Introduction Venous congestion is a pathophysiological state where high venous pressures cause organ oedema and dysfunction. Venous congestion is associated with worse outcomes, particularly acute kidney injury (AKI), for critically ill patients. Venous congestion can be measured by Doppler ultrasound at the bedside through interrogation of the inferior vena cava (IVC), hepatic vein (HV), portal vein (PV) and intrarenal veins (IRV). The objective of this study is to quantify the association between Doppler identified venous congestion and the need for renal replacement therapy (RRT) or death for patients with septic shock. Methods and analysis This study is a prespecified substudy of the ANDROMEDA-SHOCK 2 (AS-2) randomised control trial (RCT) assessing haemodynamic resuscitation in septic shock and will enrol at least 350 patients across multiple sites. We will include adult patients within 4 hours of fulfilling septic shock definition according to Sepsis-3 consensus conference. Using Doppler ultrasound, physicians will interrogate the IVC, HV, PV and IRV 6–12 hours after randomisation. Study investigators will provide web-based educational sessions to ultrasound operators and adjudicate image acquisition and interpretation. The primary outcome will be RRT or death within 28 days of septic shock. We will assess the hazard of RRT or death as a function of venous congestion using a Cox proportional hazards model. Sub-distribution HRs will describe the hazard of RRT given the competing risk of death. Ethics and dissemination We obtained ethics approval for the AS-2 RCT, including this observational substudy, from local ethics boards at all participating sites. We will report the findings of this study through open-access publication, presentation at international conferences, a coordinated dissemination strategy by investigators through social media, and an open-access workshop series in multiple languages. Trial registration number NCT05057611.

The resuscitation of a patient in shock is a highly complex endeavor that should go beyond normalizing mean arterial pressure and protocolized fluid loading. We propose a holistic, four-interface conceptual model of shock that we believe can benefit both clinicians at the bedside and researchers. The four circulatory interfaces whose uncoupling results in shock are as follows: the left ventricle to arterial, the arterial to capillary, the capillary to venular, and finally the right ventricle to pulmonary artery. We review the pathophysiology and clinical consequences behind the uncoupling of these interfaces, as well as how to assess them, and propose a strategy for approaching a patient in shock. Bedside assessment of shock may include these critical interfaces in order to avoid hemodynamic incoherence and to focus on microcirculatory restoration rather than simply mean arterial pressure. The purpose of this model is to serve as a mental model for learners as well as a framework for further resuscitation research that incorporates these concepts.

Right ventricular dysfunction (RVD) is a complication following congenital cardiac surgery in children and can lead to systemic venous congestion, low cardiac output, and organ dysfunction. Venous congestion can be transmitted backwards and adversely affect encapsulated organs such as the kidneys. To investigate the association between systemic venous congestion, as estimated by Venous Excess Ultrasound (VExUS), and the occurrence of acute kidney injury (AKI) in children with RVD following congenital heart surgery. Secondary objectives included comparing changes in VExUS scores after initiating treatment for RVD and venous congestion. This was a prospective observational study in children with RVD. The VExUS study was performed on day 1, day 2, and day 3 and categorized as VExUS-1, VExUS-2, and VExUS-3. Among 43 patients with RVD and dilated inferior vena cava, 19/43 (44%), 10/43 (23%), and 12/43 (28%) were VExUS-2 and VExUS-3, respectively. There was an association between severe RVD and elevated pulmonary artery systolic pressures and a VExUS score >2. A significant association was observed between central venous pressure (CVP) measurements and VExUS. Among 31 patients with a high VExUS score >2, 18 (58%) had AKI. Additionally, improvement in CVP and fluid balance was associated with improving VExUS scores following targeted treatment for RVD. VExUS serves as a valuable bedside tool for diagnosing and grading venous congestion through ultrasound Doppler. An elevated VExUS score was associated with the occurrence of AKI, and among the components of VExUS, portal vein pulsatility may be useful as a predictor of AKI. Natraj R, Bhaskaran AK, Rola P, Haycock K, Siuba MTT, Ranjit S. Venous Congestion Assessed by Venous Excess Ultrasound (VExUS) and Acute Kidney Injury in Children with Right Ventricular Dysfunction. Indian J Crit Care Med 2024;28(5):447–452.

Background Management of acute kidney injury (AKI) in the ED can be difficult due to uncertainty regarding the aetiology. This study investigated the diagnostic value of venous system ultrasound for determining the aetiological subtypes of AKI in the ED. Methods This multidisciplinary prospective cohort study was conducted in a single academic ED over the course of a year. Adult patients with AKI were evaluated using the venous excess ultrasound (VExUS) score, which is a four-step ultrasound protocol. The protocol begins with the inferior vena cava (IVC) measurement and examines organ flow patterns, including portal, hepatic and renal veins in the presence of dilated IVC. The AKI subtypes (hypovolaemia, cardiorenal, systemic vasodilatation and renal) were adjudicated by nephrologists and emergency physicians, considering data that became available during the hospitalisation. We determined the diagnostic test characteristics of VExUS for identifying each of the four AKI aetiological subtypes. Results 150 patients with AKI were included in the study. Hypovolaemia was the most frequent finally adjudicated cause of AKI (66%), followed by cardiorenal (18%), systemic vasodilatation (8.7%) and renal (7.3%). In diagnosing the cardiorenal subtype, the area under the curve (AUC) for VExUS grade >0 was 0.819, with 77.8% sensitivity and 80.5% specificity, and the AUC for IVC maximum diameter >20.4 mm was 0.865, with 74.1% sensitivity and 86.2% specificity. For the hypovolaemia subtype, the AUC for VExUS grade ≤0 was 0.711, with 83.8% sensitivity and 56.9% specificity, and the AUC for IVC maximum diameter ≤16.8 mm was 0.736, with 73.7% sensitivity and 68.6% specificity. None of the parameters achieved adequate test characteristics for renal and systemic vasodilatation subtypes. Conclusion The VExUS score has good diagnostic accuracy for cardiorenal AKI and fair accuracy for hypovolaemic AKI but cannot identify renal and systemic vasodilatation subtypes. It should not therefore be used in isolation to determine the cause of AKI in the ED. Trial registration number NCT04948710.

The resuscitation of the patient in shock is a highly complex endeavor which should go beyond normalizing mean arterial pressure and protocolized fluid loading. We propose a holistic, four interface conceptual model of shock which we feel can benefit both clinicians at the bedside and researchers. The four circulatory interfaces whose uncoupling result in shock are the left ventricle to arterial, the arterial to capillary, the capillary to venular and finally the right ventricle to pulmonary artery. We review the pathophysiology and clinical consequences behind the uncoupling of these interfaces as well as how to assess them and propose a strategy on how to approach the patient in shock. Bedside assessment of shock may include these critical interfaces in order to avoid hemodynamic incoherence and focus on microcirculatory restoration rather than simply mean arterial pressure. Further research may incorporate these concepts.

Critical closing pressure (CCP) and the vascular waterfall have long been used to explain perfusion failure in shock, yet their physiological meaning has been inconsistently interpreted. CCP is frequently treated as a continuous downstream pressure and inserted into formulas such as mean arterial pressure (MAP) − CCP, implying that a collapse threshold behaves like an opposing pressure even when vessels remain open. Drawing on classical vascular mechanics, whole-bed flow studies, microvascular models, and contemporary clinical physiology, we show that this interpretation is incorrect. Tone-dependent arteriolar collapse does not behave as a Starling resistor: CCP is a threshold at which smooth-muscle tension exceeds intraluminal pressure and vessels close, not a pressure governing flow in patent vessels. Perfusion becomes heterogeneous because different vascular beds reach their collapse thresholds at different pressures (via excessive tone, extrinsic compression, or profound hypotension), disconnecting macro-haemodynamics from microcirculatory flow. This explains why systemic variables such as MAP and systemic vascular resistance (SVR) may appear adequate even while tissues are under-perfused, a phenomenon now termed haemodynamic incoherence. Reframing CCP as a binary collapse threshold resolves longstanding contradictions in the literature, clarifies why MAP-centred targets often fail, and unifies the behaviour of shock states within a four-interface model of circulatory coupling. Therapeutically, the aim is not to “restore a waterfall” but to reopen closed vascular territories by lowering excessive tone, relieving external pressure, or raising truly low arterial inflow. This mechanistic reinterpretation provides a more coherent, physiologically grounded approach to personalised perfusion management in critical illness.