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USMLE Step 3 > Cardiology - Ischemic Heart Disease > Flashcards

Cardiology - Ischemic Heart Disease Flashcards

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USMLE® Step 1 flashcards
1
Q

List the 8 risk factors for coronary artery disease

A

Diabetes, HTN, Tobacco use, HLD, PAD, Obese, inactivity, family history

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2
Q

For family history to be a significant risk factor of CAD, at what age cut off does the family member have to have had a cardiovascular event?

A

Females <65 and Males <55

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3
Q

What are the three features that when presenting with chest pain, make CAD less likely?

A

Pleuritic pain (change with respiration), positional pain (change with body position), tenderness on palpation

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4
Q

What is the most common cause of chest pain that is NOT cardiac?

A

GERD

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5
Q

An alcoholic patient comes to ED with chest pain. There is n/v and epigastric tenderness. What do you recommend?

A

lipase and amylase levels

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6
Q

What cardiovascular exam finding indicates a dilated ventricle?

A

S3 gallop (rapid ventricular filling during diastole)

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7
Q

What cardiovascular exam finding indicates LVH?

A

S4 gallop (stiff noncompliant left ventricle)

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8
Q

What cardiovascular exam finding indicates mitral regurg?

A

holosystolic murmur

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9
Q

What is the most accurate test for ischemic heart disease? List two

A

CKMB and troponin

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10
Q

Which test for ischemic heart disease rises 3-6 hours after start of chest pain and lasts 1-2 days?

A

CKMB

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11
Q

Which test for ischemic heart disease rises 3-6 hours after start of chest pain and lasts 1-2 weeks?

A

troponin

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12
Q

Which troponin binds calcium to activate actin:myosin interaction?

A

Troponin C

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13
Q

Which troponin binds to tropomyosin?

A

Troponin T

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14
Q

Which troponin blocks actin:myosin interaction?

A

Troponin I

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15
Q

Which cardiac enzyme rises first after start of chest pain? CKMB, Troponin, Myoglobin?

A

Myoglobin (as early as 1-4 hours after start of chest pain)

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16
Q

What kind of patient gets dipyridamole or adenosine thallium stress test or dobutamine echo?

A

Patients who cannot exercise to target heart rate of >85% maximum (due to COPD, amputation, deconditioning, weakness/previous stroke, lower extremity ulcer, dementia, obesity)

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17
Q

What kind of patient gets exercise thallium testing or stress echo?

A

When EKG unreadable for ischemia (LBBB, dig use, pacemaker, LVH, any baseline abnormality of the ST segment on EKG)

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18
Q

What kind of patient gets a Sestamibi nuclear stress test?

A

Very obese or large breasts (radioisotope can penetrate tissue better)

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19
Q

What is worse? Reversible or fixed ischemia?

A

reversible (fixed means it’s an old infarct)

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20
Q

Decreased or increased thallium in damaged myocardium?

A

decreased uptake (Na/K normally thinks thallium is K+, healthy tissue takes it up)

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21
Q

What is the best initial therapy for all cases of ACS?

A

Aspirin (instantly inhibits platelets)

  • reduces mortality by 25% for acute MI
  • reduces mortality by 50% in “unstable angina”
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22
Q

Besides ASA, what other medications should we give for ACS that do NOT lower mortality?

A

Nitrates, morphine, Oxygen

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23
Q

What other platelet inhibitor is added to ASA for all patients with acute MI?

A

Clopidogrel (a thienopyridine) or ticagrelor

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24
Q

What platelet inhibitor is given only when angioplasty is done for acute MI?

A

Prasugrel (a thienopyridine)

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25
Q

What is the mechanism of action for clopidogrel, prasugrel, and ticagrelor?

A

P2Y12 antagonist: block platelet aggregation by blocking ADP-induced activation of P2Y12 receptor. THESE ALL LOWER MORTALITY in ACS

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26
Q

What two treatments of STEMI lower mortality AND are dependent on time?

A

thrombolytics and primary angioplasty

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27
Q

How many minutes do we have to perform a PCI upon arrival of a STEMI to the ED?

A

90 minutes

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28
Q

When are thrombolytics indicated for a patient with STEMI?

A

patient with chest pain <12 hours and has STEMI in 2 or more leads. A new LBBB is also an indication.

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29
Q

How many minutes do we have to give thrombolytics to a STEMI patient upon arrival to the ED, if PCI within 90 minutes is not an option?

A

30 min

30
Q

How do thrombolytics work?

A

Cleave plasminogen to activate into plasmin (chops fibrin into D dimers). Plasmin is inactivated by factor XIII

31
Q

Why and when do we give beta blockers in ACS?

A

We give beta blockers to lower mortality, but timing is not critical

32
Q

ACE I or ARBs lower mortality for ACS in what kind of patients?

A

YES (regardless of what EKG shows or trop/CKMB), always lower mortality!

33
Q

Should everyone with ACS get a statin?

A

Make sure to get a lipid panel to evaluate, but usually

34
Q

What is the most common cause of death in both CHF and MI?

A

ventricular arrhythmia from ischemia (beta blockers help mortality by being anti-arrhythmic and anti-ischemic)

35
Q

What are the 6 medications/interventions that ALWAYS lower mortality in ACS?

A

Aspirin, beta blockers, statins, angioplasty, clopidogrel/ticagrelor/prasugrel, thrombolytics

36
Q

Which platelet inhibitor is associated with neutropenia?

A

ticlopidine

37
Q

When are beta blockers indicated in MI/ACS and what do we give instead?

A

Patient has severe reactive airway disease (asthma), patient has cocaine-induced chest pain, patient has prinzmetal angina/coronary vasospasm. Give Ca channel blockers instead (verapamil, diltiazem)

38
Q

When do we give pacemaker in MI? (list 4 arrhythmia associated conditions)

A

Third degree AV block, mobitz II/second degree AV block, bifascicular block, new LBBB, symptomatic bradycardia

39
Q

What do we give for acute MI with vtach or vfib?

A

amiodarone or lidocaine (never as PPX though! only to treat!)

40
Q

Between prasugrel and clopidogrel, which one is more effective and which one causes more bleeding?

A

prasugrel both is more effective and causes more bleeding (ages > 75 and weighing < 60 kg)

41
Q

If a patient has cardiogenic shock after an MI, what do ou order?

A

Echo and Swan Ganz catheter to evaluate cardiac output. Treat with ACEI and urgent revascularization

42
Q

If a patient has a valve rupture as a complication after MI, what do you order?

A

Echo to evaluate. Then to stabilize you use ACEI, nitroprusside, intra-aortic balloon bridge if necessary, ultimately SURGERY to correct/repair this.

43
Q

If a patient has a septal rupture after an MI, what do you order?

A

Echo, right heart catheter. You will see step up in saturation from RA to RV which is NOT normal (there is a leak!). Then Treat with ACEI, nitroprusside, and urgent surgery

44
Q

If a patient has a myocardial wall rupture, what do you order?

A

Echo, then stabilize with pericardiocentesis. Ultimately treated with urgent cardiac repair.

45
Q

If a patient has sinus bradycardia after an MI, what do you order?

A

EKG to evaluate for arrhythmia. Use atropine at first followed by a pacemaker if symptomatic.

46
Q

If a patient has third-degree (complete) heart block after an MI, what do you order?

A

EKG to evaluate. You will see canon “a” waves. Treat with atropine and ultimately pacemaker (even if asymptomatic)

47
Q

What do you order in the case an MI patient re-infarcts in the right ventricle?

A

EKG to evaluate. Then treat with fluid loading before cath lab.

48
Q

What medications do all post-MI patients go home with?

A

Beta-blocker, statin, clopidogrel (or prasugrel), ACEI, aspirin

49
Q

Heparin and glycoprotein IIb/IIIa inhibitors are predominantly used to treat what kind of cardiac issue?

A

NSTEMI
compared to STEMI: heparin > thrombolytics, and Glycoprotein IIb/IIIa (i.e. eptifibatide, tirofiban, abciximab) significantly lower mortality

50
Q

Besides being within 12 hours of chest pain onset, what is the other clinical finding on EKG that must be present to use thrombolytics?

A

STEMI or new LBBB

51
Q

How does heparin work?

A

potentiates antithrombin (which works on almost every step of the clotting cascade)

52
Q

What two main medications lower mortality in all cases of chronic angina

A

metoprolol and aspirin

53
Q

What other comorbidities will warrant adding ACEI/ARB to medical management help stable angina?

A

CHF, systolic dysfunction, low EF

54
Q

What is angio mainly used for?

A

To evaluate for CABG, medical management doesn’t need angio, and neither does the diagnosis of CAD.

55
Q

What is the main difference between saphenous vein grafts and internal mammary artery grafts?

A

Saphenous vein lasts 5 years

internal mammary artery lasts 10

56
Q

What are the indications for CABG?

A
  • 3 vessels with >70% occlusion
  • 2-3 vessels with low EF
  • 2 vessels in a diabetic
  • left main coronary artery occluded >50-70%
57
Q

What are the two main criteria to give statin in ACS patient?

A

ANY case of CAD, or equivalent with LDL>100 mg/dL

58
Q

What is the LDL goal for a CAD patient with DM?

A

LDL < 70mg/dL

59
Q

What 10 year risk of CAD cut off means your patient is getting a statin?

A

> 7.5%

60
Q

What 5 risk factors go into determining need for statin therapy?

A

HTN (even if controlled on meds), HDL <40mg/dL, tobacco, fam h/o early CAD (female <65, male <55), age (male >45, female >55)

61
Q

Which diseases are considered CAD equivalents meaning they get a statin regardless of LDL level?

A
  • peripheral artery disease
  • aortic disease
  • carotid disease
  • cerebrovascular disease
62
Q

The most common side effect of statin therapy is…?

A

liver tox

63
Q

When do we use PCSK9 inhibitors? (evolocumab and alirocumab)

A

severely elevated LDL not controlled by statin at max dose

this drug does NOT lower mortality. This inhibitor blocks the enzyme that interferes with the clearance of LDL by the liver from the blood

64
Q

What’s the first step when a patient comes in with CHF exacerbation with acute pulmonary edema?

A

TREAT: oxygen, furosemide, nitrates, and morphine

pulmonary edema is a CLINICAL dx (orthopnea, SOB, rales, S3)

65
Q

What is the mechanism of action for carvedilol

A

anti B1, B2, and a1 - antiarrhythmic, anti-ischemic, anti-hypertensive

66
Q

What are the initial tests to be ordered for pulmonary edema/CHF exacerbation (put on first screen of CCS along with initial treatment with O2, furosemide, nitrates, and morphine)

A

CXR, EKG, oximeter (consider ABG), echocardiogram

67
Q

What is the mechanism of action of dobutamine, inamrinone, and milrinone?

A

Inamrinone and milrinone are PDE inhibitors, increasing contractility and decreasing afterload (vasodilating).

Dobutamine/dopamine just increases contractility but has a1 agonist activity which causes vasoconstriction and afterload increase

68
Q

What floor should pulm edema be admitted to?

A

ICU

69
Q

Preload reduction is usually enough to treat symptoms of CHF/pulm edema. What do you do if it is refractory?

A

Use contractility inducing agents or positive inotrope (does NOT lower mortality)

i.e. dobutamine, inamrinone, milrinone. This is further management when acute pulm edema is refractory after 30-60 min standard preload reduction. Drug of choice is dobutamine.

70
Q

What do you do if a patient has Vtach with acute pulmonary edema?

A

synchronized cardioversion.

unsynch is vtach without a pulse, or for v fib

71
Q

What is nesiritide?

A

This is a preload reducer that has NO benefit on mortality in acute pulmonary edema. Helpful for reducing SOB symptoms. It works as a synthetic analogue of atrial natriuretic peptide

USMLE Step 3 (2 decks)

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