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PY366 Heart Failure > Pharmacology of drugs used to treat heart failure > Flashcards

Pharmacology of drugs used to treat heart failure Flashcards

1
Q

when is heart failure with reduced ejection fraction initiated (1,2,3,4 answers LAQ of why do heart failure treatment drugs work)

A

initiated when an index event causes the pumping capacity of the heart to be impaired

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2
Q

what does reduced pumping capacity of the heart result in (2)

A

results in compensatory activation of the sympathetic nervous system and the renin angiotensin aldosterone system
- neurohormonal activation

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3
Q

what does neurohormonal activation lead to (3)

A

results in a series of coordinated responses that collectively work to restore cardiovascular homeostasis in the short term

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4
Q

what does sustained neurohormonal activation lead to (4)

A

drives the progression of HFrEF through the deleterious effects exerted on the circulation and myocardium

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5
Q

what forms the basis of modern therapy for HFrEF

A

Antagonism of neurohormonal systems

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6
Q

what effects does heart failure have on the sympathetic nervous system

A
  1. decreased Baroreceptor responsiveness
  2. myocyte hypertrophy
  3. increased arrhythmias
  4. impaired diastolic and systolic function
  5. reduced renal blood flow
  6. increased renin release
  7. increased tubular reabsorption of Na+
  8. increased activation of RAAS
  9. decreased response to natriuretic peptides
  10. vascular hypertrophy
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7
Q

what is the equation for cardiac output

A

cardiac output= Stroke volume x heart rate

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8
Q

describe the sympathetic response to reduced cardiac output in the neurohormonal model

A
  1. Heart is damaged which activates sympathetic system
  2. releases adrenaline which acts on B1 receptors
  3. increase frequency and force of contractability
  4. increases work load so heart is using more energy
  5. causes vasoconstriction of arterioles and this increases after load and pre load
  6. Increases In intercellular calcium and cAMP
  7. not effective in HF
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9
Q

describe the RAAS response to reduced cardiac output

A
  1. reduced cardiac output
  2. reduces renal blood flow
  3. activates RAS and angiotensin II
  4. activates aldosterone and leads to Na+ and H2o retention
  5. increases arterioconstruction
  6. Ang II works on AT1 receptors and increases afterload and preload and drives remodelling of heart
  7. increases cardiac workload
  8. NOT beneficial in the long term
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10
Q

describe the natriuretic peptide response to low cardiac output

A
  1. reduced cardiac output
  2. increased natriuretic peptides
  3. leads to veno dilation and arteriodilation
  4. decreases remodelling
  5. decreases blood pressure
  6. reduces cardiac workload
  7. Increased stretch of the heart
  8. ANP is increased
  9. Natriuretic Peptides don’t have much effect
    - when RAAS and sympathetic system are over activated, reduces the effect of natriuretic peptides
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11
Q

what is the equation for blood pressure

A

blood pressure= total peripheral resistance x cardiac output

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12
Q

what are the problems with prolonged compensation

A
  1. starlings law- overstretch leads to loss of function
  2. desensitisation of beta receptors
  3. increased angiotensin secretion leads to increased afterload which can drive remodelling of heart
  4. abnormally high levels of NA/A causes increases in heart rate (catecholamines) leading to arrhythmias
  5. myocardial hypertrophy
    - makes heart stiffer
    - muscle growth can decrease chamber size
    - muscle growth can occur faster than blood vessel supply
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13
Q

what is the 1st line treatment of heart failure

A
  • offer diuretics for congestive symptoms and fluid retention
  • for heart failure with preserved ejection fraction, manage comorbidities and offer personalised exercise based cardiac rehabilitation programme
  • for heart failure with reduced ejection fraction, offer ACE inhibitor or beta blocker
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14
Q

what are the most effective diuretics for heart failure

A

loop diuretics
- furosemide, bumetanide

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15
Q

what is the role of diuretics

A
  • provide symptomatic relief
  • decrease Na+ retention and increase H2O loss
  • decrease preload and afterload
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16
Q

what can be used to overcome resistance in diuretics

A

metalozone (thiazide like diuretic) can be used in combo with loop diuretics

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17
Q

what are the side effects of loop diuretics

A
  • dehydration/hypotension
  • loss of ions
  • hyperuricaemia and gout
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18
Q

what is the mechanism of action of loop diuretics

A
  1. blocks sodium potassium chloride cotransporter
  2. increases Na+ excretion
  3. increases K+ excretion
  4. increases Cl- excretion
  5. reduce sodium chloride reabsorption in the thick ascending limb of the loop of Henle
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19
Q

what is the role of ACE inhibitors for heart failure

A
  1. improves mortality
  2. large well conducted trials
  3. decreases preload and afterload
  4. reduces remodelling
20
Q

give examples of ACE inhibitors

A

ramipril, enalapril, captopril

21
Q

what are the side effects of ACE inhibitors

A
  1. dry cough
  2. 1st dose hypotension
  3. contraindicated in bilateral renal artery stenosis
  4. no adverse effects on serum glucose/lipids, so frontline in diabetic patients
  5. may not be as efficacious in black African/caribbean patients
22
Q

what is the mechanism of action of angiotensin receptor blockers

A
  1. block the actions of AngII on AT1-R
    - eg. losartan, candesartan
    - no cough
    - used if intolerant of ACE inhibitor
23
Q

what is the mechanism of action of ace inhibitors

A

prevent production of angiotensin II, a substance that narrows blood vessels
- This narrowing can cause high blood pressure and forces the heart to work harder

24
Q

what is the role of ARBs in heart failure

A
  1. improves mortality
  2. added into conventional therapy
  3. may be better than ACE inhibitors- less side effects
25
Q

why should an ARB be added

A
  1. ACE inhibitor therapy can lead to breakthrough due to increases in renin production and therefore Ang I
  2. there are other enzymes that convert Ang I to Ang II
26
Q

what is the role of beta blockers in heart failure

A
  1. improves mortality
  2. frontline with ACE inhibitor
  3. attenuates sympathetic drive
  4. not all BBs are equivalent
    - bisoprolol and carvedilol best supported by evidence
27
Q

what are the side effects and contraindications of Beta blockers

A
  1. potential bronchoconstriction
  2. vasoconstriction via blockade of B2-R
    - smooth muscle cell in the airways or peripheral arterioles perfusing skeletal muscle
  3. fatigue
  4. increase blood lipids
  5. hypoglycaemia/hyperglycaemia
  6. CNS side effects
  7. potentially not as efficacious in black African/americans
28
Q

what do inverse agonists have

A

negative efficacy

29
Q

what is sacubitril valsartan

A

an angiotensin receptor neprilysin inhibitor

30
Q

describe the use of vasodilators if ACE/ARB/BB not tolerated

A
  1. decrease preload
  2. decrease afterload
  3. large trials show good benefit but many side effects
31
Q

what are the side effects of vasodilators

A
  • hypotension
  • headache
  • tachycardia
32
Q

give an example of a vasodilator

A

hydralazine

33
Q

what is the mechanism of action of aldosterone antagonists (spironolactone)

A
  1. inhibits ability of aldosterone to produce new na+ channels
    - therefore causes loss of na+ and h2o
    - decrease preload and reduce blood pressure
34
Q

what is the role of spironolactone in heart failure

A
  1. improves mortality
  2. added into conventional therapy
  3. attenuates aldosterone effect
  4. only small doses required
35
Q

what are the side effects of spironolactone

A
  • hyperkalaemia
  • gynaecomastia
36
Q

when is epleronone used

A
  1. more selective for mineralocorticoid receptor- no antiandrogen effects
  2. aldosterone antagonist with reduced side effects
37
Q

what is the role of digoxin in heart failure

A
  1. used in initial trials
  2. increases myocardial contractility
  3. lost favour because of toxicity
  4. renally cleared- dependent on age, weight
38
Q

what are the side effects of digoxin

A
  • arrhythmias
  • heart block
39
Q

what is the role of ivabradine in heart failure

A

HCn channel blocker
- heart-rate-lowering agent that acts by selectively inhibiting the cardiac pacemaker current

40
Q

what other treatments can be used in heart failure

A
  1. biventricular pacing- severe CHF
    - high cost
  2. transplantation- 85% survival
41
Q

How do diuretics remove fluids from lungs

A
  • It decreases the blood volume and decreases end diastolic volume
  • will increase oncotic pressure and decrease hydrostatic pressure and both combined pulls fluid back into the cardiovascular system
42
Q

how would you monitor pulmonary congestion

A
  1. Ask how they are feeling, can lay down so not as much shortness of breath and their weight should decrease
  2. consulting points and routes of administration
  3. what formulations would you use (move from oral tablets to IV infusion)
43
Q

what should be monitored in use of ACE inhibitors

A
  • monitor blood pressure, renal impairment (effects renal blood pressure), hyperkaliemia, monitor cough, serum creatinine
  • monitor ECG
44
Q

how to reduce risk of 1st dose hypotension in ACE inhibitors

A

give initially at night, want to start on low doses because it could reduce the preload

45
Q

what does it mean if receptors are constitutively active

A

receptors are active even in absence of agonist, inverse agonist can reduce the response of the cell that are already active to stopping in the activation

46
Q

describe the 2 state receptor model

A
  1. 2 potential states: resting state and activated state
    - the receptor is moving backwards and forwards between the 2 states
    - very common in G-protein couple receptors
  2. Inverse agonist the receptor prefers to be in resting state so slowly moves to activated state and receptor moves quickly to the resting state
  3. if agonist binds, it prefers to bind in activated state and stabilize to see bigger response
  4. Inverse agonist prefer to stabilize receptor in resting state and will not drive a response
47
Q

what does remodelling involve

A
  1. can involve cardiac myocyte loss
  2. Cardiomyocyte hypertrophy
  3. Insulin resistance because cannot utilize glucose as efficiently
    - Many effects of these changes is because of aldosterone
    - increases sodium reabsorption and effects gene expression

PY366 Heart Failure (6 decks)

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