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Pharmacology > Congestive Heart Failure > Flashcards

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
Q

Direct vasodilator description/mechanism CHF

A

Increase vasodilation -> decrease preload
Increase arterial dilation -> decrease PVR and afterload
Hydralazine dilates arterioles
Nitrates dilate the veins and venules
Give in african americans

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26
Q

Direct vasodilators indication CHF

A

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
Q

Direct vasodilator adverse CHF

A

HA, dizziness, hypotension

Hydralazine can also cause tachycardia, peripheral neuritis and a lupus like syndrome

28
Q

Hydralazine adverse

A

HA, dizziness, hypotension

Tachycardia, peripheral neuritis, lupus like syndrome

29
Q

Beta blockers for CHF

A

Carvedilol

Metoprolol

30
Q

Beta blockers description CHF

A

Can reverse cardiac remodeling and reduce mortality

31
Q

Beta blockers mechanism CHF

A

Decrease HR and RAAS (-ve inotrope)
Prevents deleterious effects of NE on cardiac muscle fibers
(renin inhibition and decreased HR)

32
Q

Beta blockers indication CHF

A

Heart disease (stage B and C) in addition to an ACE-I

33
Q

Beta blockers PK CHF

A

Start at low dose -> gradually titrate to effective dose (to avoid sudden exacerbation of sx)

34
Q

Beta blockers adverse CHF

A

Initial treatment can cause fluid retention

35
Q

Beta blockers contraindication CHF

A

Use cautiously in patients with asthma or severe bradycardia

36
Q

Digoxin class

A

Inotropic agent: Cardiac glycoside

37
Q

Digoxin description CHF

A

+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
Q

Digoxin mechanism CHF

A

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
Q

Digoxin PK CHF

A

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
Q

Digoxin adverse CHF

A

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
Q

Digoxin contraindications CHF

A

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
Q

Milrinone and Inamrinone CHF description

A

Inotropic agents
PDE-3 inhibitor (phosphodiesterase inhibitors)
Good for acute/short term in increasing CO

43
Q

Milrinone and Inamrinone mechanism CHF

A

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
Q

Milrinone and Inamrinone Adverse CHF

A

Short term only, long term decreases life

Can cause thrombocytopenias

45
Q

Dopamine description CHF

A

Inotropic agent
Used in the treatment of shock that persists after volume replacement

Stimulates both adrenergic and dopaminergic receptors

46
Q

Dopamine Mechanism CHF

A

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
Q

Dobutamine Description CHF

A

Inotropic agent
Beta agonist
Recemic mixture

Used in short term management of patients with cardiac decompensation

48
Q

Dobutamine Mechanism CHF

A

+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
Q

Glucagon Description CHF

A

Inotropic agent

Acute cardiac dysfunction from beta blocker overdose

50
Q

Glucagon mechanism CHF

A

Gs-> increased cAMP -> contractility (without using beta receptors)
Inotropic and chronotropic effects
Give when you gave someone too many beta blockers

51
Q

Systolic failure

A

Want to increase volume, give inotropes

-use diuretics, beta blockers, inotropes, Spirinolactone, ACE-I, direct vasodilators

52
Q

Diastolic failure

A

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
Q

CHF Stage A

A

High risk of developing heart failure (selected patients receive ACE-I’s/ARB’s)

54
Q

CHF stage B

A

Asymptomatic heart failure (selected patients receive ACE-I’s / ARBs or beta blockers)

55
Q

CHF stage C

A

Symptomatic heart failure (routine drugs include diuretics, ACE-I and beta blocker)

56
Q

CHF stage D

A

Refractory end stage heart failure (end of life care or extraordinary measures)

57
Q

Systolic failure definition

A

Contarctility and ejection fraction are reduced

58
Q

Diastolic failure definition

A

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
Q

Symptoms of heart failure

A

tachycardia, decreased exercise tolerance, dyspnea, peripheral and pulmonary edema

60
Q

CHF

A

abnormal increase in blood volume and interstitial fluid leading to dyspnea and peripheral edema

61
Q

Physiological compensation for CHF

A

Chronic activation of SNS and RAAS associated with tissue remodeling -> additional neurohormonal activation -> vicious cycle -> death

62
Q

Goal of treatment of CHF

A

minimize the compensatory mechanisms-> reduce symptoms, slow progression and manage acute episodes

63
Q

Do not use what drugs with diastolic failure?

A

+ve inotropic agents (increase outflow obstruction)

Pharmacology (24 decks)

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