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114 Cards in this Set
- Front
- Back
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What causes an acute coronary syndrome?
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erosion or rupture of an atherosclerotic plaque with subsequent platelet adherence, activation, aggregation, and activation of the clotting cascade. Ultimately, a clot composed of fibrin and platelets forms
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What confirms diagnosis of MI?
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results of CK MB and troponin tests
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What is recommended tx fo ST segment elevation acute coronary syndrom?
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early reperfusion with primary percutaneous coronary intervention or administration of a fibrinolytic agent
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What should all pts with STEMI receive in addition to reperfusion tx within the 1st day of hospitalization?
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intranasal oxygen, ASA, clopidogrel, SL nitroglycerin, PO BB, and either unfractionated heparin or enoxaparin
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What is tx for high risk pt with non STEMI?
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early coronary angiography and revascularization with PCI or coronary artery bypass graft surgery
glycoprotein IIb/IIIa receptor blocker |
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What is tx for non STEMI?
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intranasal oxygen, ASA, SL nitro, PO BB, anticoagulant (unfractionated heparin, enoxaparin, fondaparinux, or bivalirudin), clopidogrel (most pts)
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What indefinate tx after MI without CI for secondary prevention of death, stroke, and recurrent infarction?
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ASA, BB, and ACEI
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What is goal LDL after MI?
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less than 70-100mg/dL
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When is warfarin considered?
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pts at high risk for death, reinfarction, or stroke
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What is the leading cause of death in the US?
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cardiovascular disease
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What forms of CVD cause the most death?
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unstable angina and MI
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How many acute coronary syndromes per year?
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1.5 million americans
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How many people die from MI each year?
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220,000
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What is the leading cause of of premature chronic disability in the US?
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coronary heart disease
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Are in hospital death rates higher for STEMI or nonSTEMI?
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STEMI
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Is the rate of developing heart failure in hospital for ACS increasing or decreasing?
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decreasing
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Is atherosclerosis caused only by cholesterol excess?
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no, inflammation also
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What is the earliest stage of atherosclerosis?
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endothelial dysfunction: induction and/or repression of several genes in response to stress of blood flowing over the atherosclerotic plaque on endothelial lining of the artery
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What is result of gene induction and repression?
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endothelial cells decrease synthesis of nitric oxide, increase oxidation of lipoproteins and facilitate their entry into the arterial wall, promote adherence of monocytes to the vessel wall and deposition of extracellular matrix, cause smooth muscle cell proliferation and release of local vasoconstrictor and prothrombotic substances into the blood
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What kind of organ is the endothelium in the development of atherosclerosis?
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autocrine and paracrine
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What factors are directly responsible for the development and progression of endothelial dysfunction and atherosclerosis?
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HTN, age, male, tobacco use, DM, obesity, dyslipidemias
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What is acute coronary syndromes?
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all syndromes compatible with acute myocardial ischemia from imbalance between myocardial oxygen demand and supply
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How does ACS differ from stable angina?
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results from diminished myocardial blood flow secondary to an occlusive or partially occlusive coronary artery thrombus
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What is considered NSTE ACS?
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NSTE MI and unstable angina
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What is the difference from NSTE MI and unstable angina?
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In NSTE MI ischemia is severe enough to produce myocardial necrosis, resulting in the release of a detectable amount of biochemical markers, mainly troponin I or T and creatine kinase myocardial band (CK MB) from necrotic myocytes into the bloodstream
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Are Q wave seen more often following a STEMI or nonSTEMI?
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STEMI
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What does the presence of Q waves indicate?
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transmural MI
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When is non-Q wave MI usually seen?
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nonSTEMI
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Where is a non-Q wave MI limited to?
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subendocardial myocardium
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What is the predominant cause of ACS in more than 90% of pts?
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atheromatous plaque rupture, fissuring, or erosion of an unstable atherosclerotic plaque
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Is a plaque that encompasses less than 50% of the coronary lumen or one that occludes 70-90% of the coronary artery more likely to rupture?
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less than 50%
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What are 70-90% stenoses of coronary artery characteristic of?
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stable angina
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What are characteristics of plaques that are more susceptible to rupture?
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eccentric shape, thin fibrous cap, large fatty core, high content of inflammatory cells such as macrophages and lymphocytes, limited amounts of smooth muscle, and significant compensatory enlargement
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What is compensatory enlargement?
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growth of the lesion pushing the vessel outward rather than inward plaque growth
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What can compensatory enlargement result in?
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underestimation of the atherosclerotic stenosis as measured by coronary angiography
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What results from plaque rupture?
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a partially occlusive or completely occlusive thrombus (a clot) forms on top of the ruptured plaque
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What is the result of exposure of collagen and tissue factor?
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induces platelet adhesion and activation, which promotes the release of platelet derived vasoactive substances, including ADP and thromboxane A2
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What does ADP and thromboxane A2 cause?
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vasoconstriction and potentiate platelet activation
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How does GPIIb/IIIa surface receptors of platelets change during platelet activation?
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such that platelets cross link to each other via fibrinogen bridges
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What is the final common pathway of platelet aggregation?
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change of GPIIb/IIIa surface receptors
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What other substances are known to promote platelet aggregation?
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serotonin, thrombin, and epinephrine
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What gives the clot a white appearance?
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inclusion of platelets
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What activates the extrinsic coagulation cascade pathway?
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exposure of blood components to the thrombogenic lipid core and endothelium
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What is the result of activation of the extrinsic coagulation cascade pathway?
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production of thrombin (factor IIa), which converts fibrinogen to fibrin through enzymatic activity
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What does fibrin do?
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stabilizes the clot and traps red blood cells, giving the clot a red appearance
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Does pt with ACS usually have a single ruptured atherosclerotic plaque in one major coronary artery or more than one ruptured plaque?
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single, ruptured atherosclerotic plaque in one major coronary artery
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What is prognosis if more than one ruptured plaque?
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worse
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Is a white clot more common in NSTE ACS or STE ACS?
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NSTE ACS, produces an incomplete occlusion of the coronary lumen
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Is a red clot more common in NSTE ACS or STE ACS?
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STE ACS, completely occluded, larger amounts of fibrin and RBC but smaller amount of platelets
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What can cause myocardial ischemia?
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downstream embolization of microthrombi, can produce ischemia with eventual necrosis
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What is ventricular remodeling?
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changes in size, shape, and function of the left ventricle of both the infarcted area and the remaining ventricle ultimately leading to cardiac failure
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What factors contribute to ventricular remodeling?
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neurohormonal factors (activation of renin angiotensin aldosterone and sympathetic nervous systems), hemodynamic factors, mechanical factors, changes in gene expression, and modifications in myocardial matrix metalloproteinase activity and their inhibitors
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Does ventricular remodeling cause systolic or diastolic dysfunction?
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both
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What meds can slow down or reverse ventricular remodeling through neurohormonal blockage and/or through improvement in hemodynamics (decrease preload or afterload)?
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ACEI, BB, aldosterone antagonists
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What is the most serious complication of ACS?
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cardiogenic shock, 5-6% of STEMI pts, less than 2% with NSTE ACS
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What is mortality of cardiogenic shock?
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60%
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What % of MI pts dies before reaching the hospital?
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25%, presumable of ventricular fibrillation
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What are the classic symptoms of ACS?
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midline anterior anginal chest discomfort, most often at rest, severe ne onset angina, or increasing angina at least 20 minutes in duration
chest discomfort may radiate to the shoulder, down the left arm, to the back, or to the jaw |
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What symptoms may accompany chest discomfort?
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n/v, diaphoresis, SOB
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What is main symptom of STE ACS?
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unremitting chest discomfort
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What are symptoms of NSTE ACS?
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rest angina, new onset (less than 2 months) angina, or angina that increases in frequency, duration, or intensity
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When should a 12 lead ECG be obtained?
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within 10 minutes of pt presenting to ER with symptoms of ischemic chest discomfort
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What are key findings on ECG for myocardial ischemia or MI?
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ST segment elevation, ST segment depression, and T wave inversion
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What is the appearance of a new left bundle branch block accompanied by chest discomfort highly specific for?
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acute MI
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What % of MI pts have STE on ECG?
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65%
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Can pt have MI with no ECG changes?
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yes
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What is evolving MI?
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typical rise and gradual fall (troponin) or more rapid rise and fall (CK MB) of biochemical markers of myocardial necrosis
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When do troponin and CK MB levels rise in the blood?
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following the onset of complete coronary artery occlusion subsequent to myocardial cell death
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How many times is blood drawn to test for biochemical markers?
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typically at least 3x, once in ER and twice more over the next 12-24hrs to measure troponin and CK MB
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How is MI identified based on biochemical markers?
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at least 1 troponin value greater than the MI decision limit or 2 CK MB results greater than the MI decision limit
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When does troponin and CK MB appear in the blood?
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within 6hrs of infarction
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How long does troponin stay elevated?
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up to 10 days
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When does CK MB return to normal?
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within 48hrs
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What is preferred diagnostic test for early reinfarction?
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CK MB because troponin will still be elevated from original infarction
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What ACS is at highest risk of death?
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STE
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Should troponin or CK MB be checked if STE?
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no, start tx, 97% chance of MI with biochemical markers
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What is target time for reperfusion tx with fibrinolytics for STEMI?
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30 minutes of hospital presentation
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What is target tim for PCI with STEMI?
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within 90 minutes from presentation
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What is considered to lat for reperfusion therapy?
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greater than 12hrs since onset of symptoms
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What new markers may identify pts at high risk of mortality or reinfarction?
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C-reactive protein (marker of vascular inflammation), elevated serum creatinine or reduced CrCl, and brain (B-type) natriuretic peptide
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What is 1 year mortality rate for dialysis pts following 1st MI?
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40%
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What pts are less likely to present with classic symptoms of ACS?
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elderly, diabetic, and women
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What is classic sign for ACS?
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not one, pt may present with signs of acute heart failure, including JVD, rales, and S3 sound on auscultation
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What signs of arrhythmias might pt with ACS have?
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tachycardia, bradycardia, or heart block
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Why blood chemistry measured?
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K and Mg may affect heart rhythm, glucose if elevated places pt at higher risk for morbidity and mortality
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What is echocardiogram used for?
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identify pts with low ejection fractions who are at a high risk for death following hospital discharge
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What is considered low ejection fraction?
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less than 40%
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What are short term goals of tx of ACS?
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early restoration of blood flow to the infarct related artery to prevent infarct expansion (MI) or prevent complete occlusion and MI (unstable angina)
prevention of death and other complications prevention of coronary artery reocclusion relief of ischemic chest discomfort maintenance of normoglycemia |
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What is general tx for all STE ACSs and high and intermediate risk NSTE ACS?
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admission to hospital, oxygen (if oxygen saturation is less than 90%), continuous multilead ST segment monitoring for arrhythmias and ischemia, glycemic control, frequent measurement of vital signs, bedrest for 12hrs in hemodynamically stable pt, avoidance of Valsalva maneuver (prescribe stool softeners), pain relief
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What is initial tx for STE ACS?
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efforts to reestablish coronary perfusion immediately
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What is tx for low risk pt?
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evaluated in ER, biochemical marker tests, if tests negative admit to general medical floor with ECG telemetry monitoring for ischemic changes and arrhythmias, noninvasive stress test, or d/c from ER
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What tx for high risk pt if significant coronary artery stenosis is found?
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coronary angiography within 24-48hrs and revascularization (PCI or CABG)
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What is high risk score for non STEMI?
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5-7
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What is medium risk score for nonSTEMI?
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3-4
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What is low risk score for nonSTEMI?
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0-2
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What is tx of choice for reestablishing coronary artery blood flow in STE ACS if presents within 3hrs of symptom onset?
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fibrinolysis or immediate primary PCI
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How do fibrinolysis compare to primary PCI?
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lower mortality with primary PCI, more than 90% of occluded infarct related coronary arteries are opened with primary PCI, less than 60% with fibrinolytics
lower risk of intracranial hemorrhage and major bleeding risks from primary PCI |
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What is preferred tx if pt in cardiogenic shock?
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PCI
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What is preferred tx if pt symptom onset is greater than 3hrs?
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PCI
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What is goal door to primary PCI time (time from hospital presentation to time occluded artery is opened with PCI)?
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90 minutes or less
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When is PCI used following a STEMI?
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fibrinolysis not successful, presenting later in cardiogenic shock, life threatening ventricular arrhythmias, persistent rest ischemia or signs of ischemia on stress testing following MI
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Is rescue PCI, repeated fibrinolytic administration, or conservative management superior?
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rescue PCI and resulted in fewer cardiac cerebrovascular events
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Should routine late restoration of antegrade coronary artery blood flow be performed?
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no
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What NSTE ACS should have PCI?
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high risk and consider moderate risk
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What is result of NSTE ACS PCI?
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fewer MIs, hospital readmissions for recurrent ACS, less need for additional revascularization procedures over the next year following hospitalization
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When should pt undergo evaluation of LV function for risk stratification?
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some point during hospitalization but prior to discharge
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What is most common form of LV function measurement?
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echocardiography to calculate left ventricular ejection fraction
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What is the best predictor of mortality following MI?
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LVEF less than 40% are at highest risk of death
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Who benefits from implantable cardioverterdefibrillator (ICD)?
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ventricular fibrillation or sustained ventricular tachycardia more than 2 days following MI and those with LVEF less than 30% measured at least 1 month following STEMI and 3 months after coronary artery revascularization with either PCI or CABG
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Who receives predischarge stress testing?
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moderate or low risk pts to determine which pts would benefit from coronary angiography to establish the diagnosis of CAD and pts following MI to predict intermediate and long term risk of recurrent MI and death
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What to pts with postive stress tests for coronary ischemia undergo?
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coronary angiography and subsequent revascularization of significantly occluded coronary arteries
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Is exercise stress test with addition of radionuclide imaging agent or nonpharm stress test preferred?
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exercise with radionuclide, evaluates the workload achieved with exercise as well as the occurrence of ischemia
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If pt has negative exercise stress test for ischemia, what is risk for CHD events?
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low risk, exercise stress testing has a high negative predictive value
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When should lipids be drawn?
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within 1st 24hrs of hospitalization because after that period values for cholesterol may be falsely low
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