CVS drugs

CVS drugs

ANTI-ANGINA
1. Calcium channel blockers
  1. Inhinit Ca influx through L type calcium channels, acting on CA entry into vascular SM, cardiac muscle (reduce force), SA nodal tissues (reduce rate), AV node (decrease conduction velocity)
    1. Dihydropyridine - Amlodipine
      1. vasoselective - inhibits L and T type Ca channels on primarily arterial SM --> antihypertensive effect. reduces TPR. CAUTION IN ANGINA - may cause excessive dilation - hypotension - reflex tachycardia and increase O2 demand
    2. Phenylalkalamines - verapamil
      1. Binds to open cardiac L-type channel: cardioselective. also acts as vasodilator. Indicated in angina as it reduces myocardial O2 demand and reduces coronary vasospasm. Also indicated in HTN = produces antihypertensive effect. Contraindicated in HF and with B blocker
    3. Benzothiazipines - diltiazem
      1. inhibits Ca2+ influx during membrane depolarisation of cardiac and vascular SM, interfering with slow inward depolarising current in excitable cardiac tissue. effective as anti-arrhythmic in AF, angina by reducing Oxygen demand, and can reverse coronary vasospasm.
2. Beta Blockers
  1. reduces O2 consumption by negative ionotropic and chronotropic actions
3. Nitrates/Nitrofilators
  1. MOA: mimic the actions of endogenous NO, e.g. vasodilation. Release NO in plasma or form NO within cells to cause VENOUS dilation, reducing venous pressure and preload. Reduces diastolic wall stress and cardiac work. Systemic arterial dilation reduces after load and enhances CO while also reducing ventricular wall stress and O2 demand
    1. Glyceryl Trinitrate (GTN)
      1. sublingual spray or buccal tablet - broken down quickly in stomach so not oral administration. Treatment of acute angina and relief of pain. Fast acting
    2. Isosorbide mononitrate/dinitrate
      1. oral delivery, longer onset and duration of action. More useful for long term prophylaxis and management of CAD
    3. Therapeutic uses
      1. Angina/MI
        Ischaemic pain due to decreased coronary flow and O2 delivery to the heart - vasodilation reduces preload and O2 demand, reduces systemic arterial resistance reducing after load and decrease LV wall stress, reduce wall stress, cardiac work and O2 demand.
      2. Acute.severe HF
        reduction in after load improves EF and SV, venous pressure reduction reduces oedema
Pump/Cardiac contractility
1. Calcium channel blockers
2. Centrally acting A2 agonists- Clonidine
  1. Reduces NA release at synapse - reduce sympathetic outflow, and reduces parasympathetic less. Dulls sympathetic outflow causing decreased HR and SV (due to decrease FOC) and therefore decreased CO and MAPB
3. Anti-arrhythmics
  1. B blockers- Metoprolol
    1. Inhibit binding of noradrenaline and adrenaline to beta receptors, antagonise cardiac and renal B receptors. Decrease CO and BP by both negative cardiac chronotropic and ionotropic actions. Also decreasing renin output so decrease water retention, fluid volumes in body and decrease BP
  2. Class 3 - Amiodarone
    1. MOA: Block K+ channels involved in membrane replarisation. Can modulate lipid membrane properties and affect Na+ fluxes. Plateau and AP duration are prolonged, substantially prolongs ERP so decreased chance of re-entry, prolongs atrial and ventricular replarisation
  3. Digoxin - negative ionotrope?
    1. MOA: cardiac glycoside - increases force of contraction and slows rate
Plasma/Blood volume
1. Diuretics
  1. Thiazide - Bendroflumethazide
    1. Act on distal tubule, competitively binding to Na/Cl cotransporters. Decrease reabsorption of Na and water
  2. Loop - frusemide
    1. act on thick ascending loop of heel, inhibits NKCC2 transporter by competing with Cl- for binding, reducing reabsorption of Na, K and Cl, and therefore inhibiting gradient for water to move down.
  3. Osmotic- manitol
    1. Osmotically active - filtered into tubule from glomerulus and increases osmolarity of filtrate so decreases reabsorption of whater. Also increases osmolarity of the blood, therefore increasing water flow from tissues into interstitial fluid, reducing oedema.
  4. K+ Sparing
    1. Spironolactone
      1. acts on distal tubule and collecting duct. Is an aldosterone antagonist - competes for the receptor, so no up regulation of ENax (sodium transporter) and Na/K ATPase - decreased reabsorption of sodium and therefore water
    2. Amiloride
      1. acts on distal tubule and collecting duct, inhibits ENaC, decreasing reabsorption of sodium and so decrease reabsorption of water
2. ACE inhibitors - Cilazipril
  1. Decrease angiotensin II levels being released, reduced systemic vascular resistance and vasodilation of veins. Increase levels of bradykinin (vasodilation). Downregulates AT2 provoked sympathetic activity. Blocks AT2 effect in kidney, reducing aldosterone release - increasing Na and water excretion, leads to K+ retention. also inhibit cardiac and vascular remodelling and fibrosis
  2. Therapeutic uses
    1. chronic heart failure - reduces after load, increasing SV and ejection, reduces TPR. Reduces preload, reduces sympathetic activation and prevents AT2 from cardiac remodelling
3. Angiotensin receptor blockers - Losartan
  1. Potent selective AT1 receptor antagonist. Block all effects on AT1 receptors, preventing effects of ATII on Vascular SM< aldosterone secretion, sympatheticthetic activation, pro-fibrotic pathways
Pipes (blood vessels)
1. A1 blockers - Doxazosin
  1. selectively blocks a1 receptor, causing vasodilation. reduced arteriolar resistance and increased venous capacitance, decreasing preload
2. Hyperlipidaemia
  1. Statins
  2. Fibrates
BLOOD
1. Antiplatelets and anti-coagulants
  1. Anti-platelets: Aspirin, Clopidogrel
    1. Aspirin MOA: non-selective COX inhibitor, acetylates platelet COX1, reducing TXA2 production for the lifetime of the platelet. No platelet nucleus so no transcription and production of COX1.Minimal effect on endothelial COX2 due to rapid turnover of COX2 by endothelial transcription
      1. - Prevents thrombus formation by decreasing platelet’s ability to adhere and aggregate at the site of injury
    2. Clopidogrel MOA: non-competitive blocking of ADP receptors, prevents binding of GPIIb-IIIa receptor - reduces platelet activation, and binding to each other and fibrinogen
  2. Anticoagulants e.g. Heparin, Warfarin
    1. Warfarin MOA: prevents reduction of vitamin K by inhibiting vitamin K epoxide reductase. prevents vitamin K from activating clotting factors II, IX, X and proteins C and S. Overall, reduces formation of fibrin so prevents formation of thrombus
    2. Heparin - e.g. Enoxaoarin (LMW)
      1. MOA: factor Xa is inhibited by anti-thrombin III. Heparin increases the binding of antithrombin with prothrombin (Xa) and thrombin (IIa)
2. fibrinolytics - Tenecteplase and Alteplase
  1. MOA: brings to fibrin in thrombus and converts trapped plasminogen to plasmin. Plasmin initiates local fibrinolysis
  2. Indications - acute MI: prevent thrombus or break down clot causing occlusion, ischaemic stroke - break down formed clot. used at the time of MI.

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	Created by Jasmine Appleton over 6 years ago