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J Thorac Cardiovasc Surg 1995;110:1764-1765
© 1995 Mosby, Inc.


BRIEF COMMUNICATIONS

MEASUREMENT OF LUNG OXYGEN CONSUMPTION IN A PATIENT AFTER DOUBLE-LUNG TRANSPLANT

Kang H. Lee, MA, MBBChir, MRCPa, Philippe Rico, MDa, Arthur J. Boujoukos, MDa, Robert J. Keenan, MDb, Michael R. Pinsky, MD, FCCPa


Pittsburgh, Pa.

Accepted for publication April 6, 1995. Address for reprints: Kang H. Lee, MD, Division of Critical Care Medicine, Room 604A, Scaife Hall, University of Pittsburgh Medical Center, 200 Lothrop St., Pittsburgh, PA 15213.

A 48-year woman underwent double-lung transplantation for treatment of severe emphysema. She required venous-arterial extracorporeal membrane oxygenation (ECMO; Bio-Medicus pump, model 540T; Bio-Medicus, Inc., Eden Prairie, Minn.; Medtronic/Carmeda Bioactive Surface with Maxima Hollow Fiber oxygenator CB 1380; Medtronic, Inc., Minneapolis, Minn.) to correct severe hypoxemia and cardiovascular instability. A postoperative chest radiograph demonstrated bilateral alveolar infiltrates compatible with acute lung injury.

On the second postoperative day, we measured oxygen consumption (Vo2) and carbon dioxide excretion (Vco2) by means of respiratory gas analysis with a metabolic cart (Deltatrac; SensorMedics Corp., Yorba Linda, Calif.). Blood flow through the pulmonary circulation was varied by adjusting the ECMO flow rates during the study interval. The patient was ventilated with a Puritan-Bennett 7200e ventilator (Puritan-Bennett Corp., Portable Ventilator Division, Boulder, Colo.) set on a tidal volume of 600 ml with a respiratory rate of 4 breaths/min, positive end–expiratory pressure of 10 cm H2O, and inspired oxygen fraction of 0.5. With the ECMO flow at 5 L/min, there was a nonpulsatile pulmonary arterial tracing with a mean pressure of 8 mm Hg, which was inferred to reflect no flow in the pulmonary artery. The simultaneous nonpulsatile radial arterial tracing confirmed the absence of aortic valve opening. These settings were maintained for 10 minutes, during which time the readings stabilized to yield, during a 5-minute period: Vo2, 7.8 ± 1.7 ml/min (mean ±standard deviation); and Vco2 18.3 ± 1.6 ml/min (GoTable I). Respiratory quotient (RQ) was 1.97 ± 0.05.


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Table I. Data showing the effects of changing ECMO flow rates on Vo2 and Vco2, as measured by respiratory gas analysis
 
When the ECMO flow rate was reduced gradually to 2 L/min, there was a return of pulmonary artery flow. This was evidenced by the reappearance of pulsatile pulmonary arterial and radial arterial tracings. Furthermore, a thermodilution cardiac output was measured at 3.43 L/min. Vo2 increased progressively and stabilized (after 5 minutes) at 68.7 ± 2.4 ml/min, Vco2 at 81.0 ± 1.5 ml/min, and RQ was reduced to 1.18 ± 0.05 (GoTable I).

DISCUSSION

Lung Vo2 represents the amount of oxygen consumed by the lung tissues directly from the alveoli. This volume has previously been measured directly in isolated lung preparations. Go 1 The ability of the lung tissues to extract oxygen directly from the alveoli has particular significance for the preservation of donor lungs. Preservation is better when the lung is insufflated with 100% oxygen. Go 2 Lung Vo2 has also been measured in intact animals and in human beings by assuming that it is represented by the difference between oxygen uptake through the mouth by respiratory gas analysis and the product of arteriovenous oxygen content difference and cardiac output (VO2Fick). Patients after cardiac bypass operation and patients with adult respiratory distress syndrome have also been found to have a measurable and significant lung Vo2. Go Go 3,4 This method, however, engenders thepotential error of underestimating Vo2 Fick by neglecting the bronchial circulation, which is known to have increased flow during inflammatory lung disorders. Our patient therefore provided an unique opportunity to measure true lung Vo2 because the bronchial circulation had been interrupted with the double-lung transplant and venous-arterial ECMO at the high flow rate eliminated pulmonary blood flow. In effect, we had a nonperfused lung in vivo, and any measured oxygen consumption at the mouth therefore represented true lung Vo2.

The measured lung Vo2 our patient is probably higher than normal because the lungs had obvious reperfusion injury. The actual value therefore may reflect increased metabolic activity during inflammation, or, alternatively, Vo2 for nonoxidative purposes (e.g., oxygen radical formation). We presume that if the latter were true there would be no corresponding increase in carbon dioxide production, and RQ therefore would fall. The calculated RQ was high, however, especially during conditions of no pulmonary blood flow. This RQ probably reflected the presence of anaerobic metabolism leading to metabolic acidosis and an increase in Vco2 from bicarbonate buffering of lactic acid (gas–exchange threshold) Go 5 The potential anaerobic conditions indouble–lung transplants that result from high–flow venous–arterial ECMO support without pulmonary blood flow have been a source of concern because they may lead to ischemic injury to the anastomosis site.

In summary, we have demonstrated the first direct measurement of human lung Vo2 in vivo for lungs with reperfusion injury.

Footnotes

From the Departments of Anesthesiology and Critical Care Medicine a and Surgery, b University of Pittsburgh Medical Center, Pittsburgh. Back

J THORAC CARDIOVASC SURG 1995;110:1764-5 Back

References

  1. Date H, Matsumura A, Manchester JK, Cooper JM, Lowry OH, Cooper JD. Changes in alveolar oxygen and carbon dioxide concentration and oxygen consumption during lung preservation. The maintenance of aerobic metabolism during lung preservation. J THORAC CARDIOVASC SURG 1993;105:492-501.[Abstract]
  2. Weder W, Harper BD, Shimokawa S, et al. Influence of intraalveolar oxygen concentration on lung preservation in a rabbit model. J THORAC CARDIOVASC SURG 1991;101:1037-43.[Abstract]
  3. Takala J, Keinanen O, Vaisanen P, Kari A. Measurement of gas exchange in intensive care: laboratory and clinical validation of a new device. Crit Care Med 1989;17:1041-7.[Medline]
  4. Gill RS, Cunningham DG, Sharpe MD. Oxygen consumption in sepsis: contribution of the lung [Abstract]. Am J Respir Crit Care Med 1994;149:A414.
  5. Patessio A, Casaburi R, Carone M, Appendine L, Donner CF, Wasserman K. Comparison of gas exchange, lactate and lactic acidosis thresholds in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1993;148:622-6.[Medline]



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