Alactic Base Excess, New Potential Marker Associated for Circulatory Stress Due to Hemodialysis, a Pilot Study

Indroduction: Circulatory stress increases mortality in patients with chronic kidney disease in renal replacement therapy by hemodialysis, the measurement of central venous saturation has been proposed as a useful tool for diagnosis but with limitations. We wanted to evaluate a new marker, the alactic base excess, to be applied in all types of hemodialysis patients to help diagnose this clinical condition.Methodology: An observational, analytical, prospective and longitudinal study was carried out in hemodialysis of the Instituto Mexicano del Seguro Social, in León, Guanajuato from May 2020 to June 2021 by determining the alactic base excess. The association of alactic base excess as a marker of circulatory stress in hemodialysis was proposed as a primary end point and mortality at 12 months was evaluated as a secondary end point.Results: An inverse association was found between the alactic base excess with the initial pH (r= -0.303, p= <0.05) and the final lactate (r= -0.297, p= <0.05), in addition to bicarbonate (r= 0.593, p= <0.05) and central venous saturation variability (r= 0.304, p= <0.05). In the analysis by subgroups, both lower tertiles had a higher risk of presenting the adverse event (HR= 0.817, [95% CI 0.21 to 3.05], p= 0.763). No association of mortality was found with the first (HR= 0.95, [95% CI= 0.73 to 1.2], p= 0.687) or final determination (HR= 1, [95% CI= 0.758 to 1.3], p= 0.99).Discussion: In this study we found that the alactic base excess proposed to diagnostic different types of acidosis is capable of identifying small changes related to circulatory stress, regardless of the chronicity of kidney failure, hemodynamic status or hemoglobin concentration, but not related to mortality.Conclusions: Alactic base excess is potentially useful to evaluate circulatory stress in conjunction with other tissue hypoperfusion markers, however it would be necessary to expand the sample size and introduce therapeutic variables to determine its clinical impact.

High venous to arterial CO2 gap is related to cardiovascular death in cardiogenic shock

Funding Acknowledgements Type of funding sources: None. Background Venous to arterial CO2 gap (CO2gap) is calculated by subtracting partial pressure of arterial CO2 to central venous partial pressure of CO2 (ScvCO2). This marker has been studied in septic shock and indicates hypoperfusion when exceeds 6mmHg. Its kinetics and applicability in cardiogenic shock (CS) are unclear, being mixed/central venous saturation and lactate more commonly used. Purpose The objective of the study is to describe CO2gap kinetics in patients with CS. Secondary objective is to analyze if CO2gap is as marker of prognosis in CS. Methods Prospective observational study that included patients admitted for CS in the Acute Cardiovascular Care Unit of a tertiary hospital. Gasometric samples were obtained at admission, 6, 12, 24 and 48 hours from the onset of shock. In-hospital mortality was registered. Results We included 40 patients with CS during 1 year. Most patients were male (80%), average age was 68 years. There was a high incidence of cardiac arrest (58%), most frequent cause of CS was STEMI (45%), in-hospital mortality was 45%, most cases from non-cardiovascular causes (61%). Refractory shock was frequent (28%). Average lactate peak was 6.02 mmol / L. CO2gap kinetics consisted in a peak at admission (8.8mmHg), a valley 6h (7.7mmHg), new peak at 12h (8.5mmHg) and progressive decrease at at 24 (6.8mmHg) and 48h (5.7 mmHg). Significantly, higher CO2gap values at admission (10.97mmHg vs 8.16mmHg, p = 0.007) was predictor of cardiovascular mortality. Lactate values at 6, 12 and 48 hours were also predictors of cardiovascular mortality, as well as ScvO2 at admission. Conclusions Patients with CS present with high CO2gap values during first hours of admission. The kinetics of this marker consists in two peaks at admission and 12 hours from CS onset, a valley at 6 hours and a progressive decrease at 24 and 48 hours. Its determination at admission is associated with cardiovascular mortality. We suggest the potential benefit of combining this marker, along with lactate and ScvO2 values, to guide management of patients with CS. Abstract Figure. CO2 gap and cardiovascular mortality

¿Hay factores pronósticos de mortalidad en el paciente séptico en la UCI? El valor de la tasa de eliminación de lactato sérico

La sepsis es la primera causa de muerte por infección en el mundo y el pronóstico es tiempo dependiente de un tratamiento eficaz. Existen descritos numerosos factores pronósticos en la bibliografía sin embargo hay pocos estudios que los comparen entre ellos para valorar si hay alguno con mayor peso frente a otros. El presente artículo, con una muestra de 82 pacientes, analiza diferentes factores pronósticos en las primeras 24 horas de ingreso como indicadores de supervivencia a los 28 días. Estos son: cifras de lactato, su tasa de eliminación, la saturación venosa central y la diferencia entre la saturación de oxígeno arterio-venosa central. Los resultados muestras que las cifras de lactato a las 24 horas son los que presentan una sensibilidad-especificadad mayores (punto de corte de 2,15 mmol/dl), seguido por la cifra de lactato a las 12 y a las 6 horas. ABSTRACT Are there prognostic factors for mortality in the septic patient in the ICU? The value of the serum lactate elimination rate Sepsis is the first cause of death due to infection in the world and the prognosis is time dependent on effective treatment. There are numerous prognostic factors described in the literature, however there are just a few studies comparing them among them to assess if there is one with greater weight compared to others. The present article, with a sample of 82 patients, analyzes different prognostic factors in the first 24 hours of admission as survival indicators at 28 days. These are: lactate numbers, their elimination rate, central venous saturation and the difference between central arteriovenous oxygen saturation. The results show that the lactate levels at 24 hours are the ones with higher sensitivity-specificity (cut-off point of 2.15 mmol / dl), followed by the lactate levels at 12 and at 6 hours.

A case report: a 22-year-old septic patient with central venous pO2 of 198 mmHg

Background Central venous saturation and central venous pressure can be determined with central venous catheters. Therefore, the tip of the catheter should be located in the superior vena cava. The location can be monitored by electrocardiography or X-ray. The central venous pressure curve is displayed on the monitor. The reference value of central venous saturation is &gt;70%. Venous pO2 is normally 35–45 mmHg and central venous pressure 1–9 mmHg. Case summary We treated a 22-year-old patient with septic shock. Central venous saturation was 100% with a pO2 of 198 mmHg. The arterial blood gas analysis was comparatively low with saturation of 98% and pO2 of 111 mmHg. On chest X-ray, the central venous catheter tip appeared on the left side of the heart. On echocardiography, aortic positioning was not evident. On the monitor, a ‘venous pressure-like’ curve was seen, that did not stand in exact correlation to the electrocardiogram curve. The computed tomography (CT) image showed placement of the catheter in the upper left pulmonary vein. The patient had a partial anomalous pulmonary venous return. Discussion The C-wave of the central venous pressure curve normally occurs after the R-wave of the electrocardiogram. If C-waves appeared before R-waves, the central venous catheter placement is not central venous and must be checked. In our case, the apparent ‘venous’ pO2 in blood gas examination was higher than arterial pO2. The catheter position had to be in an oxygenated vessel proximal to the left ventricle. A vascular anomaly was a possible diagnosis and was confirmed on CT imaging.

Theoretical models of changes in haemodynamic parameters and gas exchange in univentricular circulation

<!-- x-tinymce/html --><div><strong>Aim.</strong> To develop theoretical models of changes in haemodynamic parameters of patients with univentricular haemodynamics.</div><div><strong>Methods.</strong> We analysed the effects of redistributing blood flow between the two circulatory systems (pulmonary and systemic) on systemic oxygen delivery and examined changes in the arterial and venous blood gas compositions. Mathematical analyses on the basis of oxygen flow into the pulmonary circulatory system and its consumption during circulation were performed according to Fick principle for cardiac output. Calculations were performed using equations describing changes in the delivery and consumption of oxygen during univentricular circulation. Furthermore, computer simulations were employed to investigate changes in haemodynamic parameters and gas exchange associated with pathological processes such as pulmonary venous hypoxemia, reduction in systemic flow rate and mixed venous blood desaturation. Calculations were performed under conditions with oxygen concentration of &gt;0% or &lt;100%.</div><div><strong>Results.</strong> A number of theoretical models were developed, which described (i) the distribution of systemic and pulmonary blood flow and changes in arterial oxygenation depending on Qp/Qs; (ii) the ratio of systemic blood flow to Qp/Qs; (iii) changes in arterial oxygenation depending on Qp/Qs at different levels of central venous saturation; (iv) changes in pulmonary venous saturation depending on arterial saturation and Qp/Qs under conditions of normal and reduced blood flow; (v) level of central venous saturation depending on changes in Qp/Qs and SpvO₂ at systemic SaO₂ of 75% and (vi) PaO2 dynamics depending on changes in PpvO₂ and Qp/Qs.</div><div><strong>Conclusion.</strong> Changes in the oxygen status of patients with univentricular haemodynamics with sufficient combined cardiac output are indicative of the distribution of blood flow. Assessments of the developed models demonstrated that a number of additional factors affect changes in the oxygen composition of blood including (i) the initial level of arterial oxygenation; (ii) the level of oxygenation in the pulmonary veins and (iii) the ratio of pulmonary to systemic blood flow. In addition, the results indicated that PCO₂ recorded in the pulmonary veins, arteries and mixed venous blood largely depends on Qp/Qs. The theoretical models presented here can be used to compare the results of haemodynamic status assessments of patients with univentricular physiology.</div><div> </div><div>Received 22 May 2019. Revised 4 November 2019. Accepted 10 November 2019.</div><div> </div><div><strong>Funding:</strong> The study did not have sponsorship.</div><div> </div><div><strong>Conflict of interest:</strong> Authors declare no conflict of interest.</div>