12. Commonly Used Cardiac Medications Flashcards
List some categories of drugs commonly used in cardiology.
What classes of drugs are used for heart failure?
Anticoagulants: Warfarin, new oral alturnatives, aspirin, clopidogrel, heparins
Antiarrythmics: CCBs, Na+ blockers, β-blockers etc.
Heart failure
Anti anginals
GTN
Lipid modulators: e.g. statins, fibrates, niacin, orlistat.
Diuretics, spironolactone, ACE-I/ARBs, nitrates, ivrabadine, sacubitril (inhibits enzyme neprilysin which degrades ANP and BNP, two BP-lowering peptides that work mainly by reducing blood volume), inpatient; heparin, other vasodilators? digoxin?
What 4 drugs would be used to treat acute L ventricular failure?
What are the treatements for CCF (briefly list)?
What are some other options?
Nitrate infusion: causes veno relaxation, reduces preload. Smaller effect on afterload. Metabolised and release NO -> increase cGMP -> activates protein kinase G. Can cause headaches and hypotension. BUT drops BP and pt already has low BP due to HF…
IV loop diuretics
IV diamorphine (heroin)
O2
Loop diuretics, ACE-I/ARB antagonist, spironolactone, β-blocker, ivrabradine, sacubitril, ?IHD: statin, aspirin, clopidogrel, NB. salt and water.
Other vasodilators (hydralazine), digoxin, invasive methods, heart transplant, stem cells, renal denervation.
What are the 4 different types of diuretics?
How do loop diuretics work?
Briedly describe RAAS and what drugs work at which points.
- *1) Thiazide:** indapamide, metolazone (thiazide-like, for severe HF)
- *2) Loop:** bumetanide, furosemide
- *3) K+ sparing:** amiloride, triamterine
- *4) Aldosterone antagonists:** spironolactone (SE - gynaecomastia), eplenerone (both also K+ sparing)
Inhibit transport of NaCl from ascending LoH into interstitial fluid. Act on Cl- binding site. Probable veno dilator effect cf when given IV. Na+ loss (wanted), K, Mg2+ loss (unwanted), Ca2+ loss useful in hypercalcaemia. Stimulate RAAS. Poss decreased absorption with gut oedema and ascites.
What side effects can ACE-Is cause? Give examples of ACE-Is.
How do ARBs work? Any SEs? Give examples of ARBs.
How does spironolactone work? Any SEs?
Angioedema, 1st dose hypotension, high K+, dry cough. Improves prognosis. E.g. ramipril, perindopril, lisinopril. Don’t start at same time as diuretics. Can get angiodema, intermittant facial swelling.
Block A2 angiotensin receptor. Improve mortality. Like ACE-Is but no dry cough or angiodema. 1st dose hypotension. High K+. E.g. losartan, valsarten, irbesarten, candarsarten.
Aldosterone antagonist - affects RAAS. Improves mortality. Gynacomastia due to oestrogen effects. High K+. Incresed Na+ and H2O excretion. Eplenerone less oestrogen effects
Do β-blockers help diuresis? When must you only give them? Give some examples and explain how they work.
How does ivabradine work?
How does sacubitril work? What effect does it have, and is it available on its own?
No. Improve mortality. Only give when pt stable as can ppt acute LVF. Via β1 receptor, β-blockers reduce force of contraction and speed of conduction in heart. E.g. bisoprolol, atenolol, propanolol, carvedilol, metoprolol. Not for acute HF but ok once stabilised.
Causes bradycardia. Inhibits funny channels so slows pacemaker in SAN. Unlike β-blockers it can be used in asthmatics and no -ve ionotrophic effect.
Neprilysin (enzyme) inhibitor. Neprilysin normally degrades ANP and BNP (which lower BP). Thus sacubitril increases bioavailability of ANP, BNPbradykinin and substance P. Causes naturesis (Na excretion) and vasodilation. Lowers BP. Only available with valsarten (ARB) at the moment.
How is AF managed once dx?
What is digoxin used for? How does it work? What is it’s thrapeutic index like?
Decide on rate or rhythm control (rate control - want drug that increases AV block. Rhythm control - reestablish sinus rhythm). Consider surgery. Anticoagulation?
Mainly used as an antiarrhythmic (but not an antiarrhythmic!) to control AF and flutter. Doesn’t control exercise induced tachycardia. Reduces HR and increases contraction force. Inhibits Na/K pump -> Na accumulates in cell, causing Ca2+ to also accumulate, increasing contractile force. Narrow therapeutic index. Renally excreted; all elderly have renal impairment. Long T1/2 so may need loading dose. Toxicity increased by low K+ = arrhythmias, nausea, vomiting.
What is amiodarine used to treat? How does it work? What is it’s half like and why? What are some SEs?
What is the medical management of angina? (7 things)
Treats atrial and ventricular arrhythmias. Blocks Na, Ca and K channels, and antagonist of α and β adrenergic receptors. This reduces spontaneous depolarisation (automacity), slows conduction velocity, and increases refractroriness. Can cause bradycardia. Very long T1/2 due to protein binding - 6w in normal ppl, must give loading dose (or takes 6m to get to steady state). Contains iodine - may cause hypo/hyperthyroidism. SEs: pulmonary fibrosis, hepatitis, photosensitive skin rashses, corneal deposits.
β-blockers (NB, asthma). CCBs. Nitrates (tolerance and 0 bioavailability - oral, sublingual, patches). Nicorandil (K+ channel activator and NO donor). Ivabradine (acts on SAN -> bradycardia). Aspirin and statin.
Give some examples of CCBs (2 groups). How do they work? Give SEs.
Dihydropyrinidines: amlodipine, nifedipine, relatively selective for vasculature. Antiarrythmics: verapamil (more heart-selective), diltiazem. All block Ca channels (3 diff sites) thus reducing intracellular Ca2+ = muscle relaxation and vasodilation in arterial smooth muscle. In heart reduce myocardial contractility. Anti anginal and anti hypertensive. SEs: bleeding gums, amlodipine ankle swelling, verapamil constipation.