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Effects of ANS on Cardiac Conduction

Effects of ANS on Cardiac Conduction. Vagal Stimulation. Distributed to the SA and AV nodes, lesser extent to atria muscles, even less ventricular muscle Decrease strength of contraction by 20-30%. Distribution reflects direct change in heart rate rather than decrease strength of contraction.

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Effects of ANS on Cardiac Conduction

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  1. Effects of ANS on Cardiac Conduction

  2. Vagal Stimulation • Distributed to the SA and AV nodes, lesser extent to atria muscles, even less ventricular muscle • Decrease strength of contraction by 20-30%. • Distribution reflects direct change in heart rate rather than decrease strength of contraction

  3. Vagal Stimulation cont’d • Parasympathetic stimulation  acetylcholine (Ach) released at vagal endings to: 1. ↓Rhythm of SA node 2. ↓Excitability of AV junctionalfibers between atrial muscle and AV node to slow transmission of cardiac impulse to ventricles

  4. Vagal Effects: Ventricular Escape • Weak-moderate vagal stimulation slows heart rate to 50% of normal rate. • Strong vagal stimulation: completely halt excitation by the SA node or fully block transmission from atria to ventricles via the AV node. • Leading to ventricles stop beating for 15-20 secs • Purkinje fibers develop own rhythm and contract at 15-40bmp

  5. Mechanism of Vagal Effects • Ach increases permeability to K+ ions  rapid leak of K+ out of muscle fibers  increased negativity inside fibers  hyperpolarization • Tissue much less excitable! • Hyperpolarization: ↓ resting membrane to -65 to -75, compared to -55 to -65 millivolts. • Need more inward Na+ and Ca+ to reach threshold potential for excitation. • Therefore: moderate changes delays conduction and large changes blocks conduction entirely.

  6. Sympathetic Stimulation • Distributed all parts of heart but mainly to ventricles • Cardiac output can be increased 2-3x, up to 180-250 bpm. • Increase force of contraction (2x) ↑volume of blood pumped  ↑ ejection pressure

  7. Sympathetic Effects • Opposite effects as vagal stimulation • Increase rate of SA nodal discharge • Increase rate of conduction and level of excitability of entire heart. • Increases force of contraction of atrialadn ventricular muscle. • Therefore: increases overall activity of heart!

  8. Sympathetic Mechanism • Norephinephrine (NE) released at sympathetic nerve endings  ↑permeability of fiber to Na+ and Ca+  more positive resting potential in SA node to threshold level  ↑ excitability and heart rate.

  9. Sympathetic Mechanism cont’d • In AV node and AV bundles, ↑ permeability easier for AP to excite each portion of fiber bundles  decreasing conduction time from atria to ventricles. • Guyton says this is the ‘belief’, precise mechanism is “somewhat unclear”.

  10. References • Guyton & Hall. Medical Physiology, 11th Ed. 2010. Pp. 112-113, 121-122.

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