Worldwide, the 2 leading causes of mortality are heart disease and stroke, which combined, account for more than 25% of mortal events (15 million events).¹ Surprisingly, the third leading contributor to deaths on a global scale is postoperative death within 30 days, estimated to occur among 4.2 million people (7.7%) who die each year worldwide.^1,2 While it does not constitute its own category in mortality tables published by the Centers for Disease Control and Prevention, the magnitude of 30-day postoperative mortality was approximately the third leading contributor to all-cause death in the United States until COVID-19.² There are an estimated 48.4 million surgical procedures performed in the United States annually,³ and 30-day postoperative complications may arise in up to 15% of patients. These were estimated to cost hospitals more than $11 000 per case, amounting to more than $31.35 billion nationally per year.^4,5 Improving health outcomes after surgery represents an enormous opportunity, and improvement in surgical quality and health care costs is a priority for health care services and payors. Of the 15% of patients who experience complications, 50% are patients considered to be high risk.^4,5 To reduce surgical complications and improve postoperative outcomes, focus has shifted to preoperative and perioperative care for patients at high risk. However, there are few predictive tools that allow hospitals to identify these individuals with high risk in a timely and accurate manner.

Health care is undergoing major transformation with a shift from fee-for-service care to fee-for-value. The advent of new care delivery and payment models is serving as a driver for value-based care. Hospitals, payors, and patients increasingly expect physicians and healthcare systems to improve outcomes and manage costs. The impact of the coronavirus disease 2019 (COVID-19) pandemic on surgical and procedural practices further highlights the urgency and need for anesthesiologists to expand their roles in perioperative care, and to impact system improvement. While there have been substantial advances in anesthesia care, perioperative complications and mortality after surgery remain a key concern. Anesthesiologists are in a unique position to impact perioperative health care through their multitude of interactions and influences on various aspects of the perioperative domain, by using the surgical experience as the first touchpoint to reengage the patient in their own health care. Among the key interventions that are being effectively instituted by anesthesiologists include proactive engagement in preoperative optimization of patients’ health; personalization and standardization of care delivery by segmenting patients based upon their complexity and risk; and implementation of best practices that are data-driven and evidence-based and provide structure that allow the patient to return to their optimal state of functional, cognitive, and psychologic health. Through collaborative relationships with other perioperative stakeholders, anesthesiologists can consolidate their role as clinical leaders driving value-based care and healthcare transformation in the best interests of patients.

Background: Neuraxial modulation, including spinal cord stimulation, reduces cardiac sympathoexcitation and ventricular arrhythmogenesis. There is an incomplete understanding of the molecular mechanisms through which spinal cord stimulation modulates cardiospinal neural pathways. The authors hypothesize that spinal cord stimulation reduces myocardial ischemia–reperfusion—induced sympathetic excitation and ventricular arrhythmias through γ-aminobutyric acid (GABA)–mediated pathways in the thoracic spinal cord. Methods: Yorkshire pigs were randomized to control (n = 11), ischemia–reperfusion (n = 16), ischemia–reperfusion plus spinal cord stimulation (n = 17), ischemia–reperfusion plus spinal cord stimulation plus γ-aminobutyric acid type A (GABA_A) or γ-aminobutyric acid type B (GABA_B) receptor antagonist (GABA_A, n = 8; GABA_B, n = 8), and ischemia–reperfusion plus GABA transaminase inhibitor (GABAculine, n = 8). A four-pole spinal cord stimulation lead was placed epidurally (T1 to T4). GABA modulating pharmacologic agents were administered intrathecally. Spinal cord stimulation at 50 Hz was applied 30 min before ischemia. A 56-electrode epicardial mesh was used for high-resolution electrophysiologic recordings, including activation recovery intervals and ventricular arrhythmia scores. Immunohistochemistry and Western blots were performed to measure GABA receptor expression in the thoracic spinal cord. Results: Cardiac ischemia led to myocardial sympathoexcitation with reduction in activation recovery interval (mean ± SD, –42 ± 11%), which was attenuated by spinal cord stimulation (–21 ± 17%, P = 0.001). GABA_A and GABA_B receptor antagonists abolished spinal cord stimulation attenuation of sympathoexcitation (GABA_A, –9.7 ± 9.7%, P = 0.043 vs. ischemia–reperfusion plus spinal cord stimulation; GABA_B, –13 ± 14%, P = 0.012 vs. ischemia–reperfusion plus spinal cord stimulation), while GABAculine alone caused a therapeutic effect similar to spinal cord stimulation (–4.1 ± 3.7%, P = 0.038 vs. ischemia–reperfusion). The ventricular arrhythmia score supported these findings. Spinal cord stimulation during ischemia–reperfusion increased GABA_A receptor expression with no change in GABA_B receptor expression. Conclusions: Thoracic spinal cord stimulation reduces ischemia–reperfusion—induced sympathoexcitation and ventricular arrhythmias through activation of GABA signaling pathways. These data support the hypothesis that spinal cord stimulation–induced release of GABA activates inhibitory interneurons to decrease primary afferent signaling from superficial dorsal horn to sympathetic output neurons in the intermediolateral nucleus. Editor’s Perspective: What We Already Know about This Topic: What This Article Tells Us That Is New:

Introduction: Myocardial ischemia disrupts the cardio-spinal neural network that controls the cardiac sympathetic preganglionic neurons, leading to sympathoexcitation and ventricular tachyarrhythmias (VTs). Spinal cord stimulation (SCS) is capable of suppressing the sympathoexcitation caused by myocardial ischemia. However, how SCS modulates the spinal neural network is not fully known.Methods: In this pre-clinical study, we investigated the impact of SCS on the spinal neural network in mitigating myocardial ischemia-induced sympathoexcitation and arrhythmogenicity. Ten Yorkshire pigs with left circumflex coronary artery (LCX) occlusion-induced chronic myocardial infarction (MI) were anesthetized and underwent laminectomy and a sternotomy at 4−5 weeks post-MI. The activation recovery interval (ARI) and dispersion of repolarization (DOR) were analyzed to evaluate the extent of sympathoexcitation and arrhythmogenicity during the left anterior descending coronary artery (LAD) ischemia. Extracellular in vivo and in situ spinal dorsal horn (DH) and intermediolateral column (IML) neural recordings were performed using a multichannel microelectrode array inserted at the T2-T3 segment of the spinal cord. SCS was performed for 30 min at 1 kHz, 0.03 ms, 90% motor threshold. LAD ischemia was induced pre- and 1 min post-SCS to investigate how SCS modulates spinal neural network processing of myocardial ischemia. DH and IML neural interactions, including neuronal synchrony as well as cardiac sympathoexcitation and arrhythmogenicity markers were evaluated during myocardial ischemia pre- vs. post-SCS.Results: ARI shortening in the ischemic region and global DOR augmentation due to LAD ischemia was mitigated by SCS. Neural firing response of ischemia-sensitive neurons during LAD ischemia and reperfusion was blunted by SCS. Further, SCS showed a similar effect in suppressing the firing response of IML and DH neurons during LAD ischemia. SCS exhibited a similar suppressive impact on the mechanical, nociceptive and multimodal ischemia sensitive neurons. The LAD ischemia and reperfusion-induced augmentation in neuronal synchrony between DH-DH and DH-IML pairs of neurons were mitigated by the SCS.Discussion: These results suggest that SCS is decreasing the sympathoexcitation and arrhythmogenicity by suppressing the interactions between the spinal DH and IML neurons and activity of IML preganglionic sympathetic neurons.

Extracorporeal membrane oxygenation (ECMO) is a cardiac or pulmonary function support system that is used in cases of refractory organ failure in addition to conventional treatment. Currently, Level I evidence is not yet available, which reflects improved outcomes with ECMO in pregnant women, the use in pregnancy should be indicated in selected cases and only in specialized centers. We searched articles in the most important scientific databases from 2009 until 31 December 2023 consulting also the site ClinicalTrials.com to find out about studies that have been recently conducted or are currently ongoing. We matched the combination of the following keywords: “ECMO and pregnancy”, “H1N1 and pregnancy”, “COVID-19 and pregnancy”, “ARDS and pregnancy”, “ECMO and pregnancy AND (cardiac arrest)”. We selected the following number of articles for each keyword combination: “ECMO and pregnancy” (665 articles); “ECMO and influenza H1N1” (384 articles); “pregnancy and influenza H1N1” (1006 articles); “pregnancy and ARDS” (2930 articles); “ECMO and pregnancy and ARDS and influenza H1N1” (24 articles); and “[ECMO and pregnancy AND (cardiac arrest)]” (74 articles). After careful inspection, only 43 papers fitted our scope. There are two types of ECMO: venous-venous (VV-ECMO) and venous-arterial (VA-ECMO). The first-one is necessary to cope with severe hypoxia: oxygen-depleted blood is taken from the venous circulation, oxygenated, and carbon dioxide removed from the extracorporeal circuit and returned to the same venous system. The VA-ECMO is a type of mechanical assistance to the circulatory system that allows to put the failing organ at rest by ensuring adequate oxygenation and systemic de-oxygenation, avoiding multi-organ failure. The main indications for ECMO support in pregnant women are cardiogenic shock, acute respiratory distress syndrome (ARDS), pulmonary embolism, and eclampsia. There are also fetal indications for ECMO, and they are fetal distress, hypoxic-ischemic encephalopathy (HIE), and twin-to-twin transfusion syndrome (TTTS). Until now, based on the outcomes of the numerous clinical studies conducted, ECMO has been shown to be a successful therapeutic strategy in cases where medical treatment has been unsuccessful. In well-selected pregnant patients, it appears to be safe and associated with a low risk of maternal and fetal complications. The aim of this review is to report the main properties of ECMO (VV and VA) and the indications for its use in pregnant women.