BIOL 2040 – Cardiac Physiology (Lecture 6 Part 1) Comprehensive Study Notes

Introduction to the Circulatory System

• Three inseparable components form the cardiovascular (CV) circuit.

  1. Heart (Pump) – Generates the pressure gradient that drives blood. Blood always flows down its gradient \big(\Delta P = P{high} - P{low}\big).
  2. Blood Vessels (Pipes) – Closed conduits that distribute blood to every tissue and return it.
  3. Blood (Fluid Medium) – Carries gases, nutrients, wastes, hormones, heat, immune cells, etc. in dissolved or suspended form.

Gross Anatomy of the Heart

• Hollow, muscular organ ≈ size of a clenched fist; sits between sternum and vertebrae (ideal for CPR compression).
• Apex – pointed inferior tip; Base – superior surface where great vessels enter/exit.
• Positioning allows manual compression of chambers if intrinsic pumping fails.

Functional Concept: The Heart as a Dual Pump

• Two completely separate, simultaneous circuits:
• Right side → Pulmonary circulation (collects \text{O}2-poor / \text{CO}2-rich blood, sends it to lungs).
• Left side → Systemic circulation (receives freshly oxygenated blood and delivers it to all body tissues).
• The muscular septum prevents mixing of right & left blood.

Cardiac Chambers, Major Vessels & Flow Landmarks

• Each side has 2 chambers:
• Atrium – thin-walled receiving chamber; sends blood to its ventricle.
• Ventricle – thick-walled ejection chamber.
• Left ventricular wall is thicker – must overcome higher systemic resistance.
• Great vessels & flow order (trace one drop):

  1. Systemic veins → \text{Superior Vena Cava (SVC)} and \text{Inferior Vena Cava (IVC)}.
  2. Right Atrium (RA) → Right Ventricle (RV).
  3. Pulmonary Trunk → Right & Left Pulmonary Arteries → lung capillaries.
  4. Pulmonary Veins (4) → Left Atrium (LA) → Left Ventricle (LV).
  5. Aorta → systemic arterial tree → tissue capillaries → systemic veins → repeat.

Comparative Hemodynamics of Right vs. Left Pumps

• Both sides eject equal volumes per beat (stroke volume).
• Pulmonary circuit – low pressure, low resistance.
• Systemic circuit – high pressure, high resistance; therefore LV myocardium is thicker (“power pump”).
• Pressure (force on vessel wall) vs. Resistance (frictional opposition) dictate cardiac workload.

Cardiac Valves – One-Way Flow Regulators

General Principles

• Valves are thin flaps (cusps) that open/close passively as chamber pressure changes.
• Flow only permitted Atria → Ventricles → Outflow Arteries; back-flow prevented.

Atrioventricular Valves (AV)

• Right AV (Tricuspid) & Left AV (Bicuspid/Mitral).
• Chordae tendineae + papillary muscles anchor cusps; prevent prolapse during ventricular systole.
• Open when P{atria} > P{ventricle} (ventricular filling). Snap shut when P{ventricle} > P{atria} (ventricular contraction).

Semilunar Valves

• Pulmonary (RV → Pulmonary trunk) & Aortic (LV → Aorta) valves; each has three pocket-like cusps.
• Open once P{ventricle} > P{artery}; close as ventricular pressure falls & arterial blood fills cusps, forming a tight seal.

No Valves Between Atria & Veins

• Back-flow minimal because atrial pressure rarely exceeds venous pressure and venous entries are compressed during atrial systole.

Fibrous Skeleton of the Heart

• Dense connective tissue rings surrounding each valve.
• Provides structural support, electrical insulation between atria & ventricles, and anchoring for myocardium.

Layers of the Heart Wall

  1. Endocardium – thin epithelial lining continuous with vascular endothelium.
  2. Myocardium – bulk layer of cardiac muscle arranged in spiral/figure-8 bundles; wringing contraction efficiently raises pressure while shortening chamber.
  3. Epicardium – outer connective tissue; visceral layer of serous pericardium.
    • Developmentally, heart begins as a linear tube that loops into a complex spiral, explaining fiber orientation (see fetal looping diagram).

Pericardial Sac

• Double-walled: fibrous outer layer (anchors heart) + serous inner layer producing pericardial fluid (lubrication).
• Pericarditis – inflammation; reduces lubrication, creating painful friction.

Cellular Architecture of Cardiac Muscle

• Cardiomyocytes are short, branched, interconnected by intercalated discs containing:
• Desmosomes – mechanical tight links.
• Gap Junctions – low-resistance channels allowing ion flow/action potential spread → functional syncytium.
• No gap junctions between atria & ventricles (electrical separation maintained by fibrous skeleton); coordinated via specialized conduction system.
• Skeletal vs. Cardiac recruitment: Cardiac muscle contracts all-or-none each beat, but contraction strength is graded by [\text{Ca}^{2+}]_{cytosolic} (discussed later).

Autorhythmic & Contractile Cells

• Autorhythmic (≈1%) – initiate & conduct action potentials; do not contract.
• Contractile (≈99%) – generate force; normally do not self-initiate impulses.

Pacemaker (Autorhythmic) Potential

• These cells lack a stable resting potential; instead exhibit slow depolarization – pacemaker potential.
• Ion events (sequential):

  1. If ("funny") channels open on hyperpolarization ⇒ slow Na^+ & K^+ influx; first half of depolarization.
  2. T-type (transient) Ca^{2+} channels open at \approx -50\,\text{mV} ⇒ reach threshold \approx -40\,\text{mV}.
  3. Threshold triggers L-type (long-lasting) Ca^{2+} channels ⇒ action potential upstroke (slower than Na-dependent spikes).
  4. Opening of K^+ channels repolarizes cell; cycle restarts as If channels reopen.
    • Result: rhythmic self-excitation without neural input – autorhythmicity.

Specialized Conduction System & Timing

  1. Sinoatrial (SA) Node – primary pacemaker \approx 70\text{–}80\,\text{bpm}; in right atrial wall near SVC.
  2. Internodal / Interatrial Pathways – spread impulse through both atria (≈30\,\text{ms}).
  3. Atrioventricular (AV) Node – introduces AV nodal delay ≈100\,\text{ms} so atria finish emptying before ventricles contract (total atrial-ventricular offset ≈160\,\text{ms}).
  4. Bundle of His → Right & Left Bundle Branches (interventricular septum).
  5. Purkinje Fibers – spread impulse through ventricular myocardium in ≈30\,\text{ms}; ventricles contract as one.
  6. Intrinsic rates if pacemakers fail: AV Node \approx 40\text{–}60\,\text{bpm}; Purkinje \approx 20\text{–}40\,\text{bpm}.

Action Potential in Contractile Cardiomyocytes

• Resting potential \approx -80\,\text{mV}.
• Triggered by pacemaker input → sequence:

  1. Fast Na^+ influx (INa) – rapid depolarization to +50\,\text{mV}.
  2. Opening of Transient K^+ (Ito) counters with brief efflux.
  3. L-type Ca^{2+} influx (ICa,L) + Delayed Rectifier K^+ efflux (IK) create long plateau ≈200\,\text{ms}.
  4. Termination as Ca^{2+} channels inactivate; continued K^+ efflux repolarizes back to rest.
    • Purpose of plateau:
    • Maintains contraction for effective ejection.
    • Produces long refractory period ≈250\,\text{ms} preventing tetanus (vital so heart can relax & refill).

Excitation-Contraction (E-C) Coupling & Ca^{2+} Handling

• L-type channels in T-tubules admit extracellular Ca^{2+}.
• This triggers massive Ca^{2+}-induced Ca^{2+} release from sarcoplasmic reticulum (SR) (≈90\% of total).
• Ca^{2+} binds troponin → cross-bridge cycling → contraction.
• Modulating cytosolic Ca^{2+} adjusts contraction strength (inotropism):
• Less Ca^{2+} → shorter/weaker beats; more Ca^{2+} → longer/stronger beats & extended plateau.
• Drugs (e.g., calcium channel blockers, digitalis) exploit this.

Electrocardiogram (ECG/EKG)

• Surface recording of summed electrical activity transmitted through body fluids; NOT a single action potential.
• Standard waveforms:
• P wave – atrial depolarization.
• PR segment – AV nodal delay.
• QRS complex – ventricular depolarization (masks atrial repolarization).
• ST segment – ventricular systole (contraction & ejection).
• T wave – ventricular repolarization.
• TP interval – diastole (relaxation & filling).

Clinical Correlates – Rate & Rhythm Disorders

Heart Rate

• Normal (Resting): 70\text{–}80\,\text{bpm}.
• Tachycardia: >100\,\text{bpm} (stress, fever, hyperthyroid, etc.).
• Bradycardia: <60\,\text{bpm} (endurance training, vagal tone, AV block).

Rhythm (Arrhythmias)

• Extrasystole / Premature Ventricular Contraction (PVC) – early ectopic beat; sensation of “skipped” or “flutter.”
• Atrial Flutter – rapid regular atrial depolarizations 200\text{–}380\,\text{bpm}; ventricles conduct in 2{:}1 or 3{:}1 ratios → ↓ filling & output.
• Atrial Fibrillation – chaotic atrial activity; no identifiable P waves; irregular ventricular rhythm.
• Ventricular Fibrillation – lethal, random ventricular excitation; requires immediate defibrillation to reset.
• Heart Block – impaired AV conduction.
• Partial (2:1, 3:1) – some impulses fail.
• Complete – atria paced by SA node, ventricles by own slow ectopic pacemaker.

Cardiac Myopathies

• Myocardial Ischemia – insufficient \text{O}_2 supply.
• Acute Myocardial Infarction (AMI / Heart Attack) – necrosis from vessel occlusion/rupture; identified on ECG & cardiac enzymes.

Key Timing & Numerical References (all clinically significant)

• SA node intrinsic rate: 70\text{–}80\,\text{bpm}.
• Atrial excitation spread: 30\,\text{ms}.
• AV nodal delay: \approx 100\,\text{ms}.
• A-V contraction offset: \approx 160\,\text{ms}.
• Purkinje ventricular spread: \approx 30\,\text{ms}.
• Plateau duration: \approx 200\,\text{ms}.
• Refractory period: \approx 250\,\text{ms}; total systole \approx 300\,\text{ms}.

Integrative & Ethical Considerations

• Synchrony between right & left hearts is critical for matching pulmonary & systemic flows; imbalances cause pulmonary or systemic congestion.
• Understanding electrical conduction guides placement of artificial pacemakers, interpretation of ECGs, and application of defibrillation.
• CPR effectiveness relies on anatomical positioning (heart between sternum & vertebral column).
• Up-to-date knowledge on calcium handling drives pharmacologic therapy for hypertension, arrhythmia, and heart failure.
• Respect for patient data & copyrighted educational materials aligns with professional ethics and institutional policies.

Quick Study Checklist (Self-Test Prompts)

  1. Trace one red blood cell from SVC to aorta naming every chamber & valve.
  2. Explain why the AV nodal delay is life-saving.
  3. Sketch & label the pacemaker potential and a contractile cell AP; list ions involved.
  4. Correlate each ECG segment with underlying electrical & mechanical events.
  5. Predict effects of blocking L-type Ca^{2+} channels on heart rate, contractility, and AP shape.
  6. Distinguish atrial flutter vs. fibrillation vs. ventricular fibrillation on ECG and in terms of hemodynamic impact.