CVPR 03-27-14 10-11am Clinical Treatment of Heart Failure - Allen Flashcards
Goals of Any Treatment
- ↑ quantity of life (improve survival) ….. 2. ↑ quality of life (reduce symptoms) ….. 3. Decrease societal / financial burden of disease
Treatment of HF depends on…
1) acuity 2) type 3) severity
Treating Right Ventricular Failure
Hard to treat; can reduce LV failure if that’s causing the RV failure; reduce volume?
Treating acute LV Failure
Also difficult; decrease fluids, avoid sodium, etc.
Treating Chronic (stable) HFrEF (Stages B & D)
The most treatable form of HF
Specific HF Goals of Rx
- Correction of underlying cause of HF (e.g. revascularization for ischemia; not possible for many causes, such as infarcted tissue)….. 2. Elimination of precipitating factors (e.g. infection, anemia, etc)….. 3. Reduction of congestion….. 4. Improve blood flow….. 5. Modulate neurohormal activation….. 6. Devices / transplantation
Rule out reversible causes and/or precipitants of HF – primary tests
Vitals BP / HR (hypertension), EKG (tachyarrhythmia, AFib, PVCs), CMP, CBC (renal failure, liver dysfunction, anemia, infxn, DM, …), CXR (coexistant lung disease, for future comparison), BNP / NT-proBNP, troponin (prognosis), Echo (dilation, LV function, wall motion, PHTN, prognosis), Coronary angiogram v. CTA, stress testing, MRI (ischemia, scar), Thyroid function tests, Iron studies (hemochromatosis, iron deficiency)
Major classes of meds for HF
Diuretics — Vasodilators — Neurohormonal antagonists — Inotropes
Diuretics in HF – Purpose & Use
Reverses fluid retention (via Na loss); Most common HF therapy, used both chronically & acutely (typically PO dose at baseline, often IV in hospital)
Diuretics in HF – Classes
Loop diuretics (preferred due to potency, works on loop of Henle); Loop diuretics can be augmented w/a thiazide diuretic (works on distal convoluted tubule)
Loop diuretics - examples
Furosemide [Lasix], torsemide, bumetanide, ethacrinic acid
IV Diuretics – why use
Congested intestine may not absorb PO as well; W/worsening renal function, also need higher dose
Diuretics – significance & side effects
No survival data, but increased doses signify worse disease (poor HF or kidney function) ….. Side effects: dehydration, hypokalemia, sulfa, tinnitis [can go overboard w/diuretics; solve congestion, but now you’ve dropped their SV too much & they’re hypotensive, dehydrated, & unconscious)
Diuretics: Treatment of Volume Overload Mechanism
Pt compensated for low CO by increases volume, but goes overboard… To correct this, diuretics increase Salt/Water excretion —> Decrease Intravascular Fluid Volume —> Decrease Venous congestions —> Decrease Dyspnea/Edema
Furosemide vs. Bumetanide potency
Furosemide to Bumetanide = 40:1
ACE (Angiotensin Converting Enzymge) Inhibitors - examples
…prils (lisinopril, enalapril, benazepril)
ACE Inhibitors – action
Block conversion of ATI to ATII (prevents Angiotensin II’s effect to retain fluid & salt???)
ACE Inhibitors - Effects
Direct vasodilation — Decreased aldosterone activation — Other effects beyond ATII?
ACE Inhibitors - Side effects
Hypotension — Worsening renal function (afferent vasocontraction) — Hyperkalemia — COUGH (kinin potentiation): ~20% — Angioedema: <1%, can occur after months of use
ARBs (Angiotensin Receptor Blockers) - examples
…sartans (e.g. valsartan, candesartan, losartan)
ARBs – Effect
Block the receptor of angiotensin II
ARBs - Clinical use:
In studies have been equivalent to ACEI; Controversial whether use in combination (ARB + ACEI) provides added benefit (usually use one or the other); Generally used when patients develop cough to ACEI
ARBs - Side effects:
Do NOT produce kinin potentiation (no cough, as seen w/ACEIs); Otherwise side effects are similar to ACEI
Mineralocorticoid Receptor Antagonists (MRA) [aka Aldosterone agonists]- examples
Spironolactone and eplerenone
Mineralocorticoid Receptor Antagonists (MRA) - Effect:
Block mineralocorticoid (aldosterone) receptor…. Kidney = ACEI/ARB aldosterone block is incomplete (Produces additional sodium loss = diuretic)….. Other effects : Antifibrotic (anti-remodeling)
Mineralocorticoid Receptor Antagonists (MRA) - Side effects
Hyperkalemia (requires close monitoring) & Gynecomastia (spiro only)
Beta-Blockers - examples
…olols (metoprolol, carvedilol, bisoprolol)
Beta-Blockers - Effect:
Antagonize effect of sympathetic system (epinephrine/norepinephrine)… β1 blockade: Negative chronotrope (slow heart rate, less arrhythmia) & Negative inotrope (decreased metabolic demand)…. α1 blockade: vasodilation … short term, makes them feel worse (less blood flow), but good in the long-term
Beta-Blockers - Side effects:
Negative inotrope: short-term loss for long-term gain (Fluid retention, Hypotension, Decreased cardiac output, even cardiogenic shock)….. Bronchoconstriction
Adrenergic and RAAS blockers: Effects
ACEI/ARB (Vasodilation, Salt/Water Excretion), Beta Blockers (Decreased Contractility, may worsen symptoms), Aldosterone Receptor Blockade (Salt/Water Excretion, K+ retention) —> Anti-Remodeling with Decrease Hypertrophy, Fibrosis, & Apoptosis —> Reduced Mortality, Improved Survival
Arterial vasodilation (antihypertensives) - Possible benefits
Decrease in LV afterload — Reduced cardiac work — Less mitral regurgitation
Arterial vasodilation (antihypertensives) - Hydralazine / isosorbide dinitrate (ISDN) in HFREF
Hyd/ISDN < ACEI (V-HeFT II) —– Hyd/ISDN+ACEI/BB combo works well in AfAms (A-HeFT) when other drugs are good to lower BP
Venous vasodilation (venodilators) – effects
Decrease in preload
Pulmonary arterial vasodilation - effects
Decrease in RV afterload
Acute decompensated (hospitalized) HF - treatment
IV diuretics — IV vasodilators (nitrates / nitroprusside, if BP allows) — Positive pressure ventilation (CPAP/BiPAP, intubation) for hypoxia (May also reduce preload) — IV inotropes for shock only — May need to cut back on beta-blockers (only in severe cases)
Positive Inotropic Agents - Types:
Digoxin (PO) - K/Na exchange —- Dobutamine (IV) – β agonist (opposite of BB) —– Milrinone (IV) – phosphodiesterase inhibitor (effect is similar to dobutamine)
Positive Inotropic Agents – Acute Clinical Use
IV agents used short term to reverse shock (Long-term they worsen remodeling)
Positive Inotropic Agents – Chronic Clinical Use
Digoxin has no effect on mortality but may reduce symptoms & hospitalization (also some decrease in heart rate in AFib); In high doses causes dig toxicity (mostly arrhythmias)
Electrical therapies – ICD (Implanted Cardioverter Defibrillators) – reason to use
Patients with LVEF <=35% or prior dangerous heart rhythms; Abort sudden cardiac death from ventricular tachycardia / fibrillation
Electrical therapies – CRT (Cardiac Resynchronization Therapy) – what it is
Biventricular pacemakers (CRT or BiV), with LV lead placed through the coronary sinus (lead of LV wall to resynchronize it)
Electrical therapies – CRT (Cardiac Resynchronization Therapy) – why use
For pts w/electrical problems causing QRS duration > 120 msec (bundle branch block; His/Purkinji system prob); Ex: left bundle messed up—> AP doesn’t get to left wall til late, causing loss of synchronization & poor efficiency; CRT causes LV lateral wall & septal wall to contract together, which produces a more efficient contraction / ↑ stroke volume; Usually placed with ICD
Therapy depends on where a patient is in the course of the disease
Asymptomatic HF (late “prevention”) — Chronic stable HF (ambulatory) — Acute decompensated HF (hospitalized) — End-stage heart failure (advanced)
Options for end-stage HFrEF
Transplantation (limited resource, $$$, significant risk), Mechanical support (LVAD – high morbidity, $$$, significant risk), Inotrope infusion (may hasten death, but improve quality of life), Hospice (improved quality but shortened quantity of life)
Summary of HFrEF Rx options – Ways to Improve symptoms
Diuretics (furosemide) ; Digitalis PO (HFrEF with shock - dobutamine, milronone)
Summary of HFrEF Rx options – Ways to Prolong survival
ACE-I / Angiotensin Receptor Blockers —- Beta Blockers —- Aldosterone Receptor Antagonists —- Other Vasodilators (hydralazine + nitrates) —– Cardiac Resynchronization Therapy (biventricular pacing) —– Implantable Cardioverter Defibrillator (ICD)
Positive inotropic agents
Good for short-term use, good to increase HR/SV & therefore CO; Long-term use = promote remodeling & make HF worse
Beta-agonism vs. Antagonism: Acute vs. Chronic
Acute: Epinephrine, Norepinephrine, Dopamine, Dubutamine, (Milrinone), (Digoxin) ….. Chronic: Carvedilol, Metoprolol succinate, Bisoprolol
Chronic (Stable) HFrEF - Treatments
BB, ACEI/ARB, Aldosterone antagonist, Hydralazine / ISDN, +/- Digoxin, ICD/CRT
Acute (Unstable) HFrEF – Treatments
??? - IV dieresis, Nitrates (if BP allows), CPAP/BiPAP (if SOB), Pressors (if ↓↓↓CO, shock)
Chronic (Stable) HFpEF – Treatments
??? – Control risk factors (DM, HTN, obesity), Control volume status
Acute (Unstable) HFpEF – Treatments
??? – IV dieresis, Nitrates (if BP allows), CPAP/BiPAP
Therapy for HFpEF
Lack of success with neurohormonal antagonists (e.g. ACEI, ARB = only for BP control); Therapy consists of treating the underlying disorder (HTN, diabetes, kidney dysfunction); Diuretics used to keep volume normal (sodium retention is common); Vasodilators used to maintain normal BP
ARB/ACEI/MRA in HFpF vs. HFrEF
no benefit in HFpF; good effects in HFrEF
HFrEF - Rx to improve symptoms
Diuretics (furosemide), Digitalis PO (HFrEF w/shock - dobutamine, milronone)
HFrEF - Rx for prolongation of survival
ACE-I/ARBs — Beta blockers — Aldosterone Receptor Antagonists — Other Vasodilators (hydralazine + nitrates) — Cardiac Resynchronization Therapy (biventricular pacing) — Implantable Cardioverter Defibrillator (ICD)
ARB/ACEI/MRA in HFpF vs. HFrEF
no benefit in HFpF; good effects in HFrEF
Risk factors for HF
HTN, Diabetes, Hyperlipidemia, Physical inactivity, Obesity, Excessive alcohol intake, Smoking, Dietary sodium
