Acid-base disorders are pathological changes in the arterial pH and carbon dioxide partial pressure (PCO 80127, US2) and in the serum bicarbonate (HCO3-).
(See also acid-base regulation.) Acid-base disorders are pathological changes in the arterial pH and carbon dioxide partial pressure (PCO 80127, US2) and in the serum bicarbonate (HCO3-). A acidemia consists in a serum pH <7.35. A ALKALAEMIA consists in a serum pH> 7.45. Acidosis describes physiological processes that lead to acid accumulation or a base loss. Alkalosis describes physiological processes that lead to an accumulation base or an acid loss. Actual changes in pH are depending on the extent of the physiological compensation and the occurrence of several other factors. Classification Based on the clinical context and on whether the primary changes in pH are due to a change in serum HCO3- or PCO2 value are defined primary disorders of acid-base balance as a metabolic or respiratory. Metabolic acidosis is <24 mEq / L in a serum-HCO3-. Causes Increased acid production acid dietary intake Decreased renal acid excretion Gastrointestinal and renal HCO3- loss Metabolic alkalosis is a serum HCO3-> 24 mEq / l. Causes acid loss HCO3 – retention A respiratory acidosis is> 40 mmHg by a PCO2 (hypercapnia) defined. Cause reduction in minute ventilation (hypopnea) A respiratory alkalosis is at a PCO2 value <40 mmHg (hypocapnia). Cause is increasing minute ventilation (hyperventilation) Whenever an acid-base disturbance, start compensatory mechanisms to correct the pH (see Table: Primary changes and counter-regulation with simple acid-base disturbances). Compensation can not fully normalize the pH and it never comes to overcompensation. A simple (Primary) acid-base disorder is a single disturbance in acid-base balance with the consequent compensatory reaction. Mixed acid-base disorders include ? 2 primary acid-base disturbances. Tips and risks a counter-regulation in acid-base disorders can not fully normalize the pH and it never comes to overcompensation. Primary modifications and counter-regulation with simple acid-base disturbances primary disorder pH bicarbonate (HCO3-) PCO2 predictive compensation Metabolic acidosis <7.35 Primary acceptance Compensatory decrease 1.2 mm Hg decrease the PCO2 each decrease of 1 mmol / L of HCO3- or * PCO2 = (1.5 x HCO3-) + 8 (± 2) or PCO2 = HCO3- + 15 or PCO2 = the last 2 digits of the pH value × 100 Metabolic alkalosis> 7.45 Primary rise compensatory increase from 0.6 to 0.75 mmHg increase of PCO2 each increase of 1 mmol / L of HCO3- (PCO2sollte the compensatory increase above 55 mmHg rise) Respiratory acidosis <7.35 compensatory increase the primary increase in acute: 1-2 mmol / l increase of HCO3- each increase of 10 mmHg from PCO2 Chronic: 3-4 mmol / l increase of HCO3- each increase of 10 mmHg from PCO2 Respiratory alkalosis> 7.45 Compensatory decrease Primary acceptance Acute: 1-2 mmol / l decrease in HCO3- each decrease of 10 mmHg from the PCO2 Chronic: 4-5 mmol / l decrease in HCO3-per decrease of 10 mmHg from the PCO2 * Inaccurate but convenient rule of thumb. Symptoms and complaints compensated or mild disorders of acid-base balance causing few symptoms or complaints. Heavy, uncompensated disorders have numerous cardiovascular, respiratory, neurological and metabolic consequences (see Table. Clinical effects of acid-base disorders and oxyhemoglobin dissociation curve). Clinical effects of acid-base disorders system acidemia ALKALAEMIA Cardiovascular impaired cardiac contractility Arteriolar Dilation venoconstriction centralization of the blood volume increased pulmonary vascular resistance Reduced cardiac output Decreased systemic blood pressure Decreased blood flow to the kidneys and liver coronary Decreased threshold for the occurrence of cardiac arrhythmias decrease in response to catecholamines Arteriolenkonstriktion Decreased Decreased blood flow threshold for the occurrence of angina Decreased threshold for the occurrence of Her zrhythmusstörungen Metabolically insulin resistance inhibition of anaerobic glycolysis reduction in ATP synthesis hyperkalemia protein degradation bone demineralization (chronic) stimulation of anaerobic glycolysis formation of organic acids Reduced dissociation of oxyhemoglobin decreased amount of ionized calcium hypokalemia hypomagnesemia hypophosphatemia Neurological inhibition of metabolism and the regulation of cell volume disturbances of consciousness and coma tetany seizures lethargy delirium stupor Respiratory compensatory hyperventilation with possible fatigue of the respiratory muscles Compensatory hypoventilation with hypercapnia and hypoxemia diagnosis ABG serum electrolytes calculating the anion If metabolic acidosis is present, is carried out calculation of the Delta gap and application of winter formula Search compensatory changes Diagnosis by ABG and measurement of serum electrolytes. The ABG directly measures the arterial pH and PCO2. The HCO3 – levels of ABG be calculated from the Henderson-Hasselbalch equation; the HCO3 – levels of serum chemistry parameters directly measured and considered to be more accurate in case of deviations. The most accurate determination of the acid-base balance is done by measuring the pH and PCO2 of the arterial blood. In cases of circulatory failure or during cardiopulmonary resuscitation measurements can reflect the conditions on tissue level may be more accurate and a more useful guide to the bicarbonate use and ventilation needed with venous blood. Clinical calculator: Henderson-Hasselbach equation by means of pH-value can be set of the primary process (acidosis or alkalosis), although it moves with compensating for the normal range. PCO2 changes reflect the respiratory component, while reflecting changes in HCO3-metabolic component. Complex or mixed acid-base disorders comprise more than one primary process. In these mixed disorders, the values ??can be deceptively normal. It is therefore in the assessment of acid-base disturbances important to determine whether changes in the PCO2 and HCO3- show the expected compensation (see table: Primary changes and counterregulations for simple acid-base disorders). If not, then a second primary process should be suspected as a cause of the abnormal compensation. The interpretation must also take into account clinical factors (eg. As chronic lung disease, kidney failure, drug overdose). The anion (the anion) should always be calculated; an increase almost always indicates a metabolic acidosis. A normal anion having a low HCO3- (eg <24 mEq / l.) And a high chloride (Cl -) - value in the serum indicates a hyperchloremic metabolic acidosis (anion gap with normal). If metabolic acidosis is, a delta gap calculated (the anion), to detect a concurrent metabolic alkalosis. Also is determined by formula winter whether the respiratory compensation is sufficient or a second acid-base disturbance is present (predicted PCO2 = 1.5 [HCO3-] + 8 ± 2; if the PCO2 is higher, there is also a primary respiratory acidosis - if it is lower, there is a respiratory alkalosis). Clinical Calculator: anion gap Clinical Calculator: anion gap Delta Delta gradient Multicalc clinical calculator: anion gap in Hypo albumin states Clinical Calculator: Winter equation for the expected pCO2 value of clinical calculator: Arterial blood gas interpretation TreeCalc The anion The anion is the sodium concentration in serum minus the sum of chloride (Cl -) - and bicarbonate (HCO3 -) - defined concentrations; Na + - (Cl + HCO3-). The term "gap" is misleading because the law of electrical neutrality requires the same number of positive and negative charges in an open system; the gap appears in laboratory tests because certain cations (+) and anions (-) not at the lab routinely performed blood chemistry tests are measured. Therefore Na ++ unmeasured cations (UC) = Cl- + HCO3- + unmeasured anions (UA) and the anion, Na + - (Cl- + HCO3-) = UA - UC The predominant "not measured" anions are phosphate (PO43- ), sulphate (SO4), various negatively charged proteins and some organic acids, which make up 20-24 mEq / l. The predominant "measured" extracellular cations are potassium (K +), calcium (Ca ++) and magnesium (Mg ++), which account for about 11 mEq / l. Therefore, the typical anion 23-11 = 12 mEq / l. The anion may be affected by increases or decreases in the UC or the UA. Increased Anion Gap is most commonly caused by metabolic acidosis, wherein the negatively charged acids - consume HCO3- (ie be buffered characterized) - mostly ketones, lactates, sulfates, or metabolites of methanol, ethylene glycol or salicylates. Other causes of an increased anion gap include Hyperalbuminämie and uremia (increased anion) and hypocalcemia or hypomagnesemia (low cations). A decreased anion gap is not related to metabolic acidosis, but hypoalbuminemia (decreased anions), hypercalcemia, hypergammaglobulinemia, as occurs in myeloma hypermagnesemia and lithium toxicity (elevated cations), hyperviscosity or Halogenidvergiftung (bromide or iodide) gives. The effect of low albumin may be taken into account by the fact that the normal interval for the anion per decrease in albumin to 1 g / dl is shifted by 2.5 mEq / l down. A negative anion gap on in severe cases of hypernatremia, hyperlipidemia and bromide poisoning rarely occurs as a laboratory artifact. The delta gap: the difference between the anion of the patient and the normal anion gap is referred to as delta gap. This value is considered to be an equivalent of HCO3-, as for the increase of each unit of the anion should HCO3- to reduce 1 (by buffering). So if the delta gap is added to the measured HCO3-, the result of the normal range for HCO 3 should be; an increased value indicates the additional presence of a metabolic alkalosis. Example: The laboratory values ??of up vomiting, sick-looking, drunken patients show Na, 137; K, 3.8; Cl, 90; HCO3-, 22; pH 7.40; PCO2, 41; PO2, 85 the results appear unremarkable at first glance. However, calculations show an increase in the anion: 137 - (90 + 22) = 25 (normal, 10 to 12) which indicates metabolic acidosis. Respiratory compensation is calculated based on winter formula: Predicted PCO2 = 1.5 (22) + 8 ± 2 41 ± 2 = measured = predicted, so that the respiratory compensation is appropriate. Since metabolic acidosis is present, the Delta gap is calculated and the result is added to the measured HCO3-: 25 - 10 = 15 15 + 22 = 37 The resulting corrected HCO3 - value is above the normal range for HCO3-, indicating that also has a primary metabolic alkalosis is present. Thus, the patient has a mixed acid-base disorder. With clinical information could be metabolic acidosis caused by an alcoholic ketoacidosis in combination with a metabolic alkalosis by repeated vomiting with loss of Cl and volume suggest. A respiratory acidosis can be accepted at a PCO2> 40 mmHg; HCO3- should increase by 3-4 mEq / l per increase in PCO2 to 10 mmHg, which persists 4-12 h, compensate for acute (alternatively the increase may not occur or be as low as 1-2 mEq / l and slowly over several days on 3-4 mEq / l to rise). A higher increase in HCO3- indicates a primary metabolic alkalosis; lower elevations have a due to the shortness of the existence or lack of compensation or a coexistent primary metabolic acidosis out. Metabolic alkalosis can be assumed when the HCO3- is> 28 mEq / l. The PCO2 should act gegenregulatorisch by increase of about 0.6-0.75 mmHg per increase in HCO3- to 1 mEq / l (up to a maximum of about 55 mmHg). A larger increase implies concomitant respiratory acidosis; the smaller increase, however, a respiratory alkalosis. A respiratory alkalosis may be suspected if the PCO2 <38 mmHg. The HCO3- should compensate for about 4-12 h by a drop to 5 mEq / l per PCO2 drop by 10 mmHg. A weaker waste can be explained by lack of time for the compensation or the simultaneous existence of a primary metabolic alkalosis. A stronger waste takes place at a primary metabolic acidosis. Nomograms (acid-base diagrams) are an alternative for the diagnosis of disorders mixed by allowing a synchronous application of pH, HCO3, and PCO2. Summary of acidosis and alkalosis related to physiological processes which cause an accumulation or loss of acid and / or alkali; the blood pH value may be abnormal or not. Acidemia and ALKALAEMIA refer to an abnormal acidic (pH <7.35) or alkalotic (pH> 7.45) serum pH. are acid-base disorders as metabolically classified, if the change of the pH value of the primary HCO3 by a change – is carried out in serum, respiratory, if the change is primarily due to the PCO2 by a change (increase or decrease in the ventilation ). By means of pH-value can be set of the primary process (acidosis or alkalosis). PCO2Veränderungen reflect the respiratory component, changes in HCO3- show the metabolic component. All acid-base disturbances lead to compensation, which tend to normalize the pH. Metabolic acid-base disturbances lead to respiratory compensation (change in Pco2); respiratory acid-base disturbances lead to metabolic compensation (change of HCO3-). There may be more than one primary acid-base disturbance present simultaneously. It is important to identify each primary acid-base disorder, and to treat. Initial laboratory tests of acid-base disorders include ABG, serum electrolytes, and the calculation of the anion. Use one of several formulas, rules of thumb, or acid-base nomograms to determine, or whether laboratory values ??in accordance with a single acid-base disturbance (and compensation) whether a second primary acid-base disturbance is still present. Treat each primary acid-base disorder.