Ischemic heartdisease lecture made easy
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The document provides details on the anatomy, function, and pathophysiology of the heart including the structure of the heart chambers and layers, blood flow, electrical conduction system, common cardiac tests, risk factors and causes of coronary artery disease, characteristics of angina and myocardial infarction, and lifestyle and medical management of heart conditions. Key points covered include the size of the heart, blood flow rate, heart sound causes, atherosclerotic plaque formation, risk factors for coronary artery disease, signs and symptoms of angina and heart attack, and diagnostic tests like echocardiograms, EKGs, and cardiac catheterization.
Ischemic heartdisease lecture made easy
- 1. M Tayyab Student of Anesthesia kmu 1
- 2. Facts: The heart is about the size of a fist and weighs less than 1 pound The average bpm is 72 The average adult heart pumps about 6000-7500 liters of blood per day through 60,000 miles of blood vessels each minute at rest. 2
- 3. Structure Covered by pericardium Parietal Visceral (epicardium) Outer heart layer: epicardium Middle heart layer: myocardium Inner layer: endocardium
- 5. Structure (continued) Four hollow chambers Two upper, atria Two lower, ventricles Divided by septum and valves
- 6. Function Right atrium receives deoxygenated blood Right ventricle pumps blood to lungs
- 7. Function (continued) Left atrium receives oxygenated blood Left ventricle pumps oxygenated blood to body AV valve closure: S1 heart sound Semilunar valve closure: S2 heart sound Coronary circulation
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- 10. Aorta, arteries, arterioles, capillaries Venules, veins, superior and inferior vena cava Three layers Intima Media Adventitia
- 12. Function Circulation Peripheral vascular resistance: viscosity, length, diameter Blood pressure control
- 14. Mechanical SA node: pacemaker Cardiac output (CO) Heart rate (HR) Stroke volume (SV): the volume of blood pumped from one ventricle of the heart with each beat CO = HR x SV
- 16. Electrical properties: Action potential Polarization Depolarization Repolarization Refractory period
- 17. Filling and pumping Diastole – ventricular filling Systole –ventricles eject blood
- 19. Subjective Health history Chest pain SOB Leg pain Pillows to sleep Medications Lifestyle: diet, alcohol use, exercise, smoking, drugs
- 20. Objective General appearance Skin Wounds Pulses Jugular vein distention Edema Breathing
- 21. TEE (transesophageal echocardiogram) Monitor breathing, cough, gag reflex Keep NPO until gag reflex returns Doppler sonography: is a medical imaging technique that uses ultrasound enhanced by the Doppler effect and is often provide helpful information about the flow and movement of blood and inner areas of the body Monitor BP Wash extremities to remove gel after test completed
- 22. X-rays/CT scan/EBCT Electron beam computed tomography (EBCT) is used to determine coronary calcium Document client allergy to fish or shellfish Pregnancy risk Angiography/cardiac catheterization MRI Document presence of implanted electronic devices Radionuclear scans Increase fluids after the test
- 23. Telemetry/Holter monitor Teach about purpose: is a portable device for continuously monitoring various electrical activity of the central nervous system for at least 24 hours (often for two weeks at a tim Dry skin Remove hair Avoid getting unit wet When to phone the MD
- 25. Coronary Artery Disease Heart Anatomy Atherosclerotic Plaque/Atheroma Angina Pectoris Myocardial Infarction Sudden Death Overall Management 25
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- 27. CAD is the largest killer of American males and females 13 million Americans have CAD 1.1 million MI’s per year Every 26 seconds an American will suffer from a coronary event Every 60 seconds an American will die because of a coronary event @ 42% of those having a coronary event will die from it @350K people die per year because of a coronary event in the Emergency Department before even being admitted to the hospital Death Rate in 2001: 177 in 100,000 27
- 28. 84% of those who die from CAD are 65 or older If under the age of 65, 80% mortality rate with the first myocardial infarction Within 1 year of initial MI: 25% of men and 38% of women will die Within 8 years of initial MI: 50% of men and women under 65 will die An average of 11.5 years of life are lost due to an MI IMPORTANT: 50% of men and 64% of women who have died suddenly via CAD DID NOT HAVE ANY PREVIOUS SYMPTOMS Sudden Death: Those with a previous history of MI have a 5-6 times Sudden Death rate compared to the general population 28
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- 31. " Ischaemia " refers to an insufficient amount of blood. The coronary arteries are the only source of blood for the heart muscle. If this coronary arteries are blocked, the blood supply will reduce. 31
- 32. 32 Ischemic heart disease (IHD): caused by coronary atherosclerotic plaque formation which leads to imbalance between O2 supply & demand results in myocardial ischemia Chest pain: cardinal symptom of myocardial ischemia caused by coronary artery disease (CAD) 32
- 33. 33 Ischemia / infarction chest pain Diastolic Dysfunction Systolic Dysfunction cardiac output catecholamines MVO2 wall tension LV diastolic pressurepulmonary congestion pO2 (heart rate, BP)
- 34. High blood cholesterol High blood pressure Smoking Obesity Lack of physical activity 34
- 35. Uncontrollable 35 •Sex •Hereditary •Race •Age Controllable •High blood pressure •High blood cholesterol •Smoking •Physical activity •Obesity •Diabetes •Stress and anger
- 36. Why would there be an insufficient blood supply to the heart? Remember that the coronary arteries are the only source of fuel to the heart The coronary arteries may become partially/completely occluded: Atherosclerotic Plaques 36
- 37. Focal accumulation of smooth muscle cells, foam cells, cholesterol crystals and lipid under the endothelium of the artery (within the Tunica Intima) Given time, this plaque can protrude into the lumen of the vessel reducing blood flow Often develops at branch points or curves within the vasculature blood is slowed and/or turbulent 37
- 38. Where does the plaque begin? within the Tunica Intima, the innermost wall of the artery What is a plaque made of? Superficial fibrous cap made of smooth muscle cells, collagen, elastin and proteins Also contains Macrophages, Foam Cells, T Cells Foam cells are one of the first cells found at the site of the fatty streak, which is the beginning of atherosclerotic plaque formation in vessels Necrotic Center of cholesterol crystals, lipids, Apolipoprotein B LDL 38
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- 43. As the atheroma within the coronary arteries enlarges, the blood flow to the heart decreases and therefore so does the O2 supply The heart is not in danger of hypoxia until 50% of the vessel is occluded As the heart senses a decrease in O2, there is attempted compensation: Increase Heart Rate Increase Blood Pressure Aggravation/Worsening of the atheroma When 70% of the artery is occluded, Angina Pectoris will occur 43
- 44. Classification = mainly 4 types Myocardial infarction (MI) Sudden cardiac death Angina pectoris Chronic IHD with heart failure 44
- 45. At least 70% occlusion of coronary artery resulting in pain. What kind of pain? Chest pain Radiating pain to: Left shoulder Jaw Left or Right arm Usually brought on by physical exertion as the heart is trying to pump blood to the muscles, it requires more blood that is not available due to the blockage of the coronary artery(ies) Is self limiting usually stops when exertion is ceased 45
- 46. Angina Pectoris can be Stable or Unstable: Stable: The pain and pattern of events is unchanged over a period of time (months years) Unstable: The pain and pattern is changing, be it in duration, intensity or frequency A Myocardial Infarction waiting to happen 46
- 47. Partial or total occlusion of one or more of the coronary arteries due to an atheroma, thrombus or emboli resulting in cell death (infarction) of the heart muscle When an MI occurs, there is usually involvement of 3 or 4 occluded coronary vessels 47
- 48. 250,000 deaths per year. 30% mortality within the first 2 hours 45 Minutes of Ischemia: Cardiac muscle death occurs How is the Diagnosis Made? Electrocardiographic changes ST elevation Myocardial enzyme elevation Creatine kinase Troponin C Reactive Protein 48
- 49. When there is an atheroma, as mentioned before there can be rupture resulting in thrombus formation because of the build up of platelets When there is breakage of the thrombus there is emboli formation An emboli can travel to the brain (cerebral infarct) can remain in the heart (myocardial infarct) or even travel to the extremities cutting off blood supply As the area beneath the is disrupted atheroma hemorrhages, there can is increased risk of abscess formation and infection 49
- 50. Infarction leading to inability of the heart to function properly leading to Heart Failure Angina/Pain Cardiogenic shock Ventricular aneurysm and rupture Embolism Formation Arrhythmias Myocardial Infarctions can lead to Ventricular Fibrillation (shockable!) 50
- 51. Sudden Death : 250,000 deaths in the US per year are caused by what is referred to as “sudden” cardiac death Sudden Cardiac Death is also known as a “Massive Heart Attack” in which the heart converts from sinus rhythm to ventricular fibrillation In V-Fib, the heart is unable to contract fully resulting in lack of blood being pumped to the vital organs V-Fib requires shock from defibrillator “SHOCKABLE RHYTHM” 51
- 52. Many people are able to manage coronary artery disease with lifestyle changes and medications. Other people with severe coronary artery disease may need angioplasty or surgery. 52
- 53. Pharmaceuticals: Beta Blockers Act either selectively or non-selectively on Beta receptors: Beta 1 cardiac muscle increase rate and contraction Beta 2 dilates bronchial smooth muscle Ca++ Channel Blockers Acts on vasculature blocking Ca++ and causing vasodilation Nitrates Vasculature vasodilation Anti-Hypercholesterolemia HMG CoA Reductase Inhibitors reduction in “manmade” cholesterol thus helping to reduce atheroma formation Antiplatelet Medication: Clopidogrel (Plavix) Aspirin 53
- 54. 1) Stenting 2) Angioplasty (balloon) 3) Bypass surgery 54
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- 56. Lifestyle: Diet Exercise Preventive treatment • Low fat, low cholesterol diet • Cessation of smoking • Red wine (in moderation) 56
- 57. 1. 1. Gather information about all facets of the client’s activities, especially those that precede and precipitate attacks of anginal pain. 2. Assess the risk factors in the client’s history and modifications possible to reduce risk. 3. If chest discomfort is present at the time of the interview, further collection of data is delayed until pain and dysrhythmias are resolved. 4. A complete physical assessment is performed to identify the presence of chest, epigastric, jaw, back, or arm discomfort which is then rated on a subjective scale of 1 to 10 in intensity. The client is questioned regarding nausea, vomiting, diaphoresis, dizziness, weakness, palpitations, and SOB 57
- 58. 1. Pain related to myocardial ischemia. 2. Altered tissue perfusion: related to imbalance between myocardial oxygen supply and demand. 3. Anxiety related to fear of death and knowledge deficit 58
- 59. Goals 1. Prevention of pain. 2. Improved tissue perfusion as evidenced by absence of chest pain and absence of dysrhythmias. 3. Reduction of anxiety and increased knowledge of disease process. 59
- 60. 1. The nurse must teach the client the link between symptoms and activity and the need to avoid activities known to cause angina, such as sudden exertion, exposure to cold, and emotional excitement. 2. Medications used in the treatment of angina include nitrates, beta-blockers, calcium channel blockers, and platelet antiaggregants. Administer cardiac medication as prescribed and be alert for adverse side effects, particularly their effect on blood pressure. Teach the client the symptoms to be aware of and what measures to take. 3. Encourage the client to remain on bedrest in order to decrease cardiac workload and oxygen consumption. 4. Administer oxygen therapy as prescribed. 5. Evaluate vital signs hourly to determine the hemodynamic effect of the drugs and the client’s tissue perfusion. 6. Nursing care should be planned so that minimal time is spent away from the bedside due to the high level of client anxiety, as well as the unstable condition of the patient. 60
- 61. 7. Clients with unstable angina are at high risk for myocardial infarction (MI) and sudden death. The nurse watches for development of heart failure and dysrhythmias. 8. Relieving pain is the top priority for the client with an acute MI, and medication therapy is administered to accomplish this goal. 9. Maintain patent IV for administration of fluids and vasodilators and anticoagulant therapy (Nitroglycerin and heparin). They relieve pain and they aid in minimizing permanent injury to the myocardium. 10. Prepare for possible emergency heart catheterization or CABG. 61
- 62. 11. Whether CABG is planned as an elective procedure or performed on an emergency basis, the nurse should try to alleviate the client’s and the family’s anxiety and assist them in understanding the need for this life-saving procedure. 12. The nurse describes the postoperative course, emphasizing the close monitoring and use of sophisticated equipment. The client is encourage to tell the nurse about any discomfort post-op. 13. Encourage the client and family members to verbalize their fears and concerns. 14. Teach the client the nature of the illness and the facts needed to reorganize living habits in order to reduce the frequency and severity of anginal attacks, delay the progress of the disease, and avoid other complications. 62
- 63. 1. Verbalizes relief of chest pain. 2. No signs of respiratory difficulties. 3. Modifies lifestyle in order to prevent future attacks. 4. Demonstrates increased knowledge of disease process and reduction in anxiety. 5. Absence of complications. 63
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