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Patients with vasodilatory shock were randomly assigned to angiotensin II or placebo. At 3 hours, more patients in the angiotensin II group than in the placebo group had an increase in mean arterial pressure of at least 10 mm Hg or to at least 75 mm Hg.

PurposeNet ultrafiltration (UFNET) during continuous renal replacement therapy (CRRT) can control fluid balance (FB), but is usually 0 ml·h−1 in patients with vasopressors due to the risk of hemodynamic instability associated with CRRT (HIRRT). We evaluated a UFNET strategy adjusted by functional hemodynamics to control the FB of patients with vasopressors, compared to the standard of care.MethodsIn this randomized, controlled, open-label, parallel-group, multicenter, proof-of-concept trial, adults receiving vasopressors, CRRT since ≤ 24 h and cardiac output monitoring were randomized (ratio 1:1) to receive during 72 h a UFNET ≥ 100 ml·h−1, adjusted using a functional hemodynamic protocol (intervention), or a UFNET ≤ 25 ml·h−1 (control). The primary outcome was the cumulative FB at 72 h and was analyzed in patients alive at 72 h and in whom monitoring and CRRT were continuously provided (modified intention-to-treat population [mITT]). Secondary outcomes were analyzed in the intention-to-treat (ITT) population.ResultsBetween June 2021 and April 2023, 55 patients (age 69 [interquartile range, IQR: 62; 74], 35% female, Sequential Organ Failure Assessment (SOFA) 13 [11; 15]) were randomized (25 interventions, 30 controls). In the mITT population, (21 interventions, 24 controls), the 72 h FB was −2650 [−4574; −309] ml in the intervention arm, and 1841 [821; 5327] ml in controls (difference: 4942 [95% confidence interval: 2736–6902] ml, P < 0.01). Hemodynamics, oxygenation and the number of HIRRT at 72 h, and day-90 mortality did not statistically differ between arms.ConclusionIn patients with vasopressors, a UFNET fluid removal strategy secured by a hemodynamic protocol allowed active fluid balance control, compared to the standard of care.

Background No standardized index exists to assess cardiovascular responsiveness to angiotensin-II. We hypothesized that a standardized index of initial blood pressure response to angiotensin-II treatment would be associated with clinical outcomes. Methods Using data from the Angiotensin Therapy for High Output Shock (ATHOS-3) trial, we developed an Angiotensin-II Initial MAP Response Index of Treatment Effect (AIMRITE) defined as (MAP at hr1 – MAP at baseline)/study drug dose. We assessed AIMRITE continuously and, based on observed distributions, we additionally categorized patients as “responsive” or “resistant”, with responsiveness defined by an AIMRITE ≥ 0.90 mmHg/ng/kg/min. The primary clinical outcome was 28-day mortality. Secondary outcomes included days alive and vasopressor- or ventilator- or renal replacement therapy-free at day-7. Biological outcomes included baseline renin, angiotensin-II, and renin/angiotensin-II ratio, and their change at hr3. Results Of 158 placebo patients, as expected, 157 (99%) had AIMRITE < 0.90 mmHg/ng/kg/min (median AIMRITE 0.02; IQR − 0.03–0.10). In contrast, 163 patients assigned to angiotensin-II had a median AIMRITE of 1.43 mmHg/ng/kg/min (IQR 0.35–2.83). Of these, 97 (60%) were responsive (median AIMRITE 2.55; IQR 1.66–4.12) and 66 (40%) were resistant (median AIMRITE 0.24; IQR 0.10–0.52). Each 1.0-unit increase in AIMRITE was associated with a 16% lower hazard of death (HR: 0.84 per-mmHg/ng/kg/min [95% CI 0.74–0.95], p  = 0.0062). Responsive patients had half the mortality hazard than resistant patients (HR: 0.50 [95% CI 0.32–0.78], p  = 0.0026) and placebo patients (HR 0.58 [95% CI 0.40–0.86], p  = 0.0064). Resistant patients had a similar mortality hazard to placebo (HR 1.17 [95% CI 0.80–1.72], p  = 0.41). Compared to resistant patients, responsive patients had lower baseline renin and renin/angiotensin-II ratio, but a greater decrease in both at hr3. When stratified by baseline renin level, mortality was highest in placebo patients with high renin (69%) and angiotensin-II resistant patients with low renin (61%). Conclusions Among patients with catecholamine-refractory vasodilatory shock treated with angiotensin-II, the AIMRITE was associated with mortality at day-28. Responsive angiotensin-II patients had higher survival versus both angiotensin-II resistant patients and those treated with placebo plus standard vasopressors. This index may serve as a prognostic indicator and early identifier of patients most likely to benefit from angiotensin-II.

The DanGer Shock trial test the hypothesis that left ventricular (LV) mechanical circulatory support with Impella CP transvalvular microaxial flow pump improves survival in patients with ST segment elevation acute myocardial infarction complicated by cardiogenic shock (AMICS) compared to conventional guideline-driven treatment. This paper describes the rationale and design of the randomized trial, in addition to the baseline characteristics of the population screened and enrolled so far. The DanGer Shock study is a prospective, multicenter, open-label trial in patients with AMICS randomized 1:1 to Impella CP or current guideline-driven therapy with planned enrollment of 360 patients. Patients comatose after out of hospital cardiac arrest are excluded. Eligible patients are randomized immediately following shock diagnosis. Among patients randomized to receive Impella CP, the device is placed prior to angioplasty. The primary endpoint is all-cause mortality at 180 days. Baseline characteristics of patients screened and randomized in the DanGer Shock as of June 2018 are compared with 2 contemporary AMICS studies. As of end of June 2018, 314 patients were screened and 100 patients were randomized. Patients had median arterial lactate of 5.5 mmol/L (interquartile range 3.7-8.8 mmol/L), median systolic blood pressure of 76 mmHg (interquartile range 70-88 mmHg), and median LV ejection fraction of 20% (interquartile range 10%-30%). The DanGer Shock trial will be the first adequately powered randomized trial to address whether mechanical circulatory LV support with Impella CP can improve survival in AMICS. Baseline characteristics of the first 100 randomized patients indicate a population in profound cardiogenic shock.

Background Critically ill patients with shock receiving vasopressor or inotrope therapy in ICU are often exposed to relative hypotension, which is quantified as percentage blood pressure deficit relative to usual pre-illness blood pressure. Whether minimising such blood pressure deficit, by adjusting blood pressure targets according to patients’ pre-illness blood pressure (individualised blood pressure target strategy), can improve clinical outcomes remains unclear. Therefore, we are conducting a multicenter randomised controlled trial, the REACT SHOCK RCT, comparing individualised blood pressure targets to standard care among critically ill patients with shock. Methods The REACT SHOCK RCT is an international, multicenter, parallel-group, randomised, standard-care controlled, clinical superiority trial that will be conducted in up to 35 ICUs in Australia, Ireland, Singapore, UK and USA. In total, 1260 patients, receiving vasopressor therapy for non-haemorrhagic shock in ICU, will be randomly assigned to individualised mean arterial blood pressure (MAP) targets (determined as an average of 2–5 recent pre-illness blood pressure readings within last 3 years, with a MAP target range of 55 to 95 mmHg) or standard care (default MAP target of 65 mmHg) in a 1:1 ratio. The REACT SHOCK RCT is anticipated to complete recruitment by 2028. The primary endpoint is all-cause 14-day mortality. Secondary endpoints are major adverse kidney events by day 14, all-cause 90-day mortality, survival time to 14 days and 90 days, and renal replacement therapy free days by day 28. Discussion The REACT SHOCK RCT is the first international multicenter randomised clinical trial designed to ascertain whether an individualised blood pressure target strategy is superior to standard care for critically ill patients with shock. This trial will generate evidence that may influence current recommendations for MAP targets during management of shock in ICU. The pre-specified protocol summary and statistical analysis plan are presented here. Trial registration Prospectively registered on Australian and New Zealand Clinical Trials Registry (ANZCTRN 12623000044628); ClinicalTrials.gov ID NCT05850962 dated 29th April 2023.

Purpose The use of norepinephrine (NE) in patients with volume-resuscitated vasodilatory shock and acute kidney injury (AKI) remains the subject of much debate and controversy. The effects of NE-induced variations in mean arterial blood pressure (MAP) on renal blood flow (RBF), oxygen delivery (RDO 2 ), glomerular filtration rate (GFR) and the renal oxygen supply/demand relationship (renal oxygenation) in vasodilatory shock with AKI have not been previously studied. Methods Twelve post-cardiac surgery patients with NE-dependent vasodilatory shock and AKI were studied 2–6 days after surgery. NE infusion rate was randomly and sequentially titrated to target MAPs of 60, 75 and 90 mmHg. At each target MAP, data on systemic haemodynamics, RBF, GFR and renal oxygen extraction were obtained by pulmonary artery catheter, by the renal vein thermodilution technique and by renal extraction of 51 Cr-ethylenediamine tetraacetic acid ( 51 Cr-EDTA), respectively. Results At target MAP of 75 mmHg, RDO 2 (13%), GFR (27%) and urine flow were higher and renal oxygen extraction was lower (−7.4%) compared with at target MAP of 60 mmHg. However, the renal variables did not differ when compared at target MAPs of 75 and 90 mmHg. Cardiac index increased dose-dependently with NE. Conclusions Restoration of MAP from 60 to 75 mmHg improves renal oxygen delivery, GFR and the renal oxygen supply/demand relationship in post-cardiac surgery patients with vasodilatory shock and AKI. This pressure-dependent renal perfusion, filtration and oxygenation at levels of MAP below 75 mmHg reflect a more or less exhausted renal autoregulatory reserve.

PurposeMortality in circulatory shock is high. Enhanced resolution of shock may improve outcomes. We aim to determine whether adding hemodynamic monitoring with continual transesophageal echocardiography (hTEE) to usual care accelerates resolution of hemodynamic instability.Methods550 patients with circulatory shock were randomly assigned to four groups stratified using hTEE (hTEE vs usual care) and assessment frequency (minimum every 4 h vs 8 h). Primary outcome was time to resolution of hemodynamic instability, analyzed as intention-to-treat (ITT) analysis at day 6 and in a predefined secondary analysis at days 3 and 28.ResultsOf 550 randomized patients, 271 with hTEE and 274 patients with usual care were eligible and included in the ITT analysis. Time to resolution of hemodynamic instability did not differ within the first 6 days [hTEE vs usual care adjusted sub-hazard ratio (SHR) 1.20, 95% confidence interval (CI) 0.98–1.46, p = 0.067]. Time to resolution of hemodynamic instability during the 72 h of hTEE monitoring was shorter in patients with TEE (hTEE vs usual care SHR 1.26, 95% CI 1.02–1.55, p = 0.034). Assessment frequency had no influence. Time to resolution of clinical signs of hypoperfusion, duration of organ support, length of stay and mortality in the intensive care unit and hospital, and mortality at 28 days did not differ between groups.ConclusionsIn critically ill patients with shock, hTEE monitoring or hemodynamic assessment frequency did not influence resolution of hemodynamic instability or mortality within the first 6 days.Trial registration and statistical analysis planClinicalTrials.gov Identifier: NCT02048566.

Shock, the most common severe emergency syndrome, has a complicated etiopathogenesis, is difficult to identify, progresses quickly, and is dangerous. Early identification and intervention play determining roles in the final outcomes of shock patients, but no specific scoring system for shock has been established to date. We collected 292 shock patients and analyzed the correlation between 28-day prognosis and the Acute Physiologic Assessment and Chronic Health Evaluation II (APACHE II), Modified Early Warning System (MEWS), and Sequential Organ Failure Assessment scoring systems. According to the previous result, we established a new MEWS scoring system based on the conventional MEWS, which also included age and transcutaneous oxygen saturation. Some of the items with a strong correlation with the 28-day prognosis were selected to establish the new MEWS scoring system. We then evaluated the predictive efficacy of the new MEWS scoring system on 28-day prognosis and the correlation with other scoring systems. Some indexes, including age, transcutaneous oxygen saturation, arterial blood pH and blood lactic acid, serum sodium, serum potassium, HCO3, and red blood cells deposited, differed significantly between the nonsurviving and surviving groups (P<.05). The area under the curve (AUC) of the APACHE II, MEWS, shock index, and Sequential Organ Failure Assessment scoring systems for 28-day prognosis indicated a critical predictive efficacy. Receiver operating characteristic curves indicated that the MEWS AUC was 0.614, new MEWS AUC was 0.696, and APACHE II AUC was 0.785, suggesting superiority of the new MEWS to the conventional MEWS but inferiority to the APACHE II. Interestingly, the correlation efficient of the traditional MEWS and the new MEWS was 0.81. The correlation efficient of these scoring systems with other indexes, including lactic acid and hemoglobin, was less than 0.3. The new MEWS scoring system could be an independent indicator to reflect shock severity. It has higher predictive efficacy in septic shock, especially for 28-day prognosis.

In this multicenter, open-label trial, patients with septic shock were treated to maintain a mean arterial pressure target of either 80 to 85 mm Hg or 65 to 70 mm Hg. There were no significant between-group differences in 28-day mortality or in 90-day mortality. Septic shock is characterized by arterial hypotension despite adequate fluid resuscitation. The guidelines of the Surviving Sepsis Campaign 1 recommended initial resuscitation with vasopressors to reverse hypotension, with a mean arterial pressure target of at least 65 mm Hg (grade 1C, indicating a strong recommendation with a low level of evidence). This recommendation is based on the findings of small studies, which showed no significant differences in lactate levels or regional blood flow when the mean arterial pressure was elevated to more than 65 mm Hg in patients with septic shock. 2 , 3 However, as emphasized by the Surviving Sepsis Campaign guidelines, . . .

In critically ill patients, early hemodynamic assessment is essential for guiding shock resuscitation. While cardiac output (CO) is a key indicator of circulatory status, its measurement is often limited by technical and practical constraints. This perspective explores the physiological and clinical relevance of pulse pressure (PP) as a potential surrogate for stroke volume (SV), emphasizing its accessibility at the bedside. The paper discusses how factors such as arterial compliance, vascular tone, and pulse wave amplification influence the PP-SV relationship, often complicating interpretation in acute and complex hemodynamic states. It also examines the effects of vasopressors, vascular decoupling, and catheter site on PP measurements, particularly in septic shock. Despite its limitations, the review highlights how peripheral PP, when carefully interpreted, may aid in identifying low SV and guiding early resuscitation strategies.