Respiratory acidosis, hypoventilation

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... 

Hypoventilation is the opposite of hyperventilation and is eharaeterized by an inability to exerete CO9 rapidly enough to meet physioiogieai needs. Hypoventilation ean be eaused by nar-eoties, sedatives, anestheties, and depressant drugs diseases of the lung also lead to hypoventilation. Hypoventilation results in respiratory acidosis, as C09(g) aeeumulates, giving rise to H9CO3, whieh dissoeiates to form H and HCOa. ... 

In order to effectively treat respiratory acidosis, the causative process must be identified and treated. If a cause is identified, specific therapy should be started. This may include naloxone for opiate-induced hypoventilation or bronchodilator therapy for acute bronchospasm. Because respiratory acidosis represents ventilatory failure, an increase in... 

Hypoventilation causes retention of C02 by the lungs, which can lead to a respiratory acidosis. Hyperventilation can cause a respiratory alkalosis. Metabolic acidosis can result from accumulation of metabolic acids (lactic acid or the ketone bodies p-hydroxybutyric acid and acetoacetic acid), or ingestion of acids or compounds that are metabolized to acids (methanol, ethylene glycol). Metabolic alkalosis is due to increased HC03, which is accompanied by an increased pH. Acid-base disturbances lead to compensatory responses that attempt to restore normal pH. For example, a metabolic acidosis causes hyperventilation and the release of C02, which tends to lower the pH. During metabolic acidosis, the kidneys excrete NH4+, which contains H+ buffered by ammonia. 

Respiratory distress syndrome is caused by lack of surfactant (Fig. 2) and results from failure of alveolar expansion and subsequent alveolar collapse, decreased compliance and venlilation/perfusion abnormalities. Hypoventilation produces a respiratory acidosis, and hypoxaemia leads to a metabolic acidosis. The more immature the baby, the greater is the risk of respiratory distress syndrome. 

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. 

In a small number of patients whose respiratory center is depressed by long-term retention of carbon dioxide, injury, or drugs, ventilation is maintained largely by stimulation of carotid and aortic chemoreceptors, commonly referred to as the hypoxic drive. The provision of too much oxygen can depress this drive, resulting in respiratory acidosis. In these cases, supplemental oxygen should be titrated carefully to ensure adequate arterial saturation. If hypoventilation results, then mechanical ventilatory support with or without tracheal intubation should be provided. 

Respiratory acidosis is sometimes the resnlt of slow or shallow breathing (hypoventilation) caused by an overdose of narcotics or barbiturates. Anesthetists need to be particularly aware of respiratory acidosis, because most inhaled anesthetics depress respiration rates. Lung diseases, such as emphysema and pneumonia, or an object lodged in the windpipe can also result in hypoventilation. In respiratory acidosis, too little carbon dioxide is exhaled, and its concentration within the blood increases. The carbon dioxide/carbonic acid equilibrinm shifts to the left to restore the equilibrium ... 

Respiratory acidosis results when the level of CO in the blood is increased owing to hypoventilation. Slow or shallow breathing decreases the exchange of CO in the lungs and removal of this waste product from the blood. As a prime component of carbonic acid, increased CO causes a shift to the left with higher acid formation and less dissociation of the acid into component parts. 

The renal mechanisms come into play immediately the disturbance of acid-base physiology starts. However, it takes a relatively long period for the renal mechanisms to come to maximum efficiency and for the renal retention of bicarbonate to build up the concentration throughout the body. In respiratory acidosis, it takes around three days for the subject to settle to the compensated point. This is where the subject then stays so long as the same degree of hypoventilation persists. 

Figure 3.3. This shows the information of Figure 3.1 together with the new blood line of a subject who has completely compensated for the respiratory acidosis. Arrow BC indicates the change in blood chemistry if hypoventilation is suddenly corrected and the respiratory system is able to excrete the previously-accumulated COj.

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... 

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. 

The respiratory system is responsible for generating and regulating the transpulmonary pressures needed to inflate and deflate the lung. Normal gas exchange between the lung and blood requires breathing patterns that ensure appropriate alveolar ventilation. Ventilatory disorders that alter alveolar ventilation are defined as hypoventilation or hyperventilation syndromes. Hyperventilation results in an increase in the partial pressure of arterial CO2 above normal limits and can lead to acidosis, pulmonary hypertension, congestive heart failure, headache, and disturbed sleep. Hypoventilation results in a decrease in the partial pressure of arterial CO2 below normal limits and can lead to alkalosis, syncope, epileptic attacks, reduced cardiac output, and muscle weakness. 

Acidosis CO2 f pH F Hypoventilation, blockage of diffusion within lungs, respiratory center depressants... 

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. 

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