ABSTRACT
O objetivo deste artigo foi abordar as controvérsias científicas acerca dos distúrbios ácido-base nas doenças hepáticas. Nos estágios avançados da doença hepática, os distúrbios ácido-base atuam de forma complexa, comprometendo a qualidade de vida do paciente e desafiando o manejo clínico. A literatura apresenta a alcalose respiratória como uma das principais alterações, porém há uma longa discussão sobre o mecanismo fisiopatológico; em especial, citam-se a hipóxia, a hipocapnia e o nível de progesterona. Nas desordens metabólicas, com destaque para a acidose, os estudos apontam principalmente o lactato, os unmeasured ions ou íons não medidos e as alterações hidroeletrolíticas, mas cada componente desse sobressai-se dependendo da fase da doença estudada, compensada ou descompensada. As controvérsias dos distúrbios ácido-base nas doenças hepáticas devem-se ora à complexidade da fisiopatologia da própria doença, ora à necessidade de mais estudos esclarecedores.
The aim of this study is to address the scientific controversy about acid-base disorders in liver diseases. In the end stage of liver diseases, the acid-base disorder has a complex performance, impairing the patient's quality of life and challenging the clinic management. Although the literature shows respiratory alkalosis as one of the main alterations, there is a long discussion about the pathophysiological mechanism, specially regarding hypoxia, hypocapnia, and progesterone level. In metabolic disorders, especially acidosis, the studies mainly indicate the lactate, unmeasured ions, and hydroelectrolytic alterations, but, depending on the disease phase, either compensated or decompensated, each element has a particular action. The controversy about acid-base disorders in liver diseases is associated with the complexity of this condition, as well as with the necessity of more specialized research.
Subject(s)
Humans , Acid-Base Imbalance/etiology , Liver Diseases/complications , Water-Electrolyte Imbalance/physiopathology , Acidosis, Lactic/physiopathology , Alkalosis, Respiratory/physiopathology , Liver Diseases/physiopathology , Liver Diseases/metabolismABSTRACT
Estudou-se a influência da hidratação em 30 pacientes submetidos a cirurgia de pequeno e grande porte. Os pacientes foram divididos em grupos de 5 conforme o porte cirúrgico e o tipo de hidratação: restrição hídrica, segundo o balanço diário e sobrecarga hidrossalina. As alterações mais relevantes do equilíbrio ácido base foram: pré-operatório - alcalose respiratória; pós-operatório imediato - acidose respiratória; 1º, 2º e 3º dias de pós-operatório - alcalose respiratória, metabólica ou mista. Os métodos de hidratação com restrição hídrica ou segundo o balanço não afetaram o equilíbrio ácido-base, enquanto que a sobrecarga hidrossalina reduziu de modo significativo a incidência de alcalose metabólica no pós-operatório.
Subject(s)
Humans , Adult , Middle Aged , Postoperative Care/methods , Acid-Base Equilibrium/physiology , Fluid Therapy/methods , Acidosis, Respiratory/physiopathology , Alkalosis, Respiratory/physiopathology , Alkalosis/physiopathology , Blood Gas Analysis , Intraoperative Care , Water-Electrolyte Balance/physiologyABSTRACT
Se expone un caso de síndrome de Bartter en un lactante menor de dos meses de edad con antecedente prenatal de polihidramnios y parto pretérmino. Con historia de vómito, diarrea y estreñimiento ocasional, asociado con retardo pondoestatural. Este paciente presentó cuadro de bronconeumonía viral la cual evolucionó en forma tórpida con aumento del síndrome de dificultad respiratoria (SDR) y deterioro del estado general por lo cual hubo necesidad de trasladarlo a la unidad de cuidado intensivo de pediatría. Allí se corroboró la presencia de alcalosis metabólica hipokalémica e hipoclorémica con aumento de la excreción urinaria de K, Na y Cl y defecto en la habilidad de concentrar la orina. Aunado a esto se detectó hiperreninemia, poliuria y aldosterona elevada. La tensión arterial fue normal con un percentil menor de cinco para el peso y de 10 para la talla. Con base en todo lo anterior se pudo confirmar el diagnóstico de síndrome de Bartter
Subject(s)
Humans , Infant , Male , Alkalosis, Respiratory/classification , Alkalosis, Respiratory/diagnosis , Alkalosis, Respiratory/drug therapy , Alkalosis, Respiratory/nursing , Alkalosis, Respiratory/physiopathology , Bartter Syndrome/congenital , Bartter Syndrome/diagnosis , Bartter Syndrome/drug therapy , Bartter Syndrome/nursing , Bartter Syndrome/physiopathology , Bartter Syndrome/urineABSTRACT
During acute respiratory alkalosis myocardial contractility first increases but then decreases towards control levels. The mechanism of this response was investigated in isovolumic perfused rabbit hearts. Developed pressure (DP) and its first derivative (dP/dt) were measured before, during and after hypocapnia induced by equilibrating the perfusate with 2% CO2 rather than the 5% used in control. pH of the perfusate (pHo) changed from 7.36 +/- .02 to 7.71 +/- .01. After about 20 s, an increase in DP of about 20% was detected. This increase in contractility is followed by a partial recovery towards control levels. After the partial recovery a new mechanical steady state is reached in about 2 min. Neither 5-[N-ethyl-N-isopropyl]amiloride (EIPA) 10(-6) M, a blocker of the Na+/H+ exchanger, nor 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid (SITS) 10(-4) M, or 5-[aminosulfonyl]-4-chloro-2-[(2-furanylmethyl)-amino] benzoic acid (furosemide) 10(-4) M, blockers of Cl-/HCO3- exchanger, abolished the recovery in contractility towards control levels. The recovery was not abolished by replacing 50% of extracellular Cl- concentration by either sulfate or gluconate. The lack of blockade of this mechanical recovery in spite of the intervention performed suggests a mechanism other than the exchangers as the cause of the biphasic changes.
Subject(s)
Alkalosis, Respiratory/physiopathology , Hypocapnia/physiopathology , Myocardial Contraction/physiology , 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid/pharmacology , Amiloride/analogs & derivatives , Amiloride/pharmacology , Animals , Furosemide/pharmacology , Male , Myocardial Contraction/drug effects , Perfusion , Rabbits , Sodium-Hydrogen Exchangers/antagonists & inhibitorsABSTRACT
Fourteen children with congenital heart disease and associated pulmonary hypertension (preoperative mean pulmonary artery pressure (MPAP) 48 mm Hg +/- 1 SEM were examined to determine the effect of arterial carbon dioxide tension (PaCO2) and pH on pulmonary and systemic hemodynamics after surgical repair. Baseline measurements were obtained with hyperventilation to PaCO2 20 to 30 mm Hg (pH 7.56 +/- 0.01 mm Hg). The addition of carbon dioxide to inspired gas to achieve a PaCO2 40 to 45 mm Hg (pH 7.35 +/- 0.01) resulted in a significant increase in MPAP, from 32 +/- 5 mm Hg to 47 +/- 8 mm Hg (p less than 0.05). An increase in mean cardiac index (CI) from 2.7 +/- 0.3 L/min/m2 to 3.3 +/- 0.3 L/min/m2 (p less than 0.05) explained in part the associated increase in MPAP. For a subgroup of eight patients with postoperative MPAP greater than 30 mm Hg (at pH 7.35 to 7.40), pulmonary vascular resistance index (PVRI) also significantly increased (p less than 0.05) as PaCO2 was increased, implying a direct pulmonary vasodilating effect of alkalosis. Removal of carbon dioxide from inspired gas returned hemodynamic values to baseline. The higher the MPAP at physiologic pH the greater the absolute amount of MPAP reduction and PVRI reduction (p less than 0.05) with alkalosis. No complications from alkalosis were seen. We suggest that a trial of hypocarbic alkalosis in the child with severe residual pulmonary hypertension after surgical repair of congenital heart disease is warranted to reduce right ventricular afterload.
Subject(s)
Carbon Dioxide/blood , Heart Defects, Congenital/physiopathology , Hemodynamics , Hypertension, Pulmonary/physiopathology , Pulmonary Circulation , Adolescent , Alkalosis, Respiratory/physiopathology , Child , Child, Preschool , Female , Heart Defects, Congenital/blood , Heart Defects, Congenital/complications , Heart Defects, Congenital/surgery , Humans , Hydrogen-Ion Concentration , Hypertension, Pulmonary/blood , Hypertension, Pulmonary/congenital , Hypertension, Pulmonary/surgery , Infant , Male , Postoperative Period , Pulmonary Gas ExchangeABSTRACT
Twenty-three newborn infants with severe bilateral pulmonary disease and persistent pulmonary hypertension received mechanical ventilation to pH greater than 7.55 and PaCO2 less than 25 torr. Response, as defined by attainment of a PaO2 greater than 100 torr, occurred in 87% of patients. Analysis of sequential arterial pH determinations revealed a linear increase in the number of infants responding as arterial pH increased. However, individual patients varied greatly in the optimal pH necessary to correct hypoxemia (range pH 7.50 to 7.75). Sixteen patients who had received mechanical hyperventilation were observed for 11.1 +/- 2.3 months. Virtually all had normal growth and development on follow-up physical and neurologic examinations, often despite profound or prolonged alkalosis and hypocarbia. In 11 infants at a corrected gestational age of 1 year, Bayley Scales of Infant Development revealed normal mental developmental indices (mean 106.2 +/- 15.4) and normal, but significantly lower, psychomotor developmental indices (93.2 +/- 11.7) (P less than 0.005). Although response and short-term outcome of neonatal hyperventilation appear favorable, this technique should be reserved for critically ill infants, because its long-term effects on the central nervous system are unknown.