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CDL301 > Lecture 06 LV Dysfunction and HF 2 > Flashcards

Lecture 06 LV Dysfunction and HF 2 Flashcards

1. Describe the patterns of clinical presentation of LV dysfunction, chronic heart failure and acute heart failure 2. Describe neurohumoral activation in heart failure, with an understanding of the interaction between the renin-angiotensin-aldosterone and sympathetic nervous systems 3. Describe pharmacological interventions in chronic heart failure, with an emphasis on neurohumoral blockage rather than direct stimulation of cardiac contraction in patients with chronic heart failure 4. Understa

1
Q

What advantages are there for the renin-angiotensin system?

A

works well for blood loss by conserving the central blood volume and pressure and shutting down useless areas of the body

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2
Q

What is a problem of the renin-angiotensin system?

A

system doesn’t work in cases of heart failure

can’t distinguish the different between heart failure and blood loss

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3
Q

How does the renin-angiotensin system work?

A

angiotensin + renin = angiotensin I

angiotensin I + ACE = angiotensin II

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4
Q

How does the sympathetic envois system impact on the renin-angiotensin system?

A

release of noradrenaline

increases renin levels therefore increasing angiotensin II

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5
Q

What effect does angiotensin II have on the body?

A

aldosterone release
increased peripheral resistance
increased cardiac output

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6
Q

What effect does aldosterone have on the body?

A

tubular sodium reabsorption

salt and water retention

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7
Q

How does the body respond to acute blood loss?

A

tachycardia
positive inotropic effect
vasoconstriction
sodium and water retention

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8
Q

How does the body respond to LVSD?

A 
tachycardia
positive inotropic effect (NA)
vasoconstriction
sodium and water retention 
chronic adrenergic stimulation
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9
Q

What treatments can be given to a patient with LVSD?

A

diuretics
vasodilators
aldosterone antagonists
ACE inhibitors

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10
Q

Give examples of ACE Inhibitors (x4)

A

enalapril
ramipril
perindorpril
trandolapril

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11
Q

What effect did Enalapril have on patient mortality?

A

31% reduction in mortality - significant

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12
Q

Why is Enalapril beneficial to hospitals?

A

significantly reduces hospitalisation from HF significantly reducing costs

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13
Q

What other conditions can ACE inhibitors be used for?

A

hypertension and diabetic nephropathy

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14
Q

What are the adverse effects of ACE inhibitors relating to decreased angiotensin II formation?

A

hypotension
acute renal failure
hyperkalaemia
teratogenic effects in pregnancy

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15
Q

What are the adverse effects of ACE inhibitors relating to increased kinin production?

A

cough
rash
anaphylactoid reactions

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16
Q

Why is there an increase in kinin production in response to ACE inhibitors?

A

angiotensin II is responsible for the breakdown of bradykinin

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17
Q

What three beta-blockers have been shown to be beneficial in treating heart failure?

A

carvedilol
bisprolol
metoprolol

18
Q

What else can beta-blockers be used to treat?

A

IHD
angina
arrhythmia
hypertension

19
Q

What are the adverse side effects of beta-blockers?

A

CNS - fatigue, headache, sleep disturbances, nightmares
vascular - bradycardia, hypotension, cold peripheries
erectile dysfunction

20
Q

What conditions can beta-blockers make worse?

A

asthma or COPD
peripheral vascular diseases - claudication or Raynaud’s
heart failure (standard dosing)

21
Q

How are beta-blockers prescribed to avoid worsening of heart failure?

A

initially prescribed very low dose and increase the amount slowly

22
Q

What effect does Digoxin have on heart failure?

A

decreases hospitalisation but does’t decrease mortality

23
Q

How does Ivabradine work?

A

blocks the sodium funny current in the sinus node slowing the firing rate

24
Q

What is Ivabradine used to treat?

A

angina and heart failure

25
Q

What is an advantage of Ivabradine?

A

good for treating patient who can’t take beta blockers

improves rate of hospitalisation and heart failure mortality

26
Q

What is a disadvantage of Ivabradine?

A

doesn’t decrease rate of cardiovascular death

27
Q

What is an alternative to ACE inhibitors in treating HF?

28
Q

What two drugs make up Entresto?

A

sacubitril and valsartan

29
Q

How does Entresto work?

A

NEP inhibitor, increasing levels of natriuretic peptides

30
Q

Which shows more promise ACE inhibitors or Entresto?

31
Q

Who are the main sufferers of acute heart failure?

A

elderly with diastolic dysfunction

32
Q

What is the main symptom of acute heart failure? What does this cause?

A

pulmonary oedema

lungs fill with fluid decreasing oxygen uptake

33
Q

What treatments are given to those with acute heart failure? Why?

A

pure oxygen - increase oxygen gradient in lungs
diamorphine (heroin) - vasodilator and relaxant
nitrates - vasodilation and decrease preload
loop diuretics - vasodilation and diuresis

34
Q

When are Inotropes suitable for use?

A

in acute heart failure when there is a treatable problem, i.e. damaged valve

35
Q

Give two examples of Inotropes

A

adrenergic agonists

PDE III inhibitors

36
Q

Give two examples of Adrenergic Agonists

A

inoconstrictors and inodilators

37
Q

Give examples of inoconstrictors (x3). What do they do?

A

norepinephrine, epinephrine, dopamine

act on alpha receptors in periphery to achieve vasoconstriction

38
Q

Give examples of inodilators (x2). What do they do?

A

dobutamine, dopamine, isoproterenol
act on beta 1 receptors to increase force of contraction
act on beta 2 receptors in skeletal muscle to cause vasodilation

39
Q

How do PDE III inhibitors work?

A

potentiate cAMP by inhibiting PDE III

PDE II normally potentiates the breakdown of PDE III

40
Q

Give an example of a PDE III inhibitor

A

milrinone (primacor)

41
Q

Why are PDE III inhibitors unsuitable long term treatments?

A

over 18 months have been shown increase mortality compared to placebo treatment

CDL301 (14 decks)

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