Respiratory acidosis compensation

Administer through a central line at <0.2 mEq/kg/h Decrease infusion rate in the presence of respiratory compensation to avoid respiratory acidosis ° Discontinue infusion when the arterial pH reaches 7.5... 

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. 

Respiratory acidosis is caused by respiratory insufficiency resulting in an increased arterial C02 concentration. The compensation for respiratory acidosis (if present for prolonged periods) is an increase in serum HC03 . 

It is critical to differentiate acute and chronic respiratory acidosis, as the acute form is often a medical emergency that requires intubation and mechanical ventilation, whereas the chronic form is typically a stable condition. The blood gases in Case Study 2 came from a patient with advanced emphysema who is a "C02 retainer" due to ineffective ventilation. Because this patient s disease is chronic, the elevated PaC02 developed very slowly and allowed for metabolic compensation. 

The goals of therapy in patients with chronic respiratory acidosis are to maintain oxygenation and to improve alveolar ventilation if possible. Because of the presence of renal compensation it is usually not necessary to treat the pH, even in patients with severe hypercapnia. Although the specific treatment varies with the underlying disease, excessive oxygen and sedatives should be avoided, as they can worsen C02 retention. 

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. 

ABC Line AB represents a respiratory acidosis as the Paco2 has risen from 5.3 to 8kPa. Compensation is shown by line BC, which demonstrates retention of HC03. The rise in HC03 from 28 to 38mmol.l 1 (y axis) returns the pH to the normal range. 

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. 

What is the base excess in meq/L in a patient with fully compensated respiratory acidosis having an initial pH of 7.2 and [HC03 ] = 28 meq/L ... 

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). 

Compensation for respiratory acidosis occurs immediately via buffers and with time via the kidneys and, if possible, the lungs. 

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. 

The answer is e. (Murray, pp 298-307. Scriver, pp 1471-1488. Sack, pp 217-218. Wilson, pp 361-384.) In the presence of insulin deficiency, a shift to fatty acid oxidation produces the ketones such as acetoacetate that cause metabolic acidosis. The pH and bicarbonate are low, and there is frequently some respiratory compensation (hyperventilation with deep breaths) to lower the PCO2, as in choice e. A low pH with high PCO2 would represent respiratory acidosis (choices a and b—the low-normal bicarbonate values in these choices indicate partial compensation). Choice d represents respiratory alkalosis as would occur with anxious hyperventilation (high pH and low Peep, partial compensation with high bicarbonate). Choice c illustrates normal values. 

As with the metabolic acid-base disturbances, there are two cardinal respiratory acid-base disturbances respiratory acidosis and respiratory alkalosis. These disorders are generated by a primary alteration in carbon dioxide excretion, which changes the concentration of carbon dioxide, and therefore the carbonic acid concentration in body fluids. A primary reduction in PaC02 causes a rise in pH (respiratory alkalosis), and a primary increase in PaC02 causes a decrease in pH (respiratory acidosis). Unlike the metabolic disturbances, for which respiratory compensation is rapid, metabolic compensation for the respiratory disturbances is slow. Hence these disturbances can be further divided into acute disorders, with a duration of minutes to hours that is too short for metabolic compensation to have occurred, and chronic disorders, that have been present long enough for metabolic compensation to be complete. 

ACUTE RESPIRATORY ACIDOSIS IN A COMPENSATED CHRONIC RESPIRATORY ACIDOTIC PATIENT... 

In mixed respiratory and metabolic acidosis, there is a failure of compensation. The respiratory disorder prevents the compensatory decrease in PaC02 expected in the defense against metabolic acidosis. The metabolic disorder prevents the buffering and renal mechanisms from raising the bicarbonate concentration as expected in the defense against respiratory acidosis. In the absence of compensatory mechanisms, the pH decreases markedly. 

The high [H ] and PCO confirm the presence of a respiratory acidosis which, from the history, will have been expected. Note that the bicarbonate is not abnormally increased, which indicates that this is an acute development, and renal compensation for the respiratory acidosis has not had time to have a significant impact on the respiratory acidosis. 

Respiratory acidosis may be acute or chronic. Acute conditions occur within minutes or htnirs. They are uncompensated. Renal compensation has no time to develop as the mechanisms which adjust bicarbonate reabsorption take 48-72 h to become fully effective. The primary problem in acute respiratory acidosis is alveohir hypoventilation. If airflow is completely or partially reduced, the PCO, in the bltHtd will rise immediately and the H ) will rise quickly (Fig. 2). A resulting low PO, and high PCO. causes coma. If this is not reliev ed rapidly, death results. 

Chronic respiratory acidosis is usually a long-standing condition, and isaccompanied by maximal renal compensation. In a chronic respiratory acidosis the primary problem again is usually impaired alveolar ventilation, but renal compensation contributes markedly to the acid-base picture. Compensation may be partial or complete. The kidney increases hydrogen ion excretion and ECF bicarbonate levels rise. BUwtd [ll tends back towards normal (Fig., 1). 

In respiratory acidosis the blood [H ] is usually high, but may be within the reference range. The PCO, is always raised. In compensated conditions, [HCO5 ] Is also raised. 

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... 

The determination of respiratory acidosis is made when on blood-gas analysis the pH is lower than 7.35 and the Pco is above 45 mm Hg. The CO may be increased in an attempt to balance an alkiotic situation, but the pH, which governs overall state, will indicate the overall state of alkalosis or a normal range if fiilly compensated. 

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