pharmacology n.
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  1. Pharmacology • Goal of Pharmacology? • Composed of: • Pathology of conditions • The physiologic & anatomic deviations from the normal that constitute the disease • mechanisms of drugs • effects of drugs on exercise and EKG’s • individuality of patient and dose response • Foundation of the drug therapy goal • rests on pharmacokinetics and dynamics

  2. Pharmacokinetics • Bioavailability • Enteral (taken by mouth) • Parenteral (bypass GI system) • Distribution of the drug by means of the circulatory system • General or restricted • Clearance: rate of elimination by all routes • Half-life: indicates length of time the effects will last (reduced by 50%) • All of the above determine the prescribed dosage

  3. Pharmacodynamics • An understanding of the critical role of drug receptors • Most common sites for cardiac drug receptor interactions are: • Autonomic Nervous System (ANS) • Kidneys • Vascular smooth muscle

  4. Autonomic Nervous System Functional and Anatomical Divisions of ANS (most organs receive dual innervation) I. Sympathetic autonomic nervous system • Tends to activate organ II. Parasympathetic autonomic nervous system • Tends to inactivate organ

  5. Thoracic region Lumbar region

  6. Autonomic Nervous System Vascular Smooth Muscle Kidneys Sympathetic NS Parasympathetic NS Adrenergic neurotransmitters Cholinergic neurotransmitters Alpha receptors Beta receptors Muscarinic Nicotinic β1 β2 Catecholamines Decreased contractility and HR Tachycardia & HTN Contraction / Stimulation Relaxation of VSM

  7. Anti-Ischemic Drugs

  8. Physiology of Anti-Ischemic Drugs O2 supply is dependent on many factors: • coronary blood flow • O2 carrying capacity of blood • anatomy of coronary arteries (lumen size) O2 demand is affected by: • preload & afterload • wall thickness • contractility & heart rate • left ventricular volume and diameter

  9. Anti-Ischemic Drugs • Pathophysiology • Inadequate coronary blood flow results in ischemia • O2 demand is increased under conditions that increase HR, BP,or both • Most common cause of decreased supply is coronary artery disease • atherosclerotic plaque causes reduced lumen size • Clinical Assessment (Myocardial VO2) • Rate-pressure product = HR x SBP • Pharmacologic Intervention • Reestablish a balance between myocardial O2supply and demand

  10. Anti-Ischemic Drugs Decreasing myocardial O2 demand • Beta Blockers • Nitrates • Calcium channel blockers Increasing myocardial O2 supply • Antiplatelet agents • Anticoagulants • Thrombolytic agents

  11. BETA BLOCKERS Treatment • Used to treat angina, hypertension, arrhythmias • Used in acute and post MI setting Pharmacodynamics • Exert their effects by competitively blocking the beta adrenergic receptors • ß1 blockers: Inhibit cardiac stimulation • “cardioselective” if they just work on β1 receptors • ß2 blockers: Inhibit relaxation of vascular system & bronchi

  12. BETA BLOCKERS Effect of Beta Blockers • Decrease heart rate at rest and with exercise (- chronotropic effect) • Decrease myocardial contractility at rest and with exercise (- inotropic effect) • Decrease blood pressure at rest and during exercise • End result => decreased VO2 demand • Diastolic filling time increases as HR decreases

  13. BETA BLOCKERS • Side effects • Excessive fatigue • Peripheral vasoconstriction • Bronchial spasm/constriction • Significant bradycardia • May worsen lipid profile • Rebound ectopy (with abrupt withdrawal) • Generic/Brand names of β-blockers

  14. NITRATES Treatment • Used to treat hypertension & angina Pharmacodynamics • Directly relax vascular and coronary smooth muscle, thereby decreasing myocardial demand • Vasodilation on venous system (decrease venous return) => decreased volume/preload • Vasodilation of coronary arteries => decreased afterload

  15. NITRATES • Effect of Nitrates • Resting heart rate often increases • Decreased blood pressure at rest and during exercise • Increases coronary blood flow • No significant effects on exercise heart rate • patients are able to perform more exercise without developing symptoms

  16. NITRATES Administration • May be given sublingual, pill, intravaneously, transdermally Side effects of Nitrates • Patients can develop tolerance to this nitrate (desensitization of receptors) • headaches, flashing sensations, nausea • Orthostatic hypotension (and dizziness after exercise) Generic/Brand names of Nitrates

  17. CALCIUM CHANNEL BLOCKERS Treatment • Used to treat coronary vasospasm, angina, hypertension Pharmacodynamics • 2 sources of Ca++: intracellular (SR) and extracellular (plasma)

  18. CALCIUM CHANNEL BLOCKERS Pharmacodynamics • 2 sources of Ca++: intracellular (SR) and extracellular (plasma) • Act by blocking various calcium-dependent process in vascular smooth muscle & myocardial cells • Action occurs through limiting Ca++ entry into cardiac and smooth cells

  19. CALCIUM CHANNEL BLOCKERS Effect of Calcium Channel Blockers • Coronary arteries dilate (treat vasospasm) • Decreases blood pressure • arrhythmia control • Tend to decrease heart rate and blood pressure (thus, treatment of post MI angina)

  20. CALCIUM CHANNEL BLOCKERS • Side effects of Ca++ Channel Blockers • Headache • Flushing • Dizziness • Orthostatic hypotension • Syncope (fainting) Generic/Brand names of calcium channel blockers

  21. ANTIPLATELET AGENTS Pharmacodynamics • Prevent thrombus formation by decreasing the platelets’ ability to adhere and aggregate at the site of the injury Effect of platelet aggregation antagonists • Acts as a ”blood thinner” Generic/Brand names of antiplatelet agents

  22. ANTICOAGULANTS Pharmacodynamics • Inhibit the formation of thrombin and therefore negate the influence of thrombin on fibrinogen Effect of Anticoagulants • Prevent blood clot formation Generic/Brand names of anticoagulants

  23. THROMBOLYTIC AGENTS Pharmacodynamics • Facilitates the conversion of plasminogen to plasmin Effect of Fibrinolytics • Purpose is to acutely destroy (lyse) or decrease the blood clot formation that occurs within the coronary artery at the time of the myocardial infarction. • 3-4 hours from the onset of ischemia (75% success) [6 hours?]

  24. THROMBOLYTIC AGENTS Side Effects of Thrombolytic Agents • NOT tissue specific -->Blood clotting ability is markedly altered (avoid potential tissue trauma) • Cerebral vascular accidents • GI bleeding Generic/Brand names of Thrombolytics

  25. General Pharmacology • Antianginals (used to reduce chest pain assoc. with angina) • Nitrates and Nitroglycerin • Beta Blockers • Calcium Channel Blockers • Antihypertensives (used to reduce BP) • Alpha blockers • ACE Inhibitors • Beta Blockers • Calcium channel blockers • diuretics • Antiarrhythmic (used to reduce/prevent devt. of cardiac arrhythmias) • Classified by their action on cardiac tissue