Cardiac Failure Flashcards
Briefly define heart failure?
The failure of the heart to meet circulatory demands.
Describe the bodies natural compensatory mechanisms in heart failure?
Sympathetic nervous system: vasoconstriction
RAAS: Renin-angiotensin-aldosterone system: vasoconstriction, increased circulating volume and cardiac remodelling
ADH: anti diuretic hormone: increases circulating volume
ANP: atrial natriuretic peptide ~ to promote sodium loss
This causes:
Vasoconstriction = increased afterload
Increased circulating volume = increased preload and afterload
Increased peripheral resistance will lead to poor renal perfusion which will further stimulate the RAAS.
Cardiac remodelling will further decrease the efficiency of the heart.
What are the specific goals of treatment in heart failure?
Reduce cardiac workload
Increase cardiac output
Counteract maladaptation
Relieve symptoms
Describe the different drugs that will be used to achieve each of these goals?
Reduce cardiac workload: Diuretics, ACEI, Beta Blockers
Increase cardiac output: Beta Blockers
Counteract maladaptation: ACEI
Relieve symptoms: Diuretics, digoxin
Describe the drug regimen of a patient with LVF?
1st line: ACEI + Beta Blocker (Ramipril + Propanolol)
Persistent symptoms?
Add an Angiotensin receptor anatgonist (candesartan)
Or an aldosterone antagonist (spiranalactone)
Or Hydralazine + nitrate
Still persistent symptoms, or AF?
Add Digoxin
Oedema? Yes give a loop diuretic aka furosemide, you can titrate the dose up as needed.
Describe the method of action of:
ACEI
Angiotensin Receptor Antagonists (ATRA)
Beta Blockers
ACE Inhibitors:
Inhibit ACE enzyme therefore stop the actions of angiotensin II and aldosterone. Also stops bradykinin from being converted to inactive metabolites. (Bradykinin is a vasodilator but is also responsible for the side effect of dry coughs, also causes severe 1st dose hypotension)
They reduce arteriole vasoconstriction and reduce circulating volume by reducing the reabsorption of Na+.
ATRA:
Blocks binding of angiotensin to the angiotensin I receptors therefore causes the same effects as ACE I, except for the dry cough as it does not affect bradykinin.
It is therefore a good alternative for those who have poor compliance due to the dry cough.
Beta Blockers:
Block Beta receptors on the heart and reduce cardiac output therefore reducing BP.
Also reduces the amount of sympathetically stimulated renin.
Describe the beneficial effects of Aldosterone receptor antagonists (spironolactone), and digoxin?
Spironolactone:
Aldosterone causes fibrosis of the heart stiffening it and causing the hypertrophy.
Spironolactone inhibits aldosterone and therefore helps reverse these changes.
Digoxin:
Positive ianotrope by inhibiting Na+/K+ ATPase, Na+ accumulates in myocytes, exchanged with Ca2+ leading to increased contractility.
Impairs atrioventricular conduction, the heart block and bradycardia is beneficial in heart failure with atrial fibrillation. (But contraindicated in heart block)
What advice would you give a patient starting ACEI?
What would you monitor?
1st dose hypotension
You may get a dry cough
Don’t take NSAIDs
Start on a low dose then titrate up.
Monitor U/E’s before and during treatment
