Drug Treatment for IHD and HF Flashcards
(32 cards)
Digoxin is a cardiac glycosidic drug that is able to increase inotropic force and reduce HR, what is the mechanism of action of digoxin?
- inhibition of Na+/K+ ATPase
- Na+ cannot leave and ⬆️ inside cell
- Na+ leaves through Na+/Ca2+ cotransporter
- Ca2+ inside cell increases
Digoxin is able to increase Ca2+ inside cardiac cells. What is the effect of this?
- increased inotrophic force
- increased vagal tone so reduces HR
Although digoxin can be used to treat cardiac output in heart failure and does not decrease the BP, BUT it can cause side effects, what are these?
- low therapeutic window
- causes arrtymias
In heart failure what would the aim of the targeting the circled areas in the image, namely:
- blood volume
- preload
- inotrophy
- systemic vasuclar resistance
- blood volume = reduce to improve oedema
- preload = reduce to stop oedema
- inotrophy = increase or decrease
- systemic vasuclar resistance = reduce this
In angina what would the aim of the targeting the circled areas in the image, namely:
- heart rate
- preload
- inotrophy
- systemic vasuclar resistance
- heart rate = reduce workload
- preload = reduce venous blood flow
- inotrophy = reduce workload
- systemic vasuclar resistance = reduce and reduce workload on heart
What is the first line of defence drug used to treat oedema and its mechanims of action?
- loop diuretic
- furosemide
- inhibits Na+/K+/Cl- symporter
- reduces Na+/K+/Cl- and H2O reducing oedema
Although furoesmide is very effective over 6 hours, there are some side effects, what are the most common?
- dehydration
- renal impairment
- hypokalaemia (K+)
- hyponatraemia (Na+)
- hypocalcaemia (Ca2+)
- hypomagnesaemia (Mg+)
ACE inhibitors, namely Ramipril is able to act on the RAAS, what are the main effects?
- vasoconstriction = decreasing afterload
- venodilation = increased preload
- inhibit aldosterone and ADH = reduced Na+ and H2O
Are ACE inhibitors able to reduce mortality?
- yes
In addition to inhibiting the conversion of angitensin I to II, ACE inhibitors also do what?
- inhibit the breakdown of bradykinin
What are the common side effects of ACE inhibitors?
- cough due to high levels of bradykinin
- renal impairment
- hyperkalaemia (K+)
If a patient cannot be prescribed an ACE inhibitor, what could be an alternative?
- angiotensin II inhibitor Losartan
- similiar effects as ACE inhibitors
- doesnt cause dry cough
What is the role of aldosterone in the RAAS?
- released by adrenal gland
- increases Na+ and H2O retention
What aldosterone inhibitor do we need to know about?
- spirolactone
Spirolactone is an effective aldosterone inhibitor, but what are the side effects?
- gynaecomastia (man boobs)
- hyperkalaemia (K+)
Are adrenergive agonists a good thing in heart failure, essentially making the heart pump harder?
- no
- associated with increased mortality
-
In heart failure why would beta 1 blockers be used?
- reduce HR
- reduce inotrophic force
- reduce renin release
What are some common side effects of beta 1 blockers?
- fatigue
- bradycardia
- breathlessness
- cold hands
- erectile dysfunction
Which beta 1 blocker do we need to know about for heart failure?
- bisoprolol
What is the principle aim of angina treatment?
- reduce O2 demand
- increase O2 supply
What are the common drugs that are used in combination to treat angina?
- beta 1 blockers (bisoprolol) = ⬇️ inotrophic force and HR
- Ca2+ channel blockers (diltazem or amalodapine) = ⬇️ SVR
- GTN = vasodilation of blood vessels
What are the effects of glyceryl trinitrates (GTN)?
- vasodilate veins and arteries
- reduces pre and after load
What is the secondary messenger that nitrates are able to activate?
- guanylyl cycllase = increased cGMP
- reduces Ca2+
- induces vasodilation
What are some of the common side effects of nitrates?
- Headache
- Hypotension / dizziness
