Respiratory 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... 

Metabolic acidosis and alkalosis result from primary disturbances in the serum H CO., concentration. Respiratory compensation of metabolic disturbances begins within minutes and is complete within 12 hours. 

Respiratory compensation If inappropriate, see Table 25-2. cMetabolic compensation If inappropriate, see Table 25-2. dPaC02 in millimeters of mercury. 

Changes that follow the primary disorder and attempt to restore the blood pH to normal are referred to as compensatory changes. It should be stressed that compensation never normalizes the pH. Because all metabolic acid-base disorders are chronic and the normal respiratory system can quickly alter the PaC02, essentially all metabolic disorders are accompanied by some degree of respiratory compensation.3 Similarly, chronic respiratory acid-base disorders are typically accompanied by attempts at metabolic compensation.4,5 However, with acute respiratory acid-base disorders there is insufficient time for the metabolic pathways to compensate significantly.6 As such, acute respiratory derangements are essentially uncompensated. 

The manifestations of acute severe metabolic acidemia (pH less than 7.15 to 7.20) involve the cardiovascular, respiratory, and central nervous systems. Hyperventilation is often the first sign of metabolic acidosis. Respiratory compensation may occur as Kussmaul s respirations (i.e., deep, rapid respirations characteristic of diabetic ketoacidosis). 

Excess acid is partially managed by respiratory compensation, by which increased depth and speed of expiration (hyperventilation) ofC02 helps expel some of the acid, in addition to increased H excretion In the urine. 

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

The answer is C. Ingestion of an acid or excess production by the body, such as in diabetic ketoacidosis, may induce metabolic acidosis, a condition in which both pH and HCOj become depressed. In response to this condition, the carbonic acid-bicarbonate system is capable of disposing of the excess acid in the form of CO2. The equilibrium between bicarbonate and carbonic acid shifts toward formation of carbonic acid, which is converted to COj and HjO in the RBC catalyzed by carbonic anhydrase, an enzyme found mainly in the RBC. The excess CO2 is then expired by the lungs as a result of respiratory compensation for the acidosis (Figure 1-2). The main role of the kidneys in managing acidosis is through excretion of H" rather than CO2. 

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. 

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. 

An 11-year-old boy with refractory partial epilepsy who had been taking topiramate 300 mg/day for 13 months developed hyperventilation. He had a hyperchloremic metabolic acidosis with partial respiratory compensation. The hyperventilation and acidosis resolved after the administration of sodium bicarbonate and reduction of the dose of topiramate. 

When any of these conditions exists, the ratio of cHCOp CCO2 is decreased because of the primary decrease in bicarbonate. The resulting drop in pH stimulates a respiratory compensation via hyperventilation, which lowers PCO2 and thereby raises the pH. 

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

Respiratory compensation after correction of metabolic acidosis Others... 

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. 

Respiratory compensation for a primary metabolic acidosis begins rapidly (within 15 to 30 minutes) but does not reach a steady state for 12 to 24 hours after the onset of metabolic acidosis. 

Severe metabolic acidosis is usually associated with acute processes. The manifestations of severe acidemia (pH <7.15 to 7.20) involve the cardiovascular, respiratory, and central nervous systems. Hyperventilation is often the first sign of metabolic acidosis. At a pH of 7.2, pulmonary ventilation increases about fourfold and an eightfold increase has been noted at a pH of 7. Respiratory compensation may occur as Kussmaul s respirations—the deep, rapid respirations seen commonly in patients with diabetic ketoacidosis. In extremely severe acidosis (pH <6.8), central nervous system (CNS) function is disrupted to such a degree that the respiratory center is depressed. 

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. 

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. 

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. 

Where there me metabolic disorders, some compensation is possible by the lungs. This is known as respiratory compensation for the primary metabolic disorder. Respiratory compensation is quick to take effect. 

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

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

Prolonged respiratory compensation for metabolic acidosis is more likely to result in respiratory compromise and eventual failure in an older patient than in a younger patient <3 ... 

Y. Bhambhani, R. Malik, and S. Mookerjee, Cerebral Oxygenation Declines at Exercise Intensities above the Respiratory Compensation Threshold, Respir. Physiol. Neurobiol., 156,196 (2007). 

Figure 3.4. The changes in blood chemistry occurring in metabolic acidosis. Arrow NA indicates the blood buffering of the acid load, arrow AB indicates the respiratory compensation for the acidaemia and arrow BC indicates the renal contribution to compensation, with retention of bicarbonate.

For metabolic acid-base disorders, the body has two lines of defence. The first is respiratory compensation. In the case of metabolic acidosis, the fall in pH... 

It takes up to a quarter of an hour for the hyperventilation to establish a new steady state, after which point B represents the acid-base status of the subject. The situation is shown in the column of Table 3.6 labelled respiratory compensation . The respiratory compensation thus merges in time with the blood buffering. Access of the acid load to intracellular buffers takes minutes, during which time CO2 is being washed out of the body. The contribution of bone to buffering is insignificant within the time span of respiratory compensation arriving at its steady state. 

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. 

Respiratory compensation results in a change in [H ] (back towards, further away from) normal and a change in [HC03 ] (back towards, further away from) normal. It is represented by arrow. .. At this stage the PcOj is... 

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