Quiz 2 Flashcards by Med Student

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

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

o Non-bacteria thrombotic endocarditis

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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

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

o Rheumatic heart disease

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Mitral valve area; normal/stenosis

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

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Libman-sacks non-bacterial endocarditis features

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

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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

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*Aortic Regurgitation; features

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

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Infectious endocarditis

ring abscess morphology; large bulky vegetations

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Streptococcal IE tx

Penicillin or Ceftriaxone if penicillin susceptible; Vancomycin if not

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IE Prophylaxis regimen

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

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Non-bacterial Thrombotic endocarditis causes

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

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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

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

o Infective endocarditis

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• Severe Stenosis; numbers

<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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Enterococci IE Tx

Penicillin or Ampicillin or Vancomycin, with Gentamicin

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

o Libman-Sacks endocarditis

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Mitral regurgitation Tx

<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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Libman-sacks non-bacterial endocarditis cause

SLE

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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

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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)

Rheumatic fever diagnosis

ASO titers, DNAase B antibodies

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

Systolic Dysfunction Drugs

Diuretics

ACE inhibitors/ARBs/Aldosterone antagonists

Beta-blockers

Vasodilators - nitrates, hydralazine

Inotropes - Digoxin

Effects of digoxin

Direct = increased contractility, and increased vagal tone (decreased HR) Indirect = arterial and venous dilation, normalized baroreceptors

Digoxin; drug interactions

quinidine, verapamil, amiodarone

Digoxin; use

limited; LV systolic dysfunction

Other beta-agonists

dobutamine, dopamine

Beta-agonists; uses

IV; temporary hemodynamic control for acute HF

Phosphodiesterase inhibitor; what is it

Milrinone

PDE inhibitors; uses

Milrinone - IV for acute HF; positive inotrope and vasodilator

Diuretics; types and associated drugs

Loop - furosemide Thiazide - HCTZ K+ sparing - amiloride, triamterene

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

What are the mixed vasodilators

ACE inhibitors/ARBs Hydralazine/isosorbide

When to use mixed vasodilators

ACE inhibitors - first choice ARBs - intolerance to ACE inhibitors Hydralazine/isosorbide - intolerance to both ACE and ARBs

What are the aldosterone antagonists and when are they used

Spironolactone, eplerenone Severe CHF; Class III and IV

Effects of aldosterone on heart

Hypertrophy Stimulates fibrosis

Effect of aldosterone antagonists

hyperkalemia

Initial effect of beta-blockers

Can initially worsen CHF

What is neprolysin?

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

Neprolysin inhibitor/ARB combo

Superior to enalapril in preventing mortality

Diastolic HF treatment

Diuretics - to improve symptoms No mortality benefit w/ ACE inhibitors, ARBs, etc. No role for inotropes

Two most important signs of acute HF

JVD Third heart sound Presence of either = increased mortality

Most indicative lab values of mortality

BUN and creatinine - most | Troponin - also predicts mortality

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)

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

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

Diuretics in acute HF

Need higher doses than normal due to already altered renal function - furosemide = not best, cheap - butosemide, torsemide = better, more expensive

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

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

When to use vasodilators vs inotropes

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