Because of this, recent editions of the American Heart Associations Guidelines for Cardiopulmonary Resuscitation have de-emphasized the role of tracheal intubation in favor of other airway management techniques such as bag-valve-mask ventilation, the laryngeal mask airway and the Combitube. However, recent higher quality studies have shown no survival or neurological benefit with endotracheal intubation over supraglottic airway devices (Laryngeal mask or Combitube).One complication—unintentional and unrecognized intubation of the esophagus—is both common (as frequent as 25% in the hands of inexperienced personnel) and likely to result in a deleterious or even fatal outcome. In such cases, oxygen is inadvertently administered to the stomach, from where it cannot be taken up by the circulatory system, instead of the lungs. If this situation is not immediately identified and corrected, death will ensue from cerebral and cardiac anoxia. Of 4,460 claims in the American Society of Anesthesiologists (ASA) Closed Claims Project database, 266 (approximately 6%) were for airway injury. Of these 266 cases, 87% of the injuries were temporary, 5% were permanent or disabling, and 8% resulted in death. Difficult intubation, age older than 60 years, and female gender were associated with claims for perforation of the esophagus or pharynx. Early signs of perforation were present in only 51% of perforation claims, whereas late sequelae occurred in 65%.During the SARS and COVID-19 pandemics, tracheal intubation has been used with a ventilator in severe cases where the patient struggles to breathe. Performing the procedure carries a risk of the caregiver becoming infected.
HCA2 and HCA3 inhibit cyclic adenosine monophosphate (cAMP) production and thus suppress the release of free fatty acids (FFAs) from body fat, reducing their availability to the liver to synthesize the blood-circulating lipids in question. A decrease in free fatty acids also suppresses liver expression of apolipoprotein C3 and PPARg coactivator-1b, thus increasing VLDL-C turnover and reducing its production. Niacin also directly inhibits the action of diacylglycerol O-acyltransferase 2 (DGAT2) a key enzyme for triglyceride synthesis.The mechanism behind niacin increasing HDL-C is not totally understood, but seems to occur in various ways. Niacin increases apolipoprotein A1 levels by inhibiting the breakdown of this protein, which is a component of HDL-C. It also inhibits HDL-C hepatic uptake by suppressing production of the cholesterol ester transfer protein (CETP) gene. It stimulates the ABCA1 transporter in monocytes and macrophages and upregulates peroxisome proliferator-activated receptor gamma, resulting in reverse cholesterol transport. Combined with statins
Extended release niacin was combined with the lovastatin trade-named Advicor, and with simvastatin, trade-named Simcor as prescription drug combinations. Advicor was approved by the U.S. Food and Drug Administration (FDA) in 2001. Simcor was approved in 2008. Subsequently, large outcome trials using these niacin and statin therapies were unable to demonstrate incremental benefit of niacin beyond statin therapy alone. The FDA withdrew approval of both drugs in 2016.