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CVPR Unit 1 > CVPR 03-27-14 10-11am Clinical Treatment of Heart Failure - Allen > Flashcards

CVPR 03-27-14 10-11am Clinical Treatment of Heart Failure - Allen Flashcards

1
Q

Goals of Any Treatment

A
  1. ↑ quantity of life (improve survival) ….. 2. ↑ quality of life (reduce symptoms) ….. 3. Decrease societal / financial burden of disease
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2
Q

Treatment of HF depends on…

A

1) acuity 2) type 3) severity

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3
Q

Treating Right Ventricular Failure

A

Hard to treat; can reduce LV failure if that’s causing the RV failure; reduce volume?

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4
Q

Treating acute LV Failure

A

Also difficult; decrease fluids, avoid sodium, etc.

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5
Q

Treating Chronic (stable) HFrEF (Stages B & D)

A

The most treatable form of HF

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6
Q

Specific HF Goals of Rx

A
  1. 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
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7
Q

Rule out reversible causes and/or precipitants of HF – primary tests

A

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)

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8
Q

Major classes of meds for HF

A

Diuretics — Vasodilators — Neurohormonal antagonists — Inotropes

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9
Q

Diuretics in HF – Purpose & Use

A

Reverses fluid retention (via Na loss); Most common HF therapy, used both chronically & acutely (typically PO dose at baseline, often IV in hospital)

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10
Q

Diuretics in HF – Classes

A

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)

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11
Q

Loop diuretics - examples

A

Furosemide [Lasix], torsemide, bumetanide, ethacrinic acid

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12
Q

IV Diuretics – why use

A

Congested intestine may not absorb PO as well; W/worsening renal function, also need higher dose

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13
Q

Diuretics – significance & side effects

A

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)

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14
Q

Diuretics: Treatment of Volume Overload Mechanism

A

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

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15
Q

Furosemide vs. Bumetanide potency

A

Furosemide to Bumetanide = 40:1

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16
Q

ACE (Angiotensin Converting Enzymge) Inhibitors - examples

A

…prils (lisinopril, enalapril, benazepril)

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17
Q

ACE Inhibitors – action

A

Block conversion of ATI to ATII (prevents Angiotensin II’s effect to retain fluid & salt???)

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18
Q

ACE Inhibitors - Effects

A

Direct vasodilation — Decreased aldosterone activation — Other effects beyond ATII?

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19
Q

ACE Inhibitors - Side effects

A

Hypotension — Worsening renal function (afferent vasocontraction) — Hyperkalemia — COUGH (kinin potentiation): ~20% — Angioedema: <1%, can occur after months of use

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20
Q

ARBs (Angiotensin Receptor Blockers) - examples

A

…sartans (e.g. valsartan, candesartan, losartan)

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21
Q

ARBs – Effect

A

Block the receptor of angiotensin II

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22
Q

ARBs - Clinical use:

A

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

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23
Q

ARBs - Side effects:

A

Do NOT produce kinin potentiation (no cough, as seen w/ACEIs); Otherwise side effects are similar to ACEI

24
Q

Mineralocorticoid Receptor Antagonists (MRA) [aka Aldosterone agonists]- examples

A

Spironolactone and eplerenone

25
Q

Mineralocorticoid Receptor Antagonists (MRA) - Effect:

A

Block mineralocorticoid (aldosterone) receptor…. Kidney = ACEI/ARB aldosterone block is incomplete (Produces additional sodium loss = diuretic)….. Other effects : Antifibrotic (anti-remodeling)

26
Q

Mineralocorticoid Receptor Antagonists (MRA) - Side effects

A

Hyperkalemia (requires close monitoring) & Gynecomastia (spiro only)

27
Q

Beta-Blockers - examples

A

…olols (metoprolol, carvedilol, bisoprolol)

28
Q

Beta-Blockers - Effect:

A

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

29
Q

Beta-Blockers - Side effects:

A

Negative inotrope: short-term loss for long-term gain (Fluid retention, Hypotension, Decreased cardiac output, even cardiogenic shock)….. Bronchoconstriction

30
Q

Adrenergic and RAAS blockers: Effects

A

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

31
Q

Arterial vasodilation (antihypertensives) - Possible benefits

A

Decrease in LV afterload — Reduced cardiac work — Less mitral regurgitation

32
Q

Arterial vasodilation (antihypertensives) - Hydralazine / isosorbide dinitrate (ISDN) in HFREF

A

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

33
Q

Venous vasodilation (venodilators) – effects

A

Decrease in preload

34
Q

Pulmonary arterial vasodilation - effects

A

Decrease in RV afterload

35
Q

Acute decompensated (hospitalized) HF - treatment

A

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)

36
Q

Positive Inotropic Agents - Types:

A

Digoxin (PO) - K/Na exchange —- Dobutamine (IV) – β agonist (opposite of BB) —– Milrinone (IV) – phosphodiesterase inhibitor (effect is similar to dobutamine)

37
Q

Positive Inotropic Agents – Acute Clinical Use

A

IV agents used short term to reverse shock (Long-term they worsen remodeling)

38
Q

Positive Inotropic Agents – Chronic Clinical Use

A

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)

39
Q

Electrical therapies – ICD (Implanted Cardioverter Defibrillators) – reason to use

A

Patients with LVEF <=35% or prior dangerous heart rhythms; Abort sudden cardiac death from ventricular tachycardia / fibrillation

40
Q

Electrical therapies – CRT (Cardiac Resynchronization Therapy) – what it is

A

Biventricular pacemakers (CRT or BiV), with LV lead placed through the coronary sinus (lead of LV wall to resynchronize it)

41
Q

Electrical therapies – CRT (Cardiac Resynchronization Therapy) – why use

A

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

42
Q

Therapy depends on where a patient is in the course of the disease

A

Asymptomatic HF (late “prevention”) — Chronic stable HF (ambulatory) — Acute decompensated HF (hospitalized) — End-stage heart failure (advanced)

43
Q

Options for end-stage HFrEF

A

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)

44
Q

Summary of HFrEF Rx options – Ways to Improve symptoms

A

Diuretics (furosemide) ; Digitalis PO (HFrEF with shock - dobutamine, milronone)

45
Q

Summary of HFrEF Rx options – Ways to Prolong survival

A

ACE-I / Angiotensin Receptor Blockers —- Beta Blockers —- Aldosterone Receptor Antagonists —- Other Vasodilators (hydralazine + nitrates) —– Cardiac Resynchronization Therapy (biventricular pacing) —– Implantable Cardioverter Defibrillator (ICD)

46
Q

Positive inotropic agents

A

Good for short-term use, good to increase HR/SV & therefore CO; Long-term use = promote remodeling & make HF worse

47
Q

Beta-agonism vs. Antagonism: Acute vs. Chronic

A

Acute: Epinephrine, Norepinephrine, Dopamine, Dubutamine, (Milrinone), (Digoxin) ….. Chronic: Carvedilol, Metoprolol succinate, Bisoprolol

48
Q

Chronic (Stable) HFrEF - Treatments

A

BB, ACEI/ARB, Aldosterone antagonist, Hydralazine / ISDN, +/- Digoxin, ICD/CRT

49
Q

Acute (Unstable) HFrEF – Treatments

A

??? - IV dieresis, Nitrates (if BP allows), CPAP/BiPAP (if SOB), Pressors (if ↓↓↓CO, shock)

50
Q

Chronic (Stable) HFpEF – Treatments

A

??? – Control risk factors (DM, HTN, obesity), Control volume status

51
Q

Acute (Unstable) HFpEF – Treatments

A

??? – IV dieresis, Nitrates (if BP allows), CPAP/BiPAP

52
Q

Therapy for HFpEF

A

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

53
Q

ARB/ACEI/MRA in HFpF vs. HFrEF

A

no benefit in HFpF; good effects in HFrEF

54
Q

HFrEF - Rx to improve symptoms

A

Diuretics (furosemide), Digitalis PO (HFrEF w/shock - dobutamine, milronone)

55
Q

HFrEF - Rx for prolongation of survival

A

ACE-I/ARBs — Beta blockers — Aldosterone Receptor Antagonists — Other Vasodilators (hydralazine + nitrates) — Cardiac Resynchronization Therapy (biventricular pacing) — Implantable Cardioverter Defibrillator (ICD)

56
Q

ARB/ACEI/MRA in HFpF vs. HFrEF

A

no benefit in HFpF; good effects in HFrEF

57
Q

Risk factors for HF

A

HTN, Diabetes, Hyperlipidemia, Physical inactivity, Obesity, Excessive alcohol intake, Smoking, Dietary sodium

CVPR Unit 1 (28 decks)

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