Abstract
Objective
In acute respiratory failure, increased cardiac output (\(\dot Q_t \)) increase; shunt (\({{\dot Q_s } \mathord{\left/ {\vphantom {{\dot Q_s } {\dot Q_t }}} \right. \kern-\nulldelimiterspace} {\dot Q_t }}\)). We have tested if this is caused by: 1) a redistribution of blood flow towards edematous regions, or 2) a decrease of regional ventilation in the edematous region.
Design
Oleic acid edema was induced in the left lower lobe (LLL) of 11 pigs.\(\dot Q_t \) was varied with bleeding and infusion of blood and dextran. Blood flow to the LLL was measured at low and high\(\dot Q_t \) with electromagnetic low probes in 6 animals and with a gamma camera in 5. In the gamma camera pigs regional ventilation was also measured.
Measurements and results
\(\dot Q_t \) was increased by 45% (electromagnetic flow probes) and 73% (gamma camera).\({{\dot Q_s } \mathord{\left/ {\vphantom {{\dot Q_s } {\dot Q_t }}} \right. \kern-\nulldelimiterspace} {\dot Q_t }}\) increased from 24.9–31.3% (p<0.05) and from 17.6–28.8% (p<0.001) respectively. No change in fractional perfusion of LLL could be seen, neither with flow probes nor with gamma camera. A decrease in ventilation of LLL, 2.6%, was observed when Qt was increased (p<0.05).
Conclusion
Theoretically a small decrease in ventilation can explain the increase in shunt, if regions with low ventilation/perfusion (VA/\(\dot Q\)) ratio are transformed to shunt. This is, however, unlikely since earlier studies have shown that blood flow is distributed either to regions with normal VA/\(\dot Q\) ratio or to shunt regions. We conclude that the cardiac output dependent shunt is not caused by redistribution of blood flow between lobes or by decreased ventilation in the edematous region. We cannot exclude that blood flow is redistributed within the edematous lobe.
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References
Dantzker D, Lynch J, Weg JG (1980) Depression of cardiac output is a mechanism of shunt reduction in the therapy of acute respiratory failure. Chest 77:636–642
Lemaire F, Gastine H, Régner B, Teisseire B, Rapin M (1978) Perfusion changes modify intrapulmonary shunting (\({{\dot Q_s } \mathord{\left/ {\vphantom {{\dot Q_s } {\dot Q_t }}} \right. \kern-\nulldelimiterspace} {\dot Q_t }}\)) in patients with adult respiratory distress syndroxne (ARDS) (Abstract). Am Rev Respir Dis 117:144
Duke K, Ali C, Fisher CJ, Wood LDH (1980) Increased cardiac output does not redistribute towards edematous lung lobes (Abstract). Physiologist 23:665
Lynch JP, Mhyre JG, Dantzker DR (1979) Influence of cardiac output on intrapulmonary shunt. J Appl Physiol 46:315–321
Prewitt RM, Wood LDH (1981) Effect of sodium nitroprusside on cardiovascular function and pulmonary shunt in canine oleic acid pulmonary edema. Anesthesiology 55:537–541
Smith G, Cheney FW, Winter PM (1974) The effect of change in cardiac output on intrapulmonary shunting. Br J Anesth 46:337–342
Breen PH, Schumacker PT, Hedenstierna G, Ali J, Wagner PD, Wood LDH (1982) How does increased cardiac output increase shunt in pulmonary edema? J Appl Physiol 53:1273–1280
West JB (1977) Ventilation-perfusion relationships. Am Rev Respir Dis 116:919–943
Fazio R, Jones T (1975) Assessment of regional ventilation by continuous inhalation of radioactive Krypton-81m. Br Med J 3:673–676
Tucker A, McMurtry JF, Reeves JT, Alexander AF, Will AH, Grover RF (1975) Lung vascular smooth muscle as a determinant of pulmonary hypertension at high altitude. Am J Physiol 228:762–767
Velazques M, Schuster DP (1988) Pulmonary blood flow distribution after lobar oleic acid injury: a PET study. J Appl Physiol 65:2228–2235
Ali J, Wood LDH (1986) Factors affecting perfusion distribution in canine oleic acid pulmonary edema. J Appl Physiol 60:1498–1503
Bishop MJ, Cheney FW (1983) Effects of pulmonary blood flow and mixed venous O2 tension on gas exchange in dogs. Anesthesiology 58:130–135
Sandoval J, Long GR, Skoog C, Wood LDH, Oppenheimer L (1983) Independent influence of blood rate and mixed venous PO2 on shunt fraction. J Appl Physiol 55:1128–1133
Benumof JL, Wahrenbrock EA (1975) Blunted hypoxic pulmonary vasoconstriction by increased lung vascular pressures. J Appl Physiol 38:846–850
Hughes JMB (1970) Pulmonary edema and airway closure. In: Giuntini C (ed) Central hemodynamics and gas exchange. Minerva, Torino, pp 223–237
Broseghini C, Brandolese R, Poggi R, Polese G, Manzin E, Milic-Emili J, Rossi A (1988) Respiratory mechanics during the first day of mechanical ventilation in patients with pulmonary edema and chronic airway obstruction. Am Rev Respir Dis 138:355–361
Kato M, Staub NC (1966) Response of small pulmonary arteries to unilobar hypoxia and hypercarbia. Circ Res 19:426–440
Nagasaka Y, Bhatacharya F, Nanjo S, Gropper MA, Staub NC (1984) Micropuncture measurement of lung microvascular pressure profile during hypoxia in cats. Circ Res 54:90–95
Mazal D, Briscoe WA, King T (1980) The effect of severe uneven impairment of diffusing capacity on the arterial oxygen profile (Abstract). Am Rev Respir Dis 121:378
Breen PH, Schumacker PT, Sandoval J, Mayers I, Oppenheimer L, Wood LDH (1985) Increased cardiac output increases shunt: role of pulmonary edema and perfusion. J Appl Physiol 59:1313–1321
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Fredén, F., Cigarini, I., Mannting, F. et al. Dependence of shunt on cardiac output in unilobar oleic acid edema. Intensive Care Med 19, 185–190 (1993). https://doi.org/10.1007/BF01694768
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DOI: https://doi.org/10.1007/BF01694768