Term
|
Definition
| plaque formation on the inner wall of the artery. Forms a layer of scar tissue that progressively increases, occluding the lumen of the artery |
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|
Term
| what is the most commonsite of atherosclerosis |
|
Definition
|
|
Term
| what is the second most common target site of atherosclerosis |
|
Definition
|
|
Term
| what is the 3rd most common site of atherosclerosis |
|
Definition
|
|
Term
| what is the 4th most common site of atherosclerosis |
|
Definition
| aorta and associated peripheral vessels |
|
|
Term
| how can arterial spasm affect plaque in the arteries |
|
Definition
| arterial spasms may cause acute changes/symptoms as plaque breaks off |
|
|
Term
| how can acute increase in BP from exercise or anxiety affect plaque |
|
Definition
| causes shearing forces on plaque, leading to breaking off of plaque into the arteries |
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|
Term
|
Definition
|
|
Term
| what do we call documented arterial disease |
|
Definition
|
|
Term
| about how much of the artery must be stenosed before signs and symptoms occur |
|
Definition
|
|
Term
| what is the gold standard test for documenting that there is arterial disease/coronary artery disease |
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Definition
|
|
Term
| in coronary artery disease, what do clinical signs and symptoms indicate |
|
Definition
|
|
Term
| how is myocardial ischemia experiencec |
|
Definition
|
|
Term
| what are the 2 types of angina |
|
Definition
|
|
Term
| which type of angina occurs at a predictable heart rate or workload |
|
Definition
|
|
Term
| which type of angina occurs at unpredictable heart rates or workloads |
|
Definition
|
|
Term
| which type of angina is identified through stress testing and is maximally medically treated with cardiac meds |
|
Definition
|
|
Term
| which type of angina is not maximally medically controlled or treated |
|
Definition
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|
Term
| which type of angina will be documented in a patient's medical record |
|
Definition
|
|
Term
| which type of angina may or may not be documented in a patient's medical record |
|
Definition
|
|
Term
| for which type of angina can a patient take NTG if it has been prescribed |
|
Definition
|
|
Term
| if the patient has been prescribed NTG, what should we do as PTs |
|
Definition
| be sure they have it with them and that it is not expired and tell them to bring it with them to every treatment |
|
|
Term
| patients with which type of angina are candidates for cardiac rehab and exercise training |
|
Definition
|
|
Term
|
Definition
| ischemia in the heart muscle when the artery is more than 70% blocked. |
|
|
Term
| why is there referred pain in angina |
|
Definition
| autonomic and systemic nerve plexus integration for the heart muscle |
|
|
Term
| are patients with unstable angina candidates for cardiac rehab or exercise training? |
|
Definition
|
|
Term
| what should you do if a patient has angina and it is not documented as stable angina |
|
Definition
| thoroughly document the note and refer her back to her physician |
|
|
Term
| what is the difference between MI and angina (list descriptions of MI) |
|
Definition
| MI is partial or complete blockage of coronary artery. Irreversible damage occurs. Chest pressure/pain lasts hours (not minutes) and is not relieved by nitroglycerin or rest. The evolution of damage is ischemia, injury, infarct. Diagnosed with EKG and enzymes in blood |
|
|
Term
| what is the difference between MI and angina (list descriptions of angina) |
|
Definition
| pain lasts a matter of minutes. Pain relieved by nitroglycerin and/or rest. Cell death (infarction) does not occur. If chronic stable angina, it is evoked by increased myocardial demand at established level of onset. If unstable angina, it's not associated with demand and is unpredictable |
|
|
Term
| if a patient gets angina at 108 HR, what HR should you exercise them at? |
|
Definition
|
|
Term
| when a patient having a myocardial infarction first presents with ischemia, what are the clinical signs |
|
Definition
| ST segment depression or downsloping. May represent clinically as angina |
|
|
Term
| is the initial ischemic part of MI reversible, or does it cause damage? |
|
Definition
|
|
Term
| when does injury occur in an MI |
|
Definition
|
|
Term
| what happens in the injury phase of an MI |
|
Definition
| the infarction has happened and the heart goes into a healing phase |
|
|
Term
| is there permanent myocardial damage in the injury phase of a heart attack |
|
Definition
|
|
Term
| is the injury phase of an MI reversible |
|
Definition
|
|
Term
| how does the ST segment change on an EKG in the injury portion of an MI |
|
Definition
|
|
Term
| how do T waves appear during the injury phase of an MI on an EKG |
|
Definition
|
|
Term
| how do we know that a patient is in the injury phase of an MI |
|
Definition
| changes in blood enzyme levels |
|
|
Term
| what 3 enzymes have elevated levels in the injury phase of an MI |
|
Definition
|
|
Term
|
Definition
|
|
Term
| when does CPK increase following MI |
|
Definition
| increases within 3-6 hours, normalizes in 3 days |
|
|
Term
|
Definition
|
|
Term
| when are LDH levels in the blood elevated following MI |
|
Definition
| peaks within 48-72 hours, remaind elevated for 11 days |
|
|
Term
| why are there elevated plasma concentrations of troponins T and I following MI |
|
Definition
| they are muscle proteins released by damaged myocardial cells |
|
|
Term
| how does the EKG wave change following infarction |
|
Definition
|
|
Term
| when does the Q wave of an EKG change (how long after infarction) |
|
Definition
|
|
Term
| how can you tell from an EKG that a patient has had an MI at some point in the past |
|
Definition
| significant Q waves remain forever on the EKG |
|
|
Term
| what determines the seriousness of an MI |
|
Definition
| depends on where the damage occurs |
|
|
Term
| how do EKGs point to the area of the MI |
|
Definition
| there are 12 leads that we can see from doing a complete EKG. On certain leads, if we see abnormalities on the EKG, that points to locations of the MI |
|
|
Term
| if the leads affected are V2, V2, where is the MI |
|
Definition
|
|
Term
| if the leads affected are V1-4, where is the MI |
|
Definition
|
|
Term
| if the leads affected are II, III, aVF, where is the MI |
|
Definition
|
|
Term
| if the leads affected are I, aVL, where is the MI |
|
Definition
|
|
Term
| which MI location is the least clinically significant |
|
Definition
|
|
Term
| what is at the inferior part of the heart |
|
Definition
| apex, bottom of right ventricle |
|
|
Term
| which MI location is moderately signficatn |
|
Definition
|
|
Term
| what does partial thickness MI mean |
|
Definition
| the MI goes partially through the thickness of the heart muscle |
|
|
Term
| what is the most serious type of MI |
|
Definition
|
|
Term
| where is a transmural MI/what part of the heart does it go through |
|
Definition
| transmural goes through entire thickness of the heart muscle from epicardium to endocardium |
|
|
Term
| what is a subendocardial MI and what are the outcomes |
|
Definition
| subendocardial affects the inner surface of the heart muscle. Ominous outcomes |
|
|
Term
|
Definition
| patient doesn't know they had a heart attack |
|
|
Term
| in what populatoin are silent Mis common |
|
Definition
|
|
Term
| what is usually the outcome of a silent MI |
|
Definition
|
|
Term
| what factors predispose MI by increasing myocardial demand |
|
Definition
| anything that increases HR, contractility, myocardial wall tension such as: heat, cold, shock, hypoxia, stress, fear, exercise, ischemia, arrhythmias, etc. in the setting of atherosclerosis and risk factors |
|
|
Term
| what are major risk factors for coronary artery disease |
|
Definition
| hypertension, tobacco smoking, dyslipidemia, sedentary lifestyle, obesity |
|
|
Term
| what are contributing risk factors for CAD |
|
Definition
| diabetes, family history, age, gender, stress, metabolic syndrome, ETOH abuse, cocaine use, C-reactive protein, homocysteine |
|
|
Term
| what are C-reactive protien and homycysteine |
|
Definition
| enzymes in the body that are connected to heart disease and pulmonary disease |
|
|
Term
| what are modifiable risk factors for CAD |
|
Definition
| hypertension, tobacco smoking, obesity, sedentary lifestyle, excessive emotional stress, dyslipedmia, diabetes, stress, metabolic syndrome |
|
|
Term
| what are nonmodifiable risk factors for CAD |
|
Definition
| age, gender, family history |
|
|
Term
| what are signs/symptoms of metabolic syndrome |
|
Definition
| increased waist circumference, elevated triglycerides, reduced HDL, high blood pressure, high fasting glucose |
|
|
Term
| how does exercise affect the risk of MI |
|
Definition
| exercise temporarily increases myocardial demand, therefore there is a transient increased risk of MI during exercise. The more fit, the less risk of event even during exercise. decreased risk of MI at all other times if you exercise regularly. |
|
|
Term
| how does exercise affect SBP and DBP |
|
Definition
| decreases resting SBP and DBP |
|
|
Term
| how does exercise affect HDL cholesterol |
|
Definition
|
|
Term
| how does exercise affect LDL |
|
Definition
|
|
Term
| how does exercise affect total cholesterol |
|
Definition
|
|
Term
| how does exercise affect triglycerides |
|
Definition
|
|
Term
| how does exercise affect blood glucose |
|
Definition
|
|
Term
| how does exercise affect platelet aggregability |
|
Definition
|
|
Term
| how does exercise affect body fat |
|
Definition
|
|
Term
| what is the medical management summary for an MI |
|
Definition
| control pain of angina; mechanical opening of vessel/return of blood flow; decrease platelet adhesion/aggregation; anticoagulants; lipid lowering drugs; manage blood pressure; acutely administer oxygen, thrombolytics |
|
|
Term
| what are new horizons for preventing MI |
|
Definition
| prevention measures, stricter cholesterol and BP guidelines, aggressive drug therapy for BP and cholesterol, increased drug therapy to decrease platelet adhesion and/or decrease risk of re-occlusion; diet/exercise; stem cell, genomic research |
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