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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

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pharmacology
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
pharmacokinetics
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
pharmacodynamics
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
slide4

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
slide5

Thoracic region

Lumbar region

slide6

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

physiology of anti ischemic drugs
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
anti ischemic drugs9
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
anti ischemic drugs11
Anti-Ischemic Drugs

Decreasing myocardial O2 demand

  • Beta Blockers
  • Nitrates
  • Calcium channel blockers

Increasing myocardial O2 supply

  • Antiplatelet agents
  • Anticoagulants
  • Thrombolytic agents
beta blockers
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
beta blockers13
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
slide14

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
nitrates
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
nitrates16
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
nitrates17
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

calcium channel blockers
CALCIUM CHANNEL BLOCKERS

Treatment

  • Used to treat coronary vasospasm, angina, hypertension

Pharmacodynamics

  • 2 sources of Ca++: intracellular (SR) and extracellular (plasma)
calcium channel blockers20
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
calcium channel blockers21
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)
calcium channel blockers22
CALCIUM CHANNEL BLOCKERS
  • Side effects of Ca++ Channel Blockers
    • Headache
    • Flushing
    • Dizziness
    • Orthostatic hypotension
    • Syncope (fainting)

Generic/Brand names of calcium channel blockers

antiplatelet agents
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

anticoagulants
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

thrombolytic agents
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?]
thrombolytic agents26
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

general pharmacology
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