Jaime Retamal

Impact of emergency intubation on central venous oxygen saturation in critically ill patients: a multicenter observational study

IntroductionCentral venous oxygen saturation (ScvO2) has emerged as an important resuscitation goal for critically ill patients. Nevertheless, growing concerns about its limitations as a perfusion parameter have been expressed recently, including the uncommon finding of low ScvO2 values in patients in the intensive care unit (ICU). Emergency intubation may induce strong and eventually divergent effects on the physiologic determinants of oxygen transport (DO2) and oxygen consumption (VO2) and, thus, on ScvO2. Therefore, we conducted a study to determine the impact of emergency intubation on ScvO2.MethodsIn this prospective multicenter observational study, we included 103 septic and non-septic patients with a central venous catheter in place and in whom emergency intubation was required. A common intubation protocol was used and we evaluated several parameters including ScvO2 before and 15 minutes after emergency intubation. Statistical analysis included chi-square test and t test.ResultsScvO2 increased from 61.8 ± 12.6% to 68.9 ± 12.2%, with no difference between septic and non-septic patients. ScvO2 increased in 84 patients (81.6%) without correlation to changes in arterial oxygen saturation (SaO2). Seventy eight (75.7%) patients were intubated with ScvO2 less than 70% and 21 (26.9%) normalized the parameter after the intervention. Only patients with pre-intubation ScvO2 more than 70% failed to increase the parameter after intubation.ConclusionsScvO2 increases significantly in response to emergency intubation in the majority of septic and non-septic patients. When interpreting ScvO2 during early resuscitation, it is crucial to consider whether the patient has been recently intubated or is spontaneously breathing.

Non-lobar atelectasis generates inflammation and structural alveolar injury in the surrounding healthy tissue during mechanical ventilation

IntroductionWhen alveoli collapse the traction forces exerted on their walls by adjacent expanded units may increase and concentrate. These forces may promote its re-expansion at the expense of potentially injurious stresses at the interface between the collapsed and the expanded units. We developed an experimental model to test the hypothesis that a local non-lobar atelectasis can act as a stress concentrator, contributing to inflammation and structural alveolar injury in the surrounding healthy lung tissue during mechanical ventilation.MethodsA total of 35 rats were anesthetized, paralyzed and mechanically ventilated. Atelectasis was induced by bronchial blocking: after five minutes of stabilization and pre-oxygenation with FIO2 = 1.0, a silicon cylinder blocker was wedged in the terminal bronchial tree. Afterwards, the animals were randomized between two groups: 1) Tidal volume (VT) = 10 ml/kg and positive end-expiratory pressure (PEEP) = 3 cmH2O (VT10/PEEP3); and 2) VT = 20 ml/kg and PEEP = 0 cmH2O (VT20/zero end-expiratory pressure (ZEEP)). The animals were then ventilated during 180 minutes. Three series of experiments were performed: histological (n = 12); tissue cytokines (n = 12); and micro-computed tomography (microCT; n = 2). An additional six, non-ventilated, healthy animals were used as controls.ResultsAtelectasis was successfully induced in the basal region of the lung of 26 out of 29 animals. The microCT of two animals revealed that the volume of the atelectasis was 0.12 and 0.21 cm3. There were more alveolar disruption and neutrophilic infiltration in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. Edema was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in the VT20/ZEEP than VT10/PEEP3 group. The volume-to-surface ratio was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. We did not find statistical difference in tissue interleukin-1β and cytokine-induced neutrophil chemoattractant-1 between regions.ConclusionsThe present findings suggest that a local non-lobar atelectasis acts as a stress concentrator, generating structural alveolar injury and inflammation in the surrounding lung tissue.

Preliminary study of ventilation with 4 ml/kg tidal volume in acute respiratory distress syndrome: feasibility and effects on cyclic recruitment - derecruitment and hyperinflation

IntroductionCyclic recruitment-derecruitment and overdistension contribute to ventilator-induced lung injury. Tidal volume (Vt) may influence both, cyclic recruitment-derecruitment and overdistension. The goal of this study was to determine if decreasing Vt from 6 to 4 ml/kg reduces cyclic recruitment-derecruitment and hyperinflation, and if it is possible to avoid severe hypercapnia.MethodsPatients with pulmonary acute respiratory distress syndrome (ARDS) were included in a crossover study with two Vt levels: 6 and 4 ml/kg. The protocol had two parts: one bedside and other at the CT room. To avoid severe hypercapnia in the 4 ml/kg arm, we replaced the heat and moisture exchange filter by a heated humidifier, and respiratory rate was increased to keep minute ventilation constant. Data on lung mechanics and gas exchange were taken at baseline and after 30 minutes at each Vt (bedside). Thereafter, a dynamic CT (4 images/sec for 8 sec) was taken at each Vt at a fixed transverse region between the middle and lower third of the lungs. Afterward, CT images were analyzed and cyclic recruitment-derecruitment was determined as non-aerated tissue variation between inspiration and expiration, and hyperinflation as maximal hyperinflated tissue at end-inspiration, expressed as % of lung tissue weight.ResultsWe analyzed 10 patients. Decreasing Vt from 6 to 4 ml/kg consistently decreased cyclic recruitment-derecruitment from 3.6 (2.5 to 5.7) % to 2.9 (0.9 to 4.7) % (P <0.01) and end-inspiratory hyperinflation from 0.7 (0.3 to 2.2) to 0.6 (0.2 to 1.7) % (P = 0.01). No patient developed severe respiratory acidosis or severe hypercapnia when decreasing Vt to 4 ml/kg (pH 7.29 (7.21 to 7.46); PaCO2 48 (26 to 51) mmHg).ConclusionsDecreasing Vt from 6 to 4 ml/kg reduces cyclic recruitment-derecruitment and hyperinflation. Severe respiratory acidosis may be effectively prevented by decreasing instrumental dead space and by increasing respiratory rate.

Improving the Accuracy of Registration-Based Biomechanical Analysis: A Finite Element Approach to Lung Regional Strain Quantification

Tissue deformation plays an important role in lung physiology, as lung parenchyma largely deforms during spontaneous ventilation. However, excessive regional deformation may lead to lung injury, as observed in patients undergoing mechanical ventilation. Thus, the accurate estimation of regional strain has recently received great attention in the intensive care community. In this work, we assess the accuracy of regional strain maps computed from direct differentiation of B-Spline (BS) interpolations, a popular technique employed in non-rigid registration of lung computed tomography (CT) images. We show that, while BS-based registration methods give excellent results for the deformation transformation, the strain field directly computed from BS derivatives results in predictions that largely oscillate, thus introducing important errors that can even revert the sign of strain. To alleviate such spurious behavior, we present a novel finite-element (FE) method for the regional strain analysis of lung CT images. The method follows from a variational strain recovery formulation, and delivers a continuous approximation to the strain field in arbitrary domains. From analytical benchmarks, we show that the FE method results in errors that are a fraction of those found for the BS method, both in an average and pointwise sense. The application of the proposed FE method to human lung CT images results in 3D strain maps are heterogeneous and smooth, showing high consistency with specific ventilation maps reported in the literature. We envision that the proposed FE method will considerably improve the accuracy of image-based biomechanical analysis, making it reliable enough for routine medical applications.

Pressão expiratória final positiva aumenta o estiramento em pacientes com LPA/SDRA

OBJECTIVE: The objective of this study was to assess the effects of positive end-expiratory pressure on recruitment, cyclic recruitment and derecruitment and strain in patients with acute lung injury and acute respiratory distress syndrome using lung computed tomography. METHODS: This is an open, controlled, non-randomized interventional study of ten patients with acute lung injury and acute respiratory distress syndrome. Using computed tomography, single, basal slices of the lung were obtained during inspiratory and expiratory pauses at a tidal volume of 6 ml/kg and a positive end-expiratory pressure of 5, 10, 15 and 20 cmH2O. The densities of the lung parenchyma were measured in Hounsfield units. The values for positive end-expiratory pressure-induced recruitment, cyclic recruitment and derecruitment and strain were then calculated. RESULTS: Increasing levels of positive end-expiratory pressure were correlated with increased recruitment and global strain (p < 0.01), which was significantly correlated with plateau pressure (r2 = 0.97, p < 0.01). In addition, increasing levels of positive end-expiratory pressure systematically increased strain along the sternovertebral axis. CONCLUSION: While strain is an adverse effect of positive end-expiratory pressure, the decision use positive end-expiratory pressure with any patient should be balanced against the potential benefits of recruitment. Due to the small number of patients in this study, the present data should be treated as hypothesis generating and is not intended to limit the clinical application of a high level of positive end-expiratory pressure in patients with severe hypoxemia.

Driving pressure: a marker of severity, a safety limit, or a goal for mechanical ventilation?

Current guidelines for lung-protective ventilation in patients with acute respiratory distress syndrome (ARDS) suggest the use of low tidal volumes (Vt), set according to ideal body weight (IBW) of the patient [1], and higher levels of positive end-expiratory pressure (PEEP) to limit ventilator-induced lung injury (VILI) [2, 3]. However, recent studies have shown that ARDS patients who are ventilated according to these guidelines may still be exposed to forces that can induce or aggravate lung injury [4–6]. Airway driving pressure has received considerable attention after a publication by Amato et al. [7] of a complex and innovative statistical analysis of key randomized clinical trials that tested ventilatory settings in patients with ARDS. The analysis showed that driving pressure, as opposed to Vt and PEEP, was the variable that best correlated with survival in patients with ARDS [7]. Since this article, several authors have replicated this hypothesis in different clinical scenarios, to the point of suggesting that driving pressure may be a goal in itself [8]. In this Viewpoint, we review the physiological meaning of driving pressure, look at the current clinical evidence, and discuss the role of driving pressure when setting the ventilator, considering it more as a safety limit than an objective by itself. This discussion is restricted to patients undergoing controlled mechanical ventilation and without spontaneous breathing efforts. During spontaneous ventilation measurements of driving pressure will underestimate the real distending pressure of the respiratory system and it can, therefore, be misleading [9].

Trombosis venosa mayor asociada a catéter de hipotermia terapéutica en un paciente con paro cardiorrespiratorio recuperado: comunicación de un caso y revisión de la literatura

To improve survival and reduce neurological injury, the use of mild hypothermia following cardiac arrest has been recommended. We report a 65 years old woman who presented an out-of-hospital ventricular fibrillation and cardiac arrest. The patient was comatose following initial resuscitation and was admitted into the ICU, where cooling was initiated using an intravascular catheter. After 48 hours, rewarming was initiated. Although no neurological impairment was observed, physical examination of the right inguinal area and echo-Doppler examination revealed an extensive catheter-related thrombophlebitis with right ileocaval vein occlusion., with high risk of massive and life threatening pulmonary embolism. We report a clinical case and review the literature to point out the need for a high index of diagnostic suspicion of deep venous thrombosis in these specific setting.

Electrical impedance tomography in acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is a clinical entity that acutely affects the lung parenchyma, and is characterized by diffuse alveolar damage and increased pulmonary vascular permeability. Currently, computed tomography (CT) is commonly used for classifying and prognosticating ARDS. However, performing this examination in critically ill patients is complex, due to the need to transfer these patients to the CT room. Fortunately, new technologies have been developed that allow the monitoring of patients at the bedside. Electrical impedance tomography (EIT) is a monitoring tool that allows one to evaluate at the bedside the distribution of pulmonary ventilation continuously, in real time, and which has proven to be useful in optimizing mechanical ventilation parameters in critically ill patients. Several clinical applications of EIT have been developed during the last years and the technique has been generating increasing interest among researchers. However, among clinicians, there is still a lack of knowledge regarding the technical principles of EIT and potential applications in ARDS patients. The aim of this review is to present the characteristics, technical concepts, and clinical applications of EIT, which may allow better monitoring of lung function during ARDS.

O uso de níveis altos de PEEP previne a lesão pulmonar induzida pelo ventilador

A distensao excessiva e o recrutamento alveolar pelo volume corrente foram defendidos como os principais mecanismos fisicos responsaveis pela lesao pulmonar induzida pelo ventilador. A limitacao do volume corrente demonstrou beneficios quanto a sobrevivencia em pacientes com sindrome da angustia respiratoria aguda e e reconhecida como a pedra fundamental da ventilacao protetora. Em contraste, o uso de elevados niveis de pressao positiva expiratoria final em estudos clinicos gerou resultados conflitantes e ainda e um assunto controvertido. Nesta revisao, discutimos os beneficios e as limitacoes da abordagem de pulmao aberto, e debatemos alguns recentes estudos experimentais e clinicos, referentes ao uso de niveis baixos e moderados de pressao positiva expiratoria final. Tambem distinguimos o estiramento dinâmico (volume corrente) do estatico (pressao expiratoria final positiva e pressao media nas vias aereas) e discutimos seus papeis na inducao da lesao pulmonar induzida pela ventilacao. As estrategias com elevada pressao positiva expiratoria final claramente diminuem a hipoxemia refrataria em pacientes com sindrome da angustia respiratoria aguda, porem tambem aumentam o estiramento estatico, que, por sua vez, pode ser lesiva aos pacientes, especialmente para aqueles com nivel mais baixo de recrutabilidade pulmonar. Em pacientes com insuficiencia respiratoria grave, recomenda-se a titulacao da pressao positiva expiratoria final contra a gravidade da hipoxemia, ou sua aplicacao de uma forma decrescente apos manobra de recrutamento. Caso sejam observadas elevadas pressoes de plato, driving pressure ou pressao media nas vias aereas, a posicao prona ou ventilacao ultraprotetora podem ser indicadas para melhora da oxigenacao, sem estresse adicional e estiramento dos pulmoes.

Effects on Pulmonary Vascular Mechanics of Two Different Lung-Protective Ventilation Strategies in an Experimental Model of Acute Respiratory Distress Syndrome

Objectives: To compare the effects of two lung-protective ventilation strategies on pulmonary vascular mechanics in early acute respiratory distress syndrome. Design: Experimental study. Setting: University animal research laboratory. Subjects: Twelve pigs (30.8 ± 2.5 kg). Interventions: Acute respiratory distress syndrome was induced by repeated lung lavages and injurious mechanical ventilation. Thereafter, animals were randomized to 4 hours ventilation according to the Acute Respiratory Distress Syndrome Network protocol or to an open lung approach strategy. Pressure and flow sensors placed at the pulmonary artery trunk allowed continuous assessment of pulmonary artery resistance, effective elastance, compliance, and reflected pressure waves. Respiratory mechanics and gas exchange data were collected. Measurements and Main Results: Acute respiratory distress syndrome led to pulmonary vascular mechanics deterioration. Four hours after randomization, pulmonary vascular mechanics was similar in Acute Respiratory Distress Syndrome Network and open lung approach: resistance (578 ± 252 vs 626 ± 153 dyn.s/cm5; p = 0.714), effective elastance, (0.63 ± 0.22 vs 0.58 ± 0.17 mm Hg/mL; p = 0.710), compliance (1.19 ± 0.8 vs 1.50 ± 0.27 mL/mm Hg; p = 0.437), and reflection index (0.36 ± 0.04 vs 0.34 ± 0.09; p = 0.680). Open lung approach as compared to Acute Respiratory Distress Syndrome Network was associated with improved dynamic respiratory compliance (17.3 ± 2.6 vs 10.5 ± 1.3 mL/cm H2O; p < 0.001), driving pressure (9.6 ± 1.3 vs 19.3 ± 2.7 cm H2O; p < 0.001), and venous admixture (0.05 ± 0.01 vs 0.22 ± 0.03, p < 0.001) and lower mean pulmonary artery pressure (26 ± 3 vs 34 ± 7 mm Hg; p = 0.045) despite of using a higher positive end-expiratory pressure (17.4 ± 0.7 vs 9.5 ± 2.4 cm H2O; p < 0.001). Cardiac index, however, was lower in open lung approach (1.42 ± 0.16 vs 2.27 ± 0.48 L/min; p = 0.005). Conclusions: In this experimental model, Acute Respiratory Distress Syndrome Network and open lung approach affected pulmonary vascular mechanics similarly. The use of higher positive end-expiratory pressures in the open lung approach strategy did not worsen pulmonary vascular mechanics, improved lung mechanics, and gas exchange but at the expense of a lower cardiac index.