The amount of oxygen required for electrical activation of the heart is minimal, accounting for less than 1% of the total oxygen consumption of the normally working heart.
Supports prioritizing contractile over electrical efficiency in energetics research; leaves open translation to intact or diseased hearts.
The present study was undertaken to define the O 2 requirements of electrical activation of the heart. Thirteen isolated canine hearts were perfused with whole blood from which calcium had been removed with an exchange resin and to which the disodium salt of ethylenediaminetetraacetic acid had been added. Spontaneous depolarizations were suppressed by raising the plasma potassium to an average concentration of 7.5 mEq/liter, and the right ventricle was stimulated electrically at controlled frequencies. Although the stimuli produced propagated depolarizations, neither high-sensitivity strain gauge arches sutured to both ventricles, nor careful visual observation, showed any evidence of associated contractile activity. Ten of the hearts were studied with repetitive single stimuli applied in the conventional fashion, while the remaining three hearts were subjected to paired electrical stimulation. Changes of myocardial O 2 consumption (MV · O 2 ) were measured at a constant coronary blood flow and arterial O 2 content by determining changes of venous O 2 content from a continuous recording of venous PO 2 . Increases of the frequency of depolarization were uniformly accompanied by small increases of MV · O 2 , averaging 0.40 ± 0.04 (SEM) µliter/activation/100 g. The increases were of the same order of magnitude in the hearts subjected to paired electrical stimulation as in the hearts studied with single stimulation, suggesting that the altered frequency and rhythm of depolarization in paired electrical stimulation cannot account for the marked increase of MV · O 2 which this intervention produces in the intact heart. It is concluded that the amount of O 2 required for electrical activation of the heart is less than 1% of the total O 2 consumption of the normally working heart.
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Klocke et al. (1966) studied this question.
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