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CARD - 1 > Clinical Pharmacology of Heart failure > Flashcards

Clinical Pharmacology of Heart failure Flashcards

1
Q

Define heart failure.

A

Chronic heart failure is a syndrome characterised by progressive cardiac dysfunction, SoB, tiredness, neurohormonal disturbances, sudden death.

Heart failure is the state in which the heart is unable to pump blood at a rate commensurate with the requirements of the tissues or can do so only from high pressures.

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2
Q

What are the two types of heart failure?

A

Systolic heart failure (HFrEF) - decreased pumping function of the heart, which results in fluid back up in the lungs and heart failure.

Diastolic (or relaxation) heart failure (HFpEF) - 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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3
Q

Describe the epidemiology and prognosis of chronic heart failure.

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.

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4
Q

What are the risk factors for heart failure?

A

Coronary artery disease, hypertension (LVH), valvular heart disease, alcoholism, viral infection, diabetes, congenital heart defects, obesity, age, smoking, high or low hematocrits level, obstructive sleep apnea.

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5
Q

Describe the pathological progression of CV disease.

A

Coronary artery dsiease, hypertension, diabetes, cardiomyopathy, vascular disease etc… causes myocardial injury. This leads to neurohormonal stimulation and myocardial toxicity which results in pathologic remodelling –> low ejection fraction which can lead to sudden death or pump failure (chronic heart failure).

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6
Q

What happens in systolic dysfunction?

A

Frank-Starling Law - if the muscle of a healthy heart is stretched it will contract with greater force and pump out more blood.

In the failing or damaged heart this relationship is lost.
As circulatory volume increases the heart fillets, the force of contraction weakens and CO drops further.
Decreased CO then activates RAAS further. Circulatory volume increases and cardiac perform 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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7
Q

What might cause the symptoms associated with heart failure? And what are these symptoms?

A

Neurohormonal stimulation, myocardial toxicity and low ejection fraction lead to dyspnoea, fatigue and oedema.

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8
Q

When does heart failure usually occur?

A

Following sustained hypertension (diastolic dysfunction/preserved ejection fraction HF) or following myocardial damage, i.e. an MI (systolic dysfunction).

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9
Q

Summarise what essentially is happening in HF and what systems are activated in the body.

A

CO falls - body registers this as a loss in circulatory volume. Activates -
Vasoconstrictor system activation and salt and water retaining system (RAAS).

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10
Q

What does activation of the RAAS cause release of?

A

Release of renin from juxatoglomerular cells. Renin converts angiotensinogen into angiotensin I. ACE converts angiotensin I into angiotensin II. Angiotensin II is a strong peripheral vasoconstrictor (raises BP). It also stimulates release of aldosterone from the adrenal cortex.

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11
Q

What effect does the aldosterone system have on the body?

A

Increases salt and water retention, increased plasma volume, preload and cardiac workload.

Increased salt and water retention in HF patients leads to oedema and aldosterone secretion can lead to kaliuresis and fibrosis.

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12
Q

So what is the end result of the RAAS system in HF patients?

A

Salt and water retention, vasoconstriction, hypertrophy and fibrosis of cardiac myocytes.

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13
Q

What does activation of the sympathetic NS cause release of? And what do these hormones do?

A

Noradrenaline and adrenaline.

Vasoconstriction, stimulation of renin release and myocyte hypertrophy.

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14
Q

What substances may be involved in salt and water excretion and vasodilation?

A

Natriuretic peptide system - ANP/BNP.

EDRF.

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15
Q

What is ANP?

A

Atrial natriuretic peptide
Strong vasodilator and hormone secreted by heart atrial myocytes in response to high blood volume. Acts to reduce salt and water retention thus reducing BP.

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16
Q

What is BNP?

A

Brain natriuretic peptide.
Released by ventricular myocytes. Released modulated by calcium ions. When produced binds to ANP receptors and also reduce systemic vascular resistance and increase salt and water excretion.

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17
Q

What is EDRF?

A

Endothelium derived relaxing factor.

Promotes smooth muscle relaxation (vasodilatation).

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18
Q

What are the main points about atrial and brain natriuretic peptides?

A

Potent vasodilators and natriuretic peptides with short half lives.

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19
Q

How are the body’s mechanisms to excrete salt and water in comparison to those for salt and water retention?

A

Body has very strong system to retain water and salt and much weaker system to get rid of it. So ANP/BNP/EDRF easily overridden.

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20
Q

What is the final result in HF?

A

A failing heart that can’t pump out sufficient blood to supply body’s needs.
Progressive retention of salt and water –> oedema (pulmonary oedema).
Progressive myocyte death and fibrosis.
(can also build up in scrotum)

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21
Q

What do patients with HF tend to present with?

A

Severe acute breathlessness as a result of pulmonary oedema.

May also see froth coming from their mouth, stained by blood.

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22
Q

What are the two aims of modern treatment of HF? Which drugs allow these aims to be met?

A

To improve symptoms

  • Diuretics
  • Digoxin

To improve symptoms and survival

  • ACE inhibitors/ARBs
  • Spirnolactone
  • Valsartan-sacubitril

To improve survival

  • Beta-blockers
  • Ivabradine
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23
Q

What are you trying to target in symptomatic treatment of HF?

A

Inhibit detrimental neurohormonal adaptations.
Chance benefits of neurohormonal adaptations,.
Enhance cardiac function.

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24
Q

So what drugs are used for symptomatic treatment of HF?

A

Loop diuretics.
MAINSTAY of symptomatic treatment.
Furosemide or bumetanide.

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25
Q

What drugs may you use to block detrimental hormonal changes?

A

Block sympathetic activation using carvedilol, bisoprolol and metoprolol (beta-blockers which are of proven benefit in treatment of CHF).

Block RAAS activation.
Angiotensin II - ACEi e.g. ramipril or angiotensin antagonists (Valsartan, Losartan) but these are not as effective.
Aldosterone effects blocked by spironolactone (produces significant reduction in morbidity).

26
Q

How might you enhance beneficial hormonal changes?

A

ANP/BNP are metabolised by neutral endopeptidase.

Neprolysin prevents metabolism and enhances ANP/BNP actions.

27
Q

How might you enhance cardiac function in treatment of HF?

A

Positive inotropes - improve ability of heart to pump and so improve cardiac status. Digoxin only drug in common use.

Vasodilators - nitrovasodilators reduce preload and after load = improved cardiac function. Isosorbide mono or denitrate.
Hydralazine an arterial dilator also shown to improve cardiac function.

28
Q

When it the only time you would use positive inotropes (digoxin)?

A

Only used in N stage as they make the patient feel really good for about a month and then they kill them. Used only when patient is dying and just need time to say goodbye to family etc..

29
Q

How is prognosis of HF?

A

Despite treatment, mortality remains high.
ACEi reduce relative risk by 35% and beta blockers by 38%.

BUT 4 year mortality remains around 40%.

Prognosis worse than some cancers (breast, uterus, prostate and bladder).

30
Q

How does the average length of hospital admission with HF compared to other conditions?

A

2nd highest to stroke.

31
Q

How do loop diuretics such as furosemide work?

A

Induce profound diuresis by inhibiting the Na-K-Cl transporter in the Loop of Henle (work at v low glomerular filtration rates). Prevent reabsorption of 20% of filtered sodium and water.

32
Q

Why would you be more keen to give an elderly patient bumetanide as opposed to furosemide as a loop diuretic in the treatment of CHF?

A

Bumetanide more slow acting, this means that the patient won’t be running back and forth to the toilet as much as if they were on furosemide.

33
Q

What course of action must you take if the patient is diuretic resistant?

A

Use loop diuretics in combination with thiazide diuretics. This combo is powerful and may induce diuresis of 5-10L/day.

34
Q

What must you be careful of when using thiazide and loop diuretics together?

A

D-D interactions

Dehydration, hypotension, hypokalaemia, hypnonatraemia, gout, impaired glucose tolerance, diabetes.

35
Q

Why can using diuretics cause gout?

A

Can cause uric acid build up which gets deposited in the joints = gout.

36
Q

What drugs must you be furosemide?

A 
Aminoglycosides - aural and renal toxicity  
Lithium - renal toxicity 
NSAIDs - renal toxicity 
Antihypertensives - profound hypotension
Vancomycin - renal toxicity.
37
Q

So, overall how do you reduce mortality in CHF patients?

A

Angiotensin blockage
Beta receptor blockade
Aldosterone blockade
ANP/BNP enhancement

38
Q

What are ACE inhibitors and give examples of drug names?

A

Ramipril, enallapril, lisinopril.
Competitively block ACE. Prevent conversion of angiotensin I to angiotensin II (reducing preload and after load on heart).

39
Q

What are ACEi shown to significantly reduce in CHF patients?

A

Morbidity and mortality.

40
Q

What are ACEi shown to reduce in post MI patients?

A

Morbidity, mortality and onset of HF.

41
Q

What is the issue with ACEis?

A

If you block the ACE, other enzymes come into action to convert angiotensin I to II.

42
Q

What are ADRs of ACEi?

A

First dose hypotension, cough, angioedema, renal impairment, renal failure, hyperkalaemia.

43
Q

What are possible D-D interactions of ACEi?

A

NSAIDs = acute renal failure.
Potassium supplements = hyperkalaemia.
Potassium sparing diuretics = hyperkalaemia.
Hyperkalaemia can cause AF if severe enough.

44
Q

What are angiotensin receptor blockers?

A

They selectively block angiotensin II, AT1 receptor. They are effective but NOT as effective as ACEis.

45
Q

At present what are ARBs recommended for?

A

Only in patients with ACEi intolerance.

46
Q

What is the role of angiotensin II receptor AT1?

A

Vasoconstriction, vascular proliferation, aldosterone secretion, cardiac myocyte proliferation, increased sympathetic tone.

47
Q

What is the role of angiotensin II receptor AT2?

What does this mean?

A

Vasodilation, antiproliferation, apoptosis.

Selective blockade of any II at the AT1 receptor may offer advantages over nonspecific blockage of RAS (study disproved this).

48
Q

What could you use to selectively block the AT1 receptor?

A

ARB blocks AT1 receptor.
Can use combined valsartan and ARB neprilysin.

Neprilysin stops break down of ANP and ANP by neutral endopeptidases.

49
Q

What drug is an aldosterone antagonist? What does it do? What are the proven to do?

A

Spironolactone - potassium sparing diuretic, inhibits the actions of aldosterone, acts in distal tube, used in combo with loop diuretics (particularly in resistant oedema). Proven to reduce mortality when used in combo with ACEis.

50
Q

What beta blockers can be used in the treatment of HF?

A

Carvedilol, bisoprolol, metoprolol.

51
Q

Why must you take caution in using beta blockers in HF?

A

Patients must be selected carefully as their use is potentially hazardous.
They block the actions of the sympathetic NS - if you take this away and the patient is very unwell (esp if have pulm oedema) then can kill.
PUT ON ONCE STABLE.
Specialist use only.

52
Q

What have beta blockers been found to do in HF?

A

Reduce mortality and morbidity in mild/moderate and even severe HF by 30%.

53
Q

What is ivabradine?

A

A specific inhibitor of the If current in the sinoatrial node (no action on other channels in heart/vascular system).

Does not modify myocardial contractility and intracardiac conduction, even in patients with impaired systolic function.

54
Q

What are the recommendations over when to use ivabradine?

A

Beneficial to reduce HF hospitalisation for patients with symptomatic stable chronic HFrEF (LVEF <35%) who are receiving standard therapy, incl a beta blocker at max tolerated dose, and who are in sinus rhythm with a HR of 70bpm + at rest.

55
Q

What are the shown benefits/side effects of digoxin?

A

Increases availability of calcium in the myocyte. Shown to reduce no of hospitalisations. No effect on mortality.

Narrow therapeutic index, arrhythmias, nausea, confusion.

56
Q

Why might you use digoxin?

A

If patients has AF - might slow their HR.

57
Q

Why might you use anticoagulation?

A

Esp. if they have AF as this puts them at more risk of thrombus.
Use warfarin as dilated ventricle gives rise to thrombus formation and thrombi-embolic events.
Warfarin has proven value in preventing these.

58
Q

List all the medications a HF patient may be put on.

A 
Furosemide +/- thiazide  or furosemide + pulse metolazone
ACEi or ARB or ARNI
Beta blocker +/- ivabradine
MRA-spirnolactone (25mg)
Digoxin Warfarin if appropriate.
59
Q

What must you monitor regularly in HF patients and why?

A

Daily weight assessment - oedema - can increase medications according to symptoms or weight.

60
Q

What symptoms and signs can therapy offer relief from?

A

SoB, tiredness, lethargy.

Peripheral oedema, ascites, weight.

CARD - 1 (28 decks)

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