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Out-of-hospital cardiac arrests in young adults in Melbourne, Australia—Adding coronial data to a cardiac arrest registry
Resuscitation 82 (2011) 1302–1306
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Clinical paper
Out-of-hospital cardiac arrests in young adults in Melbourne, Australia—Adding coronial data to a cardiac arrest registry夽 C. Deasy a,b,c,∗,d , J.E. Bray a,d , K. Smith a,b,d , L.R. Harriss a,b,d , S.A. Bernard a,b,c,d , P. Cameron b,d a b c
Ambulance Victoria, Australia Monash University, Department of Epidemiology and Preventive Medicine, Australia Alfred Hospital, Australia
a r t i c l e
i n f o
Article history: Received 21 February 2011 Received in revised form 11 April 2011 Accepted 29 May 2011
Keywords: Cardiac arrest Coroner Autopsy Out-of-hospital Young adults CPR Cardiopulmonary resuscitation EMS
a b s t r a c t Aim: We aim to describe the coronial findings of young adults where the out-of-hospital cardiac arrest (OHCA) aetiology was ‘presumed cardiac’. Methods: Presumed cardiac aetiology OHCAs occurring in young adults aged 16–39 years were identified using the Victorian Ambulance Cardiac Arrest Registry (VACAR) and available coronial findings reviewed. Results: We identified 841 young adult OHCAs where the Utstein aetiology was ‘presumed cardiac’. Of these 740 died and 572 (77%) OHCAs were matched to coroner’s findings. On review of the coroner’s cause of death, 230 (40.2%) had a ‘confirmed cardiac’ aetiology, 221 (38.6%) were proven ‘non-cardiac’, 97 (17%) were inconclusive and 24 (4.2%) cases remained ‘open’. ‘Confirmed cardiac’ causes of OHCA were ischemic heart disease (n = 126, 55%), cardiomegaly (n = 26, 11.3%), cardiomyopathy (n = 25, 11%), congenital heart disease (n = 15, 6.5%), cardiac tamponade due to dissecting thoracic aorta aneurysm (n = 10, 4.3%), myocarditis (n = 8, 3.5%), arrhythmia (n = 7, 3%), others (n = 13, 5.7%). ‘Non-cardiac’ causes of OHCA were epilepsy/sudden unexplained death in epilepsy (SUDEP) (n = 56, 25%), pulmonary embolism (n = 29, 13%), subarachnoid haemorrhage (n = 17, 7.7%), other intracranial bleed (n = 7, 3.2%), pneumonia (n = 17, 7.7%), DKA (n = 16, 7.2%), other complications of diabetes mellitus (n = 8, 3.6%), complications of obesity (n = 9, 4%), haemorrhage (n = 12, 5.4%), sepsis (n = 8, 3.6%), peritonitis (n = 6, 2.7%), aspiration (n = 6, 2.7%), renal failure (n = 5, 2.3%), asthma (n = 5, 2.3%), complications of anorexia (n = 3) and alcohol abuse (n =2), thyrotoxicosis (n = 2), meningitis (n = 1) and others (n = 12). Compared with coroner’s diagnosed ‘non-cardiac’ OHCAs, ‘confirmed cardiac’ were more likely to be witnessed (41% vs 23%, p ≤ 0.01), receive bystander CPR (35% vs 20%, p ≤ 0.001), have a shockable rhythm (27% vs 6.3%, p < 0.001) and have EMS attempted resuscitation (62% vs 44%, p < 0.001). Discussion: Linking OHCA registries with coronial databases for aetiology of the arrest will improve the quality of the data and should be considered by all OHCA registries, particularly for young adult OHCA. © 2011 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Out-of-hospital cardiac arrest (OHCA) is presumed to be of cardiac aetiology unless, as best determined by the rescuers, it is known or likely to have been caused by trauma, submersion, drug overdose, asphyxia, exsanguination or other non cardiac cause.1 Young adults represent a minority of those who suffer an OHCA; the aetiology of cardiac arrest is likely to be different to that of older
夽 A Spanish translated version of the abstract of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2011.05.031. ∗ Corresponding author at: Monash University, Department of Epidemiology and Preventive Medicine, Alfred Hospital, Level 3 Burnet Building, 89 Commercial Road, Melbourne 3004, Australia. Tel.: +61 41 6486887. E-mail address: [email protected] (C. Deasy). d On behalf of the VACAR Steering Committee. 0300-9572/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2011.05.031
adults where ischemic heart disease is more common.2 Making an accurate clinical diagnosis in the field can be a great challenge in the young adult group of patients and the clinician’s perception of the cause of arrest can strongly influence management and the direction of treatment. Furthermore, heterogeneity in aetiology of the ‘presumed cardiac’ arrest may be responsible for the seemingly poorer results seen in this age group of patients when compared to older adults. Such heterogeneity may dilute the positive impact of initiatives designed to improve OHCA survival and outcomes as the denominator is increased by patients that were never going to survive. Determining aetiology based on clinical diagnosis has many limitations and autopsy remains the ‘gold standard’.3 However, there is little literature in the young adult age group that links cardiac arrest registry data with coronial registries that detail final diagnosis. Such information could potentially be useful for planning preventative strategies, improving emergency medical
C. Deasy et al. / Resuscitation 82 (2011) 1302–1306
service (EMS) response, planning intervention strategies and guiding future research in young adult OHCA. This paper describes the characteristics of OHCA in young adults where the OHCA aetiology was ‘presumed cardiac’ and links them with the subsequent coronial findings.
2. Methods The study setting was Melbourne, Australia, which had a population at the time of the last census (2006) of 3.59 million, of whom 1,279,980 were aged between 16 and 39 years of age with an equal male/female distribution. The EMS comprises ambulance paramedics who have some advanced life support skills (laryngeal mask airway, intravenous epinephrine) and mobile intensive care ambulance (MICA) paramedics who are authorized to perform endotracheal intubation and administer a wider range of cardiac drugs. The Advanced Medical Priority Dispatch System© is operational in Melbourne. MICA paramedics are dispatched to patients with critical illness, including patients with cardiac arrest. In addition, fire-fighters are dispatched to patients with suspected cardiac arrest in the inner two thirds of Melbourne’s area.4 The pre-hospital cardiac arrest protocols follow the recommendations of the Australian Resuscitation Council.5,6 Since December 2007, all patients attended by paramedics have patient care data collected in an electronic patient record. Previous years involved a paper patient care record (PCR). Selected data from PCRs is collected from patients in cardiac arrest and stored on the Victoria Ambulance Cardiac Arrest Registry (VACAR). Where the paramedic has not indicated the aetiology of the OHCA clinical staff within the registry make a judgment based on the details provided. The VACAR also includes some data from the hospital record for those patients transferred to hospital, including number of days in hospital, discharge direction and whether the patient survived to leave hospital. Hospital investigation results were not recorded in VACAR for the time period involved in this study. EMS response time is the time from ‘000’ telephone call to EMS arrival at scene.
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Circumstances where Ambulance Victoria paramedics may cease resuscitation efforts are detailed in Table 1.5 Under Victorian law, patients who suffer sudden death are referred to the Coroner unless a medical practitioner is able to complete a death certificate with knowledge of the cause of death. Patients referred to the Coroner generally undergo an autopsy unless there is an objection by the next-of-kin. Deaths were matched with coroner’s office records and all autopsies and coroner’s investigation notes reviewed. Cases that could not be matched included cases with missing identity or registered with alternative names and cases not reported to the coroner. The Victoria Ambulance Cardiac Arrest Registry (VACAR) was searched for all OHCAs occurring in patients aged 16–39 years. Drug overdose associated OHCA as detected at autopsy was excluded. 2.1. Ethics approval VACAR has been classified as a quality assurance project by the ethics committee at the Department of Health. The collection of cardiac arrest outcome data by VACAR was approved by the ethics committees of Victorian hospitals receiving cardiac arrests by ambulance. This study was approved by the Research Committee of Ambulance Victoria and Monash University Human Research Ethics Committee. Table 1 Circumstances where paramedics in Victoria may withhold resuscitation efforts. Where rigor mortis, decomposition or post mortem lividity is already present. Where death has been declared by a Medical Officer who is or has been at the scene. Where a refusal of treatment certificate has been completed for a current condition which most likely caused the cardiac arrest. Where the presenting rhythm was monitored as asystole for >30 s, and there has been >10 min downtime, no evidence of hypothermia, drug overdose or family/bystander objections. If advanced life support has been performed for 30 min without return of spontaneous circulation (ROSC), the rhythm is not Ventricular Fibrillation or Ventricular tachycardia, there are no signs of life, no gasps or pupillary reactions and no evidence of hypothermia or drug overdose.
Table 2 Modified Utstein template describing characteristics of ‘presumed cardiac’ OHCA in young adults. Utstein element
‘Presumed cardiac’ OHCA Young adult n (%)
Coroner confirmed ‘Cardiac’ n (%)
Coroner diagnosed ‘Non cardiac’ n (%)
Coroner findings ‘Undetermined’ n (%)
Absence of signs of circulation and/or considered for resuscitation Age median (IQR) years Male sex (%) Resuscitation attempted, n (%) Any defibrillation, n (%) First monitored rhythm, n (%) Shockable Non shockable asystole PEA Location of arrest, n (%) Home Work Street Other Arrest witnessed by layperson, n (%) Arrest not witnessed CPR before EMS arrival, n (%)* EMS response time median (IQR) (min) Where resuscitation attempted, n (%) Outcome Any ROSC Survived event Discharged from hospital alive Missing hospital outcome data, n
841 33 (27–37) 69 485 (58) 262 (31)
230 34 (30–38) 78 143 (62) 96 (41)
221 32 (26–37)* 65* 97 (44)* 23 (10.4)*
97 31 (25–35)* 60 44 (45)* 26 (26.8)*
186 (22) 549 (65) 69 (8.2)
61 (27) 140 (61) 25 (11)
149 (6.3)* 187 (85)* 12 (5)*
17 (18) 75 (77.3)* 5 (5.1)
646 (77) 24 (3) 79 (9) 92 (11) 275 (33) 529 (63) 243 (29) 7.38 (6–10)
185 (80) 8 (3.4) 15 (7) 22 (9.6) 95 (41) 132 (57) 80 (35) 7.95 (6–9.7)
189 (86) 2 (0.9) 7 (3.2)* 23 (9.9) 44 (20)* 170 (77)* 44 (20)* 7.15 (5.9–10.7)
80 (82.5) 2 (2.1) 4 (4.1) 11 (11.3) 27 (28)* 69 (71)* 29 (30) 7 (6–10)
173 (21) 148 (18) 86 (10.4) 15
22 (9.6) 12 (5.2) NA NA
17 (7.7) 12 (5.4) NA NA
3 (3) 2 (2) NA NA
*
p < 0.05.
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Fig. 1. Corner confirmed cardiac OHCA.
2.2. Statistical analysis All data were entered into an Access software cardiac arrest registry database (version 2003, Microsoft, Redmond, WA, USA). Statistical calculations were performed on STATA software (version 10.0 Stata Corporation, College Station, TX, USA). Chi-square analyses were used for categorical variables. Continuous variables were compared using the t-test (normal distribution) or Mann–Whitney. 3. Results Between the years 2000 and 2009 there were 3912 OHCAs in young adults aged 16–39 years of age. We identified 841 (21.5%) young adult OHCAs where the Utstein aetiology was ‘presumed cardiac’. Other causes of young adult OHCA were trauma (18.8%), hanging (16.6%), overdose (33.5%) and others (9.6%). There were 86 survivors (10.2%) who were not subject to coronial investigation. We were unable to ascertain survival status for 15 patients. There were 740 patients who died and 572 (77%) OHCAs were matched to coroner’s autopsy. On review of coronial findings, 230 (40.2%) had a ‘confirmed cardiac’ aetiology, 221 (38.6%) were proven ‘noncardiac’, 97 (17%) had inconclusive coronial findings and 24 (4.2%) cases remained ‘open’. Characteristics of the young adults who sustained ‘presumed cardiac’ OHCA as assigned on clinical details are shown in Table 2. Coroner confirmed cardiac and non cardiac as well as OHCAs where the coroner was unable to ascertain cause of death are also shown. The characteristics of the patients and the OHCAs they sustained were different between those who had coroner confirmed cardiac arrest and those that had a non cardiac OHCA on subsequent autopsy; coroner confirmed cardiac OHCAs were older and greater
proportions were male, witnessed, had bystander CPR, were in shockable rhythm on arrival of EMS and had an attempted resuscitation (Fig. 1). The coroner was unable to identify cause of death in 97 cases (Table 1). These cases differed from the coroner confirmed cardiac OHCA cases in being younger, a lesser proportion had EMS attempted resuscitation, less had an attempted defibrillation and less were witnessed OHCAs (Table 2). Ischemic heart disease was the cause of death on autopsy in 126 cases (22% of clinically presumed cardiac young adult OHCAs) and found present in 195 cases (34%); the median (IQR) age was 36 (31–38) years and was older than non-IHD OHCAs where the median (IQR) age was 32 (26–36) years (p < 0.001). More patients were male (83.5% vs 16.5%, p < 0.001). Ventricular fibrillation/pulseless ventricular tachycardia (VF/VT) was present in 28%, asystole in 63% and PEA in 7%. Congenital heart disease was the cause of death in 15 autopsies (2.6% of clinically ‘presumed cardiac’ OHCA). Their median (IQR) age was 31 (24–33) years. VF/VT was present in six patients on arrival of the ambulance, four patients were in PEA, and the remainder were in asystole (n = 5). Cardiac tamponade was found on autopsy in 10 cases, in all cases in association with aortic dissection; their median age was 32.5 (23–35) years. Their presenting rhythms were PEA (n = 5) and asystole (n = 5). ‘Non-cardiac’ causes of OHCA are shown in Fig. 2. Sudden unexplained death in epilepsy (SUDEP) was the autopsy cause of death in 56 cases (9.8%) who had been ‘presumed cardiac’ clinically. Their median (IQR) age was 29 (24–35.5) years. Asystole was present in 93% on arrival of EMS. Resuscitation was attempted in 20 patients (36%). Pulmonary embolism was the autopsy cause of death in 29 (5%) patients whose OHCA had been ‘presumed cardiac’ clinically. Their median (IQR) age was 30 years (28–34) years, and 59% were female. Asystole was the presenting rhythm in 17 patients (59%), VF/VT and PEA were the presenting rhythms in 4 patients each. A subarachnoid or intracranial bleed was the cause of death in 24 cases that had been presumed cardiac clinically. Their median age was 33.5 (29–37) years. Asystole was present in 18 patients (75%), PEA and VF/VT in 3 (12.5%) patients each. There were 97 patients in whom the coroner was unable to confirm cause of death. Their median (IQR) age was 31 (24–35) years, 59% were male, 29% had a witnessed arrest, 30% had bystander CPR and 45% had an EMS attempted resuscitation with 3% achieving a ROSC but subsequently not surviving. VF/VT was the presenting rhythm in 17.5%, PEA in 5% and asystole in 77%. There were 86 ‘presumed cardiac’ patients who survived and so did not have a coronial investigation. Their median age (IQR)
Fig. 2. Non cardiac cause of OHCA on coroner’s finding.
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age was 31 (24–36) years and 73% were male. Of survivors 73% were witnessed OHCAs and 40% received bystander CPR. A greater proportion of survivors sustained their OHCA in the street (24.4% vs 7.3%, p < 0.001) and less occurred in the home (48% vs 81%, p < 0.002).
4. Discussion This study shows the limitations associated with ascribing cause of OHCA on the basis of clinical details. The results of this study show that only a minority of patients had a coronial study confirming cardiac aetiology of OHCA and that the confirmed cardiac group of patients differed both in terms of patient and OHCA characteristics to those found on coronial review to be non cardiac. Accurate data is important in this area as it informs treatment and preventive strategies. Furthermore, when trying to establish the impact of initiatives such as the 2005 CPR guidelines7,8 on survival in ‘presumed cardiac’ OHCA comparing homogenous data sets is important to avoid under representing their impact. Our finding that in ‘presumed cardiac’ OHCA in this age group non-cardiac causes are frequent suggests that early echocardiography should be undertaken in patients with sudden OHCA.9–11 There were 97 cases (17%) of young adult ‘presumed cardiac’ OHCAs where the autopsy was unable to ascertain cause of death. In addition, autopsy reported 7 cases of ‘arrhythmia’ as cause of death; of these one patient had prolonged QT on a previous ECG. Most were in asystole on arrival of EMS (n = 6) with one patient in a shockable rhythm. One of the most difficult tasks in forensic medicine is deciding the cause of death in an unclear or debatable case. In general, there are three major categories that lead to difficulties: (1) co-existence of a pre-existing condition and a fatal injury; (2) competing potential causes of death; (3) historical events that may be causally relevant to death by injury.12 A ‘negative’ post-mortem may yield a default diagnosis of sudden arrhythmic death syndrome (SADS) or sudden unexplained death (SUD) syndrome after the first year of life13–15 where there are no discernible abnormalities on histopathology and a negative toxicology screen.16,17 The inherited arrhythmia syndromes (long QT, short QT, and Brugada syndromes, and familial catecholaminergic polymorphic ventricular tachycardia) may be implicated in SADS, owing to their propensity for producing ventricular tachyarrhythmia in the structurally normal heart.18 In cases where a morphological explanation for cardiac arrest is lacking, a growing number of forensic experts now resort to post-mortem genetic testing, called ‘molecular autopsy’19–21 however, at present there is no internationally established best practice concerning post-mortem genetic testing in the clinical or forensic setting.22 In at least 10% and perhaps as many as 30% of sudden deaths involving previously healthy children, adolescents, and young adults, no abnormalities are evident at autopsy15 leaving coroners, medical examiners, and forensic pathologists only to suggest that a fatal arrhythmia might be responsible for the event.23–25 Doolan et al.26 reviewed all autopsies performed on those aged <35 years between 1994 and 2002 in Sydney, Australia; they were unable to identify a cause of arrest in 60 (9.9%) cases and suggest that these cases may represent a primary arrhythmia. The actual extent of inherited arrhythmia syndromes causing OHCA is therefore at best speculative. SUDEP was the autopsy cause of death in 10% of ‘presumed cardiac’ OHCAs that had an autopsy performed. SUDEP is defined as sudden, unexpected, witnessed or unwitnessed, nontraumatic and non-drowning death in patients with epilepsy, with or without evidence for a seizure and excluding documented status epilepticus, in which post mortem examination does not reveal a toxicologic or anatomic cause of death. The incidence of SUDEP varies from 1:1000 per year to as many as 1:200 per year in those with epilepsy,
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depending upon the community surveyed. The mechanism of death in SUDEP is not clearly established. Hypoventilation and/or cardiac changes occurring during or shortly after seizure may be such mechanisms, but at the present time the precise mechanism is not known.27 The best medical intervention for OHCA is prevention. The advent of effective therapies for some of these diseases such as implantable defibrillators, antiarrhythmic treatment for long QT syndrome type 128 and low dose amiodarone for hypertrophic cardiomyopathy29,30 has prompted calls for universal screening. However, the recommended preliminary workup to prevent SUD includes a 12-lead ECG, signal-averaged ECG, transthoracic echocardiogram, exercise test, ambulatory ECG monitoring, cardiovascular magnetic resonance imaging to diagnose arrhythmogenic right ventricular cardiomyopathy or anomalous coronary arteries, a provocative challenge with a sodium channel blocker to unmask the Brugada syndrome and genetic identification of disease-causing mutations.18 It is not feasible to screen the population with this battery of investigations given the small numbers of patients that might benefit as highlighted by this study. Similarly, the likelihood of preventing SUDEP could be increased with more appropriate antiepileptic drug treatment, more comprehensive investigations and better treatment for cardiac and pulmonary disease in patients with epilepsy,31 however the requirement for routine post-ictal echocardiography, polysomnography, autonomic function tests, and loop-recorder implants as suggested by Finsterer31 is controversial32 and requires validation in studies larger than those done so far.32 Population based cardiac arrest registries linked with coronial data are important in providing the evidence needed to justify expensive preventive strategies.
5. Limitations This study has a number of limitations due to its retrospective nature. We have limited this study to ‘presumed cardiac’ aetiology OHCA as judged clinically excluding coronial diagnosed drug overdoses retrospectively; this denominator must be considered when interpreting the study outcome to avoid the over emphasis on arrhythmia or SUDEP in causation of all OHCAs that occur in young adults. We were unable to match 168 OHCAs to coroner’s autopsies (23%). A proportion of these patients had achieved ROSC (n = 31) and were transported to hospital but subsequently died. It is possible that an autopsy was not performed in these cases as the cause of death was sufficiently evident from the hospital investigations for it to be recordable on the death certificate. Reporting the aetiology of OHCA where the patient survived to reach hospital and had diagnostic investigations was beyond the scope of this study. Decisions to perform or withhold a complete autopsy are not standardized between coroners; however, in the context of young adults the threshold to perform such an investigation is low.
6. Conclusions Linking OHCA registries with coronial databases for aetiology of the arrest will improve the quality of the data, and will provide data that justifies improved diagnostic and treatment algorithms. Such linkage is particularly important in the young adult age group where there is increased heterogeneity in the aetiology of the cardiac arrest.
Conflict of interest statement No conflicts of interest to declare.
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Acknowledgements The authors would like to acknowledge Vanessa Barnes, Marian Lodder and VACAR staff; Ambulance Victoria paramedics; and Joanna Cotsonis Coroner’s office. References 1. Jacobs I, Nadkarni V, Bahr J, et al. Cardiac arrest and cardiopulmonary resuscitation outcome reports: update and simplification of the Utstein templates for resuscitation registries. A statement for healthcare professionals from a task force of the international liaison committee on resuscitation (American Heart Association, European Resuscitation Council, Australian Resuscitation Council, New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Southern Africa). Resuscitation 2004;63:233–49. 2. Zipes DP, Wellens HJ. Sudden cardiac death. Circulation 1998;98:2334–51. 3. Gow RM. Sudden cardiac death in the young. Can J Cardiol 1996;12:1157–60. 4. Smith KL, Peeters A, McNeil JJ. Results from the first 12 months of a fire firstresponder program in Australia. Resuscitation 2001;49:143–50. 5. Ambulance Victoria. Clinical practice guidelines. http://www.ambulance.vic. gov.au/Paramedics/Qualified-Paramedic-Training/Clinical-PracticeGuidelines.html. 6. Australian Resuscitation Council. Guidelines. http://www.resus.org.au. 7. Proceedings of the 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2005;67:157–341. 8. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2005;112(24 Suppl.):IV1–203. 9. Price S, Uddin S, Quinn T. Echocardiography in cardiac arrest. Curr Opin Crit Care 2010;16:211–5. 10. Niendorff DF, Rassias AJ, Palac R, Beach ML, Costa S, Greenberg M. Rapid cardiac ultrasound of inpatients suffering PEA arrest performed by nonexpert sonographers. Resuscitation 2005;67:81–7. 11. Beaulieu Y. Bedside echocardiography in the assessment of the critically ill. Crit Care Med 2007;35(5 Suppl.):S235–49. 12. Pollanen MS. Deciding the cause of death after autopsy—revisited. J Clin Forensic Med 2005;12:113–21. 13. Ellsworth EG, Ackerman MJ. The changing face of sudden cardiac death in the young. Heart Rhythm 2005;2:1283–5.
14. Morentin B, Suarez-Mier MP, Aguilera B. Sudden unexplained death among persons 1–35 years old. Forensic Sci Int 2003;135:213–7. 15. Puranik R, Chow CK, Duflou JA, Kilborn MJ, McGuire MA. Sudden death in the young. Heart Rhythm 2005;2:1277–82. 16. Behr E, Wood DA, Wright M, et al. Cardiological assessment of first-degree relatives in sudden arrhythmic death syndrome. Lancet 2003;362:1457–9. 17. Bowker TJ, Wood DA, Davies MJ, et al. Sudden, unexpected cardiac or unexplained death in England: a national survey. QJM 2003;96:269–79. 18. Sen-Chowdhry S, McKenna WJ. Sudden cardiac death in the young: a strategy for prevention by targeted evaluation. Cardiology 2006;105:196–206. 19. Tester DJ, Ackerman MJ. The role of molecular autopsy in unexplained sudden cardiac death. Curr Opin Cardiol 2006;21:166–72. 20. Tester DJ, Ackerman MJ. Postmortem long QT syndrome genetic testing for sudden unexplained death in the young. J Am Coll Cardiol 2007;49:240–6. 21. Bos JM, Ommen SR, Ackerman MJ. Genetics of hypertrophic cardiomyopathy: one, two, or more diseases? Curr Opin Cardiol 2007;22:193–9. 22. Wedekind H, Schulze-Bahr E, Debus V, Breithardt G, Brinkmann B, Bajanowski T. Cardiac arrhythmias and sudden death in infancy: implication for the medicolegal investigation. Int J Legal Med 2007;121:245–57. 23. Ackerman MJ. Cardiac channelopathies: it’s in the genes. Nat Med 2004;10:463–4. 24. Chugh SS, Kelly KL, Titus JL. Sudden cardiac death with apparently normal heart. Circulation 2000;102:649–54. 25. Wever EF, Robles de Medina EO. Sudden death in patients without structural heart disease. J Am Coll Cardiol 2004;43:1137–44. 26. Doolan A, Langlois N, Semsarian C. Causes of sudden cardiac death in young Australians. Med J Aust 2004;180:110–2. 27. Tomson T, Nashef L, Ryvlin P. Sudden unexpected death in epilepsy: current knowledge and future directions. Lancet Neurol 2008;7:1021–31. 28. Priori SG, Napolitano C, Schwartz PJ, et al. Association of long QT syndrome loci and cardiac events among patients treated with beta-blockers. JAMA 2004;292:1341–4. 29. McKenna WJ, Oakley CM, Krikler DM, Goodwin JF. Improved survival with amiodarone in patients with hypertrophic cardiomyopathy and ventricular tachycardia. Br Heart J 1985;53:412–6. 30. Al-Khatib SM, Sanders GD, Carlson M, et al. Preventing tomorrow’s sudden cardiac death today: dissemination of effective therapies for sudden cardiac death prevention. Am Heart J 2008;156:613–22. 31. Finsterer J, Stollberger C. Cardiopulmonary surveillance to prevent SUDEP. Lancet Neurol 2009;8:131–2 [author reply 132–3]. 32. Tomson T. Cardiopulmonary surveillance to prevent SUDEP—author’s reply. J Neurol 2009;8:125–216.
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Clinical paper
Out-of-hospital cardiac arrests in young adults in Melbourne, Australia—Adding coronial data to a cardiac arrest registry夽 C. Deasy a,b,c,∗,d , J.E. Bray a,d , K. Smith a,b,d , L.R. Harriss a,b,d , S.A. Bernard a,b,c,d , P. Cameron b,d a b c
Ambulance Victoria, Australia Monash University, Department of Epidemiology and Preventive Medicine, Australia Alfred Hospital, Australia
a r t i c l e
i n f o
Article history: Received 21 February 2011 Received in revised form 11 April 2011 Accepted 29 May 2011
Keywords: Cardiac arrest Coroner Autopsy Out-of-hospital Young adults CPR Cardiopulmonary resuscitation EMS
a b s t r a c t Aim: We aim to describe the coronial findings of young adults where the out-of-hospital cardiac arrest (OHCA) aetiology was ‘presumed cardiac’. Methods: Presumed cardiac aetiology OHCAs occurring in young adults aged 16–39 years were identified using the Victorian Ambulance Cardiac Arrest Registry (VACAR) and available coronial findings reviewed. Results: We identified 841 young adult OHCAs where the Utstein aetiology was ‘presumed cardiac’. Of these 740 died and 572 (77%) OHCAs were matched to coroner’s findings. On review of the coroner’s cause of death, 230 (40.2%) had a ‘confirmed cardiac’ aetiology, 221 (38.6%) were proven ‘non-cardiac’, 97 (17%) were inconclusive and 24 (4.2%) cases remained ‘open’. ‘Confirmed cardiac’ causes of OHCA were ischemic heart disease (n = 126, 55%), cardiomegaly (n = 26, 11.3%), cardiomyopathy (n = 25, 11%), congenital heart disease (n = 15, 6.5%), cardiac tamponade due to dissecting thoracic aorta aneurysm (n = 10, 4.3%), myocarditis (n = 8, 3.5%), arrhythmia (n = 7, 3%), others (n = 13, 5.7%). ‘Non-cardiac’ causes of OHCA were epilepsy/sudden unexplained death in epilepsy (SUDEP) (n = 56, 25%), pulmonary embolism (n = 29, 13%), subarachnoid haemorrhage (n = 17, 7.7%), other intracranial bleed (n = 7, 3.2%), pneumonia (n = 17, 7.7%), DKA (n = 16, 7.2%), other complications of diabetes mellitus (n = 8, 3.6%), complications of obesity (n = 9, 4%), haemorrhage (n = 12, 5.4%), sepsis (n = 8, 3.6%), peritonitis (n = 6, 2.7%), aspiration (n = 6, 2.7%), renal failure (n = 5, 2.3%), asthma (n = 5, 2.3%), complications of anorexia (n = 3) and alcohol abuse (n =2), thyrotoxicosis (n = 2), meningitis (n = 1) and others (n = 12). Compared with coroner’s diagnosed ‘non-cardiac’ OHCAs, ‘confirmed cardiac’ were more likely to be witnessed (41% vs 23%, p ≤ 0.01), receive bystander CPR (35% vs 20%, p ≤ 0.001), have a shockable rhythm (27% vs 6.3%, p < 0.001) and have EMS attempted resuscitation (62% vs 44%, p < 0.001). Discussion: Linking OHCA registries with coronial databases for aetiology of the arrest will improve the quality of the data and should be considered by all OHCA registries, particularly for young adult OHCA. © 2011 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Out-of-hospital cardiac arrest (OHCA) is presumed to be of cardiac aetiology unless, as best determined by the rescuers, it is known or likely to have been caused by trauma, submersion, drug overdose, asphyxia, exsanguination or other non cardiac cause.1 Young adults represent a minority of those who suffer an OHCA; the aetiology of cardiac arrest is likely to be different to that of older
夽 A Spanish translated version of the abstract of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2011.05.031. ∗ Corresponding author at: Monash University, Department of Epidemiology and Preventive Medicine, Alfred Hospital, Level 3 Burnet Building, 89 Commercial Road, Melbourne 3004, Australia. Tel.: +61 41 6486887. E-mail address: [email protected] (C. Deasy). d On behalf of the VACAR Steering Committee. 0300-9572/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2011.05.031
adults where ischemic heart disease is more common.2 Making an accurate clinical diagnosis in the field can be a great challenge in the young adult group of patients and the clinician’s perception of the cause of arrest can strongly influence management and the direction of treatment. Furthermore, heterogeneity in aetiology of the ‘presumed cardiac’ arrest may be responsible for the seemingly poorer results seen in this age group of patients when compared to older adults. Such heterogeneity may dilute the positive impact of initiatives designed to improve OHCA survival and outcomes as the denominator is increased by patients that were never going to survive. Determining aetiology based on clinical diagnosis has many limitations and autopsy remains the ‘gold standard’.3 However, there is little literature in the young adult age group that links cardiac arrest registry data with coronial registries that detail final diagnosis. Such information could potentially be useful for planning preventative strategies, improving emergency medical
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service (EMS) response, planning intervention strategies and guiding future research in young adult OHCA. This paper describes the characteristics of OHCA in young adults where the OHCA aetiology was ‘presumed cardiac’ and links them with the subsequent coronial findings.
2. Methods The study setting was Melbourne, Australia, which had a population at the time of the last census (2006) of 3.59 million, of whom 1,279,980 were aged between 16 and 39 years of age with an equal male/female distribution. The EMS comprises ambulance paramedics who have some advanced life support skills (laryngeal mask airway, intravenous epinephrine) and mobile intensive care ambulance (MICA) paramedics who are authorized to perform endotracheal intubation and administer a wider range of cardiac drugs. The Advanced Medical Priority Dispatch System© is operational in Melbourne. MICA paramedics are dispatched to patients with critical illness, including patients with cardiac arrest. In addition, fire-fighters are dispatched to patients with suspected cardiac arrest in the inner two thirds of Melbourne’s area.4 The pre-hospital cardiac arrest protocols follow the recommendations of the Australian Resuscitation Council.5,6 Since December 2007, all patients attended by paramedics have patient care data collected in an electronic patient record. Previous years involved a paper patient care record (PCR). Selected data from PCRs is collected from patients in cardiac arrest and stored on the Victoria Ambulance Cardiac Arrest Registry (VACAR). Where the paramedic has not indicated the aetiology of the OHCA clinical staff within the registry make a judgment based on the details provided. The VACAR also includes some data from the hospital record for those patients transferred to hospital, including number of days in hospital, discharge direction and whether the patient survived to leave hospital. Hospital investigation results were not recorded in VACAR for the time period involved in this study. EMS response time is the time from ‘000’ telephone call to EMS arrival at scene.
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Circumstances where Ambulance Victoria paramedics may cease resuscitation efforts are detailed in Table 1.5 Under Victorian law, patients who suffer sudden death are referred to the Coroner unless a medical practitioner is able to complete a death certificate with knowledge of the cause of death. Patients referred to the Coroner generally undergo an autopsy unless there is an objection by the next-of-kin. Deaths were matched with coroner’s office records and all autopsies and coroner’s investigation notes reviewed. Cases that could not be matched included cases with missing identity or registered with alternative names and cases not reported to the coroner. The Victoria Ambulance Cardiac Arrest Registry (VACAR) was searched for all OHCAs occurring in patients aged 16–39 years. Drug overdose associated OHCA as detected at autopsy was excluded. 2.1. Ethics approval VACAR has been classified as a quality assurance project by the ethics committee at the Department of Health. The collection of cardiac arrest outcome data by VACAR was approved by the ethics committees of Victorian hospitals receiving cardiac arrests by ambulance. This study was approved by the Research Committee of Ambulance Victoria and Monash University Human Research Ethics Committee. Table 1 Circumstances where paramedics in Victoria may withhold resuscitation efforts. Where rigor mortis, decomposition or post mortem lividity is already present. Where death has been declared by a Medical Officer who is or has been at the scene. Where a refusal of treatment certificate has been completed for a current condition which most likely caused the cardiac arrest. Where the presenting rhythm was monitored as asystole for >30 s, and there has been >10 min downtime, no evidence of hypothermia, drug overdose or family/bystander objections. If advanced life support has been performed for 30 min without return of spontaneous circulation (ROSC), the rhythm is not Ventricular Fibrillation or Ventricular tachycardia, there are no signs of life, no gasps or pupillary reactions and no evidence of hypothermia or drug overdose.
Table 2 Modified Utstein template describing characteristics of ‘presumed cardiac’ OHCA in young adults. Utstein element
‘Presumed cardiac’ OHCA Young adult n (%)
Coroner confirmed ‘Cardiac’ n (%)
Coroner diagnosed ‘Non cardiac’ n (%)
Coroner findings ‘Undetermined’ n (%)
Absence of signs of circulation and/or considered for resuscitation Age median (IQR) years Male sex (%) Resuscitation attempted, n (%) Any defibrillation, n (%) First monitored rhythm, n (%) Shockable Non shockable asystole PEA Location of arrest, n (%) Home Work Street Other Arrest witnessed by layperson, n (%) Arrest not witnessed CPR before EMS arrival, n (%)* EMS response time median (IQR) (min) Where resuscitation attempted, n (%) Outcome Any ROSC Survived event Discharged from hospital alive Missing hospital outcome data, n
841 33 (27–37) 69 485 (58) 262 (31)
230 34 (30–38) 78 143 (62) 96 (41)
221 32 (26–37)* 65* 97 (44)* 23 (10.4)*
97 31 (25–35)* 60 44 (45)* 26 (26.8)*
186 (22) 549 (65) 69 (8.2)
61 (27) 140 (61) 25 (11)
149 (6.3)* 187 (85)* 12 (5)*
17 (18) 75 (77.3)* 5 (5.1)
646 (77) 24 (3) 79 (9) 92 (11) 275 (33) 529 (63) 243 (29) 7.38 (6–10)
185 (80) 8 (3.4) 15 (7) 22 (9.6) 95 (41) 132 (57) 80 (35) 7.95 (6–9.7)
189 (86) 2 (0.9) 7 (3.2)* 23 (9.9) 44 (20)* 170 (77)* 44 (20)* 7.15 (5.9–10.7)
80 (82.5) 2 (2.1) 4 (4.1) 11 (11.3) 27 (28)* 69 (71)* 29 (30) 7 (6–10)
173 (21) 148 (18) 86 (10.4) 15
22 (9.6) 12 (5.2) NA NA
17 (7.7) 12 (5.4) NA NA
3 (3) 2 (2) NA NA
*
p < 0.05.
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Fig. 1. Corner confirmed cardiac OHCA.
2.2. Statistical analysis All data were entered into an Access software cardiac arrest registry database (version 2003, Microsoft, Redmond, WA, USA). Statistical calculations were performed on STATA software (version 10.0 Stata Corporation, College Station, TX, USA). Chi-square analyses were used for categorical variables. Continuous variables were compared using the t-test (normal distribution) or Mann–Whitney. 3. Results Between the years 2000 and 2009 there were 3912 OHCAs in young adults aged 16–39 years of age. We identified 841 (21.5%) young adult OHCAs where the Utstein aetiology was ‘presumed cardiac’. Other causes of young adult OHCA were trauma (18.8%), hanging (16.6%), overdose (33.5%) and others (9.6%). There were 86 survivors (10.2%) who were not subject to coronial investigation. We were unable to ascertain survival status for 15 patients. There were 740 patients who died and 572 (77%) OHCAs were matched to coroner’s autopsy. On review of coronial findings, 230 (40.2%) had a ‘confirmed cardiac’ aetiology, 221 (38.6%) were proven ‘noncardiac’, 97 (17%) had inconclusive coronial findings and 24 (4.2%) cases remained ‘open’. Characteristics of the young adults who sustained ‘presumed cardiac’ OHCA as assigned on clinical details are shown in Table 2. Coroner confirmed cardiac and non cardiac as well as OHCAs where the coroner was unable to ascertain cause of death are also shown. The characteristics of the patients and the OHCAs they sustained were different between those who had coroner confirmed cardiac arrest and those that had a non cardiac OHCA on subsequent autopsy; coroner confirmed cardiac OHCAs were older and greater
proportions were male, witnessed, had bystander CPR, were in shockable rhythm on arrival of EMS and had an attempted resuscitation (Fig. 1). The coroner was unable to identify cause of death in 97 cases (Table 1). These cases differed from the coroner confirmed cardiac OHCA cases in being younger, a lesser proportion had EMS attempted resuscitation, less had an attempted defibrillation and less were witnessed OHCAs (Table 2). Ischemic heart disease was the cause of death on autopsy in 126 cases (22% of clinically presumed cardiac young adult OHCAs) and found present in 195 cases (34%); the median (IQR) age was 36 (31–38) years and was older than non-IHD OHCAs where the median (IQR) age was 32 (26–36) years (p < 0.001). More patients were male (83.5% vs 16.5%, p < 0.001). Ventricular fibrillation/pulseless ventricular tachycardia (VF/VT) was present in 28%, asystole in 63% and PEA in 7%. Congenital heart disease was the cause of death in 15 autopsies (2.6% of clinically ‘presumed cardiac’ OHCA). Their median (IQR) age was 31 (24–33) years. VF/VT was present in six patients on arrival of the ambulance, four patients were in PEA, and the remainder were in asystole (n = 5). Cardiac tamponade was found on autopsy in 10 cases, in all cases in association with aortic dissection; their median age was 32.5 (23–35) years. Their presenting rhythms were PEA (n = 5) and asystole (n = 5). ‘Non-cardiac’ causes of OHCA are shown in Fig. 2. Sudden unexplained death in epilepsy (SUDEP) was the autopsy cause of death in 56 cases (9.8%) who had been ‘presumed cardiac’ clinically. Their median (IQR) age was 29 (24–35.5) years. Asystole was present in 93% on arrival of EMS. Resuscitation was attempted in 20 patients (36%). Pulmonary embolism was the autopsy cause of death in 29 (5%) patients whose OHCA had been ‘presumed cardiac’ clinically. Their median (IQR) age was 30 years (28–34) years, and 59% were female. Asystole was the presenting rhythm in 17 patients (59%), VF/VT and PEA were the presenting rhythms in 4 patients each. A subarachnoid or intracranial bleed was the cause of death in 24 cases that had been presumed cardiac clinically. Their median age was 33.5 (29–37) years. Asystole was present in 18 patients (75%), PEA and VF/VT in 3 (12.5%) patients each. There were 97 patients in whom the coroner was unable to confirm cause of death. Their median (IQR) age was 31 (24–35) years, 59% were male, 29% had a witnessed arrest, 30% had bystander CPR and 45% had an EMS attempted resuscitation with 3% achieving a ROSC but subsequently not surviving. VF/VT was the presenting rhythm in 17.5%, PEA in 5% and asystole in 77%. There were 86 ‘presumed cardiac’ patients who survived and so did not have a coronial investigation. Their median age (IQR)
Fig. 2. Non cardiac cause of OHCA on coroner’s finding.
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age was 31 (24–36) years and 73% were male. Of survivors 73% were witnessed OHCAs and 40% received bystander CPR. A greater proportion of survivors sustained their OHCA in the street (24.4% vs 7.3%, p < 0.001) and less occurred in the home (48% vs 81%, p < 0.002).
4. Discussion This study shows the limitations associated with ascribing cause of OHCA on the basis of clinical details. The results of this study show that only a minority of patients had a coronial study confirming cardiac aetiology of OHCA and that the confirmed cardiac group of patients differed both in terms of patient and OHCA characteristics to those found on coronial review to be non cardiac. Accurate data is important in this area as it informs treatment and preventive strategies. Furthermore, when trying to establish the impact of initiatives such as the 2005 CPR guidelines7,8 on survival in ‘presumed cardiac’ OHCA comparing homogenous data sets is important to avoid under representing their impact. Our finding that in ‘presumed cardiac’ OHCA in this age group non-cardiac causes are frequent suggests that early echocardiography should be undertaken in patients with sudden OHCA.9–11 There were 97 cases (17%) of young adult ‘presumed cardiac’ OHCAs where the autopsy was unable to ascertain cause of death. In addition, autopsy reported 7 cases of ‘arrhythmia’ as cause of death; of these one patient had prolonged QT on a previous ECG. Most were in asystole on arrival of EMS (n = 6) with one patient in a shockable rhythm. One of the most difficult tasks in forensic medicine is deciding the cause of death in an unclear or debatable case. In general, there are three major categories that lead to difficulties: (1) co-existence of a pre-existing condition and a fatal injury; (2) competing potential causes of death; (3) historical events that may be causally relevant to death by injury.12 A ‘negative’ post-mortem may yield a default diagnosis of sudden arrhythmic death syndrome (SADS) or sudden unexplained death (SUD) syndrome after the first year of life13–15 where there are no discernible abnormalities on histopathology and a negative toxicology screen.16,17 The inherited arrhythmia syndromes (long QT, short QT, and Brugada syndromes, and familial catecholaminergic polymorphic ventricular tachycardia) may be implicated in SADS, owing to their propensity for producing ventricular tachyarrhythmia in the structurally normal heart.18 In cases where a morphological explanation for cardiac arrest is lacking, a growing number of forensic experts now resort to post-mortem genetic testing, called ‘molecular autopsy’19–21 however, at present there is no internationally established best practice concerning post-mortem genetic testing in the clinical or forensic setting.22 In at least 10% and perhaps as many as 30% of sudden deaths involving previously healthy children, adolescents, and young adults, no abnormalities are evident at autopsy15 leaving coroners, medical examiners, and forensic pathologists only to suggest that a fatal arrhythmia might be responsible for the event.23–25 Doolan et al.26 reviewed all autopsies performed on those aged <35 years between 1994 and 2002 in Sydney, Australia; they were unable to identify a cause of arrest in 60 (9.9%) cases and suggest that these cases may represent a primary arrhythmia. The actual extent of inherited arrhythmia syndromes causing OHCA is therefore at best speculative. SUDEP was the autopsy cause of death in 10% of ‘presumed cardiac’ OHCAs that had an autopsy performed. SUDEP is defined as sudden, unexpected, witnessed or unwitnessed, nontraumatic and non-drowning death in patients with epilepsy, with or without evidence for a seizure and excluding documented status epilepticus, in which post mortem examination does not reveal a toxicologic or anatomic cause of death. The incidence of SUDEP varies from 1:1000 per year to as many as 1:200 per year in those with epilepsy,
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depending upon the community surveyed. The mechanism of death in SUDEP is not clearly established. Hypoventilation and/or cardiac changes occurring during or shortly after seizure may be such mechanisms, but at the present time the precise mechanism is not known.27 The best medical intervention for OHCA is prevention. The advent of effective therapies for some of these diseases such as implantable defibrillators, antiarrhythmic treatment for long QT syndrome type 128 and low dose amiodarone for hypertrophic cardiomyopathy29,30 has prompted calls for universal screening. However, the recommended preliminary workup to prevent SUD includes a 12-lead ECG, signal-averaged ECG, transthoracic echocardiogram, exercise test, ambulatory ECG monitoring, cardiovascular magnetic resonance imaging to diagnose arrhythmogenic right ventricular cardiomyopathy or anomalous coronary arteries, a provocative challenge with a sodium channel blocker to unmask the Brugada syndrome and genetic identification of disease-causing mutations.18 It is not feasible to screen the population with this battery of investigations given the small numbers of patients that might benefit as highlighted by this study. Similarly, the likelihood of preventing SUDEP could be increased with more appropriate antiepileptic drug treatment, more comprehensive investigations and better treatment for cardiac and pulmonary disease in patients with epilepsy,31 however the requirement for routine post-ictal echocardiography, polysomnography, autonomic function tests, and loop-recorder implants as suggested by Finsterer31 is controversial32 and requires validation in studies larger than those done so far.32 Population based cardiac arrest registries linked with coronial data are important in providing the evidence needed to justify expensive preventive strategies.
5. Limitations This study has a number of limitations due to its retrospective nature. We have limited this study to ‘presumed cardiac’ aetiology OHCA as judged clinically excluding coronial diagnosed drug overdoses retrospectively; this denominator must be considered when interpreting the study outcome to avoid the over emphasis on arrhythmia or SUDEP in causation of all OHCAs that occur in young adults. We were unable to match 168 OHCAs to coroner’s autopsies (23%). A proportion of these patients had achieved ROSC (n = 31) and were transported to hospital but subsequently died. It is possible that an autopsy was not performed in these cases as the cause of death was sufficiently evident from the hospital investigations for it to be recordable on the death certificate. Reporting the aetiology of OHCA where the patient survived to reach hospital and had diagnostic investigations was beyond the scope of this study. Decisions to perform or withhold a complete autopsy are not standardized between coroners; however, in the context of young adults the threshold to perform such an investigation is low.
6. Conclusions Linking OHCA registries with coronial databases for aetiology of the arrest will improve the quality of the data, and will provide data that justifies improved diagnostic and treatment algorithms. Such linkage is particularly important in the young adult age group where there is increased heterogeneity in the aetiology of the cardiac arrest.
Conflict of interest statement No conflicts of interest to declare.
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