11+C-Cardiovascular+Physiology

Heart and Circulation

• Lecturer: Dr. R. Ahangari

• Institution: University of Central Florida, Orlando

• Textbook: Human Physiology by Linda S. Constanzo

• Reference: Medline Plus

Myocardial Cells

Nodal/Conducting Cells

• Contract weakly due to few myofibrils.

• Spontaneously generate action potentials without nervous input (self-excitability).

• Rapidly conduct action potentials to heart muscle.

• Key Structures:

  • Sinoatrial node (SA node): Primary pacemaker located in upper right atrium; initiates action potentials.

  • Atrioventricular node (AV node): Receives impulses from atria before conducting to ventricles.

  • Bundle of His: Pathway for impulse transmission from AV node to ventricles.

  • Purkinje Fibers: Distributes impulse quickly throughout ventricular muscle.

Conducting System of the Heart

• Action potentials spread from SA node to both atria, leading to contraction.

• Atria electrically isolated from ventricles; impulses must pass through AV node.

• After passing through Bundle of His, impulses trigger ventricular contraction via Purkinje Fibers.

Autonomic Effects on Heart Rate and Conduction Velocity

• Chronotropic Effects:

  • Negative Chronotropic: Decreases heart rate (decreased firing of SA node).

  • Positive Chronotropic: Increases heart rate (increased firing of SA node).

• Dromotropic Effects:

  • Negative Dromotropic: Decreases conduction velocity through AV node.

  • Positive Dromotropic: Increases conduction velocity through AV node.

• Inotropic Effects:

  • Negative Inotropic: Decreases force of contraction.

  • Positive Inotropic: Increases force of contraction.

Heart and the Autonomic Nervous System

• Sympathetic Responses:

  • β1 receptors: Positive chronotropic and inotropic effects, vasodilation of coronary arteries.

• Parasympathetic Responses:

  • Negative chronotropic and inotropic effects.

Normal Heartbeat and Arrhythmias

• Normal heart beats 50-99 times/min.

• Arrhythmias: Abnormal impulse formation/conduction

  • Sinus Tachycardia: Heart rate > 100/min.

  • Sinus Bradycardia: Heart rate < 50-60/min.

Supraventricular and Ventricular Arrhythmias

• Supraventricular Arrhythmia: Extra impulses from atria or AV node cause irregular heartbeats.

  • Atrial Extrasystole: Deformed P wave, normal QRS complex.

  • Nodal Extrasystole: Retrograde stimulation, masked or late P wave.

• Ventricular Extrasystole: Ectopic impulses from distal areas of His-Purkinje system.

  • Deformity in QRS complex.

Causes of Ventricular Extrasystole

• Ischemia, certain medications (e.g., digoxin), myocarditis, cardiomyopathy, hypoxia, hypercapnia, mitral valve prolapse, substance abuse (caffeine, alcohol, cocaine), electrolyte imbalances, thyroid issues, heart attack.

Symptoms of Ventricular Extrasystole

• Chest pain, faint feelings, fatigue, hyperventilation after exercise, potential development of ventricular tachycardia from frequent PVCs.

Treatment of PVCs

• Restoration of Electrolyte Balance: Importance of magnesium and potassium.

• Pharmacological Agents:

  • Class I Agents: Sodium channel blockers (Lidocaine, Phenytoin).

  • Class II Agents: Beta-blockers (Atenolol, Propranolol, Metoprolol) decrease sympathetic activity.

  • Class III Agents: Block potassium channels (Sotalol), prolong repolarization.

  • Class IV Agents: Calcium channel blockers (Verapamil, Diltiazem) decrease contractility and conduction through AV node.

Cardiac Output and Ejection Fraction

• Definitions:

  • Stroke Volume: Volume ejected per heartbeat.

  • Cardiac Output (CO): Amount of blood pumped by each ventricle in one minute (CO = Stroke Volume x Heart Rate).

  • Ejection Fraction: Measurement of contractility (normally 55%).

Cardiac Cycle

• Steps:

  • Isovolumetric Contraction: Ventricles contract with no blood ejection.

  • Ventricular Ejection: Blood is ejected when ventricle pressure exceeds aortic pressure.

  • Isovolumetric Relaxation: Ventricles relax and pressure drops.

  • Ventricular Filling: Blood fills the ventricles once the AV valve opens.

Heart Sounds

• Heart valve closure generates sounds:

  • First sound: AV valves closure (low pitch).

  • Second sound: Aortic/pulmonary valves closure (high pitch).

  • Third sound may occur due to ventricle filling (hard to hear).

Atherosclerosis

• Formation of plaques (atheromas) in arteries leading to blockages impacting heart function.

• Risk Factors: Dyslipidemia, diabetes, smoking, sedentary lifestyle, obesity, hypertension.

Inflammatory Response in Atherosclerosis

• Initiated by endothelial injury, leading to inflammation, cell migration, plaque formation, and potential rupture.

Atrial Fibrillation and Flutter

• Irregular heart rhythms: atria out of sync with ventricles.

• Atrial flutter: fast regular atrial contractions vs. atrial fibrillation: irregular contractions.

Heart Murmurs

• Caused by turbulent blood flow, can be physiological or pathological (stenosis, valvular insufficiency).