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Oxygen Needs Interference with O2 Transport

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.

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Oxygen Needs Interference with O2 Transport

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  1. Oxygen NeedsInterference with O2 Transport

  2. Case Study

  3. Oxygen NeedsInterference with O2 Transport Coronary Artery Disease • Complications • Dysrhythmias • Pulmonary Embolism • Hypertension • Complication • Congestive Heart Failure • Peripheral Vascular / Arterial Disease

  4. Oxygen NeedsInterference with O2 Transport • Care of Patients with: • Coronary Artery Disease • Risk Factors • Myocardial Infarction • Alterations in: • Rate & Rhythm (Cardiac Conduction) • Effect on Cardiac Output

  5. Content Approach • Anatomy & Physiology Review • Demographics/occurrence • Pathophysiology • Clinical Manifestation • Medical / Surgical Management • Nursing Process (APIE) • Assessment - Nursing Actions - Education

  6. Anatomy & Physiology • Right Heart • Left Heart • Systole • Valve Closure: • Diastole • Valve Closure:

  7. Cardiac Circulation

  8. Myocardium Anterior Posterior

  9. Cardiac Cycle • 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

  10. Cardiac Cycle Phases

  11. Heart Sounds & Stethoscope Placement

  12. Coronary Arterial System

  13. 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?

  14. 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 Heart Rate 70% 60 50% 120 33% 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

  15. 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

  16. CAD - Demographics

  17. CAD - Demographics

  18. Comparison of death by CV Disease and Breast Cancer – by Women’s Age

  19. 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

  20. 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

  21. 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”

  22. Risk Factors One of the Major Modifiable Physical Inactivity

  23. 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

  24. Plasma Lipoproteins

  25. 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

  26. Progressive Atherosclerosis

  27. 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

  28. 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

  29. Coronary Thrombogenesis

  30. During an Acute Coronary Syndrome

  31. Angina

  32. Clinical ManifestationsAngina – 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

  33. 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

  34. Normal Thallium Stress Test

  35. Abnormal Thallium-Stress Test

  36. CAD - Clinical ManifestationInvasive 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

  37. CAD - Clinical ManifestationInvasive 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

  38. Right Heart Catherization

  39. Left Heart Catheterization

  40. Coronary AngiographyCoronary Blockage - LAD

  41. Cardiac CatheterizationPost 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

  42. 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

  43. Serum Cardiac Markers after MI

  44. CAD – Angina Relationship Coronary Artery Disease / \ Stable Angina Acute coronary syndrome / / \ Unstable Angina > Myocardial Infarction ST-elevated MI Non-ST-elevated MI

  45. CAD & Acute Coronary Syndrome

  46. Heart With Muscle Damage and a Blocked Artery

  47. Myocardial Infarction

  48. 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

  49. Coronary Artery Collateral Circulation

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