Compensatory mechanism respiratory

Hypercapnia (abnormally high concentration of carbon dioxide in the blood) can develop as a result of overfeeding with both dextrose and total calories.1,37 Excess carbon dioxide production and retention can lead to acute respiratory acidosis. The excess carbon dioxide also will stimulate compensatory mechanisms, resulting in an increase in respiratory rate in order to eliminate the excess carbon dioxide via the lungs. This increase in respiratory workload can cause respiratory insufficiency that may require mechanical ventilation. Reducing total calorie and dextrose intake would result in resolution of hypercapnia if due to overfeeding. 

The primary compensatory mechanism is to decrease PaCC>2 by increasing the respiratory rate. 

Arterial blood gases are the primary tools for evaluation of therapeutic outcome. They should be monitored closely to ensure resolution of simple acid-base disorders without deterioration to mixed disorders due to compensatory mechanisms. For example, arterial blood gases should be obtained every 2 to 4 hours during the acute phase of respiratory acidosis and then every 12 to 24 hours as acidosis improves. 

The buffer systems of the blood (mainly the bicarbonate/ carbonic acid buffer) minimize changes in pH. In acidoses, the bicarbonate concentration decreases to give a ratio of cHC03/cdC02 of <20 1. The respiratory compensatory mechanism responds to correct the ratio with increased rate and depth of respiration to eliminate CO2. Table 46-3 depicts expected compensation in both acidoses and alkaloses and corresponding laboratory values. 

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). 

FIGURE 24-2. Activation of compensatory mechanisms with loss of circulatory volume. Certain stages may be absent depending on a number of factors, such as age, preexisting disease states, and cause of circulatory Insufficiency. BP = blood pressure CO = cardiac output HR = heart rate PVR = peripheral vascular resistance RR = respiratory rate. 

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. 

Insults (due to drugs, biologies, or toxins) can cause detectable changes in function through multiple mechanisms depending on the namre of the insult, timing, route of dehvery (air or blood), duration of insult, and the initial respiratoiy health of the animal. The manifestation of the dysfunction will depend on which components of the respiratory system are affected and the compensatory mechanisms initiated. The pattern of dysfunction detected may reflect the primary response or may reflect the compensatory changes to the primary response. 

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. 

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. 

As a whole, the data described above reveal that gastrocnemius mitochondria from old rats, in order to produce a similar amormt of ATP, need to oxidize a smaller amount of substrate than those from yormg rats. In addition, in ageing skeletal muscle mitochondria actuate compensatory mechanisms (super-assembly of complexes and reduced proton leak) that render them more efficient despite lower levels and/or activities of respiratory complexes, thus allowing a metabolic shift toward oxidative metabohsm that is coordinated with the structural shift. 

The underlying principle assumed to govern respiratory response is the tendency of the body to induce compensatory activity to neutralize or diminish the influence of any disturbance. This principle is implemented by feedback mechanisms where the controlled variables are kept within narrow ranges of certain set points (or reference) values (see... 

Maintain an open ainway and assist ventilation if necessary (see pp 1-7). Warning Ensure adequate ventilation to prevent respiratory acidosis, and do not allow controlled mechanical ventilation to interfere with the patienf s need for compensatory efforts to maintain the semm pH. Administer supplemental oxygen. Obtain serial arterial blood gases and chest x-rays to obsenre for pulmonary edema (more common with chronic or severe intoxication). 

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