Abstract
Pulmonary pressure-flow curves can be easily generated in the intact animal by using a combination of systemic arteriovenous (a-v) fistulas and inferior vena cava (IVC) occlusion. By combining this technique with pulmonary artery occlusion, pulmonary pressure-flow curves may be studied over a broader range of pressures than has been previously been done in the intact, resting animal using pulsatile flow. Pressure-flow curves were generated by varying flow through opening and closing of the a-v fistulas in conjunction with inflating and deflating a balloon in the inferior vena cava. The pressure-flow curves were done under two conditions; (1). with both lungs perfused; (2) with the right lung excluded from the circulation (PA occlusion). PA occlusion resulted in no change in alveolar arterial oxygen tension gradient. The pressure-flow relationships for one lung and two lungs were well described by linear equations (r2 =0.83 ±0.03 and 0.82 ±0.04 respectively). The slope of the equations increased with PA occlusion (3.6 ±0.4 mmHg ·L−1 to 5.9 ±0.9 mmHg ·L−1). There was no change in the pressure axis intercept with PA occlusion (8.34 ±0.8 mmHg pre-occlusion and 8.9 ±1.3 mmHg post-occlusion). It is concluded that the pulmonary pressure-flow relationship is well described by a linear function above a mean pulmonary artery pressure (PAP) of 10–12 mmHg.
Résumé
Des courbes pression-debit pulmonaires peuvent être obtenues facilement chez l’animal intact en utilisant une combinaison de fistules artérioveineuses (a-v) systémiques et d’occlusions de la veine cave inférieure (IVC). En combinant cette technique avec l’occlusion de l’artère pulmonaire, les courbes pression-débit pulmonaires peuvent etre étudiées sur une gamme plus étendue de pression qu’auparavant chez l’’animal intact au repos par l’utilisation d’un débit pulsatile. Les courbes pression-débit ont été produites en variant le débit à trovers les fistules a-v à différents degrés d’ouverture et de fermeture, pendant temps qu’un ballon était gonflé puis dégonflé dans la veine cave inférieure. Les courbes pression-débit ont été produites sous deux conditions: 1) avec les deux poumons perfusés; 2) avec le poumon droit exclu de la circulation (occlusion PA). L’occlusion de la PA n’a produit aucun changement dans le gradient alvéolo-artériel de la tension en oxygène. Les relations pressiondébit pour un ou deux poumons étaient bien décrites par des équations linéaires (r2 = 0,83 ±0,03 et 0,82 ±0,04 respectivement). La pente des equations augmentait avec l’occlusion de la PA (3,6 ±0,4 mmHg ·L−1 à 5,9 ±0,9 mmHg ·L−1). Il n’y avait aucun changement avec l’occlusion de la PA quant à la valeur de l’intersection de la droite avec l’axe depression (8,34 ±0,8 mmHg avant l’occlusion et 8,9 ±1,3 mmHg après l’occlusion). En conclusion, la relation pression-debit pulmonaire est bien représentée par une fonction linéaire lorque la pression de l’artère pulmonaire moyenne (PAP) est au-dessus de 10 à 12 mmHg.
Article PDF
Similar content being viewed by others
References
Lategola MT. Pressure flow relationships in the dog lung during acute, subtotal pulmonary vascular occlusion. American Journal of Physiology 1958; 192(3): 613–9.
West JB, Dollery CT. Distribution of blood flow and the pressure-flow relations of the whole lung. Journal of Applied Physiology 1965; 20: 175–83.
Hyman AL. Effects of large increases in pulmonary blood flow on pulmonary venous pressure. Journal of Applied Physiology 1969; 27(2): 179–85.
Fowler NO, Holmes JC. Pulmonary arterial pressure at high pulmonary flow. Journal of Clinical Investigation 1965; 44(12): 2040–50.
Lodato RF, Michael JR, Murray PA. Multipoint pulmonary vascular pressure-cardiac output plots in conscious dogs. American Journal of Physiology 1985; 249 (Heart Circ Physiol 18):H351–57.
Ducas J, Girling L, Schick U, Prewitt RM. Pulmonary vascular effects of hydralazine in a canine preparation of pulmonary thromboembolism. Circulation 1986; 73(5): 1050–57.
Lejeune P, Deloof T, Leeman M, Mélot C, Naeije R. Multipoint pulmonary vascular pressure/flow relationships in hypoxic and normoxic dogs: effects of nitrous oxide with and without cyclooxygenase inhibition. Anesthesiology 1988; 68: 92–9.
Marshall BE, Marshall C. A model for hypoxic constriction of the pulmonary circulation. Journal of Applied Physiology 1988; 64(1): 68–77.
Bshouty Z, Younes M. Distensibility and pressure-flow relationship of the pulmonary circulation. I. Single-vessel model. Journal of Applied Physiology 1990; 68(4): 1501–13.
Bshouty Z, Younes M. Distensibility and pressure-flow relationship of the pulmonary circulation. II. Multibranched model. Journal of Applied Physiology 1990; 68(4): 1514–27.
Leeman M. The pulmonary circulation in acute lung injury: a review of some recent advances. Intensive Care Med 1991; 17:254–60.
Ducas J, Schick U, Girling L, Prewitt RM. Effects of altered left atrial pressure on pulmonary vascular pressureflow plots. Am J Physiol 1988; 255 (Heart Circ Physiol 24):H19-H25.
Hanson WL, Emhardt JD, Bartek JP, et al. Site of recruitment in the pulmonary microcirculation. Journal of Applied Physiology 1989; 66(5): 2079–83.
Smith JC, Mitzner W. Analysis of pulmonary vascular interdependence in excised dog lobes. Journal of Applied Physiology 1980; 48(3): 450–67.
Younes M, Bshouty Z, Ali J. Longitudinal distribution of pulmonary vascular resistance with very high pulmonary blood flow. J Appl Physiol 1987; 62(1): 344–58.
Craven KD, Oppenheimer L, Wood LDH. Effects of contusion and flail chest on pulmonary perfusion and oxygen exchange. Journal of Applied Physiology 1979; 47(4): 729–37.
Author information
Authors and Affiliations
Additional information
Supported by The Physician Services Incorporated Foundation of Ontario.
Rights and permissions
About this article
Cite this article
McLean, R.F., Noble, W.H. & Kolton, M. Pulmonary pressures at high flows in the intact pulsatile flow perfused lung. Can J Anaesth 39, 381–386 (1992). https://doi.org/10.1007/BF03009050
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF03009050