Laverty v Council of the City of Newcastle

CERTIFICATE OF DETERMINATION OF MEMBER
Citation:	Laverty v Council of the City of Newcastle [2022] NSWPIC 543
APPLICANT:	Susan Joy Laverty
RESPONDENT:	Council of the City of Newcastle
PRINCIPAL Member:	John Harris
DATE OF DECISION:	29 September 2022
CATCHWORDS:	WORKERS COMPENSATION - Mr Laverty died of a heart attack injury whilst participating in the certification process for a casual lifeguard employed by the respondent; the proceedings were brought by the widow for the payment of the lump sum death benefit and funeral expenses; Mr Laverty had a history of cardiac problems including two prior cardiac arrests and severe narrowing of arteries; the allegation that Mr Laverty suffered a thrombus during the swim and sustained a section 4(a) of the Workers Compensation Act 1987 (1987 Act) injury rejected as both doctors who initially provided that opinion subsequently accepted that it probably developed before the swim; medical explanation provided by Dr Clifton of the association between exercise and ischaemia the temporal connection between the swimming test and the onset of arrhythmia; consistent with Dr Herman’s evidence finding made that the exercise provoked the ischaemia through a reduced blood supply resulting in electrical instability and contributing to cardiac arrhythmia; Held – this process aggravated the underlying severe cardiac disease within the meaning of section 4(b)(ii) of the 1987 Act; no other non-work causes were relevant to the aggravation; the employment was the main contributing factor to the aggravation of the disease: AV v AW applied; the applicant had not satisfied the test in section 9B of the 1987 Act because Mr Laverty’s condition prior to the swim was critical; Mr Laverty was at very high risk of suffering an arrhythmic cardiac event without any precipitating activity; the ischaemia developed in the right coronary artery which was effectively blocked due to the pre-existent plaque and superimposed thrombus; any or nil activity with Mr Laverty’s condition could cause arrythmia; and the energy expended in the swim was not significant considering that Mr Laverty was fit for swimming and the expenditure of that type of energy was contrasted with other normal daily activities; award for the respondent.
determinations made:	1. Mr Laverty did not sustain an injury within the meaning of s 4(a) of the Workers Compensation Act 1987 (the 1987 Act). 2. The swim test provoked the ischaemia through a reduced blood supply resulting in electrical instability and contributing to cardiac arrhythmia and aggravated the underlying severe cardiac disease. The employment was the main contributing factor to the aggravation of the disease within the meaning of s 4(b)(ii) of the 1987 Act. 3. The applicant has not established, pursuant to s 9B(1) of the 1987 Act that the nature of the employment concerned gave rise to a significantly greater risk of Mr Laverty suffering the injury than had Mr Laverty not been employed in employment of that nature.
ORDERS MADE	4. Award in favour of the respondent.

STATEMENT OF REASONS

BACKGROUND

Mr Dale Laverty was employed by the Council of the City of Newcastle (the respondent) and died on 30 October 2020 whilst participating in the certification process for a casual lifeguard position.
These proceedings are brought by Ms Susan Joy Laverty seeking the lump sum death benefit and funeral expenses pursuant to the provisions of the Workers Compensation Act 1987 (the 1987 Act) in respect of the death of Mr Laverty. Ms Laverty is the surviving spouse of Mr Laverty. They have two daughters, Jessica and Emma. The parties previously noted that they were not dependent upon Mr Laverty at the time of his death.[1]
[1] Application, p 336.
The applicant was dependent upon Mr Laverty at the time of his death.
A brief statement is required for the reasons for the determination.[2]
[2] Section 294(2) of the Workplace Injury Management and Workers Compensation Act 1998 (the 1998 Act).

APPLICANT’S CLAIM OF INJURY

The injury description in the Application to Resolve a Dispute (the Application) were pleaded as:
(a)an acute thrombotic process leading to coronary ischemia and subsequent cardiac arrythmia in the context of work-related exertion (swimming);
(b)death resulted from the injury, and
(c)in the alternative, the deceased, during the course of his employment, suffered an aggravation, acceleration, exacerbation or deterioration of his pre-existing coronary heart disease.
The reference to “death resulted from the injury” is not a description of injury.
The allegations of injury articulated at the arbitration hearing were:
(a) an acute thrombotic process leading to coronary ischemia and subsequent cardiac arrhythmia (the s 4(a) allegation);[3] and/or
(b) exertion causing increases in heart rate in light of the pre-existing pathology leading to ischemia and electric disturbance (the s 4(b)(ii) allegation).[4]
[3] T, p 5.
[4] T, p 7.
In oral submissions the applicant submitted that the delay in resuscitation meant that “the outcome may have been better” but that it was not a different allegation of injury.[5]
[5] T, p 25.
In the subsequent written submissions, the applicant referred to the pleaded injuries in the Application.[6]
[6] Applicant’s submissions, [3].
Confusion has arisen in the written submissions filed after the arbitration hearing.
As noted above, the applicant articulated at the arbitration hearing the allegations of injury and stated that the delay in resuscitation was not relied upon as a separate allegation of injury. In its written submissions the applicant referred to the delay in resuscitation as a basis for finding in her favour on the s 4(b)(ii) and s 9B issues.[7] The applicant’s written submissions, when read fairly, did not contradict the pleading or what her counsel stated at the arbitration hearing.
[7] Applicant’s submissions, [54], [56], [89]-[90].
The respondent submission that the applicant’s submissions on the delay in resuscitation be “ignored” as it was beyond any issue raised in the pleadings misconstrued the applicant’s reliance on that aspect of the evidence.[8]
[8] Respondent’s submissions, [58] – [60].
The applicant’s submissions on delay in resuscitation on the s 4(b)(ii) issue also show a misunderstanding between the concept of “injury” and whether the injury caused death.
It is unfortunate that a dispute arose in the interpretation of written submissions on the particularisation of injury. The parties were advised at the hearing[9] of the need for care in formulating the allegations of injury and the observations of the Court of Appeal in Miller v State of New South Wales[10] of the necessity in identifying the particular injury. The Court then stated with reference to the inadequate particularisation of injury:[11]
“That is insufficient. That introductory section of the form narrates the way in which the deceased died, but without squarely identifying the particular “injury” which, so it was alleged, caused the death. It is one thing to describe the mechanism of death; it is another thing entirely to identify the “injury” for the purposes of a claim under s 25 of the Workers Compensation Act. As noted above, this was clarified in the parties’ oral addresses to the Arbitrator.”
[9] T, p 7.
[10] [2018] NSWCA 152 (Miller).
[11] Miller at [33].
The applicant’s written submissions do not formulate a further particular of injury. The applicant’s submissions on delay in resuscitation are considered on the issues arising under s 9B and causation of death. For the reasons provided subsequently, the delay in resuscitation is not relevant to the s 4(b)(ii) issue.

MEDICAL TERMS

The following medical terms appear in the decision:
(a)a thrombus is a clot. Thrombosis means the formation of a clot.[12] The thrombus was present on post-mortem examination in Mr Laverty’s severely diseased right coronary artery;[13]
(b)ischaemia occurs when the heart is starved of oxygen due to a reduced blood supply;[14]
(c)arrhythmia is a sudden heart rhythm disturbance;[15]
(d)a Metabolic Equivalent in Exercise Testing (MET) is a measure of energy expended in an activity.[16] One MET is approximately the expenditure of 1 kcal per kilogram of body weight per hour, and[17]
(e)Out of Hospital Cardiac Arrest (OHCA).
[12] Application, p 143.
[13] Application, p 567.
[14] Application, p 338.
[15] Application, p 135.
[16] Application, p 248.
[17] T, p 17, 42 and Application, p 142.

EVIDENCE

The matter was listed for arbitration hearing on 15 August 2022 when Mr Mueller of counsel appeared for Ms Laverty and Mr Catsanos SC appeared for the respondent.
The following material was admitted into evidence:[18]
(a) the Application and attachments, and
(b) Reply and attachments.
[18] Laverty v Council of the City of Newcastle, 15 August 2022, transcript, (T), p 1.
The respondent objected to two portions of Dr Clifton’s report (Application at page 358, paragraph 4 and at page 360, paragraph 7). The first paragraph related to the doctor’s conclusion that the exercise resulted in an acute thrombotic process and likely resulted in rhythm disturbance. The doctor concluded in the second paragraph that the swim and physical exertion placed Mr Laverty at a significantly greater risk of a sudden heart rhythm disturbance.
The objection to Dr Clifton’s “expertise” was based on Professor Keogh’s statement that
[19] Reply, p 22.
Dr Clifton, as a pathologist did “not diagnose and treat live patients, and do not interpret exercise testing”.[19]
The objections strictly went to weight and not admissibility: Bramble Industries Ltd v Bell.[20]
[20] [2010] NSWCA 162 at [19].
The paragraphs were admitted tentatively at the hearing.[21] The paragraphs subject to objection are now admitted in the proceedings. The weight that is given to the respective passages is discussed later in these reasons.
[21] T, p 4.
The hearing did not conclude on 15 August 2022 and the parties subsequently filed written submissions.

BACKGROUND FINDINGS

The following is a summary of factual matters that are not in dispute.
Mr Laverty was 57 years of age at the time of his death.[22] He had a long history of working as a lifeguard both in full-time and causal employment. Mr Laverty was also employed by Grain Corp for many years until he received a redundancy package in March 2018.
[22] Application, p 329.
In 2008 Mr Laverty experienced chest pains. Stents were then inserted into the heart arteries.[23] Mr Laverty had a family background of ischaemic heart disease.[24] In 2009 Mr Laverty developed further angina resulting in further angioplasty and the insertion of another in-stent stenosis.[25]
[23] Application, p 1.
[24] Application, p 499.
[25] Application, p 508.
According to Ms Laverty, Mr Laverty ceased taking medication for his cholesterol and heart after some time following the 2008 heart issues.[26] By at least 2010 Dr Singham recorded that Mr Laverty had ceased taking Lipitor although he remained on Aspirin.[27]
[26] Application, p 1.
[27] Application, p 510.
In 2015 Mr Laverty suffered a Non-ST-Elevation Myocardial Infarction (NSTEMI) and a further stent was inserted into the left anterior descending coronary artery.[28]
[28] Application, p 2, p 513.
In 2016 Dr Peter Hayes, cardiologist, noted that Mr Laverty was “more compliant with medications”.[29] Follow up in 2018 indicated that Mr Laverty was generally in good health with elevated cholesterol.[30] Exercise testing at that time over nine minutes reached 13.5 METS and showed normal exercise capacity.[31]
[29] Application, p 513.
[30] Application, p 520.
[31] Application, p 522.
In August 2020 Mr Laverty applied to the respondent for the position of casual lifeguard for the 2020/2021 season. Mr Laverty’s application was accepted, and he was required to complete the required testing for his annual certification and employment as a casual lifeguard.
As part of the certification process, on 26 October 2020 Mr Laverty completed the still water swim test of 800 m in under 14 minutes.[32]
[32] Application, p 553.
On 30 October 2020 Mr Laverty attended Nobbys Beach with other candidates at around
7 am to complete the Mission test component of the certification. The Mission test involved completion of an ocean swim leg, beach run, rescue board paddle and second beach run.
There is some inconsistency in the materials as to the length of the ocean swim.
The Water Safety Practice Note 15 specifies that the minimum standards for beach environments are based on nationally accredited vocational competencies and require annual proficiency every 12 months:[33]
·        800 m swim in a 25 m to 50 m pool in less than 14 minutes;
·        Lifeguard mission involving a 600 m ocean swim, 800 m beach run, 600 m rescue board paddle, and concluding with an 800 m beach run in a time set by the council, and
·        simulated board rescue and other rescues.
[33] Application, p 124.
The correspondence from the respondent indicated that the “overall distance of the swim is expected to be 600m” involving a swim of approximately 150 m to the first buoy, 150 m back to the beach and completing that leg a second time “to equal the full 600 m”.[34]
[34] Application, p 47.
The police report of death to the coroner indicated that the first swimming leg of the Mission test was 400 m and Mr Laverty was in the process of completing the second leg when he went missing.[35]
[35] Application, 553.
The applicant submitted that Mr Laverty had swum 400 m as part of the swimming leg of the Mission test. The respondent accepted that Mr Laverty had completed the first leg (300 m) and was into the second leg.[36]
[36] Transcript, pp 9-10.
As Mr Laverty was into the second leg of the ocean swim, it is accepted, as the applicant submitted, that he had swum in the order of 400 m. It was also common opinion of
Professor Keogh and Dr Herman, that Mr Laverty had expended in the order of 4-5 METs in swimming this distance.
Mr Laverty entered the water and completed the first leg of the ocean swim. He was last seen around 7.50 am. At about “ten to fifteen minutes into the Mission test” there was comment that Mr Laverty had not completed the swim and a search was initiated. Approximately five minutes later Mr Laverty was found submerged in the water showing no signs of life.[37]
[37] Application, p 553.
Mr Laverty was taken to the beach by jet ski and resuscitation efforts were commenced by lifeguards and subsequently by paramedics. The resuscitation efforts included chest compressions, two shocks from an automated external defibrillator and administration of adrenaline with no effect.[38] Mr Laverty was then conveyed to John Hunter Hospital. Shortly after 9 am, Mr Laverty’s life was pronounced extinct.
[38] Application, p 553.

Pre-existing heart condition

The Background Findings above refer to Mr Laverty’s heart symptoms and treatment since 2008.
Dr Clifton’s finding on post-mortem examination identified significant heart disease. The doctor’s findings on autopsy were:[39]
“[A] grossly enlarged heart for body size, severe coronary artery disease with multiple coronary artery stents, extensive scarring in the heart muscle (in keeping with previous ‘heart attacks’) and a thrombus or ‘clot’ in the already diseased right coronary artery. The degree of heart pathology is associated with a significant risk of death due to a sudden heart rhythm disturbance.”
[39] Application, p 567.
The coronary arteries were described as “heavily calcified with severe atherosclerosis and metal stents present” with more than “70% cross sectional luminal narrowing in unstented segments”.[40] The coronary arteries were described in further detail as:[41]
“There is severe atherosclerosis. The left anterior descending artery sections show more than 75% cross sectional luminal narrowing, the circumflex vessels show more than 70-75% cross sectional luminal narrowing and the right coronary vessel shows more than 90% cross sectional luminal narrowing with an additional almost completely occluding luminal thrombus. The plaques show thick fibrous caps, intimal thickening, extra-cellular lipid, cholesterol clefts, focal chronic inflammatory cells and florid calcification.”
[40] Application, p 570.
[41] Application, p 571.
Dr Clifton’s findings were repeated by Professor Keogh in a report dated 25 July 2021.[42] Professor Keogh described the extensive structural ischaemic disease as “extremely severe”. The Professor also opined that, apart from the known heart attack on
[42] Application, p 132.
[43] Application, p 134.
[44] Application, pp 338 - 9.
26 January 2015 affecting the front wall, there had been a second heart attack at the back of the heart at an unknown time. This conclusion was reached because there was “posteroseptal transmural scarring 50 mm extant”.[43] Dr Herman expressed a similar opinion that Mr Laverty had suffered an old heart attack.[44]
Ms Laverty stated that both she and Mr Laverty were unaware of a second heart attack. Professor Keogh explained that the evidence of the other heart attack was derived from the autopsy report and a heart attack “can be silent and unnoticed”.[45]
[45] Reply, p 12.
Dr Herman noted that the risk of arrhythmic cardiac death was high given the underlying condition. The doctor stated:[46]
“Mr Laverty almost certainly had an arrhythmic cardiac death and the risk of this happening in a gentleman with an ischaemic cardiomyopathy in addition to triple significant triple vessel coronary artery disease is extremely high.
Furthermore, Mr Laverty had evidence of a new thrombus within the right coronary artery and more than sufficient reason to have an arrhythmic event in that situation (particularly with a pre-existent ischaemic cardiomyopathy).”
[46] Application, p 342.
In a subsequent report Dr Herman described the ischaemic cardiomyopathy as severe meaning that Mr Laverty was at a “substantial risk of an arrhythmic cardiac event”.[47]
[47] Application, p 345.
Dr Clifton agreed with the opinion that Mr Laverty could have suffered a lethal cardiac arrhythmia at any time. The doctor stated:[48]
“In my opinion, this man could have suffered a sudden (potentially lethal or debilitating) cardiac arrhythmia at any time, in light of the degree of cardiac pathology identified at autopsy examination. This includes chronic ischaemic heart disease: an enlarged heart, a thickened left ventricle with chamber dilatation, myocardial scarring with microscopic regional replacement fibrosis as well as interstitial fibrosis and myocyte hypertrophy. In addition, significant coronary artery atherosclerosis in multiple major coronary arteries was present. However, further to this, there was evidence of a near occlusive acute thrombus in one of the already severely stenosed major coronary arteries.”
[48] Application, p 356.
Dr Clifton provided similar evidence orally when she stated that Mr Laverty was “at risk of having an arrhythmia at any point in time, whether they’re exerting themselves or not”.[49]
[49] T, p 56.

Cause of death

Dr Clifton certified that Mr Laverty died at Nobby Beach on 30 October 2020. The direct cause of death was ischaemic heart disease.[50] The heart disease was summarised as:
(a)    cardiomegaly with left ventricular hypertrophy;
(b)    severe triple vessel coronary artery atherosclerosis with multiple stents;
(c)    right coronary artery thrombosis, and
(d)    extensive myocardial scarring.
[50] Application, p 566.
The Deputy State Coroner dispensed with an inquest and adopted Dr Clifton’s findings on the cause of death.[51]
[51] Application, p 574.
Dr Herman opined that the cause of death was due to cardiac arrhythmia secondary to ischaemia in the setting of a probable acute occlusion of the right coronary artery.[52]
[52] Application, p 339.

MEDICAL EVIDENCE

The doctors have provided a number of reports. Their critical findings and reasons are discussed throughout the decision. The following is not intended as a summary of what are extensive opinions provided by Dr Clifton, Dr Herman and Professor Keogh.

Dr Clifton

Dr Leah Clifton, a staff specialist forensic pathologist, provided the autopsy report for the coroner.[53] The doctor’s findings on examination and cause of death are set out elsewhere. In respect of the relevance of the swim the doctor stated:[54]
“It is likely the deceased suffered a sudden heart rhythm disturbance during exertion whilst in the water due to his severe cardiac disease, rendering him unconscious and ultimately resulting in his death.”
[53] Application, p 565.
[54] Application, p 568.
Dr Clifton provided a further report dated 21 March 2022.[55]
[55] Application, p 355.
Dr Clifton opined that Mr Laverty suffered from severe pre-existing cardiac disease with superimposed thrombosis provoking near occlusion. The doctor agreed that the swim provoked the trigger for the electrical instability.
In oral evidence Dr Clifton accepted that an acute plaque rupture was not identified on the autopsy findings. The doctor couldn’t say that a plaque rupture “wasn’t present” but if just wasn’t captured in the sections of the artery examined.
The doctor accepted, the swim and physical exertion placed Mr Laverty at a significantly greater risk of a sudden heart rhythm disturbance.

Dr Herman

Dr Mark Herman, cardiologist, provided an initial report dated 28 June 2021.[56] The doctor opined that the cause of death was an arrhythmic death secondary to ischaemia probably as a result of a newly ruptured plaque with subsequent occlusive thrombosis in the right coronary artery.
[56] Application, p 337.
Dr Herman opined that the thrombosis provoked the near total occlusion triggering and provoking the ischaemia resulting in an arrhythmia and sudden cardiac arrest.
Dr Herman stated that it was difficult to speculate whether earlier resuscitation would have resulted in a better outcome noting that “the outcome may have better”.[57] The doctor opined that the trigger for the sudden episode was contributed by the haemodynamic stress of a
[57] Application, p 341.
400 m swim.
Dr Herman provided a further report dated 11 January 2022.[58] The doctor opined that the ischaemic cardiomyopathy was severe, and Mr Laverty was always at a substantial risk of an arrhythmic cardiac event. The electrical instability on the day of the event was provoked by superimposed thrombus in the right coronary artery. Dr Herman stated:[59]
“On the day of his OHCA, he had a near occlusive thrombus in the right coronary artery and on that particular day, any activity (in this case, expending at least 5 METs of energy expenditure), would, in my opinion, be sufficient to provoke ischaemia and provoke the “trigger” for the arrhythmic event.”
[58] Application, p 344.
[59] Application, p 345.
In a passage emphasised by Professor Keogh (and the respondent), Dr Herman further stated:[60]
“I differ from Professor Keogh in that, in my opinion, the electrical instability which occurred on the day of his OHCA, was provoked by ischaemia (lack of blood supply) in the right coronary artery territory which revealed a pre-existent severe blockage (up to 90%) but with a superimposed thrombus. The superimposed thrombus either occurred at the time of the swim, or probably shortly before.”
[60] Application, p 347.
Dr Herman’s interpretation of Dr Clifton’s autopsy report was that the thrombosis was an acute event rather than a chronic event because Dr Clifton referred to an “additional almost completely occluding luminal thrombosis”. Later in his opinion Dr Herman emphasised the word “additional” used by Dr Clifton as suggesting an acute event which would be best addressed by Dr Clifton.
Later in his report Dr Herman repeats that the thrombosis was present before the swim.
Dr Herman stated:[61]
“I agree with Professor Keogh that on the balance of probabilities that the deceased’s ischaemic cardiomyopathy and sudden cardiac arrhythmia could have occurred at any time and at any place at around the same time of his life.
However, I differ from Professor Keogh in that the “trigger” for this specific episode of ventricular arrhythmia and sudden cardiac death was, in my opinion, provoked by coronary ischaemia in the right coronary artery territory in a pre-existently [sic] severely stenosed vessel with superimposed thrombosis provoking near occlusion.
Mr Laverty was at a very high risk of an arrhythmic cardiac event but the swim on the day of his OHCA, provoked the trigger for the electrical instability due to ischaemia developing in the right coronary artery territory.
In my opinion, the swim itself gave risk to a significantly greater risk of Mr Laverty suffering the injury than had he not swum on the day. At that particular time, the severe narrowing of the right coronary artery with pre-existent plaque and superimposed thrombus, provoked a critical situation whereby any activity more than 4-5 METs may have provoked ischaemia and a subsequent electrical instability.”
[61] Application, p 349.
Dr Herman emphasised that Mr Laverty was in a “high-risk situation” but that the swim either provoked an acute plaque rupture with superadded thrombus was of sufficient haemodynamic stress to provoke ischaemia in the right coronary artery.

Professor Keogh

Professor Keogh provided an initial report dated 25 July 2021.[62] In that report the Professor accepted that Mr Laverty:
[62] Application, p 132.
(a)    suffered a sudden heart rhythm disturbance due to his severe cardiac disease;
(b)    the disturbance was electrical;
(c)    the degree of heart pathology is associated with a significant risk of death due to sudden rhythm disturbance;
(d)    cardiac arrest can occur at any time due to the constitutional makeup and the underlying disease;
(e)    the cardiac disease predated the employment;
(f)    Mr Laverty had a strong family history of premature coronary artery disease. He was not taking heart medication regularly and had ceased taking medication some two years before his death. Mr Laverty did not return for blood tests after March 2018 and Dr Mills noted in February 2020 that he avoided pathology testing;
(g)    the ocean swim test was well within Mr Laverty’s usual recreational activity as he swam four kilometres three times per week amongst other strenuous exercise;
(h)    one MET is equivalent to the expenditure of lying down and breathing for an hour. A maximum of 4 - 5 METs was expended during the swim;[63]
(i)    agreed with Dr Herman that cardiac arrhythmia was the final pathway for death;
(j)    Dr Clifton did not note acute plaque rupture and the there is no sense from the report of the duration of its existence, and
(k)    a delay in resuscitation did not contribute to the poor outcome. There is a 7% chance of survival if the cardiac arrest occurs at home increasing to 21% is it occurs in public, witnessed by a bystander and CPR is commenced.
[63] Application, p 145.
Professor Keogh stated:[64]
“I agree with Dr Herman that ‘Mr Laverty almost certainly had an arrhythmic cardiac death and the risk of this happening in a gentleman with an ischemic cardiomyopathy in addition to significant triple vessel disease is extremely high’. By using the phrase ‘cardiomyopathy’, Dr Herman is acknowledging the findings of wall fibrosis and left ventricular dilatation. I agree with Dr Herman that the ‘deceased had extensive, severe coronary artery disease and an ischemic cardiomyopathy and was always at very high risk of a cardiovascular event’. The risk of OHCA with the severe pathological changes seen at the deceased’s autopsy is very high.”
[64] Application, p 143.
Professor Keogh prepared a report in response to Ms Laverty’s statement.[65] In response to Ms Laverty’s comment that Mr Laverty had been compliant with his medication for the previous year, the Professor stated:[66]
“As stated previously, there is a great deal of documentation from the treating doctors, that for the majority of the 12.5 years during which Mr Laverty suffered cardiac disease, there was non-compliance or incomplete compliance with Optimal Medical Therapy.
…
Importantly, from July 2018, there was poor compliance with GP visits, many missed appointments, missed blood tests and no return for Cardiology review.”
[65] Reply, p 9.
[66] Reply, p 14.
Professor Keogh provided a further report dated 19 January 2022 in response to
Dr Herman’s report dated 11 January 2022.[67] Professor Keogh stated:[68]
“We agree that he had an ischemic cardiomyopathy (Dr Herman, page 4, para 7, report 28 June 2021) and that the ‘risk of an arrhythmic cardiac death…in ischemic cardiomyopathy and triple vessel disease is extremely high’. We agree that with the ‘ischemic cardiomyopathy (severe), he was always at a substantial risk of an arrhythmic cardiac event’ and agree that ‘the absence of Optimal Medical Therapy and the lack of cardiac defibrillator, substantially increased this risk’ (page 2, para 2, report 11 January 2022).”
[67] Reply, p 15.
[68] Reply, p 15.
Professor Keogh also noted that Dr Herman had adjusted his opinion in his second report when he opined that the “superimposed thrombus occurred at the time of the swim or probably shortly before”.
Professor Keogh opined that Mr Laverty’s thrombus was “days to weeks age”. She otherwise referred to the Victorian Ambulance Arrest Registry which shows that 98.6% of patients were resting at the time of cardiac arrest. The Professor noted that the level of exercise undertaken by Mr Laverty in the expenditure of 4-5METS was consistent with daily activities such as “mopping floors, or polishing furniture, or carrying a golf bag, or stocking shelves with light objects, or shopping and carrying groceries weighing 10kgs”.[69]
[69] Reply, p 17.
Professor Keogh provided a further report dated 10 May 2022[70] responding to Dr Clifton’s further report. The Professor noted that Dr Herman, Dr Clifton and herself all agreed “that
[70] Reply, p 20.
[71] Reply p 21.
Mr Laverty had multiple heart abnormalities and could have suffered a sudden cardiac arrhythmia at any time”.[71]
Professor Keogh disputed Dr Clifton’s suggestion that the thrombosis was acute and did not give “objective pathological justification” for why it was acute.
Professor Keogh opined that when Dr Clifton expressed an opinion on the swim provoking the trigger for the electrical instability she stepped outside her experience and speculated on the role of any exercise or exertion.

REASONS

The applicant bears the onus of proof on the balance of probabilities.[72]
[72] Nguyen v Cosmopolitan Homes (NSW) Pty Ltd [2008] NSWCA 246 per McDougall J at [44]- [55], McColl and Bell JJA (as their Honours then were) agreeing; Chen v State of New South Wales (No 2) [2016] NSWCA 292 per Leeming JA at [33]-[34]; McColl JA agreeing at [1].

Section 4(a) injury

The allegation of the s 4(a) injury referred to earlier[73] as an “acute thrombotic process” with various consequences. For the following reasons, I am not satisfied that the “acute thrombotic process” occurred either in the course of employment or arose out of the course of the employment.
[73] See xxx herein.
Dr Clifton stated that she reviewed the macroscopic photographs and histology slides and confirmed that there was acute thrombus formation within the lumen of the right coronary artery.[74] The doctor stated that the clot was “made up of fresh blood- red blood cells and also a little bit of fibrin”.[75] There was no evidence of organisation that takes days to form[76] and the process had taken “minutes to hours” but not “many hours”.[77]
[74] Application, p 361.
[75] T, p 31.
[76] T, p 32.
[77] T, p 32.
The fact that the clot was not referenced by Dr Clifton in the autopsy report as “acute” was explained in cross-examination. The doctor stated:[78]
“Catsanos: You’ve commented on in your more recent report, it’s fair to say that nowhere in your autopsy do you describe it as an acute thrombotic event. That’s fair to say, isn’t it?‑‑‑Like, I’d have to have a little look. I – I – I feel like there’s probably a bit of confusion about what I meant when I did my second report, but I probably should have articulated myself better in my initial report about the fact that it is a luminal thrombus, meaning it’s an acute process, not an organising – and I probably should have been clearer in my report, in my initial report, about that, but, yeah, it's an acute - - -
MEMBER: But to be fair to you, doctor, you’re writing a lot of reports a day and you wrote that for the purpose of the autopsy, not for legal proceedings. Is that right?‑‑‑Yeah, well, that's correct, and this is – there’s a big difference between – well, there’s a big divide between a medical report and the – what becomes legally important later down the line.
Yes?‑‑‑And I’m still learning this, five years into doing this as a staff specialist. The – it blows my mind what things become important in the wording in my reports.”
[78] T, pp 56 – 57.
In its written submissions in reply, the respondent referred to the opinion of Professor Keogh that the clot was “days to weeks of age”[79]. However, it otherwise referred to Dr Clifton’s “notable” embrace of Dr Herman’s opinion that the “the superimposed thrombus either occurred at the time of the swim, or probably shortly before”.
[79] Respondent’s submissions, [18].
I reject Professor Keogh’s evidence concerning the age of the clot. The doctor has interpreted Dr Clifton’s initial report incorrectly. Professor Keogh was otherwise unaware and did not comment on Dr Clifton’s subsequent oral evidence on what was viewed under the microscope.
Dr Clifton’s evidence was recorded. Her independence as an expert pathologist was not questioned by the respondent. That Dr Clifton viewed the clot under a microscope is clear from her evidence. The evidence is accepted as being credible and clearly within her expertise.
The issue is when and how the clot was formed in the context of whether the thrombotic process occurred during the swim test.
The applicant submitted that the increase in blood pressure caused by exertion placed stress on the arterial wall predisposing the plaque rupture and provoking acute thrombosis.[80]
[80] Applicant’s submissions, [20] - [21].
The applicant relied on the conclusions expressed by Dr Clifton in her report dated
21 March 2022 and those expressed by Dr Herman in his first report dated 28 June 2021. The doctors then expressed the opinion that plaque ruptured from the stress during swimming causing the clot.
The applicant also relied on an opinion expressed by Dr Herman in a previous decision of the Commission concerning “the pathology of a plaque rupture”.[81] That “opinion” was not tendered as evidence in this matter and was referenced in submissions in reply. No leave was sought by the applicant to adduce the evidence and objection was taken by the respondent.[82]
[81] Applicant’s submissions, [33].
[82] Respondent’s submissions, [51].
In the absence of a request for leave to adduce evidence this opinion is not before the Commission. I otherwise do not accept that the evidence further assists the applicant given Dr Herman’s opinion on the timing of the thrombus in his subsequent report.
The applicant in her written submissions failed to refer to the respondent’s defence to the
s 4(a) case that Dr Herman changed his opinion concerning when the thrombus occurred.
In his latest report Dr Herman stated:[83]
“I differ from Professor Keogh in that, in my opinion, the electrical instability which occurred on the day of his OHCA, was provoked by ischaemia (lack of blood supply) in the right coronary artery territory which revealed a pre-existent severe blockage (up to 90%) but with a superimposed thrombus. The superimposed thrombus either occurred at the time of the swim, or probably shortly before.”
[83] Application, p 347.
The respondent emphasised this part of Dr Herman’s opinion in its oral submissions[84] and noted that they were subsequently embraced by Professor Keogh as a shift in Dr Herman’s opinion.[85] The respondent submitted that Dr Herman’s subsequent opinion “can’t be read any other way”[86] and that the applicant never sought to “demur from that proposition”.[87]
[84] T, p 71.
[85] Reply, p 15.
[86] T, p 71.
[87] T, p 71.
Later in the second report Dr Herman appeared to confirm his opinion that the superimposed thrombus had probably occurred prior to the swim when the doctor referred to the “pre-existent plaque and superimposed thrombus”. The doctor stated:[88]
“In my opinion, the swim itself gave risk to a significantly greater risk of Mr Laverty suffering the injury than had he not swum on the day. At that particular time, the severe narrowing of the right coronary artery with pre-existent plaque and superimposed thrombus, provoked a critical situation whereby any activity more than 4-5 METs may have provoked ischaemia and a subsequent electrical instability.”
[88] Application, p 349.
In her oral evidence Dr Clifton initially stated that the acute thrombotic process (clot) occurred “on the day”[89] but couldn’t say although when. The process was described as “acute” and “almost completely occluded the already diseased vessel”.[90] Dr Clifton stated that the clot had not been there for “many hours” based on the observations under the microscope.
[89] T, p 30
[90] T, p 31.
In another part of her evidence Dr Clifton stated that the “acute thrombosis has happened during the swim” and Mr Laverty could not have been walking around or been symptom free.[91] Dr Clifton then stated:[92]
“I think it’s highly likely that this man had an acute thrombotic event during his swim, which has then left him in a very vulnerable position.”
[91] T, p 46.
[92] T, p 58.
Dr Clifton accepted that there was no evidence of a plaque rupture[93] which was the “most commonly understood reason why someone has a thrombus”[94] and there were other causes for a clot including the natural progression of the coronary artery disease.[95]
[93] T, p 48.
[94] T, p 58.
[95] T, p 59.
Dr Clifton then gave the following evidence:[96]
MR CATSANOS: Yes. This is what Dr Herman says. “I differ from Professor Keogh, in that in my opinion the electrical instability which occurred on the day of the OHCA was provoked by ischemia, lack of blood supply, in the right coronary artery territory, which revealed a pre‑existent blockage up to 90 per cent, with a superimposed” – emphasising superimposed – “thrombus”. He says this, “The superimposed thrombus either occurred at the time of the swim or probably shortly before.” You would accept, wouldn’t you, that proposition?‑‑‑Yes, I – I don’t disagree with that.
And so assuming, then, that it occurred before the swim, the pathological causes of that could be – I withdraw that. The causes of that might lie in the realms of a plaque rupture occurring as a product of the disease process. That’s one particular causative mechanism, would you agree with that?‑‑‑Yes. Yes.
Or a clot forming independently of any plaque rupture, but just as part of the disease process?‑‑‑Yes, that’s possible.
And once that happens, once the disease gets itself to that position, then with it comes the increased probability of a sudden cardiac arrest?‑‑‑Yes.”
[96] T, p 60.
There was no re-examination to explain the doctor’s change in her evidence on the timing of the formation of the thrombus.
In oral submissions Mr Mueller submitted that this evidence must be read with the other evidence that Mr Laverty did not suffer from any symptoms before the swim and the fact that he went for the swim lead to the inference that the thrombosis occurred during the swim.[97] Reading Dr Clifton’s evidence “in total”, it was submitted that the thrombus occurred during the swim.[98]
[97] T, p 64.
[98] T, p 68.
Dr Clifton otherwise accepted that there was no evidence of plaque rupture and there are other causes for a thrombosis.[99] The doctor stated that it was possible there was a plaque rupture, but it wasn’t seen during the autopsy.
[99] T, pp 65 – 66.
I agree with the respondent’s submission that Dr Herman’s opinion as to the occurrence of the clot changed between his first and second report. The applicant made no attempt to explain the change in the doctors’ opinion. I cannot and do not accept Dr Herman’s opinion on the timing of the clot formation given his conclusion in his second report.

Dr Clifton’s opinion on the timing of the formation of the thrombus changed over her evidence. Whilst I accept that Dr Clifton gave considered evidence why the thrombus may have occurred during the swim, the doctor then stated that she did not disagree with
Dr Herman’s opinion that it probably occurred before the swim. The doctor then gave reasons why this could have occurred at that time which included the natural progression of the underlying disease.
Professor Keogh’s opinion on the timing of the formation of the clot is of no assistance. The doctor’s evidence that the clot formed days or weeks before the swim is inconsistent with the evidence that I accept from Dr Clifton that the clot was new and had formed within hours.
I do not accept the applicant’s submission that it can be inferred that the thrombus occurred during the swim because Mr Laverty did not complain of symptoms beforehand and commenced the swim. Such an inference cannot be drawn because, as Dr Clifton noted, “some people walk around apparently unaffected by severely stenosed vessels and others don’t and I suspect it’s something to do with their usual level of activity”. [100]
[100] T, p 52.
It is otherwise unknown, as Dr Clifton stated, whether the thrombus was formed by plaque rupture or by reason of the natural progression of the cardiac disease.
The final opinions expressed by both Dr Herman and Dr Clifton do not favour a conclusion that the thrombus occurred during the swim test.
Considering the change in opinions by both Dr Clifton and Dr Herman, the applicant has not established that the thrombus occurred during the swim. For these reasons the applicant has not established injury within the meaning of s 4(a) of the 1987 Act.

Section 4(b)(ii) injury

Section 4(b)(ii) requires the applicant to establish that “the aggravation, acceleration, exacerbation or deterioration in the course of employment of any disease, but only if the employment was the main contributing factor to the aggravation, acceleration, exacerbation or deterioration of the disease”.
In AV v AW[101] Snell DP identified the following issues under s 4(b)(ii). Snell DP stated:
“The following may be taken from the above:
(a)    The test of ‘main contributing factor’ in s 4(b)(ii) is more stringent than that in s 4(b)(ii) in its previous form, which applied in conjunction with the test in s 9A. There will be one ‘main contributing factor’ to an alleged aggravation injury.
(b)    The test of ‘main contributing factor’ is one of causation. It involves consideration of the evidence overall, it is not purely a medical question. It involves an evaluative process, considering the causal factors to the aggravation, both work and non-work related. Medical evidence to address the ultimate question of whether the test of ‘main contributing factor’ is satisfied is both relevant and desirable. Its absence is not necessarily fatal, as satisfaction of the test is to be considered on the whole of the evidence.
(c)    In a matter involving s 4(b)(ii) it is necessary that the employment be the main contributing factor to the aggravation, not to the underlying disease process as a whole.”
[101] [2020] NSWWCCPD 9 (AV v AW).
During the hearing the respondent’s counsel advised that it did not rely on factors going to antecedent aggravation and Mr Laverty’s underlying condition as being relevant to the
s 4(b)(ii) allegation. That position is inconsistent with the opinion expressed by Professor Keogh. I return to this aspect shortly.
The respondent’s submissions on this issue were that there was no aggravation caused by work, and, for that reason, the applicant had not established injury under s 4(b)(ii) of the 1987 Act.[102]
[102] T, p 21.
Professor Keogh was referred to the decision of AV v AW. It is clear from her reasons that the doctor misunderstands the legal reasoning of that decision. Professor Keogh stated:[103]
“I refer to the comments of Deputy President Snell in AV v AW [2020] regarding ‘the main contributing factor’ and contrasting this with the [sic a] ‘substantial contributing factor test’ relevant to personal injury. Mr Laverty’s constitutional causal factors were the main contributing factor to his cardiac arrest.”
[103] Application, p 138.
In the quoted paragraph Professor Keogh directed attention to the “constitutional causal factors” which is said to be “main contributing factor to his cardiac arrest”. This is not the test in a s 4(b)(ii) case. The passage ignores or at least does not address whether the work was the main contributing factor to the aggravation of the disease.
In a further report Professor Keogh noted[104] that Dr Herman did not state that the swim was the “main contributing factor” to the aggravation of the cardiac disease. The Professor, with respect, showed a lack of understanding of the notion of “aggravation” of the disease by referring to six factors that aggravated the cardiac disease which were present before the allegation of injury. The factors cited by Professor Keogh included hereditary risks, underlying constitution, non-compliance, with medication and high cholesterol. All of these factors occurred prior to the period of the work aggravation and were irrelevant to the legal test described in AV v AW.
[104] Reply, p 18.
As the applicant correctly submitted, the correct question is whether the work was the main contributing factor to the aggravation of the disease.
The applicant’s case on injury was directed to the swimming leg of the Mission test. There was no evidence, and it was not suggested by the respondent, that the underlying disease was aggravated during this period by matters outside that aspect of the employment.
Accordingly, the issue is whether the employment aggravated the underlying disease during the period of the swim. If it did, then it was the only factor aggravating the underlying disease and the test of main contributing factor to the aggravation of the disease is established.
In the autopsy report Dr Clifton opined that it was likely that Mr Laverty “suffered a sudden heart rhythm disturbance during exertion whilst in the water due to his severe cardiac disease” ultimately resulting in death.[105]
[105] Application, p 567.
Dr Clifton provided the following oral evidence of the medical basis between exertion and the risk of an arrhythmia:[106]
“When you say at risk of arrhythmia, does that – why does that occur, medically? If you could tell me?‑‑‑So when you exert yourself, your blood pressure goes up, your heart rate goes up, so your heart works faster – your heart works harder, if you like. The degree of disease you have in your heart, in your coronary vessel that supplies your blood, and hence oxygen to your heart muscle itself, which is working harder, stays the same, if you’ve got critically stenosed vessels. So you’re getting less blood flow to your heart muscle, which is working harder, and because his – also because of his level of – the condition of his heart as it was, we do know that anyone with any degree of fibrosis or scarring in their heart muscles, that scar tissue itself is arrhythmogenic, so it – it predisposes you to developing an abnormal electrical activity conduction through the heart. That abnormal electrical conduction through the heart is what develops – can develop into an arrythmia, so – and it can be a benign arrhythmia – not usually. I mean, well, I – that’s not right – it can be non – inconsequential, if you like, or it can be catastrophic. So any – so does that make sense? So any sort of exertion in this man meant an increase in his blood pressure, an increase in his heart rate, more – so heart – heart – his heart had to work harder, and therefore it predisposed him to an adverse cardiac event or arrhythmia in the ultimate outcome.”
[106] T, p 35.
Dr Clifton agreed with Dr Herman’s opinion that any activity could have been sufficient to provoke ischaemia and trigger an arrhythmic event.[107]
[107] T, p 45.
Dr Herman opined that swimming in the setting of severely stenosed vessel provoked the ischaemia and arrhythmic event on that day.[108]
[108] Application, p 352.
The respondent’s counsel conceded that that the temporal connection was “a factor to consider”[109] but relied on Professor Keogh’s opinion that there was no link between exercise and the onset of arrhythmia.
[109] T, p 87.
Professor Keogh did not comment on whether an increase in blood pressure caused by exercise would lead to less blood supply to the heart and trigger an arrhythmic event. Whilst that specific evidence was first given by Dr Clifton in oral testimony, the respondent had the opportunity, which it declined, to call further evidence in response.[110]
[110] T, p 96.
Professor Keogh’s explanation that there was no causal link between exercise and cardiac arrest is based on a Victorian study that found 98.6% of patients were not exercising at the time of cardiac arrest.[111] The doctor concluded that “on the balance of probabilities, exercise is not associated with OHCA”.
[111] Reply, p 17.
The article headed “Victorian Ambulance Cardiac Arrest Registry” is an attachment to Professor Keogh’s report.[112] The article does not state the conclusion that exercise is not associated with out of hospital cardiac arrest. Professor Keogh has used general statistics to support a medical conclusion.
[112] Application, p 269.
An article headed “Physical Activity and Public Health” by Haskell et al, is also an attachment to Professor Keogh’s report.[113] The authors there noted that “risks of cardiovascular complications increase transiently during vigorous physical exertion”.[114]
[113] Application, p 145.
[114] Application, p 243 at p 250.
The concept of the use of “commonsense” inferences was recently discussed in Tudor Capital Australia Pty Ltd v Christensen[115] McColl JA (as her Honour then was) stated:[116]
“The Commission is required to draw its conclusions from material that is satisfactory, in the probative sense, in order that it act lawfully and in order that conclusions reached by it are not seen to be capricious, arbitrary or without foundational material. In cases where the experts differ, the lay tribunal must apply logic and common sense to the best of its ability in deciding which view is to be preferred or which parts of the evidence are to be accepted, an exercise which cannot be carried out without knowing the essential integers of the expert opinion.”
[115] [2017] NSWCA 260 (Christensen).
[116] at [364]-[368], Mcfarlan JA agreeing at [425].
It is common ground that Mr Laverty had severe pre-existing cardiac disease. I accept the medical evidence of Dr Clifton and Dr Herman that the arrhythmia arose out of a compromised heart structure aggravated by the reduced blood supply to the heart.
Given the medical explanation provided by Dr Clifton of the association between exercise and ischaemia, the temporal connection between the swimming test and the onset of arrhythmia, and, consistent with Dr Herman’s evidence[117], I find on the balance of probabilities that the exercise provoked the ischaemia through a reduced blood supply resulting in electrical instability and contributing to cardiac arrhythmia. This process aggravated the underlying severe cardiac disease.
[117] Application, p 353
As the claimant correctly submitted, Mr Laverty’s underlying coronary artery disease and associated symptoms were made worse during the period of employment with the respondent which satisfied the meaning of aggravation: Ogden Industries Ltd v Lucas.[118]
[118] [1967] HCA 30 at [29].
This finding of injury is consistent with the particularisation of the s 4(b)(ii) allegation at the arbitration hearing.[119]
[119] See [7].
The applicant has established that the employment was the main contributing factor to the aggravation of the disease because of the previous finding that there were no concurrent non-work factors aggravating the disease during the short period of the swim.
The applicant also referred to the delay in resuscitation as being relevant to the s 4(b)(ii) issue. For the reasons provided, the applicant succeeded on the s 4(b)(ii) issue which occurred prior to the resuscitation efforts. It is logically impossible that a subsequent event (the delay in resuscitation) could be relevant to an injury that had already occurred. I do not accept that in the present matter the delay in resuscitation is relevant to the allegation made under s 4(b)(ii).

Section 9B

Section 9B of the 1987 Act relevantly provides:
“(1) No compensation is payable under this Act in respect of an injury that consists of, is caused by, results in or is associated with a heart attack injury or stroke injury unless the nature of the employment concerned gave rise to a significantly greater risk of the worker suffering the injury than had the worker not been employed in employment of that nature.”
The parties agreed that the applicant must satisfy the requirements of s 9B as Mr Laverty suffered a heart attack injury as defined by s 9B(2) of the 1987 Act.
The applicant referred to the principles discussed in Secretary, Department of Communities and Justice v Galea[120] where Snell DP stated:
“Both parties accept that s 9B has application in the circumstances. Neither party argues that De Silva and Kim are wrongly decided. The following may be taken from those decisions:
(a) the worker carries the onus of establishing that the test in s 9B is satisfied;
(b) where the words ‘an injury’ first appear in s 9B(1), this refers to an injury asserted by a worker, in respect of which compensation is otherwise payable, subject to satisfaction of the test in s 9B;
(c) where s 9B(1) refers to ‘the nature of the employment concerned’, it refers to “what the worker in fact does in the employment that caused or contributed to the injury”;
(d) s 9B(1) requires that the relevant risk of suffering the injury in the employment concerned be significantly greater than the risk had the worker not been employed in employment of that nature. ‘Significant’ in this context means ‘important; of consequence’. The comparison involves an assessment of comparative risks and is not a true test of causation. The test involves an evaluative judgment, and
(e) the test requires satisfaction on all of the evidence. It does not necessarily “require that there be medical evidence to some particular effect”. In cases raising s 9B it is desirable that there be medical evidence addressing the requirements of the section.”
[120] [2021] NSWWCCPPD 1 (Galea) at [111].
The respondent accepted that Galea provided “a summary of the relevant principles”[121] although it did not embrace the further definition of “significant”. It noted that the “nature of the employment concerned” was the swimming undertaken by Mr Laverty.
[121] Respondent’s submissions, [35].
The respondent submitted that the evidence was “one way”, that is that Mr Laverty was “vulnerable to suffering arrhythmia having regard to his pre-existing cardiovascular disease”.[122]
[122] Respondent’s submissions, 39].
Professor Keogh stated:[123]
“Due to his ischemic cardiomyopathy, sudden cardiac arrhythmia would have occurred at any time and any place, at or around the same time of his life, irrespective of his work as a lifeguard.”
[123] Application, p 138.
Dr Clifton stated:[124]
“In my opinion, this man could have suffered a sudden (potentially lethal or debilitating) cardiac arrhythmia at any time, in light of the degree of cardiac pathology identified at autopsy examination.”
[124] Application, p 356.
In her oral evidence Dr Clifton accepted that:
(a)    Mr Laverty had pre-existing chronic disease that put him at risk of an arrhythmia;[125]
(b)    the right coronary artery had become further compromised to a critically point,
and[126]
(c)    anyone with this degree of heart pathology would be considered at risk of having an arrhythmia at any point in time.[127]
[125] T, p 30.
[126] T, p 51.
[127] T, p 56.
Dr Clifton candidly agreed that she could not comment of the degree of exertion “but any degree of exertion to me, this man was at risk of an arrhythmia or a cardiac event”.[128]
[128] T, p 35.
Dr Clifton conceded that she was unaware of the phrase METs, that she was not involved in interpreting exercise testing[129] and had no familiarity with assessing the effects of exercise on living patients with cardiac compromise.[130]
[129] T, p 38 and p 42.
[130] T, p 43.
Dr Clifton then provided a written response to a question assuming an activity of more than 4-5 METs in circumstances where the doctor subsequently accepted that she was unaware of the term and had no familiarity with assessing the effects of exercise on living patients with cardiac compromise.
Noting the concession, Dr Clifton’s opinion that the swim involved a significant increase in risk is given minimal weight.
Dr Herman in his last report stated that “any activity” would be sufficient to provoke ischaemia and provoke the trigger for the arrhythmic event.[131] Further, Dr Herman was of the view that, considering the underlying disease, Mr Laverty was always at substantial risk of an arrhythmic cardiac event which had been increased by reason of the superimposed thrombus.[132]
[131] Application, p 345.
[132] Application, p 345.
The medical evidence from both Professor Keogh and Dr Herman is that 4 to 5 METS were expended in the swimming test. Professor Keogh placed that amount of energy expended in context when she stated:[133]
“The phrase ‘Out of Hospital Cardiac Arrest at 4-5 Mets of Exercise during a swim test’ sounds impressive, quantitative and somehow very scientific. I wish to make this transparent and put 4-5 mets usage of energy into perspective with the equivalent of 4-5 mets activities in our daily lives. The equivalents are mopping floors, or polishing furniture, or carrying a golf bag, or stocking shelves with light objects, or shopping and carrying groceries weighing 10kgs.”
[133] Reply, p 17.
There was no submission suggesting evidence contradicting this passage.
Mr Laverty was a regular swimmer and had completed an 800 m swim test the previous Monday. As Professor Keogh opined and I agree, the swim test on the day was clearly within Mr Laverty’s capacity.
The applicant referred to Dr Herman’s opinion which she submitted was “well explained and based on the complete and factual foundation”.[134] It is unclear what aspect of Dr Herman’s opinion fell within his description. The opinion provided by Dr Herman to the s 9B question in his first report was as follows:[135]
“In my opinion, the deceased’s worker’s employment did give rise to a significantly greater risk of the injury than had he not been in employment of that nature.
Whilst he had extensive, severe coronary disease and an ischaemic cardiomyopathy and was always at very high risk of a cardiovascular event, the trigger for the specific episode of a sudden death was significantly contributed to by the haemodynamic stress of a 400 metres swim during a time trial.
Whilst he was always at risk of a cardiovascular event, on a particular day, his swim, as part of his Lifeguard duties gave rise to a significantly greater risk of plaque rupture and the unfortunate and tragic event.”
[134] Applicant’s submissions, [82].
[135] Application, p 342.
The first paragraph repeats the test of s 9B. The third paragraph refers to a factor (the plaque rupture) which has been found not to have caused the s 4(a) injury. It is explicable that
Dr Herman relied on this issue in his first report on the s 9B issue because at that time the doctor opined that the plaque rupture causing the thrombus occurred during the swim.
This leaves the second paragraph which relates to the stress from the 400 m swim described by Dr Herman as a trigger for the specific episode.
Dr Herman’s opinion on the application of s 9B in his second report was as follows:[136]
“I agree with Professor Keogh that on the balance of probabilities that the deceased’s ischaemic cardiomyopathy and sudden cardiac arrhythmia could have occurred at any time and at any place at around the same time of his life.
However, I differ from Professor Keogh in that the “trigger” for this specific episode of ventricular arrhythmia and sudden cardiac death was, in my opinion, provoked by coronary ischaemia in the right coronary artery territory in a pre-existently [sic] severely stenosed vessel with superimposed thrombosis provoking near occlusion.
Mr Laverty was at a very high risk of an arrhythmic cardiac event but the swim on the day of his OHCA, provoked the trigger for the electrical instability due to ischaemia developing in the right coronary artery territory.
In my opinion, the swim itself gave risk to a significantly greater risk of Mr Laverty suffering the injury than had he not swum on the day. At that particular time, the severe narrowing of the right coronary artery with pre-existent plaque and superimposed thrombus, provoked a critical situation whereby any activity more than 4-5 METs may have provoked ischaemia and a subsequent electrical instability.”
[136] Application, p 349.

The revised opinion assumes that the thrombosis was present before the swim (second and fourth paragraphs). The reasoning in the third paragraph is that whilst Mr Laverty was at “very high risk” of an arrhythmic cardiac event before the swim, the swim provoked the trigger for the electrical instability due to “ischaemia” developing in the right coronary artery.
I accept that this opinion reflects the findings on s 4(b)(ii) and involves an analysis of the actual work undertaken by Mr Laverty because “the nature of the employment concerned” refers to “what the worker in fact does in the employment that caused or contributed to the injury”. In the present case the evidence of injury is solely directed to the 400 m swim.
What is unclear from Dr Herman’s reasoning is why the s 9B test was satisfied when:
(a)    Mr Laverty’s condition prior to the swim was critical;
(b)    Mr Laverty was at very high risk of suffering an arrhythmic cardiac event without any precipitating activity;
(c)    the ischaemia developed in the right coronary artery which was effectively blocked due to the pre-existent plaque and superimposed thrombus;
(d)    any or nil activity with Mr Laverty’s condition could cause arrythmia, and
(e)    the energy expended in the swim is not significant considering that Mr Laverty was fit for swimming and the expenditure of that type of energy is contrasted with other activities discussed earlier.[137]
[137] See at [145].
I adopt the applicant’s submission on the s 9B test that:[138]
“Section 9B(1) does not require a significant risk. It requires a comparison of (1) the risk to which the nature of the employment concerned gives rise and (2) the risk had the worker not been employed in employment of that nature (De Silva [105]). It is necessary that the first of these be ‘significantly greater’ than the second if compensation is to be payable.”
[138] Applicant’s submissions, [85].
Given the matters referred to above[139] and the uncontradicted evidence that Mr Laverty was at a very high risk of suffering an arrhythmic cardiac event without any precipitating activity, the fact that the right coronary artery was blocked due to the superimposed thrombus and the modest level of energy expended in the swim test, I am not satisfied that the s 9B test is established. Mr Laverty was already at severe risk of suffering arrythmia before the swim. There was no significant increase in risk of suffering the injury by reason of the swim.
[139] See [153].
The applicant otherwise submitted that if the heart attack had occurred on land, then “the attack might not have the fatal results that followed”.[140] This submission was made in the context of s 9B although it is unclear how it relates to the operation of the section.
[140] Applicant’s submissions, [89].
The applicant referred to Dr Herman’s opinion on the delay in resuscitation. However,
Dr Herman was not decisive and opined that the “outcome may have been better” if resuscitation had occurred earlier.
Professor Keogh considered the prospects from earlier resuscitation. The doctor noted that consciousness is lost within 30 seconds[141]. Survival rates when an OHCA occurred in a public place increased to 21% (by reason of assistance from bystanders) indicating that it was more likely than not that that OHCA results in death. [142]
[141] Application, p 137.
[142] Application, p 144.
The applicant’s submission that Dr Herman provided a more persuasive opinion on this issue was unexplained. Professor Keogh explained her reasoning by reference to published statistics of likely outcomes if OHCA events occurred in public places. These figures show that it is more likely that the death will occur. In any event, given the use of the word “may”, Dr Herman was not stating on the balance of probabilities that the outcome would have been better.
I am not persuaded that earlier intervention would have on the balance of probabilities, avoided the death of Mr Laverty.
I otherwise do not accept that the delay in resuscitation is relevant to the determination of the s 9B issue. This is because the section requires an analysis of the employment concerned giving rise to a significantly greater risk of the worker suffering the injury, not whether the worker would have died. For the same reasons mentioned under s 4(b)(ii)[143], these submissions do not address the issue of “injury” as they relate to matters after the occurrence and relate to whether the death could have been prevented.
[143] See [132].

Whether death resulted from injury

It is strictly unnecessary to determine this issue as the applicant has not succeeded due to the operation of s 9B of the 1987 Act.
The applicant made submissions on whether death resulted from injury referring to dicta of Kirby P (as his Honour then was) in Kooragang Cement Pty Ltd v Bates.[144] Ms Laverty submitted that it was only necessary to establish that the “the injury found materially contributed to the death”.[145]
[144] (1994) 35 NSWLR 452 at 462, 463-4.
[145] Applicant’s submissions, [93].
The respondent made no oral or written submissions on this issue and specifically did not reply to the applicant’s submissions on whether death resulted from injury.
Given the absence of response from the respondent, for brief reasons I conclude that the injury sustained within the meaning of s 4(b)(ii) caused the death of Mr Laverty. The injury involved lack of blood supply to the heart contributing to arrythmia and resulting in loss of consciousness and death within a short time frame. In these circumstances the work-related injury caused the death of Mr Laverty noting that there was severe underlying cardiac pathology also causative of the death.

FINDINGS AND ORDERS

The findings and orders are set out in the Certificate of Determination.

[2022] NSWPIC 543

29 September 2022