title: Acidosis slows electrical conduction through the atrio-ventricular node.
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.
authors.affiliation: British Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow Glasgow, UK.
authors.forename: Ashley M
authors.initials: AM
authors.lastname: Nisbet
authors.affiliation: British Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow Glasgow, UK.
authors.forename: Francis L
authors.initials: FL
authors.lastname: Burton
authors.affiliation: British Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow Glasgow, UK.
authors.forename: Nicola L
authors.initials: NL
authors.lastname: Walker
authors.affiliation: British Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow Glasgow, UK.
authors.forename: Margaret A
authors.initials: MA
authors.lastname: Craig
authors.affiliation: School of Physiology and Pharmacology, Medical Sciences Building, University of Bristol Bristol, UK.
authors.forename: Hongwei
authors.initials: H
authors.lastname: Cheng
authors.affiliation: School of Physiology and Pharmacology, Medical Sciences Building, University of Bristol Bristol, UK.
authors.forename: Jules C
authors.initials: JC
authors.lastname: Hancox
authors.affiliation: School of Physiology and Pharmacology, Medical Sciences Building, University of Bristol Bristol, UK.
authors.forename: Clive H
authors.initials: CH
authors.lastname: Orchard
authors.affiliation: British Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow Glasgow, UK.
authors.forename: Godfrey L
authors.initials: GL
authors.lastname: Smith
keywords: acidosis; atrio-ventricular block; atrio-ventricular node; bradycardia; optical mapping; right atrium