Originally the tension of the respiratory muscles was tested in normal subjects by taking maximum pressure measurements at the mouth (Pimax),1617 while oesophageal and gastric balloon catheters allow the study of diaphragmatic strength. Contractions of the diaphragm can be obtained by electric or magnetic stimulation of the phrenic nerves.1819
In the intubated patient maximal pressure generation can be assessed during occluded maximal manoeuvres and this can be simply performed as the endotracheal tube is easily accessible. PImax was originally measured in intubated patients being weaned from mechanical ventilation by Sahn and Lakshminarayan.1 Patients with severe weakness (PImax <20 cm H2O) were unable to wean. However, as a sole indicator of the ability to breathe spontaneously, muscle strength alone may not predict success or failure. Severely weak muscles can only sustain spontaneous breathing if all other factors are entirely normal.
The measurement of respiratory muscle strength on the ICU presents more challenges.20 Firstly, generating maximal pressure with an artificial airway leads to movement of the endotracheal tube which inhibits maximal pressure generation. Secondly, many patients cannot sustain the one second plateau pressure demanded by the original PImax protocol.16 Lastly, few patients can coordinate respiration to ensure that they reach residual volume before maximum inspiratory effort.
In order to improve the ability of patients and normal subjects to perform a maximal inspiratory manoeuvre, brief inspiratory efforts were investigated during gasping against a closed airway with pressure measured in the endotracheal tube.13 21 Inspiration against an occluded airway is well tolerated by patients provided the technique is well explained and that the gasping does not continue for longer than 20 seconds. An advantage of the gasp is that maximal efforts build up over the 3-8 inspiratory efforts. This technique has been used to measure strength in patients who are not fully conscious, enabling a voluntary estimate to be made in a group of patients who were previously unable to comply with a volitional protocol.21
When the reproducibility of the measurement of inspiratory strength was assessed in intubated patients, the between observer, within day, and between day variability of inspira-tory efforts were very variable.22 The observation of a low (weak) inspiratory pressure has to be treated with caution. However, a strong effort is reassuring and unlikely to be an artifact. Finally, non-volitional magnetic stimulation of the diaphragm has been applied to the critically ill. This technique may enable studies to be performed that will address the time course and extent of respiratory and skeletal muscle weakness in critically ill patients.23
Aetiology of respiratory muscle weakness in the critically ill
Although most patients are weak, the precise cause of weakness is not always known. Causes of acute weakness include electrolyte disturbances such as hypophosphataemia and hypomagnesaemia. Although electrolyte abnormalities are relatively common on the ICU, their significance in this context is unknown. Long term weakness may be due to critical illness itself. Disuse of skeletal muscles leads to atrophy, where the reduced cross section of the muscle decreases maximum tension. This process is rapid and 7-10 days of disuse may decrease maximum pressure generation by the diaphragm by 50%.24 Critical illnesses are commonly associated with a polyneuropathy,25 with or without a myopathy.26 Such patients may present with extreme weakness, mainly in the legs, and tetraplegia is possible.27
If the muscles are weak, can we improve strength with exercise or training? Skeletal muscle responds to training regimens by increasing mass and cross sectional area. For a training regimen to be effective it must be controlled, such that the task is repetitive and supramaximal with periods of rest between training exercises.28 In addition, strength training differs conceptually and in practice from endurance training.29 For the respiratory muscles, training is ill defined and although it is felt that the respiratory muscles should behave in a similar manner to other muscle groups, definitive studies have yet to show how they may be trained. It is likely that the response to training will in part be genetically determined. The general observation that some individuals are responsive to and have ability at certain types of exercise has led to studies showing genetic differences in the response to training according to genotype.30 A genetic polymorphism of the angiotensin converting enzyme (ACE) gene has been described with a 256 base pair deletion or insertion, termed DD or II.31 In de-trained subjects there is an 11-fold difference between homozygous subgroups in response to performing a repetitive biceps exercise.30 Recently, respiratory muscle strength and endurance was studied in de-trained subjects who underwent general non-specific training. Respiratory muscle endurance was increased fivefold in the II subgroup.32
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