Quiz 2 Flashcards
<p>Aortic stenosis Tx</p>
<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>
<p>• Non-bacterial, non-destructive, non-inflammatory masses on one side</p>
<p>o Non-bacteria thrombotic endocarditis</p>
<p>Staph IE Tx</p>
<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>
<p>• Small deposits on one side of leaflet w/ inflammation – mitral valve</p>
<p>o Rheumatic heart disease</p>
<p>Mitral valve area; normal/stenosis</p>
<p>o Normal – 3-4 cm2
o Stenotic – < 2 cm2
</p>
<p>Libman-sacks non-bacterial endocarditis features</p>
<p>antiphospholipid antibodies = hypercoagulable state; fibrinous verrucae on both sides of leaflet + Inflammation</p>
<p>IE Prophylaxis; indications</p>
<p>• Need both of these to be put on prophylaxis:
• Gingival manipulation procedures
• High-risk cardiac condition – prothestic valve, congenital defects, previous infection
</p>
<p>*Aortic Regurgitation; features</p>
<p>• Widened pulse pressure
• Decrescendo diastolic murmur
• Austin-flint murmur – diastolic rumble
</p>
<p>Infectious endocarditis </p>
<p>ring abscess morphology; large bulky vegetations </p>
<p>Streptococcal IE tx</p>
<p>Penicillin or Ceftriaxone if penicillin susceptible; Vancomycin if not </p>
IE Prophylaxis regimen
- One oral dose before dental procedure – amoxicillin 2g or clindamycin 600 grams.
- IV Ampicilin 2g or ceftriaxone 1 gram
<p>Non-bacterial Thrombotic endocarditis causes</p>
<p>hypercoagulable states, pancreatic cancer, sepsis, mucos producing adenocarcinomas (Trousseau syndrome), DVTs, endocardial trauma (catheterization).
No inflammation</p>
<p>Mitral stenosis Tx</p>
<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>
<p>• Bulky, dense, destructive masses on one side of leaflet</p>
<p>o Infective endocarditis</p>
<p>• Severe Stenosis; numbers</p>
<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>
<p>Enterococci IE Tx</p>
<p>Penicillin or Ampicillin or Vancomycin, with Gentamicin </p>
<p>• Non-bacterial, inflammatory masses on one or both sides – AV valves</p>
<p>o Libman-Sacks endocarditis</p>
<p>Mitral regurgitation Tx</p>
<p>• Mitral regurgitation - MVP o Acute – surgical emergency o Chronic Asymptomatic – monitor Symptomatic – replacement Severe LV dysfunction – no treatment; poor prognosis </p>
<p>Libman-sacks non-bacterial endocarditis cause</p>
<p>SLE</p>
<p>Aortic regurgitation Tx</p>
<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>
<p>IE; non-S. aureus organisms</p>
<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>
<p>Rheumatic fever diagnosis</p>
<p>ASO titers, DNAase B antibodies</p>
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
- 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
- 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
