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Pharmacology: Mechanisms and Compliance Study Notes

Pharmacology: Mechanisms and Compliance Notes

Course and Contact Information

  • Course: HSS 3106 C - Pharmacology: Mechanisms and Compliance
  • Professor: Dr. Nehal EL-Deeb
  • Lecture Times:
    • Monday: 17:30 - 18:50
    • Wednesday: 17:30 - 18:50
  • Email: neldeeb@uottawa.ca

Cardiovascular Pharmacology Overview

  • Chapter Focus: Drugs used to treat cardiovascular conditions.
  • Key Author: Jahangir Moini, MD, MPH.

Heart Anatomy

  • Key Structures:
    • Major Veins and Arteries:
    • Superior vena cava, inferior vena cava, pulmonary arteries, aorta, coronary arteries.
    • Heart Chambers: Right atrium, left atrium, right ventricle, left ventricle.
    • Valves: Tricuspid valve, bicuspid (mitral) valve, pulmonary valve, aortic valve.

Electrical Conduction of the Heart

  • Cardiac Function Terms:
    • Inotropy: Refers to the force of heart muscle contractions; can be positive (increases strength) or negative (decreases strength).
    • Chronotropy: Refers to heart rate; positive (speeds up) or negative (slows down).
    • Dromotropy: Refers to the speed of electrical impulse conduction; positive enhances speed and negative slows it down.
    • Lusitropy: Refers to the relaxation phase of the heart muscle.

Autonomic Nervous System Regulation

  • Receptors and Their Effects:
    • Sympathetic Receptors:
    • Norepinephrine (α1, β1, β2): Increases inotropy, chronotropy, vasoconstriction (α1), vasodilation (β2).
    • Parasympathetic Receptors:
    • Acetylcholine (M2): Causes vasodilation and decreases heart rate.

ECG Interpretation

  • ECG Segments:
    • P-wave: Atrial contraction.
    • PR interval: Time for excitation from the SA node through the bundle of His.
    • QRS Complex: Ventricular contraction.
    • ST Segment: Ventricular relaxation.
    • T-wave: Ventricular repolarization.

Pharmacological Approaches to Heart Diseases

  • Dysrhythmias, Myocardial Infarction, Coronary Heart Disease:
    • Angina Pectoris: Reversible oxygen insufficiency leading to ischemia.
    • Types:
      • Classical (stable), Variant (vasospastic), Unstable angina.
  • Antianginal Drugs:
    • Classes:
    1. Organic Nitrates (Vasodilators)
    2. Beta-Blockers
    3. Calcium Channel Blockers (CCBs)

Organic Nitrates

  • Key Drug: Nitroglycerin.
    • Mechanism of Action: Forms nitric oxide, leading to vasodilation. Results in decreased cardiac oxygen demand and relief of spasms.
    • Adverse Effects: Headache, hypotension, tachycardia.
    • Long-lasting Forms: Isosorbide dinitrate, mononitrate.

Beta Blockers

  • Key Drugs: Atenolol, Metoprolol, Propranolol.
    • Mechanism: Block β1 receptors, reducing heart rate and contractility, thus lowering oxygen demand.
    • Adverse Effects: Bronchospasm, bradycardia, fatigue, diminished sex drive.
    • Contraindications: Severe asthma, pregnancy.

Myocardial Infarction (MI)

  • Mechanism: Decreased oxygenated blood flow to myocardium leads to tissue death.
  • Management Goals:
    • Limit myocardial damage using:
    • Nitroglycerin, Thrombolytics, Morphine sulfate.

Antiarrhythmic Drugs Classification

  • Class I: Sodium-channel blockers.
    • Class Ia: Intermediate onset.
    • Class Ib: Short effects.
    • Class Ic: Prolonged effects.
  • Class II: Beta-blockers.
  • Class III: Potassium-channel blockers.
  • Class IV: Calcium-channel blockers.

Antiarrhythmic Medications Overview

  • Class I (e.g., Quinidine):

    • Used for: Atrial fibrillation; slows depolarization and prolongs action potential duration.
    • Adverse Effects: Diarrhea, ventricular fibrillation risk.

  • Class II (e.g., Propranolol):

    • Used for: Tachycardia, hypertension.

  • Class III (e.g., Amiodarone):

    • Used for: Ventricular arrhythmias, prolongs action potential and slows repolarization.
    • Adverse Effects: Nausea, pulmonary fibrosis risk.

  • Class IV (e.g., Verapamil):

    • Mechanism: Slows conduction at the AV node; relaxes smooth muscle, useful for angina and hypertension.