Drugs in Heart Failure Flashcards
What are the signs and symptoms of right heart failure?
What are the signs and symptoms of left heart failure?
What are the aims of treatment in left ventricular systolic dysfunction (LVSD) (aka HFrEF)?
- Relieve symptoms
- Improve exercise tolerance
- Reduce incidence of acute exacerbations
- Reduce mortality
What are the strategies used to treat LVSD?
- ↑ 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
What are the non-pharmacological options in managing heart failure?
- Lifestyle factors - as per all CV conditions, remember mental health factors.
- ‘Device therapy’
- Pacing
- Cardiac resynchronisation therapy
- Implantable cardiac defibrillators
- Coronary revascularisation
- Heart transplant
What are the main drugs used in chronic HFrEF?
Give the 5 classes of drug and examples of each.
-
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.
What is step 1 in the treatment of chronic heart failure?
DAB
- D = diuretic if fluid retention
- A = ACE-I or ARB
- B = Beta-blocker
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.
Why would a flexible loop diuretic regime be indicated?
What is the aim of this treatment?
- 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.
What are the common side-effects of loop-diuretics?
- 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
Describe how the following drugs inhibit the RAAS:
- ACE-Is
- ARBs
What effect does this have in heart failure?
- 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.
What are the side effects of drugs inhibiting the RAAS?
-
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
What are the contra-indications to ACE-I and ARB?
- Severe bilateral renal artery stenosis
- Severe aortic stenosis
- Known hx of angioedema
- Pregnancy / risk of pregnancy
Why should you use beta-blokers in heart failure?
- 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.
What are the guidelines for prescribing beta-blockers for heart failure, and which would you use?
- 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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Describe the mechanism of action of digoxin in heart failure?
- 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.
What are the first-line drug treatments of acute heart failure?
What is the second-line treatment in acute heart failure?
- 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.
Give the locations and actions of ionotropic receptors.
Give an overview of the main points of intervention in the treatment of heart failure.
