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Cardiac Physiology and Blood Components

Prevention of Tetanus in the Heart

  • Skeletal muscle can undergo tetanus (sustained contraction) ➜ useful for posture or holding a dumb-bell.

  • Complete tetanus = sustained contraction without any relaxation.

  • In myocardium, tetanus would be catastrophic:

    • Heart could not relax/fill with blood.

    • Heart could not pump blood into systemic circulation.

  • Classic clinical image: “lock-jaw” in tetanus poisoning (botulinum toxin) ≠ desired for heart.

Electrical Activity of Myocardial Contractile Cells (MCCs)

  • Action-potential tracing has three key regions:

    • Rapid depolarization due to \text{Na}^+ influx.

    • Plateau phase (unique) caused by slow “dribble” of \text{Ca}^{2+} influx that halts early repolarization.

    • Final repolarization via massive \text{K}^+ efflux.

  • Plateau delays full repolarization ➜ prolongs refractory period.

  • Mechanical twitch (blue) vs. electrical activity (red):

    • Because of plateau, electrical & mechanical events end at ~same time.

    • Cell cannot fire a second action potential until relaxation has begun ➜ myocardium cannot tetanize.

Comparison to Skeletal Muscle

  • Skeletal muscle AP is brief; ends before peak of contraction.

  • Multiple APs can arrive before relaxation ➜ temporal summation & tetanus.

  • Cardiac plateau prevents this; safety mechanism for rhythmic pump.

Electrical Activity of Myocardial Autorhythmic Cells (MACs)

  • Cells of SA node, AV node, etc. show continuous depolarization-repolarization cycles for life.

  • No true resting membrane potential (graph oscillates between \approx -60\,\text{mV} and +20\,\text{mV}).

  • Rate in complete autonomic absence ≈ 80!\text{–}!100\;\text{times/min}.

Pacemaker Potential (PP)

  • Slow depolarizing slope from -60\,\text{mV} \rightarrow -40\,\text{mV} (threshold).

  • Carried by funny current channels (I_f):

    • Permit both \text{Na}^+ influx & \text{K}^+ efflux.

    • Net inward current because electrochemical drive for \text{Na}^+ > \text{K}^+.

  • At threshold ( -40\,\text{mV} ) ➜ voltage-gated \text{Ca}^{2+} channels open ➜ rapid upstroke to +20\,\text{mV}.

  • Repolarization: \text{K}^+ channels open ➜ return to -60\,\text{mV} and re-open $I_f$ channels.

  • Cycle repeats indefinitely (* “forever” unless pathology).

Autonomic Modulation of MACs

Parasympathetic (Vagal) Influence

  • Neurotransmitter: Acetylcholine ➜ muscarinic (M2) receptors (G-protein-coupled).

  • Effects:

    • ↑ Permeability to \text{K}^+.

    • ↓ Permeability to \text{Ca}^{2+}.

  • Graphical outcome:

    • PP slope less steep; longer time to reach -40\,\text{mV}.

    • Peak depolarization rises more slowly.

  • Functional result: intrinsic rate slowed to 60!\text{–}!80\;\text{times/min} ("vagal tone").

Sympathetic Influence

  • Neurotransmitters: Norepinephrine / Epinephrine ➜ β₁-adrenergic receptors.

  • Effects:

    • ↑ Permeability to \text{Na}^+ (steeper PP).

    • ↑ Permeability to \text{Ca}^{2+} (faster upstroke).

  • Graph output: more peaks in same time span.

  • Functional result: rate > 100\;\text{times/min} (tachycardic shift).

Summary of Rates

  • No autonomic input: 80!\text{–}!100\;\text{times/min}.

  • Dominant parasympathetic tone: 60!\text{–}!80\;\text{times/min}.

  • Dominant sympathetic drive: >100\;\text{times/min}.

Autonomic Effects on Contractile Myocardium

  • Sympathetic β₁ stimulation on MCCs ➜ ↑ \text{Ca}^{2+} influx ➜ stronger ventricular force.

  • No direct parasympathetic innervation to MCCs (force is not decreased directly; rate is slowed via MACs).

Blood Composition (≈ 5!\text{–}!6\;\text{L} total)

Centrifuged Layers

  1. Hematocrit (bottom) – \approx45\% of volume.

    • Red blood cells (RBCs; erythrocytes).

    • Function: transport \text{O}2 to tissues & \text{CO}2 from tissues.

    • Carry hemoglobin; anucleate, organelle-poor ➜ “bags of Hb.”

  2. Buffy coat – <1\% of volume.

    • Leukocytes (white blood cells): cellular immune defense.

    • Platelets (thrombocytes): fragments essential for hemostasis/clotting.

  3. Plasma (top) – \approx55\% of volume.

    • Mostly water plus dissolved constituents:

      • Ions: \text{Na}^+, \text{K}^+, \text{Ca}^{2+}, \text{Cl}^-, \text{Mg}^{2+}.

      • Nutrients: glucose, fatty acids, amino acids.

      • Gases: \text{O}2, \text{CO}2.

      • Waste: urea, creatinine, etc.

    • When clotting proteins removed ➜ called serum.

  • Collectively, erythrocytes, leukocytes, & platelets are “formed elements;” only leukocytes are true, nucleated cells.

These notes capture every major & minor point, numerical value, mechanism, and clinical/physiological implication from the video transcript for thorough exam preparation.