Professor John Alexander MacWilliam
31 July 1857 - 13 January 1937
John MacWilliam. born in Kiltarlity, Inverness-shire, was an academic “star” from the outset, enjoying a highly distinguished undergraduate career at the University of Aberdeen before graduating MB, CM with First Class Honours in 1880. He subsequently spent some time in Edinburgh, Leipzig and Berne, proceeding to MD with Highest Honours in 1882 by virtue of outstanding studies on cardiac muscle, which he then continued at University College, London until 1886. By then established as an accomplished teacher and researcher of some renown, he was appointed, at the age of 29, Professor of the Institutes of Medicine (later recognised as Physiology) at his Alma Mater.
As early as 1885 he had published an extraordinarily detailed analysis of the heart of the eel, as well as other fishes, in which he demonstrated that the contractile activity arose in the sinus venosus, propagating from there to the auricle and then the ventricle. Not only that but he described the progressively lower intrinsic contraction rates of these chambers as the impulse spread from its source and clearly describes the normal state of affairs as a sino-ventricular rhythm, controlled predominantly by the vagus nerve, and subject to interference by external electrical currents. Although he did not specifically identify the formal elements of the cardiac conduction system, there is no doubt that he understood that the primary control of heart rate rate resided at the ostial part of the sinus venosus. (The identification of the sinus node in the heart of a mole in 1906 is attributed to the then medical student Martin Flack, working with Arthur Keith – a farmer’s son from Aberdeenshire who graduated MB from the University of Aberdeen in 1888 and who may well have encountered MacWilliam as a student there).
Having overcome many technical challenges, MacWilliam was the first to establish that the mammalian heart muscle behaved in all ways similar to the cold-blooded invertebrate heart. In doing so he succeeded in maintaining the mammalian heart alive for long enough after removal from the body to make his seminal observations. Perhaps his most significant achievement was his detailed description, over the next few years, of the in vivo characteristics of ventricular fibrillation as a cause of cardiac arrest when the heart was subjected to external electrical current, describing, in 1887 “ The ventricular muscle is thrown into a state of irregular arrhythmic contraction, whilst there is a great fall in arterial blood pressure. The ventricles become dilated with blood as the rapid quivering movement of their walls is insufficient to expel their contents; the muscular action partakes of the nature of a rapid incoordinated twitching of the muscular tissue.”. That would have been dramatic enough as an observation in the laboratory animal , but he also recognised even then that this may be a potent cause of death in patients. This might not have been an altogether surprising deduction in relation to cases of sudden death by exposure to electrocution – an occurrence that was linked to the expanding use of electricity in Europe and North America. However, two years later he postulated that sudden death in man might be due to this phenomenon, especially in the presence of underlying structural or degenerative heart disease. “ instead of quiescence, there is a tumultuous activity, irregular in its character and wholly in effective as regards its results….” He specifically linked this phenomenon to coronary artery disease and especially to heart failure, a remarkable deduction, given that the prevailing wisdom at the time – and for decades to follow – was that death in those patients was always due to cardiac standstill in asystole. It should be emphasised that all of this work was done entirely without the benefit of electrocardiography (which was first applied in man in a very rudimentary form by yet another Aberdeen graduate Augustus Waller – MB 1878, MD 1881 – and developed in a much more sophisticated form a decade later by Einthoven in Leiden.) He went on to identify other factors that might trigger VF, including exertion, sleep disturbance and emotional stress, and in later years devoted a great deal of attention to investigating the relationship between these factors, the autonomic nervous system and blood pressure regulation, producing a significant contribution to the literature on these topics also.
Another pressing concern of the day was sudden unexpected death from the newly evolving anaesthetic agents, particularly chloroform. The Hyderabad Commission had concluded in 1890 that this was the result of respiratory failure, but MacWilliam introduced a new hypothesis – that this too might be the result of ventricular fibrillation – and demonstrated in his laboratory that this might be the case and in addition showed that myocardial depression could be evinced by chloroform before respiratory depression occurred.
Not only did MacWilliam describe and correctly interpret the clinical significance of ventricular fibrillation, he also described how in experimental models in cardiac arrest from this arrhythmia, recovery might be achieved after prolonged periods by rhythmic compression of the ventricles and artificial ventilation. He effectively deployed cardiopulmonary resuscitation in his experimental animals.
Ventricular fibrillation was not his only focus of attention at this time. He also turned his thoughts to asystole and, in a remarkably prescient way, outlined how an external electrical stimulus might be applied to restore the cardiac beat by application of external electrodes applied to the skin over the praecordium and on the back “so that the induction shocks may traverse the organ.” – (external defibrillation) – and ”..rhythmic compression of the ventricles, with artificial respiration..” (cardiopulmonary resuscitation).
A modest and diligent man, with less than robust good health, it was one of his later regrets that his work took so long to be recognised and applied by mainstream clinicians. At the time of many of his seminal observations, knowledge of cardiac electrophysiology, myocardial metabolism and function, and hormonal regulation of haemodynamics were virtually non-existent, but the fundamental truths of his observations are now in daily evidence around the globe. The first electrical defibrillation in man was described in 1947, the first implantable defibrillator in 1970 and the first automated external device in 1979. Implantable cardiac resynchronization therapy is now a recognised treatment for severe cardiac failure. Today many of the general public are aware of and can apply external cardiac compression as part of “routine” first aid. MacWilliam can justifiably be regarded as the father of cardiopulmonary resuscitation and it is fitting that the Resuscitation Training Room in the Suttie Centre at Aberdeen Royal Infirmary bears his name.
Testimonials to his precocious genius have since been forthcoming from many distinguished cardiologists who benefitted from his earlier work. He was elected as Fellow of the Royal Society in 1916 and received an honorary LL.B from his Alma Mater in 1928, having held his Chair there with such distinction for 41 years.
He may have been a scientist ahead of his time, but his portfolio of studies on the mammalian heart, in the eyes of many, has established John MacWilliam as the greatest medical scientist to emerge from that Institution.
Aberdeen University Review Vol XXIV 1937-37, Page 128
Image by John MacMahon; bromide print, late 19th century-early 20th century; NPG x20467 © National Portrait Gallery, London
Biography prepared from the nomination made by Prof J Webster to the University of Aberdeen 525 Alumni project.