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Congestive Heart Failure Flashcards

1
Q

Thiazide diuretic drugs

A

Chlorthalidone
Hydrocholorthiazide
Metolazone

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2
Q

Loop diuretic drugs

A

Ethacrynic acid
Furosemide
Torsemide

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3
Q

Thiazide description for CHF

A

Relieve pulmonary congestion and peripheral edema
Decrease symptoms of volume overload (orthopnea)

Decrease plasma volume -> decrease venous return (preload) -> decreased workload and O2 demand
Decrease afterload

Only give if you see edema

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4
Q

Loop Description for CHF

A

Relieve pulmonary congestion and peripheral edema
Decrease symptoms of volume overload (orthopnea)

Decrease plasma volume -> decrease venous return (preload) -> decreased workload and O2 demand
Decrease afterload

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5
Q

Loop vs Thiazide CHF

A

Loop more effective than thiazides
Thiazides: patients with hypertensive heart disease (with congestive symptoms) -ineffective by itself due to its weak diuretic effect

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6
Q

Aldosterone antagonist drugs

A

Eplerenone

Spironolactone

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7
Q

Sironolactone

A

decreases cardiac fibrosis and remodeling

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8
Q

Aldosterone antagonist description CHF

A

Prevents sodium retention, myocardial hypertrophy and potassium loss
(When combined with ACE-I’s -> decreases M & M of severe HF)

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9
Q

Aldosterone antagonist indication CHF

A

Advanced heart disease or patients with LV dysfunction after an MI (these patients have elevated aldosterone due to angiotensin stimulation and reduced hepatic clearance)

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10
Q

Aldosterone antagonist adverse CHF

A

Hyperkalemia
GI: gastritis, PUD
CNS: lethargy, confusion
Endocrine: gynecomastia, decreased libido, menstrual irregularities
Contraindicated in patients on potassium supplements

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11
Q

ACE-I drugs

A

Captopril
Enalapril
Lisinopril

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12
Q

ACE-I description CHF

A

DOC in heart failure

Dilates arterioles and veins

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13
Q

ACE - I mechanism CHF

A

Decreases PVR -> decreases BP/afterload -> increases CO
Decreases sodium and water retention -> decreases preload

Decreases long term remodeling

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14
Q

ACE-I indication CHF

A

Patients with symptomatic heart failure
Asymptomatic patients with decreased LVEF or history of MI
High risk patients: diabetes, HTN, atherosclerosis, obesity

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15
Q

ACE-I pk CHF

A

Oral- food decreases absorption

Pro-drugs except captopril

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16
Q

ACE-I adverse CHF

A 
Persistent dry cough
Hypotension
Renal insufficiency
Hyperkalemia
Angioedema
**Teratogenic**
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17
Q

ACE-I contraindications CHF

A

Pregnancy
Bilateral Renal artery stenosis
Hyperkalemia

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18
Q

ARB drugs

A

Candesartan

Valsartan

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19
Q

ARB description CHF

A

Losartan is used for HTN

Candesartan is used for CHF

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20
Q

ARB mechanism CHF

A

Block AT-I receptor

No effect on bradykinin

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21
Q

ARB Indication CHF

A

Intolerant to ACE-I’s

cough/angioedema

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22
Q

ARB adverse CHF

A 
Same as ACE-I but no cough
Hypotension
Renal insufficiency
Hyperkalemia
Teratogenic
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23
Q

ARB contraindications

A

Pregnancy
Bilateral renal artery stenosis
Hyperkalemia

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24
Q

Direct vasodilator drugs

A

Hydralazine

Nitrates (isosorbide dinitrate)

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25
Direct vasodilator description/mechanism CHF
Increase vasodilation -> decrease preload Increase arterial dilation -> decrease PVR and afterload Hydralazine dilates arterioles Nitrates dilate the veins and venules ***Give in african americans***
26
Direct vasodilators indication CHF
Patients that are intolerant to ACE-I's or Beta blockers or black patients with advanced HF (adjuvant Tx) Sustained improvement of LVEF when both oral vasodilators are combined
27
Direct vasodilator adverse CHF
HA, dizziness, hypotension | Hydralazine can also cause tachycardia, peripheral neuritis and a lupus like syndrome
28
Hydralazine adverse
HA, dizziness, hypotension | Tachycardia, peripheral neuritis, lupus like syndrome
29
Beta blockers for CHF
Carvedilol | Metoprolol
30
Beta blockers description CHF
Can reverse cardiac remodeling and reduce mortality
31
Beta blockers mechanism CHF
Decrease HR and RAAS (-ve inotrope) Prevents deleterious effects of NE on cardiac muscle fibers (renin inhibition and decreased HR)
32
Beta blockers indication CHF
Heart disease (stage B and C) in addition to an ACE-I
33
Beta blockers PK CHF
Start at low dose -> gradually titrate to effective dose (to avoid sudden exacerbation of sx)
34
Beta blockers adverse CHF
Initial treatment can cause fluid retention
35
Beta blockers contraindication CHF
Use cautiously in patients with asthma or severe bradycardia
36
Digoxin class
Inotropic agent: Cardiac glycoside
37
Digoxin description CHF
+ve inotrope -ve chronotropic From foxglove plant Widely used in the treatment of HF Very narrow therapeutic window ***Decrease sx of HF and hospitalization Increase exercise tolerance Does NOT increase survival **** Indicated in patients with ***heart failure with A fib **** along with ACE-I and beta blocker
38
Digoxin mechanism CHF
Inhibits Na/K ATPase -> decreased sodium gradient -> indirect inhibition of Na/Ca2 exchange -> **increased cytoplasmic calcium therefore increased contractility** Decreases SNS, RAAS, and PVR =-> decreases HR Enhanced vagal tone -> decreased O2 demand Decreased conduction through AV node increases the effective refractory period
39
Digoxin PK CHF
Widely distributed including the CSF Accumulates in muscle -> high Vd; requires a loading dose Sensitivity varies* between patients and may change during therapy ***Hypokalemia -> digoxin toxicity (competes with K for binding sites on ATPase) * **Hypercalcemia or decreased magnesium facilitate digoxin action * **High calcium increases chance atrial arrhythmia Mg does opposite
40
Digoxin adverse CHF
Extensive inhibition of ATPase can lead to dysrhythmias Toxicity (very common): Atrial arrhythmia-> slow Anorexia, nausea, vomiting, HA, fatigue, confusion, blurred vision, **altered color perception, halos on dark objects** Treatment of toxicity: Withdraw or reduce dose Monitor ECG, plasma concentration and K levels ***V tach-treat with lidocaine and Mg or increase potassium concentration*** severe- treat with digitalis antibodies
41
Digoxin contraindications CHF
**Diastolic or right side heart failure** Uncontrolled hypertension Bradyarrhythmias Quinidine, Verapamil and Amiodarone and NSAIDs displace digoxin from tissue protein binding sites and compete for renal excretion Digoxin levels affected by hyperthyroidism, hypothyroidism
42
Milrinone and Inamrinone CHF description
Inotropic agents PDE-3 inhibitor (phosphodiesterase inhibitors) Good for acute/short term in increasing CO
43
Milrinone and Inamrinone mechanism CHF
Inotropic agents Increase cAMP -> +ve inotropic effects and increase CO (similar to Beta 1) Systemic and pulmonary vasodilation -> decrease preload and afterload Slight increase in AV conduction
44
Milrinone and Inamrinone Adverse CHF
Short term only, long term decreases life | Can cause thrombocytopenias
45
Dopamine description CHF
Inotropic agent Used in the treatment of shock that persists after volume replacement Stimulates both adrenergic and dopaminergic receptors
46
Dopamine Mechanism CHF
Inotropic agent Low dose -> D1 dilates renal and mesenteric blood vessels ***Intermediate dose -> dopaminergic and beta 1 receptors -> increase force and rate of contraction and renal vasodilation**** High dose : alpha 1 receptors -> vasoconstriction (not helpful in CHF)
47
Dobutamine Description CHF
Inotropic agent Beta agonist Recemic mixture Used in short term management of patients with cardiac decompensation
48
Dobutamine Mechanism CHF
+ve inotropic effects and vasodilation Increased cAMP [Gs] -> phosphorylation of calcium channels with increased calcium entry into myocardium -> increased contraction Little or no effect on HR
49
Glucagon Description CHF
Inotropic agent | **Acute cardiac dysfunction from beta blocker overdose**
50
Glucagon mechanism CHF
Gs-> increased cAMP -> contractility (without using beta receptors) Inotropic and chronotropic effects Give when you gave someone too many beta blockers
51
Systolic failure
Want to increase volume, give inotropes | -use diuretics, beta blockers, inotropes, Spirinolactone, ACE-I, direct vasodilators
52
Diastolic failure
Want to slow heart, block calcium channels Use diuretics to decrease afterload Use Calcium blockers to slow heart and increase filling Use Beta blockers to slowdown heart
53
CHF Stage A
High risk of developing heart failure (selected patients receive ACE-I's/ARB's)
54
CHF stage B
Asymptomatic heart failure (selected patients receive ACE-I's / ARBs or beta blockers)
55
CHF stage C
Symptomatic heart failure (routine drugs include diuretics, ACE-I and beta blocker)
56
CHF stage D
Refractory end stage heart failure (end of life care or extraordinary measures)
57
Systolic failure definition
Contarctility and ejection fraction are reduced
58
Diastolic failure definition
Stiffening and loss of adequate relaxation -> abnormal ventricular filling and reduced CO even though the EF may be normal (does not respond to +ve inotropic agents)
59
Symptoms of heart failure
tachycardia, decreased exercise tolerance, dyspnea, peripheral and pulmonary edema
60
CHF
abnormal increase in blood volume and interstitial fluid leading to dyspnea and peripheral edema
61
Physiological compensation for CHF
Chronic activation of SNS and RAAS associated with tissue remodeling -> additional neurohormonal activation -> vicious cycle -> death
62
Goal of treatment of CHF
minimize the compensatory mechanisms-> reduce symptoms, slow progression and manage acute episodes
63
Do not use what drugs with diastolic failure?
+ve inotropic agents (increase outflow obstruction)

Pharmacology (24 decks)

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