One-lung ventilation in a patient with an organizing empyema and severe idiopathic pulmonary fibrosis.
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Biomedical subjects
Publications and source records attributed to J Pfitzner.
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At the time one-lung ventilation is initiated, nitrogen from the atmosphere may enter the non-ventilated lung via a double-lumen tube connector that has been left open to air, even momentarily. Ongoing oxygen uptake from the non-ventilated lung raises the partial pressure of nitrogen. This should lead to activation of hypoxic pulmonary vasoconstriction and a reduction in intra-pulmonary shunting. However, in spite of this, some patients still become hypoxaemic. In such cases, it may be advantageous to have excluded nitrogen from the non-ventilated lung by connecting it to an oxygen source at ambient pressure. Ongoing apnoeic oxygenation, while the airways are patent, and as the lung collapses, should delay the onset of arterial desaturation. In this paper we review the theoretical basis for apnoeic oxygenation during one-lung ventilation, and in particular on oxygen uptake by the non-ventilated lung prior to and during its subsequent collapse.
A left thoracotomy for decortication of an infected haemothorax was performed on a 52-year-old man with a partially infarcted left lower lobe that occurred as a rare complication of a pulmonary venous embolus. Before the completion of surgery, after an uncomplicated 40 minutes of one-lung ventilation, the left lung was temporarily re-expanded to assess air leak. On the resumption of one-lung ventilation the SpO2 fell rapidly to 85%, despite apnoeic oxygenation of the non-ventilated lung. In the absence of evidence of double-lumen tube displacement, intra-pulmonary shunting as a consequence of impaired hypoxic pulmonary vasoconstriction in the newly expanded markedly pathological lung is considered the most likely mechanism.
The present report describes two similar thoracoscopic procedures performed on the same 81-year-old male patient. Because acute hypoxia had developed during one-lung ventilation on the first occasion, serial blood gases were taken during the second. Also, whereas on the first occasion the non-ventilated lung had been left open to air when one-lung ventilation was initiated, on the second it was connected to an ambient pressure oxygen source with the object of theoretically enabling apnoeic oxygenation during lung collapse. It is argued that this fundamental difference in anaesthetic practice may have contributed to the improved oxygenation that was recorded during the second thoracoscopy.
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Due to the presence of major lung or extra-pulmonary pathology, which may be unilateral or bilateral, the initial placement of a double-lumen tube is not always straightforward. Although fibreoptic bronchoscopy is often used to confirm "correct" placement, a "blind" technique is frequently used for the initial insertion. The currently widely taught blind technique involves tracheal cuff inflation and ventilation of both lungs as a first manoeuvre, with a subsequent assessment of single-lung ventilation by clamping off in turn, the two limbs of the double-lumen tube double-connector: An alternative approach involves the bronchial cuff being inflated first, and then using a single-connector to transfer ventilation from one lung to the other. In this paper this technique is described and compared to the more traditional method. On a purely "number of steps" basis, the single-connector approach has several advantages. Furthermore, use of a technique that involves bronchial cuff inflation and single-lung ventilation as a first manoeuvre may reduce the risk of a temporarily malplaced double-lumen tube creating a potentially harmful ball-valve effect in a partially obstructed lobe or lung.
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Carbon dioxide insufflation into the pleural space during one-lung anaesthesia for thoracoscopic surgery is used in some centres to improve surgical access, even though this practice has been associated with well-described cardiovascular compromise. The present report is of a 35-year-old woman undergoing thoracoscopic left dorsal sympathectomy for hyperhidrosis. During one-lung anaesthesia the insufflation of carbon dioxide into the non-ventilated hemithorax for approximately 60 seconds, using a pressure-limited gas inflow, was accompanied by profound bradycardia and hypotension that resolved promptly with the release of the gas. Possible mechanisms for the cardiovascular collapse are discussed, and the role of carbon dioxide insufflation as a means of expediting lung collapse for procedures performed using single-lung ventilation is questioned.
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By enhancing gaseous uptake from the non-ventilated lung during procedures performed thoracoscopically, the rapid diffusion properties of nitrous oxide would be expected to speed lung collapse and so facilitate surgery. To assess the effect of nitrous oxide on the speed of absorptive lung collapse, a study was conducted using 11 anaesthetised sheep. Speed of collapse was assessed in an indirect manner by recording the time required in a closed-chest situation for the airway pressure distal to a single lung airway occlusion to decrease to - 1.0 kPa. The influence of nitrous oxide was assessed by comparing the time taken for this decrease in airway pressure when the animal was being mechanically ventilated with 50% nitrous oxide in oxygen with the time taken when using 100% oxygen. In all assessments, it was found that the decrease in airway pressure to - 1.0 kPa occurred in a shorter time when nitrous oxide was used. The findings lend support to the hypothesis that during thoracoscopic surgery, mechanical lung ventilation with an oxygen/nitrous oxide mixture will increase the rate of gaseous uptake from the non-ventilated lung and so hasten its absorptive collapse.
A study of 10 anaesthetised patients placed in the lateral position for thoracoscopic surgery assessed whether transient increases in pleural pressure on the side of the non-ventilated lung might increase the speed at which gas vents from that lung. The transient increases in pleural pressure were generated by the mediastinal displacement that occurs with each inspiratory phase of positive pressure ventilation of the dependent lung. When combined with a unidirectional valve allowing gas to flow out of the non-ventilated lung, and a second valve allowing ambient airflow into, but not out of, the thoracic cavity via an initial thoracoscopy access site, this mediastinal displacement could conceivably serve to 'pump' gas out of the non-ventilated lung. Using the four different combinations of valve inclusion or omission, the volume of gas that vented from the non-ventilated lung into a measuring spirometer was recorded during a 120-s measurement sequence. It was found that the speed of venting was not increased by the transient increases in pleural pressure, and that in all but one of a total of 34 measurement sequences, venting had ceased by the end of the sequence. Gas venting was a mean (SD) of 85.5 (11.9)% complete in 25 s (five breaths), and 96.6 (6.1)% complete in 60 s. This prompt partial lung collapse very likely reflected the passive elastic recoil of the lung, while the failure of transient increases in pleural pressure to result in ongoing venting of gas was probably a consequence of airways closure as the lung collapsed. It is concluded that techniques that aim to speed lung collapse by increasing pleural pressure are unlikely to be effective.
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Pulmonary alveolar proteinosis is a rare condition characterized by the abnormal accumulation of surfactant-like material within the alveolar spaces and distal bronchioles. Two cases with contrasting modes of presentation, course, and response to therapeutic whole lung lavage are described. Both cases were in hypoxaemic respiratory failure at the time the definitive diagnosis was made, and in both cases the diagnosis was made by segmental bronchoalveolar lavage following negative open lung biopsy. In neither was an underlying causative organism or agent identified. In one case the alveolar proteinosis developed in late pregnancy, a presentation that is previously unreported. Clinical improvement in this case required repeated whole lung lavages and was accompanied by a trend towards normalization of the ratios of surfactant protein-A and surfactant protein-B to disaturated phospholipid, ratios which may be useful as prognostic indicators. The response to therapeutic lavage was markedly different in the two cases, and it is postulated that this may relate to the fact that alveolar proteinosis is a heterogeneous disease and that the course and response to treatment may relate in part to the specific composition of the abnormal proteinaceous fluid.
We describe the anaesthetic management of a patient undergoing lobectomy for cavitating lung abscess complicated by haemoptysis. Surgery for lung abscess is one of the absolute indications for the use of a double-lumen tube (DLT). Because pus or blood could impede fibreoptic-assisted DLT placement, a traditional, blind placement of the DLT was performed. To protect the uninvolved parts of the operated lung, ventilation of the lung with the abscess was not performed until the resection of the involved lobe had been completed.
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