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Semester 1 Year 2 > Pharmacological treatment of cardiac failure > Flashcards

Pharmacological treatment of cardiac failure Flashcards

1
Q

What are the aims of treatment of Left Ventricular Systolic Dysfunction (LVSD) (=
Heart failure with reduced ejection fraction (HFrEF))

A
  • Relieve symptoms
  • Improve exercise tolerance
  • Reduce incidence of acute exacerbations
  • Reduce mortality
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2
Q

Discuss strategies for treatment of heart failure

A
  • ↑ cardiac contractility
  • ↓ preload and/or afterload in order to ↓ cardiac work demand
  • By relaxing vascular smooth muscle
  • By reducing blood volume
  • Inhibit the Renin-Angiotensin-Aldosterone-System (RAAS)
  • Prevent inappropriate ↑ in heart rate
  • Mobilise the oedematous fluids
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3
Q

Discuss non pharmaceutical methods of treating heart failure

A
  1. Lifestyle factors – as per all CVD conditions, remember mental health factors
  2. “Device therapy”
    • Pacing
    • Cardiac Resynchronisation Therapy
    • Implantable Cardiac Defibrillators
    • Coronary revascularisation
    • Heart transplant
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4
Q

What are the main drugs used in chronic heart failure (HFrEF)

A 
Loop diuretics
• e.g furosemide, bumetanide
ACE inhibitors
• e.g.ramipril, Lisinopril
Angiotensin II receptor blockers 
• e.g candesartan, losartan
Beta-blockers
• bisoprolol, carvedilol
Aldosterone receptor antagonists 
• e.g. spironolactone

These approaches can prolong life in heart failure and counteract some of the symptoms of heart failure…But they don’t correct the underlying fault

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5
Q

What is the basic drug use pathway in heart failure

A

ABBA Waterloo:

ACEI or ARB
Beta Blocker
Aldosterone antagonist

(diuretics sometimes)

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6
Q

Overview of treatment of chronic heart failure

A

Step 1 = “DAB”
(D = Diuretic if fluid retention) A = ACE Inhibitor or ARB
B = Beta-Blocker

A&B shown to reduce mortality (i.e. prolong life!)and improve quality of life.

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7
Q

Discuss kidney function modifiers in HF

A

Increase excretion of sodium and water

Loop diuretics (step 1)
- furosemide, bumetanide
Aldosterone receptor antagonists (step 2) - spironolactone
Further along this system you go, less diuretic effect: 
PCT = Proximal convoluted tubule 
TAL = Thick ascending loop
DT = Distal tubule
CT = Collecting tubule

So loop diuretics most effective, then thiazides, then spironolactone

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8
Q

Discuss flexible loop diuretic regimes

A

Use if clinical signs/symptoms of fluid overload/congestion
Aim to achieve a “dry” weight using the lowest diuretic dose 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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9
Q

Discuss loop diuretics common side effects

A

(e.g. furosemide, bumetanide)

  • Electrolyte disturbances –low K, Na, Mg, Ca
  • Hypotension
  • Renal impairment – measure eGFR
  • Hypovolaemia!
  • Nocturia if taken too late in day (troublesome)
  • Acute gout common with high doses
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10
Q

Discuss Renin Angiotensin System Inhibitors

A
  • Use in HF with reduced EF of all NYHA classes
  • Reduces morbidity/mortality

Angiotensin converting enzyme inhibitors
- ramipril, lisinopril

Angiotensin AT1 receptor antagonists
- candesartan, valsartan, (losartan)

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11
Q

Discuss using the ACEI and ARBs in HF

A
  • Reduce salt and water retention
  • Reduce vasoconstriction
  • Reduce vascular resistance
  • Reduce afterload
  • Improve 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

Discuss side effects/cautions of Renin-Angiotensin system inhibitors

A

Common to both
• Dizziness
• headache
• Riskofhyperkalaemia (care with drug which also raise K+)
• Renal impairment - can be reno-protective also
• Avoid in bilateral renal artery stenosis
• teratogenic

Angiotensin converting enzyme (ACE) inhibitors
• Persistentdrycough, tiredness, rare but serious – angioedema

Angiotensin AT1 receptor antagonists (ARBs)
• back/legpain

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13
Q

Why use beta blockers in HF?

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 kidney

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14
Q

Discuss beta blockers for HF

A

e.g. Carvedilol, 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, low BP (SBP<90mmHg)
- drug interactions – risk of bradycardia/AV block with: digoxin, amiodarone, verapamil, diltiazem

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15
Q

Discuss examples of beta blocker side effects

A
  • Bradycardia /Heart Block (contra-indicated)
  • Fatigue
  • Shortness of breath (Contra-indicated in Asthma)
  • Dizziness, cold peripheries, impotence/reduced libido, insomnia (more with older versions)
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16
Q

Discuss step 2 in the pathway: adding aldosterone antagonists

A

(Mineralocorticoid receptor antagonists)
• spironolactone, eplerenone
• Add in if on ACEI or ARB + Beta-blocker + diuretic (“DAB”) and still symptoms
• In NYHA class II-IV failure (effective in severe heart failure )
• low doses used
• Reduces symptoms and mortality

17
Q

Discuss common side effects of aldosterone receptor antagonists

A
  • Hyperkalaemia
  • hyponatraemia
  • Nausea
  • Hypotension
  • gynaecomastia with spironolactone •renal impairment
18
Q

Discuss management of HF drug adverse effects

A
  • Flexible dosing for DABs, may need to up and down titrate.
  • Review BP – may be low but is patient symptomatic?
  • Bradycardia – if symptomatic may need to stop beta-blocker or review any other rate controlling drugs patient on . If HR<45 BPM – stop beta-blocker, call specialist
19
Q

What is step 3 or 4

A
  • A Sacubitril(neprilysin inhibitor) – Valsartan(ARB) combination
  • Ivabradine – specialist use only – reduces heart rate but not contractility, acts on sinus node. Use only if heart rate > 75 (in SR)
20
Q

What other options for treatment should you consider if concurrent

A

Persistent sodium/water retention
– Additional diuretics (e.g. thiazides like metolazone)

Co-existing angina
– Oral nitrates
– Amlodipine (care!)

Atrial fibrillation
– Digoxin

21
Q

Discuss digoxin

A

– cardiac glycoside
• option if other treatment strategies failing
• shows no reduction in mortality rate
• narrow therapeutic window

Mechanisms of action:
• (In AF : ↑ vagal efferent ac$vity to the heart therefore ↓ SAN firing rate (↓ HR) and ↓ conduction velocity in the AV node)
• In Heart Failure: Increases 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 released results in strengthened contractility
• i.e. indirectly increases calcium levels and subsequent storage in the SR

22
Q

What are the side effects/toxicity of digoxin

A
  • GIupset
  • dizziness
  • Conduction abnormalities
  • Blurred or yellow vision
23
Q

Discuss treatment of acute (decompensated) heart failure

A

Sudden worsening of signs and symptoms of heart failure as a result of severe congestion of multiple organs.
Increased dyspnoea, oedema
Causes: MI, infection, anaemia, thyroid dysfunction, arrhythmia, uncontrolled hypertension, poor concordance

Aims:
• Normalise ventricular filling pressures
• Restore adequate tissue perfusion

First Line Drug Treatments:

IV loop diuretics
• Cause venodilation and diuresis
• Reduces pre-load

IV opiates (eg morphine)
• Reduce anxiety
• Vasodilates, reducing preload
• Reduces sympathetic drive
• Not routinely offered

IV buccal or sublingual nitrates (Glyceryl trinitrate GTN)
• Reduce preload and afterload
• vasodilates

Oxygen maintains O2 sats

Positioning - keep patient upright

REMEMBER AS LMNOP -
LOOP
MORPHINE
NITRATES
OXYGEN
POSITIONING

Second

24
Q

Discuss first and second line treatments for acute heart failure

A

First Line Drug Treatments:

IV loop diuretics
• Cause venodilation and diuresis
• Reduces pre-load

IV opiates (eg morphine)
• Reduce anxiety
• Vasodilates, reducing preload
• Reduces sympathetic drive
• Not routinely offered

IV buccal or sublingual nitrates (Glyceryl trinitrate GTN)
• Reduce preload and afterload
• vasodilates

Oxygen maintains O2 sats

Positioning - keep patient upright

REMEMBER AS LMNOP -
LOOP
MORPHINE
NITRATES
OXYGEN
POSITIONING

Second line - increasing contractility

By use of inotropic agents (examples later)
↑ contractility will ↑ stroke volume, which ↑ Cardiac output
(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

25
Q

Discuss second line drug treatments for acute HF (Only used in coronary care units and ICUs)

A

Inotropes - beta-agonists - increase myocardial contractility
– Dobutamine (beta 1&2) - in patients with cardiogenic shock to maintain
blood pressure
– 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)

Vasopressors
– Noradrenaline (alpha>beta) – cause vasoconstriction, raise BP, used in severe septic shock

26
Q

Learning outcomes

A
  • To understand the strategies for treatment of chronic heart failure
  • To understand the strategies for treatment of acute heart failure
  • To recognise how the apparently paradoxical use of beta blockers is of benefit
  • To understand the mechanism of action and uses of drugs which inhibit the renin- angiotensin-aldosterone system
  • To know the mechanism of action of digoxin and how it increases myocardial contractility
  • To know the mechanism of action and uses of inotropes

Semester 1 Year 2 (69 decks)

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