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Ventilatory response to hypoxia
Correspondence
565
S. GHOSH D. J. SNOW A. H. MOORS A. ODURO R. D. LATIMER
Department of Anaesthesia Papworth Hospital NHS Trust Cambridge 1. Snow DJ, Gray SJ, Ghosh S, Foubert L, Oduro A, Higenbottam TW, Wells FC, Latimer RD. Inhaled nitric oxide in patients with normal and raised pulmonary vascular resistance after cardiac surgery. British Journal of Anaesthesia 1994; 72: 185-189. 2. Loscalzo J. Endothelial dysfunction in pulmonary hypertension. New England Journal of Medicine 1992; 327: 117-119. 3. Frostell C, Fratacci MD, Wain JC, Jones R, Zapol WM. Inhaled nitric oxide: A selective pulmonary vasodilator reversing hypoxic pulmonary vasoconstriction. Circulation 1991; 83: 2038-2047. 4. Watkins DN, Jenkins IR, Rankin JM, Clarke GM. Inhaled nitric oxide in severe acute respiratory failure—its use in intensive care and description of a delivery system. Anaesthesia and Intensive Care 1993; 21: 861-866.
Postoperative delirium Sir,—I have read with interest the article on treatment of postoperative delirium with supplementary oxygen by Aakerlund and Rosenberg [1]. The results are interesting, but not surprising. The authors mentioned that delirium is a non-specific syndrome caused by widespread cerebral dysfunction, which may be a result of a variety of factors. However, they do not mention that acute depression may be a cause of this delirium. This is important to highlight as it is easily treated [2-4]. J. G. BROCK-UTNE
Department of Anesthesia Stanford University School of Medicine Stanford, CA, USA 1. Aakerlund LP, Rosenberg J. Postoperative delirium: treatment with supplementary oxygen. British Journal of Anaesthesia 1994; 72: 286-290.
2. Komfeld DS, Zimberg S, Malm JR. Psychiatric complication of open heart surgery. New England Journal of Medicine 1965; 273: 287-291. 3. Brock-Utne JG, Cheetham RWS, Goodwin NM. Psychiatric problems in intensive care. Anaesthesia 1976; 31: 380-384. 4. Brock-Ume JG, Goodwin NM, Hicks JC. Acute confusional states and depression treated with maprotiline mesylate. South African Medical Journal 1979; 55: 641.
Ventilatory response to hypoxia Sir,—I wish to comment on Dr Goodman's excellent and interesting editorial [1] "Volatile agents and the ventilatory response to hypoxia". In the editorial I was quoted in a personal communication note saying, "that there is no important depression specifically of the hypoxic response". The quotation is correct but needs clarification. Hypoxic ventilatory responses are traditionally expressed as changes in minute ventilation related to the degree of hypoxia. In our studies [2-6] we found that by separating minute ventilation responses into changes in tidal volume and ventilatory frequency, hypoxic ventilatory responses are achieved by increased tidal volumes (motor response) in the awake state and by increased ventilatory frequencies (chronotropic response) during isoflurane anaesthesia [6]. We therefore emphasize that motor and timing responses have to be evaluated separately. The resulting minute ventilation seems, in our hands, to be the same in awake and anaesthetized subjects, at least when a poikilocapnic approach is used. These results, from studies in humans, are currently being scrutinized in ongoing investigations in our laboratory. S. LINDAHL
Department of Anaesthesiology and Intensive Care Karolinska Institute Stockholm, Sweden 1. Goodman NW. Volatile agents and the ventilatory response to hypoxia. British Journal of Anaesthesia 1994; 72: 503-505. 2. Sjogren D, Ebberyd A, Sollevi A, Lindahl SGE. Ventilatory responses to hypoxia in awake and anesthetized humans. Anesthesiology 1991; 75: A1102. 3. Lindahl SGE, SjSgren D, Sollevi A. Isoflurane anesthesia (0.6 MAC) and hypoxic ventilatory response in humans. Anesthesiology 1993; 79: A1201. 4. Sollevi A, Sjogren D, Lindahl SGE. Effect of isoflurane anesthesia on hypoxic and hypercapnic ventilatory response in humans. Anesthesiology 1993; 79: A1202. 5. Sjogren D, Sollevi A, Ebbcryd A, Lindahl SGE. Poikilocapnic hypoxic ventilatory response in humans during 0.85 MAC isoflurane anaesthesia. Acta Anaeslhcsiologica Scandinavica 1994; 38: 149-155. 6. Sjogren D, Sollevi A, Ebberyd A, Lindahl SGE. Isoflurane anaesthesia (0.6 MAC) and hypoxic ventilatory responses in humans. Acta Anaesthesiologica Scandinavica 1994; (in press). Sir,—Professor Lindahl makes an important point. Almost all the mathematical models of ventilation ignore riming: for example, in Carley and Shannon's model [1] "breathing frequency is chosen a priori and remains constant." We also know that halothanc, enflurane and isoflurane are all ventilatory depressants but do not have identical effects on ventilatory control. There is still much to learn about the effects of anaesthesia on human breathing. N. W. GOODMAN
University Department of Anaesthesia Southmead Hospital, Bristol 1. Carley DW, Shannon DC. A minimal mathematical model of human periodic breathing. Journal of Applied Physiology 1988; 65: 1400-1409.
Risk of aspiration with the laryngeal mask Sir,—We read with interest the study by Akhtar and Street on the risk of aspiration with the laryngeal mask airway (LMA) [1]. Fifty patients were allocated randomly to receive either IPPV or spontaneous ventilation. One patient in the spontaneous ventilation group demonstrated dye staining of the pharynx, and a second patient in the IPPV group, undergoing diagnostic
Downloaded from http://bja.oxfordjournals.org/ at University of Bath Library & Learning Centre on July 16, 2015
oxygen-air, before the Brompton Manley ventilator. The concentration of nitrogen dioxide was measured in the inspiratory tubing just before the patient and was always less than 2 ppm. We are concerned that Dr Jenkins was unaware of the potential dangers of the system of introducing a high concentration of nitric oxide as a continuous flow into the inspiratory limb of an intermittent flow ventilator [4]. This technique allows a bolus of high concentration nitric oxide to be delivered to the patient which cannot be measured with the slow response analysers in current use. In order to demonstrate this danger of inadequate mixing, we have tried to simulate the dynamics of the system described [4]. In the laboratory using a test lung, we substituted carbon dioxide for nitric oxide because we have a capnograph with a sufficiently rapid response. Adding carbon dioxide before the ventilator gives adequate mixing and consequently the expected concentration. In contrast, adding carbon dioxide to the inspiratory limb can give peak concentrations of three to five times the expected concentration. Paradoxically, mixing before the ventilator delivers a lower concentration of nitrogen dioxide to the patient: although the transit time is longer, mixing is better and the dispersal of the high concentration is more rapid. We do appreciate the point that haemodynamic variables are inherently unstable in the early period after cardiac surgery and that changes in baseline measurements may potentially flaw results. We set out to study the efficacy of inhaled nitric oxide in postoperative cardiac surgical patients; within the constraints of safe and ethical practice we believe the design of our study was suited to this purpose. We hope that other groups may now feel able to conduct such a study in patients with much higher pulmonary vascular pressures and resistances with all the attendant risks. We felt that including more severely diseased patients in one of the earliest clinical studies of nitric oxide was unjustifiable.
565
S. GHOSH D. J. SNOW A. H. MOORS A. ODURO R. D. LATIMER
Department of Anaesthesia Papworth Hospital NHS Trust Cambridge 1. Snow DJ, Gray SJ, Ghosh S, Foubert L, Oduro A, Higenbottam TW, Wells FC, Latimer RD. Inhaled nitric oxide in patients with normal and raised pulmonary vascular resistance after cardiac surgery. British Journal of Anaesthesia 1994; 72: 185-189. 2. Loscalzo J. Endothelial dysfunction in pulmonary hypertension. New England Journal of Medicine 1992; 327: 117-119. 3. Frostell C, Fratacci MD, Wain JC, Jones R, Zapol WM. Inhaled nitric oxide: A selective pulmonary vasodilator reversing hypoxic pulmonary vasoconstriction. Circulation 1991; 83: 2038-2047. 4. Watkins DN, Jenkins IR, Rankin JM, Clarke GM. Inhaled nitric oxide in severe acute respiratory failure—its use in intensive care and description of a delivery system. Anaesthesia and Intensive Care 1993; 21: 861-866.
Postoperative delirium Sir,—I have read with interest the article on treatment of postoperative delirium with supplementary oxygen by Aakerlund and Rosenberg [1]. The results are interesting, but not surprising. The authors mentioned that delirium is a non-specific syndrome caused by widespread cerebral dysfunction, which may be a result of a variety of factors. However, they do not mention that acute depression may be a cause of this delirium. This is important to highlight as it is easily treated [2-4]. J. G. BROCK-UTNE
Department of Anesthesia Stanford University School of Medicine Stanford, CA, USA 1. Aakerlund LP, Rosenberg J. Postoperative delirium: treatment with supplementary oxygen. British Journal of Anaesthesia 1994; 72: 286-290.
2. Komfeld DS, Zimberg S, Malm JR. Psychiatric complication of open heart surgery. New England Journal of Medicine 1965; 273: 287-291. 3. Brock-Utne JG, Cheetham RWS, Goodwin NM. Psychiatric problems in intensive care. Anaesthesia 1976; 31: 380-384. 4. Brock-Ume JG, Goodwin NM, Hicks JC. Acute confusional states and depression treated with maprotiline mesylate. South African Medical Journal 1979; 55: 641.
Ventilatory response to hypoxia Sir,—I wish to comment on Dr Goodman's excellent and interesting editorial [1] "Volatile agents and the ventilatory response to hypoxia". In the editorial I was quoted in a personal communication note saying, "that there is no important depression specifically of the hypoxic response". The quotation is correct but needs clarification. Hypoxic ventilatory responses are traditionally expressed as changes in minute ventilation related to the degree of hypoxia. In our studies [2-6] we found that by separating minute ventilation responses into changes in tidal volume and ventilatory frequency, hypoxic ventilatory responses are achieved by increased tidal volumes (motor response) in the awake state and by increased ventilatory frequencies (chronotropic response) during isoflurane anaesthesia [6]. We therefore emphasize that motor and timing responses have to be evaluated separately. The resulting minute ventilation seems, in our hands, to be the same in awake and anaesthetized subjects, at least when a poikilocapnic approach is used. These results, from studies in humans, are currently being scrutinized in ongoing investigations in our laboratory. S. LINDAHL
Department of Anaesthesiology and Intensive Care Karolinska Institute Stockholm, Sweden 1. Goodman NW. Volatile agents and the ventilatory response to hypoxia. British Journal of Anaesthesia 1994; 72: 503-505. 2. Sjogren D, Ebberyd A, Sollevi A, Lindahl SGE. Ventilatory responses to hypoxia in awake and anesthetized humans. Anesthesiology 1991; 75: A1102. 3. Lindahl SGE, SjSgren D, Sollevi A. Isoflurane anesthesia (0.6 MAC) and hypoxic ventilatory response in humans. Anesthesiology 1993; 79: A1201. 4. Sollevi A, Sjogren D, Lindahl SGE. Effect of isoflurane anesthesia on hypoxic and hypercapnic ventilatory response in humans. Anesthesiology 1993; 79: A1202. 5. Sjogren D, Sollevi A, Ebbcryd A, Lindahl SGE. Poikilocapnic hypoxic ventilatory response in humans during 0.85 MAC isoflurane anaesthesia. Acta Anaeslhcsiologica Scandinavica 1994; 38: 149-155. 6. Sjogren D, Sollevi A, Ebberyd A, Lindahl SGE. Isoflurane anaesthesia (0.6 MAC) and hypoxic ventilatory responses in humans. Acta Anaesthesiologica Scandinavica 1994; (in press). Sir,—Professor Lindahl makes an important point. Almost all the mathematical models of ventilation ignore riming: for example, in Carley and Shannon's model [1] "breathing frequency is chosen a priori and remains constant." We also know that halothanc, enflurane and isoflurane are all ventilatory depressants but do not have identical effects on ventilatory control. There is still much to learn about the effects of anaesthesia on human breathing. N. W. GOODMAN
University Department of Anaesthesia Southmead Hospital, Bristol 1. Carley DW, Shannon DC. A minimal mathematical model of human periodic breathing. Journal of Applied Physiology 1988; 65: 1400-1409.
Risk of aspiration with the laryngeal mask Sir,—We read with interest the study by Akhtar and Street on the risk of aspiration with the laryngeal mask airway (LMA) [1]. Fifty patients were allocated randomly to receive either IPPV or spontaneous ventilation. One patient in the spontaneous ventilation group demonstrated dye staining of the pharynx, and a second patient in the IPPV group, undergoing diagnostic
Downloaded from http://bja.oxfordjournals.org/ at University of Bath Library & Learning Centre on July 16, 2015
oxygen-air, before the Brompton Manley ventilator. The concentration of nitrogen dioxide was measured in the inspiratory tubing just before the patient and was always less than 2 ppm. We are concerned that Dr Jenkins was unaware of the potential dangers of the system of introducing a high concentration of nitric oxide as a continuous flow into the inspiratory limb of an intermittent flow ventilator [4]. This technique allows a bolus of high concentration nitric oxide to be delivered to the patient which cannot be measured with the slow response analysers in current use. In order to demonstrate this danger of inadequate mixing, we have tried to simulate the dynamics of the system described [4]. In the laboratory using a test lung, we substituted carbon dioxide for nitric oxide because we have a capnograph with a sufficiently rapid response. Adding carbon dioxide before the ventilator gives adequate mixing and consequently the expected concentration. In contrast, adding carbon dioxide to the inspiratory limb can give peak concentrations of three to five times the expected concentration. Paradoxically, mixing before the ventilator delivers a lower concentration of nitrogen dioxide to the patient: although the transit time is longer, mixing is better and the dispersal of the high concentration is more rapid. We do appreciate the point that haemodynamic variables are inherently unstable in the early period after cardiac surgery and that changes in baseline measurements may potentially flaw results. We set out to study the efficacy of inhaled nitric oxide in postoperative cardiac surgical patients; within the constraints of safe and ethical practice we believe the design of our study was suited to this purpose. We hope that other groups may now feel able to conduct such a study in patients with much higher pulmonary vascular pressures and resistances with all the attendant risks. We felt that including more severely diseased patients in one of the earliest clinical studies of nitric oxide was unjustifiable.