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14 - Anti-arrhythmics

Published online by Cambridge University Press:  01 June 2010

Tom E. Peck
Affiliation:
Royal Hampshire County Hospital, Winchester
Sue Hill
Affiliation:
Southampton University Hospital
Tom Peck
Affiliation:
Consultant Anaesthetist, Royal Hampshire County Hospital, Winchester
Mark Williams
Affiliation:
Consultant Anaesthetist, Royal Perth Hospital, Australia
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Summary

Physiology

Cardiac action potential

The heart is composed of pacemaker, conducting and contractile tissue. Each has a different action potential morphology allowing the heart to function as a coordinated unit.

The SA node is in the right atrium, and of all cardiac tissue it has the fastest rate of spontaneous depolarization so that it sets the heart rate. The slow spontaneous depolarization (pre-potential or pacemaker potential) of the membrane potential is due to increased Ca2+ conductance (directed inward). At −40 mV, slow voltage-gated Ca2+ channels (L channels) open resulting in membrane depolarization. Na+ conductance changes very little. Repolarization is due to increased K+ conductance while Ca2+ channels close (Figure 14.1a).

Contractile cardiac tissue has a more stable resting potential at −80 mV. Its action potential has been divided into five phases (Figure 14.1b):

  • Phase 0 – describes the rapid depolarization (duration <1 ms) of the membrane, resulting from increased Na+ (and possibly some Ca2+) conductance through voltage-gated Na+ channels.

  • Phase 1 – represents closure of the Na+ channels while Cl is expelled.

  • Plateau phase 2 – due to Ca2+ influx via voltage-sensitive type-L Ca2+ channels and lasts up to 150 ms. This period is also known as the absolute refractory period in which the myocyte cannot be further depolarized. This prevents myocardial tetany.

  • Phase 3 – commences when the Ca2+ channels are inactivated and there is an increase in K+ conductance that returns the membrane potential to its resting value. This period is also known as the relative refractory period in which the myocyte requires a greater than normal stimulus to provoke a contraction.

  • […]

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Publisher: Cambridge University Press
Print publication year: 2008

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  • Anti-arrhythmics
    • By Tom Peck, Consultant Anaesthetist, Royal Hampshire County Hospital, Winchester, Mark Williams, Consultant Anaesthetist, Royal Perth Hospital, Australia
  • Tom E. Peck, Sue Hill
  • Book: Pharmacology for Anaesthesia and Intensive Care
  • Online publication: 01 June 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511722172.016
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  • Anti-arrhythmics
    • By Tom Peck, Consultant Anaesthetist, Royal Hampshire County Hospital, Winchester, Mark Williams, Consultant Anaesthetist, Royal Perth Hospital, Australia
  • Tom E. Peck, Sue Hill
  • Book: Pharmacology for Anaesthesia and Intensive Care
  • Online publication: 01 June 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511722172.016
Available formats
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To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

  • Anti-arrhythmics
    • By Tom Peck, Consultant Anaesthetist, Royal Hampshire County Hospital, Winchester, Mark Williams, Consultant Anaesthetist, Royal Perth Hospital, Australia
  • Tom E. Peck, Sue Hill
  • Book: Pharmacology for Anaesthesia and Intensive Care
  • Online publication: 01 June 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511722172.016
Available formats
×