Heart – Coronary Circulation

Due‐Date Logistics

  • Lecture video assignments are due at 11:59\,\text{PM} on the listed calendar date.
  • After the due‐date time passes, the lecture becomes unavailable.

Transdermal Estrogen Patch, Hormonal Birth-Control & Clotting

  • Question addressed: Why does the Zulane (transdermal) estrogen patch carry a higher clotting risk?
    • Patch delivers a higher dose of estrogen than current low-dose oral contraceptives.
    • Historical context:
    • \approx 20 years ago, oral contraceptives contained much higher estrogen doses; dosage has since decreased to reduce adverse events.
    • Empirical observation: High-dose estrogen → elevated clotting risk.
    • Mechanistic hypothesis: estrogen stimulates the liver to synthesize more clotting factors, pre-priming the coagulation cascade.
  • Comparative hormone notes:
    • Birth-control formulations may contain estrogen, progesterone, progestin, or both.
    • Progesterone downsides:
    • Historically feared for a higher association with certain cancers.
  • Two classic fears surrounding hormonal birth control:
    1. Clot formation (thrombosis / embolism).
    2. Cancer risk (especially with progesterone).

Macroscopic Heart Function – Two Circuits, One Blood

  • Heart has two functional components/circuits yet handles a single, continuous blood volume.
    1. Pulmonary circuit – sends deoxygenated blood to the lungs for gas exchange.
    2. Systemic circuit – sends oxygenated blood to the body to deliver \text{O}2 & nutrients; returns \text{CO}2-rich blood.
  • Conceptual image: a figure-8 loop with the heart located at the crossover point.
  • Flow sequence (simplified):
    • Heart → Lungs → Heart → Body → Heart → Lungs → … (repeats indefinitely).

Slide/Content Guidance (Lab vs. Lecture)

  • Slides 2–3: material required for both lab & lecture.
  • Slides 4–11 (& many others flagged skip): lab-only visuals or supplemental photographs (e.g., gross heart images) — not examinable in lecture.
  • Lecture content formally starts at slide 27 (Coronary Circulation).

Coronary Circulation

  • Definition: Network of coronary arteries & coronary veins that supply the myocardium itself.
  • Rationale: Blood inside heart chambers cannot adequately perfuse thick cardiac muscle; dedicated vessels are required.
  • Major named vessels (recognition unnecessary for lecture):
    • Right Coronary Artery (RCA).
    • Left Coronary Artery (LCA) → branches (e.g., LAD, circumflex).
    • Cardiac veins draining into the coronary sinus on the posterior heart before re-entering the right atrium.

Myocardial Infarction (Heart Attack)

  • Mechanism: Occlusion of a coronary artery → interrupted blood flow → ischemia → death of myocardial cells (infarction).
    • Common obstructive agents:
    • Atherosclerotic plaque.
    • Traveling embolus lodging in narrowed region (becomes an embolism).
  • High metabolic demand: Heart muscle survives only 1–2 minutes without \text{O}_2.
  • Distinction: Blockage occurs in coronary circulation, not the pulmonary or systemic return vessels.

Clinical Interventions

  • Stent (Balloon or Mesh)
    • Inserted via catheter to widen a narrowed coronary artery; reinforces lumen to prevent future closure.
  • Coronary Artery Bypass Grafting (CABG)
    • Surgical creation of an alternate pathway using an autologous vessel (e.g., saphenous vein, internal mammary artery).
    • Terminology:
    • Triple bypass = 3 separate grafts.
    • Quadruple bypass = 4 grafts, etc.
    • Goal: Performed prophylactically (before a large MI) or post-minor MI to restore adequate perfusion.

Diagnostic & Risk-Assessment Tools

  • Blood tests: Persistent elevation of lipids (e.g., high LDL, high triglycerides), abnormal cardiac enzymes post-event, inflammatory markers.
  • Imaging: Echocardiogram, coronary angiography, CT calcium scoring — visualizes vessel patency & detects scar tissue.
  • Risk factors
    • Genetics (primary).
    • Lifestyle / Metabolic: high BMI, poor diet (high saturated fat, processed carbs), hypertension, sedentary behavior, metabolic syndrome.
    • Endocrine influences (e.g., chronically elevated cortisol) may exacerbate lipid profile & vascular damage.

Stroke vs. Heart Attack – Shared Pathophysiology

  • Both are manifestations of an embolism in a critical organ:
    • Stroke: embolism in cerebral artery.
    • MI: embolism in coronary artery.
  • Same modifiable & non-modifiable risk spectrum governs probability of either event.

Tissue Damage, Healing & Scar Formation

  • Extent & depth of injury dictate scar formation.
    • Minor cuts → usually no scar (epithelial regeneration suffices).
    • Large/abrasive wounds (e.g., motorcycle road rash) → connective-tissue scar deposition.
  • In myocardium:
    • Necrotic cardiomyocytes removed; void filled by non-contractile scar tissue (fibrosis).
    • Scarred regions detectable years later via imaging; cannot contribute to contractile output.

Cardiac Muscle Cell (Histology Refresher)

  • Key structures:
    • Myofibrils (actin–myosin sliding filament).
    • Intercalated discs containing gap junctions & desmosomes.
    • Gap junctions enable rapid, electrically coupled action-potential propagation across myocardium.

Preview: Cardiac Action Potentials (to be covered in depth next session)

  • Students should review A&P I action-potential basics:
    • Resting-membrane potential, depolarization, repolarization phases.
    • Ionic players: \text{Na}^+ influx, \text{K}^+ efflux, role of \text{Ca}^{2+} in contractile tissue.
  • Instructor will upload \approx 10–15 refresher slides to Canvas.

Administrative / Lecture Flow Notes

  • Remaining portion of today’s lecture postponed to prevent half-covered action-potential content; will resume after upcoming test.
  • Students encouraged to spend the interim reviewing:
    • Lab worksheet (focus of practical).
    • Action-potential mechanisms.
    • Coronary-circulation clinical correlations.