Balancing carcinoid crisis and right ventricular dysfunction during tricuspid and pulmonic valve replacement for carcinoid heart disease: A case report.

INTRODUCTION AND IMPORTANCE: Carcinoid tumors are rare malignancies of neuroendocrine origin that can manifest with a constellation of systemic symptoms including right-sided cardiac involvement. Many patients with carcinoid heart disease require valve replacement, but intraoperative management of carcinoid syndrome varies within the literature. CASE PRESENTATION: A 72-year-old man with carcinoid syndrome underwent tricuspid and pulmonic valve replacement with multiple episodes of carcinoid crisis intraoperatively as well as right ventricular dysfunction after cardiopulmonary bypass. CLINICAL DISCUSSION: Octreotide is the mainstay in prevention and treatment of intraoperative carcinoid crisis, but reported dosages and timing varies significantly. The use of exogenous catecholamines is also controversial as they are thought to paradoxically worsen carcinoid symptoms. Our patient was managed successfully with both an octreotide infusion and intermittent boluses, as well as exogenous catecholamines for right ventricular support during and after cardiopulmonary bypass. CONCLUSION: The management of carcinoid syndrome in patients undergoing valve surgery for carcinoid heart disease is dependent on timely prevention and treatment of carcinoid crisis and effective mitigation of right ventricular dysfunction.

A two-circuit strategy for intraoperative extracorporeal support during single lung transplantation in a patient bridged with venovenous extracorporeal membrane oxygenation.

Venovenous extracorporeal membrane oxygenation is increasingly used as a bridging strategy in decompensating patients awaiting lung transplantation. Various approaches for continuing support intraoperatively have been previously described. A two-circuit strategy that uses the in situ venovenous extracorporeal membrane oxygenation circuit supplemented with peripheral cardiopulmonary bypass allows for diversion of native cardiac output away from the transplanted lung as well as seamless continuation of venovenous extracorporeal membrane oxygenation postoperatively.

Hydroxocobalamin for treatment of catecholamine-resistant vasoplegia during liver transplantation: A single-center series of 20 cases.

INTRODUCTION: Catecholamine-resistant vasoplegia is a potentially devastating complication during liver transplantation. Hydroxocobalamin has emerged as a treatment for vasoplegia associated with cardiac surgery, liver transplantation, and septic shock. PRESENTATION OF CASE: We performed a retrospective review of patients who underwent liver transplantation between October 2015 and May 2020 to evaluate the efficiency of hydroxocobalamin in this setting. DISCUSSION: A total of 137 patients underwent liver transplantation, of which 20 received hydroxocobalamin for vasoplegia. Administration of hydroxocobalamin increased mean arterial pressure and reduced vasoactive drug requirements. CONCLUSION: This case series adds to the previous individual reports describing the use of hydroxocobalamin during liver transplantation suggesting hydroxocobalamin can mitigate refractory hypotension from catecholamine resistant vasoplegia during liver transplantation.

Blockade of endothelial Mas receptor restores the vasomotor response to phenylephrine in human resistance arterioles pretreated with captopril and exposed to propofol.

BACKGROUND: Hypotension that is resistant to phenylephrine is a complication that occurs in anesthetized patients treated with angiotensin converting enzyme (ACE) inhibitors. We tested the hypothesis that Ang 1-7 and the endothelial Mas receptor contribute to vasodilation produced by propofol in the presence of captopril. METHODS: The internal diameters of human adipose resistance arterioles were measured before and after administration of phenylephrine (10-9 to 10-5 M) in the presence and absence of propofol (10-6 M; added 10 min before the phenylephrine) or the Mas receptor antagonist A779 (10-5 M; added 30 min before phenylephrine) in separate experimental groups. Additional groups of arterioles were incubated for 16 to 20 h with captopril (10-2 M) or Ang 1-7 (10-9 M) before experimentation with phenylephrine, propofol, and A779. RESULTS: Propofol blunted phenylephrine-induced vasoconstriction in normal vessels. Captopril pretreatment alone did not affect vasoconstriction, but the addition of propofol markedly attenuated the vasomotor response to phenylephrine. A779 alone did not affect vasoconstriction in normal vessels, but it restored vasoreactivity in arterioles pretreated with captopril and exposed to propofol. Ang 1-7 reduced the vasoconstriction in response to phenylephrine. Addition of propofol to Ang 1-7-pretreated vessels further depressed phenylephrine-induced vasoconstriction to an equivalent degree as the combination of captopril and propofol, but A779 partially reversed this effect. CONCLUSIONS: Mas receptor activation by Ang 1-7 contributes to phenylephrine-resistant vasodilation in resistance arterioles pretreated with captopril and exposed to propofol. These data suggest an alternative mechanism by which refractory hypotension may occur in anesthetized patients treated with ACE inhibitors.

A Ten-Year Analysis of Recent National Institutes of Health Funding for Anesthesiology Research in United States Medical Schools.

OBJECTIVES: The characteristics of recent National Institutes of Health (NIH) grant funding to anesthesiology researchers in United States (US) medical schools have not been systematically quantified. NIH funding to cardiac anesthesiologists has also not been estimated. The author conducted an internet-based analysis of NIH awards to anesthesiology researchers from 2011-2020 to identify the types, duration of funding, and amount of grants, and the terminal degree(s), faculty rank, gender, board certification status, and type of appointment of the grant recipients including those with an interest in cardiac anesthesiology. DESIGN: Observational study. SETTING: Internet analysis. PARTICIPANTS: NIH grants recipients. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: NIH grant recipients affiliated with anesthesiology departments were identified from the Blue Ridge Institute for Medical Research website. The number of grants, years of support, and total amount of funding were quantified for research project grants (R series), mentored career development awards (K series), and other grants (U and P series) using NIH Research Portfolio Online Reporting Tools. The terminal degree(s), faculty rank, gender, and type of appointment of grant recipients were identified using department web pages. American Board of Anesthesiology (ABA) certification, National Board of Echocardiography Advanced Perioperative Transesophageal Echocardiography (TEE) certification, and previous or current Foundation for Anesthesia Education and Research (FAER) awards to NIH grant recipients were obtained from each organization's website. A total of 532 researchers received 1250 grants with 3844 cumulative years of funding amounting to $1,676,482,440. R series grants accounted for three-quarters of all funding. PhDs were awarded more than one-half of NIH grants. MDs had lower median numbers of projects, R01 grants, and total R series grants than their colleagues with PhD or MD PhD degrees, but MDs received more K awards. One hundred ninety-eight MD and MD PhD NIH grant recipients were ABA diplomates. These physician-scientists received 26.0% and 53.1% of R and K series grants, respectively. Thirty physician-scientists also held TEE certification; these individuals with an interest in cardiac anesthesiology were awarded 4.8% of all NIH grants. Full Professors were awarded more than three-quarters of R grants and amassed more than $1.3 billion in funding, whereas assistant and associate professors received the majority of K series grants. Male investigators received greater median R grants but fewer median K awards than female researchers. One hundred-fifteen previous or current holders of FAER grants were identified; these individuals earned a total of 240 NIH awards totaling $357.7 million. CONCLUSION: PhDs, Professors, and male researchers receive the majority of R01 and other R series grants to anesthesiology departments at US medical schools. Physician-scientists, including those interested in cardiac anesthesiology, are awarded a minority of R series grants. FAER continues to provide an important stimulus for subsequent NIH funding of physician-scientists in anesthesiology.

Left hemothorax resulting from delayed right ventricular apical pacing lead perforation without hemopericardium, a case report.

INTRODUCTION AND IMPORTANCE: Right ventricular pacemaker lead perforation is a rare but well documented complication of pacemaker implantation. Lead perforation can cause an array of symptoms ranging from none to hemodynamic instability and tamponade. In previously reported cases, lead perforation has always been able to be confirmed by imaging, with computed tomography (CT) scan considered to be the gold standard diagnostic imaging modality. CASE PRESENTATION: An 80-year-old male underwent uncomplicated implantation of a dual chamber pacemaker for sick sinus syndrome as an outpatient. Thirty-nine days later, the patient presented to the emergency department complaining of new-onset, left-sided, pleuritic chest pain. He was found to have unilateral hemothorax and abnormal pacemaker lead interrogation. Pacemaker lead perforation was suspected but not confirmed with imaging. Lead perforation was only identified after surgical exploration. CLINICAL DISCUSSION: This patient had multiple risk factors for pacemaker lead perforation. However, imaging, including CT scan was unable to confirm perforation. The presence of an otherwise unexplained left hemothorax strongly suggested that surgical intervention was indicated. The lead perforation was subsequently confirmed with subxiphoid exploration of the pericardial space. The mechanism of lead perforation resulting in hemothorax in this case is not straight forward, as no direct communication between the pericardial and pleural spaces was identified. However, previously described visceral pericardial self-sealing may contribute to the small pericardial accumulation described herein. CONCLUSION: This patient's presentation and clinical course underscore the importance of maintaining a high index of suspicion for pacemaker lead perforation despite a lack of confirmation with imaging.