Compensated metabolic alkalosis

Which of the combinations of laboratory results below indicates compensated metabolic alkalosis ... 

The answer is e. (Murray, pp 15-26.) Pure metabolic acidosis (choice c) or pure metabolic alkalosis exhibits abnormal bicarbonate and normal lung function. Pure respiratory acidosis (choice d) or alkalosis (choice a) is associated with normal renal function (and normal blood acids) with a normal bicarbonate and abnormal Pccv, Thus choices b and e must involve compensation, since both the Pccv and bicarbonate are abnormal. Choice e must represent compensated metabolic alkalosis since the PCO2 is high—if it were compensated respiratory acidosis with a high PcOj, the pH would be low. 

A young man with a history of dyspepsia and excessive alcohol intake who gives a 24-hoiir history of vomiting. Blood gas results are [H ] = 28 nmol/1 PCO, = 7.2 kPa MCO., J = 48 mmol/l. This is a pariially compensated metabolic alkalosis. 

Comparison. The points for compensated respiratory acidosis and compensated metabolic alkalosis are (much closer together than, further apart than) the points representing the uncompensated disorders. Consequently, it is (easy, difficult) from the biochemistry of the blood alone to discriminate between the compensated disorders. 

Explain that the acid-base status can be deduced from the blood biochemistry in cases of uncompensated respiratory or metabolic disorder. Demonstrate examples of compensated disorders (e.g. compensated respiratory acidosis and compensated metabolic alkalosis) in which the same abnormality of blood biochemistry may be reached by different routes. Hence explain the need, in such cases, to seek each cause and evaluate its effect. 

The concentration of CO2 in blood is usually represented as FCO2, the partial pressure of CO2. Bicarbonate concentration can be regarded as the metabolic component of acid-base homeostasis while CO2 can be regarded as the respiratory component. Thus a primary change in one of these components as a result of a clinical condition can result in a compensatory change in other component. Raised blood PCO2 occurs in respiratory acidosis (as in chronic obstructive airway disease] and compensated metabolic alkalosis. Low blood PCO2 is found in respiratory alkalosis (hyperventilation) and in compensated metabolic acidosis. 

Metabolic alkalosis is the increase in pH resulting from illness or chemical ingestion. Repeated vomiting or the overuse of diuretics can cause metabolic alkalosis. Once again the body compensates, this time by decreasing the rate of respiration. 

Arterial blood gases with a normal or elevated pH indicates metabolic alkalosis that may or may not be compensated. 

Metabolic alkalosis is characterized by an increase in serum HC03A This disorder requires loss of fluid that is low in HC03 from the body or addition of HC03 to the body. The compensation for metabolic alkalosis is a decrease in ventilation with an increase in arterial C02. 

Metabolic alkalosis is characterized by an increased arterial pH, a primary increase in the HCOf concentration, and a compensatory increase in the PaC02. Patients will always hypoventilate to compensate for metabolic alkalosis—even if it results in profound hypoxemia. For a metabolic alkalosis to persist there must concurrently be a process that elevates serum HC03 concentration (gastric or renal loss of acids) and another that impairs renal HC03 excretion (hypovolemia, hypokalemia, or mineralocorticoid excess). The etiologies of metabolic alkalosis are listed in Table 25-5. 

The conclusion—respiratory acidosis must be compensated by metabolic alkalosis in order to return the pH to normal. The following table summarizes all the possibilities. Note that the directions of the arrows are always the same for pC02 and [HCO3]. Metabolic is always compensated by respiratory (and vice versa), and acidosis is always compensated by alkalosis. 

Failure of compensation is responsible for mixed acid-base disorders such as respiratory acidosis and metabolic acidosis, or respiratory alkalosis and metabolic alkalosis. In contrast, excess compensation is responsible for metabolic acidosis and respiratory alkalosis, or metabolic alkalosis and respiratory acidosis. 

AGC Line AG represents a metabolic alkalosis with a rise in HC03 to 35 mmol.l-1. Compensation occurs by hypoventilation along line GC. 

Figure 3.4 Identification of various acid-base disturbances. Acute disorders are synonymous with uncompensated disturbances, whereas chronic conditions are synonymous with partially compensated or compensated disturbances. If a specific case falls outside the shaded areas, a compound acid-base disturbance may be suspected, such as the coexistence of respiratory acidosis (partially compensated) and metabolic alkalosis. Unshaded areas may also indicate a transient state between an acute (uncompensated) state and a chronic (partially compensated) condition. (From Cogan MG, Rector FC Jr., Seldin DW. In Brenner BM, and Rector FC Jr, eds. The Kidney, 2nd ed., Vol. 1, Philadelphia WB Saunders, 1986, p. 860.)...

Solution The [H2C03] is 0.0301 x 58 = 1.75 meq/L, hence [HC03 ] = 33.8 — 1.75 = 32.05 meq/L pH = 6.1 + log 32.05/1.75 = 7.36. The patient is slightly acidotic, with both the pC02 and the [HC03 ] above normal. The patient therefore has a partly compensated respiratory acidosis. If the patient had a metabolic alkalosis with partial respiratory compensation, his or her blood pH would have been above 7.4. 

Normalization of laboratory parameters must be guaranteed (i.) regulation of serum electrolytes, acid-base equilibrium and blood sugar values, (2.) substitution of zinc, and (2.) compensation of hypovolaemia. Metabolic alkalosis should not be balanced, since it is important for the urea cycle. 

Hjqiochloremia is common in gastrointestinal disease (Svendsen et al 1979), because of the loss of gastric hydrochloric acid in high volume reflux from the stomach (in proximal enteritis and grass sickness) and the secretion and/or lack of absorption of chloride in severe colitis. It may also occur in exhausted horse syndrome, chronic compensated respiratory acidosis and following furosemide (frusemide) administration. Hypochloremia in the absence of hyponatremia results in a metabolic alkalosis (Corley Marr 1998). The alkalosis associated with hypochloremia may also result in increased cellular uptake of potassium, leading to hypokalemia (Schaer 1999). 

The compensatory mechanisms for metabolic alkalosis include both respiratory compensation and, if physiologically possible, renal compensation. 

The compensatory mechanisms respond to respiratory alkalosis in two stages. In the first stage, erythrocyte and tissue buffers provide H ions that consume a small amount of HCOT The second stage becomes operational in prolonged respiratory alkalosis and depends on the renal compensation as described for metabolic alkalosis (decreased reclamation of bicarbonate). 

The respiratory response to metabolic alkalosis is hypoventilation, which resnlts in an increased PaC02. Respiratory compensation is initiated within honrs when the central and peripheral chemoreceptors sense an increase in pH. The PaC02 increases 6 to 7 mm Hg for each 10-mEq/L increase in bicarbonate, np to a PaC02 of abont 50 to 60 mm Hg (see Table 51M) before hypoxia sensors react to prevent fnrther hypoventilation. If the PaC02 is normal or less than normal, one shonld consider the presence of a snperimposed respiratory alkalosis, which may be secondary to fever, gram-negative sepsis, or pain. 

The decrease in bicarbonate concentration that usually compensates for respiratory alkalosis is prevented by the complicating metabolic alkalosis. Likewise, the increase in PaC02 expected to compensate for metabolic alkalosis is prevented by primary respiratory alkalosis. The failure of compensation that occurs with mixed respiratory and metabolic alkalosis may result in a severe alkalemia. 

In metabolic alkalosis, the [H-] is depressed and the [HCO3 ] is always raised. Respiratory compensation results In an elevated PCOj. 

Base excess is a calculated value representing the amount of buffering anions in the blood (primarily HCO3 but also hemoglobin, proteins, phosphates, and others). The normal range of base excess is 2 mEq/L. A negative base excess (-3 mEq/L or less) indicates a deficit of base and a metabolic acidosis (i.e., ketoacidosis or lactic acidosis). A positive base excess (3 mEq/L or more) indicates metabolic alkalosis (may be present in compensation for a respiratory acidosis). 4... 

Let us now consider what happens when the effect which was secondary in the primary respiratory disorder is instead the primary disorder. This would then be a primary metabolic alkalosis, as in the vomiting of gastric contents. In the uncompensated condition, there is a positive base excess with a normal partial pressure of carbon dioxide already noted (Table 4.4C). The respiratory compensation is hypoventilation, brought about by the partial withdrawal of the normal stimulus of hydrogen ions to the peripheral chemoreceptors. The partial pressure of carbon dioxide rises, adding a respiratory component to the acid-base disorder (Table 4.4D). 

C. Respiratory compensation in metabolic alkalosis involves a fall in arterial PcOj. 

Acid-base. So, despite an extracellular metabolic alkalosis, the urine is (acid, alkaline) and (free of, loaded with) HCOj. This (helps to compensate for, exacerbates) the metabolic alkalosis it is a (positive, negative) feedback system. 

Case 4, onset high pH, PCO2 normal, positive B.E., uncompensated metabolic alkalosis. Later PCO2 now high (hypoventilation), B.E. unaltered metabolic acidosis with respiratory compensation, no renal compensation. 

Mixed disorder of acid-base pbysioiogy This expression is used with two different meanings. Some authors use it to indicate the co-existence of two primary abnormalities, e.g. respiratory acidosis and metabolic acidosis. Others use it as a synonym for compensated , when a primary disorder is accompanied by a super-added physiological response, e.g. compensated respiratory acidosis, when the primary disorder is acidosis and the renal compensation adds a physiological metabolic alkalosis. 

The condition known as alkalosis occurs when the pH of blood rises above about 7.45. Respiratory alkalosis is caused by hyperventilation, or excessive respiration. The simplest remedy consists of breathing into a paper bag in order to incresise the levels of inhcded CO2. Metabolic alkalosis may result from illness, poisoning, repeated vomiting, md overuse of diuretics. The body may compensate for the incrccise in the pH of blood by decreasing the rate of respiration. 

Respiratory acidosis and alkalosis result from primary disturbances in the arterial carbon dioxide (C02) levels. Metabolic compensation of respiratory disturbances is a slow process, often requiring days for the serum HC03 to reach the steady state. 

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