Heart failure - Pharmacotherapy for heart failure
26 important questions on Heart failure - Pharmacotherapy for heart failure
What is the percentage of EF that belongs to HFrEF?
Which percentage belongs to midly reduced EF?
Which percantage belongs to preserved EF?
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What is the effect of the compensatory mechanism RAAS?
What is the effect of arteriolar vasoconstriction? And of venous vasoconstriction?
Venous = increased venous return (preload ↑) -> ↑ stroke volume, but also edema and pulmonary congestion
What is the effect of increased sympathetic nervous activity (compensatory mechanism)?
What is the effect of ↑ antidiuretic hormone (compensatory mechanism)?
How are patients with HFrEF / mildly reduced treated?
Where do loop diuretics work on?
Where do eNaC inhibitors work on?
Where does acetazolamide work on?
Where does the SGLT2 inhibitor work on?
-> sodium-glucose co transporter 2 inhibitors
In which part of the tubuli is the reabsorption increased in HF?
How do MRA (mineralocorticoid receptor antagonists) work?
2. Na/K exchanger inhibited -> K+ concentration increases in the blood
3. The ENaC channel is also inhibited -> Na+ concentration in urine increases
--> distal tubule and collecting duct
Why are diuretics used in HF?
How doe ACE inhibitors work?
Inhibiting Ang II results in:
- no sympathetic activity
- no aldosterone secretion and thus Na retention
- no vasoconstriction
Inhibiting bradykinin conversion results in:
- vasodilatation
At a certain moment, ACE inhibitors were replaced by ARB (AT receptor antagonist), why?
Also, the vasodilatation by bradykinin is not enhanced (lowers bp)
Why are ACE inhibitors used in HF?
They also help block a substance in the blood called angiotensin that is made as a result of heart failure. Angiotensin is one of the most powerful blood vessel narrowers in the body.
How do beta blockers work?
- desensitization of ß adrenergic system
- no increase in contractility
- no increase in HR
- no cardiac remodelling (apoptosis, necrosis, fibrosis, hypertrophy)
--> those effects may be helpful in the beginning, in the end they contribute to progression of HF
--> block actions of hormones that bind to ß receptor (adrenaline and noradrenaline)
Which therapies are used in which type of HF?
Preserved = screening for and treatment of etiologies and comorbidities and diuretics for fluid retention
What are inotropic drugs?
phosphodiesterase 3 inhibitors
What is the effect of venous vasodilators?
What is the effect of phosphodiesterase 3 inhibitors?
Which treatments are used in chronic HF and in acute HF?
Acute: dependent of presence congestion/hypoperfusion = loop diuretics, vasodilators, inotropics and vasopressors
What is the problem with a patient that is warm? And cold?
Cold = reduced CO and vasoconstriction
What is the problem when the patient is dry? And wet?
wet = edema (congestion)
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