In patients who are receiving mechanical ventilation, daily interruption of sedative-drug infusions decreases the duration of mechanical ventilation and the length of stay in the intensive care unit.

June 23/30, 2020 e933 Existing American Heart Association cardiopulmonary resuscitation (CPR) guidelines do not address the challenges of providing resuscitation in the setting of the coronavirus disease 2019 (COVID-19) global pandemic, wherein rescuers must continuously balance the immediate needs of the patients with their own safety. To address this gap, the American Heart Association, in collaboration with the American Academy of Pediatrics, American Association for Respiratory Care, American College of Emergency Physicians, The Society of Critical Care Anesthesiologists, and American Society of Anesthesiologists, and with the support of the American Association of Critical Care Nurses and National Association of EMS Physicians, has compiled interim guidance to help rescuers treat individuals with cardiac arrest with suspected or confirmed COVID-19.Over the past 2 decades, there has been a steady improvement in survival after cardiac arrest occurring both inside and outside the hospital. 1 That success has relied on initiating proven resuscitation interventions such as high-quality chest compressions and defibrillation within seconds to minutes. The evolving and expanding outbreak of severe acute respiratory syndrome coronavirus 2 infections has created important challenges to such resuscitation efforts and requires potential modifications of established processes and practices. The challenge is to ensure that patients with or without COVID-19 who experience cardiac arrest get the best possible chance of survival without compromising the safety of rescuers, who will be needed to care for future patients. Complicating the emergency response to both out-of-hospital and in-hospital cardiac arrest is that COVID-19 is highly transmissible, particularly during resuscitation, and carries a high morbidity and mortality.Approximately 12% to 19% of COVID-positive patients require hospital admission, and 3% to 6% become critically ill. [2][3][4] Hypoxemic respiratory failure secondary to acute respiratory distress syndrome, myocardial injury, ventricular arrhythmias, and shock are common among critically ill patients and predispose them to cardiac arrest, [5][6][7][8] as do some of the proposed treatments such as hydroxychloroquine and azithromycin, which can prolong the QT. 9 With infections currently growing exponentially in the United States and internationally, the percentage of patients with cardiac arrests and COVID-19 is likely to increase.Healthcare workers are already the highest-risk profession for contracting the disease. 10 This risk is compounded by worldwide shortages of personal protective equipment (PPE). Resuscitations carry added risk to healthcare workers for many reasons. First, the administration of CPR involves performing numerous aerosol-generating procedures, including chest compressions, positive-pressure ventilation, and establishment of an advanced airway. During those procedures, viral particles can remain suspended in the air with a half-life of ≈1 hour and

There is a need to develop early biomarkers of acute kidney injury following cardiac surgery, where morbidity and mortality are increased by its presence. Plasma cystatin C (CyC) and plasma and urine Neutrophil Gelatinase Associated Lipocalin (NGAL) have been shown to detect kidney injury earlier than changes in plasma creatinine in critically ill patients. In order to determine the utility of urinary CyC levels as a measure of kidney injury, we prospectively collected plasma and urine from 72 adults undergoing elective cardiac surgery for analysis. Acute kidney injury was defined as a 25% or greater increase in plasma creatinine or renal replacement therapy within the first 72 hours following surgery. Plasma CyC and NGAL were not useful predictors of acute kidney injury within the first 6 hours following surgery. In contrast, both urinary CyC and NGAL were elevated in the 34 patients who later developed acute kidney injury, compared to those with no injury. The urinary NGAL at the time of ICU arrival and the urinary CyC level 6 hours after ICU admission were most useful for predicting acute kidney injury. A composite time point consisting of the maximum urinary CyC achieved in the first 6 hours following surgery outperformed all individual time points. Our study suggests that urinary CyC and NGAL are superior to conventional and novel plasma markers in the early diagnosis of acute kidney injury following adult cardiac surgery.

Our data demonstrate that intravenous methylnaltrexone can induce laxation and reverse slowing of oral cecal-transit time in subjects taking high opioid dosages. Low-dosage methylnaltrexone may have clinical utility in managing opioid-induced constipation.

Methylnaltrexone is a quaternary opioid antagonist with limited ability to cross the blood-brain barrier and the potential to antagonize the peripherally mediated effects of opioids. The effectiveness of methylnaltrexone in preventing morphine-induced changes in gastrointestinal motility and transit without affecting analgesia was evaluated in humans. Twelve healthy volunteers were given intravenous placebo, placebo plus 0.05 mg/kg morphine, or 0.45 mg/kg methylnaltrexone plus 0.05 mg/kg morphine. Oral-cecal transit time was assessed by the pulmonary hydrogen measurement technique, and analgesia was measured with use of the cold-pressor test. Morphine significantly increased oral-cecal transit time from 104.6 +/- 31.1 minutes (mean +/- SD) to 163.3 +/- 39.8 minutes (p < 0.01). Methylnaltrexone prevented 97% of morphine-induced increase in oral-cecal transit time (106.3 +/- 39.8 minutes; not significant compared with baseline; p < 0.01 compared with morphine alone). Methylnaltrexone did not affect the analgesic effect of morphine on both pain intensity and pain bothersomeness ratings. At a higher dose of morphine (0.1 mg/kg), our preliminary results indicated that 0.45 mg/kg methylnaltrexone also prevented the morphine-induced delay in oral-cecal transit time, with no effect on analgesia. Methylnaltrexone may be a useful adjunct to opioids for the relief of opioid-induced constipation.