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Treatment of CHF Flashcards

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0
Q

New Paradigm for CHF Treatment

A

Metabolic stress, apoptosis and remodeling stimulated by AT, aldosterone and NE.
Treatment focuses on inhibiting these hormones!
- early treatment with ACEI/ARBs, aldosterone antagonists, BB
- prevents decline in cardiac function (decompensation).
Prognosis improved, shifting emphasis on prevention

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1
Q

Old Paradigm for CHF Treatment

A

CHF viewed as a hemodynamic disease; treatment provided only symptomatic relief (digoxin, diuretic, bedrest). POOR PROGNOSIS because none of them addressed the underlying disease

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2
Q

NYHA Class 1

A

Symptoms - none
Presentation - low EF (<50%)
Treatment - ACE-I or ARB, BB

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3
Q

NYHA Class II

A

Symptoms - moderate exertion
Presentation - dyspnea on exertion, edema
Treatment - add diuretic

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4
Q

NYHA Class III

A

Symptoms - minimal exertion
Presentation - dyspnea, orthopnea, PND, edema
Treatment - add Digoxin and Spironolactone

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5
Q

NYHA Class IV

A

Symptoms - at rest
Presentation - refractory edema
Treatment - add IV vasodilators, transplantation/assist devices

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6
Q

Do we still use the NYHA classification?

A

No, use ACC/AHA guidelines which classifies CHF into stages A-D

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7
Q

What are the ACC/AHA stages

A

Stage A - at risk (preventive measures, ACEI/ARBs)
Stage B - NYHA I (add BB)
Stage C - NYHA II, III (add diuretic/digoxin/spironolactone)
Stage D - NYHA IV (add IV inotropes, transplant)

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8
Q

What are the primary preventative measures in CHF

A 
HTN 
Lipids
Smoking 
Diabetes 
No ETOH
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9
Q

What is the MOA and Effects of ACE-I

A

Block ATI to ATII conversion in endothelial cells of the lung to:
- Natriuresis (loss of Na+ in urine)
- Decreased TPR
- Decreased Aldosterone, Increased Na+ excretion
Also increase BRADYKININ levels due to inhibition of bradykinin metabolism. Increased prostaglandin production and increased vasorelaxation may be beneficial or may contribute to side effects

Many are prodrugs (not captopril and lisinopril)

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10
Q

Use of ACE-I

A

Decrease mortality post MI (decrease ATII, increase bradykinin)
Preserves renal function in diabetics
ADVANTAGE: little effect on lipids or sexual funciton

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11
Q

Who should not use ACE-I?

A

AA or low-renin hypertensives respond less favorably (thiazide + ACE-I is HIGHLY EFFECTIVE)

FETOTOXICITY - do not give to pregnant women, those expecting to conceive or those breastfeeding.

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12
Q

Adverse Effects of ACE-I

A

Most Common: Hypotension (1st dose), Na+ depletion
Next Common: Dry irritating cough
Hyperkalemia
Angioedema - allergic skin/mucosa disease (life threatening; incidence in AA 2-4X greater)
RENAL INSUFFICIENCY due to altered glomerular filtration
Proteinuria, rashes, reduction in blood cell counts, fever (10%), BM depression
Hepatotoxicity, pancreatitis

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13
Q

MOA of Angiotensin Receptor Antagonists (ARBs)

A

Selectively block ATI receptors, the CV targets of AngII, so have similar effects to ACE-I –> Vasodilation, Natriuresis

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14
Q

Side Effects of ARBs

A 
DO NOT CAUSE COUGH
1st dose hypotension 
Hyperkalemia
Hepatic dysfunction 
Fetotoxicity 
Olmesartan can cause spruelike enteropathy (chronic diarrhea and nausea, rare but serious)
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15
Q

What is the only renin inhibitor?

A

Aliskiren - directly inhibits protease activity of renin; causes vasodilation, natriuresis just like ACE-I/ARBs

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16
Q

Side effects of Aliskiren

A

1st dose hypotension
Hyperkalemia
Angioedema
Fetotoxicity

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17
Q

What are the DDI with Aliskiren

A

inhibits p-gp, so caution with erythromycin, amiodarone and other p-gp inhibitors

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18
Q

Endocrine effects of ACEI and ARBs

A

Prevents and reverses ANGII mitogenic effects:

  • hypertrophy of cardiac mycoytes
  • hypertrophy of vascular smooth muscle
  • cardiac and vascular fibrosis, remodeling
  • atherosclerosis
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19
Q

Which is better ACEI or ARB?

A

ACEI preferred unless patient can’t tolerate side effects. Combining shows no increased benefit.

However, evidence of “aldosterone escape” from ACEI in CHF (i.e. the reduction in aldosterone synthesis that is achieved with ACE-I therapy is eventually lost in patients).

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20
Q

Why were BBs previously contraindicated in CHF?

A

Beta adrenergic receptor activation increase inotrophy!

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21
Q

What do BBs attenuate deleterious effects of?

A

Chronic high levels of NE and EPI, which cause:

  • B-AR downregulation
  • arrhythmias (leading cause of death in class II, III CHF)
  • increased myocardial oxygen consumption/ischemia
  • myocyte apoptosis followed by cardiac fibrosis
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22
Q

What are the hemodynamic effects of BB in CHF?

A

Short-term: reduced CO, BP (PROBLEMATIC!)
Long-term: increased CO, decreased LVEDP

May see initial worsening of symptoms, then improvement (dose up slowly). USE IN EARLY STAGE CHF –> slows disease progression

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23
Q

BB should worsen CHF but…

A
  1. DIVERSE SIGNALING OF B-AR (acute vs. chronic): Beta receptor binding leads to increase cAMP and phosphorylation of contractile elements that make them more sensitive to Ca2+ (increase the force of contraction and how fast we can remove this calcium from SR)
    - Acute signaling: responding to spikes in NE and EPI (high receptor number required)
    - Chronic signaling: responding to lower but sustained levels of NE/EPI (lower receptor numbers required). When receptors are chronically stimulated, clatherin-coated pits take up receptor and internalize it so that it is no longer able to respond to circulating EPI.
  2. SIGNALING MODALITIES OF GPCR
  3. DESENSITIZATION OF B-AR

SOOO…BB reverse desensitization, increase receptor number, restore fast signaling modes (contractility) over slow signaling modes (gene expression)

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24
What are contraindications of BBs
Heart block BRadycardia Decompensated CHF/need for IV inotropes (dobutamine) Volume overload
25
What are the only 3 BBs approved for CHF?
Metoprolol Carvedilol Bisoprolol
26
Nebivolol
BB that potentiates NO in vasculature, is approved for HTN but NOT CHF.
27
What class of drugs is digitalis?
cardiac glycoside: inotrope
28
What is the MOA of digoxin ?
increased intracellular availability of Ca2+ for contractile apparatus via inhibition of Na/K+ ATPase --> increase intracellular Na+, decreased intracellular K+
29
What is the overall effects of diuretic therapy in CHF?
Promote Na+ and water excretion to reverse edema and pulmonary congestion. Reduce preload, CO NOT INCREASED! Unlike ACE-I, diuretics DO NOT improve survival or prognosis (except for spironolactone/eplerenone which block other effects of aldosterone)
30
What are some drugs used in diuretic therapy?
"High Ceiling" diuretics commonly used: Furosemide ("loop") Bumetanide Potassium sparing diuretics commonly used in combination with loop diuretics - Aldosterone antagonists: spironolactone, eplerenone - Independent of Aldo: triamterene, amiloride are not used in CHF
31
What is the toxicity of diuretics?
electrolyte distribuances, hypokalemia, hyponatremia, hypochloremic metabolic alkalosis, azotemia, dehydration, hypotension ototoxicity: tinnitus, hearing loss (loop diuretics)
32
What are the DDIs with Diuretics?
NSAIDs reduce efficacy of diuretics, promote fluid retention
33
Do ACE-I and ARBs also have diuretic effects?
YES! Reduce sodium retention by preventing aldosterone release Effect not always sufficient to prevent edema Dose of diuretic should be reduced (azotemia)
34
Do Spironolatone and Eplerenone have effects beyond just being diuretics?
YES! Aldosterone has direct mitogenic and fiborgenic effects on myocardium (combined with ATII to stimulate fibrosis). Increased aldosterone may lead to worsened LV function.
35
What is the function of arterial vasodilators?
INCREASE CO by DECREASING AFTERLOAD --> Improve hemodynamics of advanced stage HF. These should used be in combo with inotropic agents and diuretics. improve cardiac performance by reducing the resistance to outflow of blood from the LV. This shifts the pressure-volume curve upward and to the left. Preload is reduced to varying degrees depending on agent.
36
Do arterial vasodilators slow progression of CHF?
NO! Just keep patients asymptomatic
37
Direct arterial vasodilators use in CHF
REDUCE AFTERLOAD - reduced resistance to outflow of blood from LV improve ventricular performance, increase CO - improved ventricular emptying also reduces LV pressure during diastole (preload) but effect is relatively modest alone - need to combine arterial vasodilator with venodilator (nitrate) to reduce both preload and afterload
38
What is the MOA of Hydralazine
vasodilator that acts directly on arterial smooth muscle
39
Adverse effects of Hydralazine
Stimulates RAS: peripehral edema, circulatory congestion Toxicity: nausea, anorexia, drug-induced lupus (rare), can exacerbate angina (coronary steal/reflex tachycardia), +FANA (frequent)
40
When is hydralazine used?
Use limited to patients unable to tolerate ACE-I (renal insufficiency, angioedema).
41
Describe the PK of Digoxin
LOW THERAPEUTIC WINDOW!!!!!! - Excreted by kidney (unchanged in urine) - reduce dose in renal disease, elderly - Serum half-life is 36 hours. - Loading dose needed for rapid onset of action (i.e. antiarrhythmic action) - Plasma concentration correlate roughly with therapeutic effect, toxicity
42
Toxicity of Digoxin
Atrial, ventricular arrhythmias, visual changes (blurring, yellow-green halo), headache, fatigue, drowsiness, confusion, seizures Most frequent visits to emergency room because it has such a narrow therapeutic window!
43
What can be used to neutralize serum digoxin if toxicity occurs
Digibind - Ab to digoxin
44
When are nitrates used?
used to reduce preload either alone or with vasodilator - reduces pulmonary artery pressure, pulmonary congestion - reduces LV filling pressure and walls tress
45
What are IV vasodilators
Nitrates including Nitroglycerin, Nitroprusside | veno- and vasodilation reduces preload (decreases congestion) and reduces afterload
46
How do you manage advanced CHF?
IV vasodilators IV inotropic agents Nesiritide Cardiac transplantation/Extracorporeal Bridging devices
47
What are the Inotropic agents used in advanced CHF?
B Agonists: Dobutamine | PDE Inhibitors: Milrinone
48
Describe the PK of Dobutamine
B1>B2, also alpha1AR agonist, positive inotrope, vasodilator Short-term IV "bridge" or intermittent therapy Limited by Beta AR dessensitization, arrhythmias BB therapy prevents vasodilator effect of dobutamine and can even cause vasoconstriction (unopposed alpha1 agonist effect)
49
Describe the PK of Milrinone
short-term IV use (long term oral use of PDE inhibitors in CHF increases mortality)
50
MOA of Dobutamine
B1 selective agonist that activates B1 receptor in cardiac mycotes --> stimulates cAMP production --> activating through PKA --> phosphorylates several important inotropic pathways which cause greater contraction --> increased HR.
51
MOA of Milrinone
PDE inhibitor - inhibits enzyme that breaks down cAMP that is stimulated by beta adrenergic receptor activation.
52
What are the two natriuretic peptides and what do they promote in CHF?
Atrial Natriuretic Peptide (ANP) and B-type Natriuretic Peptide (BNP) PROMOTE VASODILATION
53
When are natriuretic peptides released?
Released from atria and ventricles in response to volume/pressure expansion. Naturally elevated in CHF Promotes vasodilation, venodilation and natriuresis
54
What are the hemodynamic effects of natriuretic peptides?
reduce ventricular filling pressure (preload) inhibits renin and aldosterone release inhibits sodium reabsoprtion in PCT selective afferent arteriolar vasodilation
55
What is the only BNP for CHF?
Nesiritide - recombinant human BNP; FDA approved for IV treatmetn of decompensated class IV CHF
56
Nesiritide MOA
- binds to BNP receptor in vascular smooth muscle, veno- and vasodilation (via cGMP). reduced preload/afterload - dilation of afferent renal glomerular arterioles increases GFR, filtration fraction, and decreases sodium reabsoprtion (natriuresis) - suppresses renin-angiotensin and SNS
57
Is there a benefit of Nesiritide?
Benefit comparable to IV nitroglycerin but hyptoension may persist longer; use should be limited to those who do not respond to nitroglycerin
58
OVERVIEW Digoxin
Increase inotropy Natriuretic Survival benefit
59
OVERVIEW Milrinone
Decrease afterload Increase inotropy Natriuretic NEGATIVE SURVIVAL BENEFIT
60
OVERVIEW Furosemide
Decrease preload | Natriuretic
61
OVERVIEW Hydralazine
Decreases afterload | Survival benefit
62
OVERVIEW Nitrate
Decrease preload
63
OVERVIEW ACE-I and ARBs
decrease preload and afterload anti-mitogenic natriuretic survival benefit
64
OVERVIEW Spironolactone
decrease preload anti-mitogenic natriuretic survival benefit
65
OVERVIEW Dobutamine
Increase/Decrease afterload Increase inotropy Natriuretic
66
OVERIVEW Nesiritide
decrease preload and afterload anti-mitogenic natriuretic
67
OVERVIEW BB
Increase/Decrease inotropy anti-mitogenic natriuretic survival benefit
68
What is the primary goal of pharmacology in patients with early stage (Stage A and B) CHF?
Reign in the over-activation of neurohumoral mediators such as catecholamines and ATII
69
BB are effective in treating class I-IV CHF because they...
block catecholamine-induced overdrive in the heart and restore B-AR function

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