HF Treatment

Question 1

Angiotensin | converting enzyme inhibitor (ACE)

Answer 1

Inhibit A1 to A2

A2

Question 2

Renin

Answer 2

Low cardio output in HF = ⬇️renal blood flow = ⬇️glomerular filtration = ⬆️renin

Renin convert Angiotensiongen to Angiotensin 1 , which then convert to A2 by ACE

Question 3

ACE inhibitors

*pril ending

Answer 3

Capto-pril
Enala-pril
Perindo-pril
Rami-pril

Question 4

Angiotensin 2 receptor blocker (ARB)

Answer 4

I - II not blocked but block everything that receives A II
(Antagonist at the angiotensin II receptor)

Overall effect same as ACE

DO NOT inhibit breakdown of bradykinin
⬆️brady contributes to vasodilator effects of ACE INHIBITOR
- ARB sees less vasodilation

Question 5

ARB s ( sartan)

Answer 5

Irbe-sartan

Cande-sartan

Question 6

Neprilysin inhibitor

new

Answer 6

Target neprilysin (enzyme that cleaves and inactivate naturetic protiens)

Naturetic proteins released in response to cardiac wall stress

Inhibit neprilysin = less breakdown of naturetic proteins

More proteins = more response to cardiac wall stress

Question 7

Beta- blocker in HF

MOA

Answer 7

Reduce heart rate, contractility a d afterload

Inhibit renin release from kidney to reduce preload

Slows ventricular remodelling

Question 8

Inotropes

Alters the force of muscular contraction

Answer 8

Positive : ⬆️strength of contraction

Negative : ⬇️strength of contraction
Beta-blocker

Question 9

Beta blocker drugs

End lol

Answer 9

Metopro-lol (b1 CLh)

Bisopro-lol (b1 CLr +h)

Carvedi-lol (b1,2 a1 CLh)

Question 10

Diuretics MOA in heart

Answer 10

Increased waster and sodium excretion in kidney = reduce preload

Primarily use loop diuretics

Question 11

Loop diuretics MOA

Answer 11

Inhibit reabsroption of sodium and chloride in ascending loop

Increase Na delivery to DCT, increase activity of Na/K pump
(Can cause low K+ - hypokalaemia)

Question 12

Loop diuretics drug

Answer 12

Fruosemide

Question 13

Aldosterone antagonist

MOA

Answer 13

Inhibit the promotion (caused by aldosterone) of reabsorption of Na and H2O (which increase preload )
🚫⬆️preload

Weak diuretic effect
⬇️preload
⬇️aldosterone induced myocardial or vascular damage

NO increase in K+ loss (like diuretics)

Question 14

Aldosterone drug

Answer 14

Spironolsctone

Question 15

Aldosterone AE

Answer 15

Act on progesterone/androgen receptors

• menstrual disorder
• testicular atrophy
• gynaecomastia (growth of breast)

Question 16

Site of action of fruosemide and spironolactone

Answer 16

Fruosimide - ascending loop of henle

Spironolactone - Distal convoluted tubule (active transport of Na and Cl out of tubular fluid)

Question 17

Digoxin

MOA

Answer 17

1. Inhibit the NaK pump
2. Na accumulate inside cell
3. Usually NCX passively transport 3 Na ions in for 1 Ca ion out
4. But NCX driven by gradient
5. Since ⬆️Na inside cell… NCX does not pump Ca out (accumulate in cell)
6. More Ca ++ available for troponin C ( increase contractility of cardiac muscle)

Question 18

Digoxin in HF

Answer 18

Inhibit NaK pump @ myocardial cell membrane
(⬆️Ca++ = positive inotrope)
(⬆️EF and output)

Inhibit NaK @ vascular smooth muscle

• =depolarisation = vasoC
• overall resistance ⬇️ = cardiac output ⬆️

Question 19

Digoxin AE

Related to plasma concentrations

Answer 19

GI: anorexia, nausea, vomit
Ocular: blurred/ altered vision
Cadio: arrhythmia, bradycardia, AV block
Neurological: fatigue , confusion

Narrow TI

Question 20

Digoxin drug interactions

Answer 20

• Caution with other drug that reduce heart rate ‼️
  (Arrhythmia : atrioventricular conduction ⬇️ then ⬇️heart rate)
• arrhythmia risk⬆️ in pts with hypokalaemia
• largely renally cleared (renal impairment)