Cardiology 2.0 Mksap 16 (Part 1)

Front 1

xtypical innocent–sounding heart murmurs

Back 1

1–2/6 short systolic mid–peaking murmurs along left sternal border

Front 2

When is coronary angiography indicated? (3)

Back 2

CSAP with progressive symptoms despite optimal medical therapy, difficulty tolerating medical therapy; high–risk findings on exercise testing

Front 3

How frequently should routine periodic echo be obtained in mild AS, asymptomatic patients?

Back 3

not more than every 3–5 years

Front 4

treatment of claudication symptoms that is stable

Back 4

medical therapy + exercise; NOT percutaneous or revascularization

Front 5

screening for AAA – who should be screened, how and how often?

Back 5

men 65–75 who smoked, 1–time abd US; do not repeat after a normal study

Front 6

leading cause of death in CKD patients

Back 6

CV disease

Front 7

What is the LAPS trial (Lupus Atherosclerosis Prevention Study)?

Back 7

this study failed to show benefit of statins on progression of coronary artery calcification, carotid intima media thickness, or carotid plaque over 2–years in SLE

Front 8

preferred diagnostic test in symptomatic patients with intermediate probability of CAD

Back 8

cardiac stress testing

Front 9

medication change prior to exercise stress testing

Back 9

β–Blockers should be withheld for 24 to 48 hours

Front 10

what is an "indeterminate" or "submaximal" stress test?

Back 10

negative stress test but adequate workload was not achieved

Front 11

When to use pharmacologic stressors?

Back 11

when patient cannot achieve at least 5 METS (Square dancing)

Front 12

MOA of dobutamine as pharmacologic stressor

Back 12

increases myocardial contractility and oxygen demand

Front 13

MOA of adenosine, dipyridamole, regadenoson as a pharmacologic stressor

Back 13

induce regional hypoperfusion through coronary vasodilation

Front 14

Contraindications to exercise ECG testing (6)

Back 14

(MI, arrhythmia, AS, HF, PE, Ao diss) = recent MI (<30 days), uncontrolled arrhythmia, symptomatic severe AS, acute decompensated HF, acute PE, acute aortic dissection

Front 15

radioisotopes used in SPECT studies

Back 15

thallium and technetium

Front 16

medication change prior to adenosine

Back 16

caffeine hold x 24 hours before adenosine (caffeine is an adenosine receptor antagonist)

Front 17

NOTE: Calcium AC scoring is

Back 17

sensitive but not very specific for CAD.

Front 18

cholesterol embolism – lab findings?

Back 18

urine and peripheral eosinophilia

Front 19

groin tenderness, a pulsatile mass, or a femoral bruit is present following coronary angio – Dx? Tx?

Back 19

AV fistula or pseudoaneurysm; Tx with US–guided compression, surgical repair if still bleeding, or nerve compression

Front 20

post–coronary angio, patient presents with hemodynatmic instability or rapidly decreasing Hct – next step?

Back 20

noncontrast abdominal CT

Front 21

TEE provides clearer images of these structures

Back 21

LA and MV

Front 22

TEE appropriate as initial test in these conditions (4)

Back 22

detection of LA thrombus, prosthetic valve dysfunction, and aortic dissection, high probability of endocarditis

Front 23

indication for PA catheters

Back 23

hemodynamically unstable patients, typically those requiring inotropic or vasopressor support

Front 24

goals of B blocker therapy in CSAP

Back 24

HR 55–60/min and ~75% of the heart rate that produces angina with exertion

Front 25

Absolute contraindications to β–blockers (4)

Back 25

severe bradycardia, advanced AV block, decompensated HF, severe reactive airways disease. (use calcium channel blockers instead)

Front 26

Side effects of calcium channel blockers (4)

Back 26

peripheral edema, constipation, dizziness, headache

Front 27

when is ranolazine (Ranexa) indicated?

Back 27

symptomatic CSAP despite B blockers, calcium channel blockers and nitrates

Front 28

MOA of ranolazine (Ranexa)

Back 28

selective inhibition of the late sodium channel. Txt of chronic CHF.

Front 29

S/E of ranolazine

Back 29

prolonged QT, caution with kidney or liver disease

Front 30

2 indications for combination therapy with ASA and clopidogrel

Back 30

recent MI or stent placement

Front 31

MOA of ezetimibe

Back 31

inhibits cholesterol absorption

Front 32

NOTE: Although studies have found dramatic reductions in LDL cholesterol levels,

Back 32

ezetimibe has not been shown to reduce the progression of atherosclerosis or future cardiovascular events.

Front 33

COURAGE trial

Back 33

contemporary PCI combined with aggressive medical therapy was not superior to aggressive medical therapy alone in reducing death or MI

Front 34

BARI–2D trial

Back 34

randomized type 2 DM with class I or II angina to revascularization (PCI or surgery) vs medical therapy; no difference in all–cause mortality or MI at 5 years

Front 35

coronary angiography and PCI should be reserved for

Back 35

symptomatic despite optimal medical therapy, unable to tolerate medications, high–risk findings on noninvasive imaging

Front 36

Indications for surgical revascularization in CAD

Back 36

left main disease and multivessel disease (2–3 vessels) with involvement of proximal LAD and reduced systolic function

Front 37

What is "hybrid" coronary revascularization?

Back 37

combining minimally invasive surgery and PCI; to reduce operative risk

Front 38

s/p PCI, duration of plavix (CSAP)

Back 38

1 year after DES, 1 month after BMS

Front 39

s/p PCI, duration of plavix (ACS)

Back 39

1 year

Front 40

s/p CABG duration of plavix

Back 40

CSAP not indicated, ACS 1 year

Front 41

elective noncardiac surgery in patients with CAD + stent – how long to delay surgery?

Back 41

at least 6 weeks after BMS; at least 1 year after DES

Front 42

use of TIMI risk score

Back 42

to determine aggressive medical therapy vs early invasive approach (>/=3 vs 0–2)

Front 43

how long should surgical revascularization be delayed after stopping clopidogrel?

Back 43

5–7 days

Front 44

advantages of prasugrel (Effient) over clopidogrel? "PRESUGREL"

Back 44

recently approved oral thienopyridine that does not require hepatic conversion to its active form and is more potent with a faster onset than clopidogrel

Front 45

MOA of glycoprotein IIb/IIIa inhibitors

Back 45

block the final common pathway of platelet aggregation

Front 46

trade name of prasugrel

Back 46

Effient. Replacing Plavix.

Front 47

benefit most from glycoprotein IIb/IIIa inhibitors

Back 47

intermediate or high TIMI risk score and patients who undergo an early invasive approach and receive PCI

Front 48

ACUITY and the EARLY ACS trials

Back 48

increased bleeding events and no benefit for routine early glycoprotein IIb/IIIa inhibitors in ED

Front 49

when is LMWH preferred as anticoagulation ?

Back 49

the absence of kidney disease, in planned surgical revascularization, and in those undergoing an early invasive approach

Front 50

When is unfractioned heparin (UFH) preferred as anticoagulation

Back 50

for patients being considered for an early invasive approach, those with increased bleeding risk, and in the setting of kidney disease

Front 51

when is bivaluridin an acceptable alternative to UFH?

Back 51

patients undergoing elective PCI

Front 52

The MIRACL and PROVE IT trials found that

Back 52

high–dose statin therapy initiated soon after an ACS reduced cardiovascular events at 18 months and 2 years, respectively.

Front 53

Code STEMI time goals

Back 53

PCI within 90 mins of first medical contact; if not, thrombolytics within 30 mins

Front 54

target plasma glucose in patients hospitalized with ACS

Back 54

<180

Front 55

High–risk features in patients with STEMI (8)

Back 55

cardiogenic shock, new LBBB, anterior wall MI, HF, extensive ST–segment elevation, SBP <100 mm Hg, HR>100/min, and >75 years

Front 56

therapy for high–risk patient presents to a non–PCI–capable facility

Back 56

thrombolytic therapy and immediate transfer (no waiting to determine if reperfusion has occurred)

Front 57

therapy for patients with cardiogenic shock who present to a non–PCI–capable facility

Back 57

thrombolytic therapy, placement of an intra–aortic balloon pump, and immediate transfer to a PCI facility

Front 58

guideline–suggested door–to–balloon time

Back 58

<90 minutes

Front 59

what is "rescue" PCI?

Back 59

PCI performed in the setting of failed thrombolytic therapy

Front 60

What is "facilitated" PCI?

Back 60

strategy of planned, immediate PCI after full– or half–dose thrombolytic therapy +/– glycoprotein IIb/IIIa inhibitor

Front 61

rescue PCI or facilitated PCI of use?

Back 61

rescue PCI has benefit over conservative therapy or repeat thrombolytics; facilitated PCi should be avoided (increased adverse events)

Front 62

vascular complications of PCI (4)

Back 62

hematoma, arterial pseudoaneurysm, arteriovenous fistula, and retroperitoneal bleeding

Front 63

has the lowest rate of intracerebral hemorrhage among available thrombolytic agents

Back 63

streptokinase

Front 64

the most commonly used criterion to indicate successful reperfusion

Back 64

>50 % Improvement in ST elevation on ECG 1h post tPA

Front 65

initial beta blocker dose in ACS

Back 65

Metoprolol 5mg IV q3–5m x 3 doses; if SBP >90, start metoprolol 25 or 50 mg PO q6h

Front 66

patient with ACS and significant reactive airways disease, which beta blocker to choose?

Back 66

esmolol

Front 67

which should be given early, clopidogrel or glycoprotein 2b3a inhibitors?

Back 67

clopidogrel given at the time of hospital presentation; no benefit of early glycoprotein 2b3a inhibitors ED

Front 68

arrhythmia common with inferior MI

Back 68

bradycardia +/– hypotension; treat with IV fluids, atropine or dopamine

Front 69

arrhythmia common with anterior MI

Back 69

sinus tachycardia

Front 70

implication of complete heart block after MI

Back 70

common after anterior or inferior MI, in inferior infarction, it is usually transient; temporary pacing may be required; in anterior wall MI, it indicates large infarction and poor prognostic sign; permanent pacing required

Front 71

implication of vtach after MI

Back 71

within 24 hours usually self–limited and not assoc with worse outcome; if it occurs later, associated with larger MI and higher mortality risk

Front 72

establishes diagnosis of RV infarction

Back 72

right–sided ECG showing greater than 1 mm of ST–segment elevation in leads V3R and V4R

Front 73

presents 3 to 7 days after the initial MI as hemodynamic compromise with a new holosystolic murmur typically heard along the left sternal border

Back 73

VSD

Front 74

treatment of VSD post MI

Back 74

IABP and vasopressors ffd by surgical repair (mortality >50% but medical treatment alone mortality is 95%)

Front 75

presents several days after infarction with acute pulmonary edema, a loud systolic murmur without a thrill, and rapid progression to cardiogenic shock

Back 75

papillary muscle rupture

Front 76

treatment of papillary muscle rupture after MI

Back 76

IABP, afterload reduction with sodium nitroprusside, diuretics and emergent surgery

Front 77

presents 3 to 7 days after infarction as hemopericardium with pericardial tamponade, electromechanical dissociation, and death

Back 77

rupture of LV free wall

Front 78

risk factors for LV free wall rupture

Back 78

elderly age, female sex, first MI, and anterior location of MI.

Front 79

most common location for a thrombus post anterior MI

Back 79

apex of LV

Front 80

treatment of LV thrombus after MI

Back 80

warfarin x 3–6months

Front 81

NOTE: Current ACC/AHA guidelines allow a great deal of flexibility in choice of PCI or CABG for patients with diabetes,

Back 81

although CABG may be preferred for those with multivessel disease and left ventricular systolic dysfunction.

Front 82

Initial eval of heart failure should focus on assessing

Back 82

functional capacity (NYHA class) and volume status [ by symptoms (shortness of breath, orthopnea, paroxysmal nocturnal dyspnea), physical examination findings, daily body weight monitoring, and diagnostic studies (such as B–type natriuretic peptide [BNP] level)]

Front 83

Standard laboratory evaluation for initial assessment of heart failure

Back 83

CBC, CMP, Ca, Mg, lipid profile, Uric acid, TFTs, urinalysis, (LUTU)

Front 84

utility of BNP

Back 84

differentiating HF vs pulmo disease; <100 pg/mL excludes decompensated HF, but stable heart failure may have "normal ranges" for BNP as high as 500 pg/mL

Front 85

indicated for patients with more severe heart failure (NYHA class III–IV)

Back 85

Treatment with spironolactone and hydralazine–isosorbide dinitrate (the latter specifically for black patients) IN ADDITION TO standard therapy with an ACE inhibitor and a β–blocker

Front 86

NOTE: A higher dose versus a lower dose of ACE inhibitor has not been shown to significantly affect survival

Back 86

but may reduce hospitalizations for heart failure.

Front 87

3 B–blockers that have M&M benefit in heart faliure treatment trials

Back 87

metoprolol succinate extended release, carvedilol, and bisoprolol.

Front 88

Digoxin in heart failure – benefits?

Back 88

Digoxin is not associated with a survival benefit but does decrease rates of hospitalization.

Front 89

patient on spironolactone develops gynecomastia, which alternative agent to choose

Back 89

EPLERENONE, selective aldosterone antagonist, more expensive

Front 90

guidelines for starting spironolactone based on evidence (3)

Back 90

NYHA class III–IV symptoms, K <5 and crea <2.5)

Front 91

two situations in which combined hydralazine and isosorbide dinitrate are indicated for treatment of systolic heart failure

Back 91

when ACE inhibitor or ARB therapy contraindicated (kidney disease or hyperK) and black patients with severe systolic HF (NYHA class III–IV) in addition to standard ACE inhibitor and β–blocker therapy.

Front 92

why use ISDN and not ISMN in heart failure?

Back 92

benefits seen with the hydralazine–isosorbide dinitrate combination are related to increased nitric oxide availability, because hydralazine possesses antioxidant properties and isosorbide dinitrate acts as a nitrate donor.

Front 93

causes of bradycardia

Back 93

dysfunction of sinus node, AV node, or His–Purkinje system; + reversible causes KIDLAT! (hyperK, drugs, Lyme, Thyroid disease)

Front 94

underlying cause of pathologic sinus bradycardia in most patients

Back 94

fibrotic replacement of the sinus node associated with aging (other causes – infarction, surgery damage, infiltrative processes, inc vagal tone, meds, genetic diseases)

Front 95

pathology in second degree AV blocks

Back 95

Mobitz type 1 is disease within AV node, type 2 more worrisome suggesting His Purkinje disease; HR of progressing to CHB

Front 96

two or more nonconducted P waves occur for each QRS complex

Back 96

Advanced second–degree heart block, or high–grade heart block

Front 97

pathology in CHB

Back 97

conduction block in His bundle or below

Front 98

treatment for symptomatic sinus bradycardia or heart block without reversible causes

Back 98

permanent pacemaker

Front 99

common causes of sinus tachycardia

Back 99

pain, fever, anxiety, anemia; in younger, SVTs, in older, AFib, aflutter, Vtach; any age – PACs and PVCs

Front 100

Class II and Class IV antiarrhythmics are contraindicated in

Back 100

decompensated systolic HF or WPW syndrome