Quiz 2 Flashcards

1
Q

<p>Aortic stenosis Tx</p>

A

<p>• Aortic Stenosis – calcification
o Class I = severe AS = replacement
o Class IIa = moderate AS + CABG or heart surgery = replacement
o Class III = contraindicated for replacement
</p>

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2
Q

<p>• Non-bacterial, non-destructive, non-inflammatory masses on one side</p>

A

<p>o Non-bacteria thrombotic endocarditis</p>

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2
Q

<p>Staph IE Tx</p>

A

<p>Native valve—Nafcillin or Cefazolin if methicillin-susceptible; Vancomycin or
Daptomycin if staph is methicillin-resistant or patient is penicillin allergic

Prosthetic valve—add Rifampin for synergy
</p>

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3
Q

<p>• Small deposits on one side of leaflet w/ inflammation – mitral valve</p>

A

<p>o Rheumatic heart disease</p>

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3
Q

<p>Mitral valve area; normal/stenosis</p>

A

<p>o Normal – 3-4 cm2
o Stenotic – < 2 cm2
</p>

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4
Q

<p>Libman-sacks non-bacterial endocarditis features</p>

A

<p>antiphospholipid antibodies = hypercoagulable state; fibrinous verrucae on both sides of leaflet + Inflammation</p>

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5
Q

<p>IE Prophylaxis; indications</p>

A

<p>• Need both of these to be put on prophylaxis:
• Gingival manipulation procedures
• High-risk cardiac condition – prothestic valve, congenital defects, previous infection
</p>

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6
Q

<p>*Aortic Regurgitation; features</p>

A

<p>• Widened pulse pressure
• Decrescendo diastolic murmur
• Austin-flint murmur – diastolic rumble
</p>

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7
Q

<p>Infectious endocarditis </p>

A

<p>ring abscess morphology; large bulky vegetations </p>

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9
Q

<p>Streptococcal IE tx</p>

A

<p>Penicillin or Ceftriaxone if penicillin susceptible; Vancomycin if not </p>

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10
Q

IE Prophylaxis regimen

A
  • One oral dose before dental procedure – amoxicillin 2g or clindamycin 600 grams.
  • IV Ampicilin 2g or ceftriaxone 1 gram
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12
Q

<p>Non-bacterial Thrombotic endocarditis causes</p>

A

<p>hypercoagulable states, pancreatic cancer, sepsis, mucos producing adenocarcinomas (Trousseau syndrome), DVTs, endocardial trauma (catheterization).
No inflammation</p>

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13
Q

<p>Mitral stenosis Tx</p>

A

<p>• Mitral Stenosis – Rheumatic fever
o Symptomatic w/ vascular congestion
 Diuretics
o Atrial fibrillation
 Treatment w/ beta-blockers, Ca channel blockers, digoxin
 Chronic anticoagulation therapy
• Prevent clotting due to stasis of blood in atria
o Significant pulmonary HTN or congestion
 Valve replacement
 Valvuloplasty

</p>

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14
Q

<p>• Bulky, dense, destructive masses on one side of leaflet</p>

A

<p>o Infective endocarditis</p>

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14
Q

<p>• Severe Stenosis; numbers</p>

A
<p>o	Jet velocity > 4.0 m/s
o	Mean gradient > 4.0 mmHg
o	Valve area > 1.0 seconds
o	Valve are index < 0.6
</p>
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14
Q

<p>Enterococci IE Tx</p>

A

<p>Penicillin or Ampicillin or Vancomycin, with Gentamicin </p>

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15
Q

<p>• Non-bacterial, inflammatory masses on one or both sides – AV valves</p>

A

<p>o Libman-Sacks endocarditis</p>

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17
Q

<p>Mitral regurgitation Tx</p>

A
<p>•	Mitral regurgitation - MVP
o	Acute – surgical emergency
o	Chronic
	Asymptomatic – monitor
	Symptomatic – replacement
	Severe LV dysfunction – no treatment; poor prognosis
</p>
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18
Q

<p>Libman-sacks non-bacterial endocarditis cause</p>

A

<p>SLE</p>

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20
Q

<p>Aortic regurgitation Tx</p>

A

<p>• Aortic regurgitation – root dilation
o Acute – surgical emergency
o Asymptomatic w/ LVEF >50% - monitor/observed, decrease afterload (ACE, Ca blockers)
o Asymptomatic w/ LVEF </p>

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21
Q

<p>IE; non-S. aureus organisms</p>

A

<p>• Coagulase (-) staph ¬– most common in early prosthetic IE
• Strep – most common in late prosthetic IE
• Enterococci ¬– most common in elderly; high mortality; hard to eradicate due to antibiotic resistance
• Abiotrophia ¬– nutritionally variant strep; culture-negative
• HACEK group – oral bacteria; subacute IE; culture-negative (fastidious)
</p>

22
Q

<p>Rheumatic fever diagnosis</p>

A

<p>ASO titers, DNAase B antibodies</p>

23
Q

What are the NYHA classes of heart failure

A
Class I (mild)
–Cardiac disease, but no limitation in physical activity
•
Class II (mild)
–Slight limitation of physical activity
–Dyspnea and fatigue with moderate exertion (i.e., walking up
stairs quickly)
•
Class III (moderate)
–Marked limitation of physical activity
–Dyspnea with minimal exertion (i.e., slowly walking up stairs)
–Comfortable only at rest
•
Class IV (severe)
–Severe limitation of activity
–Symptoms are present at rest
24
Q

Systolic Dysfunction Drugs

A

Diuretics

ACE inhibitors/ARBs/Aldosterone antagonists

Beta-blockers

Vasodilators - nitrates, hydralazine

Inotropes - Digoxin

25
Q

Effects of digoxin

A

Direct = increased contractility, and increased vagal tone (decreased HR)

Indirect = arterial and venous dilation, normalized baroreceptors

26
Q

Digoxin; drug interactions

A

quinidine, verapamil, amiodarone

27
Q

Digoxin; use

A

limited; LV systolic dysfunction

28
Q

Other beta-agonists

A

dobutamine, dopamine

29
Q

Beta-agonists; uses

A

IV; temporary hemodynamic control for acute HF

30
Q

Phosphodiesterase inhibitor; what is it

A

Milrinone

31
Q

PDE inhibitors; uses

A

Milrinone - IV for acute HF; positive inotrope and vasodilator

32
Q

Diuretics; types and associated drugs

A

Loop - furosemide

Thiazide - HCTZ

K+ sparing - amiloride, triamterene

33
Q

Diuretics; types and use

A

Loop - widely used; most require chronic therapy

Thiazide - rarely used alone; in combo w/ loop for those refractory to loop

K+ sparing - used to limit K+ and Mg2+ wasting

34
Q

What are the mixed vasodilators

A

ACE inhibitors/ARBs

Hydralazine/isosorbide

35
Q

When to use mixed vasodilators

A

ACE inhibitors - first choice

ARBs - intolerance to ACE inhibitors

Hydralazine/isosorbide - intolerance to both ACE and ARBs

36
Q

What are the aldosterone antagonists and when are they used

A

Spironolactone, eplerenone

Severe CHF; Class III and IV

37
Q

Effects of aldosterone on heart

A

Hypertrophy

Stimulates fibrosis

38
Q

Effect of aldosterone antagonists

A

hyperkalemia

39
Q

Initial effect of beta-blockers

A

Can initially worsen CHF

40
Q

What is neprolysin?

A

Enzyme that breaks down bradykinin, ANP, etc = decreased vasodilation

41
Q

Neprolysin inhibitor/ARB combo

A

Superior to enalapril in preventing mortality

42
Q

Diastolic HF treatment

A

Diuretics - to improve symptoms

No mortality benefit w/ ACE inhibitors, ARBs, etc.

No role for inotropes

43
Q

Two most important signs of acute HF

A

JVD
Third heart sound

Presence of either = increased mortality

44
Q

Most indicative lab values of mortality

A

BUN and creatinine - most

Troponin - also predicts mortality

45
Q

Normal Swan Ganz values and when to use

A

RA - 2-6 mmHg
RV - 25/5 mmHg
PCWP - 12-15 mmHg

When you don’t know what is going on, and when considering advanced therapy (ICD, VAD, etc)

46
Q

Cold + Dry Acute HF treatment

A

Not medically treatable; need SG catheter
-PCWP or RA less than normal - discont. diuretics, give fluids

  • PCWP or RA greater than normal - profile C
  • PCWP or RA normal; requires transplant or VAD, medications only temporary fix
47
Q

Cold + Wet Acute HF treatment

A
  1. Increase CO:
    - Diuretics = decreased volume = better pump function
    - Positive inotropes = increased contractility
    - —Beta-agonists = dobutamine, dopamine
    - —PDE inhibitors = milrinone; also vasodilates = decreased myocardial O2 demand
    - —Digoxin
    - —Levosimendan = similar to milrinone; increases troponin C sensitivity to Ca
48
Q

Diuretics in acute HF

A

Need higher doses than normal due to already altered renal function

  • furosemide = not best, cheap
  • butosemide, torsemide = better, more expensive
49
Q

Challenges to diuretics

A

Braking phenomenon - reduced ANP/BNP responses w/ long-term use

Rebound phenomenon - infrequent dosing = increased Na retention through increased RAAS

Tolerance - tubular hypertrophy

50
Q

Warm + Wet Tx

A
  1. Need to decrease filling pressures (LVEDP and PCWP)
    - Diuretics - IV diuretics
    - Vasodilators - nitrates

Do not use inotropes - increased mortality; systolic BP already high

51
Q

When to use vasodilators vs inotropes

A

SBP > 85 mmHg = vasodilators

SBP < 85 mmHg = inotropes or IABP