Extravascular lung water (EVLW) is the amount of fluid that is accumulated in the interstitial and alveolar spaces. In lung oedema, EVLW increases either because of increased lung permeability or because of increased hydrostatic pressure in the pulmonary capillaries, or both. Increased EVLW is always potentially life-threatening, mainly because it impairs gas exchange and reduces lung compliance. The only technique that provides an easy measurement of EVLW at the bedside is transpulmonary thermodilution. The validation of EVLW measurements by thermodilution was based on studies showing reasonable correlations with gravimetry or thermo-dye dilution in experimental and clinical studies. EVLW should be indexed to predicted body weight. This indexation reduces the proportion of ARDS patients for whom EVLW is in the normal range. Compared to non-indexed EVLW, indexed EVLW (EVLWI) is better correlated with the lung injury score and the oxygenation and it is a better predictor of mortality of patients with acute lung injury or acute respiratory distress syndrome (ARDS). Transpulmonary thermodilution also provides the pulmonary vascular permeability index (PVPI), which is an indirect reflection of the integrity of the alveolocapillary barrier. As clinical applications, EVLWI and PVPI may be useful to guide fluid management of patients at risk of fluid overload, as during septic shock and ARDS. High EVLWI and PVPI values predict mortality in several categories of critically ill patients, especially during ARDS. Thus, fluid administration should be limited when EVLWI is already high. Whatever the value of EVLWI, PVPI may indicate that fluid administration is particularly at risk of aggravating lung oedema. In the acute phase of haemodynamic resuscitation during septic shock and ARDS, high EVLWI and PVPI values may warn of the risk of fluid overload and prevent excessive volume expansion. At the post-resuscitation phase, they may prompt initiation of fluid removal thereby achieving a negative fluid balance.

In critically ill patients, changes in the velocity-time integral (VTI) of the left ventricular outflow tract, measured by transthoracic echocardiography (TTE), are often used to non-invasively assess the response to fluid administration or for performing tests assessing fluid responsiveness. However, the precision of TTE measurements has not yet been investigated in such patients. First, we aimed at assessing how many measurements should be averaged within one TTE examination to reach a sufficient precision for various variables. Second, we aimed at identifying the least significant change (LSC) of these variables between successive TTE examinations. We prospectively included 100 haemodynamically stable patients in whom TTE examination was planned. Three TTE examinations were performed, the first and the third by one operator and the second by another one. We calculated the precision and LSC (1) within one examination depending on the number of averaged measurements and (2) between measurements performed in two successive examinations. In patients in sinus rhythm, averaging three measurements within an examination was enough for obtaining an acceptable precision (interquartile range highest value < 10%) for VTI. In patients with atrial fibrillation, averaging five measurements was necessary. The precision of some other common TTE variables depending on the number of measurements is provided. Between two successive examinations performed by the same operator, the LSC was 11 [5–18]% for VTI. If two operators performed the examinations, the LSC for VTI significantly increased to 14 [8–26]%. The LSC between two examinations for other TTE variables is also provided. Averaging three measurements within one TTE examination is enough for obtaining precise measurements for VTI in patients in sinus rhythm but not in patients with atrial fibrillation. Between two TTE examinations performed by the same operator, the LSC of VTI is compatible with the assessment of the effects of a 500-mL fluid infusion but is not precise enough for assessing the effects of some tests predicting preload responsiveness.

A post-resuscitation shock occurs in 50–70% of patients who had a cardiac arrest. It is an early and transient complication of the post-resuscitation phase, which frequently leads to multiple-organ failure and high mortality. The pathophysiology of post-resuscitation shock is complex and results from the whole-body ischemia–reperfusion process provoked by the sequence of circulatory arrest, resuscitation manoeuvers and return of spontaneous circulation, combining a myocardial dysfunction and sepsis features, such as vasoplegia, hypovolemia and endothelial dysfunction. Similarly to septic shock, the hemodynamic management of post-resuscitation shock is based on an early and aggressive hemodynamic management, including fluid administration, vasopressors and/or inotropes. Norepinephrine should be considered as the first-line vasopressor in order to avoid arrhythmogenic effects of other catecholamines and dobutamine is the most established inotrope in this situation. Importantly, the optimal mean arterial pressure target during the post-resuscitation shock still remains unknown and may probably vary according to patients. Mechanical circulatory support by extracorporeal membrane oxygenation can be necessary in the most severe patients, when the neurological prognosis is assumed to be favourable. Other symptomatic treatments include protective lung ventilation with a target of normoxia and normocapnia and targeted temperature management by avoiding the lowest temperature targets. Early coronary angiogram and coronary reperfusion must be considered in ST-elevation myocardial infarction (STEMI) patients with preserved neurological prognosis although the timing of coronary angiogram in non-STEMI patients is still a matter of debate. Further clinical research is needed in order to explore new therapeutic opportunities regarding inflammatory, hormonal and vascular dysfunction.

Modalities of fluid management in patients sustaining the acute respiratory distress syndrome (ARDS) are challenging and controversial. Optimal fluid management should provide adequate oxygen delivery to the body, while avoiding inadvertent increase in lung edema which further impairs gas exchange. In ARDS patients, positive fluid balance has been associated with prolonged mechanical ventilation, longer ICU and hospital stay, and higher mortality. Accordingly, a restrictive strategy has been compared to a more liberal approach in randomized controlled trials conducted in various clinical settings. Restrictive strategies included fluid restriction guided by the monitoring of extravascular lung water, pulmonary capillary wedge or central venous pressure, and furosemide targeted to diuresis and/or albumin replacement in hypoproteinemic patients. Overall, restrictive strategies improved oxygenation significantly and reduced duration of mechanical ventilation, but had no significant effect on mortality. Fluid management may require different approaches depending on the time course of ARDS (i.e., early vs. late period). The effects of fluid strategy management according to ARDS phenotypes remain to be evaluated. Since ARDS is frequently associated with sepsis-induced acute circulatory failure, the prediction of fluid responsiveness is crucial in these patients to avoid hemodynamically inefficient—hence respiratory detrimental—fluid administration. Specific hemodynamic indices of fluid responsiveness or mini-fluid challenges should be preferably used. Since the positive airway pressure contributes to positive fluid balance in ventilated ARDS patients, it should be kept as low as possible. As soon as the hemodynamic status is stabilized, correction of cumulated fluid retention may rely on diuretics administration or renal replacement therapy.

The renin–angiotensin system (RAS) has long been described in the field of cardiovascular physiology as the main player in blood pressure homeostasis. However, other effects have since been described, and include proliferation, fibrosis, and inflammation. To illustrate the immunomodulatory properties of the RAS, we chose three distinct fields in which RAS may play a critical role and be the subject of specific treatments. In oncology, RAS hyperactivation has been associated with tumor migration, survival, cell proliferation, and angiogenesis; preliminary data showed promise of the benefit of RAS blockers in patients treated for certain types of cancer. In intensive care medicine, vasoplegic shock has been associated with severe macro- and microcirculatory imbalance. A relative insufficiency in angiotensin II (AngII) was associated to lethal outcomes and synthetic AngII has been suggested as a specific treatment in these cases. Finally, in solid organ transplantation, both AngI and AngII have been associated with increased rejection events, with a regional specificity in the RAS activity. These elements emphasize the complexity of the direct and indirect interactions of RAS with immunomodulatory pathways and warrant further research in the field.

Heart–lungs interactions are related to the interplay between the cardiovascular and the respiratory system. They result from the respiratory-induced changes in intrathoracic pressure, which are transmitted to the cardiac cavities and to the changes in alveolar pressure, which may impact the lung microvessels. In spontaneously breathing patients, consequences of heart–lungs interactions are during inspiration an increase in right ventricular preload and afterload, a decrease in left ventricular preload and an increase in left ventricular afterload. In mechanically ventilated patients, consequences of heart–lungs interactions are during mechanical insufflation a decrease in right ventricular preload, an increase in right ventricular afterload, an increase in left ventricular preload and a decrease in left ventricular afterload. Physiologically and during normal breathing, heart–lungs interactions do not lead to significant hemodynamic consequences. Nevertheless, in some clinical settings such as acute exacerbation of chronic obstructive pulmonary disease, acute left heart failure or acute respiratory distress syndrome, heart–lungs interactions may lead to significant hemodynamic consequences. These are linked to complex pathophysiological mechanisms, including a marked inspiratory negativity of intrathoracic pressure, a marked inspiratory increase in transpulmonary pressure and an increase in intra-abdominal pressure. The most recent application of heart–lungs interactions is the prediction of fluid responsiveness in mechanically ventilated patients. The first test to be developed using heart–lungs interactions was the respiratory variation of pulse pressure. Subsequently, many other dynamic fluid responsiveness tests using heart–lungs interactions have been developed, such as the respiratory variations of pulse contour-based stroke volume or the respiratory variations of the inferior or superior vena cava diameters. All these tests share the same limitations, the most frequent being low tidal volume ventilation, persistent spontaneous breathing activity and cardiac arrhythmia. Nevertheless, when their main limitations are properly addressed, all these tests can help intensivists in the decision-making process regarding fluid administration and fluid removal in critically ill patients.