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Effect of propofol on twitch diaphragmatic pressure
- Ping Chen (10 January 2009)
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Similar, preferably isometric, conditions are needed to assess diaphragm contractility.
- Gordon B Drummond (10 January 2009)
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Ping Chen London
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Editor- I would like to commend Dr Zhang and colleagues on their clinical study demonstrating that propofol produce a decrease in TwPdi by an inhibitory effect on diaphragmatic contractility. It was mentioned in the article that intermittent supramaximal magnetic stimuli were performed when the patients were at functional residual capacity. It is not clear how individual functional residual capacity was determined. Authors also pointed out that they did not take into account the effect of propofol on lung volume and its impact on twitch strength. Further study might required to clarify the underlying mechanism of inhibitory effect on diaphragmatic contractility. Conflict of Interest:None declared |
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Gordon B Drummond Edinburgh University
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Zhang and co-authors1, in their study of the effects of propofol on the diaphragm, state that there are no studies of the effects of propofol on peripheral neuromuscular transmission. However, Dueck and colleagues recently reported the effects of bolus doses of propofol, similar to those used by Zhang and his co-workers, on central and peripheral motor pathways.2 They measured F waves and found that although the central transmission of stimuli applied to the median nerve was progressively reduced by cumulative doses of propofol, the direct peripheral component of neuromuscular transmission (M wave) was not affected at all. A similar observation of sustained direct muscle ,responses after repeated doses of propofol was made by Kerz and co- workers.3 How then is it possible to explain the apparent effect that propofol has on the diaphragm? When peripheral muscles are studied, the EMG response is often used to assess the adequacy of neuromuscular transmission because the muscle is easily accessible. Although the diaphragm can also be studied using EMG, the study of single twitch responses is not simple, and requires suitably accurate electrode placement.4 5 If muscle contractile force is to be assessed, a peripheral muscle can be held so that contraction is isometric. Thus measurement of the force generated will indicate any possible impairment of contractility. However if the muscle shortens, then the force developed is no longer a direct index of contractility. The well-known force-length6 and force- velocity7 effects reduce the force developed if the muscle either changes its length, or is shortening when the tension is measured. Because of its shape and position, the diaphragm is a much more difficult muscle to study. In particular a single twitch is a transient event that is dynamic and particularly difficult to capture faithfully. The study that Zhang and co-workers cite by Nishina8 was of isometrically contracting isolated diaphragm strips, and did not, as they suggest, show that propofol reduced contractility. Those workers found that none of propofol, thiopental, ketamine, nor midazolam had any effect on diaphragm tension. In contrast, the studies that Zhang and his colleagues cite by Fujii9-11 were of intact dogs, where an attempt had been made to limit diaphragm movement by placing a plaster cast around the lower ribcage and abdomen. Although this is a widely used strategy to obtain “isometric” contraction, it is unlikely to do so. For example, even with airway occlusion, diaphragm contraction leads to diaphragm shortening.12 Most of the studies of diaphragm twitch and sniff have been done in conscious subjects. However the transition from consciousness to anaesthesia is an important additional factor in interpreting these studies of propofol. The mechanical interaction between the ribcage and abdomen, the resultant effects on diaphragm dimensions, and most importantly changes in ribcage flexibility are equally valid explanations for the apparent reduction in contractility reported by Fujii and indeed by Zhang and co-workers. Propofol has profound and immediate effects on ribcage dimensions13 and presumably on the stiffness of the ribcage. In conscious subjects, the ribcage muscles play an important part is sustaining rigidity of the chest wall, as has been shown in studies where the diaphragm is stimulated alone or in patients with quadriplegia.14-18 I suggest that the findings in the study by Zhang,1 as in the similar study by Shaw,19 could be caused by the effect of propofol reducing the stiffness of the ribcage. Thus the tension developing in the diaphragm would cause more distortion and allow more shortening of the diaphragm, with less resultant tension and transdiaphragmatic pressure. The only satisfactory means of establishing the validity of the method used would be to simultaneously measure ribcage dimensions to ensure that these are not affected differently by the diaphragm stimulation with and without propofol. Until we can be sure on that point, I would prefer to consider that the diaphragm will behave as other skeletal muscles,2 and not be affected directly by agents such as propofol. Reference List (1) Zhang XJ, Yu G, Wen XH, Lin ZC, Yang FQ, Zheng ZG et al. Effect of propofol on twitch diaphragmatic pressure evoked by cervical magnetic stimulation in patients. Br J Anaesth 2009; 102: 61-4. (2) Dueck MH, Oberthuer A, Wedekind C, Paul M, Boerner U. Propofol impairs the central but not the peripheral part of the motor system. Anesth Analg 2003; 96: 449-555. (3) Kerz T, Hennes HJ, Feve A, Decq P, Filipetti P, Duvaldestin P. Effects of propofol on H-reflex in humans. Anesthesiology 2001; 94: 32-7. (4) Mckenzie DK, Gandevia SC. Phrenic nerve conduction times and twitch pressures of the human diaphragm. J Appl Physiol 1985; 58: 1496- 504. (5) Gandevia SC, Mckenzie DK. Human diaphragmatic emg - changes with lung-volume and posture during supramaximal phrenic stimulation. J Appl Physiol 1986; 60: 1420-8. (6) Gordon AM, Huxley AF, Julian FJ. The variation in isometric tension with sarcomere length in vertebrate muscle fibres. J Physiol (Lond) 1966; 184: 170-92. (7) Fenn WO, Marsh BS. Muscular force at different speeds of shortening. J Physiol (Lond) 1935; 85: 277-97. (8) Nishina K, Mikawa K, Kodama S, Kagawa T, Uesugi T, Obara H. The effects of enflurane, isoflurane, and intravenous anesthetics on rat diaphragmatic function and fatigability. Anesth Analg 2003; 96: 1674-8, table. (9) Fujii Y, Hoshi T, Takahashi S, Toyooka H. Propofol decreases diaphragmatic contractility in dogs. Anesth Analg 1999; 89: 1557-60. (10) Fujii Y, Toyooka H. Midazolam versus propofol for reducing contractility of fatigued canine diaphragm. Br J Anaesth 2001; 86: 879-81. (11) Fujii Y, Uemura A, Toyooka H. The recovery profile of reduced diaphragmatic contractility induced by propofol in dogs. Anesth Analg 2004; 99: 113-6. (12) Easton PA, Fitting J-W, Grassino AE. Costal and crural diaphragm in early inspiration: free breathing and occlusion. J Appl Physiol 1987; 63: 1622-8. (13) Rutherford JS, Logan MR, Drummond GB. Changes in end-expiratory lung volume on induction of anaesthesia with thiopentone or propofol. Br J Anaesth 1994; 73: 579-82. (14) Legrand A, Schneider E, Gevenois P-A, De Troyer A. Respiratory effects of the scalene and sternomastoid muscles in humans. J Appl Physiol 2003; 94: 1467-72. (15) Danon J, Druz WS, Goldberg NB, Sharp JT. Function of the isolated paced diaphragm and the cervical accessory muscles in C1 quadriplegics. Am Rev Respir Dis 1979; 118: 373-90. (16) De Troyer A, Estenne M. Coordination between rib cage muscles and diaphragm during quiet breathing in humans. Journal of Applied Physiology Respiratory Environmental and Exercise Physiology 1984; 57: 899 -906. (17) Urmey W, Loring S, Mead J, Slutsky AS, Sarkarati M, Rossier A et al. Upper and lower rib cage deformation during breathing in quadriplegics. J Appl Physiol 1986; 60: 618-22. (18) Chihara K, Kenyon CM, Macklem PT. Human rib cage distortability. J Appl Physiol 1996; 81: 437-47. (19) Shaw IC, Mills GH, Turnbull D. The effect of propofol on airway pressures generated by magnetic stimulation of the phrenic nerves. Intensive Care Med 2002; 28: 891-7. Conflict of Interest:None declared |
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