heart failure meds Flashcards

1
Q

Pathophysiology of chronic heart failure

A

As the heart pumps become less effective, there is an increase volume of blood left in the ventricles at the end of each cycle, increasing the end-diastolic volume. Over time, the heart will be overstretched and contracts less forcefully.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are heart failure meds

A
  1. Nitrates
  2. Beta blockers
    - [non-selective] propranolol, pindolol, carvedilol
    - [beta-1 selective] atenolol, bisoprolol, metoprolol
    - [mixed - 3rd gen] nebivolol
  3. Diuretics
    - loop diuretics
    - potassium sparing diuretics
  4. hydralazine
  5. sacubitril-valsartan
  6. ivabradine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

MOA of beta blockers

A

blocks beta adrenoreceptors on cardiac myocytes
decrease adenylate cyclase
decrease ATP conversion to cAMP
decrease PKA activation
decrease opening of Ca2+ channels
decrease entry of Ca2+
decrease activation of calcium induced calcium release
decrease activation of sarcoplasmic reticulum calcium
decrease calmodulin complex activation
decrease actin-myosin complex
decrease contractility of cardiac myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MOA of loop diuretics

A

normally:
- Na+/K+/2Cl- cotransporters will reabsorb K+ from tubular lumen into the cell
- causes accumulation of K+ in the cells
- causes back diffusion of K+ into the tubular lumen
- generates a strong positive electrical potential in the tubular lumen
- creates a driving force for Ca2+ and Mg2+ reabsorption

MOA of loop diuretics:
- blocks Na+/K+/2Cl- cotransporter
- prevent accumulation of K+ in the cells
- decrease back diffusion of K+ into tubular lumen
- weakens the positive electrical potential in the tubular lumen
- decrease reabsorption of Ca2+ and Mg2+
- increase excretion of Ca2+ and Mg2+
(hypocalcaemia, hypercalciuria)
(hypomagnesemia, hypermagnaeuria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Loop diuretics induce the synthesis of?

A

renal prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Adverse effects of loop diuretics

A

Ototoxicity
Hypocalcaemia + hypercalcaeuria
Hypomagnesemia + hypermagnaeuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MOA of potassium sparing diuretics

A

Spironolactone, Eplerenone inhibits aldosterone receptor
Triamterene, Amiloride inhibits Na+ channel
-> decrease Na+ reabsorption
-> decrease K+ secretion
-> decrease blood volume
-> decrease pre-load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Between spironolactone and eplerenone, which has a slower onset of action?

A

Spironolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Between triamterene and amiloride, which has a shorter half life?

A

triamterene is metabolised in the river and has shorter half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

MOA of hydralazine

A
  • direct arteriole vasodilator
  • inhibit IP3-induced release of calcium from smooth muscle cells sarcoplasmic reticulum
  • reduces peripheral resistance + release of norepinephrine -> increase CO and venous return
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In essential hypertension, when 1st line drugs are inadequate, give…

A

hydralazine orally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In acute onset, severe peripartum or post partum hypertension, give…

A

hydralazine IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hydralazine is contraindicated in…

A

Contraindicated in patients with Coronary Artery Disease due to hydralazine’s stimulation of sympathetic nervous system -> increase CO and increase O2 demand -> myocardial ischaemia as O2 demands cannot be met

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MOA of sacubitril-valsartan

A

During heart failure
-> brain natriuretic peptide increases

Brain natriuretic peptide
-> promotes vasodilation, natriuresis, diuresis
-> antagonises RAAS
-> broken down by neprilysin

Sacubitril is a neprilysin inhibitor
-> prolong BNP effects -> good for HF

Neprilysin breaks down angiotensin II -> hence sacubitril will cause an accumulation of angiotensin II -> prolonged effects of angiotensin II -> bad for HF

Solution? Give sacubitril with valsartan (Angiotensin II Type 1 blocker)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why can’t sacubitril-valsartan be used with ACE inhibitors?

A

Neprilysin breaks down bradykinin
ACE inhibitors prevent bradykinin inactivation
-> sacubitril will lead to the accumulation of bradykinin which will lead to angioedema

Sacubitril-valsartan can replace ACE inhibitors or used with other drugs normally used with ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does neprilysin break down?

A
  1. BNP
  2. Angiotensin II
  3. Bradykinin