Teaching Hands-Only CPR (HOCPR) skills to 8th-grade students in urban Bengaluru: Development of a comprehensive Hands-Only CPR programme for high school students.

Background and Aims: Out-of-hospital cardiac arrest is one of the leading causes of death in India. Only 1.3% of these arrests receive bystander cardiopulmonary resuscitation (CPR). Bystander CPR increases a victim's chances of survival; training school children in Hands-Only CPR (HOCPR) is a proven method of increasing bystander CPR rates. Heart Rescue India is an international project working to improve care for cardiovascular diseases, and as a part of it, a ten module Cardiovascular disease (CVD) educational programme, including HOCPR training, was conducted in ten schools in 2017-18. The objective of our study was to assess the effectiveness of HOCPR training for 8th-grade high school students. Methods: Four hundred fourteen of the 530 enroled students from ten schools of Bengaluru participated in the study. The participants attended a one-hour didactic session about the recognition of cardiac arrest and HOCPR in three simple steps. Subsequently, students received hands-on training for HOCPR. The sessions included pre- and post-assessment of knowledge and skills. The results were statistically analysed using paired t-test and the McNemar test. Results: The mean overall pre-assessment score for knowledge was 62.07 ± 28.38%, and the post-assessment score was 72.42 ± 26.58% (P < 0.001). In addition, there was a statistically significant improvement in the post-training scores for HOCPR in all three parameters, namely compressions per minute, depth and chest recoil. Conclusion: The study demonstrated a simple yet effective HOCPR programme for high school children.

Wearable sensor derived decompensation index for continuous remote monitoring of COVID-19 diagnosed patients.

The COVID-19 pandemic has accelerated the adoption of innovative healthcare methods, including remote patient monitoring. In the setting of limited healthcare resources, outpatient management of individuals newly diagnosed with COVID-19 was commonly implemented, some taking advantage of various personal health technologies, but only rarely using a multi-parameter chest-patch for continuous monitoring. Here we describe the development and validation of a COVID-19 decompensation index (CDI) model based on chest patch-derived continuous sensor data to predict COVID-19 hospitalizations in outpatient-managed COVID-19 positive individuals, achieving an overall AUC of the ROC Curve of 0.84 on 308 event negative participants, and 22 event positive participants, out of an overall study cohort of 400 participants. We retrospectively compare the performance of CDI to standard of care modalities, finding that the machine learning model outperforms the standard of care modalities in terms of both numbers of events identified and with a lower false alarm rate. While only a pilot phase study, the CDI represents a promising application of machine learning within a continuous remote patient monitoring system.

Baicalein Rescues Delayed Cooling via Preservation of Akt Activation and Akt-Mediated Phospholamban Phosphorylation.

Cooling reduces the ischemia/reperfusion (I/R) injury seen in sudden cardiac arrest (SCA) by decreasing the burst of reactive oxygen species (ROS). Its cardioprotection is diminished when delay in reaching the target temperature occurs. Baicalein, a flavonoid derived from the root of ScutellariabaicalensisGeorgi, possesses antioxidant properties. Therefore, we hypothesized that baicalein can rescue cooling cardioprotection when cooling is delayed. Two murine cardiomyocyte models, an I/R model (90 min ischemia/3 h reperfusion) and stunning model (30 min ischemia/90 min reperfusion), were used to assess cell survival and contractility, respectively. Cooling (32 °C) was initiated either during ischemia or during reperfusion. Cell viability and ROS generation were measured. Cell contractility was evaluated by real-time phase-contrast imaging. Our results showed that cooling reduced cell death and ROS generation, and this effect was diminished when cooling was delayed. Baicalein (25 µM), given either at the start of reperfusion or start of cooling, resulted in a comparable reduction of cell death and ROS production. Baicalein improved phospholamban phosphorylation, contractility recovery, and cell survival. These effects were Akt-dependent. In addition, no synergistic effect was observed with the combined treatments of cooling and baicalein. Our data suggest that baicalein may serve as a novel adjunct therapeutic strategy for SCA resuscitation.

Patient acuity rating: quantifying clinical judgment regarding inpatient stability.

BACKGROUND: New resident work-hour restrictions are expected to result in further increases in the number of handoffs between inpatient care providers, a known risk factor for poor outcomes. Strategies for improving the accuracy and efficiency of provider sign-outs are needed. OBJECTIVE: To develop and test a judgment-based scale for conveying the risk of clinical deterioration. DESIGN: Prospective observational study. SETTING: University teaching hospital. SUBJECTS: Internal medicine clinicians and patients. MEASUREMENTS: The Patient Acuity Rating (PAR), a 7-point Likert score representing the likelihood of a patient experiencing a cardiac arrest or intensive care unit (ICU) transfer within the next 24 hours, was obtained from physicians and midlevel practitioners at the time of sign-out. Cross-covering physicians were blinded to the results, which were subsequently correlated with outcomes. RESULTS: Forty eligible clinicians consented to participate, providing 6034 individual scores on 3419 patient-days. Seventy-four patient-days resulted in cardiac arrest or ICU transfer within 24 hours. The average PAR was 3 ± 1 and yielded an area under the receiver operator characteristics curve (AUROC) of 0.82. Provider-specific AUROC values ranged from 0.69 for residents to 0.85 for attendings (P = 0.01). Interns and midlevels did not differ significantly from the other groups. A PAR of 4 or higher corresponded to a sensitivity of 82% and a specificity of 68% for predicting cardiac arrest or ICU transfer in the next 24 hours. CONCLUSIONS: Clinical judgment regarding patient stability can be reliably quantified in a simple score with the potential for efficiently conveying complex assessments of at-risk patients during handoffs between healthcare members.

Baicalein protects against doxorubicin-induced cardiotoxicity by attenuation of mitochondrial oxidant injury and JNK activation.

The cardiotoxicity of doxorubicin limits its clinical use in the treatment of a variety of malignancies. Previous studies suggest that doxorubicin-associated cardiotoxicity is mediated by reactive oxygen species (ROS)-induced apoptosis. We therefore investigated if baicalein, a natural antioxidant component of Scutellaria baicalensis, could attenuate ROS generation and cell death induced by doxorubicin. Using an established chick cardiomyocyte model, doxorubicin (10 µM) increased cell death in a concentration- and time-dependent manner. ROS generation was increased in a dose-response fashion and associated with loss of mitochondrial membrane potential. Doxorubicin also augmented DNA fragmentation and increased the phosphorylation of ROS-sensitive pro-apoptotic kinase c-Jun N-terminal kinase (JNK). Adjunct treatment of baicalein (25 µM) and doxorubicin for 24 h significantly reduced both ROS generation (587 ± 89 a.u. vs. 932 a.u. ± 121 a.u., P < 0.01) and cell death (30.6 ± 5.1% vs. 46.8 ± 8.3%, P < 0.01). The dissipated mitochondrial potential and increased DNA fragmentation were also ameliorated. Along with the reduction of ROS and apoptosis, baicalein attenuated phosphorylation of JNK induced by doxorubicin (1.7 ± 0.3 vs. 3.0 ± 0.4-fold, P < 0.05). Co-treatment of cardiomyocytes with doxorubicin and JNK inhibitor SP600125 (10 µM; 24 h) reduced JNK phosphorylation and enhanced cell survival, suggesting that the baicalein protection against doxorubicin cardiotoxicity was mediated by JNK activation. Importantly, concurrent baicalein treatment did not interfere with the anti-proliferative effects of doxorubicin in human breast cancer MCF-7 cells. In conclusion, baicalein adjunct treatment confers anti-apoptotic protection against doxorubicin-induced cardiotoxicity without compromising its anti-cancer efficacy.

Capnography and chest-wall impedance algorithms for ventilation detection during cardiopulmonary resuscitation.

OBJECTIVE: Hyperventilation is both common and detrimental during cardiopulmonary resuscitation (CPR). Chest-wall impedance algorithms have been developed to detect ventilations during CPR. However, impedance signals are challenged by noise artifact from multiple sources, including chest compressions. Capnography has been proposed as an alternate method to measure ventilations. We sought to assess and compare the adequacy of these two approaches. METHODS: Continuous chest-wall impedance and capnography were recorded during consecutive in-hospital cardiac arrests. Algorithms utilizing each of these data sources were compared to a manually determined "gold standard" reference ventilation rate. In addition, a combination algorithm, which utilized the highest of the impedance or capnography values in any given minute, was similarly evaluated. RESULTS: Data were collected from 37 cardiac arrests, yielding 438min of data with continuous chest compressions and concurrent recording of impedance and capnography. The manually calculated mean ventilation rate was 13.3+/-4.3/min. In comparison, the defibrillator's impedance-based algorithm yielded an average rate of 11.3+/-4.4/min (p=0.0001) while the capnography rate was 11.7+/-3.7/min (p=0.0009). There was no significant difference in sensitivity and positive predictive value between the two methods. The combination algorithm rate was 12.4+/-3.5/min (p=0.02), which yielded the highest fraction of minutes with respiratory rates within 2/min of the reference. The impedance signal was uninterpretable 19.5% of the time, compared with 9.7% for capnography. However, the signals were only simultaneously non-interpretable 0.8% of the time. CONCLUSIONS: Both the impedance and capnography-based algorithms underestimated the ventilation rate. Reliable ventilation rate determination may require a novel combination of multiple algorithms during resuscitation.

Grape seed proanthocyanidins protect cardiomyocytes from ischemia and reperfusion injury via Akt-NOS signaling.

Ischemia/reperfusion (I/R) injury in cardiomyocytes is related to excess reactive oxygen species (ROS) generation and can be modulated by nitric oxide (NO). We have previously shown that grape seed proanthocyanidin extract (GSPE), a naturally occurring antioxidant, decreased ROS and may potentially stimulate NO production. In this study, we investigated whether GSPE administration at reperfusion was associated with cardioprotection and enhanced NO production in a cardiomyocyte I/R model. GSPE attenuated I/R-induced cell death [18.0 +/- 1.8% (GSPE, 50 microg/ml) vs. 42.3 +/- 3.0% (I/R control), P < 0.001], restored contractility (6/6 vs. 0/6, respectively), and increased NO release. The NO synthase (NOS) inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME, 200 microM) significantly reduced GSPE-induced NO release and its associated cardioprotection [32.7 +/- 2.7% (GSPE + L-NAME) vs. 18.0 +/- 1.8% (GSPE alone), P < 0.01]. To determine whether GSPE induced NO production was mediated by the Akt-eNOS pathway, we utilized the Akt inhibitor API-2. API-2 (10 microM) abrogated GSPE-induced protection [44.3% +/- 2.2% (GSPE + API-2) vs. 27.0% +/- 4.3% (GSPE alone), P < 0.01], attenuated the enhanced phosphorylation of Akt at Ser473 in GSPE-treated cells and attenuated GSPE-induced NO increases. Simultaneously blocking NOS activation (L-NAME) and Akt (API-2) resulted in decreased NO levels similar to using each inhibitor independently. These data suggest that in the context of GSPE stimulation, Akt may help activate eNOS, leading to protective levels of NO. GSPE offers an alternative approach to therapeutic cardioprotection against I/R injury and may offer unique opportunities to improve cardiovascular health by enhancing NO production and increasing Akt-eNOS signaling.

Derangements in blood glucose following initial resuscitation from in-hospital cardiac arrest: a report from the national registry of cardiopulmonary resuscitation.

STUDY AIMS: Hyperglycemia is associated with poor outcomes in critically ill patients. We examined blood glucose values following in-hospital cardiac arrest (IHCA) to (1) characterize post-arrest glucose ranges, (2) develop outcomes-based thresholds of hyperglycemia and hypoglycemia, and (3) identify risk factors associated with post-arrest glucose derangements. METHODS: We retrospectively studied 17,800 adult IHCA events reported to the National Registry of Cardiopulmonary Resuscitation (NRCPR) from January 1, 2005 through February 1, 2007. RESULTS: Data were available from 3218 index events. Maximum blood glucose values were elevated in diabetics (median 226 mg/dL [IQR, 165-307 mg/dL], 12.5 mmol/L [IQR 9.2-17.0 mmol/L]) and non-diabetics (median 176 mg/dL [IQR, 135-239 mg/dL], 9.78 mmol/L [IQR 7.5-13.3 mmol/L]). Unadjusted survival to hospital discharge was higher in non-diabetics than diabetics (45.5% [95% CI, 43.3-47.6%] vs. 41.7% [95% CI, 38.9-44.5%], p=0.037). Non-diabetics displayed decreased adjusted survival odds for minimum glucose values outside the range of 71-170 mg/dL (3.9-9.4 mmol/L) and maximum values outside the range of 111-240 mg/dL (6.2-13.3 mmol/L). Diabetic survival odds decreased for minimum glucose greater than 240 mg/dL (13.3 mmol/L). In non-diabetics, arrest duration was identified as a significant factor associated with the development of hypo- and hyperglycemia. CONCLUSIONS: Hyperglycemia is common in diabetics and non-diabetics following IHCA. Survival odds in diabetics are relatively insensitive to blood glucose with decreased survival only associated with severe (>240 mg/dL, >13.3 mmol/dL) hyperglycemia. In non-diabetics, survival odds were sensitive to hypoglycemia (<70 mg/dL, <3.9 mmol/L).

Intra-arrest cooling with delayed reperfusion yields higher survival than earlier normothermic resuscitation in a mouse model of cardiac arrest.

BACKGROUND: Therapeutic hypothermia (TH) represents an important method to attenuate post-resuscitation injury after cardiac arrest. Laboratory investigations have suggested that induction of hypothermia before return of spontaneous circulation (ROSC) may confer the greatest benefit. We hypothesized that a short delay in resuscitation to induce hypothermia before ROSC, even at the expense of more prolonged ischemia, may yield both physiological and survival advantages. METHODS: Cardiac arrest was induced in C57BL/6 mice using intravenous potassium chloride; resuscitation was attempted with CPR and fluid administration. Animals were randomized into three groups (n=15 each): a normothermic control group, in which 8 min of arrest at 37 degrees C was followed by resuscitation; an early intra-arrest hypothermia group, in which 6.5 min of 37 degrees C arrest were followed by 90s of cooling, with resuscitation attempted at 30 degrees C (8 min total ischemia); and a delayed intra-arrest hypothermia group, with 90s cooling begun after 8 min of 37 degrees C ischemia, so that animals underwent resuscitation at 9.5 min. RESULTS: Animals treated with TH demonstrated improved hemodynamic variables and survival compared to normothermic controls. This was the case even when comparing the delayed intra-arrest hypothermia group with prolonged ischemia time against normothermic controls with shorter ischemia time (7-day survival, 4/15 vs. 0/15, p<0.001). CONCLUSIONS: Short resuscitation delays to allow establishment of hypothermia before ROSC appear beneficial to both cardiac function and survival. This finding supports the concept that post-resuscitation injury processes begin immediately after ROSC, and that intra-arrest cooling may serve as a useful therapeutic approach to improve survival.

Oxidant stress during simulated ischemia primes cardiomyocytes for cell death during reperfusion.

Ischemia-reperfusion injury induces oxidant stress, and the burst of reactive oxygen species (ROS) production after reperfusion of ischemic myocardium is sufficient to induce cell death. Mitochondrial oxidant production may begin during ischemia prior to reperfusion because reducing equivalents accumulate and promote superoxide production. We utilized a ratiometric redox-sensitive protein sensor (heat shock protein 33 fluorescence resonance energy transfer (HSP-FRET)) to assess oxidant stress in cardiomyocytes during simulated ischemia. HSP-FRET consists of the cyan and yellow fluorescent protein fluorophores linked by the cysteine-containing regulatory domain from bacterial HSP-33. During ischemia, ROS-mediated oxidation of HSP-FRET was observed, along with a decrease in cellular reduced glutathione levels. These findings were corroborated by measurements using redox-sensitive green fluorescent protein, another protein thiol ratiometric sensor, which became 93% oxidized by the end of simulated ischemia. However, cell death did not occur during ischemia, indicating that this oxidant stress is not sufficient to induce death before reperfusion. However, interventions that attenuate ischemic oxidant stress, including antioxidants or scavengers of residual O(2) that attenuate/prevent ROS generation during ischemia, abrogated cell death during simulated reperfusion. These findings reveal that, in isolated cardiomyocytes, sublethal H(2)O(2) generation during simulated ischemia regulates cell death during simulated reperfusion, which is mediated by the reperfusion oxidant burst.

CPR quality improvement during in-hospital cardiac arrest using a real-time audiovisual feedback system.

BACKGROUND: Cardiopulmonary resuscitation (CPR) quality during actual cardiac arrest has been found to be deficient in several recent investigations. We hypothesized that real-time feedback during CPR would improve the performance of chest compressions and ventilations during in-hospital cardiac arrest. METHODS: An investigational monitor/defibrillator with CPR-sensing and feedback capabilities was used during in-hospital cardiac arrests from December 2004 to December 2005. Chest compression and ventilation characteristics were recorded and quantified for the first 5 min of resuscitation and compared to a baseline cohort of arrest episodes without feedback, from December 2002 to April 2004. RESULTS: Data from 55 resuscitation episodes in the baseline pre-intervention group were compared to 101 resuscitations in the feedback intervention group. There was a trend toward improvement in the mean values of CPR variables in the feedback group with a statistically significant narrowing of CPR variable distributions including chest compression rate (104+/-18 to 100+/-13 min(-1); test of means, p=0.16; test of variance, p=0.003) and ventilation rate (20+/-10 to 18+/-8 min(-1); test of means, p=0.12; test of variance, p=0.04). There were no statistically significant differences between the groups in either return of spontaneous circulation or survival to hospital discharge. CONCLUSIONS: Real-time CPR-sensing and feedback technology modestly improved the quality of CPR during in-hospital cardiac arrest, and may serve as a useful adjunct for rescuers during resuscitation efforts. However, feedback specifics should be optimized for maximal benefit and additional studies will be required to assess whether gains in CPR quality translate to improvements in survival.

Effects of compression depth and pre-shock pauses predict defibrillation failure during cardiac arrest.

BACKGROUND: Cardiopulmonary resuscitation (CPR) and electrical defibrillation are the primary treatment options for ventricular fibrillation (VF). While recent studies have shown that providing CPR prior to defibrillation may improve outcomes, the effects of CPR quality remain unclear. Specifically, the clinical effects of compression depth and pauses in chest compression prior to defibrillation (pre-shock pauses) are unknown. METHODS: A prospective, multi-center, observational study of adult in-hospital and out-of-hospital cardiac resuscitations was conducted between March 2002 and December 2005. An investigational monitor/defibrillator equipped to measure compression characteristics during CPR was used. RESULTS: Data were analyzed from 60 consecutive resuscitations in which a first shock was administered for VF. The primary outcome was first shock success defined as removal of VF for at least 5s following defibrillation. A logistic regression analysis demonstrated that successful defibrillation was associated with shorter pre-shock pauses (adjusted odds ratio 1.86 for every 5s decrease; 95% confidence interval 1.10-3.15) and higher mean compression depth during the 30s of CPR preceding the pre-shock pause (adjusted odds ratio 1.99 for every 5mm increase; 95% confidence interval 1.08-3.66). CONCLUSIONS: The quality of CPR prior to defibrillation directly affects clinical outcomes. Specifically, longer pre-shock pauses and shallow chest compressions are associated with defibrillation failure. Strategies to correct these deficiencies should be developed and consideration should be made to replacing current-generation automated external defibrillators that require long pre-shock pauses for rhythm analysis.