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Guillermo Gutierrez

Publications and source records attributed to Guillermo Gutierrez.

14 recordsLinked to original sources
PubMed2006

Pulmonary alveolar proteinosis with myeloproliferative syndrome with myelodysplasia: bronchoalveolar lavage reduces white blood cell count.

Pulmonary alveolar proteinosis (PAP) is a rare disorder characterized by surfactant component accumulation in the alveolar space. Primary PAP is likely an autoimmune disorder caused by antibodies to granulocyte-macrophage colony stimulating factor (GM-CSF). When an underlying disease causes PAP, this is called secondary PAP. Hematologic malignancies are an important cause of secondary PAP. As the pathogenesis of primary PAP has become more fully understood, improvements in diagnostic and therapeutic approaches have followed. However, when PAP is secondary to an underlying hematologic malignancy, much remains unclear. Here we describe for the first time a patient with hybrid myelodysplastic syndrome/myeloproliferative syndrome and PAP who had a marked decrease in her white blood cell count following a transbronchial biopsy accompanied by bronchoalveolar lavage (BAL). Similar significant decreases in WBC count accompanied clinical improvement following two unilateral BALs. Given that patients with pulmonary alveolar proteinosis frequently have elevated GM-CSF in bronchoalveolar fluid, this observation provides a unique vantage point to understand the pathophysiology of secondary PAP.

Adult↗
PubMed2006

Future shock?

Explore the source record for details and available documents.

Critical Care↗
PubMed2005

Lactate concentration gradient from right atrium to pulmonary artery.

INTRODUCTION: We compared simultaneous measurements of blood lactate concentration ([Lac]) in the right atrium (RA) and in the pulmonary artery (PA). Our aim was to determine if the mixing of right atrial with coronary venous blood, having substantially lower [Lac], results in detectable decreases in [Lac] from the RA to the PA. METHODS: A prospective, sequential, observational study was conducted in a medical-surgical intensive care unit. We enrolled 45 critically ill adult individuals of either sex requiring pulmonary artery catheters (PACs) to guide fluid therapy. Immediately following the insertion of the PAC, one paired set of blood samples per patient was drawn in random order from the PAC's proximal and distal ports for measurement of hemoglobin concentration, O2 saturation (SO2) and [Lac]. We defined Delta[Lac] as ([Lac]ra - [Lac]pa), DeltaSO2 as (SraO2 - SpaO2) and the change in O2 consumption (DeltaVO2) as the difference in systemic VO2 calculated using Fick's equation with either SraO2 or SpaO2 in place of mixed venous SO2. Data were compared by paired Student's t-test, Spearman's correlation analysis and by the method of Bland and Altman. RESULTS: We found SraO2 > SpaO2 (74.2 +/- 9.1 versus 69.0 +/- 10.4%; p < 0.001) and [Lac]ra > [Lac]pa (3.9 +/- 3.0 versus 3.7 +/- 3.0 mmol x l-1; p < 0.001). Delta[Lac] correlated with DeltaVO2 (r2 = 0.34; p < 0.001). CONCLUSION: We found decreases in [Lac] from the RA to PA in this sample of critically ill individuals. We conclude that parallel decreases in SO2 and [Lac] from the RA to PA support the hypothesis that these gradients are produced by mixing RA with coronary venous blood of lower SO2 and [Lac]. The present study is a preliminary observation of this phenomenon and further work is needed to define the physiological and clinical significance of Delta[Lac].

Catheterization, Swan-Ganz↗
PubMed2005

Blood flow, not hypoxia, determines intramucosal PCO2.

Monitoring tissue hypoxia in critically ill patients is a challenging task. Tissue PCO2 has long been proposed as a marker of tissue hypoxia, although there is considerable controversy on whether the rise in CO2 with hypoxia is caused by anaerobic metabolism and excess CO2 production or by the accumulation of aerobically produced CO2 in the setting of blood flow stagnation. The prevention of increases in intestinal PCO2 in aggressively resuscitated septic animals supports the notion that tissue CO2 accumulation is a function of decreases in blood flow, not of tissue hypoxia.

Acidosis↗
PubMed2004

Of hemorrhagic shock, spherical cows and Aloe vera.

The central question explored in this commentary is whether the beneficial effects of an Aloe vera derived drag-reducing polymer during hemorrhagic shock is due to its O2 radical scavenging properties or to changes in blood rheology.

Aloe↗
PubMed2004

Clinical review: hemorrhagic shock.

This review addresses the pathophysiology and treatment of hemorrhagic shock - a condition produced by rapid and significant loss of intravascular volume, which may lead sequentially to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion, cellular hypoxia, organ damage, and death. Hemorrhagic shock can be rapidly fatal. The primary goals are to stop the bleeding and to restore circulating blood volume. Resuscitation may well depend on the estimated severity of hemorrhage. It now appears that patients with moderate hypotension from bleeding may benefit by delaying massive fluid resuscitation until they reach a definitive care facility. On the other hand, the use of intravenous fluids, crystalloids or colloids, and blood products can be life saving in those patients who are in severe hemorrhagic shock. The optimal method of resuscitation has not been clearly established. A hemoglobin level of 7-8 g/dl appears to be an appropriate threshold for transfusion in critically ill patients with no evidence of tissue hypoxia. However, maintaining a higher hemoglobin level of 10 g/dl is a reasonable goal in actively bleeding patients, the elderly, or individuals who are at risk for myocardial infarction. Moreover, hemoglobin concentration should not be the only therapeutic guide in actively bleeding patients. Instead, therapy should be aimed at restoring intravascular volume and adequate hemodynamic parameters.

Blood Transfusion↗
PubMed2004

Monitoring oxygen transport and tissue oxygenation.

PURPOSE OF REVIEW: To review recent publications in the field of oxygen delivery and tissue oxygenation. With few exceptions, we restricted our selection to clinical studies published in the English literature. RECENT FINDINGS: No major breakthroughs have occurred in the past decade in the diagnosis or treatment of tissue hypoxia. There is renewed interest in goal-directed resuscitation when applied early in the course of treatment. Monitoring metabolic markers of tissue hypoxia continues to hold great clinical interest, in particular, tissue PCO2, near infrared spectroscopy, base deficit and blood lactate concentration. Technical issues, however, seem to restrict the widespread use of many of these techniques. SUMMARY: There is an urgent need to develop methods to accurately and rapidly identify patients with tissue hypoxia. Perhaps the combination of gastric tonometry, near-infrared spectroscopy, urinary PO2 and continuous measures of mixed (or central) venous O2 saturation may provide the answer. An even more formidable task is that of developing effective therapy to correct tissue hypoxia while avoiding harm to the patient.

Journal Article↗
PubMed2004

Lack of equivalence between central and mixed venous oxygen saturation.

STUDY OBJECTIVE: We compared paired samples of central venous O(2) saturation (Scvo(2)) and mixed venous O(2) saturation (Svo(2)) to test the hypothesis that Scvo(2) is equivalent to Svo(2). We also compared O(2) consumption (Vo(2)) computed with Scvo(2) (Vo(2)cv) to that computed with Svo(2) (Vo(2)v). DESIGN: Prospective, sequential, observational study. SETTING: Combined medical-surgical ICU. PATIENTS: Fifty-three individuals > 18 years of age of either sex who required a pulmonary artery catheter (PAC) to guide fluid therapy. Subjects were identified as postsurgical (32 patients) or medical (21 patients) according to their ICU admission diagnosis. INTERVENTIONS: A PAC was inserted through the internal jugular or subclavian veins. Care was taken to place the PAC proximal port approximately 3 cm above the tricuspid valve. Blood samples were drawn from the proximal and distal ports in random order. An arterial blood sample also was drawn. MEASUREMENTS: Cardiac output in triplicate, systemic pressure, and central pressure. We analyzed blood samples for hemoglobin concentration and O(2) saturation (So(2)). Data were compared by correlation analysis and by the method of Bland and Altman. RESULTS: Svo(2) was consistently lower than Scvo(2) (p < 0.0001), with a mean (+/-SD) bias of -5.2 +/- 5.1%. Similar differences in Scvo(2) and Svo(2) were present within each subgroup (p < 0.001). A lower Svo(2) resulted in Vo(2)v values that were higher than the Vo(2)cv values for all patients in the study (mean Vo(2)v, 236.7 +/- 103.4 mL/min; mean Vo(2)cv, 191.1 +/- 84.0 mL/min; p < 0.001) as well as for patients within each subgroup (p < 0.001). CONCLUSIONS: Measurements of Scvo(2) and Svo(2) were not equivalent in this sample of critically ill patients. Moreover, substituting Scvo(2) for Svo(2) in the calculation of Vo(2) produced unacceptably large errors. The decrease in So(2) between Scvo(2) to Svo(2) may result from the mixing of atrial and coronary sinus blood. As such, this difference may be a marker of myocardial O(2) consumption.

Catheterization, Swan-Ganz↗
PubMed2003

A mathematical model of tissue-blood carbon dioxide exchange during hypoxia.

A two-compartment mass transport model of tissue CO(2) exchange is developed to examine the relative contributions of blood flow and cellular hypoxia (dysoxia) to increases in tissue and venous blood CO(2) concentration. The model assumes perfectly mixed homogeneous conditions, steady-state equilibrium, and CO(2) production occurring exclusively at the tissues. The behavior of the model is compared with published data derived from an isolated dog hindlimb preparation subjected to either reductions in blood flow (ischemic hypoxia) or decreases in arterial PO(2) (hypoxic hypoxia). The results of the model corroborate the experimental finding of greater venous and tissue CO(2) concentrations with ischemic hypoxia than with hypoxic hypoxia. The model also predicts increases in tissue CO(2) concentration under conditions of adequate O(2) supply if CO(2) transfer from tissue to blood becomes impaired. Consequently, from a theoretical perspective, it appears that increases in the tissue or venous blood CO(2) concentration are neither sensitive nor specific markers of tissue dysoxia. The results of the model support the notion that changes in tissue and venous blood CO(2) concentration during dysoxia reflect primarily alterations in vascular perfusion and not scarcity in cellular energy supply.

Carbon Dioxide↗
PubMed2003

Air embolism as a cause of the systemic inflammatory response syndrome: a case report.

We describe a case of systemic inflammatory response syndrome associated with air embolism following the removal of a central line catheter, coupled with a deep inspiratory maneuver. The presence of a patent foramen ovale allowed the passage of a clinically significant amount of air from the venous circulation to the systemic circulation. The interaction of air with the systemic arterial endothelium may have triggered the release of endothelium-derived cytokines, resulting in the physiologic response of systemic inflammatory response syndrome.

Aged↗