HF III - Clinical Tx of HF Flashcards
General goals of any therapy:
o ↑ Quantity of life (↑survival)
o ↑ Quality of life (↓ symptoms)
o ↓ financial/resource burden of disease
HF specific goals:
o Correction of the underlying cause of HF
o Reduction of congestion
o Optimization of cardiac function
diuretics
the sodium and fluid retention of HF
o Typically work at the far end of the frank-starling curve, such that significant decreases in pressure produce minimal changes in stroke volume (and thus CO). Thus, symptoms of congestion can be reduced without major effects on blood flow.
vasodilators
arterial, venous, and pulmonary arterial vasodilation
o Arterial: ↓ LV afterload, ↓ cardiac work, ↓ mitral regurgitation
o Venous: ↓ preload
o Pulmonary: ↓ RV afterload
ACE inhibitors:
block conversion of ATI to ATII→direct vasodilation, decreased aldosterone activation.
Side effects: hypotension, worsening renal failure, hyperkalemia, cough (kinin production), angioedema
Angiotensin receptor blockers:
block receptor of ATII→ equivalent to ACEIs, but without cough.
Aldosterone receptor blockers:
block aldosterone action in kidney→↓sodium→diuretic.
Beta-blockers:
antagonize effects of the SNS→↓chronotropy ↓inotropy (short term loss for long term gain)
Side-effects: bronchoconstriction
Inotropes
administered via IV agents short term in the ICU to reverse shock (long term—worsen remodelling ↑mortality)
o Digoxin—K/Na exchanger
o Dobutamine—beta agonist
o Milrinone—PDEi
Electrical therapies
o Defibrillators: for patients with LVEF < 35% or with prior dangerous rhythms. Implanted.
Abort sudden cardiac death from ventricular tachycardia/fibrillation.
o Resynchronization:
Left ventricular lead placed from the RA through the coronary sinus over the epicardium of the LV (3 leads: RA, RV coronary sinus/LV)
For patients with QRS > 120 msec (bundle branch block)
Cause the lateral wall and septal wall to contract together, which produces
More efficient contraction→↑stroke volume
May also improve mitral valve function→↓regurgitation
advanced therapies
o Transplantation: shortage of organs.
o Mechanical support devices: often used as a bridge to transplantation or as a destination therapy.
o Hospice: palliative advanced therapy→paradigm shift from quantity to quality of life.
stage A: definition and drugs
at risk for HF but without structural disease or symptoms
o Drugs: ACEi or ARB in appropriate patients.
Stage B: define and drugs
structural heart disease but without signs or symptoms of HF.
o Drugs: ACEi, ARB, beta-blockers
o Devices: implantable defibrillators
Stage C: define and tx
structural heart disease with prior or current symptoms of HF.
o Routine drugs: diuretics, ACEi, beta-blockers
o Drugs in selected patients: aldosterone antagonist, ARBs, digitalis, hydralazine/nitrates
o Devices: biventricular pacing, implantable defibrillators
Stage D: define and tx
refractory HF requiring specialized interventions
o Options: compassionate end-of-life care/hospice; extraordinary measures: transplant, chronic inotropes, permanent mechanical support, experimental surgery/drugs