Effects of physiotherapy during intermittent positive pressure ventilation Changes in arterial blood gas tensions

Transcription

1 Aiiaesthesia vol27 no 3 Jul-y 1972 Effects of physiotherapy during intermittent positive pressure ventilation Changes in arterial blood gas tensions J. Gormezano M. A. Branthwaite The successful maintenance of intermittent positive pressure ventilation (IPPV) over prolonged periods of time requires adequate removal of bronchial secretions 1 2. The technique of hyperinflation with manual chest compression and endotracheal suction 3 is commonly employed, but information on the acute results of this therapy is limited. A number of studies have reported hypoxia following endotracheal suction in apnoeic, anaesthetised patients4-6 and in patients receiving IPPV following cardiac surgery7. A decrease in arterial oxygen tension following pulmonary physiotherapy was reported by Holloway et a/. 8 who studied neonates with tetanus treated with paralysis and IPPV. This paper presents the results of an investigation carried out in adult patients maintained on IPPV. Changes in arterial blood gas tensions were recorded during and after pulmonary physiotherapy which included the technique of hyperinflation, manual chest compression and endotracheal suction. MATERIAL AND METHODS Forty-two patients receiving IPPV, ranging in age from 14 to 82 years, were studied on a total of 48 occasions. Twenty-nine had recently undergone cardiac surgery, 11 were suffering from respiratory failure, one had sustained neurological damage following cardiac arrest caused by a pulmonary embolus and one had recently suffered a myocardial infarction. IPPV had been employed for at least six hours in all patients, using a Brompton-Manley ventilator9 and either an endotracheal or a tracheostomy tube. Sedation with an opiate or diazepam was given when necessary to facilitate IPPV ; paralysis with pancuronium bromide was required in seven patients but no patient was totally paralysed. Inspired oxygen concentration was adjusted to maintain an arterial oxygen tension between 100 and 200mm Hg whenever possible; no patient was receiving more than SO /,, oxygen. Humidification was provided by a Cape hot-water humidifier. J. Gorinezano, FFARCS, Research Assistant irr Anaesthetics and M. A. Branth waite, MRCP, FFA RCS, Consultant Anaesthetist, Brompion Hospital, Fulhatn Road, London S W3 6HP. 258

2 Anaesthesia vol27 ti0 3 July 1972 informed consent was obtained from all fully conscious subjects but many of these patients were unable to comprehend the nature of the study and consent was not requested. In most patients, arterial cannulation had already been performed for pressure monitoring or blood sampling and the additional samples required for the study were collected from this site. There was no alteration in the duration or nature of therapy as a result of the study. Three groups were defined according to the indications for IPPV. Group I (18patients; 18 studies) These patients had no cardio-pulmonary disability at the time of treatment; 14 had been electively ventilated following cardiac surgery and were studied immediately prior to extubation. In the remaining four instances, IPPV had been instituted or continued because of neurological damage. Group 2 (13patients; 14 studies) Patients in this group were maintained on IPPV because of cardiovascular complications. In eight post-operative patients, a clinical diagnosis of low cardiac output was made on the basis of a low or unstable blood pressure, poor urinary output and peripheral vasoconstriction. Isoprenaline and other supportive therapy was required. One patient was re-studied twentyfour hours later, following the onset of a respiratory tract infection during which his cardiovascular status was still unsatisfactory. Two post-operative patients were suffering from pulmonary oedema, and one was jaundiced and in heart failure six days following mitral valve replacement. The remaining patient had suffered a cardiac arrest due to myocardial infarction the previous day. Group 3 ( I 1 patients; 16 studies) These patients were suffering from respiratory failure of varying aetiology. Three had a past history of cardiovascular pathology, but there was no circulatory embarrassment at the time of the study. Further studies were undertaken if secondary infection occurred, if pulmonary sepsis spread to give bilateral involvement or following the onset of septicaemia. Procedure In the majority of patients an arterial cannula was already in situ. In the remaining cases, a Medicut (20 gauge 2 inch-5cm) cannula was inserted percutaneously into the radial artery under local anaesthesia before treatment started. Samples were collected anaerobically and stored immediately in ice. Analysis for oxygen (Pao,) and carbon dioxide tensions (Paco2) was carried out within an hour using a Radiometer BMS 3 electrode system calibrated with known gas mixtures. The values obtained were corrected for body temperature when necessary. 2 59

3 Anaesthesia vol27 no 3 July 1972 Treatment was carried out with the patient lying supine if within the first 24 hours following operation, or if movement from side to side precipitated an alteration in cardiac rhythm or rate or blood pressure. Apart from these circumstances, all patients were treated while lying in the lateral position. Both sides were treated during one session unless hypotension, tachycardia or excessive sweating occurred. Hyperinflation was carried out using the manually-operated circuit of the ventilator and the inspired oxygen concentration therefore remained unaltered. The maximum inflation pressure used was 20cm H20 above the pressure required during the preceding period of mechanical ventilation. Hyperinflation alternated with manual compression of the chest at a frequency of approximately 20 cycles/minute. Endotracheal suction was employed as soon as secretions were audible within the air passages, if the patient attempted to cough or when the cycle of hyperinflation and manual compression had been carried out for 30 to 60 seconds. If bronchial secretions were difficult to aspirate, 1 to 2ml of normal saline were instilled into the trachea and the cycle of hyperinflation and manual compression recommenced. The total duration of treatment was 7 to 20 minutes depending on whether one or both sides were treated and whether or not copious secretions were mobilised. Arterial blood samples were collected before and at 5, 15 and 30 minutes after the completion of treatment with the patient lying in the same position on each occasion. In 31 studies, additional samples were collected during treatment in an attempt to differentiate the effects of hyperinflation with chest compression from those caused by endotracheal suction. Posture during the collection of these samples often differed from that adopted before and after treatment. RESULTS The values obtained on each occasion during and after treatment were compared with the pre-treatment figure and Student's t test was used to assess the significance of the changes observed. The results of this analysis are shown in table 1, together with figures for the mean change and standard error of the mean. The t test was also applied to the difference between the values recorded following hyperinflation and those following suction. Arterial oxygert tension Although there was a tendency for Pa02 to increase in group 1 and decrease in group 3 following treatment, there was considerable individual variation and none of the changes were significant (p> 0.1). In contrast, patients in group 2 showed a significant decrease in Pa02 at both 5 and 15 minutes (p <0.01); subsequently, Pa02 tended to rise and, by 30 minutes, did not differ significantly from the pre-treatment value (p > 0.05). 2 60

4 Anaesthesia vol27 no 3 J I I 1972 ~ TABLE 1 Changes in orteriul blood gas tensions following rreufment Mean Group 1 SEM n-18 F Mean Croup I1 SEhl n= I4 P Mean Group 111 SEM F Hyperinflation Pao* PUCO, <0.01 > >0.05 <O.Wl >o.os >o.os Suction I 5 min PUO, POCO* PUO, POCO, >0.05 > >0.05 <O.OOI >0.05 < >0.05 <O.Ool <0.01 <O.oOl >0.05 < min POO, Poco, >0.05 < <0.01 < >0.05 <O.Ol 30 min PUO, paco >O.OS >0.05 > l.2 >0.05 <0.05 Following hyperinflation alone, there was a significant increase in Pa02 in group 1 (p < 0.01) but no significant change in group 3 (p > 0.05). The mean value of Pa02 fell by 10.7mm in group 2 but this result did not reach significance (p > 0.05). Endotracheal suction caused a drop in mean P a02 in all groups. Although this additional decrease in patients in group 2 lowered Pa02 by a mean of 15mm from the pre-treatment value, the change between the value recorded following hyperinflation and that following suction was not significant in any group (p > 0.05). Arterial carbon dioxide tension. In all groups, treatment was followed by a small but significant increase in Paco2 (p <0.001) which was most marked and persistent in patients in group 3 in whom the mean value at 30 minutes was still significantlyelevated (p < 0.05). DISCUSSION Although treatment was similar in all groups, significant changes in Pa02 were largely confined to patients in group 2 who were all suffering from serious cardiac pathology. This distinction is presumed to reflect some circulatory factor which did not apply to the other groups. Several possible mechanisms could be responsible. An increase in intrathoracic pressure could lower the cardiac output so that for a given shunt effect, mixed venous P o2 and hence Pa02 would falllo. Such a mechanism would require that cardiac output fell in response to a decrease in effective filling pressure and this is less true for the failing than for the normal heart. 1 1 Such a change would also require that compensatory reflexes, which normally operate to increase venous tone and so restore ventricular filling, would be inadequate or inoperative 1 2. Alternative explanations for the fall in Pa02 in group 2 are an increase in shunt effect without any change in mixed venous Poz, or an increase in oxygen consumption without a concomitant rise in cardiac output and alveolar ventilation. Although the available evidence does not allow these 261

5 Atinesrhesia voi27 no 3 Jufy 1972 various mechanisms to be differentiated, it may be noted that none of the patients were totally paralysed at the time of treatment, and that the disturbance resulted in an increase in muscle activity so that some increase in oxygen consumption must have been inevitable. It is likely that several factors were operating simultaneously in this very unstable state, probably to a differing degree in different patients. This is borne out by the wide scatter of results. The possibility that hypoventilation contributed to the results could not be excluded, although the increases in Pacop were presumed to be due to partial rebreathing which occurs when the ventilator is manually operated. The magnitude of the decrease in Pa02 was considerable in some patients. In group 2, values for Pa02 of less than 60mm Hg were produced on four occasions, and on two more occasions, pre-treatment values less than 60mm Hg were reduced further (by 8 and 14mm Hg respectively). These values were maintained for at least 15 minutes and represent a degree of hypoxaemia which is undesirable in patients with cardiac pathology. Smaller falls in Paop which do not result in arterial desaturation, may impair tissue oxygenation if the cardiac output is also low1 3. The value of IPPV following cardiac surgery is unquestioned Pulmonary function may be disordered and considerable effort is required to maintain spontaneous respiration The hazards of IPPV include pulmonary collapse, retention of secretions and subsequent infection 19. The technique of physiotherapy used here is recommended to minimise these hazards3 but the potential value of this prophylaxis must be balanced against the danger of acute hypoxia which may result. It is suggested that the risks of therapy may outweigh the benefits unless there is definite evidence of pulmonary collapse, or secretions which cannot be mobilised readily using suction alone. If positive indications for physiotherapy exist, short frequent periods of therapy may cause less change in Paoz. In a preliminary study of five patients with signs of circulatory inadequacy following valve replacement surgery, treatment lasting less than five minutes was only followed by a fall in Pa02 in one moribund patient who had previously suffered multiple cardiac arrests. The importance of speed in the execution of endotracheal suction is confirmed by the present study. Although Pa02 fell in all groups following suction, the results were not statistically significant. The findings can be compared with those of Taylor et al. 7 who showed a significant drop in Pao2, maximal 30 seconds after disconnection from the ventilator. In the present series, the average duration of suction was 15 seconds and subsequent sampling occupied 3 seconds so that the patients were only disconnected for a total period of less than 20 seconds. In patients maintained on IPPV for reasons other than circulatory pathology (groups 1 and 3), the changes in Pa02 were variable. It was not possible to assess whether prophylactic treatment in patients in group 1 262

6 Amesthesirr ~ July 1972 (without cardio-respiratory pathology) had any influence on their subsequent clinical course. In patients with profuse bronchial secretions, the efficacy of this technique of mobilising secretions is indisputable even though significant improvement in blood gas tensions was not immediately apparent in the present series (group 3). When respiratory failure is associated with severe airways obstruction, this form of therapy may be less advisable. In two of four patients with reversible airways obstruction, there was a noticeable increase in audible spasm, together with a rise in inflation pressure following treatment. Arterial Po2 in both these patients fell by 30mm Hg or more and these values persisted for at least 30 minutes. SUMMARY The technique of manual hyperinflation with chest compression and endotracheal suction may cause a fall in arterial Po2 in some patients maintained on IPPV. It is suggested that the treatment should be employed with caution in patients with circulatory failure due to cardiac pathology or in the presence of severe airways obstruction. Short periods of treatment, lasting less than five minutes may be preferable. The importance of speed during endotracheal suction is emphasised. A ck no wledgetnoirs The authors are grateful to Miss D. Gaskell and the Staff of the Physiotherapy Department for their helpful co-operation and also to the Physicians and Surgeons of the Brompton Hospital for permission to study patients under their care. Dr J. Gormezano was supported by a grant from the Research Funds of the Board of Goveriiors, The National Heart and Chest Hospitals. Mrs A. Harrison kindly provided statistical assistance. References I Spencer,G.T. (1966). In Wylie,W.D. and Churchill-Davids0n.H.C. A Prtrctice of.4rmesthesin, 2nd edn, p London: Lloyd-Luke Ltd 2 Gilston,A. & Resnekov,L. (1971). Cardio-Respiratory Resuscifafion, 1st edn, p London : William Heinemann Medical Books Ltd 3 Clement,A.J. & Hiibsch,S.K. (1968). Chest physiotherapy by the Bag-Squeezing method: A guide to technique. Physiotherapy. 54,355 4 R0sen.M. & Hillard,E.K. (1962). The effects of negative pressure during tracheal suction. Anesthesia and Analgesia, Ciirrenf Researches, 41,50.5 Berman,I.R. & Stah1,W.M. (1968). Prevention of hypoxic complications during endotracheal suctioning. Surgery, 63,586 n Boutros,A.R. (1970). Arterial blood oxygenation during and after endotracheal wctioning in the apnoeic patient. Anesthesiology, 32, I14 7 Taylor,P.A. & Waters, H.R.(1971). Arterial oxygen tensions following endotracheal suction on 1PPV. Anaesthesia, 26,289 Holloway,R., Adams,E.B., Desai,S.D. & Thambiran,A.K. (1969). Effect of chest physiotherapy on blood gases of neonates treated by intermittent positive pressure respiration. Thorax, 24,421 9 English,I.C.W. & Manley,R.E.W. (1970). The Brompton system of artificial ventilation. Anaesthesia, 25,

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