HF Flashcards
Main aim in treating HF?
1) reduce afterload
2) reduce preload
3) reduce contractility
–> these all reduce CO
Drugs used in the Tx of HF
1st line: ACEIs
2nd line: ARBs
MoA of ACEIs in the tx of HF?
inhibits ATII/renin/aldosterone –> aretrial vasodilation –> ↓ Afterload (decreases TPR)
Clinical uses of ARBs in HF
2nd line tx –> used as an alternative to ACEIs, if not tolerated
AE of ARBs
Teratogenic (may cause odema due to H2O/ Na+ retention)
Clinical uses of ARNIs
*ARNI: angiotensin receptor-Neprilysis inhibitor
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
AE of ARNI
1) Hypotension
2) Hyperkalaemia
3) cough
4) dizziness
Beta blockers used in the tx of HF
Metoprolol
Carvedilol
Bisoprolol
Clinical uses of Beta blockers in the tx of HF
1st line tx for HF when combined w/ ACEIs, ARBs or ARNI
MoA of Beta blockers in the tx of HF
- ↓HR, ↓Bp (↓RAAS)
- ↓CA+ cycling = ↓ contractility
- ↑ Survival
Contraindications of Metoprolol, Carvedilol , Bisoprolol
Tx of ACUTE HF
tx opproach when aiming to further reduce mortality in more advanced HF?
ACEIs + β-blocker + aldosterone anatgonists (spironolactone, eplerenone)
Monitor K+ levels w/ ACEIs/ARBs/ARNI in combo w/ an Aldosterone anta.
Clinical uses of Loop/Thiazides in HF
Tx of congestion
does not prolong life
MoA of Hydralazine and Nitrate
1) Hydralazine -> ↓ TPR -> ↓Afterload
2) Nitrate –> ↓ Preload
what drug is used to improve survival in HF in px w/ low ejection fraction?
Hydralazine + Nitrate
- USED esp in black people
Tx approach in Chronic HF
Digoxin
Clinical uses of Digoxin
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
Digoxin inhibits ———- –> increases [Intracelluar/Exracelluar] Ca+ -> positive intropic agent –> [Increases/decreases]contractility
- Inhibition of Na+/K+ ATPase–> increases intracellular Ca+ –> positive inotropic agent→ Increased force of contraction.
AE of Digoxin
1) blurry,Yellow vision
2) progresses AV block
3) Ectopic beat
Contraindications of Digoxin
1) Diuretics-digoxin interactions
2) Elderly w/ renal imapairment
Tx of digoxin toxicity
Normalize K+ levels, anti-digoxin Fab
fragments, anti-arrhythmic (lidocaine-IV), pacing.
If less K+, the effect of digoxin is
[increased/decreased]
If more K+, [less/more] effective
1) increased (increased activity of Digoxin = more toxicity, arrhythmias)
2) less
Tx of Acute HF
loop diuretics –> 1st line
* if symptoms persist combo w/ IV GTN (Esp. w/ elevated Bp)
MoA of GTN in HF
Venorelaxation -> decreases preload and bp
Tx of Acute HF w/ systolic dysfunction
- 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]
Why are Diuretic contraindicated w/ Digoxin?
They cause Hypokalemia –> digoxin toxicity (w/ low K)
Antiarrythmic that reverses Digoxin toxicity?
Lidocaine (IV)
*Class IB: Na+ channel blocker
