Coronary Heart Disease/ Myocardial Infarction Flashcards
Coronary Atherosclerosis
- Atherosclerosis is the abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen
- In coronary atherosclerosis, blockages and narrowing of the coronary vessels reduce blood flow to the myocardium
- Coronary artery disease (CAD) is the most prevalent cardiovascular disease in adults
- Atherosclerosis block and narrow the coronary vessels in a way that reduces blood flow to the myocardium. Atherosclerosis involves a repetitious inflammatory response to INJURY to the vascular endothelium. The endothelium undergoes changes and stops producing the normal antithrombotic and vasodilating agents. The INJURY may be initiated by smoking, HTN, hyperlipidemia, and other factors.
Pathophysiology of Atherosclerosis
- Atherosclerosis begins as monocytes and lipids enter the intima of an injured vessel.
- Smooth muscle cells proliferate within the vessel wall contributing to the development of fatty accumulations and atheroma.
- As the plaque enlarges, the vessel narrows and blood flow decreases.
- The plaque may rupture and a thrombus might form, obstructing blood flow which leads to acute coronary syndrome (ACS) which may result in an acute myocardial infarction (MI).
- When an MI occurs, a portion of the heart muscle no longer receives blood flow and becomes necrotic.
Atherosclerosis Clinical manifestations:
- Symptoms are caused by myocardial ischemia
- Symptoms and complications are related to the location and degree of vessel obstruction
- Angina pectoris (most common manifestation)
- Other symptoms: epigastric distress, pain that radiates to jaw or left arm, SOB, atypical symptoms in women
- Myocardial infarction
- Heart failure
- Sudden cardiac death
- Ischemia is insufficient tissue oxygenation, angina pectoris refers to chest pain that is brought about by myocardial ischemia. Over time, irreversibly damaged myocardium undergoes degeneration and is replaced by scar tissue, causing various degrees of myocardial dysfunction such as low CO and HF. Sudden cardiac death (when the heart abruptly stops beating) can occur from a decrease in blood supply from CAD.
- Atypical symptoms in women include indigestion, nausea, palpitations, and numbness.
Coronary Perfusion
Left Main:
Main branch to all of LV.
Coronary Perfusion
LAD: (widow maker)
Supplies anterior LV, ventricular septum, some RV and papillary muscles of valves. High mortality.
Coronary Perfusion
Left Circumflex:
Lateral wall of LV apex, posterior wall of LV, and LA. In 40 % of population SA node, 12% AV node.
Coronary Perfusion
RCA
Inferior and posterior wall of LV, RV and RA. > 50% of population SA node, > 80% AV node.
Risk factors for Coronary Artery Disease (CAD)
- Four modifiable risk factors cited as major
— cholesterol abnormalities
— tobacco use
— HTN
— diabetes
—- People at the highest risk for having a cardiac event are those with known CAD or those with diabetes, peripheral arterial disease, abdominal aortic aneurysm or carotid artery disease. - The likelihood of having a cardiac event is also affected by factors, such as age, gender, systolic blood pressure, smoking history, level of total cholesterol, and level of high-density lipoprotein (HDL), also known as good cholesterol.
- Elevated LDL: primary target for cholesterol-lowering medication
- Framingham risk calculator
— The Framingham risk calculator is a tool commonly used to estimate the risk for having a cardiac event within the next 10 years for adults 20 years and older. - Metabolic syndrome
— Metabolic syndrome is a cluster of metabolic abnormalities including insulin resistance (fasting plasma glucose >100mg/dL), obesity (waist circumference), dyslipidemia (triglycerides>150, HDL <50 female <40 males), and HTN (BP>130/85) that increases the risk of cardiovascular disease. - hs-CRP (high-sensitivity C-reactive protein)
— CRP is known to be an inflammatory marker for cardiovascular risk, including acute coronary events and stroke. The liver produces CRP in response to a stimulus such as tissue injury, and high levels of this protein may occur in people with diabetes and those who are likely to have an acute coronary event
Prevention of CAD:
- Control cholesterol
- Four elements of fat metabolism: known to affect the development of heart disease.
— total cholesterol
— LDL
— HDL
— triglycerides
— Therapeutic Lifestyle Changes (TLC) diet, a diet low in saturated fat and high in soluble fiber including weight loss, cessation of tobacco use, and increased physical activity. Regular, moderate physical activity increases HDL levels and reduces triglyceride levels, decreasing the incidence of coronary events and reducing overall mortality risk. - Dietary measures
- Physical activity
- Medications
- Cessation of tobacco use
— Nicotinic acid in tobacco triggers the release of catecholamines, which raise HR and BP. Smoking increases the oxidation of LDL, damaging endothelium increasing platelet adhesion leading to thrombus formation. Inhalation of smoke increases the blood carbon monoxide level and decreases the supply of oxygen to the myocardium. - Manage HTN
— HTN is defined as blood measurements that repeatedly exceed 140/90. Long-standing elevated blood pressure may result in increased stiffness of the vessel walls leading to vessel injury and a resulting inflammatory response within the intima. HTN also increases the work of the left ventricle, which must pump harder to eject blood into the arteries. Overtime, increased workload causes the heart to enlarge and thicken and may eventually lead to heart failure. - Control diabetes
— Hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered red blood cell function, which can lead to thrombus formation. These metabolic alterations may impair endothelial cell—dependent vasodilation and smooth muscle function, promoting the development of atherosclerosis.
Cholesterol Medications:
- Six types of lipid-lowering agents: affect the lipid components somewhat differently
- Lipid-lowering medications can reduce CAD mortality in patients with elevated lipid levels and in at-risk patients with normal lipid levels.
- 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) (or statins) – Simvastatin, Atorvastatin
- Nicotinic acids - Niacin, lovastatin
- Fibric acids (or fibrates) -Lopid
- Bile acid sequestrants (or resins) - Questran
- Cholesterol absorption inhibitors - Zetia
- Omega-3 acid-ethyl esters – Fish oil
Angina Pectoris:
- Angina is usually caused by atherosclerotic disease. Almost invariably, angina is associated with a significant obstruction of at least one major coronary artery.
- A syndrome characterized by episodes or paroxysmal pain or pressure in the anterior chest caused by insufficient coronary blood flow
- Physical exertion or emotional stress increases myocardial oxygen demand, and the coronary vessels are unable to supply sufficient blood flow to meet the oxygen demand
- Types of angina
- Refer to Chart 27-2, page 757
Angina Pectoris Assessment Findings:
- May be described as tightness, choking, or a heavy sensation
- Frequently retrosternal (deep in the chest behind the sternum) and may radiate to neck, jaw, shoulders, back or arms (usually left)
- Anxiety frequently accompanies the pain
- Other symptoms may occur: dyspnea or shortness of breath, dizziness, nausea, and vomiting
- The pain of typical angina subsides with rest or nitroglycerin
- Unstable angina is characterized by increased frequency and severity and is not relieved by rest and nitroglycerin. Requires medical intervention!
- The patient with diabetes may not have severe pain with angina because diabetic neuropathy can blunt nociceptor transmission, dulling the perception of pain .
- Several factors are associated with typical angina pain:
- Physical exertion
- Exposure to cold
- Eating a heavy meal
- Stress
Angina Pectoris Gerontologic (Geri) Considerations:
- Diminished pain transition that occurs with aging may affect presentation of symptoms
- “Silent” CAD (no symptoms)
- Teach older adults to recognize their “chest pain–like” symptoms (i.e., weakness, shortness of breath)
- Medications should be used cautiously!
- Pharmacologic stress testing; cardiac catheterization may be used to diagnose CAD in older patients.
- Medications used to manage angina are given cautiously in older adults because they are associated with an increased risk of adverse reactions.
Angina Pectoris Treatment:
- Treatment seeks to decrease myocardial oxygen demand and increase oxygen supply
- Medications
- Oxygen
- Reduce and control risk factors
- Reperfusion therapy may also be done
- Reperfusion therapy involves Percutaneous transluminal coronary angioplasty (PTCA) and stents and CABG.
Angina Pectoris Medications:
Nitroglycerin
Beta-adrenergic blocking agents
Calcium channel blocking agents
Antiplatelet and anticoagulant medications
Aspirin
Clopidogrel and ticlopidine
Heparin
Glycoprotein IIb/IIIa agents
Angina Pectoris Medications:
Nitroglycerin
Nitrates are a standard treatment for angina pectoris. Nitroglycerin is a potent vasodilator that improves blood flow to the heart muscle and relieves pain by vasodilating primarily the veins. Dilation of the veins causes venous pooling of blood throughout the body. As a result, less blood returns to the heart, and filling pressure (preload) is reduced. Nitrates also relax the systemic arteriolar bed, lowering blood pressure and decreasing afterload. These effects decrease myocardial oxygen requirements. See chart 27-3 page 759 for self-administration of Nitroglycerin.
Angina Pectoris Medications:
Beta-adrenergic blocking agents
Beta-blockers reduce myocardial oxygen consumption by blocking beta-adrenergic sympathetic stimulation to the heart. The result is a reduction in heart rate, slowed conduction of impulses through the conduction system, decreased blood pressure, and reduced myocardial contractility (force of contraction). Because of these effects, beta-blockers balance the myocardial oxygen needs (demands) and the amount of oxygen available (supply). This helps control chest pain and delays the onset of ischemia during work or exercise. Beta blockers can mask signs of hypoglycemia and cause bronchoconstriction.
Angina Pectoris Medications:
Calcium channel blocking agents
Calcium channel blocking agents decrease sinoatrial node automaticity and atrioventricular node conduction, resulting in a slower heart rate and a decrease in the strength of myocardial contraction decreasing the workload of the heart. They also increase myocardial oxygen supply by dilating the smooth muscle wall of the coronary arterioles; they decrease myocardial oxygen demand by reducing SVR.
Angina Pectoris Medications:
Antiplatelet and anticoagulant medications
Antiplatelet medications are given to prevent platelet aggregation and subsequent thrombosis, which impedes blood flow through the coronary arteries. Dual antiplatelet therapy is recommended to be continued for 12 months post cardiac event, followed by aspirin monotherapy.
Angina Pectoris Medications:
Aspirin
- STEMI patients: Aspirin plus clopidogrel
- Post PCI with a drug-eluting stent or bare metal stent: Aspirin plus clopidogrel, prasugrel, or ticagrelor
- Patients post CABG – resume treatment prescribed post-surgery
- Aspirin prevents platelet aggregation and reduces the incidence of MI and death in patients with CAD. Because aspirin may cause GI upset and bleeding, the use of histamine-2 (H2) blockers (famotidine) or proton pump inhibitors (Prilosec) should be considered concomitant with continuous aspirin therapy.
Affects of ischemia, injury, infarction on ECG
- T- wave inversion
- Elevated ST segment
T wave inversion
Elevated ST segment
Evolution of ST segment during an MI:
Percutaneous coronary intervention:
- also known coronary angioplasty
- Opens narrowed coronary arteries
- Catheter inserted into your artery in your groin or arm and threaded to the affected artery
- Thin wire is then advanced and passes the site of blockage
- A second smaller catheter is then slid over the wire
- Ballon is then inflated opening the artery, may place permanent stent
Coronary artery bypass grafts:
Greater and lesser saphenous veins are commonly used for bypass graft procedures:
