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Cardio pharmacology

Cardio pharmacology. Angina. angina. Causes Atheroma Others: Aortic stenosis, aberrant coronary circulation, severe anaemia, arteritis Prevention Decrease metabolic demands of the heart Increase coronary blood flow Decrease cardiovascular risk factors.

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Cardio pharmacology

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  1. Cardio pharmacology • Angina

  2. angina • Causes • Atheroma • Others: Aortic stenosis, aberrant coronary circulation, severe anaemia, arteritis • Prevention • Decrease metabolic demands of the heart • Increase coronary blood flow • Decrease cardiovascular risk factors

  3. decrease cardiovascular risk factors • BP • Cholesterol • Smoking • LVH

  4. Decrease metabolic demands of the heart • 1. Decrease HR • 2. Decrease arterial pressure • 3. Decrease ventricular dimensions

  5. 1. Decrease HR • Beta adrenoreceptor blockers • Decrease sympathetic response • Not for HF • B1 • Atenolol • B2 • Propranolol

  6. Detail • 1.Drugs that ⇓ HR: • §β-adrenoreceptor blockers – atenolol (β1) - , propranolol (β2). Block β receptors ∴ attenuate the sympathetic response of the heart → slow heart rate & improve capacity for exercise. Good if cardiac function is preserved, not for HF • §Mode of action: • —⇓ HR ⇑with exercise etc. • —⇓ contractility & arterial P • —∴⇓ O2 demands of myocardium during exercise • §Side effects: • —⇑ LV dimensions∴⇑ LV work offsetting benefits • —Slow HR • —Heart failure • —Cold peripheries - Raynaud’s • §Alternatives = Ca channel blockers – verapamil & diltiazem also slow HR due to effect on calcium channels in cardiac pacemaker cells

  7. 2. decrease arterial pressure • Calcium channel blockers • Dihydropyridines • Nifedipine • Non-dihydropyridines • Diltiazem, verapamil • Mainly relax resistance arteries BP falls • Some effect on heart with... • ...Diltiazem and Verapamil?

  8. Details • 2. Drugs that ⇓ Arterial Pressure • §Ca channels blockers – verapamil, diltiazem & nifedipine (short acting) • §Mode of action: • —Diltiazem (small effects) / Verapamil (large effects) - ⇓ Ca entry into cardiac pacemaker cells → HR ⇓. ⇓ Ca entry into myocytes ∴⇓ force of contraction • —Side effects: bradycardia & heart failure (oedema) • —All - ⇓ Ca influx thru L-typevoltage-gated Ca channels in peripheral vasculature ∴⇓ peripheral resistance • —All - ⇓Ca entry into vascular myocytes → relex at arteries, TPR ⇓, BP ⇓ • Side effects: • §reflex tachycardia (Nifedipine only) in response to peripheral vasodil • §Flushing • §Headaches • §Ankle swelling

  9. 3. Decrease ventricular size • Nitrovasodilators • GTN & isosorbide mononitrate/ dinitrate • Active in 1-2 mins • Lasts for 15-20 • Metabolised to NO • Increase venous capacitance

  10. Details • 3. Drugs that ⇓ Ventricular Dimensions: • §Nitrovasodilators – glyceryl trinitrate (GTN), isosorbidemononitrate, dinitrate relax vascular & other types of smooth muscle with preferential effect on veins • —⇑ venous capacitance (& small⇓in arterial resistance) ⇓ central venous P →⇓ in ventricular dimensions & CO. The ⇓ in cardiac size & small ⇓ in TPR = ⇓ in LV work. They also dilate coronary arteries → relief from angina • §Mode of action: – nirtovasodilators metabolised to NO→ activates vsmc guanylate cyclase in vascular smooth muscle →⇑ in cGMP→⇓ in IC free Ca → vascular relaxation • §GTN – when swallowed is inactive until metabilsed in liver. If sucked under tongue absorbed rapidly, works within 1-2 mins & effects last for 15-20 mins • §Isosorbide dinitrate ISDN– converted to ISMN in liver ∴ long acting orally active form of GTN (prophylactic)

  11. Details cont. • §Side effects: • —development of tolerance, resistance of vsm: • ·In withdrawal constriction of coronary arteries may develop • ·Blood vessels may become insensitive to NO • ·Stable NO metabolite pool may become depleted • Solution = give intermittently • —Headaches due to dilation of muscular intracranial arteries • —Reflex ⇑ in HR • —Limited potential for dilating sites of atheroma, risk of steal syndrome – if one artery stenosed dilation of other = they take all the blood & leave that artery further depleted

  12. GTN ----> NO • GTN is a prodrug for NO • NO activates GC • GC converts GTP ----> cGMP • cGMP leads to smooth muscle relaxation... • ...by decrease Ca

  13. Potassium channel openers • Nicorandil • Vasodilator due to hyperpolarising of cells • Ivabradine • Acts selectively on SA node to slow HR

  14. Details • Potassium channel Openers • ·Nicorandil – ⇓ ICK+ ∴ cells become hyperpolarised - vasodilator • §Side effects: • —Severe headache • —Flushing • —Dizziness & low BP • ·Ivabradine: • §Selective action on SA node → slows HR • §Protects endothelium dependant relaxation → relax coronary arteries

  15. Combinations • Increase in heart size caused by B-blockers can be offset by... • ...nitrovasodilators • Tachycardia of nitrovasodilators or nifedipine can be prevented by giving... • ...B-blockers • Aspirin good for stopping platelets sticking • Given to everyone unless... • ...they are bleeding

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