Critical Care Simulation Education Program During the COVID-19 Pandemic.

BACKGROUND: Coronaviruses are important emerging human and animal pathogens. SARS-CoV-2, the virus that causes COVID-19, is responsible for the current global pandemic. Early in the course of the pandemic, New York City became one of the world's "hot spots" with more than 250,000 cases and more than 15,000 deaths. Although medical providers in New York were fortunate to have the knowledge gained in China and Italy before it came under siege, the magnitude and severity of the disease were unprecedented and arguably under appreciated. The surge of patients with significant COVID-19 threatened to overwhelm health care systems, as New York City health systems realized that the number of specialized critical care providers would be inadequate. A large academic medical system recognized that rapid redeployment of noncritical providers into such roles would be needed. An educational gap was therefore identified: numerous providers with minimal critical care knowledge or experience would now be required to provide critical-level patient care under supervision of intensivists. Safe provision of such high level of patient care mandated the development of "educational crash courses." METHODS: The purpose of this special article is to summarize the approach adopted by the Institute for Critical Care Medicine and Department of Anesthesiology, Perioperative and Pain Medicine's Human Emulation, Education, and Evaluation Lab for Patient Safety and Professional Study Simulation Center in developing a training program for noncritical care providers in this novel disease. RESULTS: Using this joint approach, we were able to swiftly educate a wide range of nonintensive care unit providers (such as surgical, internal medicine, nursing, and advanced practice providers) by focusing on refreshing critical care knowledge and developing essential skillsets to assist in the care of these patients. CONCLUSIONS: We believe that the practical methods reviewed here could be adopted by any health care system that is preparing for an unprecedented surge of critically ill patients.

A systematic literature search and review of sodium concentrations of body fluids
.

BACKGROUND: Wide ranges of sodium concentrations for different body fluid losses have been noted with minimal substantiating data and variability among sources, leading to use of "cumulative fluid balance" regardless of composition in hospitalized patients. AIMS: To define the sodium concentrations of fluid losses from the body. METHOD: We performed a systematic search and literature review in adult humans using PubMed database. RESULTS: Inclusion criteria were met for 107 full-text articles. Mean sodium concentrations were significantly lower for acidic (mean ± SD: 44 ± 12 mEq/L) than for alkaline (55 ± 13 mEq/L) gastric fluid, higher for bile (185 ± 24 mEq/L) or pancreatic fluid (156 ± 3 mEq/L) than for all other body fluids, and similar for intact small bowel (119 ± 14 mEq/L) and ileostomy outputs (116 ± 25 mEq/L). Sodium concentrations were significantly greater for cholera-induced diarrhea (128 ± 18 mEq/L) and lower for osmotic-induced diarrhea (28 ± 16 mEq/L) than all other causes of diarrhea. For osmotic diarrheas, sorbitol-induced diarrhea sodium concentration was higher (63 ± 17 mEq/L) than for carbohydrate malabsorption (43 ± 20 mEq/L), lactulose (26 ± 19 mEq/L), Idolax (16 ± 13 mEq/L), or polyethylene glycol (13 ± 7 mEq/L). For secretory diarrheas, sodium concentration for idiopathic causes (53 ± 22 mEq/L) was lower than for neuroendocrine and villous tumors (75 ± 13 mEq/L) or nonosmotic laxatives (88 ± 33 mEq/L). For pleural, peritoneal, and edema fluid, sodium concentrations (137 ± 13 mEq/L) were similar to plasma. No data were found for wound fluid. Sodium concentration for sweat was 44 ± 17 mEq/L. CONCLUSIONS: This is the first in-depth review of verifiable sodium concentrations of body fluids most commonly lost in hospitalized patients. Sodium concentrations are fluid-specific and consistent. Sodium concentrations for diarrhea are associated with specific mechanisms/causes. These data should be useful to more accurately replace sodium and water content for specific body fluid losses.
.

A case of apical ballooning syndrome in a male with status asthmaticus; highlighting the role of B2 agonists in the pathophysiology of a reversible cardiomyopathy.

Apical ballooning syndrome (ABS), also known as Takotsubo cardiomyopathy, was first reported by Dote and colleagues in Japanese literature in 1991 in a review of five cases. Case series have highlighted the association of severe psychological stressors as the major precipitating factors of this syndrome. Status Epilepticus and Sub-Arachnoid hemorrhage are also now established independent etiologies for this phenomenon in patients without coronary artery disease. We report a case of reversible apical ventricular dysfunction in a 50-year-old male presenting with status asthmaticus who quickly underwent intubation. Following this, he had ST elevations in precordial leads with mild cardiac enzyme leak. Subsequent cardiac catheterization revealed a left ventricular ejection fraction of 25-30% with apical aneurismal segment. No obstructive disease was observed. Three days later there was marked clinical improvement; the patient was extubated and repeat echocardiography revealed a remarkable return to normal ventricular size and systolic function. Our case demonstrates that excess use of beta-agonists may be a potential risk factor for ABS and raises the possibility of cathecholamine cardiotoxicity being mediated via beta-receptors. Furthermore, it also negates the propensity of apical ballooning so far reported only in women with respiratory distress without confounding emotional stressors.