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3rd Year (Step 2) > Cardiology 2 > Flashcards

Cardiology 2 Flashcards

1
Q

Metoprolol MOA?

A

Beta-1 specific antagonist

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2
Q

Bisoprolol MOA?

A

Beta-1 specific antagonist

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3
Q

Carvedilol MOA?

A

Nonspecific Beta-blocker + alpha-1 blocker

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4
Q

Which 3 beta-blockers actually have evidence of benefit in CHF?

A

Metoprolol, Bisoprolol, & Carvedilol

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5
Q

In CHF, when might Spironolactone be effective?

A

Only proven effective for more advanced & serious stages (class 3 & 4), where pt is SOB @ minimal exertion or @ rest

  • benefit directly related to its ability to inhibit effects of aldosterone
  • NOT used @ doses in which it has a diuretic effect
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6
Q

What do you do when a pt w/ severe CHF on Spironolactone develops gynecomastia?

A

Switch it to Eplerenone

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7
Q

Eplerenone’s role in CHF?

A

Same as Spironolactone – inhibits Aldosterone & has proven mortality benefit in stage 3 & 4 CHF – however doesn’t have gynecomastia effects

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8
Q

Digoxin’s role in CHF

A
  • Used to control symptoms of dyspnea & will reduce the number of hospitalizations
  • there is NO mortality benefit w/ Digoxin
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9
Q

Digoxin – Survival benefit in CHF?

A

NO (inotrope)

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10
Q

Spironolactone – Survival benefit in CHF?

A

YES

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11
Q

Eplerenone – Survival benefit in CHF?

A

YES

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12
Q

Beta-blockers – Survival benefit in CHF?

A

ONLY: Metoprolol, Bisoprolol, & Carvedilol

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13
Q

ACE-inhibitors – Survival benefit in CHF?

A

YES

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14
Q

ARBs – Survival benefit in CHF?

A

YES

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15
Q

Ca-channel blockers – Survival benefit in CHF?

A

NO

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16
Q

Milrinone – Survival benefit in CHF?

A

NO (no dec’d mortality in inotropes for CHF)

*MOA = PDE-3 inhibitor (dec’s cAMP brkdwn, inc’s PKA activity… this permits an increase in calcium influx into the cell. This increase in calcium influx permits increased contractility)

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17
Q

Furosemide – Survival benefit in CHF?

A

NO

  • Diuretics have NO survival benefit in CHF, they just treat symptoms when EF is low
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18
Q

Amrinone – Survival benefit in CHF?

A

NO (inotrope)

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19
Q

Dobutamine – Survival benefit in CHF?

A

NO (inotrope)

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20
Q

Hydralazine – Survival benefit in CHF?

A

YES when used in combo w/ Nitrates for systolic dysfunction

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21
Q

2 types of CHF & how to determine which it is?

A

Diastolic dysfunction:

    • preserved EF, sometimes even above normal
    • inability of heart to “relax” & receive blood

Systolic dysfunction:

    • decreased EF
    • Dilation of the heart
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22
Q

2 non-pharm treatments ass’d w/ mortality benefit in CHF?

A

Implantable Defibrillator
&
Biventricular pacemaker

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23
Q

Implantable Defibrillator – indications?

A

Ischemic cardiomyopathy & EF < 35%

  • 25% risk reduction in risk of death
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24
Q

Biventricular Pacemaker – indications?

A

Dilated cardiomyopathy & EF < 35% & wide QRS above 120 milliseconds w/ persistent symptoms

(note: biventricular diff from dual-chamber, which is atrium & ventricle)

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25
Q

Txs w/ clear mortality benefit in systolic-dysfunction CHF?

A
  • ACEi/ARBs
  • Beta-blockers
  • Spironolactone or Eplerenone
  • Hydralazine/Nitrates
  • Implantable Defibrillator

(biventricular pacemaker..?)

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26
Q

Txs w/ clear mortality benefit in diastolic-dysfunction CHF?

A

Beta blockers & diuretics

uncertain: ACEis, ARBs, & Hydralizine

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27
Q

Txs clearly NOT beneficial in diastolic dysfunction CHF?

A

Digoxin & Spironolactone

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28
Q

Worst, most severe form of CHF presents w/ what?

A

Pulmonary Edema (rapid fluid buildup in lungs)

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29
Q

Dx test that can exclude pulmonary edema as cause of SOB?

A

BNP level — if normal, excludes both Pulmonary Edema & CHF as potential causes of the SOB

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30
Q

What will you see on x-ray of Pulmonary Edema?

A

Engorged pulmonary veins above the upper half of the heart

  • filling of blood vessels towards the head, called “cephalization of flow” – b/c normally most blood flow in lungs is @ bases

In more chronic cases, there will be enlargement of heart & pleural effusions

31
Q

Pulmonary Edema - what’s expected on Oximetry/ABGs?

A
  • Hypoxia

- Respiratory alkalosis 2/2 hyperventilation — CO2 leaves more easily than oxygen enters the bloodstream

32
Q

Most important test to do in Acute Pulmonary Edema?

A

ECG – b/c can change immediate therapy if noted that plum edema is 2/2 A. fib, A. flutter, or V. tach
— would need to perform rapid, synchronized cardioversion to restore atrial systole & return atrial contribution to cardiac output

– HOWEVER first thing to do overall is give diuretics to remove fluid from lungs (if clearly SOB w/ pulm edema 2/2 CHF)

33
Q

Initial therapy of acute pulmonary edema?

A
  • Oxygen
  • Loop diuretics (furosemide, bumetinide)
  • Morphine
  • Nitrates
34
Q

Next Tx in acute pulmonary edema if SOB does not respond to preload reduction?

A

Inotropic agents:

  • – Dobutamine
  • could also use Amrinone, or Milrinone (phosphodiesterase inhibitors)
  • Digoxin, but not in acute setting as it takes weeks for it to have an inotropic effect
35
Q

Acute Pulm Edema Tx if SOB doesn’t respond to (1) preload reduction OR (2) Pos Inotropes?

A

Afterload reduction:

    • ACEi & ARBs for long-term use in pts being discharged
    • Nitroprusside & IV Hydralazine in acute setting
36
Q

What type of echo is more sensitive & specific for valvular heart disease?

A

Transesophageal > Transthoracic

37
Q

Most accurate test in valvular heart disease?

A

Catheterization (allows the most precise measurement of valvular diameter)

38
Q

Which valvular heart disease are ass’d w/ fluid overlaid in the lungs?

A

All of them.

Therefore diuretics are useful in all of them as well.

39
Q

Mitral Stenosis Tx?

A
  1. Diuretics & Na-restriction
  2. Balloon valvuloplasty (dilation) via catheter
  3. Valve replacement only when catheter cannot be done, or fails
  4. Warfarin for A. fib to an INR of 2 or 3
  5. Rate control of A. fib w/ Digoxin, Beta-blockers, Diltiazem/Verapamil
40
Q

Aortic Stenosis Tx?

A

Aortic Stenosis needs surgical removal

41
Q

Regurgitant valvular lesions Tx?

A

Respond best to vasodilator therapy, w/ ACEi/ARBs, Nifedipine, or Hydralazine

  • Surgical replacement of regurgitant lesions must be done before the heart dilates beyond repair
42
Q

What marker indicates whether valve must be replaced?

A

End-systolic diameter of the ventricle shows how much the myocardium has stretched.

Important to replace valve before it stretches too much & systolic fx is irreparable.

43
Q

Mitral Stenosis – most common cause?

A

Rheumatic Fever

(extremely uncommon in US – presents in “young adult immigrants who get pregnant” – 50% increase in blood overwhelms C/V system)

44
Q

Unique symptomatic features of Mitral Stenosis?

besides the SOB & CHF ass’d w/ all forms of valvular heart disease

A
    • Dysphagia – from LA pressing on Esophagus
    • Hoarseness – LA pressing on Laryngeal nerve
    • A. Fib – & stroke from enormous LA
    • Hemoptysis
45
Q

Mitral Stenosis murmur?

A
  • Diastole, just after an opening snap

- Squatting & leg raising increase the intensity from inc’d venous return to heart

46
Q

How does LA hypertrophy present itself on ECG in Mitral Stenosis?

A

Biphasic P wave in leads V1 & V2

47
Q 
Cause?
X-ray findings:
- Straightening of left heart border
- Elevation of left main-stem bronchus
- Second "bubble" behind the heart
A

Left Atrial Hypertrophy

2/2 Mitral Stenosis

48
Q

Aortic Stenosis murmur?

A

Systolic, crescendo-decrescendo

  • Sound dec’d w/ handgrip (dec’d EF)
  • Also dec’d w/ standing, & Valsalva (dec’d venous return to heart)
49
Q

Define “cardiac enlargement”

A

Heart greater in diameter than 50% of total transthoracic diameter

50
Q

Aortic Stenosis EKG findings?

A

LVH: S-wave in V1 plus R-wave in V5 greater than 35 millimeters

51
Q

Mitral Regurgitation causes?

A

Anything that causes the heart to dilate

i.e. HTN, endocarditis, MI w/ papillary muscle rupture

52
Q

Mitral Regurgitation murmur?

A

Pansystolic (holosystolic), obscuring both S1 & S2

  • radiates to axilla
  • Handgrip worsens the murmur (Aortic & Mitral Regurgitation murmurs b/c pushes more blood back through valve)
  • Squatting & leg raising worses MR (inc’s venous return to heart)
53
Q

Mitral Regurgitation Tx?

A
  1. Vasodilators: ACEi/ARBs are best
  2. Digoxin & diuretics can be used as in all forms of CHF
  3. Valve replacement
54
Q

Aortic Regurgitation murmur?

A

Diastolic, decrescendo murmur heard best @ LL sternal border

  • Valsalva & standing make it better
  • Handgrip makes it worse
55
Q

Aortic Regurgitation Tx?

A
  1. Vasodilators: ACEi/ARBs are best
  2. Digoxin & diuretics have little benefit
  3. Valve replacement
56
Q

Mitral Valve Prolapse Sx?

A

Usually asymptomatic, but if Sx present…

  • CHF sx absent
  • Atypical CP
  • Palpitations
  • Panic attack
57
Q

MVP murmur?

A

Midsystolic click that, when severe, is ass’d w/ a murmur just after the click from mitral regurgitation

  • Valsalva & standing worsen murmur (opp. of all other murmurs)
  • Handgrip or squatting improves murmur
58
Q

MVP Sx?

A

If symptomatic…

  • Beta-blockers
  • Valve repair (surgical)
59
Q

Cardiomyopathy: Tx common in all types except HOCM?

A

Diuretics

c/i in Hypertrophic Obstructive Cardiomyopathy

60
Q

Murmurs that do NOT increase w/ expiration?

A
  • HOCM

- MVP

61
Q

Hypertrophic Cardiomyopathy distinguishing features vs. other cardiomyopathies?

A
  • S4 gallop

- Fewer signs of RHF such as ascites & enlargement of the liver & spleen

62
Q

Most accurate test to determine precise gradients of pressure across heart chambers?

A

Catheterization

63
Q

EKG findings common in HOCM not seen in MI?

A

Septal Q waves in inferior & lateral leads

64
Q

Septal Q waves in inferior & lateral leads are common in what?

A

HOCM (Hypertrophic Obstructive CM)

  • NOT seen in MI
65
Q

Best initial Tx for HCM & HOCM?

A

Beta-blockers

66
Q

Use in HCM vs. DCM?

Beta-blockers

A

Both

67
Q

Use in HCM vs. DCM?

Diuretics

A

Both

68
Q

Use in HCM vs. DCM?

ACEi/ARBs

A

HCM = Unclear benefit

DCM = Yes

69
Q

Use in HCM vs. DCM?

Spironolactone

A

HCM = No

DCM = Yes

70
Q

Use in HCM vs. DCM?

Digoxin

A

HCM = No

DCM = Yes

71
Q

Amiodarone – MOA?

A

Beta blocker-like and potassium channel blocker-like actions on the SA and AV nodes

  • Increases the refractory period via sodium- and potassium-channel effects
  • slows intra-cardiac conduction of the cardiac action potential, via sodium-channel effects
  • Class 3 antiarrhythmic (prolongs phase 3 of the cardiac action potential, the repolarization phase where there is normally decreased calcium permeability and increased potassium permeability)
72
Q

S3 – what is it & what does it mean?

A

Sound = Blood from the left atrium striking blood that’s already present in the left ventricle, causing reverberation btwn the LV walls.

Means left ventricular failure!

73
Q

Inspiration – effect on venous return?

A

Inspiration increases venous return

Ex: in cardiac tamponade this inc’d VR causes the inter ventricular septum to deviate into the LV, dec’ing end diastolic volume, thus dec’ing stroke volume, thus dec’ing systolic BP – i.e. Pulsus paradoxus

3rd Year (Step 2) (44 decks)

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