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Oxygen Needs Interference with O2 Transport Case Study Oxygen Needs Interference with O2 Transport Coronary Artery Disease Complications Dysrhythmias Pulmonary Embolism Hypertension Complication Congestive Heart Failure Peripheral Vascular / Arterial Disease Oxygen Needs Interference with O2 Transport Care of Patients with: Coronary Artery Disease Risk Factors Myocardial Infarction Alterations in: Rate & Rhythm (Cardiac Conduction) Effect on Cardiac Output Content Approach Anatomy & Physiology Review Demographics/occurrence Pathophysiology Clinical Manifestation Medical / Surgical Management Nursing Process (APIE) Assessment - Nursing Actions - Education Anatomy & Physiology Right Heart Left Heart Systole Valve Closure: Diastole Valve Closure: Cardiac Circulation Myocardium Anterior Posterior Cardiac Cycle 1. 2. 3. 4. 5. Passive Filling – preload Atrial contraction – Aortic & Pulmonic semilunar valves close – S2 Isovolumetric ventricular contraction – all valves closed Ejection – ventricular systole – Mitral & Tricuspid valves close – S1 - afterload Isovolumetric ventricular relaxation – all valves closed Cardiac Cycle Phases Heart Sounds & Stethoscope Placement Coronary Arterial System Physiology: Oxygen Supply to the Cardiac Muscle during the Cardiac Cycle Coronary artery oxygen deficit during ventricular contraction & ejection (systole) Coronary artery filling during ventricular filling (diastole) What is the impact of heart rate on coronary artery filling? Oxygen Supply to the Cardiac Muscle during the Cardiac Cycle The actual time available for diastole shortens significantly as the heart rate increase % of a Minute 70% 50% 33% Heart Rate 60 120 188 Results: Less time for ventricular filling & coronary artery filling + as HR increases, increased oxygen is needed each minute to eject the same volume of blood. Stroke volume: volume ejected in one heart beat Cardiac Output: volume ejected in one minute Cardiac Output = Stroke Volume x Heart Rate Factors Determining Myocardial Oxygen Needs Decreased Oxygen Supply: Noncardiac: Anemia, hypoxemia, pneumonia, asthma, COPD, low blood volume Cardiac: Arrhythmias/dysrhythmias, congestive heart failure (CHF), coronary artery spasm, coronary artery thrombosis, valve disorders Increased Oxygen Demand or Consumption: Noncardiac: anxiety, cocaine use, hypertension, hyperthermia, hyperthyroidism, physical exertion Cardiac: aortic stenosis, arrhythmias, cardiomyopathy, hypertension, tachycardia CAD - Demographics CAD - Demographics Comparison of death by CV Disease and Breast Cancer – by Women’s Age 400 300 Cardiovascular Disease Breast Cancer 200 100 0 35-54 55-74 >=75 Coronary Artery Disease (CAD) Pathophysiology ASHD, IHD, CVHD = CAD AHA 1.1 mil Americans will have an MI in 2003 460,000 will die About half of those deaths occur within 1 hour of the start of symptoms and before the person reaches the hospital. Major cause: Atherosclerosis—focal deposit of cholesterol & lipids CAD – Risk Factors Unmodifiable: Age, Gender, Ethnicity, Genetic predisposition/family history Modifiable Major: Dyslipidemia--Elevated serum lipids*, hypertension*, cigarette smoking, obesity—visceral/central obesity Modifiable Contributing: Diabetes Mellitus*, stressful lifestyle * may have genetic predisposition CAD – Risk Factors Metabolic Syndrome: – – – – – – Insulin Resistance Hyperglycemia >110mg/dL Hypertension - > 130/85 Increased triglycerides >110mg/dL Decrease HDL <40 men; < 50 women Central Obesity men: waist > 40” women: waist > 35” Risk Factors One of the Major Modifiable Physical Inactivity Types of Plasma Lipoproteins HDL – Contain more protein and less lipid Carry lipids away from arteries to liver for metabolism This process prevents lipid accumulation within arterial walls Higher levels are desirable LDL – Contain more lipids than any other lipoproteins Affinity for arterial walls Increased levels correlate closely with an increased incidence of atherosclerosis Lower levels are desirable VLDL Contain of triglycerides Correlation with heart disease is uncertain Plasma Lipoproteins Atherosclerosis Elevated serum lipids Cholesterol > 200mg/dl Triglyceride > 200mg/dl HDL < 35 mg/dl – major risk 45-59 mg/dl – average risk > 60 mg/dl – negative risk LDL < 130 – desirable 130 – 159 mg/dl – borderline risk > 160 mg/dl – high risk Progressive Atherosclerosis Drug Therapy for Dyslipidemia Bile Acid Sequestrants (Questran) - Binds with bile salts Niacin - Inhibits synthesis of VLDL & LDL Fibric Acid Derivatives (Atromid)– Decrease VLDL HMG CoA Reductase Inhibitors (Statins - Lipitor, Pravachol, Zocor) – Block synthesis of cholesterol Cholesterol Absorption Inhibitor (Zetia)– Inhibits intestinal absorption of cholesterol Natural Lipid Lowering Agents Niacin - < LDL levels Omega-3 fatty acids – fish/flaxseed oil <Triglycerides & > HDL levels Milk thistle – Silymarin - > HDL levels Fiber - < Cholesterol Phytosterols - < Cholesterol Soy - < Cholesterol absorption from GI tract CoEnzyme Q10 – HMG CoA reductase inhibitors – natural statins Coronary Thrombogenesis During an Acute Coronary Syndrome Angina Clinical Manifestations Angina – Chest Pain Stable Angina Pectoris – intermittent, same pattern of onset, duration, intensity of symptoms - 3-5 mins. Silent Ischemia – 80% of patients with ischemia are asymptomatic Prinzmetal’s Angina – variant – not precipitated by physical activity – may be due to spasm Nocturnal Angina – occurs at night but not necessarily during sleep or in recumbent position Angina Decubitis – recumbent position – relieved by standing Unstable Angina – Unpredictable or may evolve from stable angina – increasing frequency, duration, intensity CAD Clinical Manifestation – Diagnostics History & Physical Examination EKG / Echocardiogram / Stress Echocardiogram Thallium Stress Test (perfusion scanning) cold spots where tissue is inadequately perfused cardiac tissue CAT scan- calcium score/CT coronary angiogram MUGA (Multiple gated radioisotope scan) – left ventricular function MRI of the heart PET (Positron emission computed tomography) – evaluate coronary artery patency Normal Thallium Stress Test Abnormal Thallium-Stress Test CAD - Clinical Manifestation Invasive Diagnostics Cardiac Catheterization Right sided: Catheter through the femoral vein through the vena cava into right atrium and right ventricle – pulmonary artery – wedge pressure Left sided: Catheter through the femoral artery through the aorta into the left atrium and left ventricle / openings of the coronary arteries Coronary arteriography: Injected dye with video & x-rays CAD - Clinical Manifestation Invasive Diagnostics Cardiac Catheterization Potential Complications Catheter looping/breaking, dysrhythmias, allergic reaction to contrast medium, arterial thrombosis, myocardial infarction, hemorrhage, infection. Patient Preparation Informed consent; allergies – shellfish/iodine; NPO x 6 hrs; explanation “flushed/tingling”; supine – absolutely still Postprocedure Care Right Heart Catherization Left Heart Catheterization Coronary Angiography Coronary Blockage - LAD Cardiac Catheterization Post Procedure Care Assess: VS q15 mins. x 2 hrs; q30 min x 2 hrs Monitor cardiac rate and rhythm Check site for bleeding Extremity: Peripheral pulse check, temperature, color, sensation, mobility Assess for chest pain, dizziness, dyspnea Nursing Action: Straight at groin x 24 hours; pressure at site x 30 mins. Maintain IV KVO for 2 hrs; IV capped x 2 hrs; then d/c Encourage oral fluids Patient/Family Education: Rationale for all nursing actions No squatting, sitting, lifting for 24 – 48 hours++ Report bleeding, swelling, discoloration, drainage Change dressing after 24 hours – small dressing to bandaid Clinical Manifestation Myocardial Infarction Lab Diagnostics Cardiac Protein – Troponin T More sensitive than CK Elevates 3 hr – peak 24-48 hrs; normal 5-14 days Cardiac Enzyme – Creatine kinase (CK-MB) Released when cardiac cells die Elevates 3 hrs – peak 12-24 hrs; normal 2-3 days Cardiac Marker - Myoglobin First to elevate Lacks cardiac specificity Normal range within 24 hours Serum Cardiac Markers after MI CAD – Angina Relationship Coronary Artery Disease / \ Stable Angina Acute coronary syndrome / / \ Unstable Angina > Myocardial Infarction ST-elevated MI Non-ST-elevated MI CAD & Acute Coronary Syndrome Heart With Muscle Damage and a Blocked Artery Myocardial Infarction Myocardial Infarction Acute Coronary Syndrome Location correlates with coronary circulation involved Inferior Wall – Right coronary artery Anterior Wall – Left anterior descending Lateral, posterior or inferior – left circumflex Healing Process Within 24 hours – leukocytes & enzymes Third day – collateral circulation developing 10-14 days – scar tissue is still weak Vulnerable time – unstable state of healing + increased activity 6 weeks – scar tissue replaces necrotic tissue Normal myocardial tissue may compensate – ventricular remodeling – can cause late congestive heart failure Coronary Artery Collateral Circulation Angina Medical Management A Aspirin / Antianginal therapy / ACE Inhibitor B b-Adrenergic blocker / blood pressure C D Diet / Diabetes E Education / Exercise Cigarette smoking / Cholesterol Angina- MI Medical Management B-Adrenergic Blockers – decreases rate, contractility, afterload Nitrates – peripheral vasodilation decreasing preload and afterload / coronary artery vasodilation Calcium Channel Blockers – Coronary & peripheral vasodilation, decreases AV conduction and myocardial contractility Morphine – analgesic – reduces preload & myocardial oxygen consumption Angiotensin-Converting Enzyme Inhibitors – Vasotec / Capoten - prevents Angiotensin I conversion to Angiotensin II – HTN, CHF Antiplatelet and Anticoagulant Agents in unstable angina and NSTEMI Oral anti-platelet agent Aspirin Initially 300 mg p.o. then 75 - 150 mg daily Clopidogrel (Plavix) Initial loading dose of 300 mg then 75 mg daily • Increased bleeding risk Heparins Heparin Sodium: Bolus: 60 U/kg IV bolus to a maximum of 4,000 units Drip: 12 units/kg/h infusion to a maximum of 1 000 units/h • Monitor PTT: keep at 50 - 70 seconds Low-molecular-weight heparin - Enoxaparin 1 mg/kg subcut q12 hr Precautions: • Peptic ulceration • Aspirin allergy • GI bleeding Antiplatelet Drugs used in unstable angina and NSTEMI Intravenous – tirofiban (Aggrastat), eptifibatide (Integrilin) New class, GP IIb/IIIa inhibitors – Abciximab (ReoPro) 0.25 mg/kg IV bolus 10 - 60 min before PCI, than 10 μg/min IV - Infusion for 12 h Precautions: • Thrombocytopenia • Bleeding disorder • Surgery < 6 weeks • Abnormal bleed < 30 d • Active GI ulceration • Puncture of a non-compressible • Prior stroke, organic CNS pathology • Any systolic BP > 180 mmHg during the acute event Thrombolytic Drugs Drugs that break down, or lyse, preformed clots Tissue plasminogen activator – plasminogen-streptokinase activator complex (APSAC) – streptokinase (Streptase) – alteplase (t-PA, Activase) – reteplase (Retavase) Angina - MI Invasive Medical Management Percutaneous Coronary Intervention – PCTA – Percutaneous transluminal coronary angioplasty Balloon-tipped catheter passed through just beyond the lesion – balloon inflated – atherosclerotic plaque is compressed Reduction in lesion size by >50% in 90% of patients Used in conjunction with thrombin inhibitors Angina- MI Invasive Medical Management Stent Placement – may be placed during PCTA – expandable meshlike structures to maintain vessel patency – placed over the angioplasty site to hold the vessel open * Stents are thrombogenic – IV antiplatelet agents ASA/Plavix Atherectomy – plaque is shaved away from the coronary artery wall Limited to use in larger portions of vessels Laser Angioplasty – “cool” laser – no heat Coronary Artery Stent Placement Coronary Atherectomy Angina - MI Invasive Medical Management Complications Abrupt closure of angioplasty site Stent thrombosis / embolization Hemorrhage / vascular damage Coronary spasm, Acute MI Need for emergent coronary artery bypass graft (CABG) Fibrinolytic Contraindications Absolute Contraindications Active internal bleeding, active inflammatory bowel disease, active peptic ulcer disease, acute pericarditis, GI/GU bleeding within 6 months, Hx of hemorrhage CVA, Neurosurgical procedure within 2 months, Pregnancy, Suspected aortic dissection, Uncontrolled HTN, >180/110 Relative Contraindications Bacterial endocarditis, chronic Coumadin Therapy, Diabetic hemorrhagic retinopathy, Poorly controlled HTN Angina - MI Surgical Management Coronary Artery Bypass Graft (CABG) construction of new vessels between the aorta to beyond the obstructed coronary artery (or arteries) Saphenous vein or internal mammary artery Palliative treatment for CAD – not a cure Postoperative care: Care of cardiac patient with chest tubes / sternotomy; pain management; short ventilator support; early ambulation; 4-5 day hospital stay Coronary Artery Bypass Coronary Artery Bypass Complications of MI Arrhythmias – lethal PVC’s within 4 hours of onset of chest pain Congestive Heart Failure Cardiogenic Shock – severe left ventricular failure – intra-aortic balloon pump & vasoactive medications Papillary Muscle Dysfunction – Mitral valve regurgitation – treat dyspnea, pulmonary edema & decreased CO Ventricular Aneurysm Pericarditis – 1-3 days post MI; pleural friction rub & fever Dressler Syndrome – pericarditis with effusion & fever 1- 4 wks post MI; elevated WBC & Sed Rate. Tx-Steroids Pulmonary Embolism Acute Coronary Syndrome Pair Share Discomfort or a heavy feeling in the chest can signal a heart attack. A. True B. False Women do not frequently experience heart attacks. A. True B. False African-American women die of heart attacks at the same rate as white women. A. True B. False Some people who are experiencing the symptoms of a heart attack may wait hours or even days before seeking needed medical care. A. True B. False Being treated within about an hour of the first symptoms can make a significant difference. A. True B. False Acute Coronary Syndrome Pair Share Many heart attack victims say their heart attack wasn’t what they’d expected. A. True B. False A family member, such as a spouse, can persuade a loved one having a heart attack to seek help immediately. A. True B. False Calling 9-1-1 for chest pain alone would probably turn out to be a waste of the emergency medical personnel’s time. A. True B. False Most heart attacks occur in people over 65. A. True B. False The major issue in delay is how long it takes for emergency medical personnel to find the address and deliver the patient to the hospital. A. True B. False Nursing Diagnoses TOP 4 ????? Nursing Process Nsg Dx: Acute Pain related to Cardiac Ischemia Assess: Chest pain—intensity, location, duration, precipitating, alleviating factors; Monitor cardiac rate & rhythm; effect of pain medication; peripheral pulses; VS; Pulse Oximetry Nsg Action: Administer O2 NC; IV access; position of comfort Patient Education: Rationale for all procedures; pain scale; instruct to report pain Nsg Dx: Ineffective Tissue Perfusion related to Myocardial Injury Assess: VS & Pulse Oximetry qh; continuous cardiac monitoring; respiratory status if Morphine IV is used; fluid balance – strict I&O peripheral edema; heart & breath sounds Nsg Action: Rest periods; Administer meds & oxygen as ordered Patient Education: Rationale for rest; energy conservation Nsg Dx: Anxiety related to perceived or actual threat of death Assess: verbal & nonverbal queues Nsg Action: Calm, reassuring approach; encourage verbalization of feelings, fears, perceptions; family involvement; Patient Education: Relaxation techniques; simple instructions Nsg Dx: Ineffective therapeutic regimen management related to lack of knowledge Assess: Current knowledge level & readiness to learn; family dynamics Nsg Action: Assist pt in identifying small successes; Assist pt is identifying lifestyle that needs to be changed; Community referrals— smoking cessation, cardiac rehab, support groups, Patient Education: Lifestyle changes, Medications—desired effect/side effects; comprehensive discharge plan—continuity with community cardiac rehabilitation Nsg Dx: Activity Intolerance related to fatigue & chest pain Assess: Monitor patient’s response to medications, activity tolerance as increased; Cardiac rate, rhythm, respiratory effort Nsg Action: Include family; advance activity as tolerated; supplement oxygen as needed Patient Education: Teach patient energy conservation – activity/rest – activities that will promote independence and decrease oxygen consumption; Cardiac Rehab: exercise & sexual activity Patient Education: Exercise Guidelines post MI Type of Exercise – regular, rhythmic & repetitive – using large muscle groups Intensity – determined by patient’s HR – should not exceed 20 beats per min > resting HR Duration – Build to 20 -30 mins Frequency -- 3-4x/week Warm-up/Cool-down – 5 mins before and after aerobic exercise. Exercise should not be stopped abruptly Cardiac Rehab – Metabolic Equivalents of Energy Expenditure Patient Education: Sexual Activity post MI Plan of resumption of sexual activity should correspond to activity prior to MI Physical training improves physical response to coitus Food & alcohol < prior to sexual activity Familiar & relaxed surroundings; positions of comfort Avoid hot or cold showers Foreplay is desirable – gradual increase in heart rate prior to orgasm Prophylactic use of nitrates decreases angina Orogenital sex places no undue strain on the heart Anal intercourse may cause undue cardiac stress – vasovagal response Emotional & Behavioral Response to Acute MI Denial – Ignores symptoms; minimizes severity; ignores activity restrictions Anger – “Why did this happen to me?” Anxiety & Fear – Fear of death & disability –apprehension, tachycardia, restlessness, hypochondria, projection of feelings Dependency – reliant on staff; hesitant to leave ICU or hospital Depression – Mourning period; realizes seriousness of situation Realistic Acceptance – Focuses on optimum rehabilitation; plans changes compatible with cardiac function
