart disease Can develop to become Chronic stable angina Acute coronary syndrome Unstable angina Myocardial infarction Can occur in any artery Prefers coronary arteries ID: 775387

coronary pain angina acs coronary pain angina acs blood risk myocardial heart care health collaborative cad cholesterol factors therapy

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Presentation Transcript

Slide1

Coronary artery disease

And nursing implications

Slide2

Most common form of heart diseaseCan develop to become:Chronic stable angina Acute coronary syndromeUnstable anginaMyocardial infarctionCan occur in any arteryPrefers coronary arteries

Etiology & Pathophysiology

Slide3

Barrier between the vessel wall and the lumen of the vesselNonreactive to platelets and leukocytes Nonreactive to coagulation, fibrinolytic, and complement factorsEndothelial wall alters as a result of inflammation and injury

Normal Endothelium & Injury Response

Slide4

Fatty Streak

Earliest lesionsCharacterized by lipid-filled smooth muscle cellsCan begin as early as age 15Potentially reversible with lowering LDL cholesterol

Slide5

Fibrous Plaque

Beginning of progressive changes in the arterial wallCan appear by age 30 and increases with ageLipoproteins transport cholesterol and other lipids into the arterial intimaFatty streak is covered by collagen, forming a fibrous plaque Narrows the artery and a reduces blood flow to the distal tissues

Slide6

Complicated Lesion

Continued inflammation resulting in plaque instability, ulceration, and rupturePlatelets accumulate and thrombus formsIncrease narrowing or total occlusion of lumen

Slide7

Factors contributing to the growth and extent of collateral circulationInherited predisposition to develop new blood vesselsPresence of chronic ischemiaWhen occlusion occurs slowly there is an increased chance of adequate collateral circulation and adequate myocardial blood flowWith rapid onset CAD or coronary spasm, there is not enough time to establish collateral vesselsDiminished arterial flow results in more severe ischemia or infarction

Collateral Circulation

Slide8

Risk factors for CAD

Slide9

AgeRisk increases with ageGenderIncidence is highest in white middle-aged menAfter age 65, incidence in men and women similarWomen tend to manifest CAD 10 years later than menWhen symptoms develop, women experience symptoms of angina rather than MI – opposite is true in men

Nonmodifiable Risk Factors

Slide10

EthnicityWhite middle-aged men have highest incidence African American women have a higher incidence and death rate compared to white womenNative Americans have mortality rates 2x high as other AmericansFamily historyFamilial hypercholesterolemiaGenetic predispositionAutosomal dominant disorder

Nonmodifiable

Risk Factors

Slide11

Elevated serum lipidsCholesterol >200 mg/dlTriglycerides >150 mg/dlLipoproteinsHDLs - high density high levels desirablelow levels associated with risk for CAD LDLs - low densityElevated levels correlate most closely with increased incidence of CAD

Modifiable Risk Factors

Slide12

Elevated blood pressureHypertension: BP > 140/90 Increases risk of atherosclerosisTobacco useNicotine can cause catecholamine release HR, peripheral vasoconstriction, BPPlatelet adhesion leading to emboli formation

Modifiable Risk Factors

Slide13

Physical inactivityPeople who are active have higher HDLsExercise increases collateral circulation & lowers BPObesityBMI > 30 kg/m2Leads to increased LDLs and triglyceridesAssociated with hypertensionPeople who are apple-shaped (store fat in abdomen) have higher incidence of CAD

Modifiable Risk Factors

Slide14

Diabetes & Metabolic syndromeIncidence of CAD 2-4x higher ObesityHypertensionElevated triglycerides, abnormal serum lipids, elevated fasting blood glucoseInsulin resistance

Modifiable Risk Factors

Slide15

Psychological statesIncrease risk of CADInclude depression, hopelessness, anxiety, hostility, & angerStress correlated with CADElevated homocysteine levelDamage the inner lining of blood vesselsPromote plaque build-upAlter the clotting mechanism to make clots more likely to occur

Modifiable Risk Factors

Slide16

Prevention & Treatment

Slide17

Health Promotion

Hypertension

Have

regular blood pressure

checkups

Take

prescribed medications for blood pressure

control

Reduce

salt

intake

Stop

tobacco use; avoid exposure to environmental tobacco (secondhand)

smoke

Control

or reduce

weight

Perform

physical activity

regularly

Slide18

Health Promotion

Elevated serum lipids

Reduce

total fat

intake

Reduce

animal (saturated) fat

intake

Take

prescribed medications for lipid

reduction

Adjust

total caloric intake to achieve and maintain ideal body

weight

Engage

in regular physical

activity

Increase

amount of complex carbohydrates and vegetable proteins in

diet

Slide19

Health Promotion

Tobacco use

Enroll

in a smoking cessation

program

Change

daily routines associated with smoking to reduce desire to

smoke

Substitute

other activities for

smoking

Ask

caregivers to support efforts to stop

smoking

Avoid

exposure to environmental tobacco

smoke

Slide20

Health Promotion

Physical Inactivity

Develop

and maintain at least 30 minutes of moderate physical activity on most days of the

week

Increase

activities to a fitness

level

Slide21

Health Promotion

Psychological State

Increase

awareness of behaviors that are detrimental to

health

Alter

patterns that are conducive to

stress

Set

realistic goals for

self

Reassess

priorities in light of health

needs

Learn

effective stress management

strategies

Seek

professional help if feeling depressed, angry

, or anxious

Plan

time for adequate rest and

sleep

Slide22

Health Promotion

Obesity

Change

eating patterns and

habits

Reduce

caloric intake to achieve

BMI of <25

Increase

physical activity to increase caloric

expenditure

Avoid

fad and crash diets, which are not effective over

time

Avoid

large, heavy

meals

Slide23

Health Promotion

Diabetes

Follow

the recommended

diet

Control

or reduce

weight

Take

prescribed

anti-diabetic medications

Monitor

blood glucose levels

regularly

Slide24

Calorie restrictionsDecrease dietary fat/cholesterolLimit saturated fats and cholesterol and emphasize complex carbohydratesFats – only about 30% of caloriesReduce or omit red meats, eggs, whole milkOmega 3 fatty acids

Nutritional Therapy

Slide25

Thorough health historyAccurate medication listPrescriptionOver the counterPresence of cardiovascular symptomsEnvironmental patterns like diet and activityValues and beliefs about health and illness

Identify people at risk

Slide26

Drugs that restrict lipoprotein productionStatinsInhibit synthesis of cholesterol in the liverNeed to monitor liver enzymesCreatine kinase assessed if myopathy suspectedNiacinInterferes with the synthesis of LDL and triglyceridesIncreases HDLCan cause flushing, pruritus, GI complaints, orthostatic hypotensionFlushing may be prevented by aspirin or NSAIDs LopidLower triglyceridesSide effects may include rashes and mild GI disturbances

Cholesterol Lowering Drug Therapy

Slide27

Drugs that increase lipoprotein removalBile acid sequestrants (e.g., cholestyramine [Questran])Increase conversion of cholesterol to bile acidsDecrease hepatic cholesterolSide effects include complaints of palatability and upper and lower GI symptomsDrugs that decrease cholesterol absorptionZetia

Cholesterol Lowering Drug Therapy

Slide28

ASA , PlavixLow dose ASA (81mg)Studies show decrease in first MI’sCan cause GI bleedUse if benefit outweighs riskPlavix has decreased risk of bleed

Antiplatelet Drug

Therapy

Slide29

Clinical Manifestations of CAD

Slide30

Temporary myocardial ischemia = Angina (chest pain)Happens when oxygen supply is less than oxygen demandCardiacNon cardiacPrimary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis

Chronic Stable Angina

Slide31

Physical exertionTemperature extremesStrong emotionsConsumption of heavy mealTobacco use or environmental tobacco smokeSexual activityStimulantsCircadian rhythm patterns

Precipitating Factors of Angina

Slide32

Referred pain in left shoulder and arm is from transmission of the pain message to the cardiac nerve rootsPain usually lasts 3 to 5 minutesPain subsides when precipitating factor relievedPain at rest is unusualECG reveals ST-segment depression and/or T-wave inversion

Chronic Stable Angina

Slide33

Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptomsConstrictiveSqueezingHeavyChokingSuffocating sensation

Chronic Stable Angina

Slide34

Angina Pain Sites

Most of the pain experienced in angina appears substernally, it may also occur in the neck May radiate to:JawShouldersDown the armsPain between the shoulder blades often is dismissed as not being heart related

Slide35

Silent IschemiaIschemia that occurs in the absence of any subjective symptoms Associated with diabetic neuropathyConfirmed by ECG changesUp to 80% of patients with ischemia are asymptomaticIschemia with or without pain has same prognosis

Types of Stable Angina

Slide36

Nocturnal anginaOccurs only at night but not necessarily during sleep or in recumbent positionAngina decubitusChest pain that occurs only while lying downRelieved by standing or sitting

Types of Stable Angina

Slide37

Prinzmetal’s AnginaOccurs at rest usually in response to spasm of major coronary arterySeen in patients with a history of migraine headaches and Raynaud’s phenomenonSpasm may occur in the absence of CAD.When spasm occursChest painMarked, transient ST-segment elevationMay occur during REM sleepMay be relieved by moderate exercise or may disappear spontaneously

Types of Stable Angina

Slide38

Microvascular AnginaMay occur in the absence of significant coronary atherosclerosis or coronary spasmSeen especially in womenPain is related to myocardial ischemia associated with abnormalities of the coronary microcirculation.

Types of Stable Angina

Slide39

Acute Coronary Syndrome

Slide40

Progression of Cardiovascular disease

Slide41

When ischemia is prolonged and is not immediately reversible, acute coronary syndrome (ACS) develops.ACS encompassesUnstable angina (UA)Non–ST-segment-elevation myocardial infarction (NSTEMI)ST-segment-elevation MI (STEMI)

Acute Coronary Syndrome

Slide42

Result Partial occlusion of coronary artery: USA or NSTEMITotal occlusion of coronary artery: STEMI

Progression of CAD

Slide43

Chest pain that is:New in onsetOccurs at restHas a worsening patternChronic stable angina can develop to unstableSignificant change in the pattern of painIncreasing frequencyEasily provoked by minimal or no exertionUnpredictable and represents a medical emergency

Unstable Angina

Slide44

Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis)Necrosis of entire thickness of myocardium takes 4 to 6 hours. Eighty percent to 90% of all acute MIs are secondary to thrombus formation

Myocardial Infarction

Slide45

Infarctions are usually described according to the location of damageAnteriorInferiorlateralposterior wall infarction

Myocardial Infarction

Slide46

The degree of altered function depends on the area of the heart involved and the size of the infarct.Contractile function of the heart is disrupted in areas of myocardial necrosis.Most MIs involve the left ventricle (LV).

Myocardial Infarction

Slide47

Pain Total occlusion → Anaerobic metabolism and lactic acid accumulation → Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administrationDescribed as heaviness, constriction, tightness, burning, pressure, or crushing Common locations: Substernal, retrosternal, or epigastric areas; pain may radiate to neck, jaw, arms

Clinical Manifestations of ACS

Slide48

Stimulation of sympathetic nervous system results in Release of glycogenDiaphoresisVasoconstriction of peripheral blood vesselsSkin: Ashen, clammy, and/or cool to touch

Clinical Manifestations of ACS

Slide49

CardiovascularInitially, ↑ HR and BP, then ↓ BP (secondary to ↓ in cardiac output) Crackles Jugular venous distentionAbnormal heart soundsS3 or S4New murmur

Clinical Manifestations of ACS

Slide50

Nausea and vomitingCan result from reflex stimulation of the vomiting center by severe painFeverSystemic manifestation of the inflammatory process caused by cell death

Clinical Manifestations of ACS

Slide51

12-lead ECGCan rule out or confirm MIChanges in QRS complex, ST segment, & T waveNot always evident shortly after infarctSerum cardiac markersReleased into blood from necrotic heart muscle after MITroponinCK-MBMyoglobinSerial

Diagnostic Studies

Slide52

ECG Changes

Slide53

ECG Changes

Slide54

Coronary angiographyCardiac catheterizationPercutaneous coronary intervention (PCI)StentBalloon angioplastyStress testingExerciseDrugPersantineAdenocardEchocardiogram

Diagnostic Studies

Slide55

DysrhythmiasAbnormal heart rhythmsMost common complicationPresent in 80% of MI patientsMost common cause of death in the pre-hospital periodLife-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock

Complications

Slide56

Heart failureA complication that occurs when the pumping power of the heart has diminishedSymptomsmild dyspnearestlessnessagitationslight tachycardia. pulmonary congestion, crackles jugular vein distention

Complications

Slide57

Cardiogenic shockOccurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failureMortality rate is highSigns and symptomsLow BPConfusionpale, clammy skinDecreased urine outputRequires aggressive managementcontrol of dysrhythmiasIntra-aortic balloon pump (IABP) therapyvasoactive drugs

Complications

Slide58

Papillary muscle dysfunctionCauses mitral valve regurgitationCondition aggravates an already compromised LVNew systolic murmur at the cardiac apexConfirmed with echocardiogramRequires surgical treatment

Complications

Slide59

Ventricular aneurysmResults when the infarcted myocardial wall becomes thinned and bulges out during contractionSigns and symptomsChest painVentricular arrhythmiasHeart failureTreatmentAnticoagulationSurgery

Complications

Slide60

Acute pericarditisAn inflammation of visceral and/or parietal pericardiumOccurs 2-3 days after MIMay result in cardiac compression, ↓ LV filling and emptying, heart failureSigns and symptomsaggravated by inspiration, coughing, and movement of the upper bodyPericardial friction rub may be heard on auscultationChest pain different from MI pain Treatment includes pain relief with aspirin or corticosteroids

Complications

Slide61

Dressler syndromeMay also occur after cardiac surgeryCharacterized by pericarditis with effusion and fever that develop 4 to 6 weeks after MIArthralgiaThought to be caused by an antigen-antibody reaction to the necrotic myocardiumTreatmentShort-term corticosteroids

Complications

Slide62

Collaborative Care of ACS

Slide63

Maintain cardiac outputTreat painAssess for complicationsIncrease activity toleranceRelieve anxietyOngoing and discharge teaching

Nursing Goals: AMI

Slide64

Emergency managementInitial interventionsRapid assessment and diagnosisAdminister oxygen therapy12 lead ECGVS, pulse oximetry Assess lung and heart soundsEstablish IV Pain managementAdminister sublingual nitroglycerinAdminister aspirin (chewable)Morphine sulfate (if nitro not effective)

Collaborative Care of ACS

Slide65

Ongoing interventionsFrequent VS and pulse oximetryBedrest for 12 – 24 hoursclear liquid dietNSTEMIASA, heparin, LovenoxPercutaneous coronary intervention (PCI) – once stabilizedSTEMIThrombolytic therapy

Collaborative Care of ACS

Slide66

Myocardial Revascularization – Emergent PCITreatment of choice for confirmed STEMI90 minute door to table timeAmbulatory 24 hours after the procedureVariety of proceduresPercutaneous transluminal coronary angioplasty (PTCA)Intracoronary stentingDrug-eluting stents

Collaborative Care of ACS

Slide67

Advantages of PCIProvide alternative to surgical interventionPerformed under local anestheticPatient ambulatory 24 hours after procedureLength of hospital stay decreased1-3 days vs. 4–6 days after CABG Rapid return to work Return to work 5–7 days vs. 2–8 weeks after CABG

Collaborative Care of ACS

Slide68

Nursing care post PCIMonitoring for signs of recurrent anginaMonitor VSEvaluating groin site for signs of bleedingMonitor for infectionAssess CMS of extremity usedAssess for hematoma formationBed rest

Collaborative Care of ACS

Slide69

Thrombolytic therapyIndications and contraindications History of or current major bleeding problem (hemorrhagic stroke, GI bleed) prevents administration2nd choice for revascularizationAdministered at facilities that do not have PCI capabilitiesMay still need PCI after thrombolytics if not fully effectiveMarker of reperfusion: Return of ST segment to baselineMajor complication: BleedingFFP is used to reverse thrombolytics

Collaborative Care of ACS

Slide70

Time is muscle; 6-hour windowSeveral thrombolytic agents available, such as:Tissue plasminogen activator (t-PA)StreptokinaseReteplaseHeparin and Lovenox

Collaborative Care of ACS

Slide71

Coronary Artery Bypass GraftingConstruction of new conduitsRequiresSternotomyCardiopulmonary bypassCommon artery used:Internal mammary artery (IMA)Saphenous vein

Collaborative Care of ACS

Slide72

Indications for CABGUnstable anginaAMIFailure of percutaneous interventionsGoals of CABGIncrease blood flow to myocardiumRelieve symptomsProlong survivalImprove quality of life

Collaborative Care of ACS

Slide73

Antiplatelet aggregation therapyChewable ASA 160 to 325 mg Nitroglycerin SLGiven q 5 minutes 3 doses total IV nitroglycerinGoal: reduce anginal pain and improve coronary blood flowImmediate onset of actionTitrated for pain reliefCommon side effects:HYPOTENSIONHEADACHE

Drug Therapy

Slide74

Morphine sulfateGiven if chest pain not relieved with nitro SLAlso acts as vasodilator and decreases myocardial oxygen consumption, reduces contractility, and decreased BP and HRAlso reduces anxiety and fearβ-adrenergic blockersDecrease myocardial oxygen demand by reducing HR, BP, and contractilityIV administration in acute phasei.e. metoprolol (Lopressor)

Drug Therapy

Slide75

Angiotensin-converting enzyme (ACE) inhibitors Prevent ventricular remodeling and prevent or slow progression of HFi.e. captopril (Capoten), enalapril (Vasotec)Antidysrhythmia drugsDysrhythmias are only treated in life threatening

Drug Therapy

Slide76

Cholesterol-lowering drugsMust first obtain fasting lipid panel If LDL is elevated, cholesterol-lowering drugs are initiatedStool softenersPromote bowel movementPrevents straining and vagal stimulation from Valsalva maneuver

Drug Therapy

Slide77

Acute PainDecreased Cardiac OutputAnxietyActivity intoleranceRisk for ineffective tissue perfusion

Nursing Diagnoses