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83 Cards in this Set
- Front
- Back
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Definition of Atherosclerosis
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Formation of fibrofatty lesions in the intimal lining of the large and medium-sized arteries
-Aorta and its branches -Coronary arteries -Large vessels that supply the brain |
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Definition of Coronary Heart Disease
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Blockages of coronary arteries by atherosclerosis
Ischemic heart disease (IHD) is the primary etiology of CHD |
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Definition of Ischemic heart disease
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Disorders of myocardial blood flow due to stable or unstable coronary atherosclerotic plaques
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Chronic IHD
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-Treated outpatient
-Chronic stable angina -Variant angina (Prinzmetal's angina) -Silent myocardial ischemia |
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Acute coronary syndrom (ACS)
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Head to hospital
Non-ST-segment elevation ACS (NTSE ACS) -Unstable angina -NSTE MI ST-segment elevation MI (STE MI) |
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Development of Atherosclerosis involves:
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-Fatty Streaks
-Fibrous atheromatous plaque -Complicated lesion |
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Fatty Streaks
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-Yellow, intimal discolorations that progressively enlarge by becoming thicker and slightly elevated as they grow in length
-Consist of macrophages and smooth muscle cells that become distended with lipid to form foam cells -Can occur as early as first decade of life -Can be genetic |
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Fibrous Atheromatous Plaque
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Accumulation of intracellular and extracellular lipid layers
Proliferation of vascular smooth muscle cells Formation of scar tissue Leads to elevated thickening of vessel intima |
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Complicated lesion
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Rupture/ulceration of plaque occurs --> Thrombus formation
-Occurs in ACS only!! -Plaque is stable (does NOT rupture) in stable angina |
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Plaque Vulnerability
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Determinants of plaque vulnerability to rupture
-Size and consistency of lipid-rick atheromatous core --Larger lipid cores within plaque increase risk of rupture --More solid consistency (calcification) stabilizes plaque decreases risk of rupture -Tickness of fibrous cap covering the core --Thin fibrous cap increases risk of rupture -Ongoing inflammation and repair withing the cap --Increased inflammation (increased macrophages and lymphocytes) increases risk of rupture -eccentric shape increases risk of rupture |
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Triggers of Plaque Rupture
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May occur spontaneously
Other factors that may serve as triggers: -Increased BP --> increased shear force -Increased force of cardiac contraction -Increased coronary blood flow Plaque rupture precipitates thrombus formation |
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Thrombus Formation
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Forms on top of ruptured plaque
Tissue factor in rupture plaque activates extrinsic coagulation pathway -Formation of thrombin --> fibrin Plates also play an important role -Adhesion to disrupted endothelium -Activation of surrounding platelets -Aggregation - linking of platelets |
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White clot
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Contains more platelets than fibrin
-Typically occurs in NSTE ACS --usually produces incomplete occlusion of coronary lumen |
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Red clot
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Contains more fibrin and red blood cells than platelets
-Fibrin stabilize clots and trap red blood cells giving a "red" appearance -Typically occurs in STE MI - Usually produces complete occlusion of coronary lumen |
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Myocardial Ischemia
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Inadequate supply of O2 to meet myocardial O2 demand (MVO2)
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Myocardial Infarction
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Results from persistent ischemia or from complete occlusion of a coronary artery
Effect on myocardium -Necrotic (nonviable) -Often dysfunctional --Often leads to heart failure |
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Major determinants of MVO2
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Heart rate (chronotropy)
-Direct relationship Myocardial contractility (inotropy) -Direct relationship Intramyocardial wall tension |
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Intramyocardial wall tension
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Intraventricular pressure, left ventricular (LV) radius (direct relationship)
-Increase BP or LV dilation --> Increase wall tension --> Increase oxygen demand Ventricular wall thickness (indirect relationship) -LV hypertrophy --> decrease wall tension --> decrease oxygen demand |
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Myocardial Ischemia
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Inadequate supply of O2 to meet myocardial O2 demand (MVO2)
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Arteriolar resistance
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increase resistance --> decrease coronary blood flow
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Myocardial Infarction
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Results from persistent ischemia or from complete occlusion of a coronary artery
Effect on myocardium -Necrotic (nonviable) -Often dysfunctional --Often leads to heart failure |
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Coronary perfusion pressure
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increase perfusion pressure --> increase coronary blood flow
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Major determinants of MVO2
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Heart rate (chronotropy)
-Direct relationship Myocardial contractility (inotropy) -Direct relationship Intramyocardial wall tension |
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the widow maker
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left main coronary artery
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Myocardial Ischemia
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Inadequate supply of O2 to meet myocardial O2 demand (MVO2)
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Intramyocardial wall tension
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Intraventricular pressure, left ventricular (LV) radius (direct relationship)
-Increase BP or LV dilation --> Increase wall tension --> Increase oxygen demand Ventricular wall thickness (indirect relationship) -LV hypertrophy --> decrease wall tension --> decrease oxygen demand |
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Arteriolar resistance
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increase resistance --> decrease coronary blood flow
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artery which travels to behind the heart
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circumflex artery
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Myocardial Infarction
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Results from persistent ischemia or from complete occlusion of a coronary artery
Effect on myocardium -Necrotic (nonviable) -Often dysfunctional --Often leads to heart failure |
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Major determinants of MVO2
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Heart rate (chronotropy)
-Direct relationship Myocardial contractility (inotropy) -Direct relationship Intramyocardial wall tension |
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artery which travels to the bottom of the heart
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diagonal branch
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Intramyocardial wall tension
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Intraventricular pressure, left ventricular (LV) radius (direct relationship)
-Increase BP or LV dilation --> Increase wall tension --> Increase oxygen demand Ventricular wall thickness (indirect relationship) -LV hypertrophy --> decrease wall tension --> decrease oxygen demand |
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Coronary perfusion pressure
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increase perfusion pressure --> increase coronary blood flow
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Myocardial Ischemia
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Inadequate supply of O2 to meet myocardial O2 demand (MVO2)
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Nonmodifiable Risk Factors
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Age
-Men >= 45 yr -Women >= 55 yr Family history of premature CAD -Includes history of MI or sudden death -Father or 1st degree male relative < 55 yr -Mother or 1st degree male relative < 65 yr |
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Arteriolar resistance
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increase resistance --> decrease coronary blood flow
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the widow maker
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left main coronary artery
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Myocardial Infarction
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Results from persistent ischemia or from complete occlusion of a coronary artery
Effect on myocardium -Necrotic (nonviable) -Often dysfunctional --Often leads to heart failure |
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Myocardial Ischemia
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Inadequate supply of O2 to meet myocardial O2 demand (MVO2)
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artery which travels to behind the heart
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circumflex artery
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Coronary perfusion pressure
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increase perfusion pressure --> increase coronary blood flow
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Major determinants of MVO2
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Heart rate (chronotropy)
-Direct relationship Myocardial contractility (inotropy) -Direct relationship Intramyocardial wall tension |
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artery which travels to the bottom of the heart
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diagonal branch
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the widow maker
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left main coronary artery
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Myocardial Infarction
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Results from persistent ischemia or from complete occlusion of a coronary artery
Effect on myocardium -Necrotic (nonviable) -Often dysfunctional --Often leads to heart failure |
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Intramyocardial wall tension
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Intraventricular pressure, left ventricular (LV) radius (direct relationship)
-Increase BP or LV dilation --> Increase wall tension --> Increase oxygen demand Ventricular wall thickness (indirect relationship) -LV hypertrophy --> decrease wall tension --> decrease oxygen demand |
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Arteriolar resistance
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increase resistance --> decrease coronary blood flow
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artery which travels to behind the heart
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circumflex artery
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Major determinants of MVO2
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Heart rate (chronotropy)
-Direct relationship Myocardial contractility (inotropy) -Direct relationship Intramyocardial wall tension |
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Coronary perfusion pressure
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increase perfusion pressure --> increase coronary blood flow
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Nonmodifiable Risk Factors
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Age
-Men >= 45 yr -Women >= 55 yr Family history of premature CAD -Includes history of MI or sudden death -Father or 1st degree male relative < 55 yr -Mother or 1st degree male relative < 65 yr |
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the widow maker
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left main coronary artery
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Intramyocardial wall tension
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Intraventricular pressure, left ventricular (LV) radius (direct relationship)
-Increase BP or LV dilation --> Increase wall tension --> Increase oxygen demand Ventricular wall thickness (indirect relationship) -LV hypertrophy --> decrease wall tension --> decrease oxygen demand |
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artery which travels to the bottom of the heart
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diagonal branch
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Arteriolar resistance
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increase resistance --> decrease coronary blood flow
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Nonmodifiable Risk Factors
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Age
-Men >= 45 yr -Women >= 55 yr Family history of premature CAD -Includes history of MI or sudden death -Father or 1st degree male relative < 55 yr -Mother or 1st degree male relative < 65 yr |
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artery which travels to behind the heart
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circumflex artery
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artery which travels to the bottom of the heart
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diagonal branch
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Nonmodifiable Risk Factors
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Age
-Men >= 45 yr -Women >= 55 yr Family history of premature CAD -Includes history of MI or sudden death -Father or 1st degree male relative < 55 yr -Mother or 1st degree male relative < 65 yr |
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Modifiable Risk Factors
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Smoking
Hypertension Dyslipidemias Diabetes mellitus Obesity Sedentary lifestyle CRP lipoprotein (a) homocysteine CKD |
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CRP
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increased C-reactive protein = serum marker for systemic inflammation
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lipoprotein (a)
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genetically determined
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homocysteine
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associated with decreased vitamin b6, b12, and folate
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What is Angina??
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Symptomatic paroxysmal chest pain or pressure sensation caused by transient myocardial ischemia
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Quality of pain
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-Heavy, squeezing, tightness, crushing, burning
-May be mistaken for indigestion -Chest "pressure" or "discomfort" -Not sharp or stabbing -Does not change with position -No relationship between severity and extent of CAD |
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Location of pain
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Usually substernal or retrosternal
Can also occur in: -Epigastrium -Neck -Shoulders -Back -Arms -Jaw |
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Radiation of chest pain and duration
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-Arms
-Shoulders -Jaw -Neck Duration = 3-5 mins |
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Precipitating factors
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-Physical activity
-Emotional distress -Cold weather -Smoking -Large meals |
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Relieving factors
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-Rest
-Sublingual nitroglycerin (SLNTG) --Within 30 seconds to 5 minutes |
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Anginal equaivalents
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May occur in absence of discomfort
-Dyspnea -Fatigue -Weakness -syncope commonly occur in women |
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Chronic Stable Angina
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Provoked by exertion or emotional stress
-Associated with certain level of physical activity Reproducible Pain is at constant level of intensity Promptly relieved with rest or nitroglycerin Caused by fixed obstruction in coronary artery that causes ischemia -the majority of patients with chronic stable angina have atherosclerotic heart disease; however, not all patients with AHD develop angina |
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Variant Angina
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Also known as Prinzmetal's angina or vasospastic angina
Coronary artery spasm = decreased blood flow Patients may or may not have underlying atherosclerotic disease Characteristics of chest pain: -Occurs at night or in early morning -Occurs at rest --Not precipitated by exertion or stress |
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Potential mechanism for vasospasm
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Hyperactive sympathetic nervous system
Defect in handling of calcium in vascular smooth muscle Alteration in nitric oxide production Imbalance between endothelium derived relaxation and contracting factors |
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Silent Myocardial Ischemia
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Ischemia is present, but anginal pain does NOT occur
Patients typically have: -Altered pain threshold -autonomic neuropathy Can occur in: -Elderly -Diabetics |
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Differential Diagnosis
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Pericarditis - stabbing chest pain
Esophageal reflux/peptic ulcer disease Aortic dissection - Ripping apart Pulmonary embolism - more like dyspnea Biliary disease Musculoskeletal disease - positional pain |
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ECG Findings
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Resting ECG normal in >= 50%
Variant angina --> ST-segment elevation Silent ischemia --> ST-segment depression or elevation Significant ischemia >= 2 mm ST-segment depression |
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Stress testing
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Types:
ETT, pharmacologic Monitor blood pressure and ECG pattern during test Can predict risk for future cardiac events and mortaility cannot determine location of obstruction usually used in conjunction with nuclear imaging |
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ETT
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PTs walk on treadmill with progressive evelation and speed
Adverse predictors -Poor exercise capacity -Exercise-induced angina -ECG finding >= 1 mm ST-segment depression -Ventricular arrhythmias |
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Pharmacologic Stress Testing
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Pharmacolgic agents used to induce "stress" to the heart
-Dipyridamole -Adenosine -Dobutamine |
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Nuclear Imaging
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Used with stress testing to help localize the area of ischemia
Patients injected with radionuclide tracers to isolate the area of ischemia Imaging then performed on 2 occasions -After exercise -At rest Looking for "cold spots" -If appear after exercise and then disappear with rest --> reversible ischemia -If appear after both --> irreversible ischemia |
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Echocardiography
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Ultrasound of the heart
Two types: =Transesophogeal echocardiography (invasive) =transthoracic echocardiography (less invasive) |
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Coronary Angiography
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"Gold standard"= used to assess presence and severity of CAD
Steps: 1)cardiac catheterizartion 2)coronary angiography Significant CAD: - >= 70% stenosis or >= 1major epicardial artery segment - >= 50% stenosis of left main coronary artery |
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Acute Coronary Syndrome
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Results primarily from diminished myocardial blood flow secondary to completely occlusive or partially occlusive coronary artery thrombus
-Due to plaque rupture |
