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array:23 [ "pii" => "S2341192919301854" "issn" => "23411929" "doi" => "10.1016/j.redare.2019.04.001" "estado" => "S300" "fechaPublicacion" => "2020-01-01" "aid" => "1041" "copyrightAnyo" => "2019" "documento" => "article" "crossmark" => 1 "subdocumento" => "rev" "cita" => "Revista Española de Anestesiología y Reanimación (English Version). 2020;67:20-34" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "Traduccion" => array:1 [ "es" => array:18 [ "pii" => "S0034935619301197" "issn" => "00349356" "doi" => "10.1016/j.redar.2019.04.001" "estado" => "S300" "fechaPublicacion" => "2020-01-01" "aid" => "1041" "documento" => "article" "crossmark" => 1 "subdocumento" => "rev" "cita" => "Rev Esp Anestesiol Reanim. 2020;67:20-34" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 365 "formatos" => array:2 [ "HTML" => 199 "PDF" => 166 ] ] "es" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Revisión</span>" "titulo" => "El algoritmo de la gasometría arterial: propuesta de un enfoque sistemático para el análisis de los trastornos del equilibrio ácido-base" "tienePdf" => "es" "tieneTextoCompleto" => "es" "tieneResumen" => array:2 [ 0 => "es" 1 => "en" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "20" "paginaFinal" => "34" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "The arterial blood gas algorithm: Proposal of a systematic approach to analysis of acid-base disorders" ] ] "contieneResumen" => array:2 [ "es" => true "en" => true ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0025" "etiqueta" => "Figura 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr5.jpeg" "Alto" => 1386 "Ancho" => 2442 "Tamanyo" => 272586 ] ] "descripcion" => array:1 [ "es" => "<p id="spar0075" class="elsevierStyleSimplePara elsevierViewall">Lista de diagnósticos diferenciales de origen renal y no renal, basada en la brecha osmolal de orina del inglés, Urine Osmolal Gap (UOG), para la acidosis metabólica con brecha aniónica normal (= acidosis metabólica hiperclorémica).</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "S. 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"apellidos" => "Fletcher" ] ] ] ] ] "idiomaDefecto" => "es" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2341192919301854" "doi" => "10.1016/j.redare.2019.04.001" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2341192919301854?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0034935619301197?idApp=UINPBA00004N" "url" => "/00349356/0000006700000001/v2_202001231002/S0034935619301197/v2_202001231002/es/main.assets" ] ] "itemSiguiente" => array:18 [ "pii" => "S2341192919301751" "issn" => "23411929" "doi" => "10.1016/j.redare.2019.08.001" "estado" => "S300" "fechaPublicacion" => "2020-01-01" "aid" => "1067" "documento" => "simple-article" "crossmark" => 1 "subdocumento" => "crp" "cita" => "Revista Española de Anestesiología y Reanimación (English Version). 2020;67:35-8" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Case report</span>" "titulo" => "Extracorporeal CO<span class="elsevierStyleInf">2</span> removal in a case of respiratory distress syndrome by sepsis" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "35" "paginaFinal" => "38" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Eliminación extracorpórea de CO<span class="elsevierStyleInf">2</span> en un caso de síndrome de distrés respiratorio por sepsis" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1000 "Ancho" => 750 "Tamanyo" => 93832 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Parallel assembly of the Prismalung® device in the extracorporeal circuit of the hemodiafiltration device.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "R. Méndez Hernández, F. Ramasco Rueda, A. Planas Roca" "autores" => array:3 [ 0 => array:2 [ "nombre" => "R." "apellidos" => "Méndez Hernández" ] 1 => array:2 [ "nombre" => "F." "apellidos" => "Ramasco Rueda" ] 2 => array:2 [ "nombre" => "A." "apellidos" => "Planas Roca" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0034935619301628" "doi" => "10.1016/j.redar.2019.08.004" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0034935619301628?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2341192919301751?idApp=UINPBA00004N" "url" => "/23411929/0000006700000001/v1_202001310725/S2341192919301751/v1_202001310725/en/main.assets" ] "itemAnterior" => array:19 [ "pii" => "S2341192919301738" "issn" => "23411929" "doi" => "10.1016/j.redare.2019.03.014" "estado" => "S300" "fechaPublicacion" => "2020-01-01" "aid" => "1026" "copyright" => "Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor" "documento" => "simple-article" "crossmark" => 1 "subdocumento" => "crp" "cita" => "Revista Española de Anestesiología y Reanimación (English Version). 2020;67:15-9" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Brief report</span>" "titulo" => "Perioperative anesthetic management of patients with malignant pleural mesothelioma undergoing cytoreductive surgery and intraoperative chemotherapy" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "15" "paginaFinal" => "19" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Manejo anestésico perioperatorio de pacientes con mesotelioma maligno pleural intervenidos mediante cirugía citorreductora y quimioterapia intratorácica" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1051 "Ancho" => 1602 "Tamanyo" => 54440 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Pain control during the early postoperative period.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "J.M. Gómez Tarradas, G. Pujol Fontrodona, M. López-Baamonde, D. Sánchez, M.J. Jiménez, R. Navarro-Ripoll" "autores" => array:6 [ 0 => array:2 [ "nombre" => "J.M." "apellidos" => "Gómez Tarradas" ] 1 => array:2 [ "nombre" => "G." "apellidos" => "Pujol Fontrodona" ] 2 => array:2 [ "nombre" => "M." "apellidos" => "López-Baamonde" ] 3 => array:2 [ "nombre" => "D." "apellidos" => "Sánchez" ] 4 => array:2 [ "nombre" => "M.J." "apellidos" => "Jiménez" ] 5 => array:2 [ "nombre" => "R." "apellidos" => "Navarro-Ripoll" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0034935619300738" "doi" => "10.1016/j.redar.2019.03.003" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0034935619300738?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2341192919301738?idApp=UINPBA00004N" "url" => "/23411929/0000006700000001/v1_202001310725/S2341192919301738/v1_202001310725/en/main.assets" ] "en" => array:20 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Review</span>" "titulo" => "The arterial blood gas algorithm: Proposal of a systematic approach to analysis of acid-base disorders" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "20" "paginaFinal" => "34" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "S. Rodríguez-Villar, B.M. Do Vale, H.M. Fletcher" "autores" => array:3 [ 0 => array:4 [ "nombre" => "S." "apellidos" => "Rodríguez-Villar" "email" => array:1 [ 0 => "sancho.villar@nhs.net" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "B.M." "apellidos" => "Do Vale" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 2 => array:3 [ "nombre" => "H.M." "apellidos" => "Fletcher" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Critical Care Department, King’s College Hospital, London, UK" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Critical Care Department, Centro Hospitalar Universitário do Porto (CHUP), Porto, Portugal" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "El algoritmo de la gasometría arterial: propuesta de un enfoque sistemático para el análisis de los trastornos del equilibrio ácido-base" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0025" "etiqueta" => "Fig. 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr5.jpeg" "Alto" => 1391 "Ancho" => 2425 "Tamanyo" => 336376 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0025" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">List of differential diagnosis of renal and non-renal origin based on the urine osmolal gap (UOG) for the metabolic acidosis with normal anion gap (=hyperchloremic metabolic acidosis).</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Approach to the analysis of acid-based disorders</span><p id="par0005" class="elsevierStylePara elsevierViewall">Our approach to the diagnosis of an acid-base disorder involves a stepwise method including 1) validation of the internal consistency of the acid-base parameters available; 2) use of information from the clinical history and physical examination; 3) calculation of the albumin-corrected serum anion gap and the change in the anion gap compared to change in serum bicarbonate (delta anion gap/delta bicarbonate); and 4) determination of the primary initiating mechanism and appropriateness of the secondary adaptive response. For some disturbances, measurements of serum osmolality and urine electrolytes are useful.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1–5</span></a> Finally, to determine the appropriate therapy, it is necessary to assess the severity of the acid-base disturbance. Currently, therapy is chosen on the basis of a study of arterial or venous blood gases, and aggressive therapy is recommended if blood pH is ≤ 7.20. However, even less severe acidemia can be associated with significant clinical abnormalities.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Normal acid-base parameters</span><p id="par0010" class="elsevierStylePara elsevierViewall">First, it is essential to identify normal acid-base parameters to establish the baseline on which changes can be described.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1–5</span></a> Based on a recent theoretical analysis and a large database review, we suggest that the mean values for serum (total CO<span class="elsevierStyleInf">2</span>/HCO3−) are approximately 25 mEq/L in healthy men and 24 mEq/L in healthy women at sea level. Additionally, a reasonable reference range for serum (total CO<span class="elsevierStyleInf">2</span>/HCO3−) is 22–30 mEq/L in healthy adults at sea level.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> Based on studies in a small number of healthy men, a plasma pH of 7.38–7.42 is considered normal.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> Values above 1500 feet, an altitude at which hypoxemia can cause hyperventilation and chronic respiratory alkalosis, have not been well established.</p><p id="par0015" class="elsevierStylePara elsevierViewall">If the baseline values (total CO<span class="elsevierStyleInf">2</span>/HCO3−) are known, those values should be used to assess the acid-base disorder. In their absence, we suggest using the mean values noted above. Values for plasma (HCO3−) will be approximately 1–1.5 mE/L lower. Thus, values < 7.38 (pH < 7.38) are termed acidemia, and values above 7.42 are termed alkalemia.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Serum (HCO3−) < 23 mEq/L is termed hypobicarbonatemia, and serum (HCO3−) > 30 mEq/L is indicative of hyperbicarbonatemia.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Assessment of acid-base disorders</span><p id="par0020" class="elsevierStylePara elsevierViewall">Errors in the measurement of plasma pH, pCO<span class="elsevierStyleInf">2</span> or serum (total CO<span class="elsevierStyleInf">2</span>/HCO3−) are not uncommon. To identify errors, it is usefule to insert the obtained values into the Henderson-Hasselbalch equation (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>).<elsevierMultimedia ident="eq0005"></elsevierMultimedia></p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">If the values do not fit, this could suggest an error in one or more of the parameters, and the measurements should be repeated (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). A focused history should be obtained, and a complete physical examination performed.<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,3</span></a> The primary initiating mechanism should be determined, and the appropriateness of the secondary adaptive response should be assessed. The serum anion gap (AG), change in the AG from baseline (ΔAG), change in serum levels (HCO3−) and change in serum (HCO3−) from baseline Δ (HCO3−) should be calculated, and the relationship between the Δ (HCO3−) and ΔAG should then be determined.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Definitions of primary acid-base disorders</span><p id="par0030" class="elsevierStylePara elsevierViewall">The four cardinal acid-base disorders are shown in <a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>. A simple acid-base disorder represents both the primary change in serum levels (HCO3−) or PaCO<span class="elsevierStyleInf">2</span> and appropriate secondary response.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> Each of the secondary responses evolves over time. For example, the immediate respiratory response to metabolic acidosis, alkalosis, or respiratory acidosis is observed within minutes, but the chronic response evolves over hours or days. Therefore, unless the clinician knows precisely when an acid-base disorder began, the written reports should reflect this uncertainty.</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Metabolic acidosis</span><p id="par0035" class="elsevierStylePara elsevierViewall">Metabolic acidosis is an acid-base disorder initiated by a reduction in plasma or serum levels (HCO3−) (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). It is associated with a secondary decrease in PCO<span class="elsevierStyleInf">2</span>, which represents the physiologic compensatory response.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> It is usually associated with a low plasma pH<span class="elsevierStyleInf">(pH<7.38)</span>.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,2,8–10</span></a></p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0040" class="elsevierStylePara elsevierViewall">Recently, patients in whom acid is retained in the interstitial compartments without a detectable change in serum levels (HCO3−) or plasma pH have been identified. This has been termed subacute or eubicarbonatemic metabolic acidosis. Importantly, these patients might present adverse effects similar to patients with overt metabolic acidosis. It is hard to identify these patients today, but appropriate methods might be available in the future.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Metabolic acidosis can also be classified according to duration. Acute metabolic acidosis is arbitrarily defined as lasting from minutes to days, and chronic metabolic acidosis lasts for weeks to years.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> This distinction has not been subject to rigorous examination, and could be redefined in the future. Importantly, the adverse effects of acute and chronic metabolic acidosis differ in many respects, as shown in <a class="elsevierStyleCrossRef" href="#tbl0015">Table 3</a>.</p><elsevierMultimedia ident="tbl0015"></elsevierMultimedia><p id="par0050" class="elsevierStylePara elsevierViewall">A priori, it has been suggested that most cases of acute, particularly severe, metabolic acidosis are due to diabetic ketoacidosis and lactic acidosis.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></p><p id="par1111" class="elsevierStylePara elsevierViewall">Non-gap metabolic acidosis is a common cause of acute metabolic acidosis, and is attributed to aggressive fluid therapy with chloride-containing solutions (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>). In addition, chronic kidney disease is probably the most common cause of normal and high anion-gap metabolic acidosis.<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">14–16</span></a></p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par1246" class="elsevierStylePara elsevierViewall">The relationship between the severity of the acidosis (as defined by serum HCO3−) and PaCO<span class="elsevierStyleInf">2</span> varies, depending on the time elapsed between onset and evaluation of the patient. Within the first 8 h, PaCO<span class="elsevierStyleInf">2</span> is reduced by 0.85 mmHg for every 1 mEq/L reduction in serum levels (HCO3−).<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> Subsequently, the adaptive response becomes more vigorous, and is complete 24 h after the onset of metabolic acidosis, although complete normalization of blood pH is not apparent.</p><p id="par0055" class="elsevierStylePara elsevierViewall">PCO<span class="elsevierStyleInf">2</span> is reduced 1–1.3 mmHg for every 1 mEq/L decrement in serum (HCO3−). The expected pCO<span class="elsevierStyleInf">2</span> can also be determined using Winter´s formula: PCO<span class="elsevierStyleInf">2</span> = 1.5 X (HCO3−) + 8 ± 2 (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). If the measured pCO<span class="elsevierStyleInf">2</span> is outside the calculated interval range, then a mixed acid-base disorder is present. Mixed disturbances common, particularly in seriously ill patients.<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7,8,18,19</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Metabolic acidosis is subcategorized into two entities based on AG. In the first entity, the AG can remain unchanged from normal: non-anion gap (hyperchloremic), and the AG (high anion gap acidosis) is increased in the second entity. The AG is calculated by subtracting the sum of chloride and bicarbonate from sodium and potassium<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,12,20</span></a> (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>):<elsevierMultimedia ident="eq0010"></elsevierMultimedia></p><p id="par0065" class="elsevierStylePara elsevierViewall">Many clinicians ignore serum potassium because its concentration is low. However, this is being re-evaluated in some studies.<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">21,22</span></a> The AG will vary with fluctuations of serum albumin concentration<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,3,7–9,20</span></a> and should be corrected for the prevailing serum albumin: corrected AG = AG + 2.5 x (4 - serum albumin g/dl).<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">The normal AG can even vary among a cohort of healthy patients (range 10 mEq/L from low to high) and between laboratories, depending on the different methods sed to measure serum chloride. Therefore, it is important for the clinician to know the normal range for their laboratory, and if possible, the normal baseline value for the particular patient.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Deviations from the prevailing normal AG value (either increases or decreases) are caused by several processes. An AG below normal is infrequent and should alert the clinician to either a laboratory error or one of several disorders (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>). A high AG is more common, and is normally associated with overproduction or decreased excretion of organic and inorganic acids.<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">The relationship between the ΔAG Δ (HCO3−) should then be determined. A 1:1 stoichiometry is often assumed between ΔAG and Δ (HCO3−), and deviations from 1:1 indicate an accompanying metabolic acid-base disorder (<a class="elsevierStyleCrossRef" href="#fig0020">Fig. 4</a>). For example, when Δ (HCO3−) exceeds the ΔAG, a normal anion gap (hyperchloremic acidosis) is said to coexist.</p><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0085" class="elsevierStylePara elsevierViewall">In contrast, when ΔAG exceeds the Δ (HCO3−), ametabolic alkalosis (or other hyperbicarbonatemic disorder) is said to coexist.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">Although the ΔAG/ Δ (HCO3−) might be 1:1 in the initial phase of an anion-gap metabolic acidosis, this ratio can potentially change when acidosis persists, and the distribution of protons extends from compartments outside the extracellular fluid can be buffered intracellularly and cause a parallel increase in the ratio.<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">8,20,25</span></a> Additionally, the 1:1 relationship found with ketoacidosis might not hold with lactic acidosis. In lactic acidosis, the relationship can be 1.6:1 early in the course of the disorder (owing to the difference between the volume of anion and proton distributions, a reduction in serum chloride secondary to its dilution by Na<span class="elsevierStyleSup">+</span>, and water in the cells during the buffering process).<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">21,22,26,27</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">Evaluation of the serum osmolal gap (SOG) can be useful, and elevation suggests toxic alcohol poisoning (<a class="elsevierStyleCrossRef" href="#fig0020">Fig. 4</a>). A simple method to determine a change in the SOG from baseline is: SOG (mOsm/kg) = (measured serum osmolality) – 2 × (Na <span class="elsevierStyleSup">++</span> K<span class="elsevierStyleSup">+</span>) + BUN (urea nitrogen) (mg/dL) /2.8 + Glucose (mg/dL)/18.</p><p id="par0100" class="elsevierStylePara elsevierViewall">Baseline values for SOG can vary from negative to close to 10–20 mOsm/kg. Additionally, the increment in SOG will depend on the molecular weight of the toxic alcohol present. Finally, time from exposure will affect the concentration of the parent alcohol. Toxic alcohol poisoning can present with elevated SOG, increased AG, an increase in both AG and SOG, or normal values for both (<a class="elsevierStyleCrossRef" href="#fig0020">Fig. 4</a>). Other disorders, such as lactic acidosis and ketoacidosis, can be associated with increased SOG and AG<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> and should be distinguished from toxic alcohol poisoning.<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">In nonanion gap metabolic acidosis, the decrease in serum (HCO3−) is matched by an equivalent increment in chloride.<a class="elsevierStyleCrossRefs" href="#bib0075"><span class="elsevierStyleSup">15,20</span></a> In fact, the AG might decrease as protons reduce their anionic equivalency.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a></p><p id="par0110" class="elsevierStylePara elsevierViewall">The main pathophysiologic processes that can cause non-anion gap metabolic acidosis are (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>) a loss of bicarbonate from the urinary or gastrointestinal tract, or a decrease in net acid excretion (primarily as the result of decreased ammonium [NH4+] excretion). In contrast to the high anion gap acidosis associated with chronic kidney disease (CKD), there is no retention of filtered anions.</p><p id="par0115" class="elsevierStylePara elsevierViewall">Disorders producing a non-anion gap acidosis are associated with either increased loss of potassium from the body and hypokalemia, or impaired renal excretion and hyperkalemia. Accordingly, non-anion gap acidosis can be divided into acidosis with high or normal serum potassium or acidosis with low serum potassium,<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> as shown in the algorithm (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>).</p><p id="par0120" class="elsevierStylePara elsevierViewall">Additionally, the kidneys can play a prominent role. Documenting whether renal bicarbonate reabsorption is impaired and ammonium excretion is appropriate will allow the clinician to identify the kidneys as a contributing factor. To establish the latter, one should assess the quantity of NH4+ excreted in urine. This can be done indirectly by calculating the urine anion or osmolal gap, as described below (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>), or urine NH4+ can be measured directly.<a class="elsevierStyleCrossRefs" href="#bib0095"><span class="elsevierStyleSup">19,29</span></a><elsevierMultimedia ident="eq0015"></elsevierMultimedia></p><p id="par0125" class="elsevierStylePara elsevierViewall">Urine Osmolal Gap (UOSMG) = measured urine osmolality – 2 x (Na<span class="elsevierStyleSup">+</span> + K<span class="elsevierStyleSup">+</span> )+ BUN (mg/dL)/2.8 + Glucose (mg/dL)/18</p><p id="par0130" class="elsevierStylePara elsevierViewall">The UAG, is negative by 30 mEq/L when NH4+ excretion is appropriate, and less negative or positive when low. Situations in which UAG is abnormal though urinary NH4 excretion is appropriate can be detected by calculating the UOSMG.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a> An UOSMG < 200 mmol/L indicates NH4+ excretion is low, whereas an UOSMG > 200 mmol/L indicates it is adequate<a class="elsevierStyleCrossRefs" href="#bib0150"><span class="elsevierStyleSup">30–32</span></a> (<a class="elsevierStyleCrossRefs" href="#fig0015">Figs. 3 and 5</a>). Urine NH4+ can be measured directly using a modification of the plasma NH4+ assay. Urine should be refrigerated to prevent urea growth from splitting pathogens.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">18–29,33</span></a></p><elsevierMultimedia ident="fig0025"></elsevierMultimedia></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Respiratory acidosis</span><p id="par0135" class="elsevierStylePara elsevierViewall">Respiratory acidosis is an acid-base disorder initiated by an elevation in pCO<span class="elsevierStyleInf">2</span> (hypercapnia). A secondary increase in serum HCO3− can occur, and represents the physiologic compensatory response<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> (<a class="elsevierStyleCrossRef" href="#fig0030">Fig. 6</a>).</p><elsevierMultimedia ident="fig0030"></elsevierMultimedia><p id="par0140" class="elsevierStylePara elsevierViewall">Respiratory acidosis results mainly from normal or increased CO<span class="elsevierStyleInf">2</span> production that cannot be adequately matched by CO<span class="elsevierStyleInf">2</span> excretion through pulmonary ventilation. As in metabolic acidosis, clinical history and physical examination should provide invaluable clues to the etiology of the disorder, and guide the appropriate diagnostic and therapeutic interventions.</p><p id="par0145" class="elsevierStylePara elsevierViewall">The adaptive rise in serum (HCO3−) in response to an increase in PCO<span class="elsevierStyleInf">2</span> can be determined from the formulae in <a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a> (see also <a class="elsevierStyleCrossRef" href="#fig0030">Fig. 6</a>). Deviations in serum (HCO3−) by > 2 mEq/L from predicted suggests the coexistence of a metabolic disorder.</p><p id="par0150" class="elsevierStylePara elsevierViewall">Hypercarbia may cause somnolence (CO<span class="elsevierStyleInf">2</span> narcosis), worsen respiratory depression, and precipitate acute respiratory arrest. Pure respiratory acidosis is easily diagnosed; the pCO<span class="elsevierStyleInf">2</span> will be elevated; arterial pH will be decreased; and the elevation in serum HCO3− will be within range of the calculated level using the respective formulas for acute or chronic hypercapnia.</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Metabolic alkalosis</span><p id="par0155" class="elsevierStylePara elsevierViewall">Metabolic alkalosis is initiated by an elevation in serum (HCO3−).<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,2,8,9</span></a><span class="elsevierStyleSup">,</span><a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> The increase in serum (HCO3−) is followed by suppression of ventilation, with a resulting increase in PaCO<span class="elsevierStyleInf">2</span>. Although this process is initiated relatively quickly after the rise in serum values (HCO3−), an established relationship between these parameters is based on observations 12–24 hours after onset, and assumes that the (HCO3−) has been relatively stable. A pCO<span class="elsevierStyleInf">2</span> within the appropriate range indicates an adequate compensatory response and a simple acid-base disturbance (<a class="elsevierStyleCrossRef" href="#fig0035">Fig. 7</a>). In contrast, if the measured PaCO<span class="elsevierStyleInf">2</span> is outside the calculated interval range, then a mixed acid-base disorder is present (if >2 mmHg of predicted value, concomitant respiratory acidosis; if <2 mmHg of predicted value, concomitant respiratory alkalosis).<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> Combined disturbances are not uncommon. Metabolic alkalosis and respiratory alkalosis are frequently seen in ICU patients with gastric drainage and infection. Similarly, metabolic alkalosis and respiratory acidosis are frequent present in patients with chronic lung disease receiving diuretics.</p><elsevierMultimedia ident="fig0035"></elsevierMultimedia><p id="par0160" class="elsevierStylePara elsevierViewall">The most common mechanisms responsible for the generation of metabolic alkalosis are either a direct loss of hydrogen, administration of bicarbonate (or its precursors, e.g., citrate) rich solutions, or volume depletion (<a class="elsevierStyleCrossRef" href="#fig0040">Fig. 8</a>).</p><elsevierMultimedia ident="fig0040"></elsevierMultimedia><p id="par0165" class="elsevierStylePara elsevierViewall">The kidney has the ability to correct metabolic alkalosis by excreting excess HCO3−. Consequently, the persistence of metabolic alkalosis requires an impairment of the kidney´s ability to excrete the excess load of HCO3−. This impairment can be due to the confluence of several factors, including a reduction in the effective circulating volume and glomerular filtration rate, chloride depletion, secondary hyperaldosteronism, and hypokalemia.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0170" class="elsevierStylePara elsevierViewall">When alkalemia is severe (pH > 7.55), mortality can reach 40 % or more. Therefore, clinicians should be vigilant in following these acute patients, and make every effort to maintain serum HCO3− levels at < 30 mmol/L (mEq/L). Additionally, as noted above, it is very common for both metabolic alkalosis and respiratory alkalosis to coexist. This combination will produce the most severe alkalemia.</p><p id="par0175" class="elsevierStylePara elsevierViewall">Metabolic alkalosis can be divided into two broad categories, based on their response to administered chloride (<a class="elsevierStyleCrossRef" href="#fig0040">Fig. 8</a>): chloride responsive (urine Cl<span class="elsevierStyleSup">−</span> concentration is usually <20 mmol/L) and chloride-resistant (urine Cl<span class="elsevierStyleSup">−</span> concentration >20 mmol/L). Serum electrolytes are similar in all cases of metabolic alkalosis, i.e., hypochloremia, elevated serum bicarbonate, and decreased serum K<span class="elsevierStyleSup">+</span>. In Cl<span class="elsevierStyleSup">−</span> responsive metabolic alkalosis associated with volume contraction, the anion gap value can be slightly elevated (by as much as 6 mmol/L).</p><p id="par0180" class="elsevierStylePara elsevierViewall">The investigation of metabolic alkalosis starts with an evaluation of the patient’s intravascular volume status based on clinical variables, such as blood pressure, heart rate, orthostatic changes in blood pressure, urine output, mentation, capillary refill time, presence of edema, urea and creatinine levels (<a class="elsevierStyleCrossRef" href="#fig0035">Fig. 7</a>). This initial evaluation should help the clinician divide these patients into two major groups: the first with normal or raised intravascular volume status, and the second with decreased intravascular volume status (<a class="elsevierStyleCrossRefs" href="#fig0040">Figs. 8 and 9</a>).</p><elsevierMultimedia ident="fig0045"></elsevierMultimedia><p id="par0185" class="elsevierStylePara elsevierViewall">The conditions most often associated with individuals in the first group are related to high mineralocorticoid pathway activity. Measurements of serum renin and aldosterone activity may provide the definitive evidence for a conclusive diagnosis (see <a class="elsevierStyleCrossRef" href="#tbl0020">Table 4</a>).</p><elsevierMultimedia ident="tbl0020"></elsevierMultimedia><p id="par0190" class="elsevierStylePara elsevierViewall">The second group of patients most often suffer from conditions associated with loss of body fluids (e.g., vomiting, diuresis, or tubular reabsorptive defects). In this setting, a measurement of urine electrolytes will be helpful in making the distinction. A low urinary Cl<span class="elsevierStyleSup">−</span>(<20 mmol/L) and a low urinary Na<span class="elsevierStyleSup">+</span> (<20 mmol/L) is suggestive of a posthypercapnic state (common among ITU treated patients in which rapid correction of pCO<span class="elsevierStyleInf">2</span> by mechanical ventilation does not allow time for the kidney to compensate), remote diuretic use, or remote non-active vomiting. Conversely, a low urinary Cl<span class="elsevierStyleSup">−</span> with a high urinary Na<span class="elsevierStyleSup">+</span> (>20 mmol/L) is suggestive of active vomiting or excretion of nonreabsorbed anions.</p><p id="par0195" class="elsevierStylePara elsevierViewall">A high urinary Cl<span class="elsevierStyleSup">−</span> (>20 mmol/L) suggests the use of diuretics, Mg<span class="elsevierStyleSup">2+</span> deficiency, Barters’ syndrome, Gitelman´s syndrome, alkali administration (such citrate) or hypokalemia.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> With normal or elevated intravascular volume, conditions associated with high mineralocorticoid activity are likely (<a class="elsevierStyleCrossRef" href="#fig0030">Fig. 6</a>).</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Respiratory alkalosis</span><p id="par0200" class="elsevierStylePara elsevierViewall">Respiratory alkalosis is initiated by a reduction in PaCO<span class="elsevierStyleInf">2</span> with a secondary decrease in serum (HCO3−). When mild, the plasma pH might be within the normal range, but when it is more severe, patients usually present with elevated plasma pH (pH > 7.42).<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,2,8,18,32</span></a></p><p id="par0205" class="elsevierStylePara elsevierViewall">Acute hypocapnia results in a more marked deviation in blood pH than chronic hypocapnia. Generally, the changes in acid-base parameters occur in two phases, similar to respiratory acidosis. Within the first 10 min, a release of protons from body buffers leads to a small decrease in serum (HCO3−) concentration. Serum HCO3− concentration is reduced by 2 mmol/L for every 10 mmHg decrease in PaCO<span class="elsevierStyleInf">2</span>. When alkalosis is prolonged by more than 24–36 hours, the suppression of respiration is more pronounced, with HCO3− being reduced by approximately 5 mmol/L for every 10 mmHg reduction of paCO<span class="elsevierStyleInf">2</span>. Of note, mild chronic hypocapnia can result in serum HCO3− and blood pH within the normal ranges, and therefore might be difficult to detect. An alkalemic pH, particularly when severe, can predispose the patient to arrhythmias due to both a decrease in ionized calcium levels and increase in cellular pH and external pH.<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4,13</span></a> (<a class="elsevierStyleCrossRef" href="#tbl0025">Table 5</a> and <a class="elsevierStyleCrossRef" href="#fig0050">Fig. 10</a>)</p><elsevierMultimedia ident="tbl0025"></elsevierMultimedia><elsevierMultimedia ident="fig0050"></elsevierMultimedia></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Mixed acid-base disorders</span><p id="par0210" class="elsevierStylePara elsevierViewall">The combination of two metabolic disturbances, a metabolic and respiratory disturbance, or two metabolic and one respiratory disturbances (triple acid-base disturbances) are common, particularly in seriously ill patients.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">18,19</span></a> (<a class="elsevierStyleCrossRef" href="#tbl0030">Table 6</a>).</p><elsevierMultimedia ident="tbl0030"></elsevierMultimedia><p id="par0215" class="elsevierStylePara elsevierViewall">In most disturbances (except for mild chronic hypocapnia), blood pH is outside normal limits. Therefore, any deviation from normal of serum (HCO3−) or PaCO<span class="elsevierStyleInf">2</span> associated with a normal plasma pH suggests the presence of a mixed acid-base disorder.</p><p id="par0220" class="elsevierStylePara elsevierViewall">The diagnosis of acid-base disorders is an essential step in the care of patients. The foregoing discussion introduced the basic concepts of acid-base analysis. An algorithm summarizing this approach is shown in <a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>. Although not perfect, it should allow the clinician to make a rapid assessment of the acid-base profile of the individual patient. However, the clinician should always be aware of the limitations of any formalized approach, and close patient follow-up is essential.</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Conclusions</span><p id="par0225" class="elsevierStylePara elsevierViewall">In this review, we attempted to provide the reader with a stepwise approach to the diagnosis of acid-base disorders using arterial blood gas as a fundamental tool, and the physiologic, bicarbonate-centric approach for analysis. Thus, by revealing and explaining some of the complexities and limitations of the arterial blood gas interpretation, we hope to equip the clinician with a framework to correctly interpret the data, maximize the information that can be extracted from it, and minimize errors or incorrect interpretations.</p><p id="par0230" class="elsevierStylePara elsevierViewall">We also discussed some of the current limitations of serum anion gap interpretations and urine anion and osmolar gap measurements; we presented future improvements that should be adopted, such as direct measurements of urinary NH4+ that will likely improve the diagnostic accuracy for renal tubular acidosis and related disorders.</p><p id="par0235" class="elsevierStylePara elsevierViewall">Arterial blood gas results must be contextualized in the clinical scenario in order to arrive at a correct diagnosis and implement the appropriate therapeutic modality.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">34</span></a> Thus, the patient’s clinical history and a detailed physical examination are indispensable for the reasoning process.</p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Funding</span><p id="par0250" class="elsevierStylePara elsevierViewall">Financial support, including any institutional departmental funds, was not sought for the study.</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Conflict of interests</span><p id="par0245" class="elsevierStylePara elsevierViewall">All faculty and staff in a position to control or affect the content of this paper have declared that they have no competing financial interests.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:17 [ 0 => array:3 [ "identificador" => "xres1294715" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1195613" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1294716" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1195612" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Approach to the analysis of acid-based disorders" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Normal acid-base parameters" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Assessment of acid-base disorders" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Definitions of primary acid-base disorders" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Metabolic acidosis" ] 9 => array:2 [ "identificador" => "sec0030" "titulo" => "Respiratory acidosis" ] 10 => array:2 [ "identificador" => "sec0035" "titulo" => "Metabolic alkalosis" ] 11 => array:2 [ "identificador" => "sec0040" "titulo" => "Respiratory alkalosis" ] 12 => array:2 [ "identificador" => "sec0045" "titulo" => "Mixed acid-base disorders" ] 13 => array:2 [ "identificador" => "sec0050" "titulo" => "Conclusions" ] 14 => array:2 [ "identificador" => "sec0065" "titulo" => "Funding" ] 15 => array:2 [ "identificador" => "sec0060" "titulo" => "Conflict of interests" ] 16 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2019-01-31" "fechaAceptado" => "2019-04-29" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1195613" "palabras" => array:3 [ 0 => "Arterial blood gas" 1 => "Acid-base disorders" 2 => "Algorithm of arterial gas analysis" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1195612" "palabras" => array:3 [ 0 => "Gasometría arterial" 1 => "Trastorno ácido-base" 2 => "Algoritmo para el análisis de gases arteriales" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0090" class="elsevierStyleSimplePara elsevierViewall">Abnormalities in the acid-base balance are common clinical problems that can have deleterious effects on cellular function, and can suggest various disorders. Therefore, it is important for the clinician to correctly diagnose the acid-base disorder (s) in order to provide the best treatment.</p><p id="spar0095" class="elsevierStyleSimplePara elsevierViewall">Three approaches have been proposed to evaluate acid-base disorders: a bicarbonate-centric approach; the Stewart approach; and the base excess approach. Although the latter two have many adherents, we will only discuss the bicarbonate-centric approach.</p><p id="spar0100" class="elsevierStyleSimplePara elsevierViewall">This approach is simpler to use at the bedside, involves a physiological evaluation of the acid-base disorder, presents an easily understandable approach to severity assessment, and provides a more solid foundation for the development of effective therapies. Therefore, the following discussion will be limited to an examination of this approach.</p><p id="spar0105" class="elsevierStyleSimplePara elsevierViewall">In this case-centric review, important new concepts will be introduced first; their benefits and limitations discussed; and then their use in the analysis of real cases will be shown.</p><p id="spar0110" class="elsevierStyleSimplePara elsevierViewall">A systematic approach algorithm that incorporates these new concepts has been generated and will be highlighted.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0115" class="elsevierStyleSimplePara elsevierViewall">Las anomalías en el equilibrio ácido-base son problemas clínicos comunes y pueden tener efectos perjudiciales en la función celular y ser el indicio de varios trastornos. Por lo tanto, es importante para el clínico, el hacer un diagnóstico preciso de los trastornos ácido-base presentes para un tratamiento adecuado.</p><p id="spar0120" class="elsevierStyleSimplePara elsevierViewall">Se han propuesto tres enfoques para evaluar los trastornos ácido-base: un enfoque centrado en el bicarbonato; El enfoque de Stewart y el enfoque de exceso de base. Aunque los dos últimos tienen muchos adeptos, sólo discutiremos el enfoque centrado en el bicarbonato.</p><p id="spar0125" class="elsevierStyleSimplePara elsevierViewall">Este enfoque es más fácil de utilizar desde el punto de vista clínico, tiene una evaluación fisiológica del trastorno ácido-base, presenta una lógica fácilmente comprensible para evaluar la gravedad y proporciona además, una base más sólida para el desarrollo de terapias efectivas. Por lo tanto, nuestro trabajo se limitará a un examen en profundidad de esta teoría.</p><p id="spar0130" class="elsevierStyleSimplePara elsevierViewall">En esta revisión, primero se introducirán conceptos importantes nuevos; sus beneficios y discusión de sus limitaciones; y luego se mostrará su utilización para analizar casos reales.</p><p id="spar0135" class="elsevierStyleSimplePara elsevierViewall">Se ha generado un algoritmo para abordar de forma sistemática el análisis que incorpora estos nuevos conceptos.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Rodríguez-Villar S, Do Vale BM, Fletcher HM. El algoritmo de la gasometría arterial: propuesta de un enfoque sistemático para el análisis de los trastornos del equilibrio ácido-base. Rev Esp Anestesiol Reanim. 2020;67:20–34.</p>" ] ] "multimedia" => array:19 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 3087 "Ancho" => 2333 "Tamanyo" => 528663 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">The first step in our approach is to identify errors and prioritize patient safety. We would start checking the arterial pH, pCO<span class="elsevierStyleInf">2</span> and serum bicarbonate for internal consistency using Henderson-Hasselbalch equation. Even an apparently “normal ABG” could potentially carry and acid-base disorder, so it is a good practice to calculate the AG (anion gap) routinely.</p>" ] ] 1 => array:8 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 3416 "Ancho" => 1567 "Tamanyo" => 494280 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0010" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Shows the systematic analysis of metabolic acidosis, initially using Winter's formula to identify the presence of a simple or complex disorder. Next, the AG (“anionic gap'') is calculated and adjusted for albumin, prevailing deviations from normal AG values (increase or decrease) are caused by several processes described in flowcharts 7 ( metabolic acidosis with high anion gap) and 8 (hyperchloraemic metabolic acidosis or normal gap anion).</p>" ] ] 2 => array:8 [ "identificador" => "fig0015" "etiqueta" => "Fig. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 4155 "Ancho" => 2059 "Tamanyo" => 926784 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0015" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Describes the main pathophysiological processes that can cause metabolic acidosis with a normal anion-gap (= hyperchloraemic metabolic acidosis): loss of bicarbonate from the urinary/gastrointestinal tract or a decrease in net acid excretion. Finally, deviations from the 200 mOsm/kg urine osmolal gap (increase or decrease) are caused by several processes that are described in flowcharts 9 and 10, and that may or may not be caused by renal dysfunction.</p>" ] ] 3 => array:8 [ "identificador" => "fig0020" "etiqueta" => "Fig. 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr4.jpeg" "Alto" => 4387 "Ancho" => 2091 "Tamanyo" => 1077034 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0020" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Flow chart for the analysis of metabolic acidosis with high gap anion. It is usually associated with overproduction or decreased excretion of organic and inorganic acids. Evaluation of this type of acidosis is based on calculating the Delta Gap, also called the Delta-Ratio , which rules out the presence of mixed acid-base disorder. Finally, the Serum Osmolal Gap is calculated. This can help identify the presence of unusual substances in plasma, such as methanol or ethylene glycol.</p>" ] ] 4 => array:8 [ "identificador" => "fig0025" "etiqueta" => "Fig. 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr5.jpeg" "Alto" => 1391 "Ancho" => 2425 "Tamanyo" => 336376 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0025" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">List of differential diagnosis of renal and non-renal origin based on the urine osmolal gap (UOG) for the metabolic acidosis with normal anion gap (=hyperchloremic metabolic acidosis).</p>" ] ] 5 => array:8 [ "identificador" => "fig0030" "etiqueta" => "Fig. 6" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr6.jpeg" "Alto" => 2664 "Ancho" => 1254 "Tamanyo" => 335920 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0030" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Respiratory acidosis results mainly from normal or increased CO<span class="elsevierStyleInf">2</span> production that cannot be adequately matched by the CO<span class="elsevierStyleInf">2</span> excretion through pulmonary ventilation. The adaptive rise in serum (HCO3−) in response to an increase in PCO<span class="elsevierStyleInf">2</span> can be determined from the formulae in <a class="elsevierStyleCrossRef" href="#fig0030">Fig. 6</a>.</p>" ] ] 6 => array:8 [ "identificador" => "fig0035" "etiqueta" => "Fig. 7" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr7.jpeg" "Alto" => 2703 "Ancho" => 1258 "Tamanyo" => 273409 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0035" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Metabolic alkalosis. pCO<span class="elsevierStyleInf">2</span> within the appropriate range indicates an adequate compensatory response and a simple acid-base disturbance. In contrast, if the measured pCO<span class="elsevierStyleInf">2</span> is outside the calculated interval range, then a mixed acid-base disorder is present. We can finally classify the aetiology of metabolic alkalosis on the basis of depleted or high/normal intravascular volume, according to flow charts 5 and 6.</p>" ] ] 7 => array:8 [ "identificador" => "fig0040" "etiqueta" => "Fig. 8" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr8.jpeg" "Alto" => 3023 "Ancho" => 2091 "Tamanyo" => 456641 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0040" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">The figure shows the differential diagnosis in the context of volume depletion, divided into two broad categories based on response to administered chloride: chloride responsive (urine Cl<span class="elsevierStyleSup">−</span>concentration is usually <20 mmol/L) and chloride-resistant (urine Cl<span class="elsevierStyleSup">−</span> concentration >20 mmol/L).</p>" ] ] 8 => array:8 [ "identificador" => "fig0045" "etiqueta" => "Fig. 9" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr9.jpeg" "Alto" => 2536 "Ancho" => 841 "Tamanyo" => 213297 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0045" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">The conditions most often associated with individuals with normal or raised intravascular volume status (metabolic alkalosis) are related to high mineralocorticoid pathway activity. Measurements of serum renin and aldosterone activity may provide the definitive evidence for a conclusive diagnosis.</p>" ] ] 9 => array:8 [ "identificador" => "fig0050" "etiqueta" => "Fig. 10" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr10.jpeg" "Alto" => 3996 "Ancho" => 1884 "Tamanyo" => 446492 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0050" "detalle" => "Fig. 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">Respiratory alkalosis is initiated by a reduction in PCO<span class="elsevierStyleInf">2</span> with a secondary decrease in serum (HCO3−). The adaptive reduction in serum (HCO3−) in response to a decrease in PCO<span class="elsevierStyleInf">2</span> can be determined from the formulae shown. HCO3− within the appropriate range indicates an adequate compensatory response and a simple acid-base disturbance. In contrast, if the measured HCO3− is outside the calculated interval range, then a mixed acid-base disorder is present.</p>" ] ] 10 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0055" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " colspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Relationship between pH & (H<span class="elsevierStyleSup">+</span>)</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">pH \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">(H<span class="elsevierStyleSup">+</span>) (nanomoles/l) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">6.8 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">158 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">6.9 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">125 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.0 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">100 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">79 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">63 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.3 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">50 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.4 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">40 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">31 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.6 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">25 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.7 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">20 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.8 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">15 \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2217364.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Validation of the internal consistency of the acid-base data.</p>" ] ] 11 => array:8 [ "identificador" => "tbl0010" "etiqueta" => "Table 2" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0060" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Acid-Base Disturbance \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Initiating factor \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Secondary compensatory response \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Metabolic Acidosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Decrease in serum (HCO3−) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">pCO<span class="elsevierStyleInf">2</span> = 1.5 × HCO3−  +8 ± 2 (Winter’s formula) or decrease in pCO<span class="elsevierStyleInf">2</span> of 1-1.3 mmHg for every 1 mEq/L decrease in serum (HCO3−) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Respiratory Acidosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Increase in pCO<span class="elsevierStyleInf">2</span> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Increase in serum [HCO3−] \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">• Acute (< 72 h): increase of 1 mEq/L in serum [HCO3−] for every 10 mmHg increase of pCO<span class="elsevierStyleInf">2</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">• Chronic (> 72 h): increase of 4 mEq/L in serum [HCO3−] for every 10 mmHg increase in pCO<span class="elsevierStyleInf">2</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Metabolic Alkalosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Increase in serum (HCO3−) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Increase in pCO<span class="elsevierStyleInf">2</span> of 4 – 7 mmHg (mean 5 mmHg) for every 10 mEq/L increase in serum [HCO3−] \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Respiratory Alkalosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Decrease in pCO<span class="elsevierStyleInf">2</span> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">• Decrease in serum [HCO3−] \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Acute (< 48 h): decrease of 2 mEq/L in serum [HCO3−] for every 10 mmHg decrease in pCO<span class="elsevierStyleInf">2</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">• Chronic (> 48 h): decrease of 5 mEq/L in serum [HCO3−] for every 10 mmHg decrease in pCO<span class="elsevierStyleInf">2</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2217360.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Primary acid-base disorders and Secondary Compensatory Response.</p>" ] ] 12 => array:8 [ "identificador" => "tbl0015" "etiqueta" => "Table 3" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0065" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "<p id="spar0070" class="elsevierStyleSimplePara elsevierViewall">2.3-DPG; 2,3 Diphosphoglycerate, Hg; Haemoglobin.</p>" "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Organ System Affected \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Pathophysiologic consequence \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Cardiovascular System \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Decreased cardiac contractilityArterial Vasodilatation HypotensionVenous Vasoconstriction with central pooling of blood \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Predisposition to cardiac arrhythmias \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Respiratory System and O2 delivery \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Stimulation of respirationEarly- decreased binding to Hg (Bohr effect)Late increased 2.3-DPG with reduced binding of O2 to Hb \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Metabolic \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Increased circulating catecholamines Reduced cellular responsiveness to catecholamines \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Changes in circulation parathyroid hormone levels \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Alterations in binding of ligand to calcium sensing receptor \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Electrolytes \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Increased ionized Ca<span class="elsevierStyleSup">2+</span>Hyperkalaemia, Hypokalaemia \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Gastrointestinal System \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Reduced gastrointestinal function \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Central Nervous System \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Decreased sensorium \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2217362.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Conditions associated with metabolic acidosis.</p>" ] ] 13 => array:8 [ "identificador" => "tbl0020" "etiqueta" => "Table 4" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0070" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col"><span class="elsevierStyleItalic">Increased renin and aldosterone activity</span> \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Renal artery stenosis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Accelerated hypertension \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Renin secreting tumors \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleItalic">Decreased renin and increased aldosterone activity</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Primary aldosteronism \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Adrenal adenoma \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Bilateral adrenal hyperplasia \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Dexamethasone responsive adrenal hyperplasia \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleItalic">Decreased renin and aldosterone activity</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Cushing syndrome \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Exogenous mineralocorticoids \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Congenital adrenal defect \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">11- -hydroxylase deficiency \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Liddle’s syndrome \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2217359.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0075" class="elsevierStyleSimplePara elsevierViewall">Conditions associated with high mineralocorticoid activity.</p>" ] ] 14 => array:8 [ "identificador" => "tbl0025" "etiqueta" => "Table 5" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0075" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col"><span class="elsevierStyleItalic">Cardiovascular</span> \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Arterial constriction \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Reduction in coronary blood flow \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Reduction in angina threshold \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Predisposition to refractory supraventricular and ventricular arrhythmias \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleItalic">Respiratory</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Hypoventilation, hypercapnia and hypoxia \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleItalic">Metabolic</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Stimulation of anaerobic glycolysis and organic acid production \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Hypokalemia \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Decreased plasma ionized calcium concentration \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Hypomagnesemia and hypophosphatemia \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleItalic">Cerebral</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Reduction in cerebral blood flow \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Tetany, seizures, lethargy, delirium and stupor \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2217363.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0080" class="elsevierStyleSimplePara elsevierViewall">Pathophysiologic consequences of severe alkalemia by organ system.</p>" ] ] 15 => array:8 [ "identificador" => "tbl0030" "etiqueta" => "Table 6" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0080" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col">Metabolic acidosis and respiratory alkalosis \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col">Severe sepsis and septic shockSalicylate toxicityCongestive heart failure and renal failure \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Metabolic acidosis and respiratory acidosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Cardiorespiratory arrestHypoxemic respiratory failure \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Metabolic alkalosis and metabolic acidosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Diuretic therapy and ketoacidosisVomiting and renal failureVomiting and lactic acidosis/ ketoacidosis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Metabolic alkalosis and respiratory alkalosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Diuretic therapy and chronic hepatic failure \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Diuretic therapy and sepsis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Metabolic alkalosis and respiratory acidosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Diuretic therapy and chronic obstructive pulmonary disease \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Vomiting and chronic obstructive pulmonary disease \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Mixed non anion gap (hyperchloremic) and high– anion gap acidosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Early chronic renal failureDiarrhea and lactic acidosis/ ketoacidosisRenal tubular acidosis and uremic acidosisHyporeninemic hypoaldosteronism and diabetic ketoacidosis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Multiple acid-base disorders \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Mixed metabolic acidosis + metabolic alkalosis + respiratory alkalosis and/or acidosis (ex: cirrhotic alcoholic patient that has a vomit episode, determining metabolic alkalosis, goes into starvation Ketoacidosis, and has concomitant respiratory alkalosis from hyperventilation secondary to liver failure). \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Any combination of the above \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2217361.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0085" class="elsevierStyleSimplePara elsevierViewall">Common mixed acid-base disorders in intensive care.</p>" ] ] 16 => array:5 [ "identificador" => "eq0005" "tipo" => "MULTIMEDIAFORMULA" "mostrarFloat" => false "mostrarDisplay" => true "Formula" => array:1 [ "Quimica" => "H+<span class="elsevierStyleHsp" style=""></span>(nEq/L)<span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span>26 X pCO<span class="elsevierStyleInf">2</span>/HCO3−" ] ] 17 => array:5 [ "identificador" => "eq0010" "tipo" => "MULTIMEDIAFORMULA" "mostrarFloat" => false "mostrarDisplay" => true "Formula" => array:1 [ "Quimica" => "AG = (Na<span class="elsevierStyleSup">+</span>+ K<span class="elsevierStyleSup">+</span>) - (Cl<span class="elsevierStyleSup">−</span> + HCO3−)." ] ] 18 => array:5 [ "identificador" => "eq0015" "tipo" => "MULTIMEDIAFORMULA" "mostrarFloat" => false "mostrarDisplay" => true "Formula" => array:1 [ "Quimica" => "Urine anion gap (UAG) = (Na<span class="elsevierStyleSup">+</span> + K<span class="elsevierStyleSup">+</span>) - Cl<span class="elsevierStyleSup">−</span>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:34 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Management of life-threatening acid-base disorders. 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