In-hospital cardiac arrest and basic life support

To improve understanding of afferent limb behaviour in acute hospital ward settings, to define and specify who needs to do what differently and to report what afferent limb behaviours should be targeted in a subsequent multi-phase, theory-based, intervention development process. Focused ethnography was used including direct observation of nursing staff enacting afferent limb behaviours and review of vital signs charts. An observation guide focused observation on "key moments" of the afferent limb. Descriptions of observations from between 7 January 2019-18 December 2019 were recorded in a field journal alongside reflexive notes. Vital signs and early warning scores from charts were reviewed and recorded. Field notes were analysed using structured content analysis. Observed behaviour was compared with expected (policy-specified) behaviour. Observation was conducted for 300hr. Four hundred and ninety-nine items of data (e.g., an episode of observation or a set of vital signs) were collected. Two hundred and eighty-nine (58%) items of data were associated with expected (i.e. policy-specified) afferent limb behaviour; 210 (42%) items of data were associated with unexpected afferent limb behaviour (i.e. alternative behaviour or no behaviour). Ten specific behaviours were identified where the behaviour observed deviated (negatively) from policy or where no action was taken when it should have been. One further behaviour was seen to expedite the assessment of a deteriorating patient by an appropriate responder and was therefore considered a positive deviance. Afferent limb failure has been described as a problem of inconsistent staff behaviour. Eleven potential target behaviours for change are reported and specified using a published framework. Clear specification of target behaviour will allow further enquiry into the determinants of these behaviours and the development of a theory-based intervention that is more likely to result in behaviour change and can be tested empirically in future research.

Part 12.1: Cardiac Arrest Associated With AsthmaAsthma is responsible for more than 2 million visits to the emergency department (ED) in the United States each year, with 1 in 4 patients requiring admission to a hospital. 1Annually there are 5,000 to 6,000 asthma-related deaths in the United States, many occurring in the prehospital setting. 2 Severe asthma accounts for approximately 2% to 20% of admissions to intensive care units, with up to one third of these patients requiring intubation and mechanical ventilation. 3This section focuses on the evaluation and treatment of patients with near-fatal asthma.Several consensus groups have developed excellent guidelines for the management of asthma that are available on the World Wide Web

To determine temporal patterns of vital sign and Cardiac Arrest Risk Triage score changes over the 48-hour period preceding cardiac arrest in an ICU setting. Vital sign instability usually occurs prior to cardiac arrest. However, few studies have been conducted on the temporal patterns of individual vital signs preceding cardiac arrest. A retrospective case-control study. The study subjects were 140 ICU patients (1 June 2011-31 December 2012): 46 died of cardiac arrest (case group), 45 died of other illnesses (control I group) and 49 were discharged after recovering (control II group). Initial detectable changes in blood pressure appeared 18-20 hours and became dramatic at 5-10 hours before cardiac arrest. Noticeable changes in heart rates began at 4 hours and became more prominent at 2 hours pre-arrest. No apparent patterns in respiratory rate changes were observed. Body temperatures usually indicated a hypothermic state pre-arrest. Cardiac Arrest Risk Triage scores were 16-18 at 48 hours pre-arrest and then continuously increased to 20. Only mean values of systolic blood pressures were significantly different between the three study groups. Mean diastolic blood pressures, heart rates, respiratory rates and Cardiac Arrest Risk Triage scores differed between the case and control II groups and between the control I and II groups. The study demonstrates vital sign instability preceded cardiac arrest and that the temporal patterns of changes in individual vital signs and Cardiac Arrest Risk Triage scores differed between groups. The findings of this study may aid the development of management strategies for cardiac arrest.

BACKGROUND: Vital signs and composite risk scores, such as the Modified Early Warning Score (MEWS), are used to identify high-risk patients, trigger rapid response teams, and assist with triage decisions. Although age-related vital sign changes are known to occur, little is known about the differences in vital signs between elderly and non-elderly patients prior to ward cardiac arrest (CA). We compared the accuracy of vital signs and the MEWS for detecting CA between elderly and non-elderly patients. METHODS: All patients hospitalized on the wards from five hospitals were included in the study. Patient characteristics and vital signs prior to CA were compared between elderly (age ≥65 years) and non-elderly (age <65 years) patients. The area under the receiver operating characteristic curve (AUC) was also calculated for vital signs and the MEWS for elderly and non-elderly ward patients for CA. RESULTS: A total of 269,956 admissions with documented age occurred during the study period, which included 422 index ward CAs. Within four hours of CA, elderly patients had significantly lower mean heart rate (88 vs. 99 beats per minute; P<0.001), diastolic blood pressure (60 vs. 66 mm Hg; P=0.007), and shock index (0.82 vs. 0.93; P<0.001), and higher pulse pressure index (0.45 vs. 0.41; P<0.001) and temperature (97.6 vs. 97.3 °F; P=0.047). The AUCs for all vital signs and the MEWS were higher for non-elderly patients than elderly patients (MEWS AUC 0.85 (95% CI 0.82-0.88) vs. 0.71 (95% CI 0.68-0.75); P<0.001). While the incidence of CA increased with age, accuracy of the MEWS decreased (Figure). CONCLUSIONS: Vital signs are much more accurate for detecting CA on the wards in non-elderly patients compared to elderly patients, which has important implications for how they are used for identifying critically ill patients. Further investigation into improving the accuracy of risk stratification for elderly patients is necessary in order to decrease their risk for this devastating event.

Classic Coronary Artery Disease in an Unlikely Patient

The recommendations for electrical therapies described in this section are designed to improve survival from SCA and life-threatening arrhythmias. Whenever defibrillation is attempted, rescuers must coordinate high-quality CPR with defibrillation to minimize interruptions in chest compressions and to ensure immediate resumption of chest compressions after shock delivery. The high first-shock efficacy of newer biphasic defibrillators led to the recommendation of single shocks plus immediate CPR instead of 3-shock sequences that were recommended prior to 2005 to treat VF. Further data are needed to refine recommendations for energy levels for defibrillation and cardioversion using biphasic waveforms.

Cardiac arrest during epidural anesthesia has been attributed to local anesthetic and opioid overdose [1], intravascular injection of local anesthetic [2], sympathetic blockade especially in the presence of hypovolemia, excessive sedation in the presence of hypoxemia [3], hypercarbia [4], or autonomic imbalance during recovery from neuraxial blockade [5]. Cardiac arrest due to psychogenic causes during extensive sympathetic blockade [6] or during establishment of spinal anesthesia [7] has rarely been described. In both reports, the patients had already received local anesthesia. In the first case [6], the patient experienced vasovagal asystole after the surgeon informed him about the poor prognosis of his vascular surgery. In the second patient [7], a presumed vasovagal arrest occurred immediately after the administration of local anesthetic. We report a patient who experienced cardiac arrest due to a vasovagal syncope that occurred during insertion of an epidural catheter and before any medication was administered epidurally. Case Report A 54-yr-old male patient (weight 78 kg, height 184 cm) was admitted for repair of an abdominal aortic aneurysm. His medical history included a vasovagal episode 3 yr before the present surgery, which occurred during proctosigmoidoscopy, and which was triggered by an emotional reaction after the endoscopist commented that he had noticed a "lesion consistent with tumor." The patient did not recall any other details about the incident, except that he was lying in the left lateral position and that he had "passed out." A review of this incident in his medical record indicated a "fainting spell" during sigmoidoscopy without any electrocardiographic or blood pressure documentation. Preoperatively, the patient's baseline electrocardiogram (ECG) was normal. A dobutamine echo stress test was negative for myocardial ischemia at 88% of maximal predicted heart rate, and left ventricular function was normal. He was taking no medications. Preoperatively, the patient appeared nervous; therefore, 1 mg of midazolam was given IV. In preparation for epidural anesthesia, the usual monitors were placed, and the patient was then positioned sitting. Oxygen was administered via a nasal cannula at a rate of 3 L/min, and 0.2 mg of glycopyrrolate was given IV. We asked the patient to warn us if he experienced any sign of lightheadedness or felt that he might faint. Epidural anesthesia was attempted at the T8-9 spinal level, and the epidural space was identified without difficulty using a loss of resistance technique. The patient's blood pressure (BP) was 134/80 mm Hg, and the heart rate was 78 bpm. During the insertion of an epidural catheter through the Touhy needle, the patient felt a paresthesia and immediately said, "I feel dizzy. I will faint." The ECG went abruptly from a normal sinus rhythm at a rate of 76 bpm to asystole; the pulse oximeter tracing ceased, and the patient had a short, generalized myoclonic movement. His eyes rolled upward; he was pale, became unresponsive, and collapsed. We quickly withdrew the epidural needle and left the catheter in, placed the patient supine, and assessed his vital signs within 30 s. At the same time, we administered 1 mg of atropine and 20 mg of ephedrine IV. As we prepared to initiate cardiopulmonary resuscitation, the ECG showed several ventricular escape beats, followed by a normal sinus rhythm. Several seconds after regaining spontaneous ECG activity, the patient awakened and asked what had happened. He did not have any neurologic deficits or stool or urine incontinence. Analysis of the ECG disclosed a 42-s period of asystole. We continued to monitor him for another 20 min. A repeat 12-lead ECG was normal; therefore, we continued with the planned surgery, which was accomplished uneventfully. Discussion Vasovagal syncope, also known as "the common faint," is a clinical disorder that is often not taken seriously by either patients or physicians. However, this condition may be serious, and syncope due to unexplained causes has been associated with a 6% mortality rate [8]. We describe a patient with severe vasovagal syncope with cardiac arrest that occurred during the insertion of an epidural catheter and before any medication was injected epidurally. This vasovagal presentation is unique in two ways. First, this is the first case reported of such a severe syncopal episode associated with epidural catheter placement. Second, the vasovagal attack was very serious, and the accompanying asystole was of unusually long duration (42 s). The patient regained consciousness and simultaneously resumed normal sinus rhythm in the supine positioning before IV atropine reached the central circulation. We believe that a vasovagal attack provoked by anxiety and nociception caused the cardiac arrest in our patient. We base this assumption on the fact that he had no history of heart disease, he had had a similar episode in the past in response to a situational stimulus, and his apparent preoperative anxiety culminated when the epidural catheter elicited paresthesia. The presentation of the syncope was typical, with a brief prodrome of dizziness, nausea, diaphoresis, and pallor, followed by sudden loss of consciousness and myoclonic movement. We also believe that cases like this are more frequent in our clinical practice than they are reported to be. Syncope most often results from a transient episode (8-10 s) of insufficient cerebral blood flow [9] The lack of an identifiable cause characterizes as much as half of recurrent syncopal attacks [10]. Situational vasovagal episodes are often described in association with injury, pain, the sight of blood, hunger, crowding, long periods of standing, fear, and/or anxiety. Any of those triggering events can cause a transient catecholamine surge that enhances myocardial contractility enough to stimulate the myocardial mechanoreceptors (C-fibers) [11]. Activation of these afferent nonmyelinated C-fibers through vigorous contraction of a relatively empty left ventricle induces bradycardia and vasodilation (Bezold-Jarisch reflex) [12,13]. Despite a substantial decrease in BP at the time of induced syncope, norepinephrine levels do not increase, whereas epinephrine levels increase severalfold [11]. Therefore, even in patients with bradycardia or asystole, hypotension is likely the primary event, whereas vagally mediated bradycardia may play only a secondary role in the pathogenesis of vasovagal syncope [11]. The cardiac mechanoreceptors erroneously sense that there is an increase in BP, and they therefore produce a neurohormonal response that causes the body's autonomic system to respond as if the individual was hypertensive, when the opposite is true. Another theory is that these individuals have hypersensitive mechanoreceptors and that any slight increase in contractility and/or pressure early during neuroautonomic compensation induced by the baroreceptors allows the body to mistakenly believe it has become fully compensated [11,14]. A standard pharmacologic treatment for the prevention of neurocardiogenic (vasovagal) syncope has not been established. However, several drug modalities have been used with success, including disopyramide (negative myocardial inotropic activity, anticholinergic, peripheral vasoconstrictive properties), beta-adrenergic blockers (to lower the discharge frequency of mechanoreceptors and to allow unopposed activation of alpha-receptors), anticholinergics, theophylline (blocking the uptake of adenosine that causes presynaptic inhibition and release of transmitters from peripheral adrenergic nerves), and selective serotonin uptake inhibitors (suppression of baroreceptor reflex) [10,15]. A mineralocorticoid, fludrocortisone, has also been used with success as a pharmacotherapy for neurocardiogenic syncope. The presumed mechanism is maintenance of intravascular volume and venous return, which can prevent the vigorous contraction of a hypovolemic ventricle that results in activation of mechanoreceptors [16]. Permanent placement of a dual chamber pacemaker has also been suggested; however, in patients with neurocardiogenic syncope, drug therapy is often effective in preventing syncope, whereas artificial pacing is not [11]. This can be explained by the pathogenesis of neurocardiogenic syncope, whereas bradycardia or asystole are secondary events. Finally, avoidance of situations that may precipitate the vasovagal episode may be advisable. Attention to a history of syncopal episodes may help to identify patients at risk of recurrent vasovagal attacks. If such an event is anticipated based on the history, one should try to prevent it with proper communication before the procedure. This may alleviate the patient's anxiety and reduce the risk imposed by the triggering event. Although performing the neuraxial blockade in the recumbent position should decrease the incidence of severe vasovagal cardiovascular collapse, our patient experienced his initial episode during a sigmoidoscopy performed in the recumbent position. In addition, adequate sedation and generous subcutaneous local anesthesia to relieve anxiety and/or pain may be a useful adjunct to successful regional block in these patients. In patients who are prone to neurogenic vasovagal attack of a malignant nature, close monitoring and liberal sedation should be used before attempting regional anesthesia. Finally, as in our case, a general anesthetic with more liberal sedative and anticholinergic premedication may be an option for avoiding any situational triggers. In conclusion, we describe a patient who experienced a vasovagal cardiac arrest during the placement of an epidural catheter. Although we anticipated the possibility of a vasovagal reaction in our patient and pretreated him with glycopyrrolate and light sedation, these medications were not sufficient to suppress the excessive vagal tone caused by our patient's anxiety, which culminated in a cardiac arrest.

Resuscitation highlights in 2011

A key limiting factor in the scale up and sustainability of HIV care and treatment programmes is the global shortage of trained health care workers. This paper discusses why it is important to move beyond conceptualising health care workers simply as 'inputs' in the delivery of HIV treatment and care, and to also consider their roles as partners and agents in the process of health care. It suggests a framework for thinking about their roles and responses in HIV care, considers the current evidence base, and concludes by identifying key areas for future research on health care workers' responses in HIV treatment and care in low and middle income settings.

This study examined records of 2566 consecutive COVID-19 patients at five Massachusetts hospitals and sought to predict level-of-care requirements based on clinical and laboratory data. Several classification methods were applied and compared against standard pneumonia severity scores. The need for hospitalization, ICU care, and mechanical ventilation were predicted with a validation accuracy of 88%, 87%, and 86%, respectively. Pneumonia severity scores achieve respective accuracies of 73% and 74% for ICU care and ventilation. When predictions are limited to patients with more complex disease, the accuracy of the ICU and ventilation prediction models achieved accuracy of 83% and 82%, respectively. Vital signs, age, BMI, dyspnea, and comorbidities were the most important predictors of hospitalization. Opacities on chest imaging, age, admission vital signs and symptoms, male gender, admission laboratory results, and diabetes were the most important risk factors for ICU admission and mechanical ventilation. The factors identified collectively form a signature of the novel COVID-19 disease.

The prediction of impending death is important for providing appropriate end-of-life care; however, limited information is currently available on the signs of impending death in non-cancer patients. Furthermore, although vital signs are routinely measured in clinical practice, changes in vital signs in the dying phase in non-cancer patients have not yet been elucidated in detail. We herein conducted a retrospective study to clarify changes in vital signs before death in noncancer patients. Non-cancer patients who died in a hospital in Japan between April 2017 and April 2018 were examined. Vital signs for up to seven days before death were analyzed, with the average value of each vital sign approximately every twelve hours being plotted. We divided data into two periods: from days -7 to -4 and from day -3 to death. We used a linear mixed model in the two periods, and t-tests were performed to assess whether the gradient of the line across the time variable significantly differed from zero. Data from 47 non-cancer patients were analyzed. Systolic blood pressure (P<0.001), diastolic blood pressure (P<0.001), and oxygen saturation (P=0.001) significantly decreased from day -3 to death, whereas no significant changes were noted in any vital sign in days -7 to -4. Based on the present results, changes in blood pressure and oxygen saturation may be useful indicators of prognosis within three days of death. Further research on clinical signs and their diagnostic characteristics for impending death in non-cancer patients is needed.

Interhospital transport of critically unwell children exacerbates physiological stress, increasing the risk of deterioration during transport. Due to the nature of illness and interventions occurring in this cohort, defining “normal” vital sign ranges is impossible, which can make identifying deterioration events difficult.A novel data-driven approach was developed to identify adverse respiratory and cardiovascular events in critically ill children during interhospital transport. In this retrospective cohort study of 1,519 transports (July 2016 to May 2021), vital signs were recorded at one-second intervals and then analysed using an adaptation of Bollinger Bands, a technique borrowed from financial market analysis. This method dynamically established each patient’s stable ranges for heart rate, blood pressure, oxygen saturation, and other respiratory parameters, and flagged adverse events when multiple parameters simultaneously fell outside their expected ranges.Adverse respiratory events were identified when oxygen saturation deviated below a dynamically defined threshold alongside at least one additional respiratory parameter. Cardiovascular events were defined by concurrent deviations in blood pressure and heart rate. Overall, 15.6 percent of transports had one or more adverse respiratory events, and 21.5 percent had at least one adverse cardiovascular event.To validate these labels, the number of adverse events and the cumulative duration of vital sign instability during transport were compared against clinical markers of deterioration. Each additional respiratory event was associated with increased odds of receiving respiratory support during transport and higher 30-day mortality, while each additional cardiovascular event was associated with increased odds of receiving vasoactive support during transport.Our method detects clinically meaningful respiratory and cardiovascular adverse events during transport. The approach is readily adaptable to other high-resolution intensive care datasets, for both retrospective labelling as well as automated, real-time identification of adverse events in the clinical setting, offering a foundation for improved monitoring and early intervention in critically ill patients.Author SummaryTransporting critically ill children between hospitals is challenging because their condition can worsen during the journey. Previously, studies have relied on fixed vital-sign cutoffs to identify “adverse events,” but these rigid thresholds may not account for individual differences in heart rate, blood pressure, and oxygen baseline levels.Here, we used a tool borrowed from financial market analysis to track minute-by-minute vital signs in over 1,500 transport episodes. Our approach identified sudden, patient-specific changes that signalled respiratory or cardiovascular problems. We found that around 15 percent of transfers had at least one breathing-related event and over 20 percent had a heart-related event. Moreover, these events were linked to worse outcomes, such as the need for extra breathing or blood-pressure support.By considering each child’s own “stable” vital sign range, this method can detect meaningful changes that standard fixed thresholds might miss. This personalised tracking of vital signs opens the door for further research on routinely collected vital-sign datasets. It could also be deployed in the clinical environment helping clinicians detect a child’s deterioration earlier and respond in real time. Although we focused on children in transport, our approach could be adapted to other intensive care settings to improve patient monitoring.

Objective: Reduction of intrathoracic pressures to -10 cm H2O during the decompression phase of cardiopulmonary resuscitation (CPR) increases cardiac preload, lowers intracranial pressures, and increases circulation and survival rates in pigs undergoing standard CPR. In this proof of concept study, we tested the hypothesis that augmentation of negative intrathoracic pressure during standard (S) CPR with intrathoracic pressure regulation (IPR) providing continuous negative intrathoracic pressure of -10 cm H2O between positive pressure ventilations will improve circulation, using end tidal (ET) CO2 as a non-invasive surrogate of organ perfusion, in patients receiving S-CPR. Methods: In this first clinical evaluation of IPR (CirQLatorTM, Advanced Circulatory Systems Inc, Roseville, MN) paramedic supervisors in Toledo OH performed CPR, applied IPR in 12 adult patients, and measured ETCO2, blood pressure and O2 saturation upon return of spontaneous circulation (ROSC) rates. IPR was continued after ROSC to help maintain perfusion. Values are expressed as mean ± SEM and statistical significance was determined by a paired Student's t-test. ETCO2 and blood pressure are expressed in mmHg. Results: IPR was used together with S-CPR to treat cardiac arrest in 12 patients: mean age 64 ± 3; 4 were male and the initial recorded rhythms were ventricular fibrillation (n=2), pulseless electrical activity (n=3), and asystole (n=7). Time from the initial 911 call to IPR application was 16±1 min. Initial ETCO2 when IPR was applied was 21± 3. Maximum ETCO2 during CPR was 44 ± 4, (p &lt; 0.001 compared with initial ETCO2). There was ROSC in 9/12 patients: 3 patients with asystole did not have ROSC. Time from IPR application to ROSC was 16 ± 3 minutes. Systolic/diastolic blood pressures immediately after ROSC were 126 ±13/72 ± 8. O2 saturation at ROSC was 96 ± 1%. IPR was used in 8/9 patients post ROSC for 8 ± 3 min. There were no observed adverse events. Conclusion: Clinical application of IPR during CPR increased ETCO2 values and resulted in ROSC in 9/12 patients, providing first clinical proof-of-concept that this new non-invasive technology increases circulation during CPR. Based upon these positive data, further study of IPR in patients in cardiac arrest is warranted.

Vital signs are an important component of monitoring the adult or child patient’s progress during hospitalization, as they allow for the prompt detection of delayed recovery or adverse events. Vital signs are measured to obtain basic indicators of a patient’s health status. The most common intervention performed in hospital medicine is a measurement of vital signs and these traditionally consist of blood pressure, temperature, pulse rate, and respiratory rate. Advanced monitoring systems incorporate a balanced combination of clinical and technological aspects to give an innovative healthcare outcome. Remote patient monitoring systems are rapidly becoming the core of healthcare deliveries. The paradigm shifted from traditional and manual recording to computer-based electronic records and further to smartphones as versatile and innovative healthcare monitoring systems. The purpose of this research is to design a Vital Sign Monitoring device for BPM and SpO2 Parameters with Notifications through the IoT-Based Telegram application. This device can monitor vital signs, especially BPM and SPO2 wherever the patient is and whenever, so that doctors or health workers, as well as patients, can find out their health condition. This display can be viewed via web thinger.io, then forwarded to telegram if an abnormal patient condition is found and there is an indicator light that will light up differently for each condition. This study uses the MAX30100 which is a digital sensor to detect oxygen saturation and heart rate. The results of this study have succeeded in displaying data on the IoT web and sending notifications to the Telegram application. And also, the resulting data has an error that does not exceed the allowable limit according to each parameter. The difference between heart rate readings and oxygen saturation values ​​on the device and patient monitor is 0.015% for heart rate and 0.01% for oxygen saturation.

Failure to detect ward hypoxaemia and hypotension: contributions of insufficient assessment frequency and patient arousal during nursing assessments