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80 Cards in this Set

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These are conditions that affect oxygen supply that cause myocardial ischemia
Atherosclerosis, thrombosis, spasm, low diastolic blood pressure, low PaO2, low hemoglobin, tachycardia
Flow (pressure and area), oxygen, time
These are conditions that affect oxygen demand that cause myocardial ischemia
Tachycardia, HTN (leading to increased wall tension), increased preload (pulmonary wedge pressure), increased inotropy (eg, sympathetic response)
These are clinical syndromes causesd by myocardial ischemia
Angina; systolic or dyastolic dysfunction (contractility); heart failure, shock (MI); arrthymias, ST-segment changes (changes in membrane polarity)
This is transient angina brought on by increase in O2 demand with existing fixed coronary obstruction.
Typical angina
This is transient angina brought about most commonly by exercise and anxiety
Typical angina
This is transient angina brought on at rest by a decrease in coronary blood flow
Variant angina (Prinzmetal's)
This is transient angina brought on most commonly by coronary spasm
Variant angina (Prinzmetal's)
These are the factors that cause "unstable" angina to be unstable.
Acute plaque rupture in an artherosclerotic vessel, leading to thrombosis; or factors that increase O2 demand (eg, sudden hypotension and tachycardia as in shock)
These syndromes are caused by decreased coronary blood flow.
Variant angina, acute MI
This syndrome is characterized by pain virtually identical to that experienced in variant angina, but of longer duration.
Acute MI
This is the mechanism of transient LV dysfunction caused by transient ischemia.
Decreased ATP available for contraction and relaxation
Transient vs. persistent LV dysfunction
Persistent LV dysfunction is caused by scarring of tissue caused by a myocardial infarction, which may result in heart failure. Transient LV dysfunction is caused by transient ischemia.
This produces ST-segment shifts
Depolarization of myocardial cell membranes, due to potassium in the extracellular space as a result of tissue damage in myocardial ischemia
These are three clinical syndromes in patients with coronary disease
Chronic coronary disease, acute coronary syndrome, sudden cardiac death
Chronic coronary disease vs. acute coronary syndrome
Stable angina and post-MI are chronic coronary diseases, whereas unstable angina, and NSTEMI and STEMI's constitute acute coronary syndromes.
Definition of NSTEMI
Non-ST-elevation myocardial infarction. Similar to unstable angina, but the ischemia is severe enough to cause MI. Diagnosed by troponin elevation.
Definition of STEMI
ST-elevation MI, caused by acute coronary thrombosis in the coronary lesion, leading to transmural (ST-elevation) ischemia
This is the most common cause of death in patients with coronary disease.
Sudden cardiac arrhytmia leading to ventricular fibrillation (sudden cardiac death).
Levine sign
Clenched fist held against the anterior chest, used by patients to describe angina
T/F: Angina is difficult for patients to localize
True.
This is the most diagnostic feature of angina
Exertional angina (esp. cold weather, after eating, emotional stress) that is relieved by rest.
T/F: Typical angina is unrelated to respiration or position.
True.
Class I severity (dyspnea, angina)
Asymptomatic
Class II severity (dyspnea, angina)
Moderate effort: >2 blocks, >1 flight
Class III severity (dyspnea, angina)
Minimal effort: <2 blocks, <1 flight
Class IV severity (dyspnea, angina)
Symptoms at rest
This is the typical duration of typical angina
2-15 minutes with rest and/or nitroglycerin
Pain lasting less than 30 sec is not angina; pain lasting 1 hr might represent MI, but is not typical angina
These are the three clinical questions used to evaluate chest pain
1) Is the chest discomfort substernal?
2) Are symptoms brought on predictably by exertion?
3) Are symptoms relieved within 30 minutes by rest or nitroglycerin?
These are the three categories of chest pain
1) Definite (or "typical") angina -- all 3 features
2) Probably (or "atypical") angina -- any 2 features
3) Nonanginal pain (none or 1 feature)
These are physical findings suggestive of coronary heart disease
Decreased LV compliance during anginal attack with S4 gallop or murmur of mitral regurgitation; HTN; type A behavior; obesity; hyperlipidemia (arcus senilis, xanthelasma, etc.).
These are nine (9) noncoronary causes of chest pain
Aortic stenosis, hypertrophic cardiomyopathy, aortic dissection, pericarditis, pleural pain, esophageal pain, GI pain, musculoskeletal pain, anxiety-hyperventilation syndrome.
Respirophasic
Describes pain that is worsened by inspiration.
This is the established test for diagnosing coronary artery disease
Coronary arteriography (angiography)
These are some of the problems with coronary arteriography
Observer variability, underestimation of disease, definition of "significant" disease (>70% obstruction), cost, morbidity and mortality (1/1000 death rate; complications: acute MI, cerebral thrombosis, allergic rxn, arterial trauma).
Indications of coronary angiogram
Diagnosis (if hx and noninvasive eval. is inconclusive) and treatment planning (CABG vs. angioplasty)
This is the most common cause of anterior wall transmural ischemia
Occlusion of the LAD
Transient spasm
Variant angina (Prinzmetal's)
Characterization of "pathological Q wave"
0.04 seconds wide, and at least 1/4 the magnitude of the remaining R wave
Transmural infarction
ST-segment depression may indicate these conditions.
Subendocardial ischemia, LVH ("strain pattern"), electrolyte abnormalities (e.g., hypokalemia), hyperventilation syndrome (resp. alkalosis w/ or w/o hypokalemia)
Segment shifts are due to shifts in membrane polarity. NEWLINE NEWLINE Even in LVH, it is because of decreased blood flow to subendocardium leading to some tissue damage releasing K+ into the EC space.
This diagnostic tool is used to detect "hot" and "cold" spots in the myocardium
Myocardial perfusion scan, with IV thallium-201, which acts like potassium
T/F: A "cold" spot in a myocardial perfusion scan denotes absolute decrease in flow
False. It is underperfused, but not necessarily completely cut off.
T/F: A positive thallium scan almost always indicates coronary artery disease
True.
T/F: Electrocardiograms are more specific for coronary disease than thallium scans
False. Thallium scans are more sensitive and specific (90% and 95%) for coronary disease than ECG, since ST-segment depression seen on ECG may be a variety of other conditions
Stress echocardiograms are conducted in this way
Dobutamine is infused, increasing inotropy and heart rate and therefore "exercising" the heart
Submaximal stress test
Patient is stopped at a target HR, marked change in BP, dangerous arrhythmia, extreme ST-segment shift
J-point
Junction between QRS complex and ST-segment
These are the data derived from stress tests
ST-segment shifts, exercise tolerance, HR and BP responses, exercise-induced arrhythmias, "soft" data (symptoms), thallium scan "cold" spots
In a stress test, "shortness of breath" may actually indicate this symptom
Angina
Indications of stress test
Diagnosis (not great, only 70% sensitivity and 85% specificity) and prognosis (better predictor than the severity of angina)
Definition of positive ST-segment depression
Any amount of flat or down-sloping ST-segment depression greater than 1 mm at 0.08 seconds after the J-point
Stress-testing for coronary artery disease is most useful for persons in whom pre-test probability is low, intermediate, or high?
Intermediate. Highs make false negatives likely, and lows make false positives likely.
"met"
A unit of measure of activity in stress tests. 1 "met" is metabolic activity at rest.
This is the classification scheme of exercise tolerance
Poor: inability to exceed 4 mets
Excellent: ability to exceed more than 10 mets
This is how ST-segment depressions are quantified
Depth (1 mm, 2mm, or greater), extent (number of leads it appears in) and duration.
These are criteria for a "markedly positive" stress test
Poor exercise tolerance (<4 mets), extensive ischemia (marked ST-segment depression in many leads), prolonged ST-segment depression, exertional hypotension
Pain is typically maximal at onset and tends to migrate (eg, from anterior chest wall to upper back to lower back)
Aortic dissection
Pain is usually related to respiration and/or position
Pericarditis
Worsened by lying flat, relieved by sitting up
Pain is usually worsened on inspiration
Pericarditis, pleural pain
Pain may be precipitated by swallowing hot or cold liquids
Esophageal pain
Pain is usually more subdiaphragmatic, with radiation through or around back
GI pain
Pain is reproduced by pressing on the chest wall
Musculoskeletal pain
These are the behavorial components of CAD treatment
Exercise (20 min 3 x/week), diet (sat. fat, cholesterol, caloric intake, carb restriction), smoking cessation, counseling to increase compliance with drug therapy
Drug therapy for CAD
Anti-HTN, cholesterol-lowering drugs
These are two effects that statins have
Cholesterol reduction, anti-inflammatory (?)
Types of cholesterol lowering drugs
HMG CoA reductase inhibitors (statins), bile acid sequestrants, nicotinic acid, fibric acids
Side effects of statins
Myopathy, increased liver enzymes
Side effects of bile acid sequestrants
GI distress, constipation, decreased absorption of other drugs
Side effects of nicotinic acid
Flushing, hyperglycemia, hyperuricemia (gout), hepatotoxicity
Side effects of fibric acids
Dyspepsia, gallstones, myopathy
Gemfibrozil
Fibric acid (cholesterol lowering)
Cholestyramine
Bile acid sequestrant (cholesterol lowering)
Colestipol
Bile acid sequestrant (cholesterol lowering)
Statins
HMG CoA reductase inhibotors (cholesterol lowering)
Mechanism and side effects of nitrates
Venodilation lowers preload and therefore also O2 demand; coronary artery dilation increase O2 supply; hypotension can cause reflex tachycardia; headaches
Includes nitroglycerin and isosorbide dinitrate
Mechanism and side effects of beta-blockers
Reduces HR and BP and therefore also O2 demand; side effects include HF, bradyarrhythmias, fatigue, depression
Includes propranolol, metoprolol, atenolol
Mechanism and side effects of calcium channel blockers
Prevents spasm to increase O2 supply (useful against variant angina); verapamil and diltiazem reduce HR, BP and inotropy to decrease O2 demand; side effects include headache and edema
Includes verapamil, diltiazem, nifedipine, amlodipine
Mechanism and side effects of late Na channel blockers
Indirect Ca channel blocker--decreases Na influx into ischemic cells, thereby reducing Ca uptake via the Na/Ca exchanger; similar to verapamil and diltiazem
Includes ranolazine
Survival benefit of CABG has been demonstrated for these two subgroups
1) Patients with left main coronary disease
2) Patients with 3-vessel disease and poor LV function
Risks and side effects of CABG
1% to 5-10% mortaility depending on LV function; acute MI, infections, arrhythmias, mental deterioration
PTCA / PCI
Percutaneous transluminal angioplasty/coronary intervention