Adaptação metabólica diante de hipercapnia persistente aguda em pacientes submetidos à ventilação mecânica por síndrome do desconforto respiratório agudo / Metabolic acid-base adaptation triggered by acute persistent hypercapnia in mechanically ventilated patients with acute respiratory distress syndrome

RESUMO Objetivo: A hipercapnia resultante da ventilação protetora na síndrome do desconforto respiratório agudo desencadeia uma compensação metabólica do pH que ainda não foi completamente caracterizada. Nosso objetivo foi descrever esta compensação metabólica. Métodos: Os dados foram recuperados a partir de uma base de dados registrada de forma prospectiva. Foram obtidas as variáveis dos pacientes no momento da admissão e quando da instalação da hipercapnia até o terceiro dia após sua instalação. Analisamos 41 pacientes com síndrome do desconforto respiratório agudo, incluindo 26 com hipercapnia persistente (pressão parcial de gás carbônico acima de 50mmHg por mais de 24 horas) e 15 sem hipercapnia (Grupo Controle). Para a realização da análise, utilizamos uma abordagem físico-química quantitativa do metabolismo acidobásico. Resultados: As médias de idade dos Grupos com Hipercapnia e Controle foram, respectivamente, de 48 ± 18 anos e 44 ± 14 anos. Após a indução da hipercapnia, o pH diminuiu acentuadamente e melhorou gradualmente nas 72 horas seguintes, de forma coerente com os aumentos observados no excesso de base padrão. A adaptação metabólica acidobásica ocorreu em razão de diminuições do lactato sérico e do strong ion gap e de aumentos na diferença aparente de strong ions inorgânicos. Além do mais, a elevação da diferença aparente de strong ions inorgânicos ocorreu por conta de ligeiros aumentos séricos de sódio, magnésio, potássio e cálcio. O cloreto sérico não diminuiu por até 72 horas após o início da hipercapnia. Conclusão: A adaptação metabólica acidobásica, que é desencadeada pela hipercapnia aguda persistente em pacientes com síndrome do desconforto respiratório agudo, foi complexa. Mais ainda, aumentos mais rápidos no excesso de base padrão em pacientes com hipercapnia envolveram diminuições séricas de lactato e íons não medidos, e aumentos na diferença aparente de strong ions inorgânicos, por meio de ligeiros aumentos séricos de sódio, magnésio, cálcio e potássio. Não ocorreu redução do cloreto sérico.

ABSTRACT Objective: Hypercapnia resulting from protective ventilation in acute respiratory distress syndrome triggers metabolic pH compensation, which is not entirely characterized. We aimed to describe this metabolic compensation. Methods: The data were retrieved from a prospective collected database. Variables from patients' admission and from hypercapnia installation until the third day after installation were gathered. Forty-one patients with acute respiratory distress syndrome were analyzed, including twenty-six with persistent hypercapnia (PaCO2 > 50mmHg > 24 hours) and 15 non-hypercapnic (control group). An acid-base quantitative physicochemical approach was used for the analysis. Results: The mean ages in the hypercapnic and control groups were 48 ± 18 years and 44 ± 14 years, respectively. After the induction of hypercapnia, pH markedly decreased and gradually improved in the ensuing 72 hours, consistent with increases in the standard base excess. The metabolic acid-base adaptation occurred because of decreases in the serum lactate and strong ion gap and increases in the inorganic apparent strong ion difference. Furthermore, the elevation in the inorganic apparent strong ion difference occurred due to slight increases in serum sodium, magnesium, potassium and calcium. Serum chloride did not decrease for up to 72 hours after the initiation of hypercapnia. Conclusion: In this explanatory study, the results indicate that metabolic acid-base adaptation, which is triggered by acute persistent hypercapnia in patients with acute respiratory distress syndrome, is complex. Furthermore, further rapid increases in the standard base excess of hypercapnic patients involve decreases in serum lactate and unmeasured anions and increases in the inorganic apparent strong ion difference by means of slight increases in serum sodium, magnesium, calcium, and potassium. Serum chloride is not reduced.

Ventilação mecânica convencional em pediatria / Conventional mechanical ventilation in pediatrics

OBJETIVO: Revisar os vários desafios existentes na ventilação mecânica de pacientes pediátricos com doenças de resistência elevada das vias aéreas, complacência pulmonar anormal ou pulmões normais. FONTES DOS DADOS: Dados originais coletados em nossa unidade de tratamento intensivo pediátrico e em nosso laboratório de pesquisa animal. Artigos pertinentes incluídos na base de dados MEDLINE durante os últimos 10 anos. Também foram incluídos capítulos de livros e estudos definitivos, a critério dos autores, sobre asma, síndrome do desconforto respiratório agudo, ventilação mecânica, lesão pulmonar induzida pelo ventilador e hipercapnia permissiva. SíNTESE DOS DADOS: O foco da ventilação mecânica de pacientes com doenças que resultam em resistência elevada das vias aéreas deve centrar-se na hipercapnia permissiva e prevenção de hiperinsuflação dinâmica, permitindo exalação total antes do início da inspiração subseqüente. A pressão expiratória final positiva deve ser usada comedidamente para evitar atelectasia e facilitar a sincronia em pacientes com respiração espontânea. A ventilação mecânica de pacientes com doenças de complacência pulmonar anormal deve levar em consideração a distribuição heterogênea da lesão pulmonar. O enfoque deve ser na prevenção de volutrauma e atelectrauma, que podem resultar em lesão pulmonar associada ao ventilador. CONCLUSÕES: A última década foi marcada por significativos avanços no manejo de insuficiência respiratória em pacientes pediátricos. A escolha da estratégia de ventilação mecânica pode influenciar significativamente o curso subseqüente da lesão pulmonar. A ventilação mecânica não pode ser vista apenas como uma mera modalidade de suporte usada para manter os pacientes vivos enquanto que tratamentos específicos à doença são empregados para melhorar a patologia de base.

OBJECTIVE: To review the various challenges of providing mechanical ventilation to pediatric patients with diseases of increased airway resistance, diseases of abnormal lung compliance or normal lungs. SOURCES: Original data from our pediatric intensive care unit and animal research laboratory. Relevant articles included in the MEDLINE electronic database during the last 10 years. Also included were book chapters and definitive studies, as judged by the authors, in the fields of asthma, acute respiratory distress syndrome, mechanical ventilation, ventilator-induced lung injury and permissive hypercapnia. SUMMARY OF THE FINDINGS: Mechanical ventilation of patients with diseases of increased airway resistance should center on avoidance of dynamic hyperinflation, allowing complete exhalation prior to the initiation of a subsequent breath and permissive hypercapnia. Positive end-expiratory pressure should be used sparingly to prevent atelectasis and facilitate synchrony in spontaneously breathing patients. Mechanical ventilation of patients with diseases of abnormal lung compliance should take into consideration the inhomogeneous distribution of lung disease. Focus should be on avoidance of volutrauma and atelectrauma that could result in ventilator-associated lung injury. CONCLUSIONS: The last decade was marked by significant advances in the management of pediatric respiratory failure. The choice of mechanical ventilation strategy can significantly influence the subsequent course of lung injury. Mechanical ventilation can no longer be viewed simply as a harmless support modality that is employed to keep patients alive while disease-specific treatments are used to ameliorate the underlying pathology.

Progressive hypoxemia, hypercarbia and hyperthermia associated with prolonged anesthesia- a case report

The authors report a case of 66-year-old female patient, 55 kg, ASA I who, under general anesthesia in supine position, developed gradual hypoxemia [from a baseline PaO[2] of 250 to 91 mmHg], carbon dioxide build up [from a baseline PaCO[2] 31 to 41 mmHg] associated with gradual hyperthermia up to 38.3°C over seven hours, intra-operatively. These observations were noted while using a semiclosed carbon dioxide absorption circuit in conjunction with the Hygroster filter at a fresh gas flow of 4 1/min of 50% nitrous oxide in oxygen. While the ventilation pattern was unchanged throughout the procedure, there was a change in exhaled tidal and minute ventilation volume with a net decrease of 28 ml and 0.4 l/min respectively. Findings are probably the result of pulmonary atelecatasis under general anesthesia due to the use of a relatively high-inspired oxygen concentration [50%]. In addition, the use of a high humidity and temperature heat moisture exchanger [HME] filter [Hygroster] in conjunction with the circle absorber system may have resulted in over humidification and aggravated the pulmonary atelecatasis over the long operative time

Mecanismos de aumento de la PCO2 tisular en el shock / Mechanisms of increased tissue PCO2 in shock

Un aumento en la PCO2 venosa o tisular podría ser provocado por un exceso de producción anaeróbica de CO2 debido al tamponamiento por bicarbonato de protones derivado de ácidos fijos, o por falta de remoción de CO2, secundaria a hipoperfusión tisular. En este Artículo, revisaremos los mecanismos fisiológicos que determinan la hipercarbia venosa y tisular, así como los estudios en los que se han comparado los gradientes venoarteriales e intramucosos arteriales de PCO2, durantes las tres formas clásicas de hipoxia: isquémica, hipóxica y anémica. De estos estudios se concluye que estos gradientes fallan para reflejar la disoxia tisular cuando el flujo sanguíneo es su principal determinante. Estos datos experimentales han sido avalados por un modelo matemático que reafirma estos conceptos. También se discute el comportamiento de los gradientes de CO2 en la situación más relevante para la terapia intensiva, la sepsis. En la sepsis clínica y experimental, el gasto cardíaco está frecuentemente normal o elevado. No obstante, la acidosis intramucosa es un hallazgo común. Esta aparente paradoja se ha intentado explicar por la presencia de alteraciones en el metabolismo ejergético celular, la llamada hipoxia citopática. Sin embargo, actualmente existen fuertes evidencias que vinculan la acidosis intramucosa a las severas alteraciones microcirculatorias que están presentes en la sepsis. Adicionalmente, se discuten modelos experimentales en los que el aumento de la perfusión previene la acidosis intramucosa, pero es incapaz de evitar alteraciones metabólicas como la acidosis por elevación del anión gap y la hiperlactacidemia. En resumen, el PCO2 no es un marcador de disoxia, sino un sensible indicador de perfusión tisular.

Acute respiratory failure and oxygen therapy.

Acute Respiratory Failure (ARF) results in an inability to maintain gas exchange at a rate commensurate with the demands of the body and results in hypoxemia and/or hypercarbia, the mechanisms of which may be different. Hypoxemia commonly occurs due to Ventilation Perfusion (V/Q) mismatching, intrapulmonary shunt, diffusion defect or hypoventilation. Hypercarpnic respiratory failure may also be multifactorial but is usually due to inhibited central respiratory drive or inefficient respiratory muscle pump. Hypercapnia may occur in upper and lower airways obstruction, respiratory muscle fatigue and occasionally due to excess CO2 production (burns and excessive glucose administration). Issues in management centre around assessment of severity, determining the need for intervention, establishing diagnosis and etiology and institution of specific treatment. Diagnosis of respiratory failure may be made clinically and confirmed by blood gas analysis. Calculation of oxygenation indices will delineate extent of hypoxemia. When evaluating a child with respiratory failure, one should be aware that a child with prominent respiratory symptoms may have non-respiratory disease (i.e. metabolic acidosis, DKA) and conversely, advanced respiratory failure may be present in a child with no respiratory distress (central hypoventilation secondary to drugs, infection) careful assessment of history, complete physical examination and evaluation of lab parameters may clarify the diagnosis. Serial assessment of sensorium, respiratory symptoms, ABG and response to treatment will provide valuable clues to determine the need for intervention. Oxygen, like any drug, must be administered in a prescribed dose, only when indicated with the potential risks borne in mind. A variety of oxygen delivery devices are available; which ever device is used, the resulting FiO2 and devisable end points must be clearly determined. Hazards of oxygen therapy range from retinal damage in premature infants, damage to the alveolar capillary membrane with resultant hypoxemia) atelectasis and decreased mucociliary activity.

Lavagem expiratória verus otimização da ventilação mecência convencional durantehipercapnia permissiva em pacientes com insuficiência respiratória aguda / Expiratory washout versus optimization of mechanical ventilation during permissive hypercapnia in patients with severe acute respiratory distress syndrome

O objetivo deste estudo foi comparar três técnicas ventilatórias para reduzir pressão arterial de CO2 em pacientes com insuficiência respiratória aguda severa e em hipercapnia permissiva...

Interactions between body temperature regulation and blood acid-base status in anuran amphibians

In vertebrate evolution, the transition from aquatic to terrestrial mode of life was associated with considerable changes in the respiratory system and CO2/pH-sensitive receptors became fundamental. The present review focuses on the combined effects of hypercapnia and body temperature in anuran amphibians, that represent a key group for the transition. Recent studies have indicated that temperature affects the hypercapnic drive to breathe. Conversely, hypercapnia modulates the range of preferred body temperature of amphibians and central (CO2/pH) receptors are likely to be involved.

Dormir en los Andes: contribución del sueño en la etiopatogenia de la enfermedad de Monge / Sleep at the Andes: contribution to dream at etiopathogeny from Monge`s disease

En las grandes alturas se han estudiado los efectos del sueño y su influencia en la etiopatogenia del soroche crónico o Enfermedad de Monge. Se hizo cateterismo cardíaco derecho durante la noche y se midió la ventilación pulmomar en voluntarios adultos normales (adaptados y en pacientes con enfermedad de Monge (desadaptados). En niños sólo se midió la ventilación pulmonar. A 4540 y a 4330 msnm. durante el sueño se producen los siguientes efectos agudos: hipoventilación, hipoxemia moderada y severa, hipercapnia, hipertensión pulmonar moderada y severa, disminuyendo el consumo de oxígeno, el débito cardíaco y el volumen de expulsión ventricular, leve incremento de la frecuencia cardíaca, acidemia y, en los desadaptados, además, se observa hipertensión diastólica sistémica. Los cambios son más acentuados en los desadaptados. En los niños el sueño ocasiona una disminución de la ventilación pulmonar siendo ésta de mayor magnitud que en los adultos. Al despertar, los residentes altoandinos están normales y sin signos, síntomas, ni ninguna condición neurológica patológica. Durante el sueño los adaptados adquieren las características que tienen los desadaptados en vigilia. Hipoventilación, hipoxemia y policitemia acentuadas, hipercapnia, hipertensión pulmonar moderada y severa son las principales características de la Enfermedad de Monge, siendo la hipoventilación el principal factor causal de ellos. Por la hipoxemia aguda durante el sueño los residentes altoandinos, teóricamente ascienden a una altura mayor que aquella en la cual están durmiendo. Desde los recién nacidos hasta la senectud la hipoventilación e hipoxemia se acentúan por el sueño, por el envejecimiento, por la mayor altitud de residencia, y más aún en las grandes alturas, la hipoxemia también se acentúa por el peculiar comportamiento fisiológico de la curva de disociación de la oxihemoglobina y, probablememte, por los mecanismos mediante los cuales la policitemia ocasiona anoxemia y viceversa y por la precoz desensibilización hipóxica de los quimiorreceptores periféricos. De esta manera, ya sea en forma aislada o asociada, el sueño y las otras variables contribuyen en la etiopatogenia de la enfermedad de Monge, condicionando que algunos adaptados vayan adquiriendo lenta y progresivamente las características que tienen los pacientes con Enfermedad de Monge. Así, la Enfermedad de Monge sería la resultante de un proceso bio-ecológico y no la de un proceso patológico

Hypoxia and its influences on the cardiovascular and respiratory systems of spontaneously breathing cats

Effects of acute systemic hypoxia on the cardiovascular system [CVS] and respiration of spontaneously breathing cats were studied in two conditions. 1]: Hypoxic air [6-8% 02 in N2] was given to the animal to induce systemic hypoxia for 20 minutes. Hyperventilation at this condition lowered arterial C02 tension [PaC02; hypocapnia]. 2]: In the second run, induction of hypocapnia was prevented by adding 3-5% C02 to hypoxic air. Comparison of the results of this study indicated that hypoxia, independent of the presence of hypocapnia, caused a significant increase in respiratory rate, aortic flow and arterial blood pressure. However, in the presence of hypocapnia, the increased respiratory rate was 10% less and a general arterial vasconstriction was observed

Gradiente venoarterial de anhídrido carbónico: valor pronóstico y relaciones con el índice cardíaco en pacientes críticos / Carbon anhydride arterial vein gradient: prognosis value and relationships with heart rate in critical patients

En 64 pacientes (P) se midió dentro de las 6 horas de la admisión, el gradiente venoarterial de CO2 (Gv-aCO2) (G) diferenciando 2 grupos A (G < a 6 mmHg) y B (> 6 mmHg) evaluándose en ellos el desarrollo de fallas múltiples (FM) y la mortalidad (M). En 35 P se midió concomitantemente el G y el índice cardíaco (IC) en 50 oportunidades correlacionándose sus valores; a la vez se midió en ellos el pHi. El desarrollo de FM y la M fueron significativamente mayores en el grupo B; la correlación entre G e IC fue débil, los niveles de IC y G en estos P definieron 4 grupos de determinaciones: I: IC < 2,7, G > 6; II: IC < 2,7, G ? 6; III: IC > 2,7, G ? a 6 y IV: IC > 2,7, G > 6 (en el último no se ubicaron mediciones). En I la X ñ DE fue significativamente menor que II y en este último que en III. El G puede ser de utilidad para establecer pronóstico en la admisión. El más reducido pHi en las determinaciones del grupo I evidencia las consecuencias de la caída efectiva del volumen circulante sumado a alteraciones en la regulación del microflujo en relación al II en el cual esas últimas estarían ausentes (similar IC con G normal)

Causas de retención de CO2 en pacientes con neumopatía obstructiva crónica / Causes of CO2 retention in patients with chronic obstructive lung disease

Los factores que llevan a la retención de CO2 en los pacientes con neumpatía obstrutiva crónica estable son complejos; es poco probable que un único factor pueda explicarla. Este artículo analiza diversos aspectos mecánicos y de intercambio gaseoso, la teoría de los luchadores vs. no luchadores, la teoría del patrón ventilatorio, la teoría del umbral de fatiga y, finalmente, se analiza la evidencia que sostiene el nuevo concepto que la hipercapnia puede desarrollarse para suprimir o prevenir la fatiga. En pacientes con EPOC estables, es muy probable que la desventaja mecánica de los músculos respiratorios sea un factor más importante que el deterioro de la relación V/Q. De gran interés son los mecanismos por los cuales el sistema de control ventilatorio cambia su estrategia de activación muscular con el objeto de prevenir la fatiga de los severa de los músculos respiratorios es el resultado del fracaso de estos complejos mecanismos compensatorios. Cuando el esfuerzo respiratorio se aproxima al umbral de fatiga, algun grado de fatiga central puede ayudar a proteger al músculo de fatiga períferica severa o aún de injuria muscular. Finalmente se hacen algunos comentarios respecto de ciertas modalidades terapéuticas tales como los estimulantes respiratorios, el entrenamiento, el reposo y en especial la oxigenoterapia y los mecanismos involucrados en el aumento de la PCO2

Anestesia en cirugía laparoscópica / Anesthesia in laparoscopic surgery

Se revisa la técnica anestésica en cirugía laparoscópica, comentando detalles, particularmente en relación a la utilización de neumoperitoneo, a la posición y sus repercusiones fisiológicas. Se detalla la técnica de anestesia de uso más habitual en nuestro Hospital. Se concluye que no siendo una técnica que requiere de una especialización particular, se acompaña de algunas alteraciones que obligan a vigilancia estrecha y monitorización especial

Mechanisms of hypercapnia in patients with chronic obstructive pulmonary disease (COPD)

A higher ventilatory drive evaluated by the inspiratory occlusion pressure (Poc) and a respiratory pattern characterized by smaller tidal volume (VT) and higher breathing frequency (f) was detected in patients with chronic obstructive pulmonary disease (COPD), in relation to normals. The purpose of this study was to identify the possible mechanisms involved in the development of hypercapnia in those patients, at rest and during exercise. We have studied 11 normocapnic (PaCO2 ( 45 mmHg) and 9 hypercapnic (PaCO2 > 45 mmHg) COPD patients. As expected, no difference in the ventilatory response and neural drive was detected between the two groups. However, the hypercapnic patients have higher values of serum HCO-3 and lower values of PaO2 at rest and values of the ratio dead volume to tidal volume (VD/VT) significantly higher at rest (0.67 vs. 0.55) and during exercise (0.54 vs. 0.38) in relation to normocapnic individuals. There was also a significant positive correlation at rest (r = 0.66*) and during exercise (r = 0.65*; *p < 0.05), between PaCO2 and VD/VT, identifying a decreased alveolar ventilatory efficiency, important in the development of hypercapnia in those patients. when the COPD patients were divided into two distinct groups (PaCO2 ( 40 and ( 50 mmHg), a respiratory pattern characterized by higher f and smaller VT was detected in the hypercapnic group during exercise. In conclusion, a higher VD/VT linked to alterations of the respiratory pattern (lower VT) and to inequalities of ventilation/perfusion (high V/Q areas), seems to explain the hypercapnia of our COPD patients, since the ventilatory response and neural drive were similar in normo and hypercapnic patients.