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Personalised Medicine - Cardiovascular > L6 - LV Dysfunction and Heart Failure II > Flashcards

L6 - LV Dysfunction and Heart Failure II Flashcards

1
Q

Why is heart failure a modern disease?

A

Our body’s mechanism for reacting to a shock to the circulation was mainly due to blood loss
Sympathetic nervous and renin-angiotensin-aldosterone system responds to this

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2
Q

How does renin get to aldosterone?

A

Renin –> angiotensin –> aldosterone

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3
Q

Which two systems work together in heart failure?

A

Renin-angiotensin-aldosterone

Sympathetic nervous system - releases noradrenaline

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4
Q

Renin-angiotensin-aldosterone and the sympathetic nervous system impact which two factors?

A

Peripheral resistance – vasoconstriction/dilation to maintain blood pressure
Cardiac out – heart rate and force of contraction

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5
Q

Does the sympathetic nervous system lead to vasodilation or vasoconstriction?

A

Vasoconstriction –> increases peripheral resistance –> maintain blood pressure
Does the best with what blood volume you have

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6
Q

Does the sympathetic nervous system lead to increased or decrease cardiac output?

A

Increases heart rate and force of contraction –> increased cardiac output

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7
Q

When is renin released from the kidney?

A

Perfusion pressure to the kidney has decreased - assumes blood loss has occured
Low levels of Na going out to the distal tubules kidneys - assumes water/Na loss

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8
Q

What converts angiotensinogen to angiotensin I?

A

Renin

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9
Q

What converts angiotensin I to angiotensin II?

A

ACE

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10
Q

What does angiotensin II lead to?

A

Vasoconstriction –> increases peripheral resistance
Aldosterone release
Tubular Na reabsorption
Na and water retention

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11
Q

What leads to aldosterone release?

A

Angiotensin II

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12
Q

How do the sympathetic nervous system and angiotensin II interact?

A

Sympathetic nervous system - activates renin release

Angiotensin II - helps the sympathetic nervous system release noradrenaline

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13
Q

Overall what does the renin-angiotensin-aldosterone system and the sympathetic nervous system do?

A

Increase peripheral resistance
Increase cardiac output
Retain Na and water

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14
Q

What can the body not distinguish between?

A

Blood loss and heart failure

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15
Q

How does the body compensate for acute blood loss?

A

Tachycardia –> increased cardiac output
Positive ionotropic effect –> increased cardiac output
Vasoconstriction –> increased blood pressure
Sodium and water retention –> increased circulatory volume

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16
Q

During acute blood loss why does vasoconstriction occur?

A

Try to preserve vital organs such as the brain and kidney, blood diverted from skin etc

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17
Q

How does the body compensate for LV systolic dysfunction?

A

Kidneys sense a loss of perfusion pressure –> think the person is losing blood
Tachycardia –> increased workload and oxygen demand of heart
Positive ionotropic effect –> increased workload and oxygen demand
Vasoconstriction –> increased afterload
Sodium and water retention –> increased preload and oedema
Chronic adrenergic stimulation –> myocyte toxicity and arrythmia

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18
Q

During LV systolic dysfunction why the faster the heart rate the less efficient the heart?

A

The faster the heart rate the less efficient the heart is in term of metabolic needs and the amount of blood it can deliver

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19
Q

During LV systolic dysfunction why is vasoconstriction bad?

A

Leads to increased after load which makes it harder for the heart to eject blood?

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20
Q

Why is the same compensation for both acute blood loss and LV systolic dysfunction bad and good?

A

Good if losing blood

Bad for heart failure

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21
Q

What are the 6 different treatments for heart failure?

A 
Diuretics 
Aldosterone antagonist
Vasodilators 
Angiotensin II receptor blockers 
ACE inhibitors 
Beta blockers
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22
Q

How do diuretics treat heart failure?

A

Release congestion

Block Na and water retention

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23
Q

How do aldosterone antagonists treat heart failure?

A

Block renin-aldosterone-angiotensin

Weak diuretics – not powerful enough to remove congestion

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24
Q

How do vasodilators treat heart failure?

A

Overcome peripheral resistance
Anything that blocks the sympathetic nervous system will act as vasodilators themselves as they block the vasoconstriction triggered by this pathway

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25
Q

How do ACE inhibitors treat heart failure?

A

Block ACE enzyme therefore angiotensin II

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26
Q

How do beta blockers treat heart failure?

A

Block sympathetic nervous system

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27
Q

What is the best treatment approach for heart failure?

A

Blocking at several different levels

28
Q

What is an example of an ACE inhibitor used to treat severe heart failure?

A

Enalapril

29
Q

What % decrease in mortality did Enalapril cause compared to placebo in severe heart failure?

A

31%

30
Q

What is an example of an ACE inhibitor used to treat mild-moderate heart failure?

A

Ramipril

31
Q

What % decrease in mortality did Ramipril cause compared to placebo in mild-moderate heart failure?

A

25%

Benefit is less as the absolute risk is less in the first place as only mild to moderate heart failure

32
Q

What is LV dysfunction without heart failure?

A

Definite impairment in contractility of the heart

No-mild heart failure symptoms

33
Q

What change in death or hospitalisation did Enalapril cause compared to placebo in LV dysfunction without heart failure?

A

Reduced all the combined end points

34
Q

What are the main clinical indicators of ACE inhibitors?

A

Hypertension
Heart failure - severe and moderate
Diabetic nephropathy
LV dysfunction with no heart failure

35
Q

What are some examples of ACE inhibitors?

A

Ramipril
Perindopril
Enalapril

36
Q

What are all the adverse effects of ACE inhibitors related to?

A

Reduced angiotensin II production

Increased kinins

37
Q

What are the adverse effects of ACE inhibitors related to reduced angiotensin II?

A

Hypotension
- Angiotensin II supports the blood pressure
Acute renal failure
- Angiotensin II restricts the efferent arteriole  increases filtration pressure in glomerulus
Hyperkalaemia
- Angiotensin II causes aldosterone release which preserves Na and loses K
- Block to get excess K in blood
Teratogenic effects in pregnancy
- ACE enzyme is important in fetal development

38
Q

What are the adverse effects of ACE inhibitors related to increased kinins?

A

Cough
- Occurs in 10% of ACE inhibitor patients
Rash
Anaphylactoid reaction

39
Q

What does ACE do?

A

Breaks down angiotensin I to angiotensin II

  • Not specific
  • Also breaks down bradykinin
  • If you block ACE you also block the breakdown of bradykinin
40
Q

What are some examples of beta blockers?

A

Carvedilol
Bisoprolol
Metoprolol

41
Q

What were the results when beta blockers were used on top of other heart failure drugs?

A

Looking for an additional benefit – either given carvedilol or placebo
12 month mortality
- Placebo - 10%
- Carvedilol – 4%
If they had a beta blocker on top of standard therapy they had better survival/event free survival

42
Q

What are the main clinical indications of beta adrenoceptor blockers?

A

Ischaemic heart disease – prevents angina
Heart failure
Arrhythmia
Hypertension

43
Q

What are some examples of beta adrenoceptor blockers?

A 
Bisoprolol 
Metoprolol 
Carvedilol 
- All important for heart failure – these have had successful trials 
- Atenolol
44
Q

What is the selectivity of different beta adrenoceptor blockers?

A 
Beta 1 selective 
- Metoprolol 
- Bisoprolol 
Beta 1/2 nonselective
- Carvedilol 
- Propranolol 
In the middle – atenolol
45
Q

As you increase the dose of beta adrenoceptor blockers the become more and more?

A

Unselective

46
Q

What does the term cardioselective imply?

A

β-1 selectivity

Inaccurate - up to 40% of cardiac β-adrenoceptors are β-2

47
Q

What are the adverse effects of beta adrenoceptor blockers?

A 
Fatigue
- Due to blocking of adrenaline 
Headache
- Can cross blood brain barrier 
Sleep disturbance/nightmares	
Bradycardia
Hypotension
Cold peripheries
- Body response to bradycardia/reduced cardiac output by preserving central blood temperature/pressure by shutting down pathways to the skin 
Erectile dysfunction
48
Q

What diseases do beta adrenoceptor blockers cause worsening of?

A

Asthma or COPD
- Due to bronchoconstriction
PVD – Claudication or Raynaud’s
- If peripheral system already compromised it can make it worse
Heart failure – if given in standard dose or acutely
- Need low starting dose and slow uptitrate over weeks

49
Q

How does digoxin help in heart failure?

A

Can slow heart rate in atrial fibrillation - positive ionotopic activity
Go to hospital less due to heart failure
Develop new heart failure less frequency

50
Q

Why might digoxin not improve death rates in heart failure patients?

A

Potentially due to side effects such as

  • Positive ionotropic effects
  • Pre-arrythmic effects
  • Off set any benefits in the longer term
51
Q

What is Ivabrine used to treat?

A

Angina – slows the heart down
Heart failure – if after adequate treatment with other drugs you still have heart rate >70bpm
- Implies you haven’t overcome the sympathetic drive

52
Q

What current does Ivabradine block to help treat heart failure?

A

Blocks the If current in the sinus node

Slows sinus node rate

53
Q

What % did Ivabradine reduce hospitalisation for heart failure?

A

26% compared to placebo

54
Q

What % did Ivabradine reduce death due to heart failure?

A

0

55
Q

What is Sacubitril?

A

Neprilysin inhibitor - potentiates AMP

  • Fluid and Na loss from kidney
  • Increases levels of natriuretic peptides
56
Q

What is Valsartan?

A

Angiotensin II blocker - vasodilator

57
Q

How well did the combined therapy of sacubitril and valsartan (Entresto) treat heart failure? - hospitalisation and death

A

Hospitalisation
- Small reduction over and above other therapies
Death from any cause
- Small reduction
Only small reductions as already been significantly reduced by other drugs previously

58
Q

What are the symptoms of acute heart failure?

A

Pressures go up –> pulmonary oedema

59
Q

What are the treatments for acute heart failure?

A

Oxygen - can’t oxygenate properly
Diamorphine/heroine - treats pain and vasodilates
Nitrates - venal and arterial dilators –> reduce preload and afterload
LOOP diuretics - helps with excess congestion and vasodilates
Inotropes
PDE III inhibitors - PDE III break down cAMP –> inhibit to allow more cAMP

60
Q

In what situations would you use inotropes to treat acute heart failure?

A

When patients can’t maintain their cardiac output

Might have to stimulate the heart over a short period of time

61
Q

What are inotropes?

A

Adrenergic agonists - mimic the sympathetic nervous system
Either
- Inoconstrictors
- Inodilators

62
Q

What do inoconstrictors do?

A

Ionotropic effects and vasoconstriction

Noradrenaline, adrenaline and dopamine

63
Q

What do inoconstrictors act on?

A

Alpha 1 – in vasculature – vasoconstriction

Beta 1 – in the heart – ionotropic

64
Q

What do inodilators do?

A

Ionotropic effects and vasodilation

Dobutamine

65
Q

What do inodilators act on?

A

Beta 2 – in vasculature – vasodilation

Beta 1 – in the heart – ionotropic

66
Q

What is an example of a PDE II inhibitor?

A

Milirinone
If used chronically - 60% mortality
40% mortality in placebo

Personalised Medicine - Cardiovascular (11 decks)

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