El algoritmo de la gasometría arterial: propuesta de un enfoque sistemático para el análisis de los trastornos del equilibrio ácido-base / The arterial blood gas algorithm: proposal of a systematic approach to analysis of acid-base disorders

Las anomalías en el equilibrio ácido-base son problemas clínicos comunes, y pueden tener efectos perjudiciales en la función celular y ser el indicio de varios trastornos. Por lo tanto, es importante para el clínico, el hacer un diagnóstico preciso de los trastornos ácido-base presentes para un tratamiento adecuado. Se han propuesto 3 enfoques para evaluar los trastornos ácido-base: un enfoque centrado en el bicarbonato, el enfoque de Stewart y el enfoque de exceso de base. Aunque los 2 últimos tienen muchos adeptos, solo discutiremos el enfoque centrado en el bicarbonato. Este enfoque es más fácil de utilizar desde el punto de vista clínico, tiene una evaluación fisiológica del trastorno ácido-base, presenta una lógica fácilmente comprensible para evaluar la gravedad y proporciona, además, una base más sólida para el desarrollo de terapias efectivas. Por lo tanto, nuestro trabajo se limitará a un examen en profundidad de esta teoría. En esta revisión, primero se introducirán nuevos conceptos importantes; sus beneficios y discusión de sus limitaciones; y luego se mostrará su utilización para analizar casos reales. Se ha generado un algoritmo para abordar de forma sistemática el análisis que incorpora estos nuevos conceptos

Abnormalities in the acid-base balance are common clinical problems and can have deleterious effects on cellular function and be a clue to various disorders. Therefore, it is important for the clinician to make a precise diagnosis of the acid-base disorder(s) present for a proper treatment. Three approaches have been proposed to evaluate acid-base disorders: a bicarbonate-centric approach; the Stewart approach, and the base excess approach. Although the latter two have many adherents, we will only discuss the bicarbonate-centric approach. This approach is simpler to utilize at the bedside, has a physiological evaluation of the acid-base disorder, presents an easily understandable approach to assess severity, and provides a more solid foundation for the development of effective therapies. Therefore, the following discussion will be limited to an examination of this approach. In this case-centric review, important new concepts will be introduced first; their benefits and limitations discussed; and then their utilization to analyze actual cases will be shown. A systematic approach algorithm that incorporates these new concepts has been generated and will be highlighted

Drug-induced acid-base disorders.

The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal anti-inflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g., anesthetics, sedatives) or hyperventilation (e.g., salicylates, epinephrine, nicotine).

Mixed acid-base disturbances.

Mixed acid-base disturbances, defined as the simultaneous presence of two or more acid-base disorders, are commonly observed in hospitalized patients, especially those in critical care units. Certain clinical settings are commonly associated with mixed acid-base disorders, including cardiorespiratory arrest, sepsis, drug intoxications, diabetes mellitus, and organ failure (especially renal, hepatic, and pulmonary failure). As a general rule, the symptoms and signs of the underlying disease that gives rise to the observed mixed acid-base disorder dominate the clinical picture. The basic principles underlying the diagnosis of mixed acid-base disorders are identical to those required for the identification of simple acid-base disturbances. The management of mixed acid-base disturbances is aimed at restoring the altered acid-base status by reversing all the elemental components present, thus it encompasses the therapy of each simple acid-base disorder.

Using quantitative acid-base analysis in the ICU.

The quantitative acid-base 'Strong Ion' calculator is a practical application of quantitative acid-base chemistry, as developed by Peter Stewart and Peter Constable. It quantifies the three independent factors that control acidity, calculates the concentration and charge of unmeasured ions, produces a report based on these calculations and displays a Gamblegram depicting measured ionic species. Used together with the medical history, quantitative acid-base analysis has advantages over traditional approaches.

Clinical review: the meaning of acid-base abnormalities in the intensive care unit part I - epidemiology.

Acid-base abnormalities are common in critically ill patients. Our ability to describe acid-base disorders must be precise. Small differences in corrections for anion gap, different types of analytical processes, and the basic approach used to diagnose acid-base aberrations can lead to markedly different interpretations and treatment strategies for the same disorder. By applying a quantitive acid-base approach, clinicians are able to account for small changes in ion distribution that may have gone unrecognized with traditional techniques of acid-base analysis. Outcome prediction based on the quantitative approach remains controversial. This is in part due to use of various technologies to measure acid-base variables, administration of fluid or medication that can alter acid-base results, and lack of standardized nomenclature. Without controlling for these factors it is difficult to appreciate the full effect that acid-base disorders have on patient outcomes, ultimately making results of outcome studies hard to compare.

Clinical review: Acid-base abnormalities in the intensive care unit -- part II.

Acid-base abnormalities are common in the critically ill. The traditional classification of acid-base abnormalities and a modern physico-chemical method of categorizing them will be explored. Specific disorders relating to mortality prediction in the intensive care unit are examined in detail. Lactic acidosis, base excess, and a strong ion gap are highlighted as markers for increased risk of death.

Interpretation of arterial blood gases: a clinical guide for nurses.

Arterial blood gas analysis has become an essential skill for all healthcare practitioners. It provides important information with regard to adequacy of ventilation, oxygen delivery to the tissues and acid-base balance. Although each patient's clinical presentation will be judged individually, situations that warrant analysis of a blood gas sample include respiratory compromise, post-cardiorespiratory arrest, evaluation of interventions such as oxygen therapy, respiratory support and as a baseline before surgery. This article reviews the different parameters that are measured by various machines, with a focus on basic measurement of arterial blood gases. These include partial pressure of carbon dioxide in arterial blood (PaCO(2)), partial pressure of oxygen in arterial blood (PaO(2)), bicarbonate levels (HC0(3)(-)) in arterial blood and base excess/deficit. The physiology of acid-base balance is reviewed and the causes and presentation of the four acid-base disturbances is described. A systematic method to aid arterial blood interpretation is identified, together with discussion regarding the importance of interpreting PaO(2) readings in relation to the amount of inspired oxygen a patient is receiving (FiO(2)), the practice of temperate correction and the relationship between standardized and actual bicarbonate readings.

Acid-base physiology: the 'traditional' and the 'modern' approaches.

The interpretation and understanding of acid-base dysfunction has recently been revisited. The 'traditional' approach developed from the pioneering work of Henderson and Hasselbalch and is still the most widely used in clinical practice. There are a number of problems identified with this approach, however. The 'modern' approach derives from Stewart's work in physical chemistry. In this review we describe the origins of the traditional approach and discusses related concepts. We then describe Stewart's approach, including how it is derived and how it may be used to classify acid-base derangements. The applications of Stewart's approach to clinical scenarios in intensive care is then discussed briefly before we examine some published clinical studies based on his work.

Diagnosis of metabolic acid-base disturbances in critically ill patients.

We compare two commonly used diagnostic approaches, one relying on plasma bicarbonate concentration and "anion gap," the other on "base excess," with a third method based on physicochemical principles, for their value in detecting complex metabolic acid-base disturbances. We analyzed arterial blood samples from 152 patients and nine normal subjects for pH, PCO(2), and concentrations of plasma electrolytes and proteins. Ninety-six percent of the patients had serum albumin concentration < or = 3 SD below the mean of the control subjects. In about one-sixth of the patients, base excess and plasma bicarbonate were normal. In a great majority of these apparently normal samples, the third method detected simultaneous presence of acidifying and alkalinizing disturbances, many of them grave. The almost ubiquitous hypoalbuminemia confounded the interpretation of acid-base data when the customary approaches were applied. Base excess missed serious acid-base abnormalities in about one-sixth of the patients; this method fails when the plasma concentrations of the nonbicarbonate buffers (mainly albumin) are abnormal. Anion gap detected a hidden "gap acidosis" in only 31% of those samples with normal plasma bicarbonate in which such acidosis was diagnosed by the third method; when adjusted for hypoalbuminemia, it reliably detected the hidden abnormal anions. The proposed third method identifies and quantifies individual components of complex acid-base abnormalities and provides insights in their pathogenesis.

Maintaining acid-base balance in organ donors.

An abnormal blood pH may cause the loss of donor organs through harmful physiological consequences. The organ procurement coordinator must correctly analyze the acid-base abnormality and treat its cause while normalizing the blood pH. We recommend that treatment of acidemia or alkalemia be first directed toward changing parameters on the mechanical ventilator, using the Paco2 to modify blood pH. Thereafter, hydrochloric acid or sodium bicarbonate may be administered to correct the calculated metabolic acid-base deficit. The types of acidosis or alkalosis, dead space effect during mechanical ventilation, base excess, base deficit, and the appropriate evaluation of blood lactate are also discussed as related to the correction of the acid-base status throughout donor care.

Principles and practice of blood gas measurement.

Homeostasis in the human body is maintained by a sophisticated process of chemical balance. The disorder of this balance results in ill health. The body has its own compensatory mechanisms but intervention may also be required. Blood gas analysis is the primary means of assessing acid base balance and is frequently required in both acute and chronic illness to assess and determine treatment. This article outlines the principles involved in blood gas analysis and acid base balance.

Acid-base disorders: classification and management strategies.

Acid-base disorders are common in clinical practice. Simple acid-base disturbances include metabolic acidosis, metabolic alkalosis, respiratory acidosis and respiratory alkalosis. Each can be clearly identified using a common clinical approach. Proper understanding of acid-base disorders requires knowledge of normal physiology. Each of the simple acid-base disorders can be diagnosed by obtaining a good history and performing a physical examination, followed by determinations of electrolyte levels, anion gap and pH. The degree and nature of compensation should then be analyzed. Finally, the ratio of the change in anion gap to the change in serum bicarbonate (delta AG/delta HCO3-) should be determined. When this diagnostic process is applied, proper identification of the disorder can be made and management can be undertaken. Mixed acid-base disorders can also be identified and managed using this method.

Stewart's quantitative acid-base chemistry: applications in biology and medicine.

We review P.A. Stewart's quantitative approach to acid-base chemistry, starting with its historical context. We outline its implications for cellular and membrane processes in acid-base physiology; discuss its contributions to the understanding and analysis of acid-base phenomena; show how it can be applied in clinical problems; and propose a classification of clinical acid-base disturbances based on this general approach.

[Clinical aspects of acid-base disorders].

Acid-base disorders are frequently recognized in a wide variety of clinical settings such as severe systemic hospitalized patients. The principal object is to assessment of acid-base equilibrium and to obtain an appropriate guide to therapy. The approach is centered to a systemic analysis of blood gas evaluation. To establish this complex matter is followed. Is an acid-base disorder present? Is the disorder a simple or a mixed abnormality? What is the primary cause? These evaluations should be obtained by accurate history taking, physical examination, and routine laboratory tests. In addition, the supporting analysises such as anion gap (AG) calculation, urine AG assessment, urine chloride concentration and so on are also useful for correct diagnosis. In view of the complexty and difficult expression of acid-base disorders, it is desirable that clinicians must have full knowledges of systemic approach to the blood gas analysis and its evaluation.

[Mixed acid-base disorders].

Maintenance of the acid-base balance is critical for keeping cellular and whole body integrity, and acid-base disturbances are commonly encountered in critically ill patients. In this chapter, the classification and the pathogenesis of mixed acid-base disorders are reviewed in order to understand and manage these abnormalities. First of all, the compensatory reactions to the primary acid-base state must be evaluated. Careful examination of the physical findings and medical history are also essential for making a correct diagnosis and to treat the patients effectively.

[Drug-induced acid-base disorders].

Drug-induced acid-base disorders may be classified into four categories with respect to the mechanism. 1. Metabolic acidosis is induced by a large acid loads incurred from exogenous sources (e.g. NH4Cl, or toxin ingestion) or endogenous acid production (e.g. generation of ketoacids or lactic acids by alcohol or phenformin) or base loss (e.g. abuse of laxatives). 2. Metabolic alkalosis results from exogenous bicarbonate loads (e.g. milk-alkali syndrome) or effective extracellular fluid contraction, potassium depletion plus hyperaldosteronism (e.g. vomiting, diuretics, or licorice). 3. Renal tubular acidosis is induced by the drugs which mainly impair proximal and/or distal tubules (e.g. vitamin D, NSAID, acetazolamide or amphotericin B). 4. Respiratory acidosis or alkalosis results from drug-induced respiratory center depression or neuromuscular impairment (e.g. anesthetic, sedative overdosage or curare) or hyperventilation (salicylates, paraldehyde, epinephrine, or nicotine).