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Mitral Stenosis and the Crescendo Presystolic Murmur
1107
by increased lung stiffness and resistance to airflow,2’ so that CO2 retention begins. Controversy also surrounds the therapeutic implicaIntermittent observations. and intraventilation (I.P.P.v.) positive-pressure venous bicarbonate were regarded as essential to the recovery of 4 patients with extreme combined acidosis tions of these
new
(arterial pH 6-87-6-99, PC02 76-120 mm. Hg),lo although conventional treatment with oxygen, digoxin, aminophylline, and a diuretic was also given. However, over a third of 55 slightly older patients died, despite all these measures, including I.P.P.V.,6 although their combined acidosis was less severe. Only 4 of ABERMAN and FULOP’s 45 patients died,! but the PCO2 never exceeded 60 mm. Hg (although pH was 7-10 or less in 6 cases). They used I.P.P.V. in only 2 patients, and bicarbonate in none. Their blood-gas results were not immediately available to guide treatment, so that morphine was given to 9 patients with C02 retention, when this was not suspected clinically. Only 2 of these patients subsequently required I.P.P.V., but it seems reasonable to withhold morphine in the first instance if the Pco2 is known to be over 60 mm. Hg, despite the valuable reduction in central blood volume 28 and dilatation of capacitance vessels 29 which probably follow its use in left ventricular failure. Clinical recognition of both severe hypoxaemia 30 and hypercapnia 1,8 is difficult in pulmonary oedema, but clouding of consciousness remains an important clinical clue to combined respiratory and metabolic acidosis.8,10 i.P.P.v. and bicarbonate can undoubtedly save lives, but should probably be reserved for patients with severe combined acidosis and PC02 levels over The prompt recognition of these 60 mm. Hg. abnormalities requires a 24-hour blood-gas diagnostic service, which will make many other contributions to the proper management of medical and surgical emergencies in the modern hospital.
Mitral Stenosis and the Crescendo Presystolic Murmur WHAT causes the presystolic murmur in mitral stenosis ? This is an old controversy,31—36 and CRILEY and his colleagues have obtained some fresh evidence. 37 They recorded the temporal relations of the Q wave of the electrocardiogram, pressure changes in the left ventricle and atrium, the first heart-sound of 27. 28. 29.
Sharp, J. T., Griffith, G. T., Bunnell, I. L., Greene, D. G. J. clin. Invest. 1958, 37, 111. Sapru, R. P. PH.D. thesis, University of Edinburgh, 1966. Vasko, J. S., Henney, R. P., Oldham, H. N., Brawley, R. K., Morrow, A. G. Am. J. Cardiol. 1966, 18, 876. Vitale, A., Dumke, P. R., Comroe, J. H. Circulation, 1954, 10, 81. Gairdner, W. T. Edinb. med. J. 1861, 7, 438. Henderson, Y., Johnson, F. E. Heart, 1912, 4, 69.
30. 31. 32. 33. Lewis, T. ibid. 1913, 4, 241. 34. Dean, A. L. Am. J. Physiol. 1916, 40, 206. 35. Alimurung, M. M., Rappaport, M. B., Sprague, H. B. New Engl. J. Med. 1948, 241, 631. 36. Gallavardin, L. J. Méd. Lyon, 1952, 33, 991. 37. Criley, J. M., Feldman, I. M., Meredith, T. Am. J. Med. 1971, 51, 456.
mitral
closure, the presystolic murmur, and the position of the anterior and posterior cusps of the valve in synchronised cine-frames. They observed, in ten out of fourteen patients in sinus rhythm, that the later portion of the presystolic murmur formed a crescendo leading to the first sound; that the crescendo followed the a-wave peak (i.e., that it happened while the atrioventricular pressure gradient was decreasing); and that it often preceded ventricular contraction and continued up to the moment of final valve closure, signalled by the first sound, which is delayed in mitral stenosis. They also noted that the murmur coincided with progressive closure of the mitral cusps. From these observations CRILEY and his co-workers concluded that the late crescendo portion of the presystolic murmur is associated with decreasing orifice size and not, as traditionally taught, with increased volume flow due to atrial contraction. To confirm that the murmur is independent of atrial systole they recorded it in four patients with tight mitral stenosis and atrial fibrillation 38 : all of them had a short crescendo presystolic murmur accompanying the initial rise of ventricular pressure. This murmur, which was present only in short diastolic periods when the end-diastolic pressure gradient was high, was thought to indicate tight stenosis with pliant Atrial systole does, however, affect the cusps. murmur. In sinus rhythm it often began before the onset of ventricular contraction, and indeed before the start of the Q wave, while in the patients with atrial fibrillation it followed the onset of pressure rise in the ventricle. CRILEY and his colleagues seem justified in associating the murmur with cusp approximation. The argument has been extended, perhaps more doubtfully, to other diastolic murmurs such as the middiastolic murmur of mitral regurgitation, the Austin Flint murmur,39 and the flow murmurs of patent ducIn all these intus and ventricular septal defect. stances it is suggested that the murmur is due to increased flow velocity as a result of narrowing of the valve orifice, rather than to increased volume flow. Intriguing as their observations are, the group’s explanation for the murmur seems hardly adequate. Why, with a falling pressure gradient, should flow velocity increase as the orifice narrows ? The Reynolds number, which describes conditions permitting turbulence to occur, includes diameter as a factor as well as velocity, and decreasing orifice diameter rather than increasing velocity may be what is important. Our understanding of the fluid mechanics of the mitral valve has been advanced through the application by EDLER 40 and others 41,42 of ultrasound technique, by which movements of the aortic cusp of the valve may be recorded, and 38. Criley, J. M., Hermer, A. J. New Engl. J. Med. 1971, 285, 1284. 39. Fortuin, N. J., Craige, E. Circulation, 1972, 45, 558. 40. Edler, I. Am. J. Cardiol. 1967, 19, 18. 41. Pridie, R. B., Oakley, C. M. Br. Heart J. 1970, 32, 203. 42. Wharton, C. F. P., Lopez Bescos, L. ibid. p. 344.
1108
through the cinematographic in-vivo studies of the valve by TAYLOR and WADE.43 Lately, the ingenious experiments on a model valve and ventricle by BELLHOUSE 44 have shown how ring-vortex formation behind the valve-cusps plays a part in moving the cusps towards each other during the later phase of diastole and how valve function can be impaired by increasing the volume of the ventricle. With the normal valve, ventricular filling takes place under a small pressure gradient and with a rapidly declining volume flow. The cusps, widely separated in early diastole, approximate in mid-diastole as flow slows and as ring-vortices form behind the cusps. Atrial systole is accompanied by brief separation of the cusps, which thereafter draw together and close almost completely just before ventricular systole. Thus, ventricular systole merely completes valve it the sole mechanism of closure, one would expect substantial systolic reversal of flow in the stream of blood through the heart. In severe mitral stenosis the narrow orifice and high atrio-ventricular pressure gradient keep the
closure;
were
valve-cusps maximally separated through diastole, and flow velocity is high. Pressure equilibration between atrium and ventricle is not completed before ventricular systole, and the effect of ring-vortex formation behind the cusps is weakened. Cusp approximation is late and rapid, and final closure of the valve, signalled by the first sound, is delayedthus happening well after reversal of the atrioventricular pressure gradient. How are the murmurs produced ? This is still a matter for speculation, but the vibrations are certainly initiated by the abnormally rapid interaction of forces in the stenotic valve. Apparently there are two types of presystolic murmur-the crescendo/ decrescendo murmur following atrial systole, which may be detected in even mild cases of mitral stenosis in sinus rhythm, and the later crescendo murmur immediately preceding the first sound, which is independent of atrial systole and indicates rapid cusp closure against a pressure gradient. The clinical importance of recognising the second type of murmur, as suggesting conditions suitable for closed mitral valvotomy, is obvious. Proof that it is present in some patients with atrial fibrillation should hearten auscultators who have been conditioned to reject the evidence of their own ears.
CONTAMINATION, CLEANING, AND COMMON SENSE MEDICAL interest in hygiene and cleaning tends to be bimodally distributed, with peaks in the zones corresponding to obsession and to apathy, and little in the central zone of reasonable and practical common sense. In a paper just published, Thomas and her co43. Taylor, D. E. M., Wade, J. D. J. Physiol., Lond. 1970, 207, 71P. 44. Bellhouse, B. J. Cardiovasc. Res. 1972, 6, 199.
workers1 describe the results of such an approach to the problem of a contaminated operating-theatre in a small, old hospital. There had been a worrying increase in gram-negative infection, from 10% to 18% among patients operated upon in a single theatre used for both clean and dirty cases. A detailed inspection and bacteriological survey was made. No significant pathogens were found in nose and throat swabs from theatre staff, and interest was concentrated in the theatre A number of matters requiring correction itself. were discovered and remedial steps were taken. Examination of the plumbing showed contamination of " sterile " water-supply and from water taps from a the ordinary mains supply, with dead pigeons in the roof tanks. Plug-holes and u-traps in basins and sinks were contaminated, and dye experiments showed how splashes from these areas could pass upwards and reach the inside of taps and faucets. Cleaning and replumbing were undertaken and sterile water was supplied from bottles. Another source of contamination was the cleaning technique. Profuse growth of pseudomonads was found in mop-heads soaking in buckets of nondescript disinfectant, and in the reservoir of an electric scrubbing machine, which could be neither completely emptied nor cleaned. Experiments with dye and with bacteria showed that a spray of dirty water was dispersed outwards and upwards from the machine for several feet, and could then fall neatly into sinks and basins. Mop-heads were regularly autoclaved and the scrubbing machine was redesigned by the hospital engineer to permit removal of the tank for cleaning and autoclaving. Other sources of contamination were a cracked terrazzo floor, which was resurfaced, the mixing of clean and dirty footwear, which was stopped, faulty sterilising equipment, which was replaced, and a general lack of maintenance, which was
improved.
As remedial measures were taken, the proportion of contaminated sites fell, and so did the number of gram-negative wound infections. Thomas et al. properly refuse to draw firm conclusions from a very limited number of cases, especially since a number of changes were introduced almost simultaneously, but they rightly claim that their results are suggestive. For the general reader, however, the message is that someone must take an interest in these mundane but important matters, that demonstration is vastly superior to exhortation, and that, given enthusiasm, honesty, and energy on the part of all concerned, great improvements can be made in the oldest and least privileged of hospitals. Among those who will need to be involved with these operations are hospital cleaning staff and domestic superintendents. For their benefit a shorter, more practical, and more readily available account of bacteriological safeguards in hospital cleaning equipment has been published.2 This could be useful in the training programmes for domestic staff now being run by regional hospital boards and others. It is is to learn that the of Health encouraging Department with the of manufacturers design scrubbing taking up Thomas, M. E. M., Piper, E., Maurer, I. M. J. Hyg., Camb. 1972, 70, 63. 2. Thomas, M. E. M., Maurer, I. M. Br. Hosp. J. soc. Serv. Rev. 1972, 82, Suppl. p. 6. 1.
by increased lung stiffness and resistance to airflow,2’ so that CO2 retention begins. Controversy also surrounds the therapeutic implicaIntermittent observations. and intraventilation (I.P.P.v.) positive-pressure venous bicarbonate were regarded as essential to the recovery of 4 patients with extreme combined acidosis tions of these
new
(arterial pH 6-87-6-99, PC02 76-120 mm. Hg),lo although conventional treatment with oxygen, digoxin, aminophylline, and a diuretic was also given. However, over a third of 55 slightly older patients died, despite all these measures, including I.P.P.V.,6 although their combined acidosis was less severe. Only 4 of ABERMAN and FULOP’s 45 patients died,! but the PCO2 never exceeded 60 mm. Hg (although pH was 7-10 or less in 6 cases). They used I.P.P.V. in only 2 patients, and bicarbonate in none. Their blood-gas results were not immediately available to guide treatment, so that morphine was given to 9 patients with C02 retention, when this was not suspected clinically. Only 2 of these patients subsequently required I.P.P.V., but it seems reasonable to withhold morphine in the first instance if the Pco2 is known to be over 60 mm. Hg, despite the valuable reduction in central blood volume 28 and dilatation of capacitance vessels 29 which probably follow its use in left ventricular failure. Clinical recognition of both severe hypoxaemia 30 and hypercapnia 1,8 is difficult in pulmonary oedema, but clouding of consciousness remains an important clinical clue to combined respiratory and metabolic acidosis.8,10 i.P.P.v. and bicarbonate can undoubtedly save lives, but should probably be reserved for patients with severe combined acidosis and PC02 levels over The prompt recognition of these 60 mm. Hg. abnormalities requires a 24-hour blood-gas diagnostic service, which will make many other contributions to the proper management of medical and surgical emergencies in the modern hospital.
Mitral Stenosis and the Crescendo Presystolic Murmur WHAT causes the presystolic murmur in mitral stenosis ? This is an old controversy,31—36 and CRILEY and his colleagues have obtained some fresh evidence. 37 They recorded the temporal relations of the Q wave of the electrocardiogram, pressure changes in the left ventricle and atrium, the first heart-sound of 27. 28. 29.
Sharp, J. T., Griffith, G. T., Bunnell, I. L., Greene, D. G. J. clin. Invest. 1958, 37, 111. Sapru, R. P. PH.D. thesis, University of Edinburgh, 1966. Vasko, J. S., Henney, R. P., Oldham, H. N., Brawley, R. K., Morrow, A. G. Am. J. Cardiol. 1966, 18, 876. Vitale, A., Dumke, P. R., Comroe, J. H. Circulation, 1954, 10, 81. Gairdner, W. T. Edinb. med. J. 1861, 7, 438. Henderson, Y., Johnson, F. E. Heart, 1912, 4, 69.
30. 31. 32. 33. Lewis, T. ibid. 1913, 4, 241. 34. Dean, A. L. Am. J. Physiol. 1916, 40, 206. 35. Alimurung, M. M., Rappaport, M. B., Sprague, H. B. New Engl. J. Med. 1948, 241, 631. 36. Gallavardin, L. J. Méd. Lyon, 1952, 33, 991. 37. Criley, J. M., Feldman, I. M., Meredith, T. Am. J. Med. 1971, 51, 456.
mitral
closure, the presystolic murmur, and the position of the anterior and posterior cusps of the valve in synchronised cine-frames. They observed, in ten out of fourteen patients in sinus rhythm, that the later portion of the presystolic murmur formed a crescendo leading to the first sound; that the crescendo followed the a-wave peak (i.e., that it happened while the atrioventricular pressure gradient was decreasing); and that it often preceded ventricular contraction and continued up to the moment of final valve closure, signalled by the first sound, which is delayed in mitral stenosis. They also noted that the murmur coincided with progressive closure of the mitral cusps. From these observations CRILEY and his co-workers concluded that the late crescendo portion of the presystolic murmur is associated with decreasing orifice size and not, as traditionally taught, with increased volume flow due to atrial contraction. To confirm that the murmur is independent of atrial systole they recorded it in four patients with tight mitral stenosis and atrial fibrillation 38 : all of them had a short crescendo presystolic murmur accompanying the initial rise of ventricular pressure. This murmur, which was present only in short diastolic periods when the end-diastolic pressure gradient was high, was thought to indicate tight stenosis with pliant Atrial systole does, however, affect the cusps. murmur. In sinus rhythm it often began before the onset of ventricular contraction, and indeed before the start of the Q wave, while in the patients with atrial fibrillation it followed the onset of pressure rise in the ventricle. CRILEY and his colleagues seem justified in associating the murmur with cusp approximation. The argument has been extended, perhaps more doubtfully, to other diastolic murmurs such as the middiastolic murmur of mitral regurgitation, the Austin Flint murmur,39 and the flow murmurs of patent ducIn all these intus and ventricular septal defect. stances it is suggested that the murmur is due to increased flow velocity as a result of narrowing of the valve orifice, rather than to increased volume flow. Intriguing as their observations are, the group’s explanation for the murmur seems hardly adequate. Why, with a falling pressure gradient, should flow velocity increase as the orifice narrows ? The Reynolds number, which describes conditions permitting turbulence to occur, includes diameter as a factor as well as velocity, and decreasing orifice diameter rather than increasing velocity may be what is important. Our understanding of the fluid mechanics of the mitral valve has been advanced through the application by EDLER 40 and others 41,42 of ultrasound technique, by which movements of the aortic cusp of the valve may be recorded, and 38. Criley, J. M., Hermer, A. J. New Engl. J. Med. 1971, 285, 1284. 39. Fortuin, N. J., Craige, E. Circulation, 1972, 45, 558. 40. Edler, I. Am. J. Cardiol. 1967, 19, 18. 41. Pridie, R. B., Oakley, C. M. Br. Heart J. 1970, 32, 203. 42. Wharton, C. F. P., Lopez Bescos, L. ibid. p. 344.
1108
through the cinematographic in-vivo studies of the valve by TAYLOR and WADE.43 Lately, the ingenious experiments on a model valve and ventricle by BELLHOUSE 44 have shown how ring-vortex formation behind the valve-cusps plays a part in moving the cusps towards each other during the later phase of diastole and how valve function can be impaired by increasing the volume of the ventricle. With the normal valve, ventricular filling takes place under a small pressure gradient and with a rapidly declining volume flow. The cusps, widely separated in early diastole, approximate in mid-diastole as flow slows and as ring-vortices form behind the cusps. Atrial systole is accompanied by brief separation of the cusps, which thereafter draw together and close almost completely just before ventricular systole. Thus, ventricular systole merely completes valve it the sole mechanism of closure, one would expect substantial systolic reversal of flow in the stream of blood through the heart. In severe mitral stenosis the narrow orifice and high atrio-ventricular pressure gradient keep the
closure;
were
valve-cusps maximally separated through diastole, and flow velocity is high. Pressure equilibration between atrium and ventricle is not completed before ventricular systole, and the effect of ring-vortex formation behind the cusps is weakened. Cusp approximation is late and rapid, and final closure of the valve, signalled by the first sound, is delayedthus happening well after reversal of the atrioventricular pressure gradient. How are the murmurs produced ? This is still a matter for speculation, but the vibrations are certainly initiated by the abnormally rapid interaction of forces in the stenotic valve. Apparently there are two types of presystolic murmur-the crescendo/ decrescendo murmur following atrial systole, which may be detected in even mild cases of mitral stenosis in sinus rhythm, and the later crescendo murmur immediately preceding the first sound, which is independent of atrial systole and indicates rapid cusp closure against a pressure gradient. The clinical importance of recognising the second type of murmur, as suggesting conditions suitable for closed mitral valvotomy, is obvious. Proof that it is present in some patients with atrial fibrillation should hearten auscultators who have been conditioned to reject the evidence of their own ears.
CONTAMINATION, CLEANING, AND COMMON SENSE MEDICAL interest in hygiene and cleaning tends to be bimodally distributed, with peaks in the zones corresponding to obsession and to apathy, and little in the central zone of reasonable and practical common sense. In a paper just published, Thomas and her co43. Taylor, D. E. M., Wade, J. D. J. Physiol., Lond. 1970, 207, 71P. 44. Bellhouse, B. J. Cardiovasc. Res. 1972, 6, 199.
workers1 describe the results of such an approach to the problem of a contaminated operating-theatre in a small, old hospital. There had been a worrying increase in gram-negative infection, from 10% to 18% among patients operated upon in a single theatre used for both clean and dirty cases. A detailed inspection and bacteriological survey was made. No significant pathogens were found in nose and throat swabs from theatre staff, and interest was concentrated in the theatre A number of matters requiring correction itself. were discovered and remedial steps were taken. Examination of the plumbing showed contamination of " sterile " water-supply and from water taps from a the ordinary mains supply, with dead pigeons in the roof tanks. Plug-holes and u-traps in basins and sinks were contaminated, and dye experiments showed how splashes from these areas could pass upwards and reach the inside of taps and faucets. Cleaning and replumbing were undertaken and sterile water was supplied from bottles. Another source of contamination was the cleaning technique. Profuse growth of pseudomonads was found in mop-heads soaking in buckets of nondescript disinfectant, and in the reservoir of an electric scrubbing machine, which could be neither completely emptied nor cleaned. Experiments with dye and with bacteria showed that a spray of dirty water was dispersed outwards and upwards from the machine for several feet, and could then fall neatly into sinks and basins. Mop-heads were regularly autoclaved and the scrubbing machine was redesigned by the hospital engineer to permit removal of the tank for cleaning and autoclaving. Other sources of contamination were a cracked terrazzo floor, which was resurfaced, the mixing of clean and dirty footwear, which was stopped, faulty sterilising equipment, which was replaced, and a general lack of maintenance, which was
improved.
As remedial measures were taken, the proportion of contaminated sites fell, and so did the number of gram-negative wound infections. Thomas et al. properly refuse to draw firm conclusions from a very limited number of cases, especially since a number of changes were introduced almost simultaneously, but they rightly claim that their results are suggestive. For the general reader, however, the message is that someone must take an interest in these mundane but important matters, that demonstration is vastly superior to exhortation, and that, given enthusiasm, honesty, and energy on the part of all concerned, great improvements can be made in the oldest and least privileged of hospitals. Among those who will need to be involved with these operations are hospital cleaning staff and domestic superintendents. For their benefit a shorter, more practical, and more readily available account of bacteriological safeguards in hospital cleaning equipment has been published.2 This could be useful in the training programmes for domestic staff now being run by regional hospital boards and others. It is is to learn that the of Health encouraging Department with the of manufacturers design scrubbing taking up Thomas, M. E. M., Piper, E., Maurer, I. M. J. Hyg., Camb. 1972, 70, 63. 2. Thomas, M. E. M., Maurer, I. M. Br. Hosp. J. soc. Serv. Rev. 1972, 82, Suppl. p. 6. 1.