No abstract

The Sodium Hydrogen Exchanger, (NHE1) is an ubiquitously expressed protein that exchanges an intracellular proton (H+) for an extracellular sodium (Na+) and regulates cell volume, intracellular pH homeostasis and cell motility. The Calceurin Homologous Protein isoforms 1 (CHP1) and isoform 2 (CHP2) each regulate NHE1. CHP1 and CHP2 share a 66% amino residue homology, yet CHP1 and CHP2 have different binding affinities for NHE1. No work has determined the differential binding site for each CHP isoform. Here we will show the binding determinates of NHE and the CHP Isoforms by mutagenesis of key amino residues in the CHP binding domain from AA 803‐845. Sequence and structural analysis demonstrated that eight amino residues may play an important role in the binding of NHE1 and the CHP isoforms. These key amino residues are Asn519Ala, Asn519Asp, Ile518Gln/Ile522Gln, Il534Lys, Il537Lys, His523Gly, His523Ile, and Asp536Gly. We have expressed and purified the c‐terminus of wild‐type NHE1 and mutations for each putative CHP interaction site. The protein interactions of recombinant CHP1 and CHP2 is determined using thermal denaturation and other biophysical methods. This work will identify potential interaction sites in common and unique for each CHP isoform and NHE1.

Background A paradoxical embolism arises when a venous thrombus passes through a cardiac right to left shunt and enters the arterial circulation. This can manifest as cardiovascular ischemia, cerebrovascular insults, increased right ventricular pressure, and/or volume overload leading to signs and symptoms of heart failure. While rare, paradoxical emboli carry high mortality and morbidity if diagnosis is missed and/or treatment is delayed. Transesophageal echocardiography can be diagnostic. Initial treatment revolves around anticoagulation and/or thrombolysis to prevent clot propagation. However, for clots in transit, emergent surgical removal is often necessary. Anesthetic induction can be tricky given the potential for rapid deterioration and the need to avoid increased right sided pressures and further clot migration. Case presentation In this report, we present a 72-year-old obese female with a history of hypertension, hyperlipidemia, gout, and diabetes found to have a paradoxical embolism caught in transit, trapped in a patent foramen ovale, and managed surgically. We describe the role of intraoperative transesophageal echocardiography in successfully treating this patient. Conclusions TEE plays an important role in the diagnosis and management of paradoxical PE. It can detect right and left heart thrombi and intracardiac shunts , can help in the successful closure of intracardiac shunts, and can impact intraoperative surgical decision making.

Congenital central hypoventilation syndrome (CCHS) is a rare neurological disease affecting the brain's response to carbon dioxide levels, resulting in dysregulation of respiration. CCHS is characterized by a diminished effort to breathe during sleep despite hypoxia and hypercapnia. Ventilation is adequate during wakeful periods but diminished during sleep. Alterations in ventilation pose a challenge to anesthesiologists in their attempts to wean these patients from ventilatory support. We describe a patient with CCHS and a complicated history of prolonged tracheal intubation, who was treated with intravenous (IV) caffeine and was able to resume adequate spontaneous ventilation and baseline mental status immediately postprocedure.

Pseudocholinesterase deficiency, commonly referred to as Butyrylcholinesterase deficiency, is a rare, inherited, or acquired condition that results in decreased or absent enzymatic activity. Pseudocholinesterase is a plasma enzyme that is responsible for the breakdown of succinylcholine and mivacurium, which are commonly used paralytic agents. People with this condition are usually unaware they have the disease, and the disease may not manifest until extubation at the end of surgery. These patients will usually have abnormally prolonged paralysis time and require mechanical ventilation well into the post anesthesia care unit because of failure to meet qualitative and quantitative extubation criteria. Treatment is mainly supportive with continued mechanical ventilation until return of muscle function because paralysis can last from minutes to hours and re-sedation to limit patient discomfort. We present two cases of prolonged paralysis after succinylcholine administration subsequently confirmed by laboratory testing to be pseudocholinesterase deficiency.