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Flashcards in Quiz 2 Deck (51):
1

Aortic stenosis Tx

• 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

2

• Non-bacterial, non-destructive, non-inflammatory masses on one side

o Non-bacteria thrombotic endocarditis

2

Staph IE Tx

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

3

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

o Rheumatic heart disease

3

Mitral valve area; normal/stenosis

o Normal – 3-4 cm2
o Stenotic – < 2 cm2

4

Libman-sacks non-bacterial endocarditis features

antiphospholipid antibodies = hypercoagulable state; fibrinous verrucae on both sides of leaflet + Inflammation

5

IE Prophylaxis; indications

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

6

*Aortic Regurgitation; features

• Widened pulse pressure
• Decrescendo diastolic murmur
• Austin-flint murmur – diastolic rumble

7

Infectious endocarditis

ring abscess morphology; large bulky vegetations

9

Streptococcal IE tx

Penicillin or Ceftriaxone if penicillin susceptible; Vancomycin if not

10

IE Prophylaxis regimen

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

12

Non-bacterial Thrombotic endocarditis causes

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

13

Mitral stenosis Tx

• 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

14

• Bulky, dense, destructive masses on one side of leaflet

o Infective endocarditis

14

• Severe Stenosis; numbers

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

14

Enterococci IE Tx

Penicillin or Ampicillin or Vancomycin, with Gentamicin

15

• Non-bacterial, inflammatory masses on one or both sides – AV valves

o Libman-Sacks endocarditis

17

Mitral regurgitation Tx

• Mitral regurgitation - MVP
o Acute – surgical emergency
o Chronic
 Asymptomatic – monitor
 Symptomatic – replacement
 Severe LV dysfunction – no treatment; poor prognosis

18

Libman-sacks non-bacterial endocarditis cause

SLE

20

Aortic regurgitation Tx

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

21

IE; non-S. aureus organisms

• 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)

22

Rheumatic fever diagnosis


ASO titers, DNAase B antibodies


23

What are the NYHA classes of heart failure

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

Systolic Dysfunction Drugs

Diuretics

ACE inhibitors/ARBs/Aldosterone antagonists

Beta-blockers

Vasodilators - nitrates, hydralazine

Inotropes - Digoxin

25

Effects of digoxin

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

Indirect = arterial and venous dilation, normalized baroreceptors

26

Digoxin; drug interactions

quinidine, verapamil, amiodarone

27

Digoxin; use

limited; LV systolic dysfunction

28

Other beta-agonists

dobutamine, dopamine

29

Beta-agonists; uses

IV; temporary hemodynamic control for acute HF

30

Phosphodiesterase inhibitor; what is it

Milrinone

31

PDE inhibitors; uses

Milrinone - IV for acute HF; positive inotrope and vasodilator

32

Diuretics; types and associated drugs

Loop - furosemide

Thiazide - HCTZ

K+ sparing - amiloride, triamterene

33

Diuretics; types and use

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

What are the mixed vasodilators

ACE inhibitors/ARBs

Hydralazine/isosorbide

35

When to use mixed vasodilators

ACE inhibitors - first choice

ARBs - intolerance to ACE inhibitors

Hydralazine/isosorbide - intolerance to both ACE and ARBs

36

What are the aldosterone antagonists and when are they used

Spironolactone, eplerenone

Severe CHF; Class III and IV

37

Effects of aldosterone on heart

Hypertrophy

Stimulates fibrosis

38

Effect of aldosterone antagonists

hyperkalemia

39

Initial effect of beta-blockers

Can initially worsen CHF

40

What is neprolysin?

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

41

Neprolysin inhibitor/ARB combo

Superior to enalapril in preventing mortality

42

Diastolic HF treatment

Diuretics - to improve symptoms

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

No role for inotropes

43

Two most important signs of acute HF

JVD
Third heart sound

Presence of either = increased mortality

44

Most indicative lab values of mortality

BUN and creatinine - most
Troponin - also predicts mortality

45

Normal Swan Ganz values and when to use

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

Cold + Dry Acute HF treatment

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

Cold + Wet Acute HF treatment

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

Diuretics in acute HF

Need higher doses than normal due to already altered renal function

-furosemide = not best, cheap
-butosemide, torsemide = better, more expensive

49

Challenges to diuretics

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

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

Tolerance - tubular hypertrophy

50

Warm + Wet Tx

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

When to use vasodilators vs inotropes

SBP > 85 mmHg = vasodilators
SBP < 85 mmHg = inotropes or IABP