A case of extreme carboxyhaemoglominemia due to vaping.

Acute carbon monoxide (CO) poisoning is known to cause neurological, metabolic and cardiorespiratory sequalae. However, data on chronic CO exposure are scant, particularly in the context of vaping, which recent literature suggests may be a greater source of CO than tobacco cigarette smoking. During a series of admissions at the time of vaping, our patient repeatedly presented with significant CO poisoning and developed pulmonary arterial hypertension with resultant high-output right heart failure. On each occasion, our patient's levels of carboxyhaemoglobin were both higher and took longer to resolve than 12 smokers who underwent arterial blood gas testing at two time points. Our observation may reveal an association between vaping, chronic carboxyhaemoglobinemia and the development of cardiorespiratory disease. Thus, further studies into the safety of vaping and chronic CO exposure are urged.

Use of CIED Generated Heart Failure Risk Score (HFRS) Alerts in an Integrated, Multi-Disciplinary Approach to HF Management-A Prospective Cohort Study.

Aim: To evaluate use of CIED-generated Heart Failure Risk Score (HFRS) alerts in an integrated, multi-disciplinary approach to HF management. Methods: We undertook a prospective, single centre outcome study of patients implanted with an HFRS-enabled Medtronic CIED, generating a "high risk" alert between November 2018 and November 2020. All patients generating a "high risk" HFRS alert were managed within an integrated HF pathway. Alerts were shared with local HF teams, prompting patient contact and appropriate intervention. Outcome data on health care utilisation (HCU) and mortality were collected. A validated questionnaire was completed by the HF teams to obtain feedback. Results: 367 "High risk" alerts were noted in 188 patients. The mean patient age was 70 and 49% had a Charlson Comorbidity Score of >6. Mean number of alerts per patients was 1.95 and 44 (23%) of patients had >3 "high risk" alerts in the follow up period. Overall, 75 (39%) patients were hospitalised in the 4−6-week period of the alert; 53 (28%) were unplanned of which 24 (13%) were for decompensated HF. A total of 33 (18%) patients died in the study period. Having three or more alerts significantly increased the risk of hospitalisation for heart failure (HR 2.5, CI 1.1−5.6 p = 0.03). The feedback on the pathway was positive. Conclusions: Patients with "high risk" alerts are co-morbid and have significant HCU. An integrated approach can facilitate timely risk stratification and intervention. Intervention in these patients is not limited to HF alone and provides the opportunity for holistic management of this complex cohort.

Knowledge gaps, lack of confidence, and system barriers to guideline implementation among European physicians managing patients with CIED lead or infection complications: a European Heart Rhythm Association/European Society of Cardiology educational needs assessment survey.

As the number of patients with cardiac implantable electronic devices (CIEDs) grows, they are likely to present with issues to diverse groups of physicians. Guideline-adherent management is associated with improved prognosis in patients with CIED infection or lead problems but is insufficiently implemented in practice. The European Heart Rhythm Association (EHRA) with the support of the European Society of Cardiology (ESC) Working Group on Cardiovascular Surgery, performed a multinational educational needs assessment study in ESC member countries, directed at physicians who might be confronted with CIED patients with complications. A total of 336 physicians from 43 countries, reached through the ESC mailing list, participated. They included a mix of electrophysiologists, cardiologists general physicians and cardiac surgeons .One hundred and twenty-nine (38%) of the respondents performed lead extraction. The survey included eight clinical cases and a self-evaluation question of knowledge and skills to apply that knowledge. The survey looked at 14 areas of care across five stages of the patient journey. Of the non-extracting physicians over 50% felt they lacked the knowledge and skills to make the diagnosis and refer for lead extraction and over 75% felt they lacked knowledge and skills to manage aspects of extraction and post-extraction care. Barriers to correct referral were logistic and attitudinal. Extracting physicians reported significantly higher rates of adequate skills and knowledge across all five stages of the patient journey (P < 0.05). We identified major gaps in physicians' knowledge and skills across all stages of CIED care. These gaps should be addressed by targeted educational activities and streamlining referral pathways.

Improving guideline-mandated care of patients with implantable cardiac defibrillators.

BACKGROUND/AIMS: Implantable cardiac defibrillators reduce the risk of sudden cardiac death in selected patients. The value of an implantable cardiac defibrillator declines as the patient's disease progresses. Guidelines suggest that the appropriateness of maintaining implantable cardiac defibrillator therapy be regularly reviewed as part of monitoring of the patient's disease trajectory. It is recommended that implantable cardiac defibrillators are deactivated as patients approach the end of life. Patients with a better understanding of their current state of health and the role that the implantable cardiac defibrillator plays within it are more likely to make informed decisions about the timing of deactivation. METHODS: A quality improvement project was undertaken on appropriate deactivation of implantable cardiac defibrillators within a large tertiary cardiac centre. This was driven by audit data showing inadequate patient communication and documentation around deactivation. Drivers for change included the introduction of electronic data records, clinical review of comorbid patients approaching elective battery change and an ongoing forum for patient and carer education. Measured outcomes included the number of deactivations performed, evidence of patient discussion and consent, and timing of deactivation of the implantable cardiac defibrillator. RESULTS: There were increased numbers of timely device deactivations undertaken following the interventions with improved documented evidence of patient discussion and consent. The educational forum was received favourably. CONCLUSIONS: Focused multidisciplinary interventions can impact favourably on appropriate implantable cardiac defibrillator deactivation and improve patient engagement.

Arterio-VENouS Intra Subject agreement for blood gases within intensive care: The AVENSIS study.

BACKGROUND: In critically ill patients, who require multiple blood gas assessments, agreement between arterial and venous blood gas values for pH and partial pressure of carbon dioxide, is not clear. Good agreement would mean that venous values could be used to assess ventilation and metabolic status of patients in intensive care unit. METHODS: All adult patients admitted to Alfred intensive care unit, Melbourne, from February 2013 to January 2014, who were likely to have arterial and central venous lines for three days, were enrolled. Patients on extra-corporeal life support and pregnant women were excluded. After enrolment, near simultaneous arterial and central venous sampling and analysis were performed at least once per nursing shift till the lines were removed or the patient died. Bland-Altman analysis for repeated measures was performed to assess the agreement between arterio-venous pH and partial pressure of carbon dioxide. RESULTS: A total of 394 paired blood gas analyses were performed from 59 participants. The median (IQR) number of samples per patient was 6 (5-9) with the median (IQR) sampling interval 9.4 (5.2-18.5) h. The mean bias for pH was + 0.036 with 95% limits of agreement ranging from - 0.005 to + 0.078. For partial pressure of carbon dioxide, the values were -2.58 and -10.43 to + 5.27 mmHg, respectively. CONCLUSIONS: The arterio-venous agreement for pH in intensive care unit patients appears to be acceptable. However, the agreement for partial pressure of carbon dioxide was poor.

Obstructive sleep apnoea predicted by the STOP-BANG questionnaire is not associated with higher rates of post-operative complications among a high-risk surgical cohort.

PURPOSE: The purpose of this study is to establish if obstructive sleep apnoea (OSA) predicted by the STOP-BANG questionnaire would be associated with higher rates of post-operative cardiac, respiratory or neurological complications among a selected high-risk population with established major comorbidities undergoing major surgery. We hypothesise that a cohort selected for major comorbidities will show a higher post-operative complication rate that may power any potential association with co-existent OSA and identify an important target group for OSA screening and treatment pathways in preparation for major surgery. METHODS: Patients attending a high-risk preadmission clinic prior to major surgery from May 2015 to November 2015 were prospectively screened for OSA using the STOP-BANG questionnaire. Patients with treated OSA were excluded. Patient data and complications were attained from the pre-admission clinic and subsequent inpatient medical record at discharge. RESULTS: Three-hundred-and-ten patients were included in the study (age 68.6 ± 13.1 years, body mass index [BMI] 30.6 ± 7.4 kg/m2; 52.9% female). Sixty-four patients (20.6%) experienced 82 post-operative complications. Seventy-five percent of the cohort had a STOP-BANG ≥ 3. There was no association between the STOP-BANG score (unadjusted and adjusted for comorbidity) with the development of post-operative complications. CONCLUSIONS: OSA predicted by the STOP-BANG score was not associated with higher rates of post-operative complications in patients with major comorbidities undergoing high-risk surgery. As the findings from this cohort contrast with other observational studies, more definitive studies are required to establish a causative link between OSA and post-operative complications and determine whether treating OSA reduces this complication rate.

Home mechanical ventilation in Australia and New Zealand.

This study aims to describe the pattern of home mechanical ventilation (HMV) usage in Australia and New Zealand. 34 centres providing HMV in the region were identified and asked to complete a questionnaire regarding centre demographics, patient diagnoses, HMV equipment and settings, staffing levels and methods employed to implement and follow-up therapy. 28 (82%) centres responded, providing data on 2,725 patients. The minimum prevalence of HMV usage was 9.9 patients per 100,000 population in Australia and 12.0 patients per 100,000 population in New Zealand. Variation existed across Australian states (range 4-13 patients per 100,000 population) correlating with population density (r=0.82; p<0.05). The commonest indications for treatment were obesity hypoventilation syndrome (OHS) (31%) and neuromuscular disease (NMD) (30%). OHS was more likely to be treated in New Zealand, in smaller, newer centres, whilst NMD was more likely to be treated in Australia, in larger, older centres. Chronic obstructive pulmonary disease was an uncommon indication (8.0%). No consensus on indications for commencing treatment was found. In conclusion, the prevalence of HMV usage varies across Australia and New Zealand according to centre location, size and experience. These findings can assist HMV service planning locally and highlight trends in usage that may be relevant in other countries.

Post-resuscitation plasma catecholamines after prolonged arrest in a swine model.

OBJECTIVE: A dramatic increase in plasma catecholamines has been demonstrated consistently following cardiac arrest and during CPR. The time course of this initial catecholamine surge after successful resuscitation has not been well studied. The purpose of this study was to measure plasma catecholamines after successful resuscitation and to determine their relationship to post-resuscitation hemodynamics. METHODS: VF cardiac arrest was induced in eight anesthetized and instrumented swine. After 5 min of VF, conventional CPR was initiated followed 2 min later by transthoracic defibrillation. Restoration of spontaneous circulation (ROSC) was achieved in six animals. Following resuscitation, hemodynamic variables and plasma catecholamines were measured at intervals. RESULTS: Myocardial contractility (peak systolic dP/dt), stoke volume, left ventricular stroke work (LVSW), and mean arterial pressure (MAP) were significantly decreased from pre-arrest values within 15 min of ROSC and remained depressed during 60 min of observation. Systemic vascular resistance (SVR) was significantly increased within 15 min and remained elevated. Significant negative correlations were observed between SVR and plasma epinephrine (adrenaline) (r=-0.72, p<0.001) and norepinephrine (noradrenaline) (r=-0.76, p<0.001). Significant negative correlations were also observed between MAP and these catecholamines. A negative correlation was also observed between norepinephrine and LVSW (r=-0.50, p=0.039). Catecholamine levels were not related to other indices of cardiac function. CONCLUSIONS: A post-resuscitation adrenergic state is driven by a decline in MAP and PVR. Although seemingly compensatory, it may also contribute to the observed decline in cardiac function.

Tumor necrosis factor-alpha is associated with early postresuscitation myocardial dysfunction.

OBJECTIVE: Left ventricular dysfunction after successful cardiopulmonary resuscitation contributes to early death following resuscitation. The stress-induced proinflammatory cytokines, particularly tumor necrosis factor-alpha and interleukin-1beta, are known to depress myocardial function. We hypothesized that tumor necrosis factor-alpha and interleukin-1beta, synthesized and released in response to the stress of global ischemia accompanying cardiac arrest, play a role in development of postresuscitation left ventricular dysfunction. METHODS: Hemodynamic variables, tumor necrosis factor-alpha , interleukin-1beta, interleukin-6 (enzyme-linked immunosorbent assay method), and ionized calcium were measured in ten anesthetized swine before and after 7 mins of cardiac arrest and during the early postresuscitation period (60-90 mins). RESULTS: Tumor necrosis factor-alpha increased three-fold within 15 mins of restoration of circulation and remained elevated throughout the observation period. A significant negative correlation was observed between tumor necrosis factor-alpha and left ventricular systolic change in pressure over time (r = -.54, p <.001). Interleukin-1beta was undetectable before and after resuscitation, and interleukin-6 was detectable in only two animals after resuscitation. Although a significant decline in ionized calcium was observed and correlated with left ventricular systolic change in pressure over time, an independent role for ionized calcium in postresuscitation left ventricular dysfunction was not demonstrated. CONCLUSION: Tumor necrosis factor-alpha increases during the early postresuscitation period and may play a role in postresuscitation myocardial dysfunction.

Milrinone facilitates resuscitation from cardiac arrest and attenuates postresuscitation myocardial dysfunction.

BACKGROUND: Left ventricular (LV) dysfunction with a low cardiac index after successful CPR contributes to early death attributable to multiorgan failure, and an effective treatment has not been identified. The purpose of this study was to investigate the use of milrinone, a selective phosphodiesterase III inhibitor, as treatment for LV dysfunction after resuscitation. METHODS AND RESULTS: Ventricular fibrillation (VF) was induced electrically in 32 swine. After 5 minutes of VF, CPR was initiated and animals were randomized to receive either saline (control group, n=16) as a bolus and infusion or milrinone 50 microg/kg as a bolus and then 0.5 microg/kg per min for 60 minutes (treatment group, n=16). After 2 minutes of CPR (total VF time, 7 minutes), countershocks were given. Coronary perfusion pressures during CPR were similar for the groups (24+/-2 versus 21+/-4 mm Hg). All animals were defibrillated; 6 of 16 control animals developed refractory postcountershock pulseless electrical activity compared with 0 of 16 treated animals (P=0.018). At 30 minutes after restoration of spontaneous circulation, stroke volume (16+/-3 versus 26+/-7 mL, P<0.01) and LV dp/dt (793+/-197 versus 1108+/-316 mm Hg/s, P<0.02) were higher in the treatment group. Similar differences were observed 60 minutes after restoration of spontaneous circulation. Significant differences in heart rates between groups were not observed, and peripheral vascular resistance was significantly greater in the control group 30 and 60 minutes after resuscitation. CONCLUSIONS: Milrinone facilitates resuscitation from prolonged VF and attenuates LV dysfunction after resuscitation without worsening major determinants of myocardial oxygen demand.

Left ventricular function after monophasic and biphasic waveform defibrillation: the impact of cardiopulmonary resuscitation time on contractile indices.

UNLABELLED: Previous work has suggested that low-energy biphasic waveform defibrillation (BWD) is followed by less post-resuscitation left ventricular (LV) dysfunction when compared with higher-energy monophasic waveform defibrillation (MWD). To the best of the authors' knowledge, the effect of cardiopulmonary resuscitation (CPR) duration and total ischemia time on LV function after countershock, controlling for waveform type, has not been evaluated. OBJECTIVE: To determine the effect of CPR duration on LV function after MWD and BWD. METHODS: VF was electrically induced in anesthetized and instrumented swine. After 5 minutes of VF, the animals were randomized to MWD (n = 22) or one of two BWDs (n = 46). If countershock terminated VF but was followed by a nonperfusing rhythm, conventional manual CPR without drug therapy was performed until restoration of spontaneous circulation (ROSC), defined as a systolic arterial pressure >60 mm Hg for 10 minutes without vasopressor support. Systolic LV pressure (LVP), LV dP/dt (first derivative of pressure measured over time), and cardiac output (CO) were measured at intervals for 60 minutes postresuscitation. CPR times (times to ROSC) and hemodynamic variables for the three groups were compared. Multivariable linear regression was performed to assess the contribution of defibrillation waveform, total joules, and CPR time on LVP, LV dP/dt, and CO at 15, 30, and 60 minutes postresuscitation. RESULTS: When analyzed as groups, significant differences in median number of shocks to terminate VF, total joules, or CPR time were not observed between waveform groups. Regression analysis demonstrated that increasing CPR time was associated with a significant effect on indices of LV function at 15 and 30 minutes postresuscitation. Global LV function was not influenced by waveform type or total joules. CONCLUSIONS: Adjustment for CPR time, a determinant of total myocardial ischemia time, is necessary when defibrillation waveforms are compared for their effect on postresuscitation cardiac function and short-term outcome.

Transthoracic impedance does not decrease with rapidly repeated countershocks in a swine cardiac arrest model.

STUDY PURPOSE: Successful defibrillation is dependent upon the delivery of adequate electrical current to the myocardium. One of the major determinant of current flow is transthoracic impedance. Prior work has suggested that impedance falls with repeated shocks during sinus rhythm. The purpose of this study was to evaluate changes in transthoracic impedance with repeated defibrillation shocks in an animal model of cardiac arrest due to ventricular fibrillation (VF). METHODS: VF was electrically induced in anesthetized swine. After 5 min of untreated VF, monophasic or biphasic waveform defibrillation was attempted using a standard sequence of 'stacked shocks' (200, 300, then 360 J, if necessary) administered via adhesive electrodes. If one of the first three shocks failed to convert VF, conventional CPR was initiated and defibrillation (360 J) attempted 1 min later. Strength-duration curves for delivered voltage and current were measured during each shock and transthoracic impedance calculated. Animals requiring a minimum of four shocks were selected for study inclusion. Impedance data from sequential shocks were analyzed using mixed linear models to account for the repeated-measures design and the variability of the initial impedance of individual animals. RESULTS: Thirteen animals (monophasic waveform, n=7, biphasic waveform, n=6) required at least four shocks to terminate VF (range 4-6). Transthoracic impedance did not change from the first shock in the 13 animals (46+/-8 Omega) to the fourth shock (46+/-9 Omega). In animals receiving more than four shocks, transthoracic impedance likewise did not change significantly from the first to the last shock, which terminated VF. The lack of a significant change in impedance was also observed when animals were analyzed according to defibrillation waveform. CONCLUSION: Transthoracic impedance does not change significantly with repeated shocks in a VF cardiac arrest model. This is likely due to the lack of reactive skin and soft tissue hyperemia and edema observed in non-arrest models.