Critically ill patients are often hemodynamically unstable (or at risk of becoming unstable) owing to hypovolemia, cardiac dysfunction, or alterations of vasomotor function, leading to organ dysfunction, deterioration into multi-organ failure, and eventually death. With hemodynamic monitoring, we aim to guide our medical management so as to prevent or treat organ failure and improve the outcomes of our patients. Therapeutic measures may include fluid resuscitation, vasopressors, or inotropic agents. Both resuscitation and de-resuscitation phases can be guided using hemodynamic monitoring. This monitoring itself includes several different techniques, each with its own advantages and disadvantages, and may range from invasive to less- and even non-invasive techniques, calibrated or non-calibrated. This article will discuss the indications and basics of monitoring, further elaborating on the different techniques of monitoring.

The causes of kidney allograft failure: more than allo-immunity. A viewpoint paper.

Over recent decades, hemodynamic monitoring has evolved from basic cardiac output monitoring techniques to a broad variety of sophisticated monitoring devices with extra parameters. In order to reduce morbidity and mortality and optimize therapeutic strategies, different monitoring techniques can be used to guide fluid resuscitation and other medical management. Generally, they can be divided in calibrated and non-calibrated techniques. In the first part of this review, the available calibrated techniques, ranging from invasive to non-invasive, will be discussed. We performed a review of the literature in order to give an overview of the current hemodynamic monitoring devices. For each monitoring system, a short overview of the physical principles, the advantages and disadvantages and the available literature with regard to validation is given. Currently, many promising hemodynamic monitoring devices are readily available in order to optimize therapeutic management in both perioperative and ICU settings. Although several of these calibrated techniques have been validated in the literature, not all techniques have been shown to reduce morbidity and mortality. Many new techniques, especially some non-calibrated devices, lack good validation data in different clinical settings (sepsis, trauma, burns, etc.). The cardiac output values obtained with these techniques need therefore to be interpreted with caution as will be discussed in the second part of this concise review. Transthoracic echocardiography forms a good initial choice to assess hemodynamics in critically ill patients after initial stabilisation. However in complex situations or in patients not responding to fluid resuscitation alone, advanced hemodynamic monitoring is recommended with the use of calibrated techniques like transpulmonary thermodilution. Calibrated techniques are preferred in patients with severe shock and changing conditions of preload, afterload and contractility. The use of the pulmonary artery catheter should be reserved for patients with right ventricular failure in order to assess the effect of medical treatment.

No abstract

on the genesis of bubbles as a result of rapid decompreBsion.

There is much evidence that fluid overload leads to adverse outcomes in perioperative and critically ill patients. Cardiac output monitoring can help us guiding initial and ongoing fluid resuscitation and can help us to assess whether a patient will be responsive to fluids when hypotensive. In recent years, many sophisticated devices that measure a variety of hemodynamic parameters have evolved on the market. We wanted to provide an overview of the different techniques available today, including their validation in different patient populations. In this second part of the review, we focus on non-calibrated techniques, both invasive and non-invasive. For each technique a short overview of the working principle, together with the advantages, disadvantages and the available validation literature is listed. Many promising minimal invasive monitoring devices can help us to further optimize our hemodynamic treatment in both the perioperative and critical care setting. However, the validation data are scarce for many of these techniques, especially in complex circumstances with changing hemodynamics (preload, afterload and contractility), as with the use of fluids and vasoactive medication. The measurements made by these devices, therefore, need to be interpreted with caution. Further improvements and more validation data are needed before these techniques can be implemented in common day practice. Moreover, in severely shocked hemodynamic unstable patients, calibrated techniques are to be preferred over those which are uncalibrated. Hence, the new techniques not only need to be accurate, but also need to be precise in order to keep track of changes.

Background The identification of complement defects as major drivers of primary atypical hemolytic uremic syndrome (HUS) has transformed the landscape of thrombotic microangiopathies (TMAs), leading to the development of targeted therapies and better patient outcomes. By contrast, little is known about the presentation, genetics, and outcomes of TMA associated with specific diseases or conditions, also referred to as secondary TMA. Methods In this study, we assessed the relative incidence, clinical and genetic spectra, and long-term outcomes of secondary TMA versus other TMAs in consecutive patients hospitalized with a first episode of TMA from 2009 to 2019 at two European reference centers. Results During the study period, 336 patients were hospitalized with a first episode of TMA. Etiologies included atypical HUS in 49 patients (15%), thrombotic thrombocytopenic purpura (TTP) in 29 (9%), shigatoxin-associated HUS in 70 (21%), and secondary TMA in 188 (56%). The main causes of secondary TMA were hematopoietic stem-cell transplantation (n=56, 30%), solid-organ transplantation (n=44, 23%), and malignant hypertension (n=25, 13%). Rare variants in complement genes were identified in 32 of 49 patients (65%) with atypical HUS and eight of 64 patients (13%) with secondary TMA; pathogenic or likely pathogenic variants were found in 24 of 49 (49%) and two of 64 (3%) of them, respectively (P < 0.001). After a median follow-up of 1157 days, death or kidney failure occurred in 14 (29%), eight (28%), five (7%), and 121 (64%) patients with atypical HUS, TTP, shigatoxin-associated HUS, and secondary TMA, respectively. Unadjusted and adjusted Cox regressions showed that patients with secondary TMA had the highest risk of death or kidney failure (unadjusted hazard ratio [HR], 3.35; 95% confidence interval [CI], 1.85 to 6.07; P < 0.001; adjusted HR, 4.11; 95% CI, 2.00 to 8.46; P < 0.001; considering atypical HUS as reference). Conclusions Secondary TMAs represent the main cause of TMA and are independently associated with a high risk of death and progression to kidney failure.

In respiratory physiology it is often desirable to maintain the end-tidal PCO2 and PO2 at adjustable levels independent of each other, e.g., when taking steady-state CO2 or O2 response curves, or when studying the ventilatory effects of exercise or drugs at constant levels of PCO2 and PO2. Based on the closed respiratory circuit described by Folgering et al. (1974), a new version was designed. The main new features of this version are that end-tidal PO2 instead of inspiratory PO2 can be kept constant, and that the correcting activity of both controllers (capnostat and oxystat) is proportional to the magnitude of the difference between the actual and the adjusted end-tidal PCO2 or PO2. An optic as well as an acoustic alarm is provided and will be switched on whenever no end-tidal PO2 is detected for an adjustable time.