Alcalosis respiratoria grave, la transformación de un cuadro funcional en orgánico. Caso clínico / Severe respiratory alkalosis due to psychogenic hyperventilation. Report of one case

Severe respiratory alkalosis is a life-threatening condition, as it induces hypo- calcaemia and extreme adrenergic sensitivity leading to cerebral and myocardial vasoconstriction. We report a 37-year-old woman with previous consultations for a conversion disorder. While she was infected with SARS-CoV-2 (without pulmonary involvement), she consulted in the emergency room due to panic attacks. On admission, she developed a new conversion crisis with progressive clinical deterioration, hyperventilation, and severe respiratory alkalosis (pH 7.68, Bicarbonate 11.8 mEq/L and PaCO2 10 mmHg). Clinically, she was in a coma, with respiratory and heart rates 55 and 180 per min, a blood pressure of 140/90 mmHg, impaired perfusion (generalized lividity, distal coldness, and severe skin mottling) and tetany. She also had electrocardiographic changes and high troponin levels suggestive of ischemia, and hyperlactatemia. She was managed in the hospital with intravenous benzodiazepines. The clinical and laboratory manifestations resolved quickly, without the need for invasive measures and without systemic repercussions.

Sistemática para el manejo del equilibrio ácido-base en pacientes graves / Systemization for the management of acid-base balance in seriously ill patients

Introducción: Las alteraciones del equilibrio ácido-base pueden ser de carácter primario. En la mayoría de los casos dependen de la complicación de una enfermedad preexistente. La frecuencia de estos trastornos es elevada, especialmente, en enfermos hospitalizados en las unidades de atención al paciente grave. Su aparición conlleva implicaciones pronósticas significativas. Objetivo: Sistematizar sobre el estado actual del manejo del equilibrio ácido-base. Método: Se realizó una revisión bibliográfica en la que se utilizaron las herramientas del método científico. Se examinó toda la bibliografía disponible publicada en los últimos cinco años y así, elaborar una síntesis crítica, acorde al criterio y las competencias de los autores sobre la temática. Resultados: Se expone la importancia de la evaluación clínica, que unida a los niveles de PCO2, y de exceso o déficit de bases en una gasometría arterial, permiten identificar el trastorno ácido base existente. Igualmente, se destaca que el CO2 tiene una función clave en el control de la ventilación, así como las modificaciones que produce al flujo sanguíneo cerebral, el pH y el tono adrenérgico. Otro aspecto importante fue la reciente práctica clínica de la "hipercapnia permisiva" para reducir el metabolismo tisular y de esta manera, mejorar la función del surfactante e impedir la nitración de las proteínas. Conclusiones: El manejo de los desequilibrios ácido-base debe ser del dominio de todos los profesionales vinculados a la asistencia médica, pues el retraso de su diagnóstico puede empeorar la evolución y el pronóstico de los pacientes graves(AU)

Introduction: Acid-base balance alterations can be of a primary nature. In most cases, they depend on the complication of a pre-existing disease. The frequency of these disorders is high, especially in patients hospitalized in critical care units. Its appearance carries significant prognostic implications. Objective: To systematize the current state of acid-base balance management. Method: A bibliographic review was carried out, for which the tools of the scientific method were used. All the available bibliography, published in the last five years, was examined; thus, a critical synthesis was prepared, according to the criteria and competences of the authors regarding the subject. Results: The importance of the clinical evaluation is exposed, which, together with PCO2 levels as well as excess or deficit of bases in an arterial blood gas, allow to identify the existing acid-base disorder. Likewise, it is highlighted that CO2 has a key function in ventilation control, together with the modifications it produces on cerebral blood flow, pH and adrenergic tone. Another important aspect was the recent clinical practice of "permissive hypercapnia" to reduce tissue metabolism and thus improve surfactant function and prevent protein nitration. Conclusions: The management of acid-base imbalances should be mastered by all professionals associated to medical care, since any delay in its diagnosis can worsen the evolution and prognosis of seriously ill patients(AU)

Acute respiratory alkalosis occurring after endoscopic third ventriculostomy: A case report / 대한마취과학회지

An endoscopic third ventriculostomy was performed in a 55-year-old man with an obstructive hydrocephalus due to aqueductal stenosis. The vital signs and laboratory studies upon admission were within the normal limits. Anesthesia was maintained with nitrous oxide in oxygen and 6% desflurane. The patient received irrigation with approximately 3,000 ml normal saline during the procedure. Anesthesia and operation were uneventful. However, he developed postoperative hyperventilation in the recovery room, and arterial blood gas analysis revealed acute respiratory alkalosis. We report a rare respiratory alkalosis that occurred after an endoscopic third ventriculostomy.

Distúrbios ácido-base na leishmaniose visceral / Acid-base disorders in visceral leishmaniasis

Defeitos na capacidade de acidificação e concentração urinárias têm sido descritos em pacientes portadores de leishmaniose visceral. Foram avaliados os distúrbios do equilíbrio ácido-base presentes nos pacientes com calazar, bem como os fatores relacionados. Metodologia: Foram estudados 59 pacientes com formas crônicas de calazar e comparados a um grupo controle. A gasometria arterial foi colhida em jejum; o pH urinário, a acidez titulável e a amônia urinária foram determinadas em urinas colhidas sob óleo mineral. A amônia foi dosada pela técnica de Berthelot e a acidez titulável, pela técnica de Palmer. Resultados: Todos os pacientes tinham hipoalbuminemia, hipergamaglobulimenia e hiponatremia. O grupo I compreendeu 75,5% dos pacientes, que apresentaram quadro misto de alcalose respiratória e alcalose metabólica. Hipocloremia ocorreu em 37,6%; hipocalemia associada a um potássio urinário elevado foi observada em 24,8% dos casos. Hipomagnesemia com perda renal de magnésio e potássio foi detectada em 44% dos casos. O grupo II, constituído por 24,5% dos pacientes, apresentou quadro de acidose metabólica. A excreção urinária de H+, a acidez titulável e a amônia foram semelhantes nos dois grupos. Um elevado pH urinário e uma carga elétrica urinária positiva confirmaram no grupo II a presença de acidose tubular renal distal. O equilíbrio ácido-base, pelo modelo stewart-Figge, mostra diminuição da diferença de íons fortes (SIDa), elevação do SIG e diminuição da concentração de ácidos fracos. Conclusões: Alcalose respiratória crônica e alcalose metabólica associada 9grupo I) foram observadas em 75.5% dos casos e relacionaram-se com o quadro de pneumonite intersticial, anemia, febre e disfunção hepática. Hipomagnesemia com depleção de potássio e magnésio estava presente.

Defects in the ability of urinary acidification and concentration have been described in patients with visceral leishmaniasis. We assessed disorders present acid-base balance in patients with kala-azar, as well as the related factors. Methodology: We studied 59 patients with chronic forms of leishmaniasis and compared to a control group. The arterial blood gas was collected in fasting, urinary pH, titratable acidity and urinary ammonium were determined in urine collected under mineral oil. Ammonia was measured by the Berthelot technique and acidity, the technique of Palmer. Results: All patients had hypoalbuminemia, and hyponatremia hipergamaglobulimenia. Group I comprised 75.5% of patients, who had mixed picture of respiratory alkalosis and metabolic alkalosis. Hypochloremia occurred in 37.6%, hypokalemia associated with a high urinary potassium was observed in 24.8% of cases. Hypomagnesemia with renal loss of magnesium and potassium was detected in 44% of cases. Group II, consisting of 24.5% of patients presented with metabolic acidosis. The urinary excretion of H +, acidity and ammonia were similar in both groups. A high urinary pH and urinary a positive electric charge in the group II confirmed the presence of distal renal tubular acidosis. The acid-base balance by Stewart-Figge model shows decrease in strong ion difference (AIDS), an increase of GIS and decreased concentration of weak acids. Conclusions: Chronic respiratory alkalosis and metabolic alkalosis associated 9grupo I) were observed in 75.5% of cases and were related to the picture of interstitial pneumonitis, anemia, fever and liver dysfunction. Hypomagnesemia with depletion of potassium and magnesium was present. Metabolic acidosis (group II) was observed in 24.5% of patients presenting with.

Effect of acute respiratory acidosis and alkalosis on the subtypes of intercalated cells in rat kidney / 대한해부학회지

Intercalated cells play a major role in proton and bicarbonate secretion in the collecting duct of kidney. A third type of intercalated cell (non A-non B cell), besides type A and B intercalated cells, and a bipolar cell are known to exist in the kidneys of the rat or the mouse. The third type cell has H(+)-ATPase in the apical membrane like the type A intercalated cell, but has no Cl(-)-HCO(3)- exchanger (AE1) on the basolateral membrane. The bipolar cell was shown to express H(+)-ATPase on both the apical and basolateral membranes. The functions of these cells, however, are not determined yet. This study was intended to know the immunohistochemical changes of the intercalated cell subtypes in the acute respiratory acidosis and alkalosis. After midline tracheostomy, respiratory acidosis and alkalosis were induced and maintained for 4 hours in the Sprague-Dawley rats (450~500 g) using a Rodent Ventilator. The kidneys were preserved for immunohistochemical studies by in vivo perfusion fixation with periodate-lysine-paraformaldehyde solution through the abdominal aorta. To identify the subtypes of intercalated cells and the tubule segments in which they are located, a triple immunolabeling procedure was used. Distal convoluted tubule cells and principal cells in the collecting duct were identified using antibody to thiazide sensitive Na(+)Cl(-) cotransporter and antibody to aquaporin-2, respectively. Antibodies to H(+)-ATPase and AE1 were used to identify subpopulation of intercalated cells. Type A cells were activated in respiratory acidosis with enhanced AE1 activity on the basolateral membrane and H(+)-ATPase reactivity moved to the apical membrane, whereas inactivated in respiratory alkalosis with decreased AE1 reactivity and H(+)-ATPase reactivity moved to the supranuclear cytoplasm. The change in reactivity of type A cells in respiratory acidosis or alkalosis was shown to differ depending on the tubular segments: most of the intercalated cells were activated in the outer medullary collecting duct while only a portion of the type A cells activated in the distal convoluted tubule, connecting tubule and cortical collecting duct. No changes were observed in type B cells in respiratory acidosis and alkalosis. In non A-non B cell which was increased in size in respiratory acidosis, H(+)-ATPase reactivity was seen on the apical membrane in respiratory acidosis, while seen in the supranuclear cytoplasm in respiratory alkalosis. These findings indicated that the renal compensation for respiratory acid-base imbalance was mediated mainly by type A cells rather than by type B or non A-non B cells. Among type A cells, more of those of outer medullary collec-ting duct were thought to be recruited compared with those of the cortical collecting duct and connecting tubule.