Drugs used in the treatment of heart failure Flashcards

1
Q

Heart failure (HF

A

Clinical syndrome associated with symptoms due to abnormalities in
cardiac structure and/or function substantiated by the presence of
increased natriuretic peptide plasma concentrations or objective
evidence of pulmonary or systemic congestion of cardiogenic origin

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2
Q

HF with reduced EF (HFrEF)

A

HF with LVEF ≤40% (0.4)

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3
Q

HF with mildly reduced EF (HFmrEF)

A

HF with LVEF 41%49% (0.41-0.49)

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4
Q

HF with preserved EF (HFpEF)

A

HF with LVEF ≥50% (0.5)

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5
Q

HF with improved EF (HFimpEF

A

HF with baseline LVEF ≤40% (0.4), a ≥10
point increase from baseline LVEF, and a
second measurement of LVEF >40% (0.4)

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6
Q

Heart failure (HFrEF)

A

Systolic dysfunction results in a decline in cardiac output leading to the activation of a number of neurohormonal compensatory responses that
attempt to maintain adequate cardiac output, including activation of:
* Sympathetic nervous system (SNS)
* Renin-angiotensin-aldosterone system (RAAS)
* other systems

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7
Q

Primary manifestations of both HFrEF and HFpEF:

A
  • Dyspnea and fatigue, which lead to exercise intolerance
  • fluid overload which can result in peripheral oedema and pulmonary congestion.
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8
Q

Class I

A

Patients with cardiac disease but without limitations of physical activity.
Ordinary physical activity does not cause undue fatigue, dyspnea, or
palpitation.

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9
Q

Class II

A

Patients with cardiac disease that results in slight limitations of physical
activity. Ordinary physical activity results in fatigue, palpitation, dyspnea, or
angina.

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10
Q

Class III

A

Patients with cardiac disease that results in marked limitation of physical
activity. Although patients are comfortable at rest, less than ordinary activity
will lead to symptoms.

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11
Q

Class IV

A

Patients with cardiac disease that results in an inability to carry on physical
activity without discomfort. Symptoms of congestive HF are present even at
rest. With any physical activity, increased discomfort is experienced.

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12
Q

CCF: goals of therapy

A
  • Improve the patient’s quality of life,
  • Relieve or reduce symptoms,
  • Prevent or minimize hospitalizations,
  • Slow progression of the disease, and
  • Prolong survival.
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13
Q

First step in the management of chronic HF is to determine

A
  • Classification of HF based upon LVEF and
  • Symptomsoms based upon NYHA functional class and/or any precipitating
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14
Q

Stepwise treatment of CCF: STGs and EML

A

Diuretic
PLUS
ACEI

Add 3rd agent:
carvedilol
OR
Spironolactone

Add 4th agent:
Carvedilol
OR
Spironolactone

Add 5th agent:
Digoxin

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15
Q

Low-ceiling diuretics Thiazides

A

Hydrochlorothiazide*

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16
Q

High-ceiling diuretics Loop

A

Furosemide*
Bumetanide
Torasemide

17
Q

Potassium-sparing Aldosterone antagonists
diuretics

A

Spironolactone*
Eplerenone

18
Q

potassium-sparing

A

Amiloride

19
Q

Angiotensin-converting
enzyme (ACE) inhibitors
(ACEI

A

Class I: captopril-like:Captopril

Class II: prodrugs
Enalapril*
Perindopril
Quinapril
Ramipril
Trandolapril

Class III: water soluble Lisinopri

20
Q

Angiotensin II receptor
blockers (ARBs)

A

Candesartan
Irbesartan
Losartan*
Telmisartan
Valsartan

21
Q

Carvedilol: pharmacokinetics

A

is a non-selective B receptor blocker with additional Alpha 1 blocking.
* Preferred in CCF (dose responsive reduction in mortality)
* Introduce cautiously…start at low dose (3.125mg bd): worsening of CF or
fluid retention may occur during up titration of carvedilol – increase diuretics,
do not increase carvedilol dose until clinically stable
* Dosing for CCF (max doses: 25mg bd – if weight is >85kg 50mg bd)
* Extensive metabolism in the liver with large first-pass effect
(lipophilic)
* Excreted mainly in the bile

22
Q
  • Adverse effects
A

postural hypotension,
dizziness, oedema of the legs

23
Q

B-blockers in HF

A
  • Carvedilol, metoprolol and bisoprolol
24
Q

Spironolactone

A

Potassium spiring: aldosterone antagonist.

Prolong survival and decrease hospitalizations in patients with HFrEF.
* Considered to reduce the risk of hospitalization in patients with
HFpEF

25
Q

Digoxin

A

Digitalis glycoside
positive inotropic effect
(an increase in the force
of contraction), a
negative chronotropic
effect (a decrease in the
heart rate), and a
negative dromotropic
effect (a decrease in
conduction velocity).

Digoxin is unique in its
ability to strengthen
cardiac contraction while
decreasing heart rate.

26
Q

Digoxin: mechanism of action

A

Mechanisms by which digoxin exerts its positive inotropic effect on the heart. Digoxin inhibits the sodium pump (ATPase) in the sarcolemma and increases the concentration of intracellular sodium. The high sodium concentration increases the activity of the sodium-calcium exchanger (Ex), thereby causing more calcium to enter or remain inside the cardiac myocyte. Calcium
activates muscle fiber shortening and increases cardiac contractility, which in turn increases stroke volume at any given fiber length

27
Q

Digoxin: Electrophysiologic and electrocardiographic effects

A

Figure 12.4 Digoxin causes an increase in parasympathetic (vagal) tone and a decrease in
sympathetic tone. These actions slow the heart rate by decreasing sinoatrial (SA) node automaticity. The increased vagal tone and decreased sympathetic tone also slows the
atrioventricular (AV) node conduction velocity while increasing the AV node refractory period. The
reduced AV conduction velocity increases the PR interval on the electrocardiogram.

28
Q

Digoxin: pharmacokinetics

A
  • Rate (but not extent) of absorption decreased by food
  • Bioavailability varies between preparations (no generic substitution)
  • Onset of action 0.5-2 hours (effects last for 6 days)
  • Half-life prolonged in renal failure; elimination is renal (50-70%
    unchanged)
  • Narrow therapeutic index: Therapeutic serum concentrations 0.65-
    1.1nmol/L
  • Individualised dosing
29
Q

Digoxin: adverse effects

A

Most common adverse effects of digoxin are gastrointestinal, cardiac,
and neurologic reactions.
* Earliest signs of toxicity are anorexia, nausea, and vomiting.
* Arrhythmias, most serious manifestation of digoxin toxicity, atrial
tachycardia with AV block is one of the most common types of
digitalis-induced arrhythmia, but digoxin can also cause ventricular
arrhythmias. Hypokalaemia can precipitate arrhythmias. * Neurologic effects: blurred vision and yellow, green, or blue
chromatopsia (a condition in which objects appear unnaturally
colored). Severe digoxin toxicity can precipitate seizures.

30
Q

Digoxin: toxicity

A

Hypokalaemia, hypomagnesaemia, and hypercalcaemia predispose to
toxicity
* Monitoring samples of steady-state serum concentration should be
taken 6-8 hours after last dose
* Patients should be aware of and report signs of toxicity: anorexia,
nauseas and vomiting. CNS signs, headache, drowsiness, facial pain,
depression, mental confusion, disturbed vision

31
Q

Digoxin: contraindications

A
  • Ventricular arrythmias without HF, Wolf-Parkinson-White syndrome,
    hypertrophic obstructive cardiomyopathy, incomplete AV nodal bloc
32
Q
A