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62 Cards in this Set
- Front
- Back
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Risk factors for stable angina |
HTN, DM, hyperlipidemia, smoking, age (men >45, women >55), fmh of CAD or MI, obesity |
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Etiology of stable angina |
Fixed atherosclerotic lesions of major coronary arteries. Occurs when oxygen demand exceeds the available blood supply |
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Possible presentations of CAD |
Asymptomatic, stable or unstable angina, MI, or sudden cardiac death |
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Target lipid levels |
LDL < 100 HDL > 40 Total < 200 Triglycerides < 150 |
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Presentation of stable angina |
Chest pain/substernal pressure lasting < 10-15 min. Brought on by exertion, relieved with rest or nitroglycerin. NOT present: pain that changes w position or breathing, chest wall tenderness |
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Physical exam of CAD pt |
Usually normal |
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Dx for CAD |
Resting ekg, stress ekg, stress echo, pharmacologic stress test if pt cannot exercise (dobutamine), holter monitor, cardiac cath (most accurate to make cardiac dx) w coronary angiography (most accurate to identify CAD) |
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Resting ekg for CAD abnormalities |
Normal in pts w stable angina. inverted T waves if prior MI/ischemia. ST segment or T wave abnormalities-- treat as unstable angina Q wave is NSTEMI |
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Stress ekg for CAD |
pt must be able to exercise reaching 85% of max heart rate (220-age) Positive stress test if ST segment depression, chest pain, hypotension, or significant arrhythmias. |
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Stress echo for CAD |
Akinesis or dyskinesis with exercise that is not present at rest. |
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Pts with positive stress test; what next? |
Cardiac catheterization |
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Pharmacologic stress test for CAD |
Done if pt cannot exercise. IV adenosine, dipyridamole, or dobutamine is used |
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Holler monitor for CAD |
Continuous ekg over 24-72 hours. Can see ekg changes not accompanied by sx |
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Coronary angiography indication |
Best test for CAD. To identify severity to determine if revascularization with PCI is needed. Significant if coronary stenosis is >70% |
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When is a CABG needed for CAD pt? |
If CAD is severe: left main or 3 vessel disease |
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Tx for risk factors for CAD |
Smoking cessation, htn control (<130/80), hyperlipidemia control (LDL<70), glycemic control in diabetics (A1c <7%), weight loss in obese pts, exercise and diet (low sat fat) |
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Standard medical tx for stable angina |
Aspirin- decreases morbidity Beta-blocker (atenolol or metoprolol)- reduces HR, BP, and contractility Nitrates for chest pain- cause generalized vasodilation May use cc blocker if bblocker and nitrates are not fully effective |
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Side effects of nitrates |
HA, orthostatic hypotension, tolerance, syncope |
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Path of unstable angina |
Blood supply is decreased secondary to reduced resting coronary flow. Oxygen demand is unchanged |
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Unstable angina presentation |
Pts with chronic angina with increased frequency, duration, or intensity of chest pain. Pts with angina at rest |
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Difference between unstable angina and NSTEMI |
Based entirely on cardiac enzymes. NSTEMI will have elevated troponins a or CK-MB |
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Dx for unstable angina |
Same as for stable angina except these Pts have higher risk for adverse events during stress testing. Should be stabilized medically before initiating or should have cardiac cath. Perform MI work up in all pts |
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Unstable angina medical management |
Hospital admission for continuous cardiac monitoring. B-blockers and nitrates are 1st line therapy. Aspirin and clopidogrel for 9-12 months. Low molecular weight heparin for 2 days (enoxaparin) More than 90% of these pts improve with this medical regimen. |
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Unstable angina surgical tx |
Done if medical therapy fails or if ekg shows ischemia that persists after 48 hours. Will have PCI done. |
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Unstable angina surgical tx |
Done if medical therapy fails or if ekg shows ischemia that persists after 48 hours. Will have PCI done. |
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Management of unstable angina after stabilized in the hospital |
Continue aspirin, B-blocker, and nitrates. Reduce risk factors same as for stable angina. |
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Hallmark of prinzmetal angina |
Transient ST segment elevation on ekg during chest pain, representing transmural ischemia |
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Definitive test for prinzmetal angina |
Coronary angiography-- displays coronary vasospasm when the pt is given IV ergonovine |
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Prinzmetal angina tx |
CC blockers and nitrates Risk factor modification like smoking cessation and lipid lowering |
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Presentation of prinzmetal angina |
Chest pain at rest associated with ventricular dysrhythmias. Classically occurs at night |
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Most common type of cardiomyopathy |
Dilated cardiomyopathy |
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Path of dilated cardiomyopathy |
Some type of insult (ischemia, infection, alcohol) causes dysfunction of left ventricular contractility |
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Etiology of Dilated cardiomyopathy |
50% are idiopathic Other causes are: CAD (w prior MI), alcohol, doxorubicin, thiamine or selenium deficiency, thyroid disease, hypophosphatemia, uremia, SLE, scleroderma, prolonged uncontrolled tachycardia, pheochromocytoma, cocaine, genetic |
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Presentation of dilated cardiomyopathy |
S/sx of left and right sided heart failure S3, S4, and murmurs of mitral or tricuspid insufficiency may be present Cardiomegaly Sudden death |
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Dx of dilated cardiomyopathy |
Consistent with CHF EKG--nonspecific but can detect ischemia or prior MI CXR--Kerley B lines, cardiomegaly, prominent interstitial markings, pleural effusion. Echo--increased ventricular volume/chamber dilation, decreased (<45%) ejection fraction |
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Tx of risk factors for dilated cardiomyopathy |
Remove offending agent if applicable. Risk factor modification: sodium <4g/day, weight loss, smoking cessation, restrict alcohol, exercise. |
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Medical tx for dilated cardiomyopathy |
Digoxin, diuretics, vasodilators (ACE inhibitors or ARBs, beta-blockers) Anticoagulation due to increased risk of embolization (especially if pt also has A fib) |
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Etiology of hypertrophic cariomyopathy |
Most are inherited (autosomal dominant). Some cases are from spontaneous mutations. |
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Path of hypertrophic cardiomyopathy |
Diastolic dysfunction is due to a stiff, hypertrophied ventricle w elevated diastolic filling pressures. Pressures increase with things that increase HR and contractility (exercise) or decrease left ventricular filling (valsalva). |
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Valsalva maneuvers |
gagging, holding your breath, bearing down, coughing, immersing face in cold water. |
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Symptoms of hypertrophic cardiomyopathy |
dyspnea on exertion, chest pain, syncope or dizziness after valsalva, palpitations, arrhythmias, cardiac failure, sudden death.
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Physical exam of hypertrophic cardiomyopathy |
Sustained PMI, loud S4. systolic ejection murmur, harsh crescendo-decrescendo (best heard at LLSB, decreases w squatting or lying down or sustained handgrip, increases with valsalva and standing)-- sounds like aortic stenosis |
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Dx of hypertrophic cardiomyopathy |
EKG may show LVH w strain, prominent Q waves, left atrial enlargement, and left axis deviation. Echo: asymmetric septal hypertrophy, RV hypertrophy, outflow obstruction. Clinical dx w FMH |
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Difference between hypertrophic cardiomyopathy and aortic stenosis |
Pulse of AS has low amplitude, it is brisk with HCM. Ejection click and aortic regurg are more common with AS, not typically seen with HCM. AS murmur decreases with valsalva, but increases in HCM. |
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Tx for hypertrophic cardiomyopathy |
If asx, no tx typically necessary, avoid strenuous exercise and dehydration Symptomatic: B-blocker, CC-blocker if b-blocker not effective. diuretics if fluid retention. Severe: myomectomy (excision of part of myocardial septum) |
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Restrictive cardiomyopathy path |
infiltration of the myocardium results in impaired diastolic ventricular filling due to decreased ventricular compliance.
less common than dilated and hypertrophic cardiomyopathy |
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Etiology of restrictive cardiomyopathy |
amyloidosis sarcoidosis hemochromatosis scleroderma carcinoid syndrome chemo or radiation induced idiopathic |
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Presentation of restrictive cardiomyopathy |
dyspnea and exercise intolerance d/t elevated filling pressures. Right sided signs and symptoms (peripheral edema--ascites, hepatomegaly) |
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Dx of restrictive cardiomyopathy |
Echo: thickened myocardium w systolic ventricular dysfunction. increased size of R and L atrium, normal LV and RV. EKG may show low voltages or conduction abnormalities, arrhythmias, A fib. Endomyocardial bx may be diagnostic |
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Tx of restrictive cardiomyopathy |
Treat underlying cause: Hemochromatosis--phlebotomy or deferoxamine. Sarcoidosis--glucocorticoids Amyloidosis--no tx available.
Give Digoxin if systolic dysfunction is present (but not w amyloidosis)
Diuretics tx sx, but may lead to decreased cardiac output (fatigue, lightheadedness)
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Path/etiology of MI |
Thrombotic occlusion of a coronary artery, which interrupts the blood supply, causing necrosis of myocardium.
Mortality rate is 30%
These pts typically have history of angina, CAD risk factors, or hx of arrhythmias |
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Risk factors for MI |
Age (men over 45, women over 55) Smoking HTN and hypercholesterolemia DM FMH of MI Sedentary lifestyle/obesity Stress Hx of preeclampsia or autoimmune condition
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Presentation of acute MI |
Chest pain that is heavy, squeezing, or crushing. -can radiate to the left arm, or other places. -pain can go up to occipital area, but not below the umbilicus. Weakness, sweating, N/V, anxiety, sense of impending doom. |
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Dx for STEMI |
EKG: Peaked T waves early ST segment elevation Q waves late T wave inversion
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Location of MI based on Leads showing st elevation on EKG + related artery |
Inferior: II, III, AVF -- Post. Descending artery Anterior: V1-V6 -- LAD, R coronary Lateral: I, AVL -- L circumflex Posterior: V1-V2 -- R coronary, L circumflex |
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EKG for NSTEMI |
May show no changes or ST depression, T wave flattening or T wave inversion. |
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Cardiac biomarkers for MI |
CK-MB: elevated 6-12 hours after onset, peak around 18-24 hours. Troponins I + T: detectable 4-6 hours after onset, peaks, then falls to lower levels for 5-7 days. |
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Prehospital MI tx |
Aspirin 162-325mg immediately Sublingual nitroglycerin |
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ER management of MI |
M: Morphine, if active chest pain O: Oxygen 2-4 L/min N: Nitroglycerin, if not already given A: Aspirin, if not already given B: Beta blocker, unless hypotension, bradycardia, or asthma A: Ace inhibitor w/in 24 hours S: Statin soon after, and indefinitely H: Heparin x48 hours |
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Definitive tx of MI |
If w/in first 1-3 hours--fibrinolysis After, tx of choice is PCI w stenting |
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#1 risk factor for acute MI |
DM, risk is same as someone without DM with previous MI |
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what to not use in a pt with kidney stones (calcium) |
Loops |
