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array:23 [ "pii" => "S2173572711000087" "issn" => "21735727" "doi" => "10.1016/j.medine.2010.11.001" "estado" => "S300" "fechaPublicacion" => "2011-06-01" "aid" => "235" "copyright" => "Elsevier España, S.L. and SEMICYUC" "copyrightAnyo" => "2010" "documento" => "article" "crossmark" => 0 "subdocumento" => "ssu" "cita" => "Med Intensiva. 2011;35:288-98" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 28492 "formatos" => array:3 [ "EPUB" => 199 "HTML" => 23310 "PDF" => 4983 ] ] "itemSiguiente" => array:18 [ "pii" => "S2173572711000075" "issn" => "21735727" "doi" => "10.1016/j.medine.2011.03.003" "estado" => "S300" "fechaPublicacion" => "2011-06-01" "aid" => "277" "copyright" => "Elsevier España, S.L. and SEMICYUC" "documento" => "article" "crossmark" => 0 "subdocumento" => "sco" "cita" => "Med Intensiva. 2011;35:299-306" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 8300 "formatos" => array:3 [ "EPUB" => 159 "HTML" => 7221 "PDF" => 920 ] ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Update in Intensive Care Medicine: News in Resuscitation</span>" "titulo" => "News in basic life support and semi-automated external defibrillation" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "299" "paginaFinal" => "306" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Novedades en soporte vital básico y desfibrilación externa semiautomática" ] ] "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" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 3798 "Ancho" => 2500 "Tamanyo" => 807160 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Sequence of intervention in BLS.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "J.B. López-Messa, P. Herrero-Ansola, J.L. Pérez-Vela, H. Martín-Hernández" "autores" => array:4 [ 0 => array:2 [ "nombre" => "J.B." "apellidos" => "López-Messa" ] 1 => array:2 [ "nombre" => "P." "apellidos" => "Herrero-Ansola" ] 2 => array:2 [ "nombre" => "J.L." "apellidos" => "Pérez-Vela" ] 3 => array:2 [ "nombre" => "H." "apellidos" => "Martín-Hernández" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2173572711000075?idApp=WMIE" "url" => "/21735727/0000003500000005/v2_201212101038/S2173572711000075/v2_201212101038/en/main.assets" ] "itemAnterior" => array:18 [ "pii" => "S217357271100004X" "issn" => "21735727" "doi" => "10.1016/j.medine.2011.01.002" "estado" => "S300" "fechaPublicacion" => "2011-06-01" "aid" => "261" "copyright" => "Elsevier España, S.L. and SEMICYUC" "documento" => "article" "crossmark" => 0 "subdocumento" => "sco" "cita" => "Med Intensiva. 2011;35:286-7" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 3320 "formatos" => array:3 [ "EPUB" => 150 "HTML" => 2299 "PDF" => 871 ] ] "en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Point of view</span>" "titulo" => "Tranexamic Acid Therapy Decreases Mortality of Traumatic Hemorrhagic Shock" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "286" "paginaFinal" => "287" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "El ácido tranexámico disminuye la mortalidad del <span class="elsevierStyleItalic">shock</span> hemorrágico traumático" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "A. Muñoz-Sánchez, F. Murillo-Cabezas" "autores" => array:2 [ 0 => array:2 [ "nombre" => "A." "apellidos" => "Muñoz-Sánchez" ] 1 => array:2 [ "nombre" => "F." "apellidos" => "Murillo-Cabezas" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S217357271100004X?idApp=WMIE" "url" => "/21735727/0000003500000005/v2_201212101038/S217357271100004X/v2_201212101038/en/main.assets" ] "en" => array:20 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Review</span>" "titulo" => "Invasive Mechanical Ventilation in COPD and Asthma" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "288" "paginaFinal" => "298" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "E. García Vicente, J.C. Sandoval Almengor, L.A. Díaz Caballero, J.C. Salgado Campo" "autores" => array:4 [ 0 => array:4 [ "nombre" => "E." "apellidos" => "García Vicente" "email" => array:1 [ 0 => "ernesdino@yahoo.es" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">¿</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "J.C." "apellidos" => "Sandoval Almengor" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 2 => array:3 [ "nombre" => "L.A." "apellidos" => "Díaz Caballero" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] 3 => array:3 [ "nombre" => "J.C." "apellidos" => "Salgado Campo" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">d</span>" "identificador" => "aff0020" ] ] ] ] "afiliaciones" => array:4 [ 0 => array:3 [ "entidad" => "Hospital de Santa Bárbara, Soria, Spain" "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Centro Médico ABC, Mexico City, Mexico" "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Geisinger Health System, Danville, PA, United States" "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] 3 => array:3 [ "entidad" => "University of Pittsburgh Medical Center, Pittsburgh, PA, United States" "etiqueta" => "<span class="elsevierStyleSup">d</span>" "identificador" => "aff0020" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Ventilación mecánica invasiva en EPOC y asma" ] ] "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" => 1458 "Ancho" => 1674 "Tamanyo" => 76926 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Occlusion of the expiratory valve.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Chronic obstructive airway disease includes not only chronic obstructive pulmonary disease (COPD) and chronic asthma but also disorders such as bronchiectasis, pneumoconiosis and post-tuberculosis lung disease. COPD is a major health and economical problem of growing prevalence; in the year 1990 it represented the sixth most common cause of deaths worldwide, and by 2020 the disease is expected to become the third most common cause of death. Mortality associated to asthma is also considerable, with an estimated 1–8 deaths per 100,000 inhabitants and year. Adequate triage or screening for admission to the Intensive Care Unit (ICU) is therefore essential among patients at risk.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Although a general indication for almost all conditions, patients of this kind should not receive invasive mechanical ventilatory support, since mortality increases significantly as a result. However, the failure of noninvasive mechanical ventilation (effective in at least 75% of the cases, particularly in COPD), or the prescription of surgery, can lead to a fatal outcome. Heterogeneity and the presence of mixed variants are the rule in patients of this kind, with the frequent combination of physiopathological characteristics of asthma (inflammation of the bronchial tree and bronchospasm), emphysema (loss of parenchymal compliance) and chronic bronchitis (presence of mucosal hypersecretion). The adoption of rigid general strategies for the ventilation of these patients therefore can lead to dangerous simplifications in management approach. Moreover, it must be remembered that patients with emphysema and chronic bronchitis typically have serious comorbidities that add further elements to be taken into account when planning treatment—our objective being to improve gas exchange and ensure recovery of the respiratory muscles. In addition to ventilatory support, immediate medical treatment should be started (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>). Oxygen must be administered to correct the hypoxemia in acute asthma, as well as in COPD—though in this case it is essential to avoid the increase in pCO<span class="elsevierStyleInf">2</span> and consequent hypercapnic narcosis; the correct titration of FiO<span class="elsevierStyleInf">2</span> is therefore essential,<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> making sure that SaO<span class="elsevierStyleInf">2</span> does not exceed 90%. If worsening of the respiratory acidosis occurs despite these measures, then ventilation support is clearly indicated.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Once such support has been started, a differential diagnosis should be established among the possible causes of respiratory failure (e.g., pulmonary thromboembolism, pneumothorax, and upper airway obstruction), with identification of the etiological factor triggering the episode. It should be remembered that heart failure (particularly right-side failure) is often present in decompensated COPD.</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">No system has been developed allowing prediction of the survival or success/failure rate in the weaning of patients with COPD exacerbation. Thus, unless we have prior written patient rejection of intubation, ventilation support is to be provided when necessary. Respiratory arrest constitutes the terminal event of COPD and asthma, and is preceded by certain warning signs: lethargy, obnubilation, auscultation silence, bradycardia and hypotension. However, it is difficult to determine the severity of the process before arrest occurs; the medical history, clinical findings and initial response to treatment are therefore useful:<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">–</span><p id="par0020" class="elsevierStylePara elsevierViewall">The medical history will define the prognosis in acute COPD—fundamental considerations being the basal condition of the patient (evaluated by spirometry) and the presence of significant comorbidities. In asthma, antecedents of mechanical ventilation are indicative of a poor prognosis, in the same way as deterioration despite optimum treatment including oral corticosteroids and beta-agonists. It is important to point out that this latter disease can manifest gradually, with a slow and insufficient response to medical treatment and with important airway secretions and inflammation, or alternatively in a sudden manner, with a predominance of bronchospasm and progression towards respiratory arrest in a matter of minutes or hours (in rare cases).<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">–</span><p id="par0025" class="elsevierStylePara elsevierViewall">The clinical findings in COPD (drowsiness, intercostal space retraction, paradoxical breathing, etc.) are fundamental for patient stratification, and respiratory acidosis is the best predictor of patient exhaustion. Arterial blood gas determinations are essential, as well as comparison with previous samples. Clinical signs of severe asthma are taken to be tachycardia, tachypnea, paradoxical pulse, incapacity to end a phrase in a single breath, and peak expiratory flow rate (PEFR)<span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>50% of the theoretical normal or best normal value (<200<span class="elsevierStyleHsp" style=""></span>l/min if not known). Signs of life-threatening situations are auscultation silence, cyanosis, confusion or coma, bradycardia and hypotension, and a non-quantifiable PEFR. It must be remembered that the measurement of PEFR may prove dangerous in severe and sudden onset asthma; although fatal worsening of bronchospasm has been described, it is very useful for assessing the efficacy of treatment once the acute phase has been passed.</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">–</span><p id="par0030" class="elsevierStylePara elsevierViewall">The initial response to treatment in asthma patients is an important prognostic factor. If the patient does not improve clinically, physiologically (blood gases) and mechanically (PEFR) within 1–2<span class="elsevierStyleHsp" style=""></span>h, ventilation support should be considered, and it is essential to repeat evaluation of the patient (initially every hour).<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> In COPD, the prognostic significance is not the same as in asthma, since the response to treatment is slower. These concepts are summarized in <a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>.</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia></li></ul></p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Physiopathological Concepts</span><p id="par0035" class="elsevierStylePara elsevierViewall">Patients of this kind present a series of coinciding factors, such as increased airway resistance (due fundamentally to edema, secretions, bronchospasm and collapse), pulmonary hyperinsufflation (reduction of lung and chest wall compliance), and a large physiological dead space—with the consequent increase in respiratory effort. If the ventilatory demand exceeds the capacity of the respiratory muscles, acute respiratory failure results.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> Although the lung mechanics are similar in both conditions, there are some physiopathological differences that should be mentioned. In effect, COPD is characterized by greater airway collapse, due fundamentally to destruction of the lung parenchyma (particularly in emphysema), as well as by a loss of elastic rebound of the lungs,<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> while asthma is characterized by hypertrophy of the airway walls secondary to inflammation, lesser airway collapse despite the considerable decrease in airway caliber (central involvement versus peripheral involvement in COPD), and generally reversible obstruction—which can be minimal or lacking in long-evolving asthma.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> Likewise, and particularly in the asthmatic lung, the non-uniform distribution of the disease is a typical feature, together with important variability in the pulmonary distribution of obstruction within one same individual, who may experience substantial changes in a matter of minutes. It is necessary to take this element into account when selecting the ventilatory mode (volume control in favor of pressure control, fundamentally),<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> since its consequences may be: (1) abnormal distribution of the ventilation/perfusion ratio due to the redistribution of blood towards normally ventilated zones; (2) increased risk of barotrauma; and (3) venous return difficulties with hemodynamic alterations, shock and cardiorespiratory arrest.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> Furthermore, a reduction in the diameter of the glottis during expiration may be added to all these conditions.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> It must be mentioned that in contrast to patients with COPD, patients with bronchial asthma typically present high peak inspiratory pressures (as a result of which the presence of pneumothorax, mucus plugs or acute lung edema should always be suspected), and usually require greater ventilation support to correct or improve their pH.</p><p id="par0040" class="elsevierStylePara elsevierViewall">The limitation of airflow influences the efficacy of the respiratory mechanics in the following ways: (1) it increases the variation in pressure needed to overcome airway resistance for a given flow; (2) it causes hyperinsufflation, which partially counters the increase in resistance by expanding the airway diameter but also reduces the compliance of the system; (3) the hyperinsufflation (and destruction of the lung parenchyma) increases the ventilatory dead space, and therefore, also the minute-volume required for correct alveolar ventilation; (4) auto-PEEP or intrinsic PEEP (iPEEP) causes greater respiratory effort for activating the respiratory trigger; and (5) muscle capacity to cope with the increase in respiratory effort is altered (alteration of chest wall-diaphragm geometry, metabolic alteration due to hypoxemia-acidosis, cachexia in the COPD patient, etc.).</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Mechanical Ventilation in COPD and Asthma</span><p id="par0045" class="elsevierStylePara elsevierViewall">Once the respiratory muscles are no longer able to meet the ventilatory demand, the patient gradually becomes exhausted. This is the point where ventilation support is indicated in order to disrupt the vicious circle. The purpose of mechanical ventilation is to offer some rest to the respiratory muscles until treatment is started to deal with the cause of the exacerbation and revert the bronchial obstruction.</p><p id="par0050" class="elsevierStylePara elsevierViewall">In severe COPD exacerbation with respiratory acidosis, it is generally accepted that ventilation support initially must be provided on a noninvasive basis, as this has been shown to reduce the intubation rate, the duration of stay in intensive care, and patient mortality. Only when this measure fails (with exceptions, e.g., the performance of surgery) is patient intubation indicated.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> Conclusions based on a sufficient level of evidence have not been drawn in the case of asthma. Although there are no clearly defined criteria for starting such support in COPD and asthma, the indications could comprise at least two of the following conditions: (1) moderate–severe dyspnea, with use of the accessory muscles and abdominal breathing; (2) hypercapnic acidosis (pH<span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>7.35); and (3) tachypnea (>25<span class="elsevierStyleHsp" style=""></span>rpm). The most widely employed ventilatory modes are supportive pressure with PEEP and the BIPAP modes if the respiratory stimulus proves insufficient.<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13–16</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">There are no clearly defined criteria for the start of invasive mechanical ventilation in COPD and asthma. In COPD, the most widely adopted approach is patient intubation if noninvasive mechanical ventilation fails after 1<span class="elsevierStyleHsp" style=""></span>h (clinical and blood gas worsening). In asthma, intubation should not be delayed for too long (always based on clinical criteria, e.g., diminished consciousness and respiratory frequency), since the main objective of mechanical ventilation is to maintain oxygenation and avoid respiratory arrest. Once the decision to intubate has been taken, full control of patient cardiorespiratory arrest is the priority concern, and the technique should be carried out by the clinician with the greatest experience—using the largest orotracheal tube diameter possible in order to reduce the resistances and optimize clearance of the secretions.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">The factors associated to ventilator-induced lung damage to be considered and avoided when initially programming the machine are volutrauma/barotrauma, atelectrauma and oxygen therapy-related toxicity (FiO<span class="elsevierStyleInf">2</span><span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>0.5–0.6). In this sense it is important to underscore the concept of controlled hypoventilation as a general ventilatory strategy in application to both diseases – limiting the objectives to maintaining the oxygenation and minute-volume essential for avoiding severe acidosis. To this effect it is necessary to reach deep sedation, and (particularly in the case of asthma) the administration of short half-life neuromuscular relaxants entails a risk of myopathy in these patients (particularly when on corticosteroids); bolus dose administration with train of four (TOF) monitoring is therefore preferable.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">The initially programmed ventilator parameters can be very similar in both diseases, and we must choose a controlled or passive condition mode (there being no consensus regarding the concrete ventilatory mode)—attempting to prolong the expiratory time as far as possible by means of a low respiratory frequency (10–14<span class="elsevierStyleHsp" style=""></span>rpm) and I:E ratio, in order to minimize iPEEP and air trapping. The general strategy is to combine a relatively low minute-volume (<115<span class="elsevierStyleHsp" style=""></span>ml/kg) with a high inspiratory flow (80–100<span class="elsevierStyleHsp" style=""></span>l/min) in order to ensure a short inspiratory time and therefore a low I:E ratio.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> No benefit has been demonstrated for an expiratory time of longer than 4<span class="elsevierStyleHsp" style=""></span>s.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Ventilation should be sufficient to maintain pH<span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>7.15, with a low volume tidal (5–8<span class="elsevierStyleHsp" style=""></span>ml/kg) in order to avoid plateau pressures<span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>30<span class="elsevierStyleHsp" style=""></span>mmHg. The indication of bicarbonate to resolve respiratory acidosis is questionable to say the least, and should be accompanied by caution—particularly if the patient suffers hemodynamic instability or intracranial hypertension. The guiding parameter is pH, not pCO<span class="elsevierStyleInf">2</span>, avoiding alkalemia, particularly in chronic retainers.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">21</span></a> Adjustment of the trigger is essential for both diseases, usually adjusting by −1 to 2<span class="elsevierStyleHsp" style=""></span>cmH<span class="elsevierStyleInf">2</span>O for pressure and 2<span class="elsevierStyleHsp" style=""></span>l/min for flow. Too sensitive a trigger will activate more cycles than necessary, giving rise to respiratory alkalosis, while too “hard” a trigger will increase respiratory effort. The benefits of flow versus pressure trigger are clear in the intermittent mandatory ventilation (IMV) mode, not so decisive in the pressure support ventilation (PSV) mode, and without differences in the rest of ventilatory modes.<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a> Titrating FiO<span class="elsevierStyleInf">2</span> not only serves to reduce toxicity associated to high oxygen concentrations but in the case of COPD also reduces the degree of respiratory center suppression. In this case FiO<span class="elsevierStyleInf">2</span> should be titrated to reach SatO<span class="elsevierStyleInf">2</span><span class="elsevierStyleHsp" style=""></span>≥<span class="elsevierStyleHsp" style=""></span>88%.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Dynamic Hyperinsufflation and Auto-PEEP</span><p id="par0075" class="elsevierStylePara elsevierViewall">Dynamic hyperinsufflation appears when the pulmonary volume at the end of expiration is greater than the functional residual capacity (FRC) as a consequence of insufficient emptying of the lung, by starting inspiration before completing the preceding expiration.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a> A vicious circle is created, and if the latter is not resolved, the patient gradually becomes exhausted until cardiovascular and respiratory collapse occurs in a way similar to that produced by tension pneumothorax. The only measure that has been shown to predict the complications of hyperinsufflation is the determination of end-inspiratory volume (<span class="elsevierStyleItalic">V</span><span class="elsevierStyleInf">ei</span>) over functional residual capacity, calculating the total volume of gas exhaled in a patient with muscle paralysis after 60<span class="elsevierStyleHsp" style=""></span>s of apnea.<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> In this context, <span class="elsevierStyleItalic">V</span><span class="elsevierStyleInf">ei</span><span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>20<span class="elsevierStyleHsp" style=""></span>ml/kg is considered to be predictive of complications such as hypotension and barotrauma. Assuming that the compliance of the respiratory system remains constant, <span class="elsevierStyleItalic">V</span><span class="elsevierStyleInf">ei</span> could be calculated from the following formula, though the latter has not yet been validated:<elsevierMultimedia ident="eq0005"></elsevierMultimedia>Because of the limitations in calculating <span class="elsevierStyleItalic">V</span><span class="elsevierStyleInf">ei</span> in clinical practice, iPEEP and <span class="elsevierStyleItalic">P</span><span class="elsevierStyleInf">plateau</span> are used in its place, since both increase in situations of dynamic hyperinsufflation. <span class="elsevierStyleItalic">P</span><span class="elsevierStyleInf">peak</span> also increases, but lacks clinical value, since it increases with the rise in airway resistance and high inspiratory flows—with dissipation upon reaching the alveolus. iPEEP is defined as the spontaneous appearance of positive pressure at the end of expiration at alveolar level, due to insufficient expiratory time, and may appear with or without airflow limitation. The former group would include patients with asthma/bronchospasm and COPD, while in the absence of an increase in airway resistance a shortening of expiratory time due to disproportionate tachypnea can generate auto-PEEP (e.g., metabolic acidosis with compensatory hyperventilation, and primary respiratory alkalosis). It is the lowest mean alveolar pressure reached during the respiratory cycle, and is best measured during the sustained expiratory valve occlusion maneuver in the relaxed (not necessarily paralyzed) patient.<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">25</span></a> During this maneuver there is no flow in the airway, and a pressure balance is found in the system, with determination of the mean end-expiratory alveolar pressure (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). The presence of auto-PEEP can also be detected when the inspiratory efforts of the patient for activating the trigger are excessive or even ineffective<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a>; when active expiration continues at the start of the next inspiration; and, using the flow-time plot of the ventilator, when expiratory airflow persists at the end of inspiration (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>).<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> It can also be detected by applying successive increments of 3<span class="elsevierStyleHsp" style=""></span>cmH<span class="elsevierStyleInf">2</span>O of extrinsic PEEP, since at the point when the plateau and peak pressures increase, extrinsic PEEP will have exceeded auto-PEEP.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0080" class="elsevierStylePara elsevierViewall">The calculation of iPEEP in a spontaneously breathing patient is much more complex and difficult to extend to clinical practice, due to the frequent contribution of the respiratory muscles during active expiration. Through the determination of esophageal pressure (<span class="elsevierStyleItalic">P</span><span class="elsevierStyleInf">esoph</span>), an approximation can be obtained via the negative inflexion of <span class="elsevierStyleItalic">P</span><span class="elsevierStyleInf">esoph</span> immediately before activating the trigger in each inspiration. The existence of hyperinsufflation is suspected, since inspiration begins before the expiratory flow returns to zero. The value calculated by this procedure is usually lower than that confirmed from sustained expiration on detecting the lowest iPEEP value, while the second yields the mean value.<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a> There is no iPEEP value predictive of barotrauma, though successive and increasing determinations of iPEEP reflect growing hyperinsufflation. There is general agreement that in order to minimize the risk of volutrauma and barotrauma, <span class="elsevierStyleItalic">P</span><span class="elsevierStyleInf">plateau</span> must be kept below 30<span class="elsevierStyleHsp" style=""></span>mmHg.<a class="elsevierStyleCrossRefs" href="#bib0075"><span class="elsevierStyleSup">15,16,29,30</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">The application of extrinsic or external PEEP (ePEEP) should be made whenever there is iPEEP, with the purpose of reducing the efforts for activating the trigger. The attempts to exceed iPEEP constitute one of the main causes of respiratory failure in COPD exacerbation, and moreover represent a major cause of failure in the weaning of patients with airflow obstruction. ePEEP can be useful for countering iPEEP. However, ePEEP should not be applied to patients with COPD while under controlled ventilatory modes with the purpose of maximizing exhalation and of preventing regional overdistension—reserving it for when the assisted mode is resumed, to thus reduce the patient triggering effort. ePEEP should not be used in severe asthma.<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">31</span></a> It is not easy to calculate the adequate amount of ePEEP to be administered. Taking into account the waterfall principle, equaling ePEEP to iPEEP would imply a maximum decrease in inspiratory effort without the risk of hyperinsufflation.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a> However, there are two reasons why ePEEP should be lower than iPEEP: (1) there may be situations characterized by the coexistence of a limitation in airflow and conditions without such limitation and (2) the distribution of iPEEP in COPD and asthma is usually not homogeneous, and in certain areas of the lung the effective iPEEP may be lower than the calculated static iPEEP. These two possibilities may give rise to an increase in total PEEP if ePEEP<span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span>iPEEP, with the consequent barotrauma. Although adequate scientific evidence is lacking, there is an agreement that ePEEP should be 80% of iPEEP.</p><p id="par0090" class="elsevierStylePara elsevierViewall">If the above were not enough, there is still another problem: iPEEP varies in relation to the respiratory parameters (respiratory frequency and ventilation), the position of the patient, and the changes in respiratory mechanics related to the course of the disease and treatment response. Therefore, the values of iPEEP measured under controlled ventilation in a relaxed patient may be very different from those calculated under spontaneous ventilation—the situation in which we wish to apply ePEEP. In clinical practice it is useful to ask the patient about his or her degree of comfort and dyspnea while we very gradually increase ePEEP, so that the patient is personally aware of the relief in effort as a result of counterbalancing of the iPEEP until hyperinflation increases (the dyspnea will be proportional to <span class="elsevierStyleItalic">V</span><span class="elsevierStyleInf">ei</span>, as a result of which the patient can notice the increase in hyperinsufflation). Thus, in a patient with bronchial obstruction subjected to mechanical ventilation, we must determine auto-PEEP, apply different levels of ePEEP (=<span class="elsevierStyleHsp" style=""></span>iPEEP), and observe the changes in total PEEP.</p><p id="par0095" class="elsevierStylePara elsevierViewall">The concept of cardiopulmonary interaction is intimately linked to that of dynamic hyperinsufflation, since the lungs, heart and pulmonary circulation are located in the same compartment (chest cavity), with the consequence changes in cardiac function as a result of the variations in intrapleural pressure.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a> Hyperinsufflation increases the positive intrathoracic pressure, accentuating the decrease in venous return and preloading of both ventricles, and increasing the pulmonary vascular resistances and thus right ventricle post-loading. Hypotension is the most common effect of diminished preload, and is accentuated by hypovolemia. In this context, situations of electromechanical dissociation have been described<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">34</span></a>; as a result, if hyperinsufflation is suspected in a patient subjected to mechanical ventilation, it is advisable to disconnect the respirator for 20–30<span class="elsevierStyleHsp" style=""></span>s. Because of the increase in right ventricular post-loading, hyperinsufflation can give rise to acute failure with dilatation of the right ventricle – causing displacement of the interventricular septum and reduction of left ventricle filling, due to the interdependence between both ventricles. The intrathoracic pressure is partially transmitted to the circulation, and therefore influences the measured values of central venous pressure and wedge pressure—a fact that must be taken into account in hemodynamic monitoring.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Weaning from Mechanical Ventilation</span><p id="par0100" class="elsevierStylePara elsevierViewall">Weaning from mechanical ventilation is one of the main challenges for the intensivist. Prospective studies<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a> have shown the application of protocols to accelerate the process without increasing the failure rate. The use of merely intuitive clinical criteria is insufficient for taking decisions (sensitivity 35%; specificity 79%).<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">36</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">Mechanical ventilation is associated with many side effects. It is therefore advisable to start weaning as soon as possible, particularly in COPD. In order to assess the adequate moment for starting the process, due consideration is required of the possible causes of respirator dependency and of difficulties during weaning (<a class="elsevierStyleCrossRef" href="#tbl0015">Table 3</a>), as well as of the factors allowing us to predict successful weaning (<a class="elsevierStyleCrossRef" href="#tbl0020">Table 4</a>). Particularly in COPD and in difficult situations, the use of noninvasive mechanical ventilation is recommended after extubation, with a view to avoid the need for reintubation.<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">37–39</span></a></p><elsevierMultimedia ident="tbl0015"></elsevierMultimedia><elsevierMultimedia ident="tbl0020"></elsevierMultimedia><p id="par0110" class="elsevierStylePara elsevierViewall">Apart from the new assisted ventilation systems offering potential advantages for these patients in the transition phase, such as proportional assisted ventilation (PAV) or the more recent neurally adjusted ventilatory assist (NAVA), a number of mechanical ventilation weaning methods are available. While the superiority of one concrete option over another has not been demonstrated, it is advisable to establish protocolized use of the selected method<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a>:<ul class="elsevierStyleList" id="lis0010"><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">–</span><p id="par0115" class="elsevierStylePara elsevierViewall">Progressive reduction of ventilatory support: FiO<span class="elsevierStyleInf">2</span>, PEEP and the supportive pressure level can be gradually reduced, based on the respiratory pattern, the adequacy of gas exchange, and patient hemodynamic stability and comfort. It should be remembered that adjustment of the supportive pressure level to the respiratory frequency is dangerous, due to the great risk of over-assisting these patients and thus of promoting patient-ventilator synchrony and its complications—as has been recently demonstrated.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a> It is interesting that the greater the level of assistance, the greater the incidence of patient failure to activate the trigger—probably as a result of hyperinsufflation, which can be reduced by applying ePEEP, though there is controversy in the literature regarding the application of this maneuver.<a class="elsevierStyleCrossRefs" href="#bib0210"><span class="elsevierStyleSup">42,43</span></a> In clinical practice, ineffective attempts to activate the trigger should not prevent us from continuing the weaning process, though an ePEEP addition test should be made, and it is even possible to speak with the patient to try and establish the ideal PEEP, using different levels of supportive pressure in the course of the day.</p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">–</span><p id="par0120" class="elsevierStylePara elsevierViewall">Multiple daily <span class="elsevierStyleItalic">t</span>-tests: in the <span class="elsevierStyleItalic">t</span>-test the patient breathes spontaneously, and a success rate of 70% has been demonstrated after 30<span class="elsevierStyleHsp" style=""></span>min of disconnection.<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">44</span></a> It is not advisable to exceed 120<span class="elsevierStyleHsp" style=""></span>min, in order to avoid fatigue, since the orotracheal tube increases breathing effort. The use of minimum supportive pressure (e.g., 5<span class="elsevierStyleHsp" style=""></span>mmHg) is recommended to avoid tube resistance, though this technique has not been evaluated in any clinical trial to date.<a class="elsevierStyleCrossRefs" href="#bib0225"><span class="elsevierStyleSup">45,46</span></a> Another alternative is to use the ventilator without supportive pressure, preserving the alarm system as safety mechanism.</p></li><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">–</span><p id="par0125" class="elsevierStylePara elsevierViewall">SIMV (synchronized intermittent mandatory ventilation): the respiratory frequency and tidal volume/supportive pressure in controlled mode and supportive pressure/trigger level in spontaneous breathing are programmed in the respirator, with the gradual reduction of assistance. This method has revealed lesser efficacy in the recent literature and is now no longer recommended.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a></p></li></ul></p><p id="par0130" class="elsevierStylePara elsevierViewall">If the weaning process fails, immediate re-evaluation of the possible causes is required (<a class="elsevierStyleCrossRef" href="#tbl0015">Table 3</a>), with the adoption of specific measures<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">47</span></a>, and taking into account that with the exception of patients who are recovering from the effects of sedation, muscle relaxation, pneumothorax and atelectasis, respiratory alterations are only rarely resolved in a short period of time (e.g., several hours). The patients who do not pass the weaning test should have a rest period in a comfortable ventilation mode for at least 24<span class="elsevierStyleHsp" style=""></span>h. The controlled modes are usually required to relax the patient, though use should be made of the assisted modes with high supportive pressure levels, because they allow better ventilator-patient synchrony and prevent muscle atrophy. After 24<span class="elsevierStyleHsp" style=""></span>h of rest, a new weaning protocol should be reinitiated. When it becomes obvious that the patient will need long-term assisted ventilation, a tracheotomy should be considered. The impact of the timing of the latter upon the duration of mechanical ventilation remains unclear.<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a></p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Non-ventilatory Support and Management of Complications</span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Drug Treatment</span><p id="par0135" class="elsevierStylePara elsevierViewall">Although in COPD the degree of reversibility of airflow obstruction is less than in asthma, the bronchodilators play an important role (representing first-choice treatment in asthma); in this context, inhalatory β<span class="elsevierStyleInf">2</span> agonists are recommended, in combination with anticholinergic drugs every 1–2<span class="elsevierStyleHsp" style=""></span>h initially, followed by reduction according to the response obtained. Intravenous administration is not indicated in COPD (risk of arrhythmias, hypopotassemia, tremor and lactic acidosis), though it is accepted in asthmatics with a poor response to the inhalatory form. The usefulness of anticholinergic drugs in the asthmatic patient is less predictable than in COPD. Theophylline has shown minimal or no added efficacy, and adrenalin does not offer greater bronchodilating potency than the beta-mimetic drugs, and should not be used (either nebulized or via the systemic route), because of its many side effects. Both nebulizers and metered dose inhalers (MDIs) can be used for the administration of β<span class="elsevierStyleInf">2</span> agonists in patients subjected to mechanical ventilation, with grade A recommendation. The advantages of MDIs are their low cost, the absence of contamination, and improved dosing. The use of nebulizations is more comfortable and involves a lesser workload.<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">49</span></a> The administration of aerosols in patients subjected to mechanical ventilation is problematic, since the medications tend to accumulate in the tubulators and in the endotracheal tube. This can be resolved by administering large amounts of bronchodilators with a nebulizer installed in the actual circuit—though the use of MDIs improves the efficiency of the procedure, and at a lesser cost. Four puffs elicit the maximum bronchodilator effect, though the technique must be correctly executed, i.e., we must ensure sufficient tidal volume (at least 500<span class="elsevierStyleHsp" style=""></span>ml), an inspiratory time representing over 30% of the total cycle, correct ventilator-patient synchronization, activation of the device at the start of inspiration, and maintenance of an end-inspiratory pause of 3–5<span class="elsevierStyleHsp" style=""></span>s, allowing passive expiration and repetition of the technique every 20–30<span class="elsevierStyleHsp" style=""></span>s until the total dose is reached. It is worth mentioning that in the study published by Dhand et al.<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">50</span></a>, the drug dose deposited in the airway was found to be greater than with MDIs. The only study involving nebulizations in which the amount of drug deposited proved greater was carried out without a humidifier installed in the circuit.</p><p id="par0140" class="elsevierStylePara elsevierViewall">Systemic corticosteroids have demonstrated their efficacy in severe COPD exacerbation characterized by a poor response to bronchodilators, and although there is no agreement on the dose to be administered, a regimen of 0.5<span class="elsevierStyleHsp" style=""></span>mg/kg/6–8<span class="elsevierStyleHsp" style=""></span>h of methylprednisolone is advised, with rapid reduction of the dose, and taking care not to exceed two weeks of treatment.<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a> Since inflammation of the airway wall is central to the pathogenesis of the disorder, corticosteroids constitute the first line of treatment in asthma; efficacy has been demonstrated both for hydrocortisone and for methylprednisolone, and a starting dose of the latter of 125<span class="elsevierStyleHsp" style=""></span>mg/6–8<span class="elsevierStyleHsp" style=""></span>h is advised in the maximum severity phase.</p><p id="par0145" class="elsevierStylePara elsevierViewall">Regarding the use of other bronchodilators, opiates are not advised in induction and during the rest of the course—particularly morphic chloride (due to its associated histamine release and consequent bronchial constricting effect). In this sense the preferred drugs are propofol and ketamine, both of which have bronchodilating effects, though propofol causes principally hypotension (in some cases intense) and ketamine is associated with hallucinations, increased secretions, arterial and intracranial hypertension, and sometimes laryngeal spasms.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a> Short-acting benzodiazepines (midazolam and lorazepam) are commonly used, though they have no bronchodilatory effects, and high doses are needed to suppress the respiratory stimulus. A number of randomized and controlled trials warrant the use of magnesium sulfate (even with normal serum magnesium concentrations) in acute severe asthma, due to its bronchodilator capacity secondary to inhibition of the calcium channels, at repeated doses of 2<span class="elsevierStyleHsp" style=""></span>g/30<span class="elsevierStyleHsp" style=""></span>min (maximum total dose 10<span class="elsevierStyleHsp" style=""></span>g).<a class="elsevierStyleCrossRefs" href="#bib0265"><span class="elsevierStyleSup">53,54</span></a> The use of inhalatory anesthetics (halothane, isoflurane, etc.) has often been described in the literature, though they pose the inconveniences of rebound bronchospasm on interrupting administration, and the scarce flow which the anesthesia respiratory are able to deliver.<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">55</span></a> Heliox (an 80:20 mixture of helium and oxygen) may be considered in patients in which the conventional treatments have failed, though there is no solid scientific evidence clearly supporting their use.<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">56</span></a> Some studies have been published on the use of extracorporeal membrane oxygenation (ECMO) in severe asthma refractory to conventional treatment.<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">57</span></a></p><p id="par0150" class="elsevierStylePara elsevierViewall">Regarding anti-infectious treatment, it must be remembered that bronchial infections are the main cause of COPD exacerbation—a considerable number of these infections being produced by viruses (e.g., rhinovirus). Between 25 and 50% of these patients present bacterial colonization of the lower airways, associated to an increased inflammatory component. If the patient shows initial symptoms in the form of increased dyspnea and/or sputum secretion, or a worsening of their characteristics, active antibiotic treatment must be started against <span class="elsevierStyleItalic">Haemophilus influenzae</span>, <span class="elsevierStyleItalic">Streptococcus pneumoniae</span>, <span class="elsevierStyleItalic">Moraxella catarrhalis</span> and atypical bacteria, checking the immunization status of the patient. It should be remembered that the macrolides afford a greater antiinflammatory activity, improve action against <span class="elsevierStyleItalic">Streptococcus pneumoniae</span>, and inhibit the production of cytokines in the airway stimulated by rhinovirus overinfections. In contrast, in asthma antibiotic treatment should only be started if there is clear evidence of infection (despite the usual sputum purulence due to eosinophilia), since the triggering factors are not usually of an infectious nature. Mucolytic agents (e.g., N-acetylcysteine) are not used in the management of acute COPD and asthma.</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Correction of Water–Electrolyte and Acid–Base Imbalances</span><p id="par0155" class="elsevierStylePara elsevierViewall">The chronic inflammatory component in patients with COPD and in asthmatics leads to lung remodeling, and ultimately to emphysema. Lung edema is more likely, due to the alteration of lymphatic drainage, even with moderate volume replacement. Although there may be coexisting metabolic acidosis (e.g., lactic acidosis), most patients with COPD exacerbation and asthmatics present respiratory acidosis. The rise in pCO<span class="elsevierStyleInf">2</span> implies an increase in brain blood flow and in intracranial pressure, cardiac output and circulating catecholamine concentrations, pulmonary artery pressure and right ventricle overload, as well as a decrease in peripheral vascular tone. As has been mentioned, the indication of bicarbonate administration is debatable, and it is preferable first to optimize mechanical ventilation and the cardiocirculatory condition of the patient. Iatrogenic respiratory alkalosis due to hyperventilation can worsen compensatory metabolic alkalosis in COPD with chronic hypercapnia subjected to mechanical ventilation. The symptoms appear with pH<span class="elsevierStyleHsp" style=""></span>≥<span class="elsevierStyleHsp" style=""></span>7.55, while above pH 7.7 the patient may experience seizures, coma, arrhythmias and cardiac arrest.<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">58</span></a></p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Nutritional Support</span><p id="par0160" class="elsevierStylePara elsevierViewall">While asthmatics rarely present nutritional deficits, COPD patients often suffer imbalances between energy intake and expenditure, due to the chronic inflammation and extra constant effort required, and moreover show a loss of muscle mass and even cachexia. Early nutritional support, preferably via the enteral route, aims to compensate the metabolic needs of these patients, though care is required not to administer excessive amounts of carbohydrate supplements, since they increase the production of CO<span class="elsevierStyleInf">2</span> and O<span class="elsevierStyleInf">2</span> consumption.</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Treatment of Complications</span><p id="par0165" class="elsevierStylePara elsevierViewall">Since these are inflammatory syndromes, fever is a common presence in COPD and asthma; infections and overinfections are further factors to be taken into account during patient admission. Most patients with COPD show bacterial colonization of the lower airways, and asthmatics in turn are frequently affected by sinusitis and the microaspirations secondary to gastroesophageal reflux. Logically, all other potential causes of fever must be excluded. Atelectasis persistently exerts a negative influence on the clinical course of these individuals. Apart from the hypoxemia resulting from the intrapulmonary shunt (abnormal ventilation/perfusion ratio), atelectasis poses an added risk of pulmonary infection. The causal mechanisms are the following: (1) chronic hyperinsufflation with the reduction of diaphragm function; (2) diminished lung and chest wall compliance due to general anesthesia; (3) alveolar collapse secondary to high concentrations of O<span class="elsevierStyleInf">2</span>; (4) extrapulmonary compression (pneumothorax, pleural effusion, etc.), and (5) increased production and accumulation of bronchial secretions (this being the most common finding). In order to avoid atelectasis as far as possible, early weaning from mechanical ventilation should be started, and if this is not possible, then a spontaneous ventilation mode should be selected with a high tidal volume and PEEP, with the reduction of patient sedation. If the tracheobronchial secretions are abundant, endotracheal aspirations should be performed—attempting not to damage the tracheobronchial mucosa, oxygenating the patient before and after in order to avoid hypoxia, and taking care not to aspirate too often (loss of surfactant) or too little (aspiration atelectasis). Respiratory physiotherapy is advisable, with postural drainage, and in cooperative and non-intubated patients, forced spirometry and assisted cough are indicated. Optic fibrobronchoscopy with aspiration can prove harmful, since it may induce bronchial collapse and mucosal damage. It is not recommended in the presence of hemodynamic instability or severe hypoxia.<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">59</span></a></p><p id="par0170" class="elsevierStylePara elsevierViewall">Patients with COPD exacerbation or severe asthma are very susceptible to sinusal tachycardia and tachyarrhythmias as a result of hypoxia, stress, respiratory effort, sympathomimetic drug treatment, etc. The lung–heart interactions due to pulmonary hyperinsufflation affect cardiac output, resulting in hypotension and shock. In COPD, pulmonary hypertension usually implies cardiomyopathy, right heart failure and coronary insufficiency. Treatment is based on the control of these factors (sedation, titration of β<span class="elsevierStyleInf">2</span> agonists, avoidance of hyperinsufflation, the exclusion of ischemic heart disease, etc.).</p></span></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Conflicts of Interest</span><p id="par0175" class="elsevierStylePara elsevierViewall">The authors declare no conflicts of interest and assume responsibility for the data reflected in this manuscript.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:12 [ 0 => array:2 [ "identificador" => "xres9186" "titulo" => "Abstract" ] 1 => array:2 [ "identificador" => "xpalclavsec10626" "titulo" => "Keywords" ] 2 => array:2 [ "identificador" => "xres9187" "titulo" => "Resumen" ] 3 => array:2 [ "identificador" => "xpalclavsec10627" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Physiopathological Concepts" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Mechanical Ventilation in COPD and Asthma" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Dynamic Hyperinsufflation and Auto-PEEP" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Weaning from Mechanical Ventilation" ] 9 => array:3 [ "identificador" => "sec0030" "titulo" => "Non-ventilatory Support and Management of Complications" "secciones" => array:4 [ 0 => array:2 [ "identificador" => "sec0035" "titulo" => "Drug Treatment" ] 1 => array:2 [ "identificador" => "sec0040" "titulo" => "Correction of Water–Electrolyte and Acid–Base Imbalances" ] 2 => array:2 [ "identificador" => "sec0045" "titulo" => "Nutritional Support" ] 3 => array:2 [ "identificador" => "sec0050" "titulo" => "Treatment of Complications" ] ] ] 10 => array:2 [ "identificador" => "sec0055" "titulo" => "Conflicts of Interest" ] 11 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2010-04-24" "fechaAceptado" => "2010-11-03" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec10626" "palabras" => array:8 [ 0 => "COPD" 1 => "Asthma" 2 => "Mechanical ventilation" 3 => "Intubation" 4 => "Intensive care" 5 => "Dynamic hyperinflation" 6 => "Auto-PEEP" 7 => "Air-trapping" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec10627" "palabras" => array:8 [ 0 => "EPOC" 1 => "Asma" 2 => "Ventilación mecánica" 3 => "Intubación" 4 => "Medicina intensiva" 5 => "Hiperinsuflación dinámica" 6 => "Auto-PEEP" 7 => "Atrapamiento aéreo" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">COPD and asthmatic patients use a substantial proportion of mechanical ventilation in the ICU, and their overall mortality with ventilatory support can be significant. From the pathophysiological standpoint, they have increased airway resistance, pulmonary hyperinflation, and high pulmonary dead space, leading to increased work of breathing. If ventilatory demand exceeds work output of the respiratory muscles, acute respiratory failure follows.</p><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">The main goal of mechanical ventilation in these kinds of patients is to improve pulmonary gas exchange and to allow for sufficient rest of compromised respiratory muscles to recover from the fatigued state. The current evidence supports the use of noninvasive positive-pressure ventilation for these patients (especially in COPD), but invasive ventilation also is required frequently in patients who have more severe disease. The physician must be cautious to avoid complications related to mechanical ventilation during ventilatory support. One major cause of the morbidity and mortality arising during mechanical ventilation in these patients is excessive dynamic pulmonary hyperinflation (DH) with intrinsic positive end-expiratory pressure (intrinsic PEEP or auto-PEEP). The purpose of this article is to provide a concise update of the most relevant aspects for the optimal ventilatory management in these patients.</p>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Los pacientes con EPOC y asmáticos utilizan una proporción sustancial de ventilación mecánica en la UCI, y su mortalidad global en tratamiento con ventilación mecánica puede ser significativa. Desde el punto de vista fisiopatológico muestran un incremento de la resistencia de la vía aérea, hiperinsuflación pulmonar, y elevado espacio muerto anatómico, lo que conduce a un mayor trabajo respiratorio. Si la demanda ventilatoria sobrepasa a la capacidad de la musculatura respiratoria, se producirá el fracaso respiratorio agudo.</p><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">El principal objetivo de la ventilación mecánica en este tipo de pacientes es proporcionar una mejora en el intercambio gaseoso así como el suficiente descanso para la musculatura respiratoria tras un período de agotamiento. La evidencia actual apoya el uso de la ventilación mecánica no invasiva en estos pacientes (especialmente en el EPOC), pero con frecuencia se precisa de la ventilación mecánica invasiva para los pacientes con enfermedad más severa. El clínico debe ser muy cauto de cara a evitar complicaciones relacionadas con la ventilación mecánica durante el soporte ventilatorio. Una causa mayor de morbilidad y mortalidad en estos pacientes es la excesiva hiperinsuflación dinámica pulmonar con presión positiva al final de la espiración (PEEP intrínseca o auto-PEEP). El objetivo de este artículo es proporcionar una concisa actualización de los aspectos más relevantes para el óptimo manejo ventilatorio en estos pacientes.</p>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara">Please cite this article as: García Vicente E, et al. Ventilación mecánica invasiva en EPOC y asma. Med Intensiva. 2011;35:288–98.</p>" ] ] "multimedia" => array:7 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1458 "Ancho" => 1674 "Tamanyo" => 76926 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Occlusion of the expiratory valve.</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1097 "Ancho" => 1944 "Tamanyo" => 80695 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Auto-PEEP.</p>" ] ] 2 => array:7 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "tabla" => array:2 [ "leyenda" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">++: good level of evidence; +: relatively good level of evidence; −: without evidence.</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"><td class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t" style="border-bottom: 2px solid black"> \t\t\t\t\t\t\n \t\t\t\t</td><td 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" style="border-bottom: 2px solid black">Asthma \t\t\t\t\t\t\n \t\t\t\t</td><td 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" style="border-bottom: 2px solid black">COPD \t\t\t\t\t\t\n \t\t\t\t</td></tr></thead><tbody title="tbody"><tr title="table-row"><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">Inhalatory β agonists \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">++ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Inhalatory anticholinergic agents \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">++ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Systemic corticosteroids \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">+ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Antibiotics \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">+ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Oxygen \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">+ (carefully titrate FiO<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" 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">Noninvasive ventilation \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">++ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Theophylline \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">− \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Mucolytic agents \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">− \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab8780.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Medical treatment in asthma and COPD.</p>" ] ] 3 => array:7 [ "identificador" => "tbl0010" "etiqueta" => "Table 2" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "tabla" => array:2 [ "leyenda" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">FVC: forced vital capacity; FEV1: forced expiratory volume in 1<span class="elsevierStyleHsp" style=""></span>s.</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"><td class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t" style="border-bottom: 2px solid black"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " colspan="3" align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" style="border-bottom: 2px solid black">COPD</td><td class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" style="border-bottom: 2px solid black">Asthma \t\t\t\t\t\t\n \t\t\t\t</td></tr></thead><tbody title="tbody"><tr title="table-row"><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">Clinical history \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 " colspan="3" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Comorbidities</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">Previous admission to ICU \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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 " colspan="3" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" style="border-bottom: 2px solid black">Basal severity (spirometry)</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">Mechanical ventilation \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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" style="border-bottom: 2px solid black">Severity \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" style="border-bottom: 2px solid black">Following bronchodilation (FEV<span class="elsevierStyleInf">1</span>/FVC) \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" style="border-bottom: 2px solid black">FEV<span class="elsevierStyleInf">1</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">Worsening despite optimum medical treatment including oral corticosteroids. Increase in the use of β agonists in the last days \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">At risk \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">>0.7 \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">≥80 \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="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Mild \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"><0.7 \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">≥80 \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="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Moderate \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"><0.7 \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">50–80 \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="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Severe \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"><0.7 \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">30–49 \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="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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" style="border-bottom: 2px solid black">Very severe \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" style="border-bottom: 2px solid black"><0.7 \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" style="border-bottom: 2px solid black"><30 \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="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="5" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><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">Clinical signs \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 " colspan="3" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Severity of dyspnea: respiratory frequency, accessory muscle use</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">Severity of dyspnea: respiratory frequency, accessory muscle use \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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="" 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="" 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="" 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">Auscultation silence \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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="" 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="" 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="" 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">Hemodynamic alterations: tachycardia, paradoxical pulse \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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="" 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="" 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="" 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">Diaphoresis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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="" 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="" 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="" 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">Restlessness, anxiety or stupor, coma \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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 " colspan="3" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Futile peak forced expiratory flow</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">Without improvement 1–2<span class="elsevierStyleHsp" style=""></span>h after the start of treatment \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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="" 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="" 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="" 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">Useful peak forced expiratory flow \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="5" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><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">Arterial blood gases \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 " colspan="3" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Respiratory acidosis</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">Normocapnic or hypercapnic hypoxemia \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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 " colspan="3" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">No improvement with treatment</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">No reduction in pCO<span class="elsevierStyleInf">2</span> with treatment or correction of hypoxemia \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab8779.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Grading of the severity-risk association in respiratory failure.</p>" ] ] 4 => array:7 [ "identificador" => "tbl0015" "etiqueta" => "Table 3" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "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=""><tbody title="tbody"><tr title="table-row"><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">Gas exchange \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">Ventilation-perfusion imbalance \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Shunts (atelectasis, pulmonary thromboembolism) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Altered breathing pattern (increased dead space) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><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">Respiratory muscles \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">Fatigue and muscle atrophy \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Hyperinsufflation \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Increased resistances with high respiratory effort \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><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">Ventilator \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">High resistance to flow through the orotracheal tube and tubulators, humidifiers and valves \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><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">Metabolism \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">Overfeed with excess CO<span class="elsevierStyleInf">2</span> production \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Denutrition with protein hypercatabolism \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Electrolyte defects (phosphate, magnesium) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Hormone alterations (hypothyroidism, insulin/glucagon/adrenal corticoid dysfunction \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><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">Cardiovascular \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">Left heart failure with acute lung edema \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Pulmonary hypertension with right ventricle failure \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Variations in pre- and post-loading \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><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">Neurological \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">Cortical dysfunction due to sedation and toxic-metabolic factors \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Sleep apnea syndrome \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Polymyoneuropathy of the critical patient \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" 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">Severe restlessness and delirium \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab8778.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Causes of respirator dependency and obstacles in weaning.</p>" ] ] 5 => array:7 [ "identificador" => "tbl0020" "etiqueta" => "Table 4" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "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"><td 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" style="border-bottom: 2px solid black">Correction of the underlying cause</td></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " rowspan="5" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Respiratory criteria</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">PaO<span class="elsevierStyleInf">2</span>/FiO<span class="elsevierStyleInf">2</span><span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>150–200 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">PEEP<span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>15<span class="elsevierStyleHsp" style=""></span>cmH<span class="elsevierStyleInf">2</span>O, <5<span class="elsevierStyleHsp" style=""></span>cmH<span class="elsevierStyleInf">2</span>O for extubation \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">pH<span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>7.3 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Rapid shallow breathing index<span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>100 [RF/tidal volume (l)] \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Other factors: maximum inspiratory pressure<span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>−20 to 30<span class="elsevierStyleHsp" style=""></span>cmH<span class="elsevierStyleInf">2</span>O; occlusion pressure after 100<span class="elsevierStyleHsp" style=""></span>ms<span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>6<span class="elsevierStyleHsp" style=""></span>mbar \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " rowspan="4" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Hemodynamic stability</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">Correct cardiac output \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Without lung edema \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Without relevant arrhythmias \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Without myocardial ischemia \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " rowspan="6" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Adequate respiratory coordination and strength</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">Without thoracic instability \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Normal intra-abdominal pressure \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">Capacity for inspiratory effort/cough \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">No use of accessory muscles \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">No paradoxical breathing \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><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">No relevant hyperinsufflation/auto-PEEP \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab8777.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Weaning success prognostic factors.</p>" ] ] 6 => array:5 [ "identificador" => "eq0005" "tipo" => "MULTIMEDIAFORMULA" "mostrarFloat" => false "mostrarDisplay" => true "Formula" => array:5 [ "Matematica" => "Vei=(Vtidal×Pplateau)(Pplateau−iPEEP)" "Fichero" => "si1.jpeg" "Tamanyo" => 2795 "Alto" => 40 "Ancho" => 163 ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:59 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: National Heart, Lung, and Blood Institute and World 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2023 August | 250 | 138 | 388 |
2023 July | 272 | 57 | 329 |
2023 June | 207 | 56 | 263 |
2023 May | 91 | 23 | 114 |