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Objectives:. To construct a highly detailed yet practical, attainable roadmap for enhancing the likelihood of neurologically intact survival following sudden cardiac arrest. Design, Setting, and Patients:. Population-based outcomes following out-of-hospital cardiac arrest were collated for 10 U.S. counties in Alaska, California, Florida, Ohio, Minnesota, Utah, and Washington. The 10 identified emergency medical services systems were those that had recently reported significant improvements in neurologically intact survival after introducing a more comprehensive approach involving citizens, hospitals, and evolving strategies for incorporating technology-based, highly choreographed care and training. Detailed inventories of in-common elements were collated from the ten 9-1-1 agencies and assimilated. For reference, combined averaged outcomes for out-of-hospital cardiac arrest occurring January 1, 2017, to February 28, 2018, were compared with concurrent U.S. outcomes reported by the well-established Cardiac Arrest Registry to Enhance Survival. Interventions:. Most commonly, interventions and components from the ten 9-1-1 systems consistently included extensive public cardiopulmonary resuscitation training, 9-1-1 system-connected smart phone applications, expedited dispatcher procedures, cardiopulmonary resuscitation quality monitoring, mechanical cardiopulmonary resuscitation, devices for enhancing negative intrathoracic pressure regulation, extracorporeal membrane oxygenation protocols, body temperature management procedures, rapid cardiac angiography, and intensive involvement of medical directors, operational and quality assurance officers, and training staff. Measurements and Main Results:. Compared with Cardiac Arrest Registry to Enhance Survival (n = 78,704), the cohorts from the 10 emergency medical services agencies examined (n = 2,911) demonstrated significantly increased likelihoods of return of spontaneous circulation (mean 37.4% vs 31.5%; p < 0.001) and neurologically favorable hospital discharge, particularly after witnessed collapses involving bystander cardiopulmonary resuscitation and shockable cardiac rhythms (mean 10.7% vs 8.4%; p < 0.001; and 41.6% vs 29.2%; p < 0.001, respectively). Conclusions:. The likelihood of neurologically favorable survival following out-of-hospital cardiac arrest can improve substantially in communities that conscientiously and meticulously introduce a well-sequenced, highly choreographed, system-wide portfolio of both traditional and nonconventional approaches to training, technologies, and physiologic management. The commonalities found in the analyzed systems create a compelling case that other communities can also improve out-of-hospital cardiac arrest outcomes significantly by conscientiously exploring and adopting similar bundles of system organization and care.

Abstract Background Reducing intrathoracic pressure in the setting of compromised cerebral perfusion due to acute brain injury has been associated with reduced intracranial pressure and enhanced cerebral perfusion pressure and blood flow in animals. Noninvasive active intrathoracic pressure regulation lowers intrathoracic pressure, increases preload, reduces the volume of venous blood and cerebral spinal fluid in the skull, and enhances cerebral blood flow. We examined the feasibility of active intrathoracic pressure regulation therapy in patients with brain injury. We hypothesized that active intrathoracic pressure regulation therapy would be associated with lowered intracranial pressure and increased cerebral perfusion pressure in these patients. Methods At three institutions, active intrathoracic pressure regulation therapy (CirQlator™, ZOLL) was utilized for 2 consecutive hours in five mechanically ventilated patients with brain injury. A 30-minute interval was used to collect baseline data and determine persistence of effects after device use. End-tidal carbon dioxide was controlled by respiratory rate changes during device use. The intracranial pressure, mean arterial pressure, and cerebral perfusion pressure were recorded at 5-minute intervals throughout all three periods of the protocol. Results for each interval are reported as mean and standard deviation. Results Intracranial pressure was decreased in all five patients by an average of 21% during (15 ± 4 mmHg) compared to before active intrathoracic pressure regulation (19 ± 4) (p = 0.005). This effect on intracranial pressure (15 ± 6) was still present in four of the five patients 30 minutes after therapy was discontinued (p = 0.89). As a result, cerebral perfusion pressure was 16% higher during (81 ± 10) compared to before active intrathoracic pressure regulation (70 ± 14) (p = 0.04) and this effect remained present 30 minutes after therapy was discontinued. No adverse events were reported. Conclusions These data support the notion that active intrathoracic pressure regulation, in this limited evaluation, can successfully augment cerebral perfusion by lowering intracranial pressure and increasing mean arterial pressure in patients with mild brain injury. The measured effects were immediate on administration of the therapy and persisted to some degree after the therapy was terminated.

Abstract Background Intrathoracic pressure regulation (IPR) therapy has been shown to increase blood pressure in hypotensive patients. The potential value of this therapy in patients with hypotension secondary to trauma with bleeding is not well understood. We hypothesized that IPR would non-invasively and safely enhance blood pressure in spontaneously breathing patients with trauma-induced hypotension. Methods This prospective observational cohort study assessed vital signs from hypotensive patients with a systolic blood pressure (SBP) ≤90 mmHg secondary to trauma treated with IPR (ResQGARD™, ZOLL Medical) by pre-hospital emergency medical personnel in three large US metropolitan areas. Upon determination of hypotension, facemask-based IPR was initiated as long as bleeding was controlled. Vital signs were recorded before, during, and after IPR. An increased SBP with IPR use was the primary study endpoint. Device tolerance and ease of use were also reported. Results A total of 54 patients with hypotension secondary to trauma were treated from 2009 to 2016. The mean ± SD SBP increased from 80.9 ± 12.2 mmHg to 106.6 ± 19.2 mmHg with IPR (p

OBJECTIVE:: An inspiratory impedance threshold device was evaluated in spontaneously breathing animals with hypotension to determine whether it could help improve systemic arterial pressures when fluid replacement was not immediately available. DESIGN:: Prospective, randomized. SETTING:: Animal laboratory. SUBJECTS:: Thirty-nine female farm pigs (weight, 28 –33 kg). INTERVENTIONS:: A total of 39 anesthetized spontaneously breathing pigs were treated with an impedance threshold device, with cracking pressures from 0 to −20 cm H2O. Four separate experimental protocols were performed: protocol A, in which the hemodynamics of seven pigs were examined during application of an impedance threshold device at various levels of inspiratory impedance (−5, −10, −15, and −20 cm H2O), both before and after a severe, controlled hemorrhage to a systolic blood pressure of 50 –55 mm Hg; protocol B, in which nine pigs bled to systolic blood pressure of 50 –55 mm Hg were treated with an impedance threshold device set at −12 cm H2O and were compared with nine others treated with a sham device; protocol C, in which the effects of the impedance threshold device on mixed venous gases were measured in seven hemorrhaged pigs; and protocol D, in which the effects of the impedance threshold device on cardiac output in seven hemorrhaged pigs were measured. METHODS AND MAIN RESULTS:: During initial studies with both normovolemic and hypovolemic pigs, sequential increases in inspiratory impedance resulted in a significant increase in systolic blood pressure, whereas diastolic left ventricular and right atrial pressures decreased significantly and proportionally to the level of impedance. When comparing the sham vs. active impedance threshold device (−12 cm H2O) in hypotensive pigs, systolic blood pressure (mean ± sem) with active impedance threshold device treatment increased from 70 ± 2 mm Hg to 105 ± 4 mm Hg (p < .01). Pressures in the control group remained at 70 ± 4 mm Hg (p < .01). Cardiac output increased by nearly 25% (p < .01) with the active impedance threshold device when calculated using the mixed gas equation and when determined by thermodilution. CONCLUSIONS:: These studies demonstrate that it is feasible to use a device that creates inspiratory impedance in spontaneously breathing normotensive and hypotensive pigs to increase blood pressure and enhance cardiopulmonary circulation in the absence of immediate fluid resuscitation. Further studies are needed to evaluate the potential long-term effects and limitations of this new approach to treat hypovolemic hypotension. [ABSTRACT FROM AUTHOR]

Symptoms arising from cardiac arrhythmias are often transient. Consequently, defining the responsible rhythm disturbance remains a challenge. However, absent a confident diagnosis of the arrhythmic basis for the symptoms, it is not possible to develop an effective treatment strategy. The implantable loop recorder (ILR) has become a valuable element in the evaluation of patients with suspected intermittent arrhythmia related symptoms. In this regard, clinical studies have not only demonstrated its superior effectiveness compared to other monitoring modalities, but even suggest that it may be cost-effective for the ILR to be used at an earlier stage of the evaluation strategy. [ABSTRACT FROM AUTHOR]