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ACEM Primary Written > Cardiovascular: Pharmacology - Heart failure > Flashcards

Cardiovascular: Pharmacology - Heart failure Flashcards

1
Q

List 7 classes of treatments used in the management of chronic systolic HF. Which of these confer a mortality benefit and reduction in hospitalisations?

A
  1. Diuretics
  2. Aldosterone receptor antagonists*
  3. ACEIs/ARBs
  4. B-blockers*
  5. Cardiac glycosides
  6. Vasodilators
  7. Resynchronisation, cardioversion
  • mortality benefit and reduction in hospitalisations (certain B-blockers only)
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2
Q

List 6 classes of treatments used in the management of acute HF

A
  1. Diuretics
  2. Vasodilators
  3. B-agonists
  4. Bipyridines
  5. Natriuretic peptide
  6. LVAD
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3
Q

What is the effect of B-agonists in acute vs chronic HF?

A

Used in treatment of acute HF but reduce survival in chronic HF

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4
Q

What’s the most common cause of HF?

A

CAD

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5
Q

What are the three types of HF? Describe each briefly

A
  1. Systolic failure: decreased contractility, HFrEF
  2. Diastolic failure: stiffening and decreased relaxation leading to reduced filling and reduced SV/CO, often HFpEF, more common with increasing age and in women
  3. High-output failure
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6
Q

List 4 causes of high-output HF

A
  1. Hyperthyroidism
  2. Anaemia
  3. Beriberi
  4. AV shunts
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7
Q

What are four main pathophysiological features of HF? What causes each

A
  1. Increased preload: due to increased Na+/H2O retention, venous tone
  2. Increased afterload: due to increased TPR
  3. Reduce contractility: due to remodelling, cell apoptosis
  4. Increased HR: due to B-adrenergic stimulation
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8
Q

What are the effects of tachycardia in HF?

A

Reduced filling time and coronary blood flow

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9
Q

Describe the pathophysiology of HF

A
  1. Reduced CO results in reduced carotid sinus firing and reduced renal blood flow
  2. Reduced carotid sinus firing causes increased sympathetic discharge: increased contractility, HR and preload
  3. Reduced renal blood flow activates RAAS: angiotensin II increases afterload and further increases sympathetic discharge
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10
Q

What is the effect of HF on the baroreceptor reflex?

A

Baroreceptor reflex is reset with lower sensitivity to arterial pressure
Decreased stimulation of vasomotor centre increases sympathetic outflow and decreases parasympathetic outflow

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11
Q

What class of drug is digitalis/digoxin?

A

Cardiac glycoside

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12
Q

Describe the pharmacokinetics of digitalis in terms of its chemical structure and ADME

A

Chemical structure: steroid nucleus, lacks easily ionisable group so solubility is not pH-dependent
Absorption: bioavailability 65-80%
Distribution: widely distributed (including CNS) with 20-30% protein binding
Metabolism: 2/3 excreted unchanged by kidneys, t1/2 = 36-40hrs with normal renal function
Elimination: proportional to CrCl

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13
Q

List four drugs which inhibit excretion of digitalis

A

Amiodarone
Verapamil
Quinidine
Spironolactone

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14
Q

What is the mechanism of action of digitalis?

A

Inhibits Na+/K+ ATPase
Causes increased intracellular Na+, which produces decrease Ca2+ efflux via Na+/Ca2+ antiport
Increased cytosolic Ca2+ increases contractility

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15
Q

Describe the effects of digitalis on intracellular K+

A

Initially: increased K+ conductance due to increased Ca2+ causes reduced action potential duration
At higher doses: decreased K+ due to Na+/K+/ATPase pump inhibition causes resting membrane potential to become less negative, can get delayed after-depolarisations which cause ectopics if they reach thresholds -> further increase in dose produces tachyarrhythmias

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16
Q

Describe the autonomic effects of digitalis

A

Low therapeutic doses increase parasympathetic effects (predominantly in SA and AV nodes as there is less cholinergic innervation in ventricles)
At toxic doses increases sympathetic outflow

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17
Q

What are the three cardiac effects of digitalis?

A
  1. Positive inotropy
  2. Negative chronotropy (decreased SA node firing and conduction velocity)
  3. Negative dromotropy (increased AV block)
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18
Q

What are two extra-cardiac effects of digitalis?

A

GI: increased motility (N+V, diarrohoea), anorexia
CNS: vagal and chemoreceptor trigger zone stimulation, disorientation, hallucination, visual disturbance

19
Q

What is the effect of K+, Ca2+ and Mg2+ on risk of digoxin toxicity?

A

Decreased K+, decreased Mg2+ and increased Ca2+ all increase digoxin toxicity

20
Q

What arrhythmias can be induced by digoxin?

A

AV junctional rhythm
PVCs
Bigeminy
VT
2nd degree AVB

21
Q

How is digoxin toxicity treated?

A

Digibind (sheep Ab)

22
Q

What is the clinical application for digoxin?

A

Used in patients with HF and AF

23
Q

What is the mechanism of action of bipyridines?

A

Inhibits PDE-3
Increased contractility by increased Ca2+ influx during action potential
Also vasodilates

24
Q

Give an example of a bipyridine

A

Milrinone

25
Q

Milrinone half-life

A

3-6hrs

26
Q

Describe the excretion of milrinone

A

10-40% excreted in urine

27
Q

Give an example of a B-agonist used in the management of acute HF

A

Dobutamine

28
Q

What is the mechanism of action of dobutamine?

A

Selective B1-agonist
Increases CO, decreases ventricular filling pressure
May cause tachycardia and increased O2 demand

29
Q

What are the clinical applications of dobutamine?

A

Acute HF
HF with HTN

30
Q

What is the mechanism of action of aldosterone receptor antagonists in the management of HF?

A

Reduces preload by reducing Na+/H2O retention
Also decreases afterload by reducing BP in setting of HF with HTN

31
Q

What is the mechanism of action of ACEIs/ARBs in the management of HF?

A

Reduces afterload by reducing TPR
Reduces preload by reducing Na+/H2O retention
Reduces cardiac and vessel remodelling

32
Q

When should ACEIs/ARBs be used first-line in the management of HTN?

A

In the setting of LV dysfunction without oedema

33
Q

What is the mechanism of action of vasodilators (e.g. nitrates, hydralazine) in the management of HF?

A

Reduced preload by venodilation (e.g. nitrates)
Reduced afterload by arteriolar dilation (e.g. hydralazine)

34
Q

List 4 B-blockers which confer a mortality benefit in HF

A
  1. Bisoprolol
  2. Carvedilol
  3. Metoprolol
  4. Nebivolol
35
Q

What is the mechanism of action of B-blockers in the management of HF?

A

Up-regulation of B-receptors
Attenuation of effects of increased catecholamines (including apoptosis)
Decreased remodelling by inhibition of mitogenic activity of catecholamines
Decreased HR

36
Q

Outline the AHA stages of CHF

A

A: no symptoms, risk factors present
B: symptoms with severe exercise
C: symptoms with marked or mild exercise
D: severe symptoms at rest

37
Q

Outline the NYHA classes of CHF

A

Prefailure: no symptoms, risk factors present
I: symptoms with severe exercise
II: symptoms with marked exercise
III: symptoms with mild exercise
IV: severe symptoms at rest

38
Q

Outline the management of CHF as per the AHA/NYHA stages

A

A/prefailure: treat risk factors (obesity, HTN, DM, hyperlipidaemia)
B/I: ACEI/ARB, B-blocker, diuretic
C/II/III: add aldosterone antagonist, digoxin; CRT, ARNI (angiotensin receptor/neprilysin inhibitor), hydralazine/nitrate
D/IV: transplant, LVAD

39
Q

List 7 classes of anti-anginals. Which can be used to treat variant angina caused by coronary vasospasm?

A
  1. Nitrates*
  2. Nicorandil
  3. CCBs*
  4. B-blockers
  5. Perhexiline
  6. Ivabradine
  7. Allopurinol
  • used in variant angina
40
Q

What is the mechanism of action of nicorandil as an anti-anginal?

A

K+ channel activator
Vasodilatory in normal coronaries
Likely decreases preload and afterload

41
Q

What is the mechanism of action of perhexiline as an anti-anginal?

A

Inhibits mitochondrial enzyme to increase ATP and improve myocardial efficiency

42
Q

What is the mechanism of action of ivabradine as an anti-anginal?

A

Inhibits If Na+ channel
Decreases HR

43
Q

What is the mechanism of action of allopurinol as an anti-anginal?

A

XO inhibitor
Appears to cause increased vasodilation

ACEM Primary Written (150 decks)

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