Current Opinion in Critical Care最新文献

Purpose of review: Mechanical ventilation may have adverse effects on diaphragm and lung function. Lung- and diaphragm-protective ventilation is an approach that challenges the clinician to facilitate physiological respiratory efforts, while maintaining minimal lung stress and strain. Here, we discuss the latest advances in monitoring and interventions to achieve lung- and diaphragm protective ventilation.

Recent findings: Noninvasive ventilator maneuvers (P0.1, airway occlusion pressure, pressure-muscle index) can accurately detect low and excessive respiratory efforts and high lung stress. Additional monitoring techniques include esophageal manometry, ultrasound, electrical activity of the diaphragm, and electrical impedance tomography. Recent trials demonstrate that a systematic approach to titrating inspiratory support and sedation facilitates lung- and diaphragm protective ventilation. Titration of positive-end expiratory pressure and, if available, veno-venous extracorporeal membrane oxygenation sweep gas flow may further modulate neural respiratory drive and effort to facilitate lung- and diaphragm protective ventilation.

Summary: Achieving lung- and diaphragm-protective ventilation may require more than a single intervention; it demands a comprehensive understanding of the (neuro)physiology of breathing and mechanical ventilation, along with the application of a series of interventions under close monitoring. We suggest a bedside-approach to achieve lung- and diaphragm protective ventilation targets.

Purpose of review: Respiratory drive is frequently deranged in the ICU, being associated with adverse clinical outcomes. Monitoring and modulating respiratory drive to prevent potentially injurious consequences merits attention. This review gives a general overview of the available monitoring tools and interventions to modulate drive.

Recent findings: Airway occlusion pressure (P0.1) is an excellent measure of drive and is displayed on ventilators. Respiratory drive can also be estimated based on the electrical activity of respiratory muscles and measures of respiratory effort; however, high respiratory drive might be present in the context of low effort with neuromuscular weakness. Modulating a deranged drive requires a multifaceted intervention, prioritizing treatment of the underlying cause and adjusting ventilator settings for comfort. Additional tools include changes in PEEP, peak inspiratory flow, fraction of inspired oxygen, and sweep gas flow (in patients receiving extracorporeal life-support). Sedatives and opioids have differential effects on drive according to drug category. Monitoring response to any intervention is warranted and modulating drive should not preclude readiness to wean assessment or delay ventilation liberation.

Summary: Monitoring and modulating respiratory drive are feasible based on physiological principles presented in this review. However, evidence arising from clinical trials will help determine precise thresholds and optimal interventions.

Purpose of review: Venovenous extracorporeal membrane oxygenation (VV-ECMO) provides gas exchange for patients with advanced respiratory failure who cannot maintain adequate oxygenation or carbon dioxide (CO2) clearance through conventional mechanical ventilation. This review examines clinical applications of VV-ECMO with a focus on optimizing oxygen delivery and CO2 removal.

Recent findings: Over the past two decades, VV-ECMO utilization has expanded, now serving as a bridge to recovery in cases of severe hypoxemic and hypercapnic respiratory failure, as procedural support, and as a bridge to lung transplantation. Recent data have corroborated the role of VV-ECMO in managing acute respiratory distress syndrome (ARDS), and guidelines from the American Thoracic Society (ATS) and the European Society of Intensive Care Medicine (ESICM) now recommend it be considered for severe ARDS.

Summary: This review aims to provide insights into the evolving role of VV-ECMO in the management of critical respiratory failure. Key determinants of oxygenation are discussed, particularly optimizing the ratio of VV-ECMO blood flow to cardiac output (CO). We analyze factors influencing CO2 clearance and review available VV-ECMO configurations and their effects on gas exchange. We discuss practical targets for oxygenation and CO2 removal in VV-ECMO, along with adjunctive techniques for refractory hypoxemia and hypercapnia.

Purpose of review: The increasing use of prone position, in intubated patients with acute respiratory distress syndrome as well as in patients with acute hypoxemic respiratory failure receiving noninvasive respiratory support, mandates a better definition and monitoring of the response to the manoeuvre. This review will first discuss the definition of the response to prone positioning, which is still largely based on its effect on oxygenation. We will then address monitoring respiratory and hemodynamic responses to prone positioning in intubated patients. Finally, we will also discuss monitoring inspiratory effort in nonintubated patients with acute hypoxemic respiratory failure who breathe spontaneously and receive noninvasive respiratory support.

Recent findings: The response to prone positioning should be enriched by data pertaining to lung protection beyond oxygenation. These include trans-pulmonary pressure, driving pressure, mechanical power, distribution of aeration and ventilation and assessment of potential for lung recruitment before the pronation.

Summary: The implications of present findings are to: better select those patients who will benefit from proning in physiological terms, better indicate the timing of onset and end of the sessions, and strengthen the relationship between physiological response and patient outcome.

Purpose of review: This review aims to examine recent advances in the understanding of injury-induced endotheliopathy and therapeutics to mitigate its development in critically injured patients.

Recent findings: Clinical studies have clearly demonstrated that syndecan-1 ectodomains can be found in circulation after various types of trauma and injury and correlates with worse outcomes. As the mechanisms of endotheliopathy are better understood, pathologic hyperadhesive forms of von Willebrand factor, along with a relative deficiency of its cleaving enzyme, a disintegrin and metalloprotease with thrombospondin type I motifs, member 13 (ADAMTS13), have emerged as additional biomarkers. Therapeutics to date have focused primarily on the protective effects of fresh frozen plasma and its constituents to restore the glycocalyx. Human recombinant ADAMTS13 holds promise, as do synthetic variants of heparan sulfate and activated protein C, although all data to date are preclinical.

Summary: Injury-induced endotheliopathy represents an important pathologic response to trauma. Key biomarkers, such as syndecan-1, can aid in the diagnosis, but testing is not yet available clinically. As the mechanisms of endotheliopathy are better understood, therapeutics are being identified and show promise. To date, plasma has been the most widely studied; however, like all therapeutics for injury-induced endotheliopathy, it has primarily been studied in the preclinical setting.

Purpose of review: This review discusses novel concepts of acute kidney injury (AKI), including subphenotyping, which may facilitate the development of target treatment strategies for specific subgroups of patients to achieve precision medicine.

Recent findings: AKI is a multifaceted syndrome with a major impact on morbidity and mortality. As efforts to identify treatment strategies have largely failed, it is becoming increasingly apparent that there are different subphenotypes that require different treatment strategies. Various ways of subphenotyping AKI have been investigated, including the use of novel renal biomarkers, machine learning and artificial intelligence, some of which have already been implemented in the clinical setting. Thus, novel renal biomarkers have been recommended for inclusion in new definition criteria for AKI and for the use of biomarker bundled strategies for the prevention of AKI. Computational models have been explored and require future research.

Summary: Subphenotyping of AKI may provide a new understanding of this syndrome and guide targeted treatment strategies in order to improve patient outcomes.

Purpose of review: Acute kidney injury (AKI) is commonly encountered in critical care medicine as is intravenous fluid therapy. It is accepted that there is interplay between fluid use and AKI, both potentially positive and negative. An understanding of the physiological rationale for fluid is important to help clinicians when considering fluid therapy in patients with, or at risk for AKI; this includes understanding choice of fluid, method of monitoring, administration and clinical sequelae.

Recent findings: There is increasing interest in combining both static and dynamic measures to assess fluid balance, fluid responsiveness effects of fluid therapy, which are areas requiring ongoing study to translate this theory into clinically useful practice at the bedside. Whilst the debate of choice of crystalloid in ICU practice continues, further evidence for benefits for balanced solutions emerges in the form of international guidelines and patient data meta-analysis of previously performed trials.

Summary: This review assesses the physiological rationale for fluid use in ICU cohorts with AKI of various types, as well as a systematic approach for choice of fluid therapy using a number of different variables, which aims to help guide clinicians in managing fluid use and fluid balance in critically ill patients with AKI.

Purpose of review: The aim of this study was to outline recent developments in calcium channel blocker (CCB) poisoning. The dihydropyridine CCB amlodipine is commonly prescribed in the United States, and amlodipine poisoning is increasing in frequency, presenting new challenges for clinicians because current paradigms of CCB poisoning management arose from literature on non-dihydropyridine agents.

Recent findings: Amlodipine is now the most common CCB involved in poisoning. High-dose insulin is a potent inotrope and vasodilator; as such, it should be used cautiously, and typically in conjunction with vasopressors, as it theoretically may worsen vasodilation in amlodipine poisoning. High-dose insulin is best used when some degree of cardiogenic shock is suspected. Venoarterial extracorporeal membrane oxygenation utilization in CCB poisoning appears to be increasing, but high flow rates may be needed to combat amlodipine-induced vasoplegia. Intravenous lipid emulsion cannot be routinely recommended but may have a role in peri-arrest situations. Adjunct treatments such as angiotensin II, methylene blue, and hydroxocobalamin offer theoretical benefit but warrant further study.

Summary: Amlodipine causes most cases of CCB poisoning and can induce both cardiogenic and distributive shock through multiple mechanisms. Clinicians should tailor treatment to suspected shock etiology, be aware of adjunct treatments for refractory shock, and consult an expert in poisoning.