BACKGROUND: Sodium glucose cotransporter-2 (SGLT-2) inhibitors are known to reduce hospitalization and cardiovascular mortality in various heart failure (HF) populations, potentially through enhanced excretion of water and sodium. However, there are concerns regarding the risk of acute kidney injury (AKI) associated with their use. This meta-analysis aimed to unravel the effects of SGLT-2 inhibitors on risk of AKI in a variety of patients with HF.
METHODS: This study conducted a comprehensive literature search using PubMed, EMBASE, Cochrane Library, and clinicaltrials.gov for studies published up to January 1, 2024. Data were analyzed using both random-effects or fixed-effects models to estimate the overall relative risk (RR) with a 95% confidence interval (CI).
RESULTS: Our analysis included 25,172 patients with HF from 16 randomized controlled trials. Treatment with SGLT-2 inhibitors led to a 28% reduction in the risk of AKI progression compared to placebo (RR 0.72, 95% CI 0.61-0.85, p<0.0001), without an increased risk of hypotension (RR 1.21, 95% CI 0.87-1.70, p = 0.26) and hypovolemia (RR 2.26, 95% CI: 0.70-7.33, p = 0.17). Notably, SGLT-2 inhibitors significantly decreased AKI in specific subgroups, including patients with HF with reduced ejection fraction (RR 0.59, 95% CI 0.43-0.80, p = 0.0007), those treated with empagliflozin (RR 0.70, 95% CI 0.57-0.88, p = 0.002) or dapagliflozin (RR 0.74, 95% CI 0.57-0.98, p = 0.04), in studies with a follow-up of at least 1 year (RR 0.67, 95% CI 0.55-0.82, p = 0.0001), and in patients aged 65 years or older (RR 0.72, 95% CI 0.61-0.85, p < 0.0001).
CONCLUSIONS: Use of SGLT-2 inhibitors did not increase the incidence of AKI regardless of the ejection fraction environment (chronic and acute), type of SGLT-2 inhibitors, or patient age.

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The compensatory reserve index (CRI), derived from machine learning algorithms from peripherally obtained photoplethysmography signals, provides a non-invasive assessment of cardiovascular stability, that may be useful clinically. Briefly, the CRI device provides a value between 0 and 1, with 1 reflecting full compensable capabilities and 0 reflecting little to no compensable capabilities. However, the CRI algorithm was developed in younger to middle aged adults, such that it is unknown if older age modulates CRI responses to cardiovascular challenges. In young and older subjects, we compared CRI responses to normothermic and hyperthermic progressive lower body negative pressure (LBNP), and volume loading with saline infusion. Eleven younger (20-36 years) and 10 older (61-75 years) healthy participants underwent (1) graded normothermic LBNP up to 30 mmHg, (2) graded hyperthermic (1.5°C increase in blood temperature) LBNP up to 30 mmHg, and (3) infusion of 15 mL/kg saline (volume loading) with hyperthermia maintained. CRI was obtained throughout each procedure. CRI at 30 mmHg LBNP was 0.18 and 0.24 units greater in the older group during normothermic and hyperthermic LBNP, respectively. However, CRI was not different between age groups at any other LBNP stage, nor did CRI change with volume loading regardless of age. In response to passive hyperthermia alone, regression analyses showed that heart rate was the strongest predictor of CRI. Blood temperature, rate pressure product, and stroke volume were also predictive of CRI but to a lesser extent. In conclusion, age attenuates the reduction in CRI during progressive normothermic and hyperthermic LBNP, but only at 30 mmHg. Second, the CRI was unchanged during volume loading in all subjects. Future studies should determine whether the age differences in CRI reflect age differences in LBNP tolerance.

Idiopathic capillary leak syndrome, also known as Clarkson\'s Disease, is a rare cause of hypovolemic shock that physicians should be aware of. It is characterized by a state of hypovolemia with features of widespread fluid third spacing and poses diagnostic and therapeutic challenges. Here, we present a challenging case of a 36-year-old woman who experienced recurrent episodes of widespread edema and hypovolemic shock symptoms suggestive of capillary leak syndrome. The resuscitative and therapeutic measures employed in managing this disease are described in this case report.

Introduction: Centhaquine is a resuscitative agent that acts on α2B adrenergic receptors. Its effect on cardiac output in hypovolemic shock patients has not been reported. Methods: This pilot study was conducted in 12 hypovolemic shock patients treated with centhaquine who participated in an open-label phase IV study (NCT05956418). Echocardiography was utilized to measure stroke volume (SV), cardiac output (CO), left ventricular outflow tract velocity time integral (LVOT-VTI) and diameter (LVOTd), heart rate (HR), left ventricular ejection fraction (LVEF) and fractional shortening (LVFS), and inferior vena cava (IVC) diameter before (0 min) and 60, 120, and 300 min after centhaquine (0.01 mg/kg) iv infusion for 60 min. Results: SV was significantly increased after 60, 120, and 300 min. CO increased significantly after 120 and 300 min despite a decrease in HR. IVC diameter and LVOT-VTI at these time points significantly increased, indicating the increased venous return. LVEF and LVFS did not change, while the mean arterial pressure (MAP, mmHg) increased after 120 and 300 min. Positive correlations between IVC diameter and SV (R2 = 0.9556) and between IVC diameter and MAP (R2 = 0.8928) were observed, which indicated the effects of an increase in venous return on SV, CO, and MAP. Conclusions: Centhaquine-mediated increase in venous return is critical in enhancing SV, CO, and MAP in patients with hypovolemic shock; these changes could be pivotal for reducing shock-mediated circulatory failure, promoting tissue perfusion, and improving patient outcomes. Trial Registration: CTRI/2021/01/030263 and NCT05956418.

OBJECTIVE: The current study investigated whether sustained mild dehydration affects thermoregulatory function and cognitive performance during prolonged exercise.
METHODS: Twelve young adults performed a test consisting of three sets of 20-min exercise with 2-min intervals under euhydrated (control, CON) and mildly dehydrated conditions (MDEH) at an ambient temperature of 30 °C and 60% relative humidity. MDEH was established by restricting water intake for 24 h, resulting in urine specific gravity of ≥ 1.020. Heart rate (HR), mean arterial blood pressure (MAP), skin blood flow (SkBF), sweat rate (SR) on the chest and forearm, and ear canal and mean skin surface temperatures (Tear and mean Tskin, respectively) were continuously recorded. For each exercise set, thermal and humid sensations and thermal discomfort were assessed using visual analog scales (VAS), and the rating of perceived exertion (RPE) was estimated. Cognitive performance on the Go/No-Go (easy) and incongruent Stroop (difficult) tasks was assessed before and after the test.
RESULTS: No differences were observed in HR, MAP, SkBF, SR, Tear, and mean Tskin between the CON and MDEH. Thermal and humidity sensations, thermal discomfort, and RPE were higher in MDEH than in CON. Moreover, response time to the Stroop task was prolonged in MDEH.
CONCLUSIONS: These findings suggest that sustained mild dehydration does not affect autonomic thermoregulation during exercise. Augmented thermal perception and perceived exertion, which are necessary for behavioral thermoregulation, were noted; however, cognitive function may be attenuated under MDEH.

Adrenal insufficiency (AI) is a rare but potentially life-threatening endocrine disorder characterized by inadequate production or impaired response to adrenal hormones. Symptoms may range from acute emergent crisis presenting as hemodynamic shock or may be more chronic in presentation with a gradual onset of nonspecific symptoms. These vague symptoms are often accompanied by typical laboratory findings, such as hyponatremia, hypotension, and hyperkalemia, and point toward a diagnosis of chronic AI. In this case presentation, we demonstrate chronic AI presenting with severe hyponatremia, which was revealed after return to an euvolemic baseline. Because of an insidious presentation, AI can be both an incidental finding and easily missed. This case highlights the importance of evaluating suspected cases of AI at a baseline metabolic and hemodynamic state, including volume status. High clinical suspicion is warranted in these patients to avoid potential emergent adrenal crisis and to provide appropriate replacement therapy once etiology is established.

Evaluating fluid responsiveness with dynamic parameters is recommended for fluid management. However, in hemodynamically stable patients who are breathing spontaneously, accurately measuring stroke volume variation via echocardiography and passive leg raising is challenging due to subtle SV changes. This study aimed to identify normal SV changes in healthy volunteers and evaluate the precision of hemodynamic parameters in screening mild hypovolemia in patients. This prospective, repeated-measures, cross-sectional study screened 269 subjects via echocardiography. Initially, 45 healthy volunteers underwent a fluid challenge test, the outcomes of which served as criteria to screen 215 ICU patients. Among these patients, 53 underwent additional fluid challenge testing. Hemodynamic parameters, including medians of maximum velocity time integrals (VTImaxs), peak velocity of VTImax (PV), internal jugular vein diameters (IJVD), and area (IJVA) were repeatedly measured first at a 60° upper body elevation (UBE), second in a supine position, third at UBE, fourth in a supine position, and lastly in a supine position after fluid loading. The hemodynamic responses to the position changes were compared between 83 fluid non-responders and 15 fluid responders. Fluid responsiveness was defined as fluid-induced medians\' change of VTImaxs (fluid-induced median VTImax change) ≥ 10%. None of the healthy volunteers showed the mean value of repeatedly measured medians of VTImaxs ≥ 7%, following either UBE position (UBE-induced median VTImax change) or fluid loading (fluid-induced median VTImax change). UBE-induced median VTImax and PV changes were significantly correlated with fluid responsiveness (p < 0.001, AUC 0.959; p < 0.001, AUC 0.804). The significant correlations were demonstrated via multivariable analysis using binary logistic regression (p = 0.001, OR 90.1) and the correlation coefficient (R2 = 0.793) using linear regression analysis. UBE-induced median VTImax changes (≥ 11.8% and 7.98%) predicted fluid-induced median VTImax changes ≥ 10% and 7% (AUC 0.959 and 0.939). The collapsibility and variation of IJVD and IJVA showed no significant correlation. An increase in the mean value of medians of repeatedly measured VTImaxs transitioning from an UBE to a supine position, effectively screened mild hypovolemia and demonstrated a significant correlation with fluid responsiveness in spontaneously breathing patients maintaining hemodynamic stability.

The use of ultrasound while caring for critically ill patients has been increasing exponentially in the last two decades and now is an essential component of intensive care practice. Abdominal ultrasound is an established technique in other specialties, but its use in intensive care has lagged behind other ultrasound modalities. However, its potential role in the diagnosis and management of patients will make it an invaluable tool for intensivists. The main use of abdominal ultrasound at the bedside is for free fluid detection in trauma patients. But abdominal ultrasound can also help us diagnose patients with abdominal pain, hypovolemia or anuria, and it can guide us during procedures such as paracentesis or bladder catheter and gastric tube placement.