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Clinical pharmacology of heart failure Flashcards

1
Q

What is chronic heart failure characterised by (symptoms)?

A
  • By progressive cardiac dysfunction
  • Breathlessness
  • Tiredness
  • Neurohormonal disturbances
  • Sudden death
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2
Q

What are the 2 types of heart failure

A
  • Systolic heart failure (HFrEF)
  • Diastolic (or relaxation) heart failure (HFpEF)

Know systolic, not diastolic!!

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3
Q

Features of Systolic heart failure (HFrEF)

A

Decreased pumping function of the heart, which results in fluid back up in the lungs and heart failure

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4
Q

Features of Diastolic heart failure (HFpEF)

A
  • Involves a thickened and stiff heart muscle
  • As a result, the heart does not fill with blood properly
  • This results in fluid backup in the lungs and heart failure
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5
Q

What is the Ejection fraction?

A

Volume of blood ejected from the ventricle with each beat

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6
Q

Chronic heart failure facts

A
  • Affects 2-10% of the population
  • Incidence rises with increasing age
  • Has a poor prognosis with a 5 year mortality of 50% rising to 80% in a year for some patients
  • Patients are often very symptomatic
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7
Q

Risk factors for heart failure

A
  • Coronary artery disease
  • Hyperension (LVH)
  • Valvular heart disease
  • Alcoholism
  • Infection (viral)
  • Congenital heart defects
  • Diabetes
  • Other: obesity, age, smoking, high or low haematocrit level, obstructive sleep apnoea
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8
Q

What is the no.1 risk factor for Heart failure?

A

Hypertension

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9
Q

What is the Frank-Starling Law?

A

If the muscle of a healthy heart is stretched it will contract with greater force and pump out more blood.

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10
Q

Features of Systolic Dysfunction

A
  • Frank-Starling law
  • In the failing or damaged heart this relationship is lost
  • As circulatory volume increases the heart dilates, the force of contraction weakens and cardiac output drops further
  • Cardiac output then activates the RAAS further
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11
Q

What is the result of systolic dysfunction?

A
  • The result is a vicious cycle in which the RAAS is activated, circulatory volume increases and cardiac performance deteriorates further.
  • As the heart starts to dilate the cardiac myocytes undergo hypertrophy and then fibrosis and thus the heart is further weakened.
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12
Q

What is activated fir salt and water retention and vasoconstriction?

A

Renin-Angiotensin-Aldosterone System

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13
Q

What does the activation of the sympathetic system cause the release of?

A

Noradrenaline and Adrenaline

  • Vasoconstriction
  • Stimulate renin release
  • Myocyte hypertrophy
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14
Q

What is used for salt and water excretion and vasodilatation?

A
  • Natriuretic peptide system ANP/BNP

- EDRF

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15
Q

Features of atrial and brain natriuretic peptides

A
  • Potent vasodilators and natriuretic peptides

- Short half-life

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16
Q

What are the 2 main aims of heart failure treatment?

A

To improve symptoms and improve survival

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17
Q

Treatment used to improve symptoms

A
  • Diuretics (loop diuretics)

- Digoxin

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18
Q

Treatment used to improve symptoms and survival

A
  • ACE inhibitors/ARBs
  • Spironolactone
  • Valsartan-sacubitril
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19
Q

Treatment used to improve survival

A
  • Beta-blockers

- Ivabradine

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20
Q

What is used for blocking detrimental hormonal changes?

A

Sympathetic activation

- Carvedilol, Bisoprolol and Metoprolol are beta blockers which are of proven benefit in the treatment of CHF.

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21
Q

RAAS activation: inhibition of Angiotensin II

A
  • Two groups of drugs available to block the effects of angiotensin II
  • ACE inhibitors (Ramipril)
  • Angiotensin antagonists (Valsartan, Losartan_ but these are not as effective (ELITE II)
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22
Q

RAAS activation: Aldosterone inhibition

A
  • Effects blocked by Spironolactone

- Produces a significant reduction in morbidity (RALES)

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23
Q

What treatments are used for enhancing beneficial hormonal changes?

A
  • Natriuretic peptide system
  • ANP/BNP: atrial natriuretic and brain peptides are potent natriuretic agents and vasodilators
  • Metabolised by neutral endopeptidase
  • Neprolysin prevents metabolism and enhances ANP/BNP actions
24
Q

What treatments are used for enhancement of cardiac function?

A
  • Positive Inotropes

- Vasodilators

25
Features of positive inotropes
- These drugs improve the ability of the heart to pump and so improve cardiac status - Digoxin is the only drug in common use
26
Features of Vasodilators
- The nitrovasodilators by reducing preload and afterload improve cardiac function (Isosorbide mono or Dinitrate) - Hydralazine an arterial dilator has also been shown to improve cardiac function
27
By how much do ACEi and beta blockers reduce mortality and hospitalisation?
ACEi - relative risk reduction 35% Beta Blockers - relative risk reduction 38%
28
Features of Loop Diuretics (Furosemide)
- The main stay of treatment - Removes excess salt and water - The loop diuretics induce profound diuresis - Inhibit the Na-K-Cl transporter in the Loop of Henle - Work at very low glomerular filtration rates - Prevent the reabsorption of 20% of filtered sodium and water
29
Adverse drug reactions of diuretics
- Dehydration - Hypotension - Hypokalaemia, Hyponatraemia - Gout - Impaired glucose tolerance, diabetes
30
Drug-Drugs interactions: Frusemide and aminoglycosides
Aural and renal toxicity
31
Drug-Drugs interactions: Frusemide and Lithium
Renal toxicity
32
Drug-Drugs interactions: Frusemide and NSAIDs
Renal toxicity
33
Drug-Drugs interactions: Frusemide and antihypertensives
Profound hypotension
34
Drug-Drugs interactions: Frusemide and Vancomycin
Renal toxicity
35
Mechanism to reducing mortality
- Angiotensin blockade - Beta receptor blockade - Aldosterone blockade - ANP/BNP enhancement
36
Does local angiotensin II synthesis require ACE inhibitors?
No it is independent of ACE
37
Examples of Angiotensin converting enzyme inhibitors
- Ramipril - Enalapril - Lisinopril
38
Features of Angiotensin converting enzyme inhibitors
- Completely block angiotensin converting enzyme - Prevent the conversion of angiotensin I to angiotensin II - Reduce preload and afterload on the heart
39
Features of ACE inhibitors
- In CHF patients significantly reduce: morbidity, mortality - Post MI patients to reduce: morbidity, mortality, onset of heart failure - Main studies CONSENSUS, SOLVD, SAVE, AIRE, ISSIS-4
40
Adverse drug reactions of ACE inhibitors
- First dose hypotension - Cough - Angioedema - Renal impairment - Renal failure - Hyperkalaemia
41
ACE inhibitor drug-drug interactions
NSAIDs - acute renal failure Potassium supplements - hyperkalaemia Potassium sparing diuretics - hyperkalaemia
42
Features of Angiotensin receptor blockers
- ARBs selectively block the angiotensin II, AT1 receptor - They are effective, but not as effective as ACEi's - At present recommended for use in ACEi intolerant patients
43
What are the roles of AT1 receptors?
- Vasoconstriction - Vascular proliferation - Aldosterone secretion - Cardiac myocyte proliferation - Increased sympathetic tone
44
What are the roles of AT2 receptors?
- Vasodilation - Antiproliferation - Apoptosis
45
According to studies, is ACEi therapy good?
No, greatest benefits in patients not on ACE inhibitor therapy
46
Features of Valsartan-Sacubitril (ARNI)
- Combined valsartan and ARB and Neprilysin - ARB blocks AT1 receptor - Neprilysin stops break down of ANP and BNP by neutral endopeptidases
47
Features of Aldosterone Antangonists (Spirolactone)
Spironolactone - Potassium sparing diuretic - Inhibits the actions of aldosterone - Acts in the distal tubule - Used in combination with loop diuretics - Particularly useful in resistant oedema Proven to reduce mortality when used in combinations with ACEi's
48
Examples of Beta-Blockers in treatment of CHF
- Carvedilol - Bisoprolol - Metoprolol
49
Features of Beta-blockers in treatment of CHF
- Use of beta-blockers in this treatment of CHF is potentially hazardous and patients must be selected carefully - Block the actions of the sympathetic system - May precipitate severe deterioration in CHF - Have been demonstrated to reduce morbidity and mortality in mild/moderate and severe heart failure by 30% - Should be used only when a patient has been stabilised and not during an acute presentation - Specialist use only
50
Features of Ivabradine
- Ivabradine is a specific inhibitor of the If current in the sinoatrial node. - No action on other channels in the heart or vascular system. - Does not modify myocardial contractility and intracardiac conduction, even in patients with impaired systolic function.
51
When is Ivabradine recommended?
It can be beneficial to reduce HF hospitalisation for patients with symptomatic (NYHA class II-III) stable chronic HFrEF (LVEF <35%) who are receiving standard therapy, including a beta blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70bpm or greater at rest.
52
Features of Positive Inotropes (Digoxin)
Digoxin (the DIG study) - Increases availability of calcium in the myocyte - Shown to reduce number of hospitalisations - No effect on mortality - Narrow therapeutic index - Arrhythmias - Nausea - Confusion
53
Features of Anticoagulants (Warfarin)
Warfarin - Dilated ventricle gives rise to thrombus formation and thrombo-embolic events - Warfarin has proven to prevent these events - Anticoagulant use if high risk of thromboembolic disease
54
What is the therapeutic regime for heart failure?
- Furosemide +- thiazide, appropriate dose - Furosemide + pulsed metolazone - ACE inhibitor, appropriate dose - Angiotensin receptor blocker - ARNI - Beta-blocker +- Ivabradine - MRA-spironolactone, 25mg - Digoxin, TDM - Warfarin, TDM
55
Monitoring benefit of treatment
- Symptomatic relief: SOB, tiredness, lethargy - Clinical relief: peripheral oedema, ascites, weight - Monitor weight regularly: patient performs daily weight assessment, Increase medication according to symptoms or weight - Patient education

Cardiovascular System (36 decks)

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