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101 Cards in this Set
- Front
- Back
What should be included in the differential for ischemic heart disease presenting as chest pain?
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1. Unstable angina
2. Acute MI 3. Pulmonary Embolism 4. Aortic Dissection 5. Pneumothorax 6. Aortic Aneurysm |
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Chest wall tenderness presents in what % of people w/ ischemic heart pain?
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5%
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Describe the symptoms of ischemic heart disease and the location & radiation of the pain.
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Sx's: diaphoresis, nausea,
dyspnea, palpitations, syncope; Location & radiation: substernal, radiates to neck, shoulder (L or R-more commonly L), back, epigastrium. |
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**What are some risk factors for ischemic heart disease?
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family history, smoking, HTN, DM, elevated cholesterol, male sex (but females are on the rise), obesity, cocaine, type A personality.
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On a PE, what signs would indicate cardiac abnoralities?
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-Vitals: tachycardia, HTN
-Cardiac exam: -->NEW S4-noncompetent ventricle -->NEW S3-congestive heart failure -->NEW murmur: papillary muscle dysfxn or rupture -->Interventricular septal rupture -->New friction rub=pericardial inflamamtion |
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What evaluation and diagnostic studies should be done on a patient w/ chest pain/ischemic heart disease?
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-ECG; abnl in <1/2 of pts in ED w/ ischemic CP; Can be abnl w/ pericarditis, myocarditis, aortic dissection, electrolyte abnormalities, & cardiac hypertrophy;
-CXR: helpful to evaluate aortic dissection or pulmonary dz. -Evaluate heart size: will tell you cardiothoracic ration. (get an old EKG to compare to new findings) |
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Describe the changes in the cardiac enzymes in ischemic heart disease.***
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-Myoglobin + early in 1/2-2 hrs but nonspecific (b/c can inc just from putting in IV or IM injections but also goes up w/ MI)
-Troponin (#1 test now! nl < .05) + in 2-6 hrs & specific for cardiac injury. -CPK MB (#2): + 3-8 hrs, less specific than troponin. -Enzymes + only w/ infarction & myocardial cell death -Nl w/ ischemic heart dz or angina. Can be nl early even in MI and + w/ myocarditis, myositis, renal failure. |
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Define angina.
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Myocardiac oxygen demand exceeds supply
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What are the 2 classifications of ischemic chest pain?
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A: dec oxygen supply, obstruction of coronary supply from atherosclerotic lesions (everyone has some!) or arterial spasm, systemic hypotension (if you have a dec in BP & you're pursuing oxygen supply,it can lead to MI), severe anemia (don't have O2 carrying capacity in blood).
B: Inc oxygen demand, tachycardia, systemic HTN (if your afterload has inc and yourheart is trying to pump against that), inc contractility of drugs. |
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What usually occurs on an EKG indicating an MI?
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ST wave elevation
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What are the 3 types of acute coronary syndrome?
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1) ST segment MI
2) Non ST segment MI 3) Unstable angina |
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Describe what a complex atheroma looks like when examining a coronary artery.
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Calcification, thrombosis, hemorrhage. (Calcification can make a coronary angioplasty difficult)
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What are the symptoms of unstable angina.
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Pain new onset, at rest, or crescendo pattern (inc frequency or w/ less exertion); 40% infarction w/in 90 days
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What are the 8 types of treatment for unstable angina?
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1. Aspirin
2. Heparin (LMWH) 3. Nitrates 4. Beta blockers 5. Calcium Channel Blockers 6. Glycoprotein IIb/IIIa inhibitor 7. Clopidogrel (plavix) 8. ACE inhibitor: helps remodeling of heart. |
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What is the mechanism of aspirin?
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Inhibits cyclo-oxygenase & dec thromboxane A2 (1st line of treatment), decreases platelet aggregation---1st line treatment!
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What is the mechanism of low molecular weight heparin?
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Inhibits coagulation; its simpler to administer, monitor, & effective.
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What is the fxn of Nitrates?
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-Systemic and coronary vasodilation;
-Inc collateral flow, dec wall tension. |
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What is the fxn of beta blockers?
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-reduction in heart flow & contractility reduces myocardial oxygen demand.
-decreases dysrhythmias. -may inc risk of CHF & heart block. |
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What is the fxn of Ca channel blockers?
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decreases contractility, little evidence decreases mortality in ischemia.
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When should Glycoprotein IIb/IIIa inhibitor IV be used?
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Pre-catheterization, otherwise not given routinely. Oral may inc mortality, IV may be beneficial.
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What is the mechanism of Clopidogrel (plavix)?
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-blocks adenopsine diphosphate receptor, inhibits platelet activation & aggregation; combo therapy w/ aspirin reduces risk of adverse cardiac events esp in pts undergoing percutaneous coronary intervention so they don't occlude coronary artery.
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What is the fxn of an ACE inhibitor?
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-helps remodeling of heart.
-administer w/in first 24 hrs. -reduces mortality & incidence of CHF. |
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What is Prinzmetal's (Variant) Angina? When does the pain occur? What relieves the pain?
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-spasm of coronary artery.
-transient lg ST elevation -2/3 have non-significant fixed coronary lesions -Usually occur @ rest, may result in acute MI. -Usually relieved w/ nitrates (to try to reverse them but don't let them leave b/c you don't know if they have coronary vascular dz) |
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What are the symptoms of acute myocardial infarction? This is secondary to what?
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-sx's similar to unstable angina except more prolonged.
-usually secondary to atherosclerotic plaque causing thrombosis. |
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Describe the treatments for Acute Myocardial Infarction.
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-Goal preservation of heart muscle-->pick this up b/c tx's can reserve this.
-20-25% loss causes CHF, 34-40% cardiogenic shock. -re-open coronary artery to preserve myocardium 1. Thrombolysis vs 2. Angioplasty. -PTCA better outcome & fewer complications w/ experienced angiographers in busy centers. -benefit of PTCA (Percutaneous Coronary Angioplasty) lost w/ timy delay: open up coronary arteries mechanically. |
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In which 2 conditions is it common to get significant narrowing of distal portion of coronary artery?
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DM or Familial Hypercholesterolemia.
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What is the #1 complication of an MI?
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dysrhythmia.
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What do normal myocardial fibers looks like?
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Central nuclei & syncytial arrangement of fibers, some have pink intercalated discs.
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How do you determine what type of surgical procedure should be done in a patient w/ severe atherosclerosis?
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Pre-operative catheterization is done.
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In an artery where is the atherosclerosis worse?
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proximal-where arterial blood flow is more turbulent.
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An aneurysm in the heart (formed from healing post infarction)predisposes to what?
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Mural thrombosis. The aneurysm is non-contractile tissue that reduces stroke volume & strains remaining myocardium.
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What are the 3 types of thrombolytic agents?
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1. tissue plasminogen activators (tPA)
2. Urokinase 3. Streptokinase (comparable early in infections, tPA may be more efficacious in some groups & less side effects. |
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What are the contraindications to using thrombolytic agents?***
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1. Recent major surgery (<10d)
2. Recent GI bleed 3. Recent trauma 4. HTN (BP>180/110) 5. Pericarditis 6. Clotting abnormalities 7. Prior receipt of streptokinase (only tPA)-foreign protein (previous neurosurgery, previous stroke) |
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What does a Q wave on EKG indicate?
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sign of MI in past.
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What on an EKG indicates death of a tissue?
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T wave inversions & Q waves.
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How do endocardial and transmural injuries differ on an EKG?
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-endocardial injury: ST depression;
-transmural injury: ST elevation (>1mm in 2 leads)-->this is an indication for thrombolytic; |
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Do Q waves always develop post MI?
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No, depending on size & location of ischemia, Q waves may not develop (non-Q wave infarctions)
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What is the earliest change post MI?
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peaked or 'hyper-acute' T waves.
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In an inferior wall MI, you should be cautious of giving a patient what?
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-pt may be volume dependent for cardiac output.
-caution w/ nitrates or vasodilators esp if assoc R ventricular infarction (diagnose by right sided leads V3R and V4R) |
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What does a posterior wall MI show on EKG?
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-Large R wave in VI and V2 w/ ST depression, also may place posterior leads.
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What is probably the cause of nearly all out-of-hospital mortality from an acute MI?
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arrhythmias, nearly any rhythm can occur, treat like any other dysrhythmia.
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**What is an accelerated idioventricular rhythm? How do you treat it?
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-occurs primarily in setting of acute MI;
-resembles VT except slow rate (40-90/min) -usually transient & self-limited NOT requiring therapy-->treatment may result in ASYSTOLE! |
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Is most CHF R ventricular, L ventricular, or biventricular?
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biventricular
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Most R ventricular failure is secondary to what?
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Left failure.
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What are the signs & sx's of R ventricular failure?
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JVD (jugular venous distention), dependent edema, liver congestion
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What are the causes of R ventricular failure?
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-Mitral stenosis/regurgiations
-Pulmonary HTN (-->R ventricular P) -pulmonary stenosis/regurgiation -Cardiomyopathy-can involve R & L ventricular walls -R ventricular infarction (portal |
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What are the signs & sx's of L ventricular failure?
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-Pulmonary edema (you hear rhales, wet sounds)
-Orthopnea (ask pts how many pillows they use to sleep) -Paroxysmal nocturnal dyspnea (wake up in middle of night gasping) -Pulsus alterans (BP varies w/ inspiration & expiration) -S3 gallop |
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What are the causes of L ventricular failure?
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1. Mitral regurgitation
2. Systemic HTN 3. Aortic stenosis/regurgitation 4. Cardiomyopathy (on both sides, dz of muscle itself) 5. Left ventricular infarction |
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What are the causes of high output CHF?
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Hyperthyroidism, Septic shock, Beri Beri (thiamine deficiency), AV fistula, Severe Paget's dz, severe anemia, pregnancy.
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What are the causes of low output CHF? What happens to the Starling curve?
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-acute decompensation w/ minor stress dietary, tachydysrhythmia, infection, hypoxia, meds or lack of meds, ischemia, pulmonary embolism.
-Starling curve: exceeds capacity of inc filling pressures to inc CO. |
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What diagnostic testing is done for CHF?**
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1. CXR: Cardiomegaly, Cephalization (venous distribution), Kerley B lines (lymphatic vessels--help to drain back up of fluid on periphery of lung), interstitial peri-hilar infiltrates, Pleural effusion (R>L). X ray may identify other cause of SOB.
2. ECG: useful if etiology is acute ischemia or prior infarction, usually non-specific. 3. B-naturetic peptide (BNP): elevated in CHF value, may reflex severity of dz., useful to discriminate COPD & pulm dz from CHF. |
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What is the tx for CHF?
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-oxygen,
-inotropic agents (dobutamine, amrinone), -reduced filling pressures (reduce pre-load)-->diuretics (lasix), nitrates, morphine (vasodilates), sitting upright (b/c short of breath), Nesiritide (BNP)(really good drug, calming, allows urination, no breathing problems, very justifying drug); Inc outflow (reduced after-load)-->nitrates, nitroprusside (or other anti-HTN) given IV, titratable, but light senstivie so needs to be covered from light. |
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Why should you not overaggressively treat HTN?
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Can lead to stroke or renal failure
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What is asymptomatic HTN? How should you treat it?
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-Diastolic <130-140, no sx's, no signs of end organ injury;
-Education, follow-up w/in 1week, initiation of outpatient therapy; |
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How do you define a hypertensive emergency?
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Elevation of DBP>130 w/ systemic complication or problem (but don't really go by numbers)
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What are some examples of hypertensive emergencies?***
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1. Hypertensive encephalopathy
2. Intracerebral hemorrhage 3. Left ventricular failure or cardiac ischemia. 4. Aortic dissection 5. Malignant HTN, papilledema, seizure, confusion, coma. 6. Eclampsia 7. Renal failure |
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Define hypertensive urgency (Grey zone). How should you treat it?
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-Asymptomatic pts w/ severe or recently inc BP
-No sign of any end organ acute injury. -Diastolic >130-140 mm Hg -BP should be gradually reduced over 24 hrs |
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How would you tx someone w/ a hypertensive emergency?
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-reduce DMP by 30% in 1st hour (but not below 90-100). Normalize BP over next 8-24 hrs.
-IV meds preferable (quickly titratable) |
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What are the sx's of hypertensive encephalopathy? How would you tx it?
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Sx's: HEADACHE!, N, V, confusion, seizure, focal neuro deficits, papilledema or coma.
-Nl cerebral vascular autoregulation is lost. -Lower BP gradually-->1) nitroprusside, 2) labetalol, 3) nicardipine. |
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What are the sx's of an intracerebral hemorrhage?
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-HA, N, V, confusion, seizure, focal neuro deficits, papilledema, coma.
-tx severe HTN gradually |
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Which is tolerated better: mild-moderate HTN or Hypotension?
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HTN
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Whats the most common place for an intracerebral hemorrhage?
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-60% ICH-basal ganglia in location, 20% infratentorial (18% cerebellum, 2% brainstem)
[ie if its supratentorial-->its in basal ganglia; if in infratentorial-->its in cerebellum |
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If someone has an intracerebral hemorrhage, do you want to decrease their blood pressure?
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NO--you need for your BP to cover for ICP.
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Why are there often bleeds at the lenticular striate arteries?
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b/c they're at right angles to anterior & middle cerebral arteries.
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In an ischemic CVA, how can the HTN be treated?
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gradual reduction!
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What is considered the 'angina of blood pressure'?
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Malignant HTN-Hypertensive emergency!
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What are the characteristics of Malignant HTN?
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Accelerated HTN, papilledema, renal dysfxn (azothemia, proteinuria, red cells)
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In Cardiac ischemia or CHF, what happens to the myocardial oxygen demands and the cardiac output?
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Myocardial oxygen demands inc, cardiac output decreases due to high afterload.
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What are the sx's of cardiac ischemia or CHF?
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-chest pain, shortness of breath, bipedal edema
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What is the tx for cardiac ischemia or CHF?
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nitroglycerin, morphine, diuretics.
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What are some causes of catecholamine excess?
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MAO inhibitors, pheochromocytomas, clonidine withdrawal, stimulant drug ingestion, alcohol withdrawal
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10% of those w/ alcohol withdrawal get what emergency
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delirium tremens;
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What should be avoided to prevent catecholamine excess?
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Avoid beta blockers alone (unopposed alpha receptor stimulation may lead to inc BP)
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What is the tx of an aortic dissection?
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-Needs AGGRESSIVE lowering of BP w/ beta blockers & nitroprusside or w/ labetalol (has alpha & beta blockage)
-Dec SBP to 90-100 (as tolerate to dec stress on intimal flap) |
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What is the difference b/w an aneurysm and an aortic dissection?
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Aneurysm: involves all layers vs Aortic dissection which involves only intima.
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What is an aortic dissection?
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-Intimal tear in artery lining that allows blood to leak into media of artery wall.
-Lining of artery separates from wall, dissection of lining propagates proximally & distally. -Aortic dissection is NOT an aneursym. (aneurysm is balloon like dilatation of all layers of artery) |
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What are the risk factors for an aortic dissection?
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atherosclerosis, age>50 y/o, males, HTN (70-90% of all pts), connective tissue d/o (Marfans/ Ehlers Danlos--type III collagen deficiency), Hyperdynamic states (pregnancy, hyperthyroidism, cocaine), trauma, congenital dz (bicuspid aortic valve, coarctation), prosthetic aortic valve.
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What is the prognosis of someone who has an aortic dissection?
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-most don't die immediately
-most have time to seek medical care as dissection propagates -Mortality: 28% in 24 hrs -50% in 48 hrs -90% in 3 months |
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What are the 2 classifications for aortic dissections?
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1. Debakey: Type I-ascending & descending aorta involved, Type II, ascending aorta only, Type III-descending aorta only.
2. Stanford:Type A: involves ascending aorta (includes Debakey type II), type B: involves only descending aorta. |
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What are the sx's of someone w/ an aortic dissection?
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This condition EVOLVES as condition progresses, migrates depending on where dissection is going on.
-Pain=most common presenting sx (70-90%) -starts abruptly, excrutiating & maximal at onset -Migrates as dissection flap propagates -may be located in back, epigastrium, chest upper back, mid back, lower back, flank, legs; -others sx's occur as aortic branch vessels are occluded by intimal flap -CVA (Carotid vessels) -Paraplegia (spinal artery) -Cold, pulseless extremity -CHF, CP, Pulmonary edema (coronary artery) -Abdominal pain (mesenteric arteries) -Flank pain & hematuria (renal artery) -Syncope |
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What are the clinical findings of someone w/ an aortic dissection?
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HTN, tachycardia, clammy, diaphoretic, unequal pulses (>20 mm Hg) rarely occurs, aortic insuffiency murmur, tamponade (muffled heart sound)
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What is the differential diagnosis of an aortic dissection?
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Acute MI, pulmonary embolism, abdominal aortic aneurysm, stroke, CVGA, systemic embolic disease
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________ occurs when inner lining of aorta tears & blood flow dissects b/w layers of aortic wall, it bursts into pericardium.
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Aortic dissection
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If a tear progresses down to and occludes coronary artery, what do you have?
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MI
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If a valve disrupts aortic valve producing acute valvular insufficiency, what condition do you get?
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CHF
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***What should be seen on an X-ray indicating an aortic dissection?
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1) widened mediastinum
2) Aortic border >5mm beyond calcific intimal shadow 3) blurred aortic knob 4) pleural apical cap 5) pleural effusion |
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Besides the X-ray what are some other imaging modalities are diagnosing aortic dissection?
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-no labs
-EKG: to rule out MI but dissection can lead to MI if it goes down to coronaries; -Transesophageal Echo: sensitivity & specificity approach 100%, visualizes pericardium & aortic valve, only real disadvantage: requires special equipment & trained operators (often not in hospital) |
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What is the disadvantage of using an MRI to view an aortic dissection since its specificity and sensitivity approach 100%?
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needs long time to scan
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What are the adv and disadv of using a CT scan for aortic dissection?
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ADV: sensi & specificty of 95-98%, can help ID other causes for chest pain, readily available.
DISADV: can't do in ED, doesn't reveal aortic regurgitation or coronary artery involvement. |
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What are the adv and disadv of using an aortography for an aortic dissection?
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used to be thought of as 'gold standard';
disadv: invasive, specialized personnel, contrast media allergies, can't be performed in ED |
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What is the tx for someone w/ aortic dissection?
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TREAT QUICKLY!
-Control of BP & rate of change of pulse P w/ each beat (dP/dT) -Beta blocker + Nitroprusside or labetalol -Goal: reduce systolic to 90-100 mm Hg. Hypotension managed w/ fluid or blood products but don't want to overburden heart. -Long term tx: surgical management |
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What is the difference in the surgical mortality in someone w/ a type A vs type B aortic dissection?
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type A (involves ASC aorta) surgical tx lowest mortality.
type B (invovles Desc Aorta) surgical mortality exceeds medical management mortality. -minimal invasive grafts. |
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What is an aortic aneurysm? It may lead to what?
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deterioration of elastic fibers in aorta leads to localized stretching & dilatation of all 3 layers of aorta;
-may lead to aortic rupture-->can kill your patient. Rupture risk inc w/ size of aneurysm |
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Where are the majority of aortic aneurysms located?
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abdominal and intra-renal
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What are the risk factors for an aortic aneurysm?
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advanced age, males, HTN, smoking, hx of atherosclerotic dz, fam hx of aortic aneurysm.
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How does pt w/ aortic aneurysm present? may radiate to what?
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sudden onset of severe abdominal, chest, back or flank pain.May radiate to groin. Syncope from pain or blood loss w/ rupture. May be dull in nature & radiate to groin or legs.
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Diagnosis of aortic aneurysm often confused w/ what?
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renal stone or musculoskeletal pain (mimics sciatic or kidney stone)
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how much does an aoric aneurysm grow/yr?
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once its stretched >3cm, it grows by 4mm/yr
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What will be found on PE of pts w/ aortic aneurysm?
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pulsatile mass palpable in 3/4 of pts, may not be palpable if pt hypotensive, small aneurysm, fat pt; unequal pulses, less than 1/2 are hypotensive,
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What imaging technique is used in 100% of detection of aneurysms but can't detect if aneurysm has ruptured or leaked
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ultrasound (this CAN be done by CT)
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What imaging technique is superior to CT for detecting and evaluating aneurysms but it takes too long?
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MRI
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