Experimental study demonstrates that arterial carbon dioxide tension and airway pressure independently modulate cardiac output in anesthetized dogs, highlighting metabolic influences on blood flow.
Hemodynamic effects of changes in arterial carbon dioxide tension during intermittent positive pressure ventilation (IPPV) were studied in lightly anesthetized dogs following recovery from implantation of pulsed ultrasonic flow transducers on aorta and vena cava. Alveolar ventilation was maintained in excess of normal, and arterial PCO2 was varied by alteration of inspired CO2 concentration. Data were obtained at PaCO2 20, 40 and 60 torr, and at each PaCO2 high (peak airway pressure 30 cm. of water, inspiratory to expiratory ratio of 2:1) and low (peak airway pressure 10 cm. of water, inspiratory to expiratory ratio of 1:2) levels of ventilation were employed. Two separate hemodynamic effects were observed, the effects of changes in intrathoracic pressure and those produced by alterations in PaCO2 At each PaCO2 high level of ventilation decreased stroke volume and cardiac output compared to low level of ventilation. At each level of ventilation, stroke volume and cardiac output were decreased during respiratory alkalosis and increased during respiratory acidosis.
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Morgan et al. (1967) studied this question.
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