Effects of oxygen administration, bicarbonate infusions, and brief hyperventilation on patients with pulmonary vascular obstructive disease.

Abstract

In an attempt to clarify further the mechanisms underlying labile rise in pulmonary vascular resistance, the effects of administering high oxygen concentrations, briefvoluntary hyperventilation, and correction of acidosis were studied in 16 patients in whom congenital heart disease was associated with pulmonary vascular disease. On breathing 100 per cent oxygen thele was a significant fall in pulmonary vascular resistance from 21 8 ± 4.6 to 12.9 3-6 units/M2 (P < 0.001), with a rise in pulmonary blood flow from 4-4 ± 0-6 to 8-8 ± 2-0 1/min per m2 (P < 0 025) and a fall in pulmonary artery pressure from #67.8 ± 2.8 to 61 8 ± 4 0 mmHg (P < 0 025). The changes occurring on sodium bicarbonate adninistra-;tion in 6 patients did not reach levels of significance, but the size of each individual response was closely correlated with the response to oxygen administration. No significant changes occurred either on voluntary hyperventilation or, in the systemic circulation, with any intervention. However, systemic vascular resistance was positively correlated with pulmonary vascular resistance (P < 0.01). As a result of this, though age was correlated positively with both pulmonary artery mean pressure (P < 0 025) and vascular resistance (P < 0.025), it was not correlated with the ratio of pulmonary to systemic resistance. Since pulmonary vascular disease is progressive, these results cast some doubt on the validity ofresistance ratio as a measure of its severity.

Incidence of secondary pulmonary hypertension in adults with atrial septal or sinus venosus defects

“…A mean pulmonary artery pressure of > 30 mm Hg was arbitrarily considered to represent pulmonary hypertension. Pulmonary and systemic blood flows were measured by the Fick method 7. Mixed venous saturation was obtained from the superior and inferior venae cavae (SVC and IVC) and calculated as [(3 × SVC) + (1 × IVC) saturation]/4 7…”

“…The ratio between pulmonary and systemic vascular resistances (resistance index, Rp/Rs) was calculated; we regarded this as the most important indicator of pulmonary vascular resistance because errors in oxygen capacity cancel out8 and the use of the ratio avoids the need to index for flows and resistances 7. An Rp/Rs ratio greater than 0.3 was arbitrarily considered to represent raised pulmonary vascular resistance.…”

Assessment of operability in d-transposition of great arteries with ventricular septal defect: A practical method

“…It is well known that oxygen reduces pulmonary arterial pressure and PVR[ 18 19 ] especially where irreversible PVOD has still not set in. This effect of oxygen is typically tested in the catheterization lab.…”

Patients with Congenital Atrial Septal Defects: Effect of Age at Repair and Defect Size on Pulmonary Artery Pressures Prior to Repair

“…Pressures were measured with standard fluid-filled catheters coupled to a Statham transducer. Pulmonary and systemic blood flows were measured by the Fick method [12]. All patients with pulmonary artery systolic pressure (PASP) greater than 40 mmHg were classified as having PAH [13,14].…”