HF

Question 1

Main aim in treating HF?

Answer 1

1) reduce afterload
2) reduce preload
3) reduce contractility
–> these all reduce CO

Question 2

Drugs used in the Tx of HF

Answer 2

1st line: ACEIs
2nd line: ARBs

Question 3

MoA of ACEIs in the tx of HF?

Answer 3

inhibits ATII/renin/aldosterone –> aretrial vasodilation –> ↓ Afterload (decreases TPR)

Question 4

Clinical uses of ARBs in HF

Answer 4

2nd line tx –> used as an alternative to ACEIs, if not tolerated

Question 5

AE of ARBs

Answer 5

Teratogenic (may cause odema due to H2O/ Na+ retention)

Question 6

Clinical uses of ARNIs

*ARNI: angiotensin receptor-Neprilysis inhibitor

Answer 6

1) Current or prior elevated BNP level or N-terminal proBNP.
2) Haemodynamic stability (BP>100 mmHg), as ARNI may cause Hypotension
3) no Hx of angioedema,
4) access to medication

Question 7

AE of ARNI

Answer 7

1) Hypotension
2) Hyperkalaemia
3) cough
4) dizziness

Question 8

Beta blockers used in the tx of HF

Answer 8

Metoprolol
Carvedilol
Bisoprolol

Question 9

Clinical uses of Beta blockers in the tx of HF

Answer 9

1st line tx for HF when combined w/ ACEIs, ARBs or ARNI

Question 10

MoA of Beta blockers in the tx of HF

Answer 10

• ↓HR, ↓Bp (↓RAAS)
• ↓CA+ cycling = ↓ contractility
• ↑ Survival

Question 11

Contraindications of Metoprolol, Carvedilol , Bisoprolol

Answer 11

Tx of ACUTE HF

Question 12

tx opproach when aiming to further reduce mortality in more advanced HF?

Answer 12

ACEIs + β-blocker + aldosterone anatgonists (spironolactone, eplerenone)

Monitor K+ levels w/ ACEIs/ARBs/ARNI in combo w/ an Aldosterone anta.

Question 13

Clinical uses of Loop/Thiazides in HF

Answer 13

Tx of congestion
does not prolong life

Question 14

MoA of Hydralazine and Nitrate

Answer 14

1) Hydralazine -> ↓ TPR -> ↓Afterload
2) Nitrate –> ↓ Preload

Question 15

what drug is used to improve survival in HF in px w/ low ejection fraction?

Answer 15

Hydralazine + Nitrate

• USED esp in black people

Question 16

Tx approach in Chronic HF

Answer 16

Digoxin

Question 17

Clinical uses of Digoxin

Answer 17

Tx of Chronic HF –> ↓ Hospitalization
only short-term use
1) Tx HF in patients who remain symptomatic despite optimal use of ACEIs and diuretics
2) AFib due to AV conduction slowing

Question 18

Digoxin inhibits ———- –> increases [Intracelluar/Exracelluar] Ca+ -> positive intropic agent –> [Increases/decreases]contractility

Answer 18

• Inhibition of Na+/K+ ATPase–> increases intracellular Ca+ –> positive inotropic agent→ Increased force of contraction.

Question 19

AE of Digoxin

Answer 19

1) blurry,Yellow vision
2) progresses AV block
3) Ectopic beat

Question 20

Contraindications of Digoxin

Answer 20

1) Diuretics-digoxin interactions
2) Elderly w/ renal imapairment

Question 21

Tx of digoxin toxicity

Answer 21

Normalize K+ levels, anti-digoxin Fab
fragments, anti-arrhythmic (lidocaine-IV), pacing.

Question 22

If less K+, the effect of digoxin is
[increased/decreased]
If more K+, [less/more] effective

Answer 22

1) increased (increased activity of Digoxin = more toxicity, arrhythmias)
2) less

Question 23

Tx of Acute HF

Answer 23

loop diuretics –> 1st line
* if symptoms persist combo w/ IV GTN (Esp. w/ elevated Bp)

Question 24

MoA of GTN in HF

Answer 24

Venorelaxation -> decreases preload and bp

Question 25

Tx of Acute HF w/ systolic dysfunction

Answer 25

• 1st line: Dobutamine –> increases contractility
• 2nd line: Dopamine (if Doputamine is not tolerated) –> positive introp, may increase renal blood flow (benifits patients w/ kidney dys.)
• less preferred :PDE3 inhibitors: Amrinone, Milrinone →increase cAMP in heart muscle
  & smooth muscle: positive inotropy, decreased TPR. [Improve haemodynamic indices, worsen survival: arrhythmias]

Question 26

Why are Diuretic contraindicated w/ Digoxin?

Answer 26

They cause Hypokalemia –> digoxin toxicity (w/ low K)

Question 27

Antiarrythmic that reverses Digoxin toxicity?

Answer 27

Lidocaine (IV)

*Class IB: Na+ channel blocker