Interaction between effects of hypoxia and hypercapnia on altering left ventricular relaxation and chamber stiffness in dogs.

Abstract

Left ventricular (LV) isovolumic relaxation and chamber stiffness were examined in dogs to see how hypoxemia and hypercapnia occurring during an acute exacerbation of chronic obstructive lung disease could directly affect diastolic performance. Measurements were obtained during baseline (arterial PO2 approximately 200 mm Hg; PCO2 approximately 35 mm Hg; pH approximately 7.35), hypoxia (PO2 approximately 35 mm Hg; PCO2 approximately 35 mm Hg; pH approximately 7.35), and hypoxia-hypercapnia (PO2 approximately 35 mm Hg; PCO2 approximately 60 mm Hg; pH approximately 7.15) in an open-chest, open-pericardium preparation. Changes in LV diastolic performance during hypoxic and hypercapnic interventions were contrasted with those caused by ventricular interdependence in which pulmonary artery occlusion was used to produce a right to left ventricular septal shift. Subendocardial ultrasonic crystal transducers were placed along the three orthogonal axes of the left ventricle to measure dimensions by sonomicrometry. Along each axis, LV end-diastolic dimension-pressure relations were constructed in the various conditions; the slope of this relationship, obtained over a linear portion of the curve, was used as an index of diastolic dimensional distensibility (DD). The results showed that during hypoxia, DD appeared decreased along the three axes, with a reduction in filling primarily along the anterior-posterior and apex-base axes. The addition of hypercapnia to hypoxia completely abolished the hypoxic effect. On the other hand, during pulmonary artery occlusion, LV DD were not changed along the latter two dimensions. We conclude that during respiratory failure, LV diastolic performance may be directly affected by arterial blood gas tensions, which by altering the interaction between the contractile filaments modulate LV filling.