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Nisbet AM, Burton FL, Walker NL, et al. Acidosis slows electrical conduction through the atrio-ventricular node. Front Physiol. 2014;5:233doi: 10.3389/fphys.2014.00233.
Nisbet, A. M., Burton, F. L., Walker, N. L., Craig, M. A., Cheng, H., Hancox, J. C., Orchard, C. H., & Smith, G. L. (2014). Acidosis slows electrical conduction through the atrio-ventricular node. Frontiers in physiology, 5233. https://doi.org/10.3389/fphys.2014.00233
Nisbet, Ashley M, et al. "Acidosis slows electrical conduction through the atrio-ventricular node." Frontiers in physiology vol. 5 (2014): 233. doi: https://doi.org/10.3389/fphys.2014.00233
Nisbet AM, Burton FL, Walker NL, Craig MA, Cheng H, Hancox JC, Orchard CH, Smith GL. Acidosis slows electrical conduction through the atrio-ventricular node. Front Physiol. 2014 Jun 25;5:233. doi: 10.3389/fphys.2014.00233. eCollection 2014. PMID: 25009505; PMCID: PMC4070392.
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Front Physiol. 2014 Jun 25;5:233. doi: 10.3389/fphys.2014.00233. eCollection 2014.

Acidosis slows electrical conduction through the atrio-ventricular node.

Frontiers in physiology

Ashley M Nisbet, Francis L Burton, Nicola L Walker, Margaret A Craig, Hongwei Cheng, Jules C Hancox, Clive H Orchard, Godfrey L Smith

Affiliations

  1. British Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow Glasgow, UK.
  2. School of Physiology and Pharmacology, Medical Sciences Building, University of Bristol Bristol, UK.

PMID: 25009505 PMCID: PMC4070392 DOI: 10.3389/fphys.2014.00233

Abstract

Acidosis affects the mechanical and electrical activity of mammalian hearts but comparatively little is known about its effects on the function of the atrio-ventricular node (AVN). In this study, the electrical activity of the epicardial surface of the left ventricle of isolated Langendorff-perfused rabbit hearts was examined using optical methods. Perfusion with hypercapnic Tyrode's solution (20% CO2, pH 6.7) increased the time of earliest activation (Tact) from 100.5 ± 7.9 to 166.1 ± 7.2 ms (n = 8) at a pacing cycle length (PCL) of 300 ms (37°C). Tact increased at shorter PCL, and the hypercapnic solution prolonged Tact further: at 150 ms PCL, Tact was prolonged from 131.0 ± 5.2 to 174.9 ± 16.3 ms. 2:1 AVN block was common at shorter cycle lengths. Atrial and ventricular conduction times were not significantly affected by the hypercapnic solution suggesting that the increased delay originated in the AVN. Isolated right atrial preparations were superfused with Tyrode's solutions at pH 7.4 (control), 6.8 and 6.3. Low pH prolonged the atrial-Hisian (AH) interval, the AVN effective and functional refractory periods and Wenckebach cycle length significantly. Complete AVN block occurred in 6 out of 9 preparations. Optical imaging of conduction at the AV junction revealed increased conduction delay in the region of the AVN, with less marked effects in atrial and ventricular tissue. Thus acidosis can dramatically prolong the AVN delay, and in combination with short cycle lengths, this can cause partial or complete AVN block and is therefore implicated in the development of brady-arrhythmias in conditions of local or systemic acidosis.

Keywords: acidosis; atrio-ventricular block; atrio-ventricular node; bradycardia; optical mapping; right atrium

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