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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
How do ACE inhibitors treat heart failure?
Block ACE enzyme therefore angiotensin II
26
How do beta blockers treat heart failure?
Block sympathetic nervous system
27
What is the best treatment approach for heart failure?
Blocking at several different levels
28
What is an example of an ACE inhibitor used to treat severe heart failure?
Enalapril
29
What % decrease in mortality did Enalapril cause compared to placebo in severe heart failure?
31%
30
What is an example of an ACE inhibitor used to treat mild-moderate heart failure?
Ramipril
31
What % decrease in mortality did Ramipril cause compared to placebo in mild-moderate heart failure?
25% | Benefit is less as the absolute risk is less in the first place as only mild to moderate heart failure
32
What is LV dysfunction without heart failure?
Definite impairment in contractility of the heart | No-mild heart failure symptoms
33
What change in death or hospitalisation did Enalapril cause compared to placebo in LV dysfunction without heart failure?
Reduced all the combined end points
34
What are the main clinical indicators of ACE inhibitors?
Hypertension Heart failure - severe and moderate Diabetic nephropathy LV dysfunction with no heart failure
35
What are some examples of ACE inhibitors?
Ramipril Perindopril Enalapril
36
What are all the adverse effects of ACE inhibitors related to?
Reduced angiotensin II production | Increased kinins
37
What are the adverse effects of ACE inhibitors related to reduced angiotensin II?
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
What are the adverse effects of ACE inhibitors related to increased kinins?
Cough - Occurs in 10% of ACE inhibitor patients Rash Anaphylactoid reaction
39
What does ACE do?
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
What are some examples of beta blockers?
Carvedilol Bisoprolol Metoprolol
41
What were the results when beta blockers were used on top of other heart failure drugs?
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
What are the main clinical indications of beta adrenoceptor blockers?
Ischaemic heart disease – prevents angina Heart failure Arrhythmia Hypertension
43
What are some examples of beta adrenoceptor blockers?
``` Bisoprolol Metoprolol Carvedilol - All important for heart failure – these have had successful trials - Atenolol ```
44
What is the selectivity of different beta adrenoceptor blockers?
``` Beta 1 selective - Metoprolol - Bisoprolol Beta 1/2 nonselective - Carvedilol - Propranolol In the middle – atenolol ```
45
As you increase the dose of beta adrenoceptor blockers the become more and more?
Unselective
46
What does the term cardioselective imply?
β-1 selectivity | Inaccurate - up to 40% of cardiac β-adrenoceptors are β-2
47
What are the adverse effects of beta adrenoceptor blockers?
``` 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
What diseases do beta adrenoceptor blockers cause worsening of?
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
How does digoxin help in heart failure?
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
Why might digoxin not improve death rates in heart failure patients?
Potentially due to side effects such as - Positive ionotropic effects - Pre-arrythmic effects - Off set any benefits in the longer term
51
What is Ivabrine used to treat?
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
What current does Ivabradine block to help treat heart failure?
Blocks the If current in the sinus node | Slows sinus node rate
53
What % did Ivabradine reduce hospitalisation for heart failure?
26% compared to placebo
54
What % did Ivabradine reduce death due to heart failure?
0
55
What is Sacubitril?
Neprilysin inhibitor - potentiates AMP - Fluid and Na loss from kidney - Increases levels of natriuretic peptides
56
What is Valsartan?
Angiotensin II blocker - vasodilator
57
How well did the combined therapy of sacubitril and valsartan (Entresto) treat heart failure? - hospitalisation and death
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
What are the symptoms of acute heart failure?
Pressures go up --> pulmonary oedema
59
What are the treatments for acute heart failure?
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
In what situations would you use inotropes to treat acute heart failure?
When patients can’t maintain their cardiac output | Might have to stimulate the heart over a short period of time
61
What are inotropes?
Adrenergic agonists - mimic the sympathetic nervous system Either - Inoconstrictors - Inodilators
62
What do inoconstrictors do?
Ionotropic effects and vasoconstriction | Noradrenaline, adrenaline and dopamine
63
What do inoconstrictors act on?
Alpha 1 – in vasculature – vasoconstriction | Beta 1 – in the heart – ionotropic
64
What do inodilators do?
Ionotropic effects and vasodilation | Dobutamine
65
What do inodilators act on?
Beta 2 – in vasculature – vasodilation | Beta 1 – in the heart – ionotropic
66
What is an example of a PDE II inhibitor?
Milirinone If used chronically - 60% mortality 40% mortality in placebo

Personalised Medicine - Cardiovascular (11 decks)

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