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 influx.
Plateau phase (unique) caused by slow “dribble” of influx that halts early repolarization.
Final repolarization via massive 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 and ).
Rate in complete autonomic absence ≈ .
Pacemaker Potential (PP)
Slow depolarizing slope from (threshold).
Carried by funny current channels ():
Permit both influx & efflux.
Net inward current because electrochemical drive for > .
At threshold ( ) ➜ voltage-gated channels open ➜ rapid upstroke to .
Repolarization: channels open ➜ return to 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 .
↓ Permeability to .
Graphical outcome:
PP slope less steep; longer time to reach .
Peak depolarization rises more slowly.
Functional result: intrinsic rate slowed to ("vagal tone").
Sympathetic Influence
Neurotransmitters: Norepinephrine / Epinephrine ➜ β₁-adrenergic receptors.
Effects:
↑ Permeability to (steeper PP).
↑ Permeability to (faster upstroke).
Graph output: more peaks in same time span.
Functional result: rate > (tachycardic shift).
Summary of Rates
No autonomic input: .
Dominant parasympathetic tone: .
Dominant sympathetic drive: >100\;\text{times/min}.
Autonomic Effects on Contractile Myocardium
Sympathetic β₁ stimulation on MCCs ➜ ↑ influx ➜ stronger ventricular force.
No direct parasympathetic innervation to MCCs (force is not decreased directly; rate is slowed via MACs).
Blood Composition (≈ total)
Centrifuged Layers
Hematocrit (bottom) – of volume.
Red blood cells (RBCs; erythrocytes).
Function: transport to tissues & from tissues.
Carry hemoglobin; anucleate, organelle-poor ➜ “bags of Hb.”
Buffy coat – <1\% of volume.
Leukocytes (white blood cells): cellular immune defense.
Platelets (thrombocytes): fragments essential for hemostasis/clotting.
Plasma (top) – of volume.
Mostly water plus dissolved constituents:
Ions: , , , , .
Nutrients: glucose, fatty acids, amino acids.
Gases: , .
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.