G-0967 Coronary Arte..
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Transcript of G-0967 Coronary Arte..
Coronary Artery Disease, Coronary Artery Disease, Angina, Myocardial Angina, Myocardial
Infarction, and Congestive Infarction, and Congestive Heart FailureHeart Failure
Provided Courtesy of RD411.comWhere dietitians go for information
Review Date 3/09 G-0967
A Review of the Basics
•Smoking•High intake of alcohol•Obesity•Sedentary lifestyle•Diabetes•Hypercholestrolemia•Hyperlipidemia
Risk Factors For Coronary Artery Disease, Angina, Myocardial Infarction, and Congestive Heart Failure
•More than 45 years old for males and 55 years old for females (risk increases after menopause)
•Family history—genetics •Hypertension•Stress/personality type
Risk Factors (cont’d) For Coronary Artery Disease, Angina, Myocardial Infarction, and Congestive Heart Failure
•High low-density lipoprotein (LDL) cholesterol
•Low high-density lipoprotein (HDL) cholesterol
•Left ventricular hypertrophy
Risk Factors (cont’d) For Coronary Artery Disease, Angina, Myocardial Infarction, and Congestive Heart Failure
•Anyone with cardiac conditions– Coronary artery disease (CAD)– Myocardial infarction (MI)– Postcoronary bypass
•Hypertension•Left ventricular hypertrophy•Diabetes•Chronic obstructive pulmonary disease
Risk Factors For Congestive Heart Failure
•Pulmonary hypertension•Anemia•Hypothyroidism•Hyperthyroidism•Overweight or obesity•Alcoholism
Risk Factors (cont’d) For Congestive Heart Failure
•Blood flow to the vessels surrounding the heart is blocked
•The major underlying cause of CAD is atherosclerosis
Coronary Artery Disease: An Overview
•Elevated cholesterol and triglyceride levels
•Hypertension•Infection that initiates the inflammatory response
Plaque Development
Many factors speed up plaque development:
•Elevated iron levels—carry free radicals that damage lining
•Elevated homocysteine level•Cigarette smoking•Diabetes•Obesity•Oxidized LDL cholesterol
Plaque Development (cont’d)
Many factors speed up plaque development:
•Buildup of smooth muscle cells, macrophages, and lymphocytes
•Smooth muscle cells form a matrix of connective tissue
•Lipid and cholesterol accumulates in the matrix
The Atherosclerotic Process
•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
The Atherosclerotic Process (cont’d)
•Fatty streaks form, often in people younger than 30 years of age
•People are asymptomatic during this first stage of CAD
•Plasma LDL enters the injured endothelial wall and forms a plaque that sometimes is prone to rupture
Development of Coronary Artery Disease
Steps to development of CAD:
•Acute, complicated lesions with rupture and either nonocclusive or occlusive thrombus form– Occlusive often results in MI and
sudden death•Hemorrhage into plaque produces thrombi; thrombus formation within arterial lumen initiated
Development of Coronary Artery Disease (cont’d)
Steps to development of CAD:
•Progressive narrowing of lumen•Insufficient blood flow to myocardium (ischemia) results
•Chest pain or angina pectoris occurs
Development of Coronary Artery Disease (cont’d)
Steps to development of CAD:
•Chest pain•Hypertension•Increased pulse•Increased respiration•Dyspnea on exertion•Pallor of skin•Lightheadedness with exertion
Signs and Symptoms of Coronary Artery Disease
•Diminished peripheral pulses•Intermittent claudication—cramping of the lower extremities
Signs and Symptoms of Coronary Artery Disease (cont’d)
•Antihyperlipidemic agents•Medications that lower triglycerides
•Antiplatelets (aspirin)•Antihypertensives•Antianginals (nitroglycerin)•Antimicrobials
Treatment of Coronary Artery Disease
•Chest pain caused by myocardial ischemia from reduced blood flow and/or reduced oxygen supply to myocardium
•Angina is a warning sign that a heart attack (MI) may occur
Angina Pectoris: An Overview
•Aerobic metabolism switches to anaerobic metabolism:– Lactic acid buildup– Release of histamine, bradykinins,
and enzymes, which stimulate nerve fibers in myocardium, sending pain impulses to the central nervous system
Angina Pectoris: An Overview (cont’d)
•Other causes of decreased oxygen supply to myocardium:– Congestive heart failure– Congenital heart defects– Pulmonary hypertension– Left ventricular hypertrophy– Cardiomyopathy– Severe hypertension– Narrowing of aortic valve
Angina Pectoris: An Overview (cont’d)
•Other causes of decreased oxygen supply to myocardium (cont’d):– Leakage of the aortic valve– Ventricle wall thickening– Atheroma leading to arterial
narrowing•Silent ischemia—decreased oxygen supply with no pain
Angina Pectoris: An Overview (cont’d)
•Anemia•Exercise•Thyrotoxicosis•Substance abuse, particularly cocaine
•Hyperthyroidism•Emotional stress
Causes of Increased Oxygen Demand of Myocardium
•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
Four Types of Angina
•Prinzmetal’s (variant):– No identified cause– May occur at same time of day– May intensify or worsen over time– Usual cause is coronary artery
spasm•Angina decubitus:
– Occurs when a person is lying down with no cause
– Occurs because gravity redistributes body fluids
Four Types of Angina (cont’d)
•Form of angina caused by neither spasm or blockage of the large coronary arteries
•Temporary narrowing of the small coronary arteries possibly responsible
•Reasons for temporary narrowing are unknown, but possibly because of chemical imbalance in the heart or abnormal functioning of the small arteries
Syndrome X
•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
Signs and Symptoms of Angina
•Light-headedness•Hypotension•Pulse changes•Indigestion
Signs and Symptoms of Angina (cont’d)
•Antianginals (nitroglycerin)•Antiplatelets (aspirin)•ACE inhibitors•Beta-blockers•Calcium channel-blockers•Thrombolytic therapy (if thrombi are cause)
Treatment of Angina
•Stool softeners•Oxygen administration•Percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft (CABG) to prevent MI
Treatment of Angina (cont’d)
•Death of cells in the myocardium, usually related to prolonged or severe ischemia
•Necrosis, tissue damage, and sometimes death result
Myocardial Infarction: An Overview
•Cause of MI include:– Sudden onset of ventricular fibrillation– Embolus (most common cause)– Thrombosis– Artherosclerotic occlusion– Prolonged vasospasm
Myocardial Infarction: An Overview (cont’d)
•Cellular injury occurs from lack of oxygen; if prolonged, will lead to cell death
•Scar replaces muscle, but can not contract or conduct impulses; location of damage is determined by which artery is blocked
•Damage begins at subendocardial level; will progress to the epicadium with 1-6 hours
Progression of Myocardial Infarction
•Damaged cells lead to decreased contractility– Less blood ejected by left ventricle
with each beat– Decreased blood pressure– Decreased tissue perfusion
Progression of Myocardial Infarction (cont’d)
•Pain—typical is middle of chest, radiating to jaws, arms (usually the left), abdomen, and/or shoulders, and lasting about 20 minutes– Possible to have no pain or atypical
pain (particularly in females) – Sudden onset of pain, not associated
with activity
Signs and Symptoms of Myocardial Infarction
•Tachycardia•Excessive perspiration•Painful breathing and/or difficulty breathing
•Anxiety/panic•Nausea/vomiting•Fever•Stomach pain, often confused with indigestion
Signs and Symptoms of Myocardial Infarction (cont’d)
•Creatinine phosphokinase (CPK):– Not elevated in blood serum, unless
injury has occurred– CPK II is present in heart tissue and is
elevated if MI has occurred
Cardiac Enzymes
•Lactic dehydrogenase (LDH):– LDH I is present in cardiac muscle, and
LDH II is present in the reticuloendothelial system
– Usually LDH I is greater than LDH II, but following a MI, LDH II is greater than LDH I
•Troponin:– Involved in muscle contraction and
released when cells are damaged
Cardiac Enzymes (cont’d)
•If more than 50% of heart tissue is damaged, severe disability or death will result
•Pericarditis may develop up to 2 months later:– Fever– Pericardial effusion– Pleurisy– Pleural effusion– Joint pain
Complications of Myocardial Infarction
•Rupture of heart muscle•Ventricular aneurysm•Blood clots•Hypotension
Complications of Myocardial Infarction (cont’d)
•Antianginals (nitroglycerin)•Analgesics•Stool softener•Electrolyte replacement•Calcium channel-blockers•Beta-blockers•Antihypertensives•Anticoagulants
Treatment Following Myocardial Infarction
•Antiarrhythmics•Thrombolytics•Oxygen•Mild antianxiety agents
Treatment Following Myocardial Infarction (cont’d)
•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
Congestive Heart Failure: An Overview
•MI•Hypertension•Myocarditis•Pulmonary embolism•CAD•Kidney failure•Cardiomyopathies
Causes of Congestive Heart Failure
•Valve disorders•Inflammatory conditions•Water intoxication•Side effects of medicine, such as corticosteroids
Causes of Congestive Heart Failure (cont’d)
•Damage to the heart leads to decreased output and tissue perfusion
•Andrenergic nervous system, renin-angiotensin system, and cytokine system are activated to compensate for the damage
Development of Congestive Heart Failure
•Decreased cardiac output causes release of norepinepherine to increase heart rate and contractility– Causes vasoconstriction– Increases cardiac output
Development of Congestive Heart Failure (cont’d)
•Decreased cardiac output decreases renal perfusion and activation of the renin-angiotensin-aldosterone system– Causes vasoconstriction and leads to
the production of aldosterone and antidiuretic hormone (ADH)
– Aldosterone causes sodium reabsorption and water retention—blood pressure increases
– ADH inhibits water excretion and raises blood pressure
Development of Congestive Heart Failure (cont’d)
•Vasoconstriction causes increased blood return to heart:*– Causing more stretch of the heart
muscle and enlargement of the heart chambers
– Increasing cardiac output in the short term
Development of Congestive Heart Failure (cont’d)
*Frank-Starling law: The greater the stretch of cardiac muscle fibers, the greater the force of contraction.
•Ventricular hypertrophy results from excess fluid and pressure:– First leads to an increase in
contraction– With time, leads to a decrease in
contraction•Increased heart rate leads to ischemia and decreased cardiac output
Development of Congestive Heart Failure (cont’d)
•Beta-receptors in heart become less sensitive to sympathetic-nervous-system stimulation, decreasing heart rate and contractility
•Alpha-receptors on peripheral blood vessels have increased sensitivity:– Promoting vasoconstriction– Increasing cardiac workload
Development of Congestive Heart Failure (cont’d)
•Ventricular dilation leads to ventricular wall thinning, degeneration, and loss of contractility
Development of Congestive Heart Failure (cont’d)
•Systolic dysfunction: – Heart contracts with less force and
can not pump out as much blood to the rest of the body as normal
– Blood accumulates in the ventricles and veins
Types of Congestive Heart Failure
•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
Types of Congestive Heart Failure (cont’d)
•Left sided: – More common– Fluid backs into lungs– Signs and symptoms include:
Types of Congestive Heart Failure (cont’d)
• Fatigue • Coughing• Activity intolerance
• Pulmonary crackles
• Dizziness • Tachycardia• Syncope • urine output• Dyspnea • Shortness of breath
when lying down
•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:
Types of Congestive Heart Failure (cont’d)
• Lower extremity edema in the ambulatory
• Sacral edema in the bedridden
• Liver engorgement and right upper quadrant pain
• Anorexia and nausea• Jugular venous
distension
•Biventricular (signs and symptoms of both left and right heart failure):– Signs and symptoms:
Types of Congestive Heart Failure (cont’d)
• 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
•35%-55% of patients with moderately severe congestive heart failure (CHF) develop cardiac cachexia
•Loss of lean body mass >10% of total weight
•Resultant loss of cardiac muscle mass
•Impaired fat absorption
Cardiac Cachexia
•Many other metabolic changes:– Decreased sodium– Increased catabolic catecholamines– Tumor necrosis factor—causes weight
loss in animals and is increased in CHF patients
Cardiac Cachexia (cont’d)
•Diuretics•Dopamine•Analgesics•Antihypertensives•ACE inhibitors•Direct vasodilators•Antidysrhythmics•Cardiac glycosides (digitalis)•Aldosterone agonists
Treatment of Coronary Heart Disease
•Antibiotics, if necessary•Iron supplementation, if necessary•Supplemental oxygen•Nitrates•Beta blockers•Anticoagulants
Treatment of Coronary Heart Disease (cont’d)
References and Recommended Readings
•Arnold M. Heart failure. In: Merck Manual of Medical Information, Second Home Edition. Whitehouse Station, NJ: Merck Research Laboratories; 2003:150-158.
•Hogan MA, Hill K. Pathophysiology: Reviews and Rationales. Upper Saddle River, NJ: Pearson Education; 2004:43-61.
•Krummel DA. Medical nutrition therapy for heart failure and transplant. In: Mahan LK, Escott-Stump S. Krause’s Food, Nutrition, and Diet Therapy. 11th ed. Philadelphia, PA: WB Saunders; 2004:919-935.
•Krummel DA. Medical nutrition therapy in cardiovascular disease. In: Mahan LK, Escott-Stump S. Krause’s Food, Nutrition, and Diet Therapy. 11th ed. Philadelphia, PA: WB Saunders; 2004:860-899.
•Warnica JW. Coronary artery disease. In: Merck Manual of Medical Information, Second Home Edition. Whitehouse Station, NJ: Merck Research Laboratories; 2003:199-215.