England and Wales High Court (Queen's Bench Division) Decisions

IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION
MANCHESTER DISTRICT REGISTRY

		Manchester Civil Justice Centre 1 Bridge Street West Manchester M3 3FX
		17/12/2014

Mr Justice Kenneth Parker:

Introduction

1. The Claimant in this action is Mrs Jennifer Davies, widow and administratrix of the estate of John Davies. The Defendant is the Countess of Chester Hospital NHS Foundation Trust, which has responsibility for the Countess of Chester Hospital ("the hospital").
2. Mr Davies attended the hospital on 4 January 2010. He was in ventricular tachycardia. Synchronised cardioversion was carried out under sedation; one shock at 50 joules, two shocks at 100 joules and one shock at 150 joules were administered. Mr Davies remained in ventricular tachycardia. Cardiology advice was sought and, as a result of a serious error, 8mg of magnesium was administered as a bolus, being four times the intended and appropriate dose. Mr Davies then suffered a fatal cardiac arrest. The pharmacology experts have agreed that the immediate cause of death was the excess dose of magnesium.
3. Although the immediate cause of death was as described above, the hospital maintains that by the time the magnesium was administered, the condition of Mr Davies was such that, within minutes or at least shortly thereafter, he would have died in any event. The Claimant denies that that was the case. Furthermore, the Claimant contends that the hospital was already in breach of duty towards Mr Davies before the fatal dose of magnesium was delivered; that that breach of duty caused, or materially contributed to, his condition; and that if Mr Davies had been treated with reasonable care he would, firstly, have been brought out of the ventricular tachycardia and, secondly, would have survived to live for about another five years.

The Basic Facts

4. Mr Davies was 57 years old when he died. He had a number of risk factors for cardiac illness. His father died aged 48 after myocardial infarction. He had been morbidly obese since at least 1998. At his death he weighed over 20 stone, and his body mass index was 48.2kg/m². He was a persistent smoker, and was hypertensive. In July 1998 he had an acute myocardial infarction. In May 2001 he had developed atrial fibrillation. In July 2006 he was admitted to hospital feeling lightheaded, the symptoms being attributed to a bradycardia induced by beta-blocker treatment. He was being considered for bariatric surgery at the end of 2009 and he had apparently expressed a recent resolution to give up smoking.
5. On the morning of 4 January 2010 he set off for work at about 8:10am. En route he began to feel unwell, faint and sweaty with palpitations and shortness of breath. He drove himself to the hospital, parked and walked into the Accident and Emergency ("A&E") unit. He complained of chest pain and was sweating.
6. He was triaged at 8:18am. An electrocardiogram ("ECG") was performed. He had ventricular tachycardia with a heart rate of 235bpm. In ventricular tachycardia the heart beats so rapidly that it cannot fill properly and cardiac output drops so low that it cannot provide sufficient circulation to vital organs. Ventricular tachycardia is the most serious of the cardiac arrhythmias because it can degenerate to ventricular fibrillation and cardiac arrest. Most people who develop ventricular tachycardia do so because of underlying heart disease, especially a previous myocardial infarction (resulting in scar tissue) and left ventricular hypertrophy, which is associated with scar tissue. In particular a myocardial scar can form a potential abnormal electrical circuit in the heart. The circuit produces a broad complex tachycardia, which may degenerate to fibrillation and cardiac arrest.
7. Mr Davies was assessed by Dr Khan, then a specialist registrar in A&E but shortly to become a consultant at a different hospital. Dr Khan noted that Mr Davies had presented at A&E complaining of chest pain and feeling light-headed. Dr Khan reviewed the ECG and noted the ventricular tachycardia. Mr Davies was alert and talking. He was able to give Dr Khan a history of his presentation. He was complaining of chest pain.
8. Given Mr Davies' complaint of chest pain and his abnormal cardiac rhythm, Dr Khan made a decision to treat him by way of synchronised cardioversion.
9. In external cardioversion, a direct current discharge is fired between two electrodes placed on the chest wall. The aim is to cause depolarisation of all the myocardial cells so that the cells are electrically silent. When the cells have recovered (re-polarised), they become receptive to the normal intrinsic pacemaker. In other words, cardioversion is intended to stop the abnormal heart rate and shock it back to normal rhythm.
10. Dr Khan sought the assistance of an anaesthetist, Dr Fanning. Dr Fanning came to the resuscitation area and found Mr Davies on a trolley, with ECG, blood pressure and pulse oximetry monitoring in place. An initial airway, breathing, circulation, disability and exposure assessment was carried out. Blood pressure was 140/62, and Mr Davies was alert and oriented. Dr Fanning noted the ventricular tachycardia with associated chest pain and sweatiness. Dr Fanning took from Mr Davies a pre-anaesthetic history. Dr Fanning considered him high risk of anaesthesia because of his high body mass index, large neck (rendering intubation difficult), large face and goatee beard (impeding a mask to the face). Having made this assessment, Dr Fanning called for anaesthetic assistance.
11. At this point a second patient was brought into the resuscitation area with an impending upper airway obstruction. This was an anaesthetic emergency. Without swift specialised intervention by a skilled anaesthetist the patient would almost certainly die. Dr Khan assessed the relative needs of the two patients and told Dr Fanning that it was appropriate for him to treat the second patient. Dr Khan informed Dr Fanning that in view of the extraordinary nature of Mr Davies' situation and the urgency of Mr Davies' condition, he would carry out cardioversion under sedation, and that he would administer the sedation. Dr Fanning proposed to Dr Khan that Mr Davies should be placed in a lateral and slightly head-down position when Dr Khan administered the sedation and performed the cardioversion, in order to reduce the risk of aspiration of stomach contents.
12. Dr Khan called for Dr Parkinson, a relatively recently qualified physician, to assist with sedation. Nurse Rachel Griffiths, who was in attendance, drew up the sedative drug fentanyl, an opiate similar to morphine, and Dr Parkinson administered 1ml and then 5ml of fentanyl. The first cardioversion of 50 joules was then delivered.
13. This was not effective. Nurse Griffiths then drew up the sedative drug midazolam which Dr Parkinson again administered, 5mg in three divided doses. Mr Davies became drowsy but could communicate if spoken to. A second cardioversion of 100 joules was delivered. That also was not effective. Dr Khan paged for assistance and Dr McClements, the on call medical registrar, arrived to assist, either just before the third cardioversion was delivered at 100 joules or as it was being delivered. Dr McClements had been "fast bleeped" at exactly 9:17am. Nurse Griffiths drew up amiodarone and infusion began. A further cardioversion was delivered at 150 joules. There was a slight pause on the ECG before the ventricular tachycardia began again. Dr Khan asked Dr McClements to discuss the situation with Dr Peter Reid, the on-call consultant cardiologist. Dr McClements returned and told Dr Khan that Dr Reid had advised that magnesium should be administered. Dr Fanning returned at this point to the bay, observing that Mr Davies remained in ventricular tachycardia, his condition deteriorating, with blood pressure dropping, and hands feeling cool and capillary refill time prolonged. As Dr Fanning was helping with inserting the central venous catheter, the fatal dose of magnesium was administered. Mr Davies complained immediately of an unpleasant burning sensation, and then went into cardiac arrest. Notwithstanding a number of attempts at resuscitation, including the use of two defibrillators simultaneously, none was successful and Mr Davies' death was confirmed at 10:36am. The post mortem showed that Mr Davies' heart was massively enlarged. There was coronary atheroma with small areas of over 75 per cent occlusion in both the LAD and right coronary artery. There was no evidence of recent myocardial infarction.

The Issue of Timing

14. The Claimant accepted that if I found that Mr Davies' condition was rapidly deteriorating on his presentation at hospital, then the decision to carry out cardioversion as an absolute emergency would not have been wrong. In other words the Claimant:

"… accepts that if the deceased's blood pressure had dropped to the level recorded at 9am … before the decision was made or the process started, then that deterioration would justify the decision on commencement." (closing written submissions, paragraph 7)

15. There was produced in evidence a chart showing that at 9am Mr Davies' blood pressure had dropped to 80/40. I accept Professor Channer's evidence that the drugs used to sedate Mr. Davies may have caused a slight lowering of blood pressure but would not have caused the profound hypotension recorded at 9am. The profound drop in blood pressure was the result of the ventricular cardioversion. The experts all agreed that if blood pressure had at that time dropped to such an extent, a decision to carry out cardioversion at that time would have been justified. The relevant question then arises: at what time was the decision to carry out cardioversion taken, and at what time did actual cardioversion take place? The sequence of events as such was not in dispute.
16. The most emphatic witness as to timing was Dr Fanning, the specialist doctor in anaesthesia to whom reference has already been made. In his witness statement he said:

"At 8:50 hours on 4 January 2010, I was informed that there had been a call from the Emergency Department, who were requesting an anaesthetic review with regards to sedation for synchronised cardioversion.

I attended the Emergency Department at approximately 9:00 hours …."

17. Cardioversion did not begin before Dr Fanning arrived at the emergency department or before he had turned his attention shortly thereafter to the critically affected patient in another bay. Dr Fanning was pressed very hard on his timing. However, at 11am that morning he made a note describing his involvement with Mr Davies, and the timing on the note is entirely consistent with his evidence. Furthermore, he retained a clear recollection of his routine on that specific morning, and in particular of how he had been told at 8:50am by an on-call anaesthetist (who had received an urgent call) that an anaesthetist had been requested by the Emergency Department in respect of a contemplated cardioversion. Any hypothesis that he had arrived in the Emergency Department at any time significantly before 9am was simply not consistent with his clear recollection of the chronology of the routine that he had followed that specific morning. Dr Fanning has maintained that position from the outset; he appeared to me to have thought about the matter very carefully (especially in the light of its emerging significance in these proceedings), but he did not waiver in his conviction.
18. Dr Fanning was pressed in particular on the contents of his note (see paragraph 17 above) and about the later descriptions that he gave of Mr Davies' condition when he first saw him. Dr Fanning first explained that, in the light of the other critical emergency that had suddenly arisen (see paragraph 11 above), he had had a relatively limited opportunity to assess Mr Davies' condition. He accepted that he had told the coroner that his assessment was "satisfactory apart from the VT [ventricular tachycardia] with associated chest pain and sweatiness which we were looking to treat"; that "he [Mr Davies] did look clammy but although unwell not kind of critically unwell at the time"; and that he had noted that Mr Davies "had started to deteriorate" when he returned to the bay. However, he maintained that his (almost) contemporary notes and the statements that he had later made were consistent with the view that he had formed at the time, namely, that Mr Davies' condition was very serious indeed and that cardioversion was justified. In colloquial terms he explained that treatment of some patients, even if urgently required, could be deferred for a time, but in some cases the urgency was with a capital "U", and immediate treatment was demanded. At the time he assessed the condition of Mr Davies as so serious that it compelled "Urgent" treatment. He added that as a clinician he had wider responsibilities, and if, given his assessment of the seriousness of Mr Davies' condition, he had had any significant reservations about the appropriateness of Dr Khan's decision to cardiovert, he would have intervened to voice his concern.
19. As to his later statements, I believe that it is important to bear in mind the context in which they were made. Dr Fanning had been faced with a dilemma, two patients in the Emergency Department needing his urgent attention. He chose to leave Mr Davies in order to tend the other patient, deciding that without specialist anaesthetic intervention that patient could well die within moments, whereas Mr Davies did not appear to be at that extreme level of risk, and, in particular, did not demand his continued presence as an anaesthetist. From that perspective his statements were understandable and not inconsistent with his assessment, made perforce rapidly, that the condition of Mr Davies appeared life threatening, and with his view, as an involved and responsible clinician, that Dr Khan's proposed action was not unreasonable in the circumstances confronting him.
20. The matter does not end there, because there was evidence that directly contradicted Dr Fanning's chronology. According to a contemporaneous document, a patient audit trail, Nurse Rachel Griffiths became involved in the care of Mr Davies at 8:44am at the point when he was transferred to the resuscitation room. It appears from her statement that Nurse Griffiths kept a contemporary note of the sedative drugs (fentanyl and midazolam) that were administered to Mr Davies. In the note as produced in evidence times are set beside the drugs indicating the time when each was made ready and administered. What is less clear from her statement (she did not give oral evidence) is whether she entered the times contemporaneously or why she would have done so. Certainly her retrospective note of her care of Mr Davies does not mention any timing for the giving of drugs, but simply gives a description of events (consistent with other evidence), specifying the sedative drugs that were administered to Mr Davies.
21. The document produced in evidence gives a timing of 8:35 hours for the administering of the first 150mg of fentanyl. That timing is difficult to reconcile with the patient audit (see paragraph 19 above) and is, of course, significantly out of line with Dr Fanning's chronology. Times of 8:40am and 8:45am are also given for the second dose of fentanyl and the 5ml of midazolam, times again that are wholly inconsistent with Dr Fanning's chronology. Dr Parkinson, who was called to assist Dr Khan with the cardioversion, did not make any independent note of timings. She was first interviewed about the present events on 7 January 2010 and said only that she arrived on duty at 8:00am and attended the area at "approximately 20:30hrs" (plainly meaning 8:30am). In a statement made much later on 14 August 2010 she does refer to relevant timings, but these are all exactly the same as those set out in Nurse Griffiths' note, and the inference is inescapable that they are based, directly or indirectly, on that note, and do not, therefore, provide independent corroboration of Nurse Griffith's timings.
22. Dr Fanning was asked about Nurse Griffith's timings. He said that they did not correspond with his clear recollection of the chronology and were just wrong. Given Dr Fanning's unwavering and sure evidence, and the uncertainties surrounding Nurse Griffiths' note, I must prefer the chronology advanced by Dr Fanning which, in my view, is consistent with the sequence of events and with the evidence bearing on the nature of those events as they developed. I am reinforced in that conclusion by the fact that the note of Nurse Griffiths contains a legend, as a warning to anyone who might seek later to rely on the document, in the following terms and format:

"(ALL TIMES APPROXIMATE)"

23. It follows inexorably from this finding of fact that Mr Davies' blood pressure had dipped to the level recorded at 9am before the process of cardioversion at least had started, and that that deterioration justified the commencement of cardioversion.
24. However, I also wish to make clear what conclusion I would have reached even if I had found that cardioversion began before 9am, consistent with the timing stated in Nurse Griffiths' note.
25. In this case I had evidence from experts in accident and emergency practice and procedure, and in cardiology. In A&E I had reports and heard oral evidence from Dr Nigel Zoltie (Claimant) and from Dr Philip Randall (Defendant); in cardiology, from Dr Richard Cooke (Claimant) and Professor Kevin Channer (Defendant). All the experts were very well qualified and experienced. In my view, each was genuinely seeking to assist the Court, even if they differed in their assessment.
26. The expert evidence indicated that Mr Davies' condition on presentation in the A&E department (ventricular tachycardia at 230bpm) justified, indeed required, cardioversion. However, Dr Zoltie and Dr Cooke considered that cardioversion was not immediately justified and that Dr Khan, by commencing cardioversion before 9am (on the present hypothesis), failed to exercise the reasonable level of care that could be expected of a competent medical practitioner in his situation. Dr Randall and Professor Channer, however, believed that Dr Khan's immediate action was reasonably justified in the circumstances confronting him, and that he did not fail to exercise reasonable care.
27. In my judgment, the correct analytical framework for resolving the issue dividing the respective experts is to seek to balance the medical risks that Dr Khan would have run if he had not begun cardioversion immediately against the risks of acting as he did. In that context it must be remembered that Dr Khan was a registrar in A&E. He had before him a patient who, on any view, was very ill with a very serious condition, ventricular tachycardia. That condition was capable of leading rapidly to myocardial infarction (heart attack) and death. Mr Davies had had a heart attack in the past. Dr Khan had to make a relatively speedy evaluation of the patient in front of him. If immediate cardioversion was required, and he failed to deliver it, the risk of imminent death was high. The overall context was one of life or death.
28. There is no doubt that the procedure of cardioversion carries inherent risks. It may exacerbate the condition: the electrical shock may destabilise the heart rhythm by accelerating the ventricular tachycardia, induce ventricular fibrillation or cause the heart to stop. In particular, and of considerable present relevance, the risks are increased if cardioversion is carried out under sub-optimal conditions. Best practice would indicate the presence of a skilled anaesthetist with a competent assistant. As Dr Cooke said in his report:

"Mr Davies was morbidly obese, was taking morphine and was obviously going to present a challenge in achieving sedation and analgesia while maintaining ventilation and protecting his airway …"

29. However, it is important to keep the degree of this particular risk in this case in perspective. Dr Cooke accepted that an anaesthetist was the appropriate practitioner to determine the extent of risk. The only anaesthetist who gave evidence was Dr Fanning, who was clear and concise. He did not suggest in any way that, given Mr Davies' condition, he would have managed the situation differently if he had been able to remain and provide appropriate support. He did not criticise in any way Dr Khan's decision to sedate, rather than to anaesthetise, Mr Davies, or question the sedative drugs selected by Dr Khan, or the quantities in which they were administered. On the last point Dr Cooke stated that the level of sedation was inadequate, but he also said that sedatives could lower blood pressure, and Dr Fanning fairly pointed out that, if that indeed was the case, increasing the quantity of sedatives might not have been entirely risk free. Furthermore, Dr Fanning in no way suggested that Dr Khan, as a registrar in A&E, was not appropriately competent and adequately supported safely to carry out the sedation of Mr Davies for the purposes of cardioversion. It was suggested that Dr Parkinson (with the help, of course, of Nurse Griffiths), as a Foundation Year 2 doctor having qualified in 2008, was not up to the task assigned to her by Dr Khan, but Dr Fanning gave no support for that suggestion, and Professor Channer, from his enormous experience of carrying out cardioversion in emergency situations, was positively scathing in rejecting it.
30. It seems to me, therefore, that, from an anaesthetic viewpoint, the actual extent of the risk in the case of Mr Davies was very limited, and from that viewpoint Dr Khan was entitled to proceed on the basis that, if he were to continue with cardioversion in the absence of Dr Fanning (and his regular support), assisted by Dr Parkinson and Nurse Griffiths, he would not be substantially increasing such risk as in any case would arise. Put differently, I do not believe on the evidence that Dr Fanning would have managed Mr Davies in a manner significantly different from that in fact followed by Dr Khan.
31. The second relevant risk arises from performance of cardioversion by a practitioner who is not a cardiologist. In some cases the delivery of the electric shock can no doubt be inexpertly delivered, with actual or potential detrimental effects. That was a risk that Dr Khan was entitled to discount because he was fully trained and experienced to carry out the physical procedure, and no witness suggested the contrary. However, the extent of shock is of considerable significance. All the experts agreed that, by reason of Mr Davies' morbid obesity, the level of electric shock was inadequate and was very likely to fail: 150 joules were required, and that level was not attained until Mr Davies had had three cardioversions at lower levels. Objectively seen, there was a risk that Dr Khan, not being a cardiologist, would administer an inadequate level of cardioversion that would be likely to fail and would in itself increase the risk of exacerbating the condition and of causing death.
32. However, in evaluating that risk, I must again return to the context. Dr Khan in his evidence said that, in acting as he did, he was simply following his training as an A&E practitioner, and adhering to applicable protocol. That was not challenged. Indeed the experts agreed that, as an A&E practitioner, Dr Khan acted reasonably in administering the level of cardioversion that he did. In other words, in deciding to cardiovert, although Dr Khan did not appreciate the relevant objective risk of failure, he had no good reason, as an A&E registrar, to perceive that he was incurring such a risk.
33. I conclude, therefore, that both relevant risks – absence of anaesthetist and of cardiologist – were, so far as concerned Dr Khan, relatively limited in this case. What were then the counterbalancing risks of not carrying out cardioversion? Yet again I must return to context. Dr Khan had in front of him a man who had had a previous heart attack, who was complaining of chest pain, who was sweating profusely, and who had ventricular tachycardia of 230bpm. In Dr Khan's own estimation, given in evidence, he was looking at a man whose next condition would be ventricular fibrillation, cardiac arrest and death. The experts were divided on this question. Dr Zoltie and Dr Cooke did not believe that Mr Davies' condition was as critical as that put forward by Dr Randall and Professor Channer.
34. On this issue much focus was placed at the trial on Mr Davies' chest pain. Dr Cooke was convinced that the "pain" was likely to be no more than "mild chest tightness" or discomfort ordinarily associated with ventricular tachycardia. Professor Channer disagreed: in his view, the chest pain was caused by myocardial ischaemia which he strongly stated could reasonably be expected in this case, given the duration and incidence of ventricular tachycardia and the condition of Mr Davies' heart, as disclosed by the autopsy.
35. The foregoing debate was set in the context of the Guidance, Advanced Life Support, Fifth Edition, June 2008. In that Guidance "adverse features" of tachyarrhythmia included:

"

heart rate > 150/min

chest pain

"

36. The Guidance then stated:

"… if the patient is unstable and deteriorating with adverse features caused by the tachycardia, attempt synchronised cardioversion immediately." (emphasis added)

37. The Claimant's experts contended that, before 9am, Mr Davies was "stable" and not "deteriorating", because his condition had not worsened since his presentation in the A&E Department. Professor Channer, by contrast contended that the purpose of the Guidance was to assist a practitioner to identify whether the condition of the patient was so serious as to justify immediate cardioversion. In his view, given that purpose, and given Mr Davies' tachycardia of 230bpm and chest pain (caused in all probability by myocardia ischaemia), he could not sensibly be described as "stable" and his condition had already "deteriorated" to the point where immediate cardioversion was necessary.
38. I do not think that it is correct to downplay Mr Davies' complaints of chest pain. It is correct that he did not complain of chest pain to Mrs Davies, but perhaps he simply did not wish to alarm her, in the light of his previous heart attack. What is clear is that on admission to the hospital he complained immediately of chest pain, and he repeated that complaint, as noted both by Dr Khan and Dr Fanning. He was also sweating profusely. In my view, it was entirely reasonable for Dr Khan to proceed on the basis that the chest pain constituted an adverse feature within the guideline, and that it was indicative, given the ventricular tachycardia and the patient's history, of myocardial ischaemia, creating a real risk of imminent cardiac arrest. That was the reasoned opinion in this case of Professor Channer, a very experienced cardiologist. He might, of course, have been wrong in his diagnosis. Dr Cooke, who, in my view, did downplay without sufficient justification the chest pain to chest "discomfort", might have been correct in denying that there was in fact myocardia ischaemia. But Dr Khan had the patient in front of him in an emergency situation and made a judgment, supported in retrospect by Professor Channer, that was reasonably justified in all the circumstances.
39. I have already considered the extent of the risks if Dr Khan carried out cardioversion. Given that Dr Khan's assessment of Mr Davies' condition was reasonably justified, as I have found above, the risks of not carrying out immediate cardioversion were substantial: heart failure and death. Weighing these respective risks in the balance, I am not able to conclude that, in deciding to carry out cardioversion, and in carrying out the cardioversion as he did, Dr Khan failed to exercise such skill and judgment as could reasonably be expected of a competent practitioner in the circumstances as they were presented to him. For the avoidance of doubt I should add that I accept Professor Channer's interpretation of the Guidance (see paragraph 36 above): whether a patient is "unstable and deteriorating" requires the exercise of judgment and an assessment of whether the "adverse features" are so adverse as to justify, in the reasonable opinion of the treating practitioner, resort to immediate cardioversion. Dr Khan was reasonably justified in believing that in this case the adverse features (extent of ventricular tachycardia, chest pain in a patient with unfavourable clinical history, profuse sweating) indicated immediate cardioversion, and, on a balance of risk, that course of action was reasonably pursued.
40. I believe that this conclusion is also supported by the evidence of Dr Fanning. It must be remembered that this physician also had the patient in front of him in an emergency situation. He knew what Dr Khan intended to do. He did not intervene to suggest that immediate cardioversion was inappropriate, or even to invite Dr Khan to re-consider his contemplated course of action. Dr Fanning was not, of course, a cardiologist or a practitioner in A&E. But he pointed out in his evidence to the Court that he had sufficient general medical training and experience to form his own assessment of Mr Davies' condition, and that with such training and experience and being a clinician immediately involved with the patient he had an ethical duty to intervene if he had reason to believe that Dr Khan's proposed course of action was inappropriate. Dr Fanning in fact at the time unequivocally shared Dr Khan's assessment that Mr Davies' condition required immediate cardioversion and, as already noted, did not suggest that Dr Khan could not adequately carry out the anaesthetic element of such a procedure.
41. The pharmacology experts have agreed that the immediate cause of Mr Davies' death was the administration of magnesium, and that the administration was a serious clinical failure. However, the Claimant, to succeed on this claim, would have to show, on a balance of probabilities, that Mr Davies would have survived for a substantial period if the magnesium had not been administered. On the footing that I found (as I have done) that cardioversion did not commence until 9am when Mr Davies' condition had already seriously deteriorated and/or that there was in any event no breach of duty and no opportunity for controlled cardioversion (including involvement of an anaesthetist and cardiologist), my understanding was that the Claimant accepted that she faced an uphill task on this last aspect.
42. Mr Davies was already in a critical condition when cardioversion began (see paragraph 22 above). Cardioversion had been tried on four occasions, once with the efficacy which all the experts agreed was appropriate in the circumstances, but without success. Mr Davies' condition continued to deteriorate. Even if cardioversion had started earlier (see paragraph 23 above), by the time that the magnesium was administered Mr Davies' condition had very seriously deteriorated. This serious deterioration was the result of the ventricular tachycardia. I accept the evidence of Professor Channer that in these circumstances Mr Davies was unlikely to have survived. Dr Cooke was more sanguine, essentially because he considered that cardioversion is always successful. Professor Channer, drawing on his considerable practical experience, including cardioversion performed in emergency situations, did not agree and firmly believed that given the state of Mr Davies' heart (as described in the post mortem) and the extent of deterioration brought about by ventricular tachycardia, which had not responded to cardioversion, further attempts at cardioversion would not have avoided degeneration into ventricular fibrillation and death. Professor Channer considered that the failure of the cardioversion was largely attributable to Mr Davies' morbid obesity, a conclusion that he based on his experience and knowledge and which he sought to support by a learned paper (Saliba and others JACC 199; 34: 2031-4). Dr Cooke challenged the finding of that paper, on the footing that it concerned monophasic defibrillators and did not give a reliable indicator of likely success in the modern era of biphasic defibrillators. Dr Cooke referred to a paper by White and others (2004 Critical Care Medicine), supporting a view that the success of cardioversion did not depend significantly on weight. However, Professor Channer countered by showing that the White paper was based on a small sample of 68 patients (with body weight available for 62), in which body weight was normally distributed and 4 percent were identified as extremely obese (BMI over 40kg/m²). The individual with the greatest weight weighed less than 140kg, whereas Mr Davies weighed 165kg on post mortem, with a BMI of 48.2kg/m². I am not convinced that a reliable statistical conclusion can be drawn from the limited White study, and in the end on this issue I accept the opinion of Professor Channer, with his great experience, especially in the context of emergency situations, of the likely success of cardioversion, even in the modern era of technology, in patients presenting with Mr Davies' condition who are morbidly obese.
43. I conclude on this aspect that Mr Davies would not have survived for any significant time even if the Defendant, in serious breach of duty, had not administered the fatal dose of magnesium.
44. For these reasons, I must dismiss this claim.