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Pharmacology > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Drugs used for systolic heart failure?

A
  • Diuretics
  • Spironolactone
  • Inhibitors of angiotensin (ACE-inhibitors / ARBs)
  • Direct vasodilators
  • b-adrenoceptor antagonists (b-blockers)
  • Inotropic agents
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2
Q

Drugs used for diastolic heart failure?

A
  • Diuretics
  • ACEI /ARBs
  • b-adrenoceptor antagonists (b-blockers)
  • Calcium-channel antagonists
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3
Q

Diuretic MOA in HF?

A

• Relieve pulmonary congestion & peripheral edema
• Reduce symptoms of volume overload (eg,
orthopnea)
• plasma volume à venous return to the heart
(preload)
à cardiac workload & O2 demand
• Also afterload (reducing plasma volume à BP)

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4
Q

Diuretic clinical applications in heart failure?

A

• Integral component of treatment for congestive symptoms
and/or intravascular volume overload
• No evidence of a mortality benefit with thiazide or
loop diuretics alone
Thiazide diuretics : patients with hypertensive heart
disease (with congestive symptoms). Often ineffective as
monotherapy due to weak diuretic effect
Loop diuretics : more effective diuretics than thiazides
(useful if edema present)

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5
Q

ACE inhibitor role in heart failure?

A

• Agents of choice in HF
decrease vascular resistance & BP à cardiac output (afterload)
decrease salt & H20 retention ( preload)
decrease long-term remodeling of the heart
ACE inhibitors improve symptoms in patients with HF,
decrease incidence of hospitalization & MI, and
prolong survival

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6
Q

ACE inhibitors recommended and suggested for who in regards to HF?

A

Captopril / Enalapril / Lisinopril
Recommended for all patients with:
• symptomatic heart failure
• asymptomatic patients with decreased LVEF or
history of MI
Suggested for patients:
• at high risk of developing heart failure due to
atherosclerotic disease, obesity, diabetes
mellitus or hypertension

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7
Q

ACE inhibitor AE?

A 
• Hypotension,
• Persistent dry cough
• Hyperkalemia
• Angioedema
• Acute renal failure (patients with bilateral renal artery
stenosis)
• Teratogenic
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8
Q

ARB moa, use, and AE in heart failure?

A 
Candesartan / Valsartan
Potent competitive antagonists of angiotensin type I
receptor
DO NOT affect bradykinin levels
Clinical Application In HF
Substitute for patients who can’t tolerate ACE
inhibitors (severe cough or angioedema)
Adverse Effects
Similar to ACE inhibitors (no cough)
Teratogenic
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9
Q

Direct vasodilators MOA in HF?

A

Hydralazine + isosorbide dinitrate
increase vasodilation -> decrease cardiac preload
increase arterial dilation -> systemic arteriolar resistance & decrease afterload
• Concurrent use of two oral vasodilators: hydralazine
& isosorbide dinitrate can produce sustained
improvement in LVEF
Vasodilator Site of Dilating Action
Hydralazine- Arterioles
Nitrates- Veins and Venules
ACE inhibitors- Arterioles and Veins

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10
Q

Direct vasodilators clinical applications?

A

• Concurrent use of hydralazine & isosorbide dinitrate
recommended for use in patients:
• who cannot tolerate ACEI or ARB
or,
• in African American patients with advanced
heart failure as an adjunct to standard therapy

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11
Q

Direct vasodilators AE?

A

Hydralazine & isosorbide dinitrate
Headache, dizziness

Hydralazine
Tachycardia, peripheral neuritis, lupus-like syndrome

Contraindications
Sildenafil

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12
Q

Beta blocker use in HF?

A

Studies demonstrate reverse cardiac remodeling &
reduction in mortality & hospitalization (30-40% in
patients with NYHA II-IV HF)
• decrease HR and decrease contractility & inhibition of renin release (b1 receptors)
• Prevent deleterious effects of norepinephrine on cardiac
muscle fibers -> decrease remodeling, hypertrophy etc
• Can get initial exacerbation of symptoms (start at low
dose & gradually increase over several weeks)

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13
Q

Clinical applications of beta blockers in HF?

A

Recommended in addition to an ACEI for patients with:
- symptomatic heart failure
- asymptomatic patients with a decreased LVEF
or history of MI
NB. USE CAUTIOUSLY in decompensated HF and are
contraindicated in cardiogenic shock

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14
Q

Beta blocker AE?

A

• Same as all b-blockers
• Use cautiously in asthmatics and patients with severe
bradycardia
• Fluid retention (upon initial treatment) – an increasing
dose of concurrent diuretic may help

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15
Q

Spironolactone role and moa in heart failure?

A

Patients with advanced heart disease have elevated
aldosterone levels due to:
• angiotensin stimulation
• reduced hepatic clearance
MOA
Aldosterone antagonist à prevents Na+ retention,
myocardial hypertrophy & hypokalemia

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16
Q

Spironolactone clinical applications and AE in HF?

A

Clinical Application in HF
+ ACE inhibitors are shown to decrease
morbidity & mortality in patients with severe
heart failure
Adverse Effects
Hyperkalemia (esp. in patients taking ACEIs/ARBs,
K+ supplements or who have renal failure)
GI disturbances (gastritis, peptic ulcer)
CNS effects (lethargy, confusion)
Endocrine abnormalities (gynecomastia, decreased
libido, menstrual irregularities)

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17
Q

What is digoxin?

A

Ionotropic agent
• Cardiac glycoside
• Derived from digitalis (foxglove) plant
• Widely used in treatment of HF
• Digoxin can decrease the symptoms of heart failure,
increase exercise tolerance and decrease rate of
hospitalization, but DOES NOT increase survival

18
Q

Disadvantages of Digoxin?

A

Disadvantages
• Narrow therapeutic margin
• Unfavourable, complicated pharmacokinetics
• Drug sensitivity varies between patients
• Drug sensitivity may change during therapy
• Severe, potentially lethal adverse effects

19
Q

Digoxin MOA?

A

Positively inotropic
• Increases force of heart contraction
Negatively chronotropic
• Decreases heart rate

• Inotropic action : increase cytoplasmic Ca2+ concentration that enhances contractility of cardiac muscle and -> increases cardiac output
• also
• enhances vagal tone -> decrease HR
• reduces sympathetic activity
• reduces peripheral resistance
-> decrease myocardial O2 demand
20
Q

Digoxin MOA on membrane and flux calcium?

A

• [Ca2+]i must be lowered for cardiac muscle to relax
• Na+/Ca2+ exchanger extrudes Ca2+ from myocyte
• Concentration gradient determines net ion movement
• Inhibiting active transport of Na+ decreases Na+
concentration gradient & ability for Ca2+ to leave cell
• Increased cellular Na+ is exchanged for Ca2+
• Ca2+ is retained intracellularly -> increased [Ca2+]i
• If Na+/K+ ATPase is extensively inhibited ->
dysrhythmias

21
Q

Summary of Digoxin effects?

A

• Effects of digoxin result from direct action on cardiac
muscle as well as indirect actions (autonomic
effects):
• increase force and velocity of myocardial systolic
contraction (+ve inotropic action)
• decrease in the degree of activation of SNS & renin angiotensin system (-ve chronotropic action)
• Slowing of the HR & decrease conduction velocity through AV node (-ve chronotropic and –ve dromotropic
action)

22
Q

Digoxin clinical applications?

A

• HF with atrial fibrillation (main application)
• Can be used (in addition to ACEI & b-blocker) to
decrease symptoms, increase exercise tolerance &
decrease rate of hospitalization

23
Q

Digoxin PK?

A 
• Very potent (narrow safety margin)
• Widely distributed (including CSF)
• t ½ = ~36-40 h
• Accumulates in muscle à large Vd (loading dose
required)
24
Q

Digoxin AE?

A

Digoxin toxicity = one of most common ADRs
• Cardiac effects: arrhythmias, characterized by slowing of
AV conduction (atrial arrhythmias)
• GI effects: anorexia, nausea & vomiting
• CNS effects: headache, fatigue, confusion, blurred vision,
alteration of color perception, halos on dark objects

25
Q

Precipitating factors of digoxin toxicity?

A
  • Hypokalemia
  • Drug accumulation / relative overdose
  • Hypomagnesemia or hypercalcemia
  • Hyperthyreosis
  • Abnormal renal function
  • Respiratory disease
  • Acid-base imbalances
  • …. age above 65, low body weight, fever etc
26
Q

Digoxin interactions?

A

K+ Digoxin & K+ inhibit each others binding to Na+/K+
ATPase
-> hyperkalemia reduces digoxin activity
-> hypokalemia facilitates digoxin activity

Ca2+ Accelerates overloading of Ca2+ stores
-> facilitates toxic actions of digoxin, esp. arrhythmias

Mg2+ Opposite to Ca2+ (Mg2+ antagonizes effects of Ca2+)

27
Q

Factors predisposing to digoxin toxicity?

A
  • K+-depleting diuretics
  • Corticosteroids
  • Hypothyroidism
  • Hypoxia
  • Renal failure
  • Myocarditis
28
Q

Drugs predisposing to digoxin toxicity?

A

Quinidine, verapamil & amiodarone can cause
digoxin toxicity by displacement from tissue
protein-binding sites & competition for renal
excretion – digoxin levels can increase by 70-100%

29
Q

Treatment of digoxin toxicity?

A

• Withdraw drug for some days and/or reduce dose
• Monitor plasma digoxin and K+ levels, ECG
• Adjust electrolyte status (K+ supplements)
• Ventricular tachyarrhythmia: lidocaine,
magnesium, adjust K+ to high normal

30
Q

Severe digoxin interaction?

A

• Bradyarrhythmias, suppressed automaticity ->
temporary cardiac pacemaker
• Treat with digitalis antibodies (Digoxine immune
fab, Digibind)

31
Q

Severe digoxin interactions?

A
  • In patients with diastolic or right-sided HF
  • In presence of uncontrolled hypertension
  • In presence of bradyarrhythmias
  • In non-responders or intolerant patients
32
Q

criteria for systolic dysfunction and treatment of HF?

A

All patients with HF & systolic dysfunction (LVEF
<40%) should take (unless a specific contraindication):
ACE inhibitor and a b-blocker & a diuretic (if volume
overloaded)

33
Q 
HFrEF Stage C
NYHA Class I-IV
Treatment:
ACEI (or ARB)
AND b-blocker
What are criteria for add on?
A 
For all volume overload, NYHA class II-IV patients
Loop diuretic
For persistently symptomatic African Americans, NYHA class III-IV patients
Hydralazine+ isosorbide dinitrate
For NYHA class II-IV patients, provided estimated creatinine >30ml/min &amp; K+ <5.0mEq/dL
Spironolactone
34
Q

HF conclusions when to use ARBS, aldosterone antagonists, digoxin, and vasodilators?

A

• ARBS – patients who cannot tolerate an ACEI
• Aldosterone antagonist – addition can be beneficial for
patients with moderately-severe to severe HF or patients
with LV dysfunction after an MI
• Hydralazine/isosorbide dinitrate – addition can be
beneficial
• Digoxin – addition can decrease symptoms but not
increase survival

35
Q

Agents used in diastolic HF?

A

Diuretics
Can be used to treat any resulting pulmonary edema; must be used cautiously (do not want stroke volume to decrease)

ACEI/ARBs
Same benefits as in HFrEF

Calcium-channel blockers
In diastolic failure inotropy can be normal so Ca2+-
channel blockers do not impair stroke volume. Shown to be beneficial in improving ventricular relaxation and reducing heart rate

b-blockers
Similar beneficial effects to Ca2+-channel blockers

36
Q

AGENTS NOT USED in diastolic HF?

A

AGENTS NOT USED
• Positive inotropes (increasing inotropy can lead to
increased outflow obstruction)

37
Q

PDE 3 inhibitors moa and uses?

A

Inamrinone, Milrinone
• Inhibit myocardial cAMP PDE activity -> increased cAMP
levels (+ve inotropic effect and increased cardiac output)
• Possess systemic & pulmonary vasodilator effects
(reduce both preload and afterload)
• Shown to increase AV conduction slightly
• Used for short-term therapy in patients with
intractable heart failure

38
Q

Dopamine used in acute HF?

A

Stimulates both adrenergic & dopaminergic receptors
• Lower doses = mainly dopaminergic stimulating
(produce renal and mesenteric vasodilation)
• Higher doses = both dopaminergic & b1
stimulating (produce cardiac stimulation & renal
vasodilation)
• Large doses = stimulate a receptors
(vasoconstriction)
• Used in the treatment of shock (eg, MI, open heart
surgery, renal failure, cardiac decompensation) which
persists after adequate fluid volume replacement.
Dopamine also promotes diuresis.

39
Q

Dobutamine use in HF?

A

Dobutamine is administered as a racemic mixture
• (-) isomer is an a1-receptor agonist and a weak b1
agonist
• (+) isomer is an a1-antagonist, a potent b1 agonist
and a mild b2 agonist
• At therapeutic levels the stimulation of b1-receptors
predominate, leading to a potent inotropic effect (with
little change in heart rate). Net vascular effect is mild
vasodilation (b2-receptors)
• Used to increase cardiac output in acute management
of heart failure (eg, MI)

40
Q

Glucagon use in HF?

A

Stimulates adenylyl cyclase to produce increased cAMP
(by binding to GPCR), leading to potent inotropic and
chronotropic effects
• Produces similar effect to b-agonists, without
requiring functioning b-receptors
• Used as a cardiac stimulant in management of severe
cases of b-blocker overdosage

Pharmacology (49 decks)

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