Respiratory renal 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. 

Increased plasma Cl" concentration, Uke increased Na concentration, occurs with dehydration, RTA, acute renal failure, metabohc acidosis associated with prolonged diarrhea and loss of sodium bicarbonate, DI, states of adrenocortical hyperfimction, and overtreatment with saline solutions. A slight rise in Cl" concentration may also be seen in respiratory alkalosis due to the renal compensation of excreting... 

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). 

Metabolic compensation occurs when respiratory alkalosis persists for more than 6 to 12 hours. In response to the alkalemia, proximal tubular bicarbonate reabsorption is inhibited and the serum bicarbonate concentration falls. Renal compensation is usually complete within 1 to 2 days. The renal bicarbonaturia, as well as decreased NH4+ and titratable acid excretion, are direct effects of the reduced PaC02 and pH on renal reabsorption of chloride and bicarbonate. The... 

High therapeutic mild uncoupling of oxidative phosphorylation leads to T respiration ->4 pC02 > respiratory alkalosis — renal compensation — T HCO , elimination —> compensated respiratory alkalosis (pH — normal, -1 HCOj 4 pC02). 

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. 

The simple relationships of the bicarbrinatc buffer system are complicated by physiological mechanisms which have evolved to try to return a disordered [ 1 P to normal. Where lung function is compromised, the body attempts to increase the excretion of hydrogen ion via the renal route. This is known as renal compensation for the primary respiratory disorder. Renal compensation is slow to take effect. 

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). 

Respiratory alkalosis is much less common than acidosis but can occur when respiration is stimulated or is no longer subjcci to feedback control (Fig. 4). Usually these are acute conditions, and there is no renal compensation. The treatment is to inhibit or remove the cause of the hyperventilation, and the acid-base balance should return to normal. Examples are ... 

In contrast to respiratory compensation in metabolic disorders, the renal compensating mechanisms are much slower to take effect. 

High therapeutic mid uncoupling of oxidative phosphorylation —respiration —>4 PCO2 —> respiratory alkalosis —> renal compensation —HCOj" elimination —> compensated respiratory alkalosis (pH = normal, 4 HCO3U 4 PCO2)... 

Figure 3.1. Bicarbonate concentration as a function of PCO2. The normal blood line is shown and the oblique line representing a normal extracellular hydrogen ion concentration. Point N is a typical point representing normal acid-base status. Arrow NA indicates the change accompanying uncompensated respiratory acidosis and arrow AB indicates renal compensation.

Figure 3.2. The degrees of renal compensation of respiratory acidosis. In partial compensation the hydrogen ion concentration is partially restored towards normal, in complete compensation the hydrogen ion concentration is fully restored and in over-compensation, the renal retention of bicarbonate has more than compensated for the rise in PCO2.

This nomenclature is now applied to the sequence of events in hypoventilation. Within half an hour, the subject moves to a point which is described as acute or uncompensated respiratory acidosis . There is acidaemia. Over the course of the ensuing days, renal compensation occurs and the patient s blood is represented by a point which is described as compensated respiratory... 

Case 3, onset low pH, PCO2 normal, negative B.E., uncompensated metabolic acidosis. Later PCO2 now low (hyperventilation) negative B.E. but less negative than before metabolic acidosis with respiratory and renal compensation. 

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. 

If symptoms do not improve, the patient should be evaluated for persistent infection. There are many reasons for poor patient outcome with intraabdominal infection improper antimicrobial selection is only one. The patient maybe immunocompromised, which decreases the likelihood of successful outcome with any regimen. It is impossible for antimicrobials to compensate for a nonfunctioning immune system. There may be surgical reasons for poor patient outcome. Failure to identify all intraabdominal foci of infection or leaks from a GI anastomosis may cause continued intraabdominal infection. Even when intraabdominal infection is controlled, accompanying organ system failure, most often renal or respiratory, may lead to patient demise. 

Excess HCOf is managed to some extent by respiratory compensation (hypoventilation) but mainly by an increase in renal HCOf excretion. 

Q7 Yes. The renal and respiratory compensations can normally rectify the changes in pH and blood gases, unless there are also problems within the lung or heart which limit normal gas exchange and cardiac output. Many stroke patients unfortunately also have concomitant conditions such as heart failure, atherosclerosis or diabetes, since strokes are more common in the elderly population. 

If sites in the brain that control respiration are damaged, respiration and blood gas tensions will be disrupted. It is also possible that assisted ventilation is required by a stroke patient, and this can alter blood gas tensions temporarily. Renal and respiratory compensations rectify these changes during recovery. 

In acute exposure prompt medical attention is critical. The victim should be immediately removed to fresh air and away from the source of exposure. Oxygen should be provided if there is a respiratory distress. Initial therapy should be directed at stopping the ongoing hemolysis by performing exchange transfusion. Currently there is no other treatment to decrease arsine hemolysis however, studies in vitro have shown that some dithiol chelators (meso-2,3-dimercaptosuccinic acid, DMSA 2,3-dimercapto-l-propanesulfonic acid, DMPS and 2,3-butanedithiol) are effective (see Further Reading). This should be followed by aims to restore renal function or compensate for lost renal function (hemodialysis). This process does not remove any formed arsenic from the exposed body. Administration of dimercaprol (British Anti-Lewisite, BAL) has no effect on arsine hemolysis, but it lowers blood arsenic levels resulting from arsine exposure. The use of chelators must be... 

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. 

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. 

This mixed disorder is often seen in patients with advanced liver disease, salicylate intoxication, and pulmonary-renal syndromes. The respiratory alkalosis decreases the PaC02 beyond the appropriate range of the respiratory compensation for metabolic acidosis. The plasma bicarbonate concentration also falls below the level expected in compensation for a simple respiratory alkalosis. In a sense, the defense of pH for either disorder alone is enhanced thus the pH may be normal or close to normal, with a low PaC02 and a low [HCOj]. Treatment of this disorder should be directed at the underlying cause. Because of the enhanced compensation, the pH is usually closer to normal than in either of the two simple disorders. 

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