Heart failure treatment Flashcards
(28 cards)
Pros and cons of using diuretics to treat heart failure
Pros:
-
Pros and cons of ACE inhibitors in treatment of heart failure
What role does renal and hepatic dysfunction have on adverse drug reactions and drug drug interactions?
What are the hormonal responses to heart failure?
Sympathetic and RAAS activated
What are the physiological responses to heart failure?
Where are the potential sites for therapeutic intervention?
What are the strengths and weaknesses of beta blockade in the treatment of heart failure?
HFrEf VS HfpEF
HFrEF = Heart Failure with Reduced Ejection Fraction (systolic dysfunction, can’t pump out enough blood so it backs up) - common with MI
HfpEF = Heart Failure with Preserved Ejection Fraction (diastolic dysfunction - can’t fill up enough with blood, eg due to hypertension causing thickening and stiffening of the ventricle wall
2 major risk factors for HFrEF
Previous MI and Hypertension
Why are the sympathetic and raas (renin- algiotensin - aldosterone systems) activated and what do they lead to?
They are activated due to a reduced cardiac output causing (due to reduced ability to contract - thickened wall/scarring/fibrosis).
Leads to venoconstriction and increased heart rate.
This then increases preload, but as the heart muscle is damaged, the stretch doens’t increase contractility but instead just kind of flops open and dilates.
This means the heart is unable to contract as hard and so leads to further reduction in CO, stimulating sympathetic and RAAS system
Further salt and water retention and peripheral vasoconstriction
Why is Furosemide mainstay of treatment for patients with salt and water retension? How and where do they work? What type of drug is it?
It is a loop diuretic, works by inhibiting the Na - K - Cl transporter in loop of Henle on cells in the kidney, preventing the reabsorption of 20% of filtered sodium and water. Works at very low glomerular filtration rates (often the case for heart failure patients)
Very effective in treating all their symptoms and improving quality of life
Why can resistance to loop diuretics occur? How do we overcome this?
Oedema can cause thickening of small bowel wall and this prevents absorption of the diuretic. Alternatively it can open up alternative transport channels for salt and water to pass through.
So use loop diuretic with thiazide diuretic eg benzothiadiazine/metolazone -produces profound reaction.
What can be the adverse drug reactions of diuretics?
Hypotension, dehydration
Hypokalaemia,Hyponatraemia
Gout
Impaired glucose tolerance/diabetics
Frusemide interactions with?
NSAIDs, vancomycin and lithium (Renal toxicity)
Aminoglycosides (aural and renal toxicity)
Anti-hypertensives - profound hypertension
Neuro-hormonal antagonists
RAAS:
ACE inhibitors, Angiotensin Receptor Blockers, Mineralocorticoid Receptor Blockers (inhibit Aldosterone)
Sympathetic:
Beta Blockers
Combined angiotensin blockage plus ANP(Atria Natriuretic Peptide/BNP (Brain Natriuretic Peptide) enhancement
ANP/BNP = naturally produced and cause significant vasodilation and water loss, but naturally have short half life
ACE inhibitors affects and eg. results in CHF patients:
Competitively block angiotensin converting enzyme, preventing conversion angiotensin I to angiotensin II, reducing pre and after load on the heart. Significantly reduce mobidity and mortality.
EG -PRIL so ramiPRIL, enalaPRIL and lisinoPRIL
ACE inhibitors adr and drug drug interactions
COUGH! Angioedema, renal impairment/failure, hyperkalaemia
NSAIDS (acute renal failure)
Potassium supplements/Potassium sparing diuretics (hyperkalaemia)
Angiotensin receptor blockers only used when currently? Why?
Only used if intollerant to ACE inhibitor, not as popular as haven’t been consistantly able to prove a reduction in HFrEF mortality and morbidity and aren’t proven to be as effective as ACE inhibitors.
What is Valsartan- Sacubitril? When is it recommenfded?
Valsartan = AT1 (angiotensin type 1) receptor blocker (block the affects of angiotensin II on the body, decreasing bp) Sacubitril = ANP/BNP enhancer - basically natural diuretic and vasodilator
Recommended:
NYHA classes II+ (any limitation on physical activity),
Left vent EF 35% or less
Who are already on stable does of ACE/ARBs (Angiotension II receptor-blockers)
What are the issues with Valsartan- Sacubitril?
Can produce significant hypotension, so important to take care when uptitrating
What type of drugs are spironolactone and eplerenone? how do they work and where? Recommended for who? And inconjunction with what?
MRA (Mineralcorticoid receptor antagonist)
Block aldosterone and other steroid hormone receptors
Potassium sparing diuretic
Acts in distal tubule
Patients presenting with symptoms despite treatment with ACEI and beta blocker, with LVEF 35%+
Which BBlockers are licensed for HF? When used?
CarvdiLOL, BisoproLOL
Only when patient stabilised, not during acute presentation as can deteriorate patient if they are in fluid overload.
When is Ivabradine used?
Only used in patients in sinus rhythm 70bpm+, on standard therapy and still NYHA class II or class III
Slows heart rate by blocking If (funny Na+ channel) in sinus node.
What positive ionotrope can we use? Issues with it? What good effects does it have?
Digoxin - increases availability of Ca2+ in myocytes
Issues: Narrow therapeutic index, can cause nausea and confusion esp in elderly patients
Reduces no. hospitalisations so Quality of life but doesn’t improve mortality/morbidity rates etc
