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Cardiac Muscle & Circulatory Physiology Review

Circulatory Overview

  • Primary role of the heart: generate pressure to move blood ➔ maintains two distinct but linked circuits.
    • Systemic circulation = oxygen-rich blood delivery to entire body.
    • Pulmonary circulation = oxygen-poor blood to lungs for gas exchange.
  • Sequence (starting in systemic side for orientation):
    • Left ventricle (LV) contracts ➔ ejects blood into aorta.
    • Aorta repeatedly bifurcates → arteries → arterioles → capillary beds serving all tissues ("big toe, brain, GI tract, pancreas, skeletal muscle, kidneys," and even the myocardium itself via coronary arteries).
    • After oxygen drop-off & waste pick-up, de-oxygenated blood returns via superior + inferior vena cavae to right atrium (RA) ➔ right ventricle (RV).
    • RV pumps through pulmonary arteries → lungs (located lateral to heart in thoracic cavity/mediastinum) ➔ CO₂ unloaded, O₂ loaded.
    • Oxygen-rich blood moves through pulmonary veins → left atrium (LA) ➔ LV and the cycle repeats.
  • Side distinction shorthand:
    • Right side = "oxygen-poor".
    • Left side = "oxygen-rich".

Heart Anatomy & Spatial Orientation

  • Human-anatomy convention: described from specimen’s point of view (patient facing you). Your left hand = specimen’s right side, etc.
  • Chambers
    • 2 atria (RA, LA)
    • 2 ventricles (RV, LV)
  • Atria—especially LA—are more posterior; anterior heart views mainly show both ventricles + RA auricle.
  • Heart sits in mediastinum between right & left lungs inside thoracic cavity.
  • Drawings sometimes place aorta exit anteriorly for clarity; reality: aorta ascends from LV’s superior border and arches posteriorly.

Systemic vs Pulmonary Circuit Pressures

  • Blood flows down pressure gradients (higher ➔ lower); absolute value less important than relative difference.
  • Typical systemic arterial blood pressure: 120\,\text{mmHg}/80\,\text{mmHg}
    • 120 = LV systolic (contracted)
    • 80 = LV diastolic (relaxed)
  • Returning venous pressure to RA is single-digit mmHg.
  • RV/pulmonary circuit operates at much lower peak pressures than LV/systemic circuit.

Physics of Pressure–Volume Relationships

  • Two distinct “volumes” to track:
    1. Volume of the container (chamber or vessel diameter changes).
    2. Volume of the fluid (amount of blood present).
  • Container rule (inverse relationship):
    • ↑ Chamber volume ➔ ↓ Pressure.
    • ↓ Chamber volume (e.g.
      ventricular systole) ➔ ↑ Pressure.
  • Fluid rule (direct relationship):
    • ↑ Blood volume ➔ ↑ Pressure (balloon filling analogy).
    • ↓ Blood volume ➔ ↓ Pressure (hemorrhage → hypovolemia → hypotension).
  • Water-balloon metaphors illustrate both:
    • Adding water (fluid increase) raises pressure until balloon bursts.
    • Squeezing fixed-volume balloon (container decrease) likewise raises internal pressure until rupture.

Phases of the Left Ventricular Cycle

  • End-Systolic Volume (ESV)
    • Blood remaining in LV immediately after contraction.
  • Passive Ventricular Filling (early diastole)
    • Blood flows LA → LV mainly via gravity + pressure gradient while LV pressure is lower than LA pressure.
  • Atrial Systole (late diastole)
    • LA contracts to push final blood into LV once LV pressure nears LA pressure.
  • End-Diastolic Volume (EDV)
    • Max blood in LV just before it contracts.
    • Aortic pressure still > LV pressure, so aortic valve closed.
  • Ventricular Systole / Ejection
    • LV muscle contracts (container shrinks) + has full EDV (fluid increase) ➔ rapid pressure rise.
    • When P{LV} > P{aorta}, aortic valve opens; blood ejected into systemic circulation.
  • Dual mechanisms raising LV pressure before ejection:
    1. Increased fluid volume (EDV).
    2. Decreased chamber size (muscle contraction).

Cardiac Output (CO) Calculations

  • Definition: Volume of blood pumped by LV per unit time (≈ L · min⁻¹).
  • Formula: CO = HR \times SV
    • HR = heart rate (beats · min⁻¹)
    • SV = stroke volume (mL · beat⁻¹)
  • SV = EDV - ESV
  • Numerical example from transcript:
    • Given EDV = 100\,\text{mL}
    • ESV = 20\,\text{mL}
    • SV = 100 - 20 = 80\,\text{mL}
    • Assume HR = 70\,\text{beats·min}^{-1}
    • CO = 70\,\text{beats·min}^{-1} \times 80\,\text{mL·beat}^{-1} = 5600\,\text{mL·min}^{-1}
    • Convert: 5600\,\text{mL} = 5.6\,\text{L} ➔ CO \approx 5.6\,\text{L·min}^{-1}
    • Matches total blood volume (≈5-6 L) ➔ entire blood volume circulates once per minute.

Cardiac Muscle Cell Types

  • Myocardium ("myo" = muscle, "cardium" = heart) contains two cell classes:
    1. Myocardial Contractile Cells (MCCs)
    • Perform force generation & ejection, analogous to skeletal muscle fibers.
    1. Myocardial Autorhythmic Cells (MACs)
    • Generate & propagate electrical impulses that dictate timing/rate; covered in later lecture.

Excitation–Contraction Coupling in MCCs

  • Structural parallels to skeletal muscle
    • Sarcoplasmic reticulum (SR)
    • T-tubules
    • Troponin/tropomyosin regulated thin filaments
  • Key molecular players (with cardiac twists):
    1. Voltage-gated Calcium Channel (VGCC) in T-tubule membrane (analogue of DHP receptor).
    • Voltage-sensitive but permits actual Ca²⁺ influx (unlike skeletal DHP which is voltage sensor only).
    1. Ryanodine Receptor (RyR) on SR membrane is ligand-gated (not mechanically gated).
    • Ligand = Ca²⁺ (coming from VGCC ingress).
  • Process (Calcium-Induced Calcium Release, CICR):
    • MAC depolarization reaches MCC ➔ action potential travels along sarcolemma/T-tubule.
    • VGCC opens ➔ extracellular Ca²⁺ enters cell.
    • Ca²⁺ binds RyR ➔ SR releases large Ca²⁺ pool into cytosol.
    • Cytosolic Ca²⁺ binds troponin ➔ tropomyosin moves ➔ cross-bridge cycling & contraction (sliding-filament theory same as skeletal muscle from here).

Ion Removal & Homeostasis Post-Contraction

  • SR Ca²⁺-ATPase (SERCA) pumps Ca²⁺ back into SR (primary active transport).
  • Na⁺/K⁺-ATPase restores Na⁺ & K⁺ gradients (3 Na⁺ out / 2 K⁺ in per ATP).
  • NCX (Na⁺/Ca²⁺ Exchanger)
    • Secondary active antiporter: 3 Na⁺ in (down gradient) drive 1 Ca²⁺ out (against gradient).
    • Prevents cytosolic Ca²⁺ overload & permits relaxation.
    • Potential depolarizing Na⁺ influx instantly countered by Na⁺/K⁺-ATPase to avoid unintended action potentials; ensures MCCs fire only when orchestrated by MACs.

Skeletal vs Cardiac Muscle – Key Differences Highlighted

  • Skeletal: Mechanical coupling between DHP & RyR; no need for external Ca²⁺ entry.
  • Cardiac: CICR—requires initial extracellular Ca²⁺ influx; RyR is Ca²⁺-gated.
  • Functional consequence: Cardiac muscle cannot enter tetanus because refractory period matches contraction length (topic foreshadowed for future lecture).

Examples, Analogies, & Real-World Relevance

  • Water-balloon analogy used twice: illustrates both fluid-volume–pressure (fluid addition) and container-volume–pressure (squeezing) principles.
  • Hypovolemia (severe bleed) ➔ ↓ plasma volume ➔ ↓ pressure gradients ➔ impaired tissue perfusion.
  • Coronary arteries = systemic branches specifically serving myocardium (heart "feeds itself").
  • Understanding LV pressure/volume important for diagnosing heart failure, calculating ejection fraction, and managing blood pressure therapeutically (e.g., antihypertensives target systemic pressure).
  • Normal CO ≈ 5 – 6 L·min⁻¹ reaffirms why alterations in HR or SV (exercise, disease) have systemic implications.

Ethical & Clinical Considerations (Implicit)

  • Maintaining adequate perfusion critical for organ health; rapid recognition/management of hypovolemia can be lifesaving.
  • Pharmacologic manipulation of Ca²⁺ channels or NCX affects contractility—therapeutic potential (e.g., calcium channel blockers) but requires caution to avoid compromising CO.