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Coronary Heart Disease, Myocardial Infarction, and Heart Failure Provided Courtesy of Nutrition.com Review Date 12/13 G-0967 A Review of the Basics.

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Presentation on theme: "Coronary Heart Disease, Myocardial Infarction, and Heart Failure Provided Courtesy of Nutrition.com Review Date 12/13 G-0967 A Review of the Basics."— Presentation transcript:

1 Coronary Heart Disease, Myocardial Infarction, and Heart Failure Provided Courtesy of Nutrition.com Review Date 12/13 G-0967 A Review of the Basics

2 Defining Heart Disease Heart disease is a broad term used to describe a range of diseases that affect your heart, such as: Coronary heart disease (CHD) Atherosclerosis Myocardial infarction (MI) Heart failure (formerly called congestive heart failure)

3 Risk Factors for CHD and MI Smoking High intake of alcohol Obesity Sedentary lifestyle Diabetes Hypertension

4 Risk Factors for CHD and MI (cont’d) More than 34 years of age for males and 55 years of age for females (risk increases after menopause) Family history—genetics Hypertension Stress Chronic kidney disease

5 Risk Factors for CHD and MI (cont’d) High low-density lipoprotein (LDL) cholesterol Low high-density lipoprotein (HDL) cholesterol Left ventricular hypertrophy

6 Risk Factors for Heart Failure Obesity Hypertension Overweight or obesity Ischemic heart disease Changes in cardiovascular structure, such as diseases to the heart valves or muscle

7 Coronary Heart Disease: An Overview Blood flow to the vessels surrounding the heart is blocked The major underlying cause of CHD is atherosclerosis or a buildup of plaque in the arteries

8 Plaque Development Many factors speed up plaque development: ̶Elevated cholesterol and triglyceride levels ̶Hypertension ̶Infection that initiates the inflammatory response ̶Elevated iron levels—carry free radicals that damage lining ̶Elevated homocysteine level ̶Cigarette smoking ̶Diabetes ̶Obesity ̶Oxidized (LDL) levels

9 The Atherosclerotic Process Buildup of smooth muscle cells, macrophages, and lymphocytes Smooth muscle cells form a matrix of connective tissue Lipid and cholesterol accumulates in the matrix

10 The Atherosclerotic Process (cont’d) Lipid deposits and other materials (including cellular waste, fibrin, and calcium) build up and form a plaque After injury, platelets adhere to the arterial wall and release growth factors, which promote lesion development

11 Coronary Heart Disease Development Steps to development of CHD: ̶Fatty streaks form, often in people younger than 30 years of age ̶People are asymptomatic during this first stage of CHD ̶Plasma LDL enters the injured endothelial wall and forms a plaque that sometimes is prone to rupture ̶Acute, complicated lesions with rupture and either nonocclusive or occlusive thrombus form (occlusive form often results in MI and sudden death) ̶Hemorrhage into plaque produces thrombi—thrombus formation with arterial lumen initiated

12 Coronary Heart Disease Development (cont’d) Steps to development of CHD (cont’d): ̶Progressive narrowing of lumen ̶Insufficient blood flow to myocardium (ischemia) results ̶Chest pain or angina pectoris occurs

13 Signs and Symptoms of Coronary Heart Disease Chest pain Hypertension Increased pulse Increased respiration Dyspnea on exertion Pallor of skin Light-headedness with exertion Diminished peripheral pulses Intermittent claudication—cramping of the lower extremities

14 Treatment of Coronary Heart Disease Antihyperlipidemic agents Medications that lower triglycerides Antiplatelets (aspirin) Antihypertensives Antianginals (nitroglycerin) Antimicrobials

15 Angina Pectoris: An Overview Chest pain caused by myocardial ischemia from reduced blood flow and/or reduced oxygen supply to the myocardium Angina is a warning sign that a heart attack (MI) may occur

16 Angina Pectoris: An Overview (cont’d) Aerobic metabolism switches to anaerobic metabolism: ̶Lactic acid buildup ̶Release of histamine, bradykinins, and enzymes, which stimulate nerve fibers in the myocardium, sending pain impulses to the central nervous system

17 Angina Pectoris: An Overview (cont’d) Other causes of decreased oxygen supply to the myocardium: ̶Congestive heart failure ̶Congenital heart defects ̶Pulmonary hypertension ̶Left ventricular hypertrophy ̶Cardiomyopathy ̶Severe hypertension ̶Narrowing of the aortic valve

18 Angina Pectoris: An Overview (cont’d) Other causes of decreased oxygen supply to the myocardium (cont’d): ̶Leakage of the aortic valve ̶Ventricle wall thickening ̶Atheroma leading to arterial narrowing Silent ischemia—decreased oxygen supply with no pain

19 Causes of Increased Oxygen Demand Causes of increased oxygen demand on the myocardium: ̶Anemia ̶Exercise ̶Thyrotoxicosis ̶Substance abuse, particularly cocaine ̶Hyperthyroidism ̶Emotional stress

20 Four Types of Angina Stable: ̶Caused by specific amount of activity ̶Predictable ̶Relieved with rest and nitrates Unstable: ̶Pain occurs with increasing frequency, severity, and duration over time ̶Unpredictable ̶May occur at rest ̶High risk for MI

21 Four Types of Angina (cont’d) Prinzmetal’s (variant): ̶Has no identified cause ̶May occur at same time of day ̶May intensify or worsen over time ̶Is usually caused by coronary artery spasm Angina decubitus: ̶Occurs when a person is lying down with no cause ̶Occurs because gravity redistributes body fluids

22 Signs and Symptoms of Angina Pressure or heaviness in chest beneath breastbone—women are likely to have unusual types of chest discomfort Pain may occur down shoulder or inside of arms, or in the throat, jaw, or teeth Stomach pain, especially after eating Sweating

23 Signs and Symptoms of Angina (cont’d) Light-headedness Hypotension Pulse changes Indigestion

24 Treatment of Angina Antianginals (nitroglycerin) Antiplatelets (aspirin) ACE inhibitors Beta-blockers Calcium channel blockers Thrombolytic therapy (if thrombi are the cause) Oxygen administration Percutaneous transluminal coronary angioplasty or coronary artery bypass graft to prevent MI

25 Myocardial Infarction: An Overview Death of cells in the myocardium, usually related to prolonged or severe ischemia Necrosis, tissue damage, and sometimes death results Cause of MI include: ̶Sudden onset of ventricular fibrillation ̶Embolus (most common cause) ̶Thrombosis ̶Atherosclerotic occlusion ̶Prolonged vasospasm

26 Myocardial Infarction Progression Cellular injury occurs from lack of oxygen: ̶If prolonged, will lead to cell death Scar replaces muscle, but cannot contract or conduct impulses: ̶Location of damage is determined by which artery is blocked Damage begins at subendocardial level: ̶Will progress to the epicardium within 1 to 6 hours

27 Myocardial Infarction Progression (cont’d) Damaged cells lead to decreased contractility: ̶Less blood ejected by left ventricle with each beat ̶Decreased blood pressure ̶Decreased tissue perfusion

28 Pain, typically in middle of chest, radiating to jaws, arms (usually the left), abdomen, and/or shoulders, and lasting 20 minutes: ̶Possible to have no pain or atypical pan (particularly in females) ̶Sudden onset of pain, not associated with activity Myocardial Infarction: Signs and Symptoms

29 Myocardial Infarction: Signs and Symptoms (cont’d) Tachycardia Excessive perspiration Painful breathing and/or difficulty breathing Anxiety/panic Nausea/vomiting Fever Stomach pain, often confused with indigestion

30 Laboratory Evaluation Creatinine kinase Trophin Myoglobin

31 Myocardial Infarction Complications If more than 50% of heart tissue is damaged, severe disability or death will result

32 Myocardial Infarction Complications (cont’d) Pericarditis may develop up to 2 months later: ̶Fever ̶Pericardial effusion ̶Pleurisy ̶Pleural effusion ̶Joint pain ̶Rupture of heart muscle ̶Ventricular aneurysm ̶Blood clots ̶Hypotension

33 Treatment Following Myocardial Infarction Antianginals (nitroglycerin) Analgesics Electrolyte replacement Calcium channel blockers Beta-blockers Antihypertensives Anticoagulants

34 Treatment Following Myocardial Infarction (cont’d) Antiarrhythmics Thrombolytics Oxygen Mild antianxiety agents

35 Heart Failure: An Overview Inability of the heart to pump sufficiently to meet metabolic needs, leading to decreased tissue perfusion as a result of decreased cardiac output Acute or chronic Left sided or right sided Systolic or diastolic

36 Causes of Heart Failure Hypertension MI Cardiomyopathies Congenital heart disease Valve disorders Side effect of medication or alcohol

37 Types of Heart Failure Systolic dysfunction: ̶Heart contracts with less force and cannot pump out as much blood to the rest of the body as normal ̶Blood accumulates in the ventricles and veins Diastolic dysfunction: ̶Heart is stiff and does not relax after contracting ̶Heart does not allow as much blood to enter its chambers from the veins, and the blood accumulates in the veins

38 Types of Heart Failure (cont’d) Left sided: ̶More common ̶Fluid backs into lungs ̶Signs and symptoms include: Fatigue Activity intolerance Dizziness Syncope Dyspnea Coughing Pulmonary crackles Tacycardia  urine output Shortness of breath when lying down

39 Types of Heart Failure (cont’d) Right sided: ̶Caused by pulmonary hypertension or right ventricular infarction ̶Fluid backs into rest of body, with abdominal organ congestion and peripheral edema ̶Signs and symptoms include: Lower extremity edema in the ambulatory Sacral edema in the bedridden Liver engorgement and right upper quadrant pain Anorexia and nausea Jugular venous distension

40 Types of Heart Failure (cont’d) Biventricular (signs and symptoms of both left and right heart failure): ̶Signs and symptoms include: All symptoms of right and left heart failure Dyspnea at rest Hepatomegaly and splenomegaly Abdominal pressure Ascites Anorexia Nausea and vomiting  digestion and absorption of nutrients Dysrhythmias Cardiogenic shock or acute pulmonary edema

41 Cardiac Cachexia 10% to 15% of patients with heart failure develop cardiac cachexia Loss of 6% of nonedematous body weight over 6 months Concurrent loss of cardiac muscle mass as a result

42 Cardiac Cachexia (cont’d) Many other metabolic changes: ̶Increased catabolic catecholamines ̶Tumor necrosis factor is increased, contributing to a lower body mass index and catabolic state

43 Treatment of Coronary Heart Disease Diuretics Dopamine Analgesics Antihypertensives ACE inhibitors Direct vasodilators Antidysrhythmics Cardiac glycosides (digitalis) Aldosterone agonists

44 Treatment of Coronary Heart Disease (cont’d) Antibiotics, if necessary Iron supplementation, if necessary Supplemental oxygen Nitrates Beta-blockers Anticoagulants

45 References Academy of Nutrition and Dietetics. Nutrition Care Manual ® [by subscription]. Nutrition Care Manual Web site. www.nutritioncaremanual.org. Accessed December 1, 2013. www.nutritioncaremanual.org Cleveland Clinic. Acute myocardial infarction. Cleveland Clinic Center of Continuing Education Web site. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/ cardiology/acute-myocardial-infarction/. Accessed December 1, 2013. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/ cardiology/acute-myocardial-infarction/ Cleveland Clinic. Heart failure. Cleveland Clinic Center for Continuing Education Web site. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/ cardiology/heart-failure. Accessed December 1, 2013. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/ cardiology/heart-failure

46 References (cont’d) Raymond JL, Couch SC. Medical nutrition therapy for cardiovascular disease. In: Mahan, LK, Escott-Stump S, Raymond JL. Krause’s Food and the Nutrition Care Process. 13th ed. St Louis, MO: Elsevier Saunders; 2012:742-781. The Merck Manual for Health Care Professionals. Cardiovascular disorders. Merck Manuals Web site. http://www.merckmanuals.com/professional/cardiovascular_disorders.ht ml. Accessed December 1, 2013. http://www.merckmanuals.com/professional/cardiovascular_disorders.ht ml What is angina? National Heart, Lung, and Blood Institute Web site. http://www.nhlbi.nih.gov/health/health-topics/topics/angina/. Accessed December 1, 2013. http://www.nhlbi.nih.gov/health/health-topics/topics/angina/


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