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Chronic and Life Limiting Illnesses > Drugs in Heart Failure > Flashcards

Drugs in Heart Failure Flashcards

1
Q

What are the signs and symptoms of right heart failure?

A
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2
Q

What are the signs and symptoms of left heart failure?

A
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3
Q

What are the aims of treatment in left ventricular systolic dysfunction (LVSD) (aka HFrEF)?

A
  • Relieve symptoms
  • Improve exercise tolerance
  • Reduce incidence of acute exacerbations
  • Reduce mortality
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4
Q

What are the strategies used to treat LVSD?

A
  • ↑ cardiac contractility.
  • ↓ preload and / or afterload in order to ↓ cardiac work demand
    • by relaxing vascular smooth muscle
    • by reducing blood volume
  • Inhibit the RAAS
  • Prevent inappropriate ↑ in heart rate
  • Mobilise the oedematous fluids
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5
Q

What are the non-pharmacological options in managing heart failure?

A
  1. Lifestyle factors - as per all CV conditions, remember mental health factors.
  2. ‘Device therapy’
    • Pacing
    • Cardiac resynchronisation therapy
    • Implantable cardiac defibrillators
    • Coronary revascularisation
    • Heart transplant
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6
Q

What are the main drugs used in chronic HFrEF?

Give the 5 classes of drug and examples of each.

A
  • Loop diuretics
    • Furosemide
    • Bumetanide
  • ACE-Inhibitors
    • Ramipril
    • Lisinopril
  • Angiotensin II receptor blockers
    • Candesartan
    • Losartan
  • Beta-blockers
    • Bisoprolol
    • Carvedilol
  • Aldosterone receptor antagonists
    • Spironolactone

These approaches can prolong life in heart failure and counteract some of the symptoms of heart failure… BUT they do not correct the underlying fault.

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7
Q

What is step 1 in the treatment of chronic heart failure?

A

DAB

  • D = diuretic if fluid retention
  • A = ACE-I or ARB
  • B = Beta-blocker
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8
Q

Explain the kidney function modification caused by drugs used in heart failure, specifically:

  • Loop diuretics
  • Thiazides
  • Aldosterone receptor antagonists

State where in the kidney each of these act.

A
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9
Q

Why would a flexible loop diuretic regime be indicated?

What is the aim of this treatment?

A
  • Use if clinical signs / symptoms of fluid overload or congestion.
  • Aim to achieve a ‘dry’ weight using the lowest diuretic possible.
  • Patient self-management with education:
    • Daily weights - if varies in either direction, alter dose.
    • Symptom review - breathlessness, peripheral oedema.
    • Thirst level, dizziness, ‘washed’out’.
  • GP - blood chemistry checks within a week of any dose change.
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10
Q

What are the common side-effects of loop-diuretics?

A
  • Electrolyte disturbance
    • Low K+
    • Low Na+
    • Low Mg+
    • Low Ca2+
  • Hypotension
  • Renal impairment - measure eGFR
  • Hypovolaemia!
  • Nocturia if taken too late in the day (troublesome)
  • Acute gout common with high doses
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11
Q

Describe how the following drugs inhibit the RAAS:

  • ACE-Is
  • ARBs

What effect does this have in heart failure?

A
  • RAAS inhibition - used in HFrEF of all NHYA classes.
    • Reduces morbidity / mortality
  • Reduces salt and water retention.
  • Reduces vasoconstriction.
  • Reduces vascular resistance.
  • Reduces afterload.
  • Improves tissue perfusion.
  • Reduces ventricular remodelling and hypertrophy.
  • Less effective in African or Caribbean ethnicity (try hydralazine + nitrate).
  • Start low dose, monitoring BP, blood chemistry and symptoms and uptitrating to maximum tolerated or target doses.
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12
Q

What are the side effects of drugs inhibiting the RAAS?

A
  • ACE-I:
    • Persistent dry cough
    • Tireness
    • Rare but serious - angioedema
  • ARB:
    • Back / leg pain
  • Common to both:
    • Dizziness
    • Headache
    • Risk of hyperkalaemia (care with drugs which also raise K+)
    • Renal impairment - can be reno-protective also
    • Avoid in bilateral renal artery stenosis
    • Teratogenic
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13
Q

What are the contra-indications to ACE-I and ARB?

A
  • Severe bilateral renal artery stenosis
  • Severe aortic stenosis
  • Known hx of angioedema
  • Pregnancy / risk of pregnancy
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14
Q

Why should you use beta-blokers in heart failure?

A
  • Bad news - may slow HR which could decrease CO.
  • Good news:
    • ​Allows ventricle to fill more completely during diastole.
    • Some beta-blockers (e.g. carvedilol) cause vasodilation through blockage of alpha receptors, therefore ↓ afterload.
    • Reduce renin release by the kidney.
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15
Q

What are the guidelines for prescribing beta-blockers for heart failure, and which would you use?

A
  • Carvedilol or Bisoprolol
  • Start if reduced ejection fraction but stable NYHA class II-IV.
  • Start low, go slow.
  • Reduces mortality.
  • Seek specialist advice if severe HF, current exacerbation of HF, heart block or bradycardia, persisting signs of fluid overload, or low BP (SBP <90mmHg).
    *
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16
Q

What are the important interactions to remember with beta-blockers in HF?

A
  • Risk of bradycardia / AV block with:
    • Digoxin
    • Amiodarone
    • Verapamil
    • Diltiazem
17
Q

What are the side effects of beta-blockers?

A
  • Bradycardia / heart block (contraindicated)
  • Fatigue
  • Dyspnoea (contraindicated in asthma)
  • Dizziness, cold peripheries, impotence / reduced libido, insomnia (more with older versions)
18
Q

What is step 2 in the treatment of chronic heart failure?

A
  • Adding aldosterone antagonists (mineralocorticoid receptor antagonists).
    • Spironolactone
    • Eplerenone
  • Add in if already on ‘DAB’ and still symptomatic.
  • In NYHA class II-IV failure (effective in severe heart failure).
  • Low doses used.
  • Reduces symptoms and mortality.
19
Q

What are the common side effects of aldosterone antagonists?

A
  • Hyperkalaemia
  • Hyponatraemia
  • Nausea
  • Hypotension
  • Gynaecomastia with spironolactone
  • Renal impairment
20
Q

What is step 3/4 in the treatment of chronic heart failure?

A
  • Sacubitral (Neprilysin inhibitor) - valsartan (ARB) combination.
  • Ivabradine - specialist use only - ↓ HR but not contractility, acts on sinus node. Use only if HR >75 (in sinur rhythm).
21
Q

What should you consider if there is:

  • Persistent sodium / water retention?
  • Co-existing angina?
  • Atrial fibrillation?
A
  • Persistent sodium / water retention
    • Additional diuretics
      • Thiazides like metolazone
  • Co-existing angina
    • Oral nitrates
    • Amlodipine (take care!)
  • Atrial fibrillation
    • Digoxin
22
Q

Describe the mechanism of action of digoxin in heart failure?

A
  • DIGOXIN = CARDIAC GLYCOSIDE
  • This is another option if other treatment strategies are failing.
  • Shows no reduction in mortality rate, and has narrow therapeutic window.
  • Mechanism of action:
    • ​In heart failure - increases the force of myocardial contraction.
    • Inhibits Na+ / K+ ATP-ase pump, thus affecting Na/Ca exchanger, elevating intracellular calcium levels in sarcoplasmic reticulum then when calcium is released, results in strengthened contractility.
      • I.e. indirectly increases calcium levels and subsequent storage in the SR.
  • In AF: ↑ vagal efferent activity to the heart, therefore ↓ SAN firing rate (↓HR) and ↓ conduction velocity in the AV node.
23
Q

What is acute decompensated heart failure and what symptoms does it commonly cause?

A
  • Sudden worsening of signs and symptoms of heart failure as a result of severe congestion of multiple organs.
  • Symptoms:
    • Increased dyspnoea
    • Increased oedema
24
Q

What are the causes of acute decompensated heart failure?

A
  • MI
  • Infection
  • Anaemia
  • Thyroid dysfunction
  • Arrhythmia
  • Uncontrolled HTN
  • Poor concordance
25
Q

What are the aims of treatment in acute decompensated heart failure?

A
  • Normalise ventricular filling pressures.
  • Restore adequate tissue perfusion.
26
Q

What are the first-line drug treatments of acute heart failure?

27
Q

What is the second-line treatment in acute heart failure?

A
  • Increasing contractility​!
  • By use of ionotropic agents.
  • ↑ contractility will ​↑ SV, which ​↑ CO so ​↑ clearance of pooled blood in the ventricles.
  • As CO increases, baroreceptors sense change in MABP and ↓ sympathetic drive and so ​↓ HR and ↓ TPR.
28
Q

Give the locations and actions of ionotropic receptors.

29
Q

Describe the use of ionotropes in the second-line drug treatment of acute HF.

A
  • Intensive care / CCU only.
  • Ionotropes - act on sympathomimetic system to increase myocardial contractility.
    • Dobutamine (beta1 > beta 2) - in patients with cardiogenic shock to maintain BP.
    • Dopamine (DA > beta > alpha) - increases renal perfusion at low doses, can increase BP at high doses.
    • Isoprenaline - in bradycardia / heart block emergencies.
    • Adrenaline (beta > alpha).
    • Noradrenaline (alpha > beta) - a vasopressor, cause vasoconstriction, raises BP, used in severe septic shock.
30
Q

After ionotropes, what is the other option in second-line management of acute HF?

A
  • Milrinone​
    • ​Phosphodiesterase 3 inhibitor.
    • Increases intracellular calcium causing vasodilation and increased myocardial conractility.
31
Q

Give an overview of the main points of intervention in the treatment of heart failure.

Chronic and Life Limiting Illnesses (36 decks)

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