You searched for:"Fernando Godinho Zampieri"
We found (28) results for your search.Abstract
Crit Care Sci. 2024;36:e20240210en
DOI 10.62675/2965-2774.20240210-en
Driving pressure has been suggested to be the main driver of ventilator-induced lung injury and mortality in observational studies of acute respiratory distress syndrome. Whether a driving pressure-limiting strategy can improve clinical outcomes is unclear.
To describe the protocol and statistical analysis plan that will be used to test whether a driving pressure-limiting strategy including positive end-expiratory pressure titration according to the best respiratory compliance and reduction in tidal volume is superior to a standard strategy involving the use of the ARDSNet low-positive end-expiratory pressure table in terms of increasing the number of ventilator-free days in patients with acute respiratory distress syndrome due to community-acquired pneumonia.
The ventilator STrAtegy for coMmunIty acquired pNeumoniA (STAMINA) study is a randomized, multicenter, open-label trial that compares a driving pressure-limiting strategy to the ARDSnet low-positive end-expiratory pressure table in patients with moderate-to-severe acute respiratory distress syndrome due to community-acquired pneumonia admitted to intensive care units. We expect to recruit 500 patients from 20 Brazilian and 2 Colombian intensive care units. They will be randomized to a driving pressure-limiting strategy group or to a standard strategy using the ARDSNet low-positive end-expiratory pressure table. In the driving pressure-limiting strategy group, positive end-expiratory pressure will be titrated according to the best respiratory system compliance.
The primary outcome is the number of ventilator-free days within 28 days. The secondary outcomes are in-hospital and intensive care unit mortality and the need for rescue therapies such as extracorporeal life support, recruitment maneuvers and inhaled nitric oxide.
STAMINA is designed to provide evidence on whether a driving pressure-limiting strategy is superior to the ARDSNet low-positive end-expiratory pressure table strategy for increasing the number of ventilator-free days within 28 days in patients with moderate-to-severe acute respiratory distress syndrome. Here, we describe the rationale, design and status of the trial.
Abstract
Rev Bras Ter Intensiva. 2016;28(2):120-131
DOI 10.5935/0103-507X.20160026
The aim of this study was to investigate the clinical and laboratorial factors associated with serum sodium variation during continuous renal replacement therapy and to assess whether the perfect admixture formula could predict 24-hour sodium variation.
Thirty-six continuous renal replacement therapy sessions of 33 patients, in which the affluent prescription was unchanged during the first 24 hours, were retrieved from a prospective collected database and then analyzed. A mixed linear model was performed to investigate the factors associated with large serum sodium variations (≥ 8mEq/L), and a Bland-Altman plot was generated to assess the agreement between the predicted and observed variations.
In continuous renal replacement therapy 24-hour sessions, SAPS 3 (p = 0.022) and baseline hypernatremia (p = 0.023) were statistically significant predictors of serum sodium variations ≥ 8mEq/L in univariate analysis, but only hypernatremia demonstrated an independent association (β = 0.429, p < 0.001). The perfect admixture formula for sodium prediction at 24 hours demonstrated poor agreement with the observed values.
Hypernatremia at the time of continuous renal replacement therapy initiation is an important factor associated with clinically significant serum sodium variation. The use of 4% citrate or acid citrate dextrose - formula A 2.2% as anticoagulants was not associated with higher serum sodium variations. A mathematical prediction for the serum sodium concentration after 24 hours was not feasible.
Abstract
Rev Bras Ter Intensiva. 2015;27(2):141-148
DOI 10.5935/0103-507X.20150025
To evaluate the impact of body mass index on the short-term prognosis of non-surgical critically ill patients while controlling for performance status and comorbidities.
We performed a retrospective analysis on a two-year single-center database including 1943 patients. We evaluated the impact of body mass index on hospital mortality using a gradient-boosted model that also included comorbidities and was assessed by Charlson’s comorbidity index, performance status and illness severity, which was measured by the SAPS3 score. The SAPS3 score was adjusted to avoid including the same variable twice in the model. We also assessed the impact of body mass index on the length of stay in the hospital after intensive care unit admission using multiple linear regressions.
A low value (< 20kg/m2) was associated with a sharp increase in hospital mortality. Mortality tended to subsequently decrease as body mass index increased, but the impact of a high body mass index in defining mortality was low. Mortality increased as the burden of comorbidities increased and as the performance status decreased. Body mass index interacted with the impact of SAPS3 on patient outcome, but there was no significant interaction between body mass index, performance status and comorbidities. There was no apparent association between body mass index and the length of stay at the hospital after intensive care unit admission.
Body mass index does appear to influence the shortterm outcomes of critically ill medical patients, who are generally underweight. This association was independent of comorbidities and performance status.
Abstract
Rev Bras Ter Intensiva. 2011;23(2):164-169
DOI 10.1590/S0103-507X2011000200008
OBJECTIVE: To evaluate the effects of hemodynamic, respiratory and metabolic changes on intracranial pressure in a model of acute lung injury and abdominal compartment syndrome. METHODS: Eight Agroceres pigs were submitted to five different clinical scenarios after instrumentation: 1) a baseline condition with low intra-abdominal pressure and healthy lungs; 2) pneumoperitoneum with 20 mmHg intra-abdominal pressure; 3) acute lung injury induced by pulmonary lavage with surfactant deactivation; 4) pneumoperitoneum with 20 mmHg intra-abdominal pressure with lung pulmonary injury and low positive end-expiratory pressure; and 5) 27 cmH2O positive end-expiratory pressure with pneumoperitoneum and acute lung injury. Respiratory and hemodynamic variables were collected. A multivariate analysis was conducted to search for variables associated with increased intracranial pressure in the five scenarios. RESULTS: Only plateau airway pressure showed a positive correlation with intracranial pressure in the multivariate analysis. In the models with acute lung injury, plateau airway pressure, CO2 arterial pressure, end tidal CO2 and central venous pressure were positively correlated with increased intracranial pressure. CONCLUSION: In a model of multiple organ dysfunction with associated clinical conditions causing increased intra-thoracic and abdominal pressure, increased intracranial pressure triggered by elevated intra-abdominal pressure is apparently caused by worsened respiratory system compliance and a reduced brain venous drainage gradient due to increased central venous pressure.
Abstract
Rev Bras Ter Intensiva. 2011;23(2):176-182
DOI 10.1590/S0103-507X2011000200010
OBJECTIVE: The aim of this study was to characterize and quantify metabolic acidosis that was caused by initial volume expansion during the reanimation of patients with severe sepsis and septic shock. METHODS: A blood sample was drawn for physicochemical characterization of the patient's acid-base equilibrium both before and after volume expansion using 30 mL/kg 0.9% saline solution. The diagnosis and quantification of metabolic acidosis were based on the standard base excess (SBE). RESULTS: Eight patients with a mean age of 58 ± 13 years and mean APACHE II scores of 20 ± 4 were expanded using 2,000 ± 370 mL of 0.9% saline solution. Blood pH dropped from 7.404 ± 0.080 to 7.367 ± 0.086 (p=0.018), and PC O2 increased from 30 ± 5 to 32 ± 2 mmHg (p=0.215); SBE dropped from -4.4 ± 5.6 to -6.0 ± 5.7 mEq/L (p=0.039). The drop in SBE was associated with the acidifying power of two factors, namely, a significant increase in the strong ion gap (SIG) from 6.1 ± 3.4 to 7.7 ± 4.0 mEq/L (p = 0.134) and a non-significant drop in the apparent inorganic strong ion differences (SIDai) from 40 ± 5 to 38 ± 4 mEq/L (p = 0.318). Conversely, the serum albumin levels decreased from 3.1 ± 1.0 to 2.6 ± 0.8 mEq/L (p = 0.003) with an alkalinizing effect on SBE. Increased serum chloride levels from 103 ± 10 to 106 ± 7 mEq/L (p < 0.001) led to a drop in SIDai. CONCLUSION: Initial resuscitation using 30 mL/kg of 0.9% saline solution for patients with severe sepsis and septic shock is associated with worsened metabolic acidosis, as measured by SBE. This worsened SBE can be ascribed to a serum increase in the levels of unmeasurable anions and chloride.
Abstract
Rev Bras Ter Intensiva. 2016;28(1):19-26
DOI 10.5935/0103-507X.20160009
Hypercapnia resulting from protective ventilation in acute respiratory distress syndrome triggers metabolic pH compensation, which is not entirely characterized. We aimed to describe this metabolic compensation.
The data were retrieved from a prospective collected database. Variables from patients' admission and from hypercapnia installation until the third day after installation were gathered. Forty-one patients with acute respiratory distress syndrome were analyzed, including twenty-six with persistent hypercapnia (PaCO2 > 50mmHg > 24 hours) and 15 non-hypercapnic (control group). An acid-base quantitative physicochemical approach was used for the analysis.
The mean ages in the hypercapnic and control groups were 48 ± 18 years and 44 ± 14 years, respectively. After the induction of hypercapnia, pH markedly decreased and gradually improved in the ensuing 72 hours, consistent with increases in the standard base excess. The metabolic acid-base adaptation occurred because of decreases in the serum lactate and strong ion gap and increases in the inorganic apparent strong ion difference. Furthermore, the elevation in the inorganic apparent strong ion difference occurred due to slight increases in serum sodium, magnesium, potassium and calcium. Serum chloride did not decrease for up to 72 hours after the initiation of hypercapnia.
In this explanatory study, the results indicate that metabolic acid-base adaptation, which is triggered by acute persistent hypercapnia in patients with acute respiratory distress syndrome, is complex. Furthermore, further rapid increases in the standard base excess of hypercapnic patients involve decreases in serum lactate and unmeasured anions and increases in the inorganic apparent strong ion difference by means of slight increases in serum sodium, magnesium, calcium, and potassium. Serum chloride is not reduced.
Abstract
Rev Bras Ter Intensiva. 2020;32(2):203-206
DOI 10.5935/0103-507X.20200040