Hypercapnia chronic

In advanced COPD, caution should be used since overly aggressive administration of oxygen to patients with chronic hypercapnia may result in respiratory depression and respiratory failure. In these patients, mild hypoxemia, rather than carbon dioxide accumulation, triggers their drive to breathe. 

The goals of therapy in patients with chronic respiratory acidosis are to maintain oxygenation and to improve alveolar ventilation if possible. Because of the presence of renal compensation it is usually not necessary to treat the pH, even in patients with severe hypercapnia. Although the specific treatment varies with the underlying disease, excessive oxygen and sedatives should be avoided, as they can worsen C02 retention. 

Polak A, Haynie GD, Hays RM, Schwartz WB. Effects of chronic hypercapnia on electrolyte and acid-base equilibrium. J Clin Invest 1961 40 1223-1237. 

Patients with chronic pulmonary disorders may exhibit lethargy, confusion, memory loss and stupor. The combined insults of hypoxia and hypercapnia, which result in C02 retention, contribute to the encephalopathy but neurological symptoms correlate best with the degree of C02 retention. Acute moderate hypercapnia associated with 5-10% C02 in the expired air, leads to arousal and excitability whereas higher C02 concentrations, >35% in the expired air, are anesthetic. 

Significant changes in arterial blood gases are not usually present until the FEV is less than 1 L. At this stage, hypoxemia and hypercapnia may become chronic problems. Hypoxemia usually occurs initially with exercise but develops at rest as the disease progresses. 

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. 

Epidural/Intrathecal administration Limit epidural or intrathecal administration of preservative-free morphine and sufentanil to the lumbar area. Intrathecal use has been associated with a higher incidence of respiratory depression than epidural use. Asthma and other respiratory conditions The use of bisulfites is contraindicated in asthmatic patients. Bisulfites and morphine may potentiate each other, preventing use by causing severe adverse reactions. Use with extreme caution in patients having an acute asthmatic attack, bronchial asthma, chronic obstructive pulmonary disease or cor pulmonale, a substantially decreased respiratory reserve, and preexisting respiratory depression, hypoxia, or hypercapnia. Even usual therapeutic doses of narcotics may decrease respiratory drive while simultaneously increasing airway resistance to the point of apnea. Reserve use for those whose conditions require endotracheal intubation and respiratory support or control of ventilation. In these patients, consider alternative nonopioid analgesics, and employ only under careful medical supervision at the lowest effective dose. 

Administration of oxygen-rich gas mixtures is useful in hypoxia, but 100% 02 is not often used. In chronic bronchitis, hypoxia and hypercapnia coexist, the respiratory centre in the medulla becomes tolerant to the high C02 content of blood and is relatively insensitive to it. Respiratory drive is maintained by hypoxia acting via chemoreceptors in the aorta and carotid body. Removal of the hypoxic stimulus to the respiratory centre in the medulla may actually stop the patient breathing. 

There has been one case report of reduced ventilatory response to hypercapnia after nortriptyline in a woman with chronic obstructive pulmonary disease (SEDA-18,19). 

If pafienf has severe chronic hypercapnia, myasfhenia gravis, severe respiratory insufficiency, sleep apnea, or severe hepafic insufficiency... 

Chronic bronchitis is a persistent inflammation of the bronchi because of excess mucous production that irritates the bronchial and results in a persistent productive cough. Smoking is a common cause of chronic bronchitis and is aggravated by air pollution, infection, and allergies. Patients with chronic bronchitis have rhonchi (a gurgling sound) on inspiration and expiration, caused by airway blockage from excess mucus. This excess results in hypercapnia (buildup of carbon dioxide in the blood) and hypoxemia (decreased oxygen in the blood). The patient experiences respiratory acidosis. 

Henderson-Hasselbalch equation, Chapter 1). It may result from central depression of respiration (e.g., narcotic or barbiturate overdose, trauma, infection, cerebrovascular accident) or from pulmonary disease (e.g., asthma, obstructive lung disease, infection). Increased [H+] is in part buffered by cellular uptake of H+ with corresponding loss of intracellular K" ". In acute hypercapnia, the primary compensatory mechanism is tissue buffering. In chronic hypercapnia, the kidneys respond to elevated plasma Pcoj increasing the amount of HCO formed by carbonic an-hydrase in the tubules and by excreting more H+. 

Respiratory acidosis may produce neuromuscular symptoms, including altered mental status, abnormal behavior, seizures, stupor, and coma. Hypercapnia may mimic stroke or CNS tumors by producing headache, papilledema, focal paresis, and abnormal reflexes. Carbon dioxide acts as a vasodilator in the brain, thus causing an increase in cerebral blood flow. This increase in cerebral blood flow is thought to be partially responsible for the CNS symptoms. The CNS response to hypercapnia is extremely variable between patients and is also influenced by the acuity of presentation. Chronic hypercapnia blunts the usual respiratory stimulus resulting from increased PaC02. In patients with severe chronic respiratory acidosis, hypoxemia rather than hypercapnia provides the primary ventilatory stimulus. ... 

Doxapram (0.5 to 1 mg/kg) is used as a postanesthesia respiratory stimulation, in drug-induced CNS depression, and in acute hypercapnia associated with chronic obstructive pulmonary disease. 

In chronic hypercapnia, the full compensatory mechanism is placed in gear. The central events are increased acid secretion by the kidney (ammonium plus titrable acid) and increased reabsorption of bicarbonate (HCO3). Indeed, the maximum renal reabsorption of bicarbonate rises with the increase in Pco2 levels in blood. 

Oxycodone should be used with caution in patients with significant chronic obstructive pulmonary disease or cor pulmonale, and in patients having decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression. In such patients, even usual therapeutic doses may decrease respiratory drive to the point of apnea. 

Serious adverse events respiratory depression, similar to other potent injectable opioids particularly in elderly or debilitated patients. Predisposing conditions include hypoxia, hypercapnia, or decreased respiratory reserve such as asthma, chronic obstructive pulmonary disease or cor pulmonale, severe obesity, sleep apnea syndrome, myxedema, kyphoscoliosis, central nervous system (CNS) depression, or coma. 

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). 

Table 2 Causes of Chronic Hypoxemia with Hypercapnia...

Begin P, Grassino A. Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. Am Rev Respir Dis 1991 143 905-912. 

Gay PC, Edmonds LC. Severe hypercapnia after low-flow oxygen therapy in patients with neuromuscular disease and diaphragmatic dysfunction. Mayo Clin Proc 1995 70 327-330. Mannino D. Chronic obstructive pulmonary disease in 2025 where are we headed Eur Respir J 2005 26 189. 

---