Lecture: Drugs Affecting the Cardiovascular and Hematological System

Cardiac Cycle

• Duration: From the beginning of one heartbeat to the next.
• Systole: Ventricles contract, increasing pressure; mitral and tricuspid valves close; blood ejected into aorta and pulmonary artery.
• Diastole: Ventricles relax, mitral and tricuspid valves open, blood flows into atria.
• Atrial contraction pushes blood into ventricles.
• Blood flow sequence:
  • Unoxygenated blood returns to right atrium via vena cava.
  • To right ventricle, then to lungs via pulmonary artery.
  • Oxygenated blood returns to left atrium, then left ventricle.
  • Blood is ejected to body via aorta.

Stroke Volume

• Amount of blood leaving left ventricle per contraction (~75 ml).
• Dependent on:
  • Preload: Stretching force by blood in heart at end of diastole.
    • Affected by venous return, atrial contractility, and ventricular blood volume.
  • Contractility: Force of ventricular contraction.
    • Influenced by heart muscle health and catecholamine concentration.
  • Afterload: Resistance left ventricle must overcome to eject blood.

Cardiac Output

• Volume of blood leaving the left ventricle in 1 minute.
• Calculated by: Stroke Volume x Heart Rate
• Compensatory mechanisms adjust heart rate or stroke volume to maintain cardiac output.

Heart Failure

• Low cardiac output; heart unable to meet body's metabolic demands.
• Compensatory Mechanisms: Chronic sympathetic nervous system activation, RAAS system.
  • RAAS System: Renin release triggers angiotensin I conversion to angiotensin II.
    • Leads to vasoconstriction and sodium retention.
• Drug Therapy: Aims to improve cardiac function by altering heart's influencing factors.
  • ACE Inhibitors & ARBs: Interrupt RAAS, reduce vasoconstriction, fluid retention.
  • Beta-Blockers: Decrease heart workload and oxygen needs.
  • Calcium Channel Blockers & Digoxin: Affect contraction force and efficiency.
  • Diuretics: Reduce fluid retention.

Drug Classes and Their Effects

ACE Inhibitors

• Example: Captopril
• Mechanism: Inhibits angiotensin-converting enzyme, reducing angiotensin II production.
• Effects: Vasodilation, decreased blood volume, improved cardiac output.
• Adverse Effects: Cough, hyperkalemia, angioedema, neutropenia.
• Contraindications: Pregnancy, risk of teratogenicity.

Beta-Adrenergic Blockers

• Types: Non-selective (Propranolol), Selective (Metoprolol)
• Mechanism: Block beta receptors, reducing heart rate, contractility.
• Effects: Lowered cardiac output, blood pressure, oxygen demand.
• Adverse Effects: Bronchospasms, hypotension, hypoglycemia.
• Usage: Hypertension, angina, heart failure.

Cardiac Glycosides

• Example: Digoxin
• Mechanism: Increases cardiac contractility by affecting calcium movement.
• Effects: Increased cardiac output, delayed AV node conduction.
• Adverse Effects: Toxicity risks with electrolyte imbalance, bradycardia.
• Usage: Heart failure, atrial fibrillation.

Nursing Considerations

• Patient Education: Importance of medication adherence, monitoring blood pressure, heart rate.
• Monitoring: Electrolyte levels, signs of toxicity, kidney function.

Newer Drug Classes

Nesiritide

• Mechanism: Vasodilator, similar to B-natriuretic peptide.
• Usage: Acute heart failure management.

Angiotensin Receptor Neprilysin Inhibitors

• Example: Entresto
• Mechanism: Modulates natriuretic system, inhibits neprilysin.
• Effects: Decreased preload, afterload, improved heart failure symptoms.