Cardiac Muscle Properties

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Cardiac Muscle Histology - Tiny Heart Builders

  • Myocytes: Short, branched, striated; central single nucleus (occasionally two).
  • Intercalated Discs: Unique step-like junctions connecting myocytes.
    • Gap Junctions (Longitudinal): Rapid electrical spread; key to functional syncytium.
    • Desmosomes (Transverse/Longitudinal): Bind cells, resist mechanical stress.
    • Fascia Adherens (Transverse): Anchor actin to sarcolemma.
  • Sarcoplasmic Reticulum: Less developed; forms dyads (not triads) with T-tubules.
  • T-tubules: Larger diameter, at Z-lines (one per sarcomere).
  • Mitochondria: Abundant (up to 40% cell volume), for high energy needs. Cardiac Muscle Micrograph with Key Features Labeled

⭐ Intercalated discs with gap junctions allow cardiac muscle to function as a syncytium.

Cardiac Electrophysiology - Spark of Life

  • Resting Membrane Potential (RMP):
    • Ventricular: -90 mV; SA Node: -55 to -60 mV.
    • Maintained by $K^+$ efflux ($I_{K1}$).
  • Ventricular Action Potential (AP): Duration ~250-300 ms.
    • Phase 0: Rapid Depolarization (↑ Na+ influx).
    • Phase 1: Early Repolarization (↑ K+ efflux, $I_{to}$).
    • Phase 2: Plateau (↑ $Ca^{2+}$ L-type vs K+ efflux).
    • Phase 3: Rapid Repolarization (↑ K+ efflux).
    • Phase 4: RMP.
  • Pacemaker Potential (SA/AV Node): Automaticity.
    • Phase 4: Spontaneous Depolarization (↑$I_f$ Na$^+$; ↑T-type $Ca^{2+}$).
    • Phase 0: Depolarization (↑L-type $Ca^{2+}$).
    • Phase 3: Repolarization (↑ K+ efflux).

⭐ Phase 0 of ventricular action potential is due to rapid Na+ influx, while in SA node it's due to $Ca^{2+}$ influx (L-type channels). 📌 Sodium for Strong (ventricular), Calcium for Commencement (SA node).

Cardiac action potential phases and ion flow

Excitation-Contraction Coupling - The Cardiac Hug

  • Initiation: Action potential (AP) travels down sarcolemma & T-tubules.
  • Ca2+ Entry: Depolarization opens L-type Ca2+ channels (Dihydropyridine receptors - DHPR).
    • Influx of extracellular Ca2+ ("trigger calcium").
  • CICR (Calcium-Induced Calcium Release):
    • Trigger Ca2+ activates Ryanodine Receptors (RyR2) on Sarcoplasmic Reticulum (SR).
    • Massive Ca2+ release from SR into cytosol.

    ⭐ Cardiac muscle relies on Calcium-Induced Calcium Release (CICR) from the sarcoplasmic reticulum for contraction.

  • Contraction Cascade:
    • Ca2+ binds Troponin C (TnC).
    • Conformational change in Troponin complex.
    • Tropomyosin shifts, exposing myosin-binding sites on actin.
    • Actin-myosin cross-bridge cycling → muscle contraction.
  • Relaxation:
    • Ca2+ reuptake into SR by SERCA2a pump (ATP-dependent).
    • Ca2+ extrusion from cell by Na+/Ca2+ exchanger (NCX) & Plasma Membrane Ca2+-ATPase (PMCA).

Cardiac Muscle Excitation-Contraction Coupling

Mechanical Properties & Regulation - Pumping Powerhouse

  • Contractility (Inotropy): Myocardial force generation capability.
    • ↑ by: Sympathetic (β1 receptors), Catecholamines, Ca²⁺, Digitalis.
    • ↓ by: Parasympathetic (M2 receptors, mainly atria), Hypoxia, Acidosis.
  • Frank-Starling Law: ↑ Preload (End-Diastolic Volume, EDV) → ↑ Stroke Volume (SV).

    ⭐ The Frank-Starling mechanism states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the ventricles (the end diastolic volume) when all other factors remain constant.

  • Preload: Stretch on ventricle at end-diastole.
  • Afterload: Resistance ventricle overcomes to eject blood.
  • Key Metrics:
    • Cardiac Output (CO): $CO = SV \times HR$.
    • Ejection Fraction (EF): $EF = (SV / EDV) \times 100$. Normal: 55-70%.
  • Autonomic Nervous System (ANS) Control:
    SystemHR (Chronotropy)Inotropy (Contractility)Dromotropy (Conduction)Lusitropy (Relaxation)
    Sympathetic (β1)↑ (AV Node)
    Parasympathetic (M2)↓ (Atria)↓ (AV Node)Negligible
    📌 Sympathetic = Speeds up & Strengthens heart.

Autonomic regulation of cardiac muscle

High‑Yield Points - ⚡ Biggest Takeaways

  • Cardiac muscle: a functional syncytium via gap junctions in intercalated discs for coordinated contraction.
  • Autorhythmicity from unstable pacemaker potentials in specialized cardiac cells.
  • The entire myocardium adheres to the all-or-none law.
  • Long absolute refractory period (ARP) is crucial to prevent cardiac tetany.
  • Excitation-contraction coupling depends on Calcium-Induced Calcium Release (CICR).
  • Frank-Starling mechanism allows adaptation to changing preload (venous return).
  • Extracellular Ca²⁺ influx during plateau phase is vital for contractile force.

Practice Questions: Cardiac Muscle Properties

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What is the role of gap junctions in cardiac muscle function?

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Flashcards: Cardiac Muscle Properties

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Which type of muscle fibres undergo hypertrophy ONLY?_____

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Which type of muscle fibres undergo hypertrophy ONLY?_____

Skeletal, Cardiac

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