ABSTRACT
BACKGROUND: Early in the coronavirus disease 2019 (COVID-19) pandemic, there was serious concern that the United States would encounter a shortfall of mechanical ventilators. In response, the US government, using the Defense Production Act, ordered the development of 200,000 ventilators from 11 different manufacturers. These ventilators have different capabilities, and whether all are able to support COVID-19 patients is not evident. RESEARCH QUESTION: Evaluate ventilator requirements for affected COVID-19 patients, assess the clinical performance of current US Strategic National Stockpile (SNS) ventilators employed during the pandemic, and finally, compare ordered ventilators' functionality based on COVID-19 patient needs. STUDY DESIGN AND METHODS: Current published literature, publicly available documents, and lay press articles were reviewed by a diverse team of disaster experts. Data were assembled into tabular format, which formed the basis for analysis and future recommendations. RESULTS: COVID-19 patients often develop severe hypoxemic acute respiratory failure and adult respiratory defense syndrome (ARDS), requiring high levels of ventilator support. Current SNS ventilators were unable to fully support all COVID-19 patients, and only approximately half of newly ordered ventilators have the capacity to support the most severely affected patients; ventilators with less capacity for providing high-level support are still of significant value in caring for many patients. INTERPRETATION: Current SNS ventilators and those on order are capable of supporting most but not all COVID-19 patients. Technologic, logistic, and educational challenges encountered from current SNS ventilators are summarized, with potential next-generation SNS ventilator updates offered.
Subject(s)
COVID-19/therapy , Respiration, Artificial/methods , Respiratory Distress Syndrome/therapy , Respiratory Insufficiency/therapy , Strategic Stockpile , Ventilators, Mechanical/statistics & numerical data , Humans , Intensive Care Units , Respiration, Artificial/instrumentation , SARS-CoV-2 , United States , Ventilators, Mechanical/standards , Ventilators, Mechanical/supply & distributionABSTRACT
Obtaining intravenous (i.v.) access for fluid administration is a critical step in treating hemorrhage. However, expertise, supplies, and personnel to accomplish this task can be delayed or even absent in austere environments. An alternative approach that can "buy time" and improve circulation when i.v. fluids are absent is needed. Preclinical studies show that intrathoracic pressure regulation (ITPR) can increase perfusion in hypovolemia in the absence of i.v. fluid. We compared ITPR with placebo in humans undergoing a 15% hemorrhage under general anesthesia. Paired healthy volunteers (n = 7, aged 21 - 35 years) received either ITPR or placebo on different study days. Institutional review board informed consent was obtained. Subjects were anesthetized using propofol, intubated, and mechanically ventilated and hemorrhaged (10 mL/kg). Twenty minutes after hemorrhage, ITPR (-12 cm H2O vacuum) or placebo (device but no vacuum) was administered for another 60 min. Intravenous fluid was administered when systolic blood pressure was less than 85 mmHg. Hemodynamics, cardiac function by echocardiography, and volumetric data were compared. Data were expressed in Δmean ± SEM before and after ITPR/placebo intervention. There were no differences in mean arterial pressure (ITPR, 2.1 ± 3 mmHg; placebo, -0.7 ± 3 mmHg) or fluid infused (ITPR, 17.4 ± 4 mL/kg; placebo, 18.6 ± 5 mL/kg). Urinary output and plasma volume also were not significantly different. Intrathoracic pressure regulation augmented stroke volume (ITPR, 22 ± 5 mL, placebo, 6 ± 4 mL; P < 0.05), ejection fraction (ITPR, 4% ± 1%; placebo, 0% ± 1%), and diastolic function (ΔE/e') (ITPR, -0.8 ± 0.4 vs. placebo, +0.81 ± 0.6; P < 0.05). Intrathoracic pressure regulation did not improve mean arterial pressure in healthy volunteers aged 21 to 35 years. However, ITPR augmented stroke volume, which could be caused by improved ventricular function.