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CARDIOLOGY Flashcards

1
Q

guidelines for PCI for STEMI

A

within 12 hours of symptom onset AND within 90 minutes of 1st medical contact to device time at PCI-capable facility (door to balloon time)
OR
within 120 min of 1st medical contact to device time at non-PCI capable facility (to allow transport time to PCI capable facility)

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2
Q

what is recommendation for STEMI at non-PCI-capable facility

A

fibrinolysis within 12 hrs of symptom onset

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3
Q

Acute Mitral Regurgitation

  • etiology
  • clinical features
  • mgmt
A

etiology:
1. ruptured mitral chordae tendineae (flail leaflet): mitral prolapse, trauma, rheumatic heart disease, mitral valve prolapse
2. papillary muscle rupture due to MI or trauma (usually 2-7 days post MI)

clinical features: rapid pulmonary edema, hypotension–>cariogenic shock, pulmonary HTN

PE: diaphoresis & pallor, cool extremities, signs of right ventricular pressure, hyper dynamic cardiac impulse, decrescendo systolic murmur at lower left sternal border

mgmt: echo and surgery

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4
Q

Ehlers-Danlos

  • what is it
  • skin
  • MSK
  • cardiac
  • other
  • genetics
A
  • what is it: connective tissue disorder characterized by joint hyper mobility, hyper extensibility with easy bruising, delayed healing with atrophic scars.
  • skin: transparent, hyperextensible, eary bruising, poor wound healing, velvety (“dough”) fragile with atrophy & scarring
  • MSK: joint hypermobility, joint dislocations, pectus excavatum, high & arched palate, premature degenerative joint disease, scoliosis
  • cardiac: mitral valve prolapse with myxomatous degeneration of valvular apparatus–>chordae tendineae rupture & acute mitral regurgitation
  • other: hernias, cervical insufficiency & uterine prolapse
  • genetics: COL5A1 & COL5A2 gene mutations, autosomal dominant
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5
Q

Marfan Syndrome

  • what is it
  • skin
  • MSK
  • cardiac
  • other
  • genetics
A

skin: no characteristic features
- MSK: joint hyper mobility, pectus carinatum, disproportionately tall stature & long extremities, scoliosis
- cardiac: progressive aortic root dilation–> rupture/dissection
- other: lens dislocation., retinal detachment, spontaneous pneumothorax
- genetics: FGN1 gene mutation, autosomal dominant

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6
Q

Acute Coronary Syndrome

-what do you do if EKG inconsistent with ACS

A

-obtain CXR, if negative then: serial cardiac biomarkers (troponin and/or CK-MB) & repeat EKG, assess pericarditis, aortic dissection, PE

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7
Q

Neurocardiogenic (Vasovagal) Syncope

  • clinical presentation
  • diagnosis
  • treatment
  • autonomic prodrome
A
  • clinical presentation: inciting event (prolonged standing, stress)
  • diagnosis: clinical, tilt-table
  • treatment: reassure, avoid triggers, counterpressure techniques for recurrent episodes
  • autonomic prodrome: nausea, pallor, diaphoresis, gerneralized warmth. NOT PALPITATIONS–USUALLY INDICATIVE OF CARDIOGENIC SYNCOPE
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8
Q

Valve Replacement in aortic stenosis

  • severe aortic stenosis criteria
  • indications for valve replacement
A

-severe aortic stenosis criteria: aortic jet velocity>4.0m/sec
OR mean transvalvular pressure gradient >40mmHg, valve area is usually <1cm

  • indications for valve replacement (decreased mortality): severe aortic stenosis & 1 or more:
    1. symptoms (angina, syncope)
    2. LVEF<50%
    3. undergoing other cardiac sx (CABG)
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9
Q

multifocal atrial tachycardia

  • typical patient
  • etiology
  • clinical findings
  • treatment
A
  • typical patient: elderly patient who is hospitalized with acute exacerbation of underlying pulmonary dx.
  • etiology: exacerbation of pulmonary dx, electrolyte disturbance (hypokalemia), catecholamine surge (sepsis)
  • clinical findings: usually asymptomatic, rapid, irregular pulse

EKG: 3 OR MORE P WAVE MORPHOLOGIES, atrial rate >100/min, IRREGULAR R-R INTERVALS

-treatment correct underlying disturbance FIRST, AV nodal blockade (verapamil) if persistent

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10
Q

trastuzumab
-cardiotoxicity

vs anthracycline cardiotoxicity

A

=mab tragets HER2.
-cardiotoxicity: loss of myocardial contractility (myocardial hibernation) leading to decreased LVEF which is usually REVERSIBLE

anthracycline (doxorubicin) cardiotoxicity is irreversible

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11
Q 
Hypertrophic cardiomyopathy: 
1. effect of maneuver on hypertrophic cardiomyopathy: 
valsalva
abrupt standing 
nitroglycerin
sustained hand grip 
squatting 
passive leg raise
  1. management
  2. genetics
  3. what medication could worsen condition
A

valsalva, abrupt standing & nitroglycerin–> decrease preload & increase murmur intensity

sustained hand grip–> increase after load & decrease murmur intensity

squatting–>increase preload & after load, decrease murmur intensity

passive leg raise–> increase preload & decrease murmur intensity

  1. negative ionotrpic agents : b-blockers initial therapy then verapamil or disopyramide. note: implantable cardioverter-defibrillator placement indicated for preventing SCD in patients with HCM and increased risk (family hx SCD, prior cardiac arrest/sustained spontaneous Vtach, hypotension with exercise, extreme LVH, non sustained VT)
  2. autosomal dominant genetic disorder of cardiac sarcomere
  3. ACE-I/ARBs and vasodilators cause reduction in systemic vascular resistance, potentially worsening LV outflow tract gradient in patients with HCM
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12
Q

Guidelines for lipid lowering therapy

  • indications
  • recommended therapy
A
  • indications
    1. clinically significant atherosclerotic disease (ACS, MI, stable/unstable angina, coronary/other arterial revascularization, stroke, TIA, PAD); mgmt: <75 yrs high intensity statin, >75yrs moderate intensity statin
  1. LDL >190mg/dL–>high intensity statin
  2. 40-75 yrs with dbts
    - risk>7.5% high intensity statin
    - risk<7.5% mod intensity statin
  3. est 10yr ASCVD risk> 7.5%, mgmt mod to high intensity statin
    - recommended therapy:
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13
Q

Peripheral Artery disease

  1. presentation
  2. testing
  3. treatment
A
  1. claudication, smooth/shiny skin (no hair or sweat glands), loss of pedal pulses
  2. ABI >.9
    angiography most accurate
  3. mgmt:
    -risk factor control (statin therapy, BP, dbts, smoking cessation, antiPLT therapy (aspirin, clopidogrel)
    -exercise program
    -if exercise doesn’t work than cilostazol
    -revascularization if limb-threatening dx or persistent functional limitation on above therapy (angioplasty with stent, bypass graft)
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14
Q

TCA overdose

clinical presentation

A

CNS: mental status changes, seizure, respiratory depression
CV:sinus tach, hypotension, prolonged PR/QRS/QT, arrhythmias
anticholinergic: dry mouth, blurry vision, dilated pupils, urinary retention, flushing, hyperthermia

mgmt: IV fluids, O2, intubation, activated charcoal for patients within 2 hrs of ingestion (unless ileum), IV sodium braced for QRS widening or ventricular arrhythmia

TCS inhibit fast sodium channels in His-Purkinje tissue and myocardium to decrease conduction speed, increase phase 0 depolarization, and prolong refractory period

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15
Q

Antithrombotic therapy in patient with mechanical heart valves

A

ASA in all patients with aortic or mitral valve replacement

warfarin (goal INR 2-3) aortic valve replacement w/o risk factors

warfarin (goal INR 2.5-3.5) mitral valve replacement, aortic valve replacement w/ risk factors, in 1st 3mo after aortic valve replacement

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16
Q

anti arrhythmic therapy to maintain sinus rhythm in afib:

  1. no structural heart dx
  2. LVH
  3. CAD w/o heart failure
  4. heart failure
  5. recurrent AF symptoms refractory to anti arrhythmic drugs
A
  1. no structural heart dx: flecainide
  2. LVH: amiodarone, dronedarone
  3. CAD w/o heart failure: stall, dronedarone
  4. heart failure: amiodarone, dofetilide
  5. recurrent AF symptoms refractory to anti arrhythmic drugs:radiofrequency catheter ablation

*afib needs anticoagulation and rate control with AV node blockers (b-blockers), or rhythm control with antiarrhythmics

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17
Q

what is major side effect of nitroprusside . signs

A

cyanide accumulation & toxicity . treat with sodium thiosulfate.
main signs, flushing,, altered mental status, metabolic acidosis. nitroprusside is potent vasodilator that works on arterial and venous circulation and is used for HTN emergency, it is metabolized to cyanide, which may accumulate and can be toxic

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18
Q

Bacterial Endocarditis prophylaxis

  • high risk procedures
  • indicated procedures & appropriate coverage
A

-high risk procedures: prosthetic heart valve, previous infective endocarditis, structural valve abnormality in transplanted heart, unrepaired cyanotic congenital heart disease, repaired congenital heart disease with residual defect

*don’d need prophylaxis for GI or GU procedures
unless active GI/GU infection

  • indicated procedures & appropriate coverage:
  • gingival or respiratory: viridans group strep coverage –>amoxicillin
  • GU/GI active infection: enterococcus coverage (ampicillin)
  • sx of infected skin/muscle: staph coverage (vanc)
  • sx placement of prosthetic cardiac material: staph (vanc)
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19
Q

alternative treatment for patient on menopausal hormone therapy if patient develops venous thromboembolism

A

SSRI or SNRI

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20
Q

treatment of acute DVT/PE

A

oral factor Xa inhibitors
-onset 2-4 hours, no overlap, no monitoring
(use LMWH if patient has cancer)

warfarin
-vit K antagonist, onset 5-7 days, need overlap with UFH or LMWH for 5 days, need PTT/INR monitoring

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21
Q

what is stongly associated with AAA formation, expansion and rupture

A

cigarette smoking

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22
Q

maternal hyperglycemia effects on fetal myocardium

A

excessive glycogen deposition –>hypertrophic cardiomyopathy –>CHF

interventricular myocardial hypertrophy & outflow obstruction typically resolves spontaneously

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23
Q

Anticoagulation in nonvalvular afib

A 
mgmt of new onset AF includes assessing for rate-vs rhythm control strategy and preventing systemic embolization.  hemodynamically unstable-->cardiovert.  need to CHADSVASC score to see if anticoagulant is needed. 
CHF (1)
HTN (1)
Age >75yrs (2)
DM (1)
Stroke/TIA/thromboemb.(2)
Vascular dx (1)
Age 65-74 (1)
Sec category (women) (1)
max score 9

0=low score risk, no anticoag
1=intermed, maybe anticoag
2+=high, warfarin or rivaroxaban

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24
Q

Ischemic Heart Disease (CAD)

  1. risk factors
  2. 3 features that can r/o CAD
  3. mgmt
A
  1. diabetes (worst risk factor), HTN, tobacco use, hyperlipidemia, PAD, inactivity, obesity, family history (women <65, men <55)
  2. pleuritic pain, positional pain, tenderness
  3. EKG, ASA first
    cardiac enzymes
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25
Q

cardiac enzymes

A
  • troponins: rise w/in 3-6 hours, stay elevated 1-2 wks
  • CK-MB: rise w/in 3-6hrs, elevated 1-2days (good measure of reinfarction)
  • myoglobin rises 1-4 hours, otherwise not too useful
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26
Q

CAD stress testing

  1. when/why. reversible vs fixed
  2. when dipyridamole or adenosine stress test, or dobutamine echo
  3. when thallium testing (what is mechanism) or stress echo
  4. when sestamibi nuclear stress test
A

1.stress test increases sensitivity of detection of CAD beyond EKG and enzymes. use for f/u in non-acute cases. reversible ischemia most dangerous (will do angiography). if test shows fixed defects than no change between rest and exercise (no angiography needed)

2.patients that can’t exercise to target HR >85% of max
COPD, amputation, deconditioning, weakness/previous stroke, obesity, dementia, lower extremity ulcer

  1. EKG unreadable b/c digoxin use, LVH, pacemaker, LBBB, baseline abnormality of ST segment . mechanism of thallium=nuclear isotopes picked up by Na/K ATPase of normal myocardium. decreased upstate = damage
  2. obesity, large breasts
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27
Q

What is next step after abnormal stress test for CAD

A

angiography following reversible ischemia found on stress testing

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28
Q

Acute Coronary Syndrome

  1. definition. what is it based on
  2. EKG
  3. treatment
    a. what lowers mortality and should be given first
    b. what else can you give
    c. when do you add clopidogrel, tigrelor, prasugrel
  4. role & effect of angioplasty and thrombolytics . How much time do you have for each? what is indiction for thrombolytics
  5. should you do angioplasty for stable angina?
  6. role of beta-blockers
  7. role ACE-I/ARBs
  8. role of statins
  9. stent thrombosis
A

ACS: umbrella term for situations where the blood supplied to the heart muscle is suddenly blocked.

  1. based on hx of acute chest pain at rest or with exercise suggestive of ischemic dx. NOT BASED ON ENZYME LEVELS, ANGIOGRAPHY, STRESS TEST RESULTS
  2. may have ST segment elevation, ST segment depression or normal EKG
  3. a. ASPIRIN LOWERS MORTALITY! instantly inhibits PLTs
    b. can give nitrates & morphine but won’t lower mortality
    c. clopidogrel or tigrelor added to aspirin for acute MI. prasugrel given for angioplasty. (they inhibit ADP activation of PLTs)
  4. DURING STEMI:
    PRIMARY ANGIOPLASTY (type of PCI) LOWERS MORTALITY & MUST DO WITHIN 9OMIN ARRIVAL IN ED

NO PCI THEN THROMBOLYTICS!

THROMBOLYTICS WHICH ALSO LOWERS MORTALITY AND MUST DO WITHIN 30MIN OF ARRIVAL IN ED
indications: within 12 hrs onset of chest pain & ST elevation in 2 or leads on EKG or new LBBB

  1. angioplasty doesn’t decrease mortality more than medical therapy (ASA, b-blockers, statins) for stable angina
  2. beta-blockers lower mortality but timing isn’t critical. should give metoprolol but not as urgent as ASA
  3. ACE-I/ARBs should be given to all patients with ACS, but only lower mortality if there is LV/systolic dysfunction
  4. statins should be given to all patients with ACS
  5. biggest risk factor: premature cessation of dual antiPLT therapy with aspirin & clopidogrel/prasugrel/ticagrelor
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29
Q

effect of therapy used in ACS

  1. which meds always lower mortality
  2. which meds lower mortality in certain conditions
  3. which don’t lower mortality at all
A
  1. ASA, thrombolytics, PCI, metoprolol, statins, clopidogrel, prasugrel, ticagrelor
  2. ACE-I/ARBs if LVEF is low
  3. O2, morphine, nitrates, CCBs, lidocaine, amiodarone
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30
Q 
ACS
when do you use:
1. prasugrel, clopidogreal, ticagrelor 
2. CCBs (diltiazem, verapamil)
3.pacemaker
4.lidocaine, amiodarone
A
  1. prasugrel, clopidogreal, ticagrelor:
    ASA allergy, acute MI, angioplasty
  2. CCBs (diltiazem, verapamil):
    intolerance to b-blockers, cocaine induced chest pain, prinzmetal’s angina

3.pacemaker:
bifasicular block, 2nd or 3rd degree AV block, new LBBB, symptomatic bradycardia

4.lidocaine, amiodarone:
only if VTACH or VFIB
not used preventatively

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31
Q 
Complications of MI
diag-diag test-treatment 
1.cardiogenic shock 
2.septal rupture 
3. myocardial wall rupture
4. sinus bradycardia
5. 3rd degree (complete) heart block 
6. right ventricular infarction 
7. valve rupture
A
  1. cardiogenic shock –>echo, swanz-ganz cath–>ACEI, urgent revascularization
  2. septal rupture–>echo, swan-ganz cath showing step up in saturation from RA to RV–> ACEI, nitroprusside & urgent surgery
  3. myocardial wall rupture–>echo–>pericardiocentesis, urgent cardiac repair
  4. sinus bradycardia–>ekg–>atropine, followed by pacemaker if symptoms persist
  5. 3rd degree (complete) heart block (canon “a” waves) –>atropine & a pacemaker even if symptoms resolve
  6. right ventricular infarction–>EKG showing right ventricular leads–>fluid loading
  7. valve rupture –>echo–>ACEI, nitroprusside, intra-aortic ballon pump as BRIDGE to surgery
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32
Q

post-MI discharge instructions

A

d/c on ASA, statin, metoprolol, ACEI, clopidogrel (or prasugrel). wait 2-6 wks before sex

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33
Q

what difference managing STEMI vs NSTEMI

A

NSTEMI:

  • no thrombolytics
  • HEPARIN: LOWERS MORTALITY. stops new clots from forming by potentiating antithrombin
  • glycoprotein IIb/IIIa lowers mortality when used in combination with angioplasty and send placement
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34
Q

Chronic Angina

  • treatment
  • when do you use ACEI/ARBs
  • why is coronary angiography used
  • what can be added for pain despite optimized treatment
A
  • aspirin & metoprolol lowers mortality!
  • nitrates for anginal pain but doesn’t lower mortality
  • ACEI/ARBs for stable cases involving heart failure, systolic dysfunction, low LVEF
  • coronary angiography used to see who is candidate for CABG
  • statin
  • use clopidogrel/prasugrel/ticarelor if acute MI or intolerant of ASA
  • add ranolazine or ivabradine for persistent pain
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35
Q

Coronary Artery Bypass Graft
indications
major difference between saphenous vein and internal mammary artery grafts

A 
indications: 
3 coronary vessels with > 70% stenosis 
left main coronary artery stenosis > 50-70%
2 vessels in a diabetic 
2-3 vessels with low ejection fraction

saphenous vein grafts become occluded after 5 yrs vs internal mammary artery grafts occlude after 10 yrs

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36
Q

Lipid Management

  1. what is strongest indication for lipid lowering agent
  2. LDL goal of therapy CAD
  3. risk factors
  4. toxicity statins
  5. role of evolocumab & alirocumab
A
  1. ACS strong indication for statin . STATIN THERAPY FOR ANYBODY WITH CAD OR AN EQUIVALENT WITH LDL >100!
  2. goal of therapy CAD +/- dbts LDL < 70
  3. risk factors: smoking cigs, HTN, low HDL, FH early CAD (male relatives >65yrs, female rel. >55yrs), age (men >45yrs, wmn > 55yrs)
  4. check LFTS on statins
  5. role of evolocumab & alirocumab = PCSK9 inhibitors that increase clearance of LDL from bloodstream. THEY DON’T LOWER MORTALITY! use when statin therapy maxed out. they’re injectable
37
Q

CAD equivalents

A
  1. diabetes mellitus
  2. PAD
  3. aortic dx
  4. carotid dx
38
Q

Acute Congestive Heart Failure

  1. a. Management of acute pulmonary edema
    b. no response to preload reduction with diuretics
    c. drug that should never give
    d. how to manage if Vtach
  2. diagnostic tests CHF
  3. role of nesiritide
A
  1. a. O2, furosemida, nitrates and morphine
    b. no response to preload reduction with diuretics then use + inotropic agents dobutamine, imamrinone, milrinone
    c. never digoxin in setting of acute pull edema
    d. unstable pt with pulse–>synchronized cardioversion unstable pt w/o pulse–>unsynchronized cardiovernsion
    stable patient–> lidocaine/amiodarone/procainamide
  2. EKG–>sinus tach, atrial and ventricular arrhythmia

CXR: cephalization of flow, effusion, pulm vasc congestion, cardiomegaly

oximetry (may want ABGs too): hypoxia, respiratory alkalosis

Echo: diastolic vs systolic dysfunction

  1. nesiritide=synthetic atrial natruiretic peptide that’s used for acute pulmonary edema as part of preload reduction
39
Q

Chronic CHF Management

  1. Systolic dysfunction (low LVEF)
  2. diastolic dysfunction
  3. side effect spironolactone
  4. what if pt still dyspneic after optimized therapy
  5. what is most common cause of death in CHF
  6. biventricular pacemaker
  7. absolute contraindication to b-blockers
A
  1. Systolic dysfunction (low LVEF)
    ACEI/ARB–LOWERS MORTALITY
    metoproplol/carvedilol/bisproprolol–LOWERS MORTALITY
    sprionolactone–LOWERS MORTALITY if advanced CHF
    diuretics
    digoxin
    hydralazine/nitrates (if can’t use ACEI/ARB)
  2. diastolic dysfunction
    metoproplol/carvedilol/bisproprolol–LOWERS MORTALITY
    diuretic
  3. antiandrogenic. causes erectile dysfunction and gynecomastia. can switch to eplerenone. lowers mortality
  4. ivabradine: inhibits funny channels SA node
    sacubitril/valsartan: alternative to ACEI. inhibits nerprilysin that degrades bradykinin and BNP. lower mortality
  5. sudden death from arrhythmia. if LVEF <35% that persists than implantable defibrillator.
  6. decreases mortality if pt still dyspneic & wide QRS (>120). LVEF <35%. “cardiac resynchronization therapy”
  7. symptomatic bradycardia
40
Q

acquired long QT

A
  • diruetics (electrolye imbalanaces)
  • antiemtics (ondansetron)
  • antipsychotics (haloperidol, quetiapine, risperidone)
  • tricyclic antidepressants
  • SSRI (citalopram)
  • antiarrhythmics (amiodarone, sotalol, flecainide)
  • antianginal drugs (ranolazine)
  • anti-infective drgus (macrolides, flouroquinolones, antifungals)

metabolic disorders: starvation, electrolyte imbalances, hypothyroidism

bradyarrhythmias: sinus nose dysfunction, AV block
others: HIV infections, intracranial dx, MI, myocardial ischemia, hypothermia

41
Q

Wolff-Parkinson White

A
  • cardiac preexcitation due to accessory pathway that conducts faster than AV node and excites ventricles prematurely.
  • EKD: short PR, delta wave, wide QRS (>.12 sec)
  • can be asymptomatic but some people develop tachyarrhythmias (most commonly paroxsymal SVT). if WPW pt develops afib can conduct down accessory pathway quickly leading to syncope. EtOH triggers afib
  • consider catheter ablation, esp if tachyarrhythmias
42
Q

Treatment peri-infarction pericarditis

A

high dose aspirin

43
Q

What are patients with bicuspid aortic valve at risk of developing

A
  • bicuspid aortic valve = most common congenital heart dx in adults.
  • aortic dilation, aortic aneurysm, aortic dissection
44
Q

Mitral Stenosis

A

PE: loud S1, opening snap, mid-diastolic rumble

CXRL pulmonary blood flow redistribution to upper lobes, dilated pulmonary vessels, LAE, flattened left heart border

EKG: “p mitrale” (broad, notched p waves

TTEL MV thickening/calcification

45
Q

Pulseless electrical Activity

A

presence of organized EKG rhythm (i.e. afib with rapid ventricular rate) without sufficient cardiac output to produce palpable pulse or measurable BP

  • need CPR immediately .
  • defibrillation or cardioversion not indicated to PEA
46
Q

Compartment Syndrome

  1. common complication
  2. how do you diagnose
  3. treatment
A
  1. pts may develop rhabdomyolysis and release myoglobin. heme pigment from myoglobin is nephrotoxic. patients may develop acute renal failure, especially if they’re volume depleted
  2. direct measurement of compartment or tissue pressure.
  3. if improving can observe. otherwise fasciotomy. clinical assessments are unreliable indicator of dx severity
47
Q

investigating blunt chest injury

A

stabilize and then CXR and then EKG

48
Q

what is most common arrhythmia associated with inferior wall MI

A

sinus brady . should treat with IV atropine . if persistent then think vol. depletion and give IV fluids

49
Q

cocaine related chest pain

A

-most acute cardiovascular effect of cocaine due to inhibition of presynaptic repute of NE –>overstim of alpha and beta receptors –>tachy, increase contractility, casoconstriction, HTN. leads to increase myocardial demand and decrease in supply resulting in myocardial ischemia and ACS. the HTN can lead to aortic dissection. cocaine also stimulated PLT activity and potentiates thrombus formation–>thrombotic occlusion of coronary arteries can happen. so ASA should be given early. if ST elevation persists despite initial medical therapy then do coronary angiography with percutaneous coronary intervention!

benzos are preferred initial treatment since b-blockers are contraindicated.

b-blockers are contraindicated for cocaine ingestions b/c risk of excessive alpha-1 receptor mediated vasoconstriction.

50
Q

Pediatric dyslipidemia

-screening recommendation

A

all people 9-11 and 17-21 should be screened. if risk factors perform at age >2 years and every 2 years after that

51
Q

HTN

effects of lifestyle modifications

A

weight loss most effective nonpharmacologic measure to decrease BP in overweight people. then DASH diet, exercise, reduced NA, cut back EtOH

52
Q

aortic Stenosis

A
  • soft, single S2
  • delayed and diminished carotid pulse “pervious and trades”
  • loud and late peaking systolic murmur
53
Q

common side effect of CCBs

A

peripheral edema. ACEI can cause angioedema (face, upper airway, lips)

54
Q

Acute Aortic dissection

  1. diagnosis
  2. treatment
A
  1. diagnosis
    CXR: mediastinal widening
    EKG:normal or nonspecific ST & T wave changes
    CT angiography or TEE for definitive diagnosis
  2. treatment
    - morphine for pain
    - IV b-blockers: esmolol
    - Na nitroprusside* if SBP >120mmHG
    - surgical repair

b-blockers preferred initial therapy. nitroprusside used in add’n if BP remains high

55
Q

Cardiac Tamponade

  1. Etiology
  2. Clinical signs
  3. Diagnosis
  4. treatment
  5. what is most dangerous therapy
A
  1. Etiology
    - aortic aneurysm/post MI
    - malignancy/radiation therapy
    - infection (viral, Tb)
    - connectie tissue dx
    - CV surgery
  2. Clinical signs
    - pulsus paradoxus (SBP lowers >10mmHg on inspiration)
    - shortness of breath, hypotension, JVD
  3. Diagnosis
    EKG: low voltage QRS, electrical alternans
    CXR:big cardiac silhouette, clear lungs
    Echo: right atrial and ventricular collapse, IVC plethora
    right heart catheterization will show equalization of pressures in heart during diastole
  4. treatment:immediate pericardiocentesis . long term: pericardial window placement.
  5. most dangerous therapy diuretics!
56
Q

Pulmonary HTN

  1. initial evaluation test
  2. treatment if idiopathic
A
  1. initial evaluation test
    TTE for pulmonary arterial pressure
  2. treatment if idiopathic: endothelin receptor antagonists (bosentan, ambrisentan). endothelin, which is a vasoconstricting hormone made by endothelia cells and endothelin receptors are abundant in pulmonary arteries
57
Q

difference in treatment strategies for bradyarrhythmias associated with acute inferior vs acute anterior MIs

A

1.inferior MI commonly associated with AV block and sinus brady. bradyarrhythmias associated with acute inferior MI are usually transient and respond to IV atropine.

in contrast, bradyarrhythmias associated with anterior MI usually due to damage to the conduction system below AV node. AV block in the setting of anterior MI is BAD. will not respond to atropine. NEED pacing

58
Q

Warfarin Interactions

  1. increase warfarin effect (increase INR)
  2. decrease warfarin effeect (decrease INR)
  3. INR-independent interaction
A
  1. increase warfarin effect (increase INR)
    a. metronidazolem quinolones (alter intestinal flora)
    b. azoles, amiodarone (CYP2C9 inihibition)
    c. acetaminophen (decrease Vit K recycling)
  2. decrease warfarin effeect (decrease INR)
    a.rifampin, phenytoin, SJW (CYP2C9 induction)
    b.oral contraceptives
    (increase coagulation factors)
    c.green leafy vegetables (increase vit K ingestion)
  3. INR-independent interaction
    a. NSAIDs, clopidogreal inhibit PLT fxn
    b. ginkgo biloba increases bleeding
59
Q

Mitral regurgitation

1. recommendation for valvular surgery

A
  1. symptomatic MR and LVEF <60%
60
Q
  1. Systolic Murmurs
  2. Diastolic Murmurs
  3. effect of inhaling on murmurs
A
  1. Systolic Murmurs: aortic stenosis, mitral regurgitation, mitral valve prolapse, HCOM
  2. Diastolic Murmurs: aortic regurgitation, mitral stenosis
  3. left sided murmurs decrease in intensity, while right sided murmurs increase
61
Q

effect on murmur:

  1. Valsalva and standing
  2. squatting and leg raise
A

effect on murmur:

  1. Valsalva and standing: decrease venous return, decrease murmur intensity EXCEPT HCOM and MVP
  2. squatting and leg raise: increase venous return, increase murmur intensity except HCOM and MVP
62
Q

effects on AR, MR, VSD, MVP, HCOM

  1. handgrip: worsens/lessens
  2. amyl nitrate: worsens/lessens
A
  1. worsens murmur of AR, MR, VSD because increased afterload pushing more blood backwards.

improves MVP and HCOM (these lessen when LV is fuller. increased afterload means LV doesn’t empty and bigger LV lessens obstruction in HCOM)

  1. amyl nitrate is vasodilator that decreases afterload so improves AR, MR, VSD

worsens MVP and HCOM because it increases ventricular emptying and decreases size on LV

63
Q

effect of hand grip and amyl nitrate on aortic stenosis

A

hand grip: you cant have a murmur if blood isn’t leaving ventricle so hand grip (increased afterload) softens murmur of aortic stenosis.

amyl nitrate: AS murmur depends on pressure gradient between LV and aorta. amyl nitrate decrease afterload and decreases the pressure at the aorta causing increased gradient between LV and aorta so murmur will get louder.

64
Q

what is best initial diagnostic test for a murmur? what is most accurate test

A

initial: echo
accurate: left heart catheterization (can also measure P)

65
Q

treatment of murmurs:

  1. regurgitant
  2. stenotic
  3. typically, what is indicated if Valsalva improves murmur, amyl nitrate improves murmur
A
  1. regurgitant
    get better with vasodilator therapy, ACEI/ARBs, nifedipine. slows progression.. if murmur gets worse with handgrip then ACEI. if no improvement then valve replacement.
  2. stenotic
    anatomic repair. diuretics can decrease pulmonary vascular congestion
    MS: balloon valvuloplasty
    AS: surgery
  3. if Valsalva improves murmur–>diuretics
    if amyl nitrate improves murmur–>ACEI
66
Q

treatment of murmurs:

  1. regurgitant
  2. stenotic
  3. typically, what is indicated if Valsalva improves murmur, amyl nitrate improves murmur
A
  1. regurgitant
    get better with vasodilator therapy, ACEI/ARBs, nifedipine. slows progression.. if murmur gets worse with handgrip then ACEI. if no improvement then valve replacement.
  2. stenotic
    anatomic repair. diuretics can decrease pulmonary vascular congestion
    MS: balloon valvuloplasty
    AS: surgery
  3. if Valsalva improves murmur–>diuretics
    if amyl nitrate improves murmur–>ACEI
67
Q

Aortic Stenosis
PE:
diagnosis
treatment

A

PE: frequently present with chest pain.
rescendo-decrescendo systolic murmur best heard at 2nd right intercostal space, radiating to carotid artery

diagnosis: TTE best initial, TEE more accurate, left catheterization most accurate and can get pressures. LVH on CXR and EKG

treatment:
valve replacement
-bioprostheic valves last 10 years, no warfarin
-mechanical valves last longer but need warfarin

also give diuretics but won’t alter long term prognosis

68
Q

Aortic Regurgitation

  1. possible causes
  2. PE:
  3. diagnosis
  4. treatment
A
  1. possible causes: HTN, rheumatic heart dc, endocarditis, cystic medial necrosis. shortness of breath, fatigue
  2. PE: diastolic decrescendo murmur best heard at left sternal border. rare: bounding pulses “water hammer”, head bobbing
  3. diagnosis:TTE best initial, TEE more accurate, left catheterization most accurate. LVH on CXR and EKG
  4. treatment: ACEI/ARBs, nifedipine. can add loop diuretic. surgery when LVEF <55%
69
Q

Mitral Stenosis

  1. possible causes
  2. PE:
  3. diagnosis
  4. treatment
A
  1. possible causes: rheumatic fever most common
  2. PE:
    dysphagia (big LA pressing on esophagus)
    hoarseness (pressure on recurrent laryngeal)
    afib (can lead to stroke)
    diastolic rumble after OPENING SNAP (extra sound during diastole)
  3. diagnosis:TTE best initial, TEE more accurate, left catheterization most accurate. left atrial hypertrophy, straightening of left heart border and elevation on left mainstem bronchus on CXR
  4. treatment: give diuretics but they don’t alter progression so will need balloon valvuloplasty (pregnancy not a contraind)
70
Q

Mitral Regurgitation

  1. possible causes
  2. PE:
  3. diagnosis
  4. treatment
A
  1. possible causes: HTN, ischemic heart dx, or anything that makes heart dilate. cant have dilation of heart without mitral valve leaflets separating
  2. PE: dyspnea on exertion common presentation. holosystolic and obscures s1, s2. best heard at apex and radiates to axilla
  3. diagnosis: TTE best initial, TEE more accurate
  4. treatment: ACEI/ARBs, nifedipine. can add loop diuretic. surgery (valve replacement) when LVEF <60
71
Q

VSD

  1. PE:
  2. diagnosis
  3. treatment
A
  1. PE: holosystolic at left sternal border. if big then shortness of breath
  2. diagnosis: echo. catheterization can determine degree of left–>right shunting
  3. mechanical closure if large
72
Q

ASD

  1. PE:
  2. diagnosis
  3. treatment
A
  1. PE: if large then shortness of breath, parasternal heave signs of right ventricular failure. FIXED SPLITTING OF S2
  2. diagnosis:echo
  3. treatment: percutaneous or catheter device. repair wen shunt ratios > 1.5 to 1
73
Q

S2 splitting

  • fixed
  • wide, P2 delayed
  • paradoxical, A2 delayed
A
  • fixed: ASD
  • wide, P2 delayed: RBBB, pulmonic stenosis, RVH, pulmonary HTN
  • paradoxical, A2 delayed: LBBB, aortic stenosis, LVH, HTN
74
Q

Dilated Cardiomyopathy

  • common causes
  • management
  • diagnostic testing
  • treatment
A
  • common causes: ischemia, EtOH, radiation, Chagas, Adriamycin
  • management: same as CHF
  • diagnostic testing: echo
  • treatment: ACEI/ARBs, b-blockers and spironolactone (decrease heart’s work), digoxin, ivabradine if HR>70
75
Q

Hypertrophic Cardiomyopathy

  • typical presentation
  • diagnostic testing
  • treatment
A
  • typical presentation: S4 gallop, shortness of breath on exertion
  • diagnostic testing: echo
  • treatment: b-blockers and diuretics
76
Q

Restrictive Cardiomyopathy

  • typical presentation
  • diagnostic testing
  • treatment
A

-typical presentation: usually shortness of breath with hx of sarcoidosis, amyloidosis, cancer, myocardial fibrosis, hematochromatosis, glycogen storage dx. Kussmaul’s sign: shortness of breath on inhalation

-diagnostic testing:
cardiac catheterization : rapid x and y descent
EKG: low voltage
echo mainstay!
endomyocardial biopsy most accurate

-treatment diuretics and correct underlying cause

77
Q

Takotsubo Cardiomyopathy

  • typical presentation
  • diagnostic testing
  • treatment
A
  • typical presentation: sudden systolic dysfunction brought on by extreme emotions. typically post-menopausal woman with sudden psychological stress. present like acute MI with ventricular dysfunction except coronaries are normal.
  • treatment: ACEI,diuretics, b-blockers
78
Q

Pericarditis

  1. possible causes
  2. PE:
  3. diagnosis
  4. treatment
A
  1. possible causes: most are viral
  2. PE: pleuritic & positional chest pain that’s sharp & brief. friction rub
  3. diagnosis: EKG showing diffuse ST elevation
  4. treatment: NSAID (high dose aspirin, indomethacin, naproxen, ibuprofen+ colchicine). if persistent pain then oral prednisone.
79
Q

Constrictive Pericarditis

  1. possible causes
  2. PE:
  3. diagnosis
  4. treatment
A
  1. possible causes
  2. PE: shortness of breath, signs of right heart failure (edema, JVD, ascites, hepatospelonomegaly).
    - kussmals sign: increase JVP on inhalation
    - pericardial knock: extra diastolic sound from heart hitting calcified thickened pericardium
  3. diagnosis:
    CXR: calcification
    EKG: low voltage
    CT, MRI: thick pericardium
  4. treatment
    diuretic best initial
    pericardial stripping most effective
80
Q

Aortic Dissection

  1. PE:
  2. diagnosis
  3. treatment
A

1.. PE: severe/ripping chest pain radiating to back, difference in BP between arms

  1. diagnosis :
    initial CXR showing wide mediastinum.
    most accurate CT angiography
    EKG
  2. treatment: b-blockers, then nitroprusside for BP control. need surgical correction
81
Q

Abdominal Aortic Aneurysm

screening

A

screening: abdominal u/s all 65-75 yo men who are former or current smokers. repair if >5cm

82
Q

Atrial Fibrillation

  1. presentation
  2. diagnosis
  3. treatment
  4. Atrial Flutter management
A
  1. presentation: palpations, irregular pulse in patient with hxof cardiomyopathy, ischemia, HTN. EtOH can trigger
  2. diagnosis: EKG, if negative then overnight telemetry. if stable can do holter
  3. treatment
    unstable (confusion, SBP<90, CHF, chest pain): synchronized electrical cardioversion
    stable:
    a. rate control b-blockers (metoprolol, carvedolol), CCBs (diltiazem), digoxin

after rate control give anticoag

a. managed the same as afib

83
Q

How to pick right rate control med for Afib or Aflutter

b-blockers vs CCBs vs digoxin

A

B-blockers (metoprolol): pheocytochromocytoma, migraines, graves dx, ischemic heart dx

CCBs (diltiazem): asthma, migraine

digoxin: borderline hypotension

84
Q

Multifocal Atrial Tachycardia

  1. presentation
  2. diagnosis
  3. treatment
A
  1. presentation: like an atrial arrhythmia associated with COPD/emphysema
  2. diagnosis
    EKG: polymorphic p waves, tachy, irreg chaotic rhythm
  3. treatment: 1st oxygen then diltiazem
    NO B-BLOCKERS!
85
Q

Supraventricular Tachycardia

  1. presentation
  2. diagnosis
  3. treatment
A
  1. presentation: palpitations, tachy, sometimes syncope
  2. diagnosis: regular rhythm with ventricular rate 160-180
    if EKG normal then Holter or telemetry
  3. treatment:
    unstable: synchronized cardioversion
    stable:
    1st vagal maneuvers
    2nd IV adenosine
    long term: ablation
86
Q

Wolff Parkinson White Syndrome

  1. presentation
  2. diagnosis
  3. treatment
A
  1. presentation: SVT that alternates with Vtach. gets worse after CCB or digoxin
  2. diagnosis
    EKGL delta wave
  3. treatment
    procainamide
    long term: radiofrequency ablation
87
Q

Ventricular Tachycardia

  1. presentation
  2. diagnosis
  3. treatment
  4. torsades
A
  1. presentation: syncope, chest pain, sudden death or palpitations
  2. diagnosis:if EKG normal then telemetry
  3. treatment
    unstable: synchronized cardioversion
    stable: amiodarone, lidocaine, Mg, procainamide
  4. torsades is vtach with undulating amplitude. ALWAYS GIVE MG
88
Q

Ventricular Fibrillation

  1. presentation
  2. diagnosis
  3. treatment
A
  1. presentation: sudden death
  2. diagnosis: EKG
  3. treatment: ALWAYS unsynchronized cardioversion first! vfib defib

Step 3 (22 decks)

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