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Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction ...
Dr. R. W. Winters conducted an experiment in the 1960s on 60 patients with varying degrees of metabolic acidosis. He aimed to empirically determine a mathematical expression representing the effect of respiratory compensation during metabolic acidosis. He measured the blood pH, plasma PCO2, blood base excess, and plasma bicarbonate concentrations.
Since carbon dioxide is in equilibrium with carbonic acid in the blood, hypercapnia drives serum pH down, resulting in respiratory acidosis. Clinically, the effect of hypercapnia on pH is estimated using the ratio of the arterial pressure of carbon dioxide to the concentration of bicarbonate ion, P a C O 2 / H C O 3 − {\displaystyle {P_{a_{CO ...
As indicated by the Davenport diagram, respiratory depression, which results in a high P CO 2, will lower blood pH. Hyperventilation will have the opposite effects. A decrease in blood pH due to respiratory depression is called respiratory acidosis. An increase in blood pH due to hyperventilation is called respiratory alkalosis (Fig. 11).
The amount of respiratory compensation in metabolic acidosis can be estimated using Winters' formula. [2] Hyperventilation due to the compensation for metabolic acidosis persists for 24 to 48 hours after correction of the acidosis, and can lead to respiratory alkalosis. [3] This compensation process can occur within minutes. [4]
Respiratory failure is classified as either Type 1 or Type 2, based on whether there is a high carbon dioxide level, and can be acute or chronic. In clinical trials, the definition of respiratory failure usually includes increased respiratory rate, abnormal blood gases (hypoxemia, hypercapnia, or both), and evidence of increased work of breathing.
It is a good indicator of respiratory function and the closely related factor of acid–base homeostasis, reflecting the amount of acid in the blood (without lactic acid). Normal values for humans are in the range 35–45 mmHg. Values less than this may indicate hyperventilation and (if blood pH is greater than 7.45) respiratory alkalosis.
The partial pressure of carbon dioxide, along with the pH, can be used to differentiate between metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. Hypoventilation exists when the ratio of carbon dioxide production to alveolar ventilation increases above normal values – greater than 45mmHg.