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Coronary Artery Disease &Acute Coronary Syndrome Kelly Marchant
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Learning Objectives At The Completion of this presentation, the nursing student will be able to successfully Describe Coronary Circulation Apply the pathophysiology of atherosclerosis to development of CAD and ACS Differentiate between Myocardial Injury, Ischemia, and Infarction Evaluate physical symptoms, and patients at risk for development of ACS Prioritize Nursing Assessments and Interventions for patients in ACS
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Cardiac Circulation
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Review Cardiac Circulation Cardiac circulation provides blood for cardiac tissue Occurs during systole Left Coronary Artery (LAD, LCx) Left Anterior Descending supplies anterior 2/3 of Intraventricular Septum, most of R & L Bundle Branches, the anterior and lateral wall of Left Ventricle Left Circumflex artery supplies Left Atrial Wall, lateral and posterior wall of Left Ventricle Right Coronary Artery Supplies Right Atrial & Ventricular Walls, the AV Node, Bundle of His, and interior wall of Left Ventricle
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Coronary Artery Disease Type of blood vessel disease Major cause is atherosclerosis “hardening of the arteries” Progressive Disease that develops over many years Leading cause of death in US (AHA, 2014) 17,000,000 patients 800,000 new heat attacks annually 320,000 recurrent attacks annually
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Atherosclerosis Most common cause of CAD Deposits of fat in the intima of the artery that harden with age Deposit of fat causes endothelial injury and inflammation 3 Stages Fatty Streak Fibrous Plaque (leads to instability, rupture, & plaque) Complicated Lesion (platelets accumulate, thrombus formation, reduces circulation) Collateral Circulation
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Types of Plaques STABLE Plaque is fixed Obstructs blood flow= stable angina Collateral circulation UNSTABLE Plaque can rupture and cause platelet adhesion and thrombus formation (complicated lesion) Unstable angina Myocardial infarction
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Pathophysiology of Plaque FIG 34-1
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3 Determinants of Plaque Vulnerability to Rupture “Size of the lipid rich core and the stability of its fibrous cap” “The presence of inflammation within the plaque” “The lack of smooth muscle cells with impaired healing and plaque stabilization”
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Coronary Thrombogenesis Secondary to Plaque Deterioration
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Modifiable Risk Factors Serum Lipids Hypertension Diabetes Tobacco Use Physical Inactivity Obesity Diabetes Psychological state
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Elevated Serum Lipid Risk of CAD associated with Total Cholesterol >200 Triglycerides > 150 LDL > 160 HDL <40 (men), <50 women
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Hypertension Increases risk of MI 10 fold in all populations Defined as Blood Pressure > 140/90 >130/80 if patient has DM or CKD Stress of HTN increases rate of atherosclerosis development (shearing stress) Salt intake (increased intravascular volume, increase SVR) Treat with Beta Blockers, ACE Inhibitors, CCB
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Tobacco Use Risk of developing CAD is 2-6 times higher in those who smoke or use smokeless tobacco than non-users CAD mortality drops to that of a nonsmoker within 12 months of quitting
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Physical Inactivity & Obesity Physical Inactivity Exercise increase thrombolytic activity May encourage collateral circulation formation Obesity Defined as BMI > 30kg/m2 Pear-shaped Increased insulin resistance
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Diabetes Incidence of CAD 2-4 times more likely for patient with diabetes (even when well controlled) Increased tendency for diabetics toward endothelial dysfunction Diabetics have altered lipid metabolism, higher cholesterol and triglycerides
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Psychological State Framingham Heart Study “Type A” Stressful State; Depression, Acute & Chronic Stress, Anxiety, Anger & Hostility, Lack of Support Stressful State stimulates SNS, increased catacholamine levels lead to increased HR & myocardial O2 demand
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Non Modifiable Risk Factors Increased Age Gender (more common in men until age 65) Ethnicity (more common in whites than AA) Genetic predisposition and family Hx
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Identification & Management of HR Patients Proper Identification of HR patients can prevent, modify, or slow progression of disease Risk Screening Includes Health Hx (DM, HTN, CHO) Family Hx Cardiovascular Symptoms Environmental Factors, diet, exercise, Smoking, ETOH, psychological stressors Management Lifestyle Modification, Diet & Exercise, smoking cessation Lipid Lowering Agents Antiplatelet therapy
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Myocardial Ischemia Occurs when demand for myocardial oxygen exceeds coronary arteries’ ability to supply oxygen to the heart Angina clinical term for reversible chest pain For ischemia secondary to atherosclerosis to occur >75% of vessel must be occluded Myocardial cell hypoxia occurs within 10 seconds of coronary occlusion Delay in depolarization and repolarization of cardiac cells In ischemic conditions, cardiac cells are viable for 20 minutes
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Ischemia Algorithm https://evolve.elsevier.com/cs/store?role=student
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Types of Angina Table 34-9 Chronic Stable Angina; CAD Episodic pain, last 5-15 minutes, provoked by exertion, relieved by rest or NTG Prinzmetal’s Angina; Coronary Vasospasm, Occurs at rest, triggered by smoking or other substance (histamine, epi) Microvascular Angina; Microvascular Ds affecting distal branches of CA More common in women, triggered by everyday activities, may respond to NTG Unstable Angina; Rupture of Plaque New onset CP, occurs with minimal exertion, does not respond to NTG
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Myocardial Injury When Ischemia is prolonged anoxic cardiac cells sustain injury Hypoxia prevents generation or conduction of electrical impulses (EKG Changes), leads to inability to contract Ability to recover to normal function is related to the length and degree of injury
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Myocardial Infarction Occurs because of severe sustained ischemia Persistent hypoxia secondary to increased supply, and decreased demand 80-90% of acute MI caused by thrombus, No Blood Flow distal to thrombus No electrical current Cell Death is Irreversible, necrosis and scarring Described by location of damage
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Acute Coronary Syndromes Term used to describe cases of acute, prolonged ischemia that is not immediately reversible Medical Emergency Includes Unstable Angina Non ST Elevation Myocardial Infarction (NSTEMI) ST Elevation Myocardial Infarction (STEMI) ST segment elevation on EKG, patients have complete coronary occlusion on angiography
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EKG Changes EKG Changes Occur with ACS T wave inversion ST segment elevation Abnormal Q wave Changes vary with duration, location, and extent of ischemia
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Location of Infarction Septal MI; LAD Anterior MI; LAD Anteroseptal MI; LAD Anterolateral MI; LAD or L Cx Inferior MI; RCA or L Cx
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Acute Septal MI 12 Lead
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Anterior MI 12 LEAD EKG
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Acute Anterior MI 12 LEAD Sinus Rhythm 60, with sinus arrhythmia St Segment Elevation V1-V4 Interpretation; Acute Anterior MI
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Acute Inferior MI 12 LEAD Sinus Rhythm 88 ST Segment Elevations V2-V4 Interpretation Inferior MI
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Acute Anterolateral MI 12 LEAD Sinus Rhythm 80 QRS 0.10 St Segment Elevation I, aVL, V2-V6, ST Segment Depression II, III, aVF Interpretation Acute Anterolateral MI
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Acute Interior MI 12 Lead Sinus Tacchycardia 115 with unifocal PVCs ST Segment Elevation II, III, aVF, ST Segment Depression I, aVL Interpretation Acute Inferior MI
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Acute Coronary Syndrome Gender Differences Men Average age of onset Men 64.5 Present with Acute MI more frequently as first manifestation of CAD Develop greater collateral circulation Women Average age of onset 70.4 Risk of MI quadruples post menopause Do not present with classic symptoms Increased rate of “silent MI” Increased rates of fatal MI
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ACS Gender
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Gerontologic Considerations Incidence of CAD increased in older adults, and is leading cause of death Risk factor reduction efforts are effective but frequently nor prescribed Aggressive Risk Factor Management antidyslipemic, antihypertensives, planned pprogram of physical activity, Most likely to consider lifestyle changes When hospitalized When symptomatic
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Nursing Care & Considerations
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Expected Signs & Symptoms Pain Palpitations Dyspnea Cough Wheezing Anorexia Nausea Vomiting
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Location of CP
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Chronic Stable Angina Education Lifestyle Modification Nitroglycerine Short acting, Sublingual Long Acting Isosorbide Dinitrate Statins Beta Blockers, ACE Inhibitors, CCB
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Clinical Manifestations of MI Result of sustained ischemia Causes irreversible myocardial necrosis Necrosis of entire thickness of myocardium occurs after 4 hours, can take up to 12 hours Degree of altered cardiac function related to location, duration, and size of the infarct Contractile function of heart is disrupted in areas of myocardial necrosis Most MIs involve Left Ventricle
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Objective Symptoms Vital Signs Rate and Rhythm changes, tacchypnea, BP changes Apperance of Skin Cold, sweaty, clammy, cyanotic Cardiovascular Signs Distant Heart Sounds, S3 S4, edema Respiratory signs Rales, rhonchi, wheezing, dyspnea
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Lab Values Myoglobin Elevation indicates skeletal OR cardiac muscle injury CK-MB More specific to cardiac muscle injury May be useful in re-infarction Troponin Gold Standard for Cardiac Injury Distinguishes cardiac from skeletal muscle injury Remains elevated for 5-14 days Takes 30 minutes to appear in serum
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Cardiac Biomarkers Elevation
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Management of ACS Prompt Response All chest pain assumed cardiac until ruled out Goal is Repurfusion Fibrinolytic Administration Antiplatelets (ASA, Clopidogrel) Anticoagulants (Heparin, lovenox) Thrombolytic Agents, (tPA) Converts plasmin into plasminogen, dissolves the fibrin binding platelets
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Nursing Interventions Maintain Airway Administer O2 via NC Obtain 12 Lead EKG Insert two PIV Medicate for Pain (Morphine, NTG) Continuous ECG monitoring Obtain Lab Studies Portable Chest Xray Frequent VS; document response to treatments Provide Reassurance Advanced Directives
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Complications of MI Dysrhythmias Heart Failure Cardiogenic Shock Papillary Muscle Dysfunction Rare, has high mortality rate Control Dysrhythmias, IABP& vasoactive drugs to support contractility Ventricular Aneurysm; infacrted Myocardial wall bulges during contraction HF, dysrhythmia, angina Thrombus formation, increased risk of stroke Pericarditis; inflammation of visceral or parietal myocardium Occurs 2-3 days post MI CP aggrivated by DP, cough EKG shows diffuse ST elevation Tx NSAIDS, corticosteroids Dressler Syndrome; pericarditis with effusion and fever, develops 4-6 wk post MI Ag/Ab rection to necrotic myocardium Pericardial pain, fever, friction rub, pericardial effusion, arthralgia Tx, ST corticosteroids
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Percutaneous Transluminal Coronary Angioplasty PTCA Insertion of Balloon-tipped Catheter into occluded CA Followed by inflation of Balloon Fractures plaque and dilates arterial lumen Can be done with or without stent
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Balloon Angioplasty
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Coronary Artery Stenting
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Surgical Revascularization CABG OPCAB MIDCAB Can be with or without IABP
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Reperfusion Therapy Emergent PCI, Thrombolytic Therapy, or Surgical Interventions Assess Time & Risk Assess Intervention
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“Fibrinolynic Therapy” AKA Thrombolytic Therapy Especially Important in facilities without interventional cardiac catheterization lab Breaks up fibrin meshwork in clots Gal of administration is 30 minutes from arrival to ED Review Contraindications (Table 34-14) Active internal bleeding, HX cerebral aneurysm or AV malformation, known intracranial neoplasm, HX cerebral hemorrhage, ischemic stoke in last 3 months, suspected aortic dissection
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Pharmacology in Acute MI IV Nitroglycerine Morphine Sulfate Beta Blockers ACE Inhibitors Antidysrhythmics Cholesterol Lowering Agents Stool Softeners
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Patient Teaching Table 34- 17 Signs & Symptoms of an MI, and what to do if they occur When & How to seek help (EMS) A&P of Heart Cause & Effect of Atherosclerosis ID and Plans to reduce Risk Factors Rationale for Tests & Tx Recovery & Rehabilitation Plan Resumption of ADLs (work, physical & sexual activity)
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Sudden Cardiac Death Unexpected death resulting from a variety of cardiac causes Sudden disruption in cardiac functioning and abrupt loss of CO and cerebral blood flow Estimated 382,800 deaths annually 56% occur outside hospital Of patients that survive SCD approximately 80% sustain neurological impairment Majority of SCD caused by acute ventricular dysrhythmias
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References Lewis et al., (2014). Medical Surgical Nursing; assessment and Management of Clinical Problems, Chapter 34 McCance et al., (2010). Pathophysiology; The Basis for Disease in Adults and Children, Chapter 30 American heart Association http://circ.ahajournals.org/content/129/3/e28.fig ures-only
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