‘The True Value of IPPV'
Dr Neil Soni, Chelsea and Westminster Hospital, London
The meeting was opened by Dr John Chambers who was standing in for Professor Hunter who was unable to attend due to a prior engagement. Dr Chambers started the meeting by informing the audience that David Gray would be raising a cheque for £1000 on behalf of the MSA as a donation to the LSA in appreciation for the contribution made to the first FCARCSI Primary OSCE/Orals course earlier this month. He then introduced the speaker, Dr Neil Soni from the Chelsea and Westminster Hospital, London.
Dr Soni started his talk entitled ‘The True Value of IPPV’ by looking at the 1952 Polio epidemic in Copenhagen where mortality fell from 87% to 40% by the administration of IPPV by medical students. He said there were three principle problems; hypoxia, hypercapnia and sputum production. The first two were overcome by positive pressure ventilation and the third by the insertion of a tracheostomy. He emphasized that ventilatory failure was different from respiratory failure. He said that as an oxygenator, the lung had both a large surface area and perfusion and therefore had huge redundancy. He then pointed out the ‘West’ zones of ventilation which were produced by spontaneous ventilation through low negative pressures and that under these conditions, surfactant works well and the circulation is advantaged. He then looked at the lymphatics which he thought were an important lung defence mechanism and worked best during spontaneous breathing because of the pump effect on these low pressure vessels. He demonstrated the effects of positive pressure on lymphatic drainage and showed that this was impeded and made the lymphatics become leaky.
Dr Soni then examined the effects of positive pressure ventilation on the distribution of gas and blood flow within the lung and demonstrated the pressure differences particularly in ventilated patients in the Intensive Care Unit. In simple terms, he thought there were two types of alveoli in the patient with respiratory failure. Firstly those that had collapsed due to infection and inflammation and secondly those relatively normal alveolar that would be hyper-inflated due to the high pressures used in an attempt to recruit alveoli in these sick patients. He then looked at the haemodynamics of ventilation and said that the reduction in venous return due to the high intra-thoracic pressure could easily be compensated by increasing preload. He commented that in good areas of the lung transmission of pressures will be more easily facilitated by the relatively high compliance and therefore barotrauma will be more common in these areas. He then looked at surfactant and said that its distribution was different in positive pressure ventilation leading to pooling and therefore abnormal function leading to further alveolar collapse. The combination of positive pressure and poor surfactant commonly leads to over inflation or no inflation.
Dr Soni then spoke about hypercarbia and demonstrated from one paper that permissive hypercarbia improved outcome and in another in the BMJ from 1925, CO2 had been used as a treatment for shock. He reiterated his view that in ARDS, lung zones were either collapsed or over-expanded. Dr Soni then looked at the effects of positive pressure ventilation on other organ systems such as the kidney with a reduction in renal plasma flow and other deleterious effects on renal function. These could be reversed by spontaneous respiration and greater preload. There was also a reduction in hepatosplanchnic blood flow which could be corrected with fluid although this could lead to venous stasis.
Dr Soni then looked at positive pressure ventilation and lymphatic flow within the lungs. His conclusion was that lymphatic flow was greatly impeded by positive pressure and made even worse by the relatively high venous pressure in the SVC. This would inevitably lead to pooling within the interstitial space of the lungs. He then asked why have we used positive pressure ventilation when it is less efficient in terms of gas exchange than spontaneous respiration and causes inflammation and cardiac depression? It also disrupts surfactant which worsens inflammatory processes and impairs lymphatic production and drainage. He thought the combination of fluid stasis; inflammation and time usually lead to secondary infection. In ARDS he said that patients don’t usually die of hypoxia they more commonly die of infection and multi-organ failure. He thought that with modern ventilators, we are now at the limits of what is possible with this therapy. He wondered whether the focus on hypoxia was wrong when it had been demonstrated by the extreme Everest expedition that a significant degree of hypoxia could be tolerated without causing highly significant organ dysfunction.
Dr Soni discussed the possible alternatives. He thought that rather than using positive pressure ventilation to its limits, in fact the lung would be better served by resting it. It should still be ventilated but at physiological pressures. What we really need are new technologies to improve oxygenation and remove carbon dioxide but outside the lung. There are currently two new technologies PECLA (pumpless extra corporeal lung assist) and ECMO (extra corporeal membrane oxygenation). He thought both techniques had promise however, he compared them with the dialysis machines of 20 years ago which were associated with poor patient outcome and the current technology of haemodiafiltration which was far safer in the critically ill.
Dr Soni concluded with his thoughts that in measuring patient oxygenation, we may be measuring the wrong parameter and positive pressure ventilation may only give a short term gain. Lymphatic function had been ignored in the past because it was difficult to study. Dr Soni then covered a couple of other points; firstly he thought taking the ‘P’ out of CPAP would be a good idea because some of his recent work had shown that the real benefit of CPAP was the tight fitting mask and the avoidance of air-entrainment so that patients were actually getting additional oxygen. Another concept he was developing was that of ‘Ventilatory Ratio’. The numerator is the product of the measured minute volume and arterial pCO2 over the predicted value. This should normally be one and a higher value will clearly show a rise in dead space and deterioration in lung function.
Dr Soni took some questions from the floor. In answer to one question about the role of negative pressure ventilation, he quoted an Italian study that showed there was a lower infection rate in patients who were ventilated with this method compared with conventional ventilation. He thought that in 20 years time patients would be ventilated with a negative pressure technique with additional oxygen delivery and CO2 extraction by a technique such as ECMO. Dr Soni was asked if he had any experience with the oscillator and whether it was any better than the Novo Lung. He said he had no experience with the former however the Novo Lung would allow gentler ventilation by reducing the pCO2 if relative hypoxia was accepted. Dr Richard Nelson gave the vote of thanks and the meeting concluded at 20:30.