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higher and that a large number of babies are at increased risk of developing hypernatraemia.Clearly the problem is one of education of mothers beginning in the maternity unit and continuing through the advice of health visitors and family doctors. The use of written, illustrated instructions and practical lessons in the maternity unit and clinics where mothers can be shown and then practise how to reconstitute dried milk should be more widespread. Manufacturers of dried milk could improve the mixing instructions by illustrating the procedure step by step on the packet, as is done by one major manufacturer. The information on some packets that 1 fl. oz. (28-4 ml) equals two tablespoons could probably best be discarded and replaced by a statement that quantities must be measured accurately in a measuring jug. The volumes of tablespoons are variable and the strength of the milk will vary accordingly. As infant-feeding practices are largely influenced by tradition, folk-lore, and advertising pressures considerable educational effort may be needed to avert the trend to obesity and the dangers of hypernatraemia to which many infants seem to be exposed. I wish to thank Dr. J. H. Briscoe-Smith, medical officer of health for the City of Westminster, for permission to interview mothers attending infant welfare clinics.

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The selection of patients with mitral stenosis for valvotomy is considerably influenced by the degree of dyspncea of which the patient complains, and in many cases the history of progressive dyspncea with episodes of acute pulmonary cedema or haemoptysis makes the need for operation obvious. In some cases, however, fatigue is confused with dyspncea as a reason for limiting physical activity or the synmptoms of the effort syndrome may be superimposed so that some objective measurement of the degree of disability might be of value. Attempts to correlate the degree of dyspncea with the circulatory changes in the heart and lungs, measured by means of the cardiac catheter, or with results of tests of respiratory efficiency have given conflicting results. Most of these studies have been carried out with the patient at rest but even when repeated during steady exercise the same lack of correlation has been reported (West et al., 1953).Pathologists have long been familiar with the fact that the lungs of patients dying in heart failure were more rigid than normal lungs, but it was not until 1934 that Christie and Meakins (1934) measured in vivo the distensibility of the lungs in patients with congestive heart failure by means of simultaneous tracings of the tidal air and the intrapleural pressure fluctuations. They showed that in heart failure the lungs were more rigid than normal, probably because of pulmonary congestion, and that with clinical improvement the distensibility of the lungs improved. There was thought to be a direct relationship between the degree of lung rigidity and the amount of dyspncea and it was later suggested that cardiac dyspncea was reflex in origin, the increased lung rigidity through the Hering-Breuer reflex causing the rapid shallow breathing of heart failure (Christie, 1938). Because of the necessity of inducing a small pneumothorax to record the changes in intrapleural pressure little use has been made of the method of Christie and Meakins (1934) of measuring the pulmonary distensibility in cardiac patients. Dornhorst and Leathart (1952) have shown that an accurate record of changes in intrathoracic pressure can be obtained by recording the pressure changes in the cesophagus and this method has been used to study on a larger scale changes in lung distensibility and respiratory work in heart failure (Marshall et al., 1954).If the degree of cardiac dyspncea is directly related to the increased rigidity of the lungs, the measurement of pulmonary distensibility might be of help in assessing the amount of disability. In this investigation the relationship between dyspncea and pulmonary distensibility and respiratory work has been studied in 30 patients with mitral stenosis. Measurements were made at rest, and during and immediately after exercise, and in 6 patients were repeated 3-6 months after mitral valvotomy. METHODSChanges in intrathoracic pressure were measured using an cesophageal catheter and these were recorded simultaneously with records of the tidal air obtained with the pneumotacho...

, were reviewed from one to three years after operation. These patients had presented with serious mitral valve disease and there was a high incidence of severe dyspnoea and persistent congestive failure before operation. There were four operative deaths, and two survivors had poor results due to regurgitation alongside the prosthesis. The remaining 10 patients showed considerable improvement. Although no diuretics were given after operation there was little dyspnoea and congestive failure resolved. Anticoagulant therapy is given after operation, and there have been few embolic incidents. The pulmonary vascular resistance was raised to between 6 and 11 units before operation in six patients. There was no undue mortality in this group, and post-operative cardiac catheterization showed a considerable fall in resistance and an increase in cardiac output, suggesting resolution of the pulmonary vascular obstruction. Tricuspid incompetence in these patients disappeared post-operatively. We conclude that mitral valve replacement can restore a patient severely disabled by mitral valve disease to a nearly normal life. We do not regard pulmonary hypertension as a contraindication to operation. Starr and Edwards (1961) showed that it was possible to correct the mechanical abnormalities in mitral valve disease by replacing the valve with a mechanical prosthesis, and they demonstrated that the procedure gave effective relief of symptoms in patients with serious disability. Replacement of the mitral valve with the Starr-Edwards prosthesis has been performed in 50 patients at St. Bartholomew's Hospital since the end of 1963, and there are 39 survivors, a mortality rate of 22 %. Our first successful mitral valve replacement was performed as a desperate measure in a severely ill patient with considerable pulmonary vascular obstruction (Fig. 1). Following this experience we have continued to operate on such patients, and we do not regard the presence of pulmonary vascular disease as a contraindication to mitral valve replacement. As a result of this policy many of our patients have had serious congestive heart failure with tricuspid incompetence at the time of operation. There has been a gratifying improvement in the pulmonary vascular obstruction and in the congestive failure after operation in these patients.The present report is based on the post-operative evaluation of the 16 patients operated on before October 1965. Four of these patients died at operation. The 12 survivors have been followed for from one to three years, with particular reference to the fall in pulmonary vascular resistance which has followed the operation. METHODSClinical features before and after operation have been classified as slight, moderate, severe or gross abnormalities and coded from 0 (for normal) to 4 on this basis. Congestive failure was regarded as slight if the venous pressure was controlled by diuretic therapy, and as gross if hepatic puls-ation or severe oedema persisted in spite of this treatment. Right and left ventricular hypertrophy were...