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Y2S1 CARDIO. > Pharmacological Treatment of Cardiac Failure > Flashcards

Pharmacological Treatment of Cardiac Failure Flashcards

1
Q

Left Ventricular Systolic Dysfunction (LVSD) =
Heart failure with reduced ejection fraction (HFrEF)

Aims for treatment

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

LVSD strategies fro treatment

A
  • ↑ cardiac contrac$lity
  • ↓ preload and/or a’erload 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

non-pharmalogical treatment of LVSD

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

Main Drugs Used in chronic Heart Failure (HFrEF)

THINK ABBA Waterloo

A
  • loop diuretics
  • ACE inhibitors
  • angiotensin II receptor blockers
  • beta-blockers
  • aldosterone receptor antagonists
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5
Q

step 1 in treatment of chronic heart failure

THINK DAB

A

(Diuretics if they are experiencing fluid retention)
A = ace inhibitors or ARB)
B = Beta Blocker

Waterloo = diuretics sometimes

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6
Q

Kidney function modifiers in HF

A

Increase excretion of sodium and water

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7
Q

two steps in the process which increases the excretion of sodium and water in HF

A 
Loop diuretics (step 1)
- furosemide, bumetanide
Aldosterone receptor antagonists (step 2) - spironolactone
PCT = Proximal convoluted tubule 
TAL = Thick ascending loop
DT = Distal tubule
CT = Collecting tubule
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8
Q

Patient self-management with education

A
  • daily weights – if varies in either direction, alter dose
  • Symptom review – breathlessness, peripheral oedema
  • Thirst level, dizziness, “washed out”
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9
Q

Loop Diuretics (e.g. furosemide, bumetanide) common side-effects

A
  • 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

Renin Angiotensin System Inhibitors

A
  • Use in HF with reduced EF of all NYHA classes

* Reduces morbidity/mortality

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11
Q

Angiotensin converting enzyme inhibitors

A
  • ramipril, lisinopril
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12
Q

Angiotensin AT1 receptor antagonists

A
  • candesartan, valsartan, (losartan)
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13
Q

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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14
Q

renin-Angiotensin system inhibitors : Side effects/cautions

A

• Dizziness
• headache
• Persistentdrycough, tiredness, rare but serious – angioedema
•Risk of hyperkalaemia (care with drug which also raise K+)
• Renal impairment - can be reno-protective also
Angiotensin AT1 receptor antagonists (ARBs)
• Avoid in bilateral renal artery stenosis
• back/legpain
• teratogenic

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15
Q

angiotensin coveting enzyme inhibitors side effects

A

• Persistent dry cough, tiredness, rare but serious – angioedema

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16
Q

Angiotensin AT1 receptor antagonists (ARBs) side effects

A

back/leg pain

17
Q

Why Use Beta-Blockers in HF?

A

may slow HR, which could decrease CO

  • allows ventricle to fill more completely during diastole
  • Some Beta-blockers (e.g. carvedilol) cause vasodilation through blockage of alpha-receptors,  ↓ afterload
  • Reduce renin release by kidney
18
Q

Beta-blockers for HF

A

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)
19
Q
  • drug interactions of beta blockers
A

– risk of bradycardia/AV block with: digoxin, amiodarone, verapamil, diltiazem

20
Q

Beta-blockers side-effect examples

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)
21
Q

adding aldosterone antagonists

A
  • 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
22
Q

Aldosterone Receptor Antagonists - Common side effects

A
  • Hyperkalaemia
  • hyponatraemia
  • Nausea
  • Hypotension
  • gynaecomastia with spironolactone •renal impairment
23
Q

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
24
Q

Step3or4 in treatment of HF

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)
25
Q

Persistent sodium/water retention

A

– Additional diuretics (e.g. thiazides like metolazone)

26
Q

Co-existing angina

A

– Oral nitrates

– Amlodipine (care!)

27
Q

Atrial fibrillation

A

– Digoxin
• shows no reduction in mortality rate
• narrow therapeutic window

28
Q

mechanism of action in digoxin in AF

A

↑ vagal efferent activity to the heart  ↓ SAN firing rate (↓ HR) and ↓ conduction velocity in the AV node

29
Q

mechanism of action in digoxin in heart failure

A

Increases force of myocardial contraction
– Inhibits Na/KATP-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

30
Q

Digoxin side-

effects/toxicity

A
  • GIupset
  • dizziness
  • Conduction abnormalities
  • Blurred or yellow vision
31
Q

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

32
Q

Acute (decompensated) Heart Failure causes

A

MI, infection, anaemia, thyroid dysfunction, arrhythmia, uncontrolled hypertension, poor concordance

33
Q

Acute (decompensated) Heart Failure aims of the treatment

A
  • Normalise ventricular filling pressures

* Restore adequate tissue perfusion

34
Q

Treatment of Acute Heart Failure: First Line Drug Treatments:

A

LMNOP

35
Q

Treatment of Acute Heart Failure: second line

A

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 ↓ sympathe$c drive and so ↓ HR and ↓ TPR

36
Q

Inotropes - beta-agonists - increase myocardial contractility

A

– 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)

37
Q

Vasopressors

A

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

Y2S1 CARDIO. (47 decks)

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