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101 Cards in this Set

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What should be included in the differential for ischemic heart disease presenting as chest pain?
1. Unstable angina
2. Acute MI
3. Pulmonary Embolism
4. Aortic Dissection
5. Pneumothorax
6. Aortic Aneurysm
Chest wall tenderness presents in what % of people w/ ischemic heart pain?
Describe the symptoms of ischemic heart disease and the location & radiation of the pain.
Sx's: diaphoresis, nausea,
dyspnea, palpitations, syncope;
Location & radiation: substernal, radiates to neck, shoulder (L or R-more commonly L), back, epigastrium.
**What are some risk factors for ischemic heart disease?
family history, smoking, HTN, DM, elevated cholesterol, male sex (but females are on the rise), obesity, cocaine, type A personality.
On a PE, what signs would indicate cardiac abnoralities?
-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
What evaluation and diagnostic studies should be done on a patient w/ chest pain/ischemic heart disease?
-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)
Describe the changes in the cardiac enzymes in ischemic heart disease.***
-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.
Define angina.
Myocardiac oxygen demand exceeds supply
What are the 2 classifications of ischemic chest pain?
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.
What usually occurs on an EKG indicating an MI?
ST wave elevation
What are the 3 types of acute coronary syndrome?
1) ST segment MI
2) Non ST segment MI
3) Unstable angina
Describe what a complex atheroma looks like when examining a coronary artery.
Calcification, thrombosis, hemorrhage. (Calcification can make a coronary angioplasty difficult)
What are the symptoms of unstable angina.
Pain new onset, at rest, or crescendo pattern (inc frequency or w/ less exertion); 40% infarction w/in 90 days
What are the 8 types of treatment for unstable angina?
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.
What is the mechanism of aspirin?
Inhibits cyclo-oxygenase & dec thromboxane A2 (1st line of treatment), decreases platelet aggregation---1st line treatment!
What is the mechanism of low molecular weight heparin?
Inhibits coagulation; its simpler to administer, monitor, & effective.
What is the fxn of Nitrates?
-Systemic and coronary vasodilation;
-Inc collateral flow, dec wall tension.
What is the fxn of beta blockers?
-reduction in heart flow & contractility reduces myocardial oxygen demand.
-decreases dysrhythmias.
-may inc risk of CHF & heart block.
What is the fxn of Ca channel blockers?
decreases contractility, little evidence decreases mortality in ischemia.
When should Glycoprotein IIb/IIIa inhibitor IV be used?
Pre-catheterization, otherwise not given routinely. Oral may inc mortality, IV may be beneficial.
What is the mechanism of Clopidogrel (plavix)?
-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.
What is the fxn of an ACE inhibitor?
-helps remodeling of heart.
-administer w/in first 24 hrs.
-reduces mortality & incidence of CHF.
What is Prinzmetal's (Variant) Angina? When does the pain occur? What relieves the pain?
-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)
What are the symptoms of acute myocardial infarction? This is secondary to what?
-sx's similar to unstable angina except more prolonged.
-usually secondary to atherosclerotic plaque causing thrombosis.
Describe the treatments for Acute Myocardial Infarction.
-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.
In which 2 conditions is it common to get significant narrowing of distal portion of coronary artery?
DM or Familial Hypercholesterolemia.
What is the #1 complication of an MI?
What do normal myocardial fibers looks like?
Central nuclei & syncytial arrangement of fibers, some have pink intercalated discs.
How do you determine what type of surgical procedure should be done in a patient w/ severe atherosclerosis?
Pre-operative catheterization is done.
In an artery where is the atherosclerosis worse?
proximal-where arterial blood flow is more turbulent.
An aneurysm in the heart (formed from healing post infarction)predisposes to what?
Mural thrombosis. The aneurysm is non-contractile tissue that reduces stroke volume & strains remaining myocardium.
What are the 3 types of thrombolytic agents?
1. tissue plasminogen activators (tPA)
2. Urokinase
3. Streptokinase
(comparable early in infections, tPA may be more efficacious in some groups & less side effects.
What are the contraindications to using thrombolytic agents?***
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)
What does a Q wave on EKG indicate?
sign of MI in past.
What on an EKG indicates death of a tissue?
T wave inversions & Q waves.
How do endocardial and transmural injuries differ on an EKG?
-endocardial injury: ST depression;
-transmural injury: ST elevation (>1mm in 2 leads)-->this is an indication for thrombolytic;
Do Q waves always develop post MI?
No, depending on size & location of ischemia, Q waves may not develop (non-Q wave infarctions)
What is the earliest change post MI?
peaked or 'hyper-acute' T waves.
In an inferior wall MI, you should be cautious of giving a patient what?
-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)
What does a posterior wall MI show on EKG?
-Large R wave in VI and V2 w/ ST depression, also may place posterior leads.
What is probably the cause of nearly all out-of-hospital mortality from an acute MI?
arrhythmias, nearly any rhythm can occur, treat like any other dysrhythmia.
**What is an accelerated idioventricular rhythm? How do you treat it?
-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!
Is most CHF R ventricular, L ventricular, or biventricular?
Most R ventricular failure is secondary to what?
Left failure.
What are the signs & sx's of R ventricular failure?
JVD (jugular venous distention), dependent edema, liver congestion
What are the causes of R ventricular failure?
-Mitral stenosis/regurgiations
-Pulmonary HTN (-->R ventricular P)
-pulmonary stenosis/regurgiation
-Cardiomyopathy-can involve R & L ventricular walls
-R ventricular infarction
What are the signs & sx's of L ventricular failure?
-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
What are the causes of L ventricular failure?
1. Mitral regurgitation
2. Systemic HTN
3. Aortic stenosis/regurgitation
4. Cardiomyopathy (on both sides, dz of muscle itself)
5. Left ventricular infarction
What are the causes of high output CHF?
Hyperthyroidism, Septic shock, Beri Beri (thiamine deficiency), AV fistula, Severe Paget's dz, severe anemia, pregnancy.
What are the causes of low output CHF? What happens to the Starling curve?
-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.
What diagnostic testing is done for CHF?**
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.
What is the tx for CHF?
-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.
Why should you not overaggressively treat HTN?
Can lead to stroke or renal failure
What is asymptomatic HTN? How should you treat it?
-Diastolic <130-140, no sx's, no signs of end organ injury;
-Education, follow-up w/in 1week, initiation of outpatient therapy;
How do you define a hypertensive emergency?
Elevation of DBP>130 w/ systemic complication or problem (but don't really go by numbers)
What are some examples of hypertensive emergencies?***
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
Define hypertensive urgency (Grey zone). How should you treat it?
-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
How would you tx someone w/ a hypertensive emergency?
-reduce DMP by 30% in 1st hour (but not below 90-100). Normalize BP over next 8-24 hrs.
-IV meds preferable (quickly titratable)
What are the sx's of hypertensive encephalopathy? How would you tx it?
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.
What are the sx's of an intracerebral hemorrhage?
-HA, N, V, confusion, seizure, focal neuro deficits, papilledema, coma.
-tx severe HTN gradually
Which is tolerated better: mild-moderate HTN or Hypotension?
Whats the most common place for an intracerebral hemorrhage?
-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
If someone has an intracerebral hemorrhage, do you want to decrease their blood pressure?
NO--you need for your BP to cover for ICP.
Why are there often bleeds at the lenticular striate arteries?
b/c they're at right angles to anterior & middle cerebral arteries.
In an ischemic CVA, how can the HTN be treated?
gradual reduction!
What is considered the 'angina of blood pressure'?
Malignant HTN-Hypertensive emergency!
What are the characteristics of Malignant HTN?
Accelerated HTN, papilledema, renal dysfxn (azothemia, proteinuria, red cells)
In Cardiac ischemia or CHF, what happens to the myocardial oxygen demands and the cardiac output?
Myocardial oxygen demands inc, cardiac output decreases due to high afterload.
What are the sx's of cardiac ischemia or CHF?
-chest pain, shortness of breath, bipedal edema
What is the tx for cardiac ischemia or CHF?
nitroglycerin, morphine, diuretics.
What are some causes of catecholamine excess?
MAO inhibitors, pheochromocytomas, clonidine withdrawal, stimulant drug ingestion, alcohol withdrawal
10% of those w/ alcohol withdrawal get what emergency
delirium tremens;
What should be avoided to prevent catecholamine excess?
Avoid beta blockers alone (unopposed alpha receptor stimulation may lead to inc BP)
What is the tx of an aortic dissection?
-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)
What is the difference b/w an aneurysm and an aortic dissection?
Aneurysm: involves all layers vs Aortic dissection which involves only intima.
What is an aortic dissection?
-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)
What are the risk factors for an aortic dissection?
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.
What is the prognosis of someone who has an aortic dissection?
-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
What are the 2 classifications for aortic dissections?
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.
What are the sx's of someone w/ an aortic dissection?
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)
What are the clinical findings of someone w/ an aortic dissection?
HTN, tachycardia, clammy, diaphoretic, unequal pulses (>20 mm Hg) rarely occurs, aortic insuffiency murmur, tamponade (muffled heart sound)
What is the differential diagnosis of an aortic dissection?
Acute MI, pulmonary embolism, abdominal aortic aneurysm, stroke, CVGA, systemic embolic disease
________ occurs when inner lining of aorta tears & blood flow dissects b/w layers of aortic wall, it bursts into pericardium.
Aortic dissection
If a tear progresses down to and occludes coronary artery, what do you have?
If a valve disrupts aortic valve producing acute valvular insufficiency, what condition do you get?
***What should be seen on an X-ray indicating an aortic dissection?
1) widened mediastinum
2) Aortic border >5mm beyond calcific intimal shadow
3) blurred aortic knob
4) pleural apical cap
5) pleural effusion
Besides the X-ray what are some other imaging modalities are diagnosing aortic dissection?
-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)
What is the disadvantage of using an MRI to view an aortic dissection since its specificity and sensitivity approach 100%?
needs long time to scan
What are the adv and disadv of using a CT scan for aortic dissection?
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.
What are the adv and disadv of using an aortography for an aortic dissection?
used to be thought of as 'gold standard';
disadv: invasive, specialized personnel, contrast media allergies, can't be performed in ED
What is the tx for someone w/ aortic dissection?
-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
What is the difference in the surgical mortality in someone w/ a type A vs type B aortic dissection?
type A (involves ASC aorta) surgical tx lowest mortality.
type B (invovles Desc Aorta) surgical mortality exceeds medical management mortality.
-minimal invasive grafts.
What is an aortic aneurysm? It may lead to what?
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
Where are the majority of aortic aneurysms located?
abdominal and intra-renal
What are the risk factors for an aortic aneurysm?
advanced age, males, HTN, smoking, hx of atherosclerotic dz, fam hx of aortic aneurysm.
How does pt w/ aortic aneurysm present? may radiate to what?
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.
Diagnosis of aortic aneurysm often confused w/ what?
renal stone or musculoskeletal pain (mimics sciatic or kidney stone)
how much does an aoric aneurysm grow/yr?
once its stretched >3cm, it grows by 4mm/yr
What will be found on PE of pts w/ aortic aneurysm?
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,
What imaging technique is used in 100% of detection of aneurysms but can't detect if aneurysm has ruptured or leaked
ultrasound (this CAN be done by CT)
What imaging technique is superior to CT for detecting and evaluating aneurysms but it takes too long?