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Increased PVRI: Due to hypoxia?
LETI'ERS TO THE EDITOR
619
Increased PVRI: Due to Hypoxia? To the Editor: The report from Weyland et al ~ describing a transpulmonary double indicator dilution method to measure cardiac index, pulmonary vascular resistance index (PVRI) and extravascular lung water in children with a univentricular physiology after cavopulmonary anastomosis has provided a new potentially valuable tool for objectively evaluating these children perioperatively. However, there were some questions left unanswered by the published report. The authors noted a remarkable increase m PVRI in the children studied after extubation in whom the PVRI increased from 107 to 190 dyne/s/cm-5/m 2. This would not be intuitively expected because mean airway pressure should be expected to decrease, even if the children were on only minimal ventilatory settings beforehand. Oxygenation data after extubatlon showed a drop in mean PO2 from 99 + 12 to 83 + 127 mmHg. Although these data appear to be displayed in a manner suggesting scientific validity, the large standard deviation displayed after extubation suggests that the individual patient values did not assume a normal Gaussian distribution. It also suggests that the majority of patients had a high PO2 after extubation, but that a small minority had a very low PO2, which brought the overall mean down. Because hypoxia is a potent pulmonary vasoconstrictor, the PVRI Increases may have simply been related to this. These comments are certainly borne out by the graphs of PVRI in which only two of the patients appeared to show any type of increase in PVRI after extubation. The authors stated conclusions, therefore, that PVRI increases after extubation should not be viewed as inevitable. Indeed this may not be applicable to the clinical situation in which careful attention is paid to ventilatory status.
Nancy Setzer, MD Associate Professor of Anesthesiology (Clinical) University of Florida College of Medicine Gainesville, F L REFERENCE
1. Weyland A, Buhre W, Hoeft A, et al" AppllcaUon of transpulmonary double indicator dilution method for postoperative assessment of cardiac index, pulmonary vascular resistance index and
extravascular lung water in children undergoing total cavopulmonary anastomosis" Preliminary results in six patients. J Cardiothor Vasc Anesth 8:636-641, 1994
Reply I very much appreciate the interest in our study by Setzer and thank her for the careful reading of our article. Unfortunately, a printing error that occurred despite correction in the galley proofs most probably was the primary reason for the doubts about the normal distribution of PaO2 values. In Table 2, the values of PaO2 after extubation appear as 83 + 127. These values should read: 83 --- 12. The standard deviation of PaO2 thus did not differ from the value before extubation. Because of the well-known effect of hypoxemia on pulmonary vascular resistance, we agree that a decrease in mean PaO2 should be considered as a potential reason for the observed changes in PVRI following extubation. The slight alteration of oxygenation, however, seems indeed unlikely to explain the 78% increase in mean PVRI. Although this increase in PVRI was not the principal finding of our methodologic study, it raises important questions with respect to the underlying reasons and to possible therapeutic consequences of these hemodynamic changes. Based on previous recommendations on the ventilatory management of patients after total cavo-pulmonary anastomosis, improved venous return and a subsequent increase in cardiac index could be expected after weaning from positive- pressure ventilation. Because of the concomitant changes in PVRI, this was not observed in our patients. We believe that the mterplay of ventilation, intravascular volume status, pulmonary vascular resistance, and ventricular function is not yet completely understood in patients with cavopulmonary continuity.
Andreas Weyland, MD Department of Anesthesiology, Emergency and Intensive Care Medicine University of Gottingen Germany
619
Increased PVRI: Due to Hypoxia? To the Editor: The report from Weyland et al ~ describing a transpulmonary double indicator dilution method to measure cardiac index, pulmonary vascular resistance index (PVRI) and extravascular lung water in children with a univentricular physiology after cavopulmonary anastomosis has provided a new potentially valuable tool for objectively evaluating these children perioperatively. However, there were some questions left unanswered by the published report. The authors noted a remarkable increase m PVRI in the children studied after extubation in whom the PVRI increased from 107 to 190 dyne/s/cm-5/m 2. This would not be intuitively expected because mean airway pressure should be expected to decrease, even if the children were on only minimal ventilatory settings beforehand. Oxygenation data after extubatlon showed a drop in mean PO2 from 99 + 12 to 83 + 127 mmHg. Although these data appear to be displayed in a manner suggesting scientific validity, the large standard deviation displayed after extubation suggests that the individual patient values did not assume a normal Gaussian distribution. It also suggests that the majority of patients had a high PO2 after extubation, but that a small minority had a very low PO2, which brought the overall mean down. Because hypoxia is a potent pulmonary vasoconstrictor, the PVRI Increases may have simply been related to this. These comments are certainly borne out by the graphs of PVRI in which only two of the patients appeared to show any type of increase in PVRI after extubation. The authors stated conclusions, therefore, that PVRI increases after extubation should not be viewed as inevitable. Indeed this may not be applicable to the clinical situation in which careful attention is paid to ventilatory status.
Nancy Setzer, MD Associate Professor of Anesthesiology (Clinical) University of Florida College of Medicine Gainesville, F L REFERENCE
1. Weyland A, Buhre W, Hoeft A, et al" AppllcaUon of transpulmonary double indicator dilution method for postoperative assessment of cardiac index, pulmonary vascular resistance index and
extravascular lung water in children undergoing total cavopulmonary anastomosis" Preliminary results in six patients. J Cardiothor Vasc Anesth 8:636-641, 1994
Reply I very much appreciate the interest in our study by Setzer and thank her for the careful reading of our article. Unfortunately, a printing error that occurred despite correction in the galley proofs most probably was the primary reason for the doubts about the normal distribution of PaO2 values. In Table 2, the values of PaO2 after extubation appear as 83 + 127. These values should read: 83 --- 12. The standard deviation of PaO2 thus did not differ from the value before extubation. Because of the well-known effect of hypoxemia on pulmonary vascular resistance, we agree that a decrease in mean PaO2 should be considered as a potential reason for the observed changes in PVRI following extubation. The slight alteration of oxygenation, however, seems indeed unlikely to explain the 78% increase in mean PVRI. Although this increase in PVRI was not the principal finding of our methodologic study, it raises important questions with respect to the underlying reasons and to possible therapeutic consequences of these hemodynamic changes. Based on previous recommendations on the ventilatory management of patients after total cavo-pulmonary anastomosis, improved venous return and a subsequent increase in cardiac index could be expected after weaning from positive- pressure ventilation. Because of the concomitant changes in PVRI, this was not observed in our patients. We believe that the mterplay of ventilation, intravascular volume status, pulmonary vascular resistance, and ventricular function is not yet completely understood in patients with cavopulmonary continuity.
Andreas Weyland, MD Department of Anesthesiology, Emergency and Intensive Care Medicine University of Gottingen Germany