Heart failure 3 Flashcards

1
Q

What are the renin-angiotensin system inhibitors used for managing heart failure with reduced ejection fraction (HFrEF)?

A

The renin-angiotensin system inhibitors used for HFrEF are:

  • angiotensin-receptor neprilysin inhibitor (ARNI) sacubitril+valsartan
  • angiotensin converting enzyme inhibitors (ACEIs)
  • angiotensin II receptor blockers (ARBs)

These medications improve symptoms and reduce cardiovascular mortality and hospitalisation for heart failure.

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2
Q

When should a renin-angiotensin system inhibitor be started in patients diagnosed with HFrEF?

A

A renin-angiotensin system inhibitor should be started at diagnosis or within 2 to 4 weeks of diagnosis of HFrEF.

This initiation should occur alongside a beta blocker, mineralocorticoid receptor antagonist, and sodium-glucose co-transporter 2 inhibitor.

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3
Q

How does sacubitril+valsartan compare to ACEIs in terms of effectiveness for symptomatic HFrEF?

A

Sacubitril+valsartan is more effective in reducing the risk of death and hospitalisation for heart failure compared to ACEI in symptomatic HFrEF patients.

However, sacubitril+valsartan is more likely to cause symptomatic hypotension.

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4
Q

What should be substituted if a patient with persistent HFrEF is on an ACEI or ARB?

A

Substitute with sacubitril+valsartan (ARNI)

Do not use more than one renin-angiotensin system inhibitor concurrently.

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5
Q

What should be monitored in patients taking a renin-angiotensin system inhibitor?

A

Hypotension, kidney impairment, and hyperkalaemia

An asymptomatic fall in blood pressure or a small rise in serum creatinine or serum potassium can occur when therapy is started or the dose is increased.

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6
Q

What may occur when therapy with a renin-angiotensin system inhibitor is initiated?

A

An asymptomatic fall in blood pressure or a small rise in serum creatinine or serum potassium

These changes may be transient and should not necessarily prompt dose reduction or cessation.
the risk of first dose hypotension is increased in patients with severely acutely decompensated heart failure but is minimised by starting therapy with a low dose

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7
Q

True or False: An ARB can be used concurrently with an ACEI.

A

False

Only one renin-angiotensin system inhibitor should be used at a time.

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8
Q

Fill in the blank: An ARB is usually used if an ACEI or _______ is not tolerated.

A

sacubitril+valsartan (ARNI)

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9
Q

list some ACE inhibitor examples

A

captopril
enalapril
fosinopril
lisinopril
perindopril (arginine or erbumine)
quinapril

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10
Q

list some ARBs

A

candesartan
eprosartan
irbesartan
losartan
olmesartan
telmisartan
valsartan

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11
Q

examples of beta blockers approved for heart failure

A

Beta blockers that improve clinical outcomes in HFrEF are
bisoprolol
carvedilol
metoprolol succinate
nebivolol
Patients already taking a different beta blocker for a comorbidity (eg angina, hypertension) should be switched to one of these heart failure–specific beta blockers.

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12
Q

why does beta-blocker therapy initially worsen symptoms in heart failure?

A

Blocking sympathetic nervous system support for the failing heart

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13
Q

When should beta-blocker therapy not be started?

A

During a period of acute decompensation or if the patient has signs of congestion

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14
Q

How often should a patient’s weight be measured during beta-blocker therapy?

A

Daily

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15
Q

What can the combination of a mineralocorticoid receptor antagonist and a renin-angiotensin system inhibitor cause in patients with kidney impairment?

A

Life-threatening hyperkalaemia

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16
Q

What should be considered when treating patients with kidney impairment using mineralocorticoid receptor antagonists?

A

Starting with a lower dose

Lower doses help mitigate the risk of adverse effects such as hyperkalaemia.

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17
Q

What may occur when therapy with a mineralocorticoid receptor antagonist is initiated or the dose is increased?

A

A small rise in serum potassium

This rise is typically within the normal range and may be transient, and should not necessarily prompt dose reduction or cessation

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18
Q

What is the mechanism of action of ACE inhibitors?

A

Block conversion of angiotensin I to angiotensin II and inhibit the breakdown of bradykinin, leading to reduced angiotensin II mediated vasoconstriction, sodium retention and aldosterone release.

ACE inhibitors improve heart failure outcomes by reducing vascular resistance and fluid retention.

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19
Q

What is a common side effect of ACE inhibitors?

A

Dry annoying cough.

This side effect is frequently reported by patients taking ACE inhibitors.

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20
Q

What is a rare but serious side effect of ACE inhibitors?

A

Angioedema.

Occurs in 0.1-1% of patients taking ACE inhibitors.

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21
Q

In what condition should ACE inhibitors be avoided?

A

Bilateral renal artery stenosis (or unilateral to single functioning kidney).

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22
Q

List some drugs classified as ACE inhibitors.

A
  • captopril
  • enalapril
  • fosinopril
  • lisinopril
  • perindopril
  • quinapril
  • ramipril
  • trandolapril
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23
Q

What is the mechanism of action of heart failure beta blockers?

A

Competitively block beta receptors in heart and peripheral vasculature to reduce heart rate, blood pressure, and cardiac contractility.

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24
Q

What are potential safety issues associated with heart failure beta blockers?

A
  • Hypotension
  • Dizziness
  • Worsening of heart failure
    these are transient effects and can be minimised through slow dose titration
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25
Q

List some heart failure beta blockers.

A
  • Bisoprolol
  • Carvedilol
  • Metoprolol succinate controlled-release
  • Nebivolol
26
Q

What should be monitored when introducing a heart failure beta blocker?

A
  • Worsening heart failure
  • Hypotension
  • Adverse reactions (fatigue, sexual dysfunction, depression)
27
Q

angiotensin II receptor blockers are also called

A

Sartans
ARBs
angiotensin II receptor antagonists

28
Q

What is the mechanism of action of angiotensin II receptor blockers?

A

Competitively block angiotensin II binding to type 1 angiotensin receptors, reducing vasoconstriction, sodium reabsorption, and aldosterone release.

29
Q

What laboratory values should be monitored at baseline and 1 to 2 weeks after starting treatment with angiotensin II receptor blockers?

A

Serum creatinine and electrolytes.

30
Q

True or False: Sartans are more likely to cause cough than ACE inhibitors.

31
Q

Have sartans been shown to be superior to ACE inhibitors for chronic heart failure?

A

No, they have not been shown to be superior.

32
Q

What is a benefit of sartans for patients who cannot tolerate ACE inhibitors?

A

They improve prognosis and serve as an alternative.

33
Q

Which sartans are approved by the Australian Therapeutic Goods Administration (TGA) for treatment of heart failure?

A

Candesartan and valsartan.

34
Q

List the drugs included in the class of angiotensin II receptor blockers.

A
  • candesartan
  • eprosartan
  • irbesartan
  • losartan
  • olmesartan
  • telmisartan
  • valsartan
35
Q

What is the mechanism of action of thiazide diuretics?

A

They inhibit reabsorption of sodium and chloride in the proximal segment of the distal convoluted tubule, increasing sodium delivery to the collecting tubules and potassium excretion.

36
Q

What is the primary indication for thiazide diuretics?

A

Oedema associated with heart failure.

37
Q

What safety issues should be monitored when using thiazide diuretics?

A

Electrolytes, renal function, blood pressure, and volume status.

38
Q

Can thiazide diuretics be used in combination with other diuretics?

A

Yes, they can be used with loop diuretics.

39
Q

In what setting are thiazide diuretics typically combined with loop diuretics?

A

In the setting of decompensated heart failure where the patient is maintained on regular high doses of furosemide which can result in diuretic resistance

40
Q

What can result from the combination of thiazide and loop diuretics?

A

A powerful diuretic response due to blockade of sodium uptake in distal renal tubules.

41
Q

What combination may be considered for patients with HFrEF if ACE inhibitors and sartans are contraindicated?

A

Thiazide diuretic (hydralazine) plus nitrates.

42
Q

Name a drug in the thiazide diuretics class.

A

Hydrochlorothiazide or indapamide.

43
Q

Fill in the blank: The diuretic effect of thiazide diuretics is dependent on adequate _______.

A

renal function.

44
Q

What is the mechanism of action of SGLT2 inhibitors?

A

Inhibit sodium-glucose co-transporter 2, reducing glucose reabsorption by the kidney and increasing its excretion into urine, water follows.

45
Q

What are common safety issues associated with SGLT2 inhibitors?

A

due to glycosuria, can cause genital infections, polyuria, dysuria, urinary tract infections.

46
Q

What are other common side effects of SGLT2 inhibitors?

A

Dyslipidaemia, increased haematocrit, constipation, nausea, thirst, renal impairment.

47
Q

What are the short-term effects of SGLT2 inhibitors on weight and blood pressure?

A

Produce modest weight loss and slight reduction in blood pressure.

48
Q

When should SGLT2 inhibitors be stopped before surgery?

A

3 days before surgery due to perioperative risks.

49
Q

What are some perioperative risks associated with SGLT2 inhibitors?

A

Dehydration, urinary tract infections, renal impairment, increased risk of ketoacidosis.

50
Q

Name two drugs in the SGLT2 inhibitor class.

A
  • dapagliflozin
  • empagliflozin
51
Q

Fill in the blank: SGLT2 inhibitors increase the excretion of glucose into _______.

52
Q

aldosterone antagonists are also called

A

mineralocorticoid receptor antagonists

53
Q

What is the mechanism of action of aldosterone antagonists?

A

Inhibit sodium absorption in the distal tubule by antagonising aldosterone, increasing sodium and water excretion and reducing potassium excretion

They are weak diuretics and improve outcomes in heart failure by reducing aldosterone activity.

54
Q

What safety issue is associated with the addition of an MRA to ACE inhibitors or sartans?

A

May result in life-threatening hyperkalaemia in patients who have renal impairment

Monitoring for hyperkalaemia is essential.

55
Q

What are the anti-androgenic adverse effects of spironolactone?

A

spironolactone is not selective for aldosterone receptors so can cause anti-androgenic side effects

  • Gynaecomastia
  • Menstrual changes
  • Sexual dysfunction

Eplerenone does not cause these adverse effects but is more costly.

56
Q

What is the effect of low-dose spironolactone on patients with NYHA III or IV heart failure?

A

Reduces mortality and hospitalisations for patients with LVEF of less than or equal to 35% on top of background therapy

Background therapy included prescription rates of more than 80% for diuretics and ACE inhibitors.

57
Q

What is the effect of low-dose eplerenone on patients with NYHA II heart failure?

A

Decreases mortality and hospitalisations for patients with LVEF of less than or equal to 35% on top of background therapy

Background therapy included prescription rates of more than 80% for diuretics, ACE inhibitors or sartans, and beta blockers.

58
Q

What are the two drugs in the aldosterone antagonist class mentioned?

A
  • Eplerenone - tablet
  • Spironolactone - tablet

Both are used in the treatment of heart failure.

59
Q

True or False: Eplerenone causes anti-androgenic adverse effects.

A

False

Eplerenone does not cause these adverse effects unlike spironolactone.

60
Q

Fill in the blank: Aldosterone antagonists improve survival and decrease hospitalisations for heart failure with _______.

A

reduced ejection fraction

They should be used with standard treatment.