Central hypoxemia

Respiratory acidosis is characterized by a reduced arterial pH, a primary increase in the arterial PaC02 and, when present for sufficient time, a compensatory rise in the HCOf concentration. Because increased C02 is a potent respiratory stimulus, respiratory acidosis represents ventilatory failure or impaired central control of ventilation as opposed to an increase in C02 production. As such, most patients will have hypoxemia in addition to hypercapnia. The most common etiologies of respiratory acidosis are listed in Table 25-6. 

Chemoreceptor response to decreased arterial P02. Hypoxia has a direct depressant effect on central chemoreceptors as well as on the medullary respiratory center. In fact, hypoxia tends to inhibit activity in all regions of the brain. Therefore, the ventilatory response to hypoxemia is elicited only by the peripheral chemoreceptors. 

Some patients lose the ability to increase the rate or depth or respiration in response to persistent hypoxemia. This decreased ventilatory drive may be due to abnormal peripheral or central respiratory receptor responses. This relative hypoventilation leads to hypercapnia in this situation the central respiratory response to a chronically increased PaC02 can be blunted. Because these changes in Pa02 and PaC02 are subtle and progress over many years, the pH is usually near normal because the kidneys compensate by retaining bicarbonate. 

Lee, K.-N., Lee, H.-J., Shin, W.W., Webb, W.R. Hypoxemia and hver cirrhosis (hepatopulmonary syndrome) in eight patients comparison of the central and peripheral pulmonary vasculature. Radiology 1999 211 549-553... 

The time of death after a single acute exposure may range from <5 minutes to nearly 24 hours, depending on the dose, route, agent, and other factors. The cause of death primarily is respiratory failure, usually accompanied by a secondary cardiovascular component. Peripheral muscarinic and nicotinic as well as central actions all contribute to respiratory compromise effects include laryngospasm, bronchoconstriction, increased tracheobronchial and salivary secretions, compromised voluntary control of the diaphragm and intercostal muscles, and central respiratory depression. Blood pressure may fall to alarmingly low levels and cardiac arrhythmias intervene. These effects usually result from hypoxemia and often are reversed by assisted pulmonary ventilation. 

Of six patients with central sleep apnea, who were receiving opioids (morphine equivalent doses of 120 20 mg/day) for chronic pain, four achieved symptomatic improvement when treated with bi-level ventilation, correcting nocturnal hypoxemia and reducing sleep fragmentation P ]. 

Numerous physiological and clinical conditions are associated with hypoxemia, ranging from acute episodes of hypoxia (asthma) to chronic sustained hypoxia (ascent to high altitude, COPD) or chronic intermittent hypoxia (OSA). During these episodes of hypoxia, activation of both peripheral and central sites likely occurs, with the net response refiecting a coordination of these drives by the pattern-generating network. 

Respiratory failure may be classified as hypoxemic (type 1) or hypercapnic (type II or ventilatory failure) (3), either of which may be acute and chronic. Hypoxemic respiratory failure is due to failure of the lungs, caused by acute (cardiogenic pulmonary edema, pneumonia, acute respiratory distress syndrome) or chronic (emphysema, interstitial limg disorders) diseases (Tables 1 and 2). It is characterized by hypoxemia with normocapnia or hypocapnia. In these conditions central respiratory drive is high and there is sufficient alveolar ventilation (VA) to eliminate CO2 and prevent hypercapnia. 

Hypercapnic respiratory failure is due to failure of the ventilatory pump caused by acute (drug overdose, acute neuromuscular diseases) or chronic (chest wall abnormalities, chronic neuromuscular diseases) disorders. It is characterized by alveolar hypoventilation, which leads to hypercapnia with coexistent, usually mild, hypoxemia. The central drive may be globally reduced with the fall in Pa02 resulting from the increase in alveolar CO2. More commonly, the drive remains high, but the mechanical load on the respiratory systan is too great or the capacity of the muscles too low to ensure efficient CO2 elimination (Fig. 1). 

Children with achondroplasia often have sleep-related respiratory disturbances, primarily hypoxemia (8). A substantial minority of them have obstructive or central apnea,... 

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