Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
80 Cards in this Set
- Front
- Back
- 3rd side (hint)
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
|
|