Congestive Heart Failure Flashcards
When to start aldosterone antagonists in heart failure?
When there’s symptomatic heart failure in NYHA functional class II, III, IV and LVEF<35%
Post STEMI and LV EF <40% and symptomatic heart failure or DM2
This stops aldosterone driven cardiac remodeling and also has potassium sparing effect on K wasting of loop and thiazide diuretics and so lowers risk for hypokalemic induced arrhythmia.
So avoid in CrCl pts <30 or K>5
NYHA HF class 1
no symptoms of limitation of physical activity
NYHA HF class 2
slight limitation in physical activity (dyspnea w/ climbing stairs)
NYHA HF class 3
marked limitation of physical activity (dyspnea with house chores)
NYHA HF class 4
inability to perform physical activity without significant discomfort
When should aldosterone antagonists should be avoided in pts with heart failure?
Cr <30 or pts with K >5
When do we give metolazone in patients with heart failure?
when pts who have heart failure and their peripheral edema is refractory to loop diuretics.
They work on a different part of renal tubule
who needs to be on combination of hydralazine and oral nitrates
AA with NYHA classes III and IV heart failure.
When to get cardiac resynchronization therapy with biventricular pacing?
sinus rhythm with persistent symptoms and optimal medical care who have EF<35% or QRS duration >150 msec and LBBB.
When can you use combo of hydralzine and nitrate therapy in addition to goal directed therapy for CHF?
There is a symptomatic and mortality benefit in AA pts with NYHA III and IV HF and have EF<40%
indications for cardiac resynchronization therapy (CRT)
LVEF<35% and sinus rhythm with one of the following: QRS duration >150 msec and NYHA class III and IV symptoms on optimal medical therapy (Grade IA) ORS duration >120 msec but <150 msec and NYHA class III or IV symptoms on on optimal medical therapy undergoing pacemaker or ICD implantation with anticipated frequent ventricular pacing LVEF<30% and QRS duration >150 msec with LBBB, NYHA class I or II symptoms on optical medical therapy.
bivendricular pacing has helped to do what for pts with heart failure?
increase exercise tolerance, reduce need for hospitalization and decrease overal mortality and they decrease risk for sudden cardiac death.
in acute heart failure when do we initiate inotropes to help with augment forward flow and assist in ventricular offloading
when there’s acute heart failure exacerbation and volume overload, reduced cardiac index and lack of response to high dose IV diuretics. Start with milrinone or dobutamine. Dobutamine is favored in renal dysfunction.
Side effect of milrionone?
renally metabolized and accumulation can lead to hypotension
indications for ICD (implantable cardioverter defibrillator) placement for primary prevention and secondary prevention of VT?
primary prevention:
prior MI with LVEF<30%
NYHA class II or III and LVEF<35%
Secondary prevention:
prior VF or unstable VT without reversible cause
prior sustained VT with underlying cardiomyopathy
ICD placement in primary prevention should be done to prevent in sudden cardiac death in pts who are at least _(list a time duration)_ from post MI
Need to be at least 40 days post MI or 3 months post CABG/PCI.
do we worry about beta blockers in pts who have CHF and asthma or COPD?
no as long as you use cardioselective beta blockers like metorpolol and bisoprolol and there’s no increased respiratory symptoms or
CHF review chart
Stages in development of heart failure
heart failure with perserved LV EF
causes and management of HFpEF
HFpEF or left ventricular diastolic dysfunction accounts for
Management is based off:
BP and HR Goals for management are:
1/2 of all decompensated heart failure exacerbations. See elevated filling pressures.
NO evidence that the BB, ACEi, ARB or aldosterone agonists help with morbidity or mortality
Management is based on controlling BP’s <140/90
controlling heart rate: 80-90 HR esp if has afib
management of fluid volume with appropriate dosing of diuretics
coronary revascularization for pts who need it
what is brain natriuretic peptide and where is from and why is it released?
prohormone N terminal pro BNP (NT-proBNP) is released from ventricles during increased ventricular filling pressures
Both BNP and NTproBNP help diagnose both heart failure, asymptomatic or symptomatic left ventricular dysfunction. Seen elevated in dyspena (cor pulmonale, PE and pulmonary HTN
what values of BNP and NTproBNP help exclude heart failure?
What cutoffs are highly suggestive of heart failure.
What can cause falsely high levels and what can cause falsely low levels?
BNP<100 pg/ml and NT-proBNP<300 pg/ml levels rule out HF
BNP>400 and NT-pro BNP>900 are suggestive of heart failure
CKD and age >65 can cause elevations in BNP and NT-pro BNP.
Obese pts can have a falsely low BNP and Nt-pro BNP.
How to estimate central venous pressure CVP
what is milrinone?
NOT the same thing as metalazone (which is a diuretic that you use if loop diuretic doesn’t work anymore)
Milrinone is a phosphodiesterase inhibitor that decreases cyclic AMP and acts a arterial and venous dilator.
It increases ceullular calcium influx and intraceulluar calcium concentration and see myocardial contractility increase and this helps improve hemodynamics and dypsnea for pts who have symptomatic advanced CHF, low output state (NYHA III AND IV) and marginal systolic BP.
why do we not use milirone long term?
chronic use of oral milrinone is associated with increased mortality of CHF pts in in-hospital and 60 day mortality
see more number of hypotensive pts that required discontinuation, increased arterial or ventricular arrhytmias and increased in pt and 60 day mortality with them. ischemic cardiomyopathy did significantly worsen due to milrione provoked ischemia from increased myocardial oxygen demand and consumption.
mainstay of treatment in acute CHF exacerbation:
hemodynamic stabilization
supplemental oxygen and ventilation
optimization of volume status
congestion improvement
identification and correction of precipitation factors
symptomatic relief.
cor pulmonale
