Uncompensated respiratory

If acute respiratory distress develops (e.g., due to pneumonia or a COPD exacerbation) the PaC02 may rise sharply resulting in an uncompensated respiratory acidosis. 

F-xamples of acute, and hence uncompensated, respiratory acidosis are ... 

The phase of primary respiratory alkalosis rarely is recognized in children with salicylate toxicity. They usually present in a state of mixed respiratory and renal acidosis, characterized by a decrease in blood pH, a low plasma bicarbonate concentration, and normal or nearly normal plasma PCO2. Direct salicylate-induced depression of respiration prevents adequate respiratory hyperventilation to match the increased peripheral production of CO2- Consequently, plasma PCO2 increases and blood pH decreases. Because the concentration of bicarbonate in plasma already is low due to increased renal bicarbonate excretion, the acid-base status at this stage essentially is an uncompensated respiratory acidosis. Superimposed, however, is a true metabolic acidosis caused by accumulation of acids as a result of three processes. First, toxic concentrations of salicylates displace 2-3 mEq/L of plasma bicarbonate. Second, vasomotor depression caused by toxic doses of salicylates impairs renal function, with consequent accumulation of sulfuric and phosphoric acids. Third, salicylates in toxic doses may decrease aerobic metabolism as a result of inhibition of various enzymes. This derangement of carbohydrate metabolism leads to the accumulation of organic acids, especially pyruvic, lactic, and acetoacetic acids. 

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.

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... 

Respiratory acidosis Hypoventilation of acute onset results in a change of blood biochemistry (along the normal, to a different) blood line, as shown by arrow. .. In the resultant uncompensated respiratory acidosis the alveolar PCO2 is... 

C. Blood from a patient with an uncompensated respiratory alkalosis would yield a point lying on the normal blood line . 

A. Yes. At the uncompensated stage, a move along the blood line to the right unambiguously indicates a primary uncompensated respiratory acidosis. 

Case 1, onset high PcOj, B.E. zero, uncompensated respiratory acidosis. Later, PCO2 still high, B.E. positive compensated respiratory acidosis. 

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. 

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. 

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.)...

High pH, normal [HC03-], and low pC02 are consistent with uncompensated (pure) respiratory alkalosis (see Figure 3.3). 

Lactic acidosis, respiratory dysfunction, uncompensated metabolic alkalosis, hypocalcemia, hypokalemia, hypercapnia... 

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. 

When fixed acid accumulates in the body because of diabetes, the accumulation is in many cases very slow, over the course of days, weeks or months. Compensatory mechanisms are called up as the accumulation proceeds. So it is uncommon to meet patients with the sudden uncompensated condition as is sometimes the case with respiratory disorders. However, to understand the different components of a metabolic disorder, it is instructive to follow the sequence of events in the artificial situation of a rapid injection of fixed acid, for instance of hydrochloric acid intravenously, into an anaesthetized animal. Such a situation has occurred in a human when, by tragic accident, a strong acid has been infused and even then, the phases of the responses of the body run into each other. It will nevertheless be easier if we consider the phases as if they occurred separately. 

The need for a better measure of the metabolic component of an acid-base disorder. At first sight, w e might think that the deviation of the standard bicarbonate from the value for normal blood is all the information that we need about the non-respiratory component of an acid- base disorder. However, the change in standard bicarbonate underestimates the non-respiratory component of the acid base disorder. To illustrate this, consider uncompensated metabolic alkalosis, produced by the addition of alkali, such as sodium hydroxide, to the blood. Each of the buffer acids in the blood (protein buffer acid and CO2) buffers some of the added alkali as shown in the two chemical reactions in Table 4.2A. Protein buffer acid combines with some of the alkali to yield water and protein buffer base CO2 from metabolism combines with most of the rest of the alkali to yield bicarbonate. The result is an increase in concentration both of non-bicarbonate buffer base Pr and of bicarbonate. 

In the initial stages of a disturbance of acid-base physiology, the condition is uncompensated, which essentially means that chemical buffering alone is operating. At this stage therefore, there is only one component to the disorder. This component is respiratory in respiratory disorders and metabolic in metabolic disorders. In the respiratory disorder the subject moves along the normal blood line. The partial pressure of carbon dioxide is abnormal but the base excess, the measure of metabolic component, is zero. This is shown in Table 4.4A. For an uncompensated metabolic disorder (Table 4.4C), it is the... 

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). 

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. 

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. 

On the graph of PCO2 [HCO3 ], indicate the immediate effects of hypoventilation and hyperventilation and deduce the effects on [HC03 ] and [H" ]. Also on the graph, indicate and explain the delayed effects, mediated by the kidney, occurring if the primary respiratory disorder persists. Hence define uncompensated and compensated respiratory acidosis and alkalosis. 

A condition in which there is loss of base or accumulation of acid capable of causing a fall in pH to below nornial limits (an uncompensated acidosis). If this has been corrected by compensatory mechanisms (see below) it is known as a compensated acidosis. Acidosis can be classified into either a primary metabolic or respiratory disorder, although occasionally mixed types may occur. 

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