In hypercapnia

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. 

Poon, C.-S. 1987b. Ventilatory control in hypercapnia and exercise optimization hypothesis. J. Appl. 

In other words, the hydrogen ion concentration is proportional to the ratio of the amount of COj to bicarbonate concentration in the blood. Hence, in hypercapnia (high blood COj concentration) such as in respiratory acidosis, the ratio of pC02 to HCOj" is abnormally high, therefore the [H is high (i.e. pH is low). 

Primary disorder lung disease causes Impaired ventilation or gas diffusion resulting in hypercapnia (increased arterial PCO2). Alternatively, non-pulmonary hypercapnia is caused by failure of the CNS respiratory centre to stimulate the respiratory muscles, see below... 

PhiUis JW, O Regan MH, Song D. Further evidence for the role of adenosine in hypercapnia/acidosis-evoked coronary flow regulation. Gen Pharmacol 1999 33 431-7. 

Bianchi AL, St John WM. Changes in antidromic latencies of medullary respiratory neurons in hypercapnia and hypoxia. J Appl Physiol 1985 59 1208-1213. 

The efficacy of end-tidal CO2 and transcutaneous CO2 measurements are extremely close for older children and adults. With currently available sensors, the latter has been shown to correlate extremely well with Pac02. Although both can be accurate in assessing stable Paco2 during mechanical ventilation, both can underestimate increases in hypercapnia and can be an optimal evaluation for therapy (19,43,44). 

In advanced COPD, airflow obstruction, damaged bronchioles and alveoli, and pulmonary vascular abnormalities lead to impaired gas exchange. This results in hypoxemia and eventually hypercapnia. Hypoxemia is initially present only during exercise but occurs at rest as the disease progresses. Inequality in the ventilation/perfusion ratio (VAQ) is the major mechanism behind hypoxemia in COPD. 

The goal of oxygen therapy is to maintain Pao2 above 60 mm Hg (8 kPa) or Sao2 above 90% in order to prevent tissue hypoxia and preserve cellular oxygenation.1 Increasing the Pao2 much further confers little added benefit and may increase the risk of C02 retention, which may lead to respiratory acidosis. An arterial blood gas should be obtained after 1 to 2 hours to assess for hypercapnia. 

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. 

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. 

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. 

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. 

Hypercapnia Abnormally high concentration of carbon dioxide in the blood. 

Chemoreceptors. The peripheral chemoreceptors include the carotid bodies, located at the bifurcation of the common carotid arteries, and the aortic bodies, located in the aortic arch. These receptors are stimulated by a decrease in arterial oxygen (hypoxia), an increase in arterial carbon dioxide (hypercapnia),... 

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. 

Although C02 is a normal metabolite, it is toxic at elevated levels. C02 exists in equilibrium with carbonic acid (H2C03) and with bicarbonate (HCO, ), a major H+ buffer. Renal conservation of HCO, is generally sufficient to buffer hypercapnia however, an added insult, such as... 

The combination of hypoxia and hypercapnia in pulmonary insufficiency results in cerebral vasodilation and increased CBF and may lead to increased intracranial pressure. Arteriovenous differences for oxygen across the brain generally decrease as a function of increased CBF, leaving CMR02 unchanged [6]. 

Neuromuscular symptoms include altered mental status, abnormal behavior, seizures, stupor, and coma. Hypercapnia can mimic a stroke or CNS tumor by producing headache, papilledema, focal paresis, and abnormal reflexes. CNS symptoms are caused by increased cerebral blood flow and are variable, depending in part on the acuity of onset. 

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. 

The most common cause of acute respiratory failure in COPD is acute exacerbation of bronchitis with an increase in sputum volume and viscosity. This serves to worsen obstruction and further impair alveolar ventilation, resulting in worsening hypoxemia and hypercapnia. Additional causes are pneumonia, pulmonary embolism, left ventricular failure, pneumothorax, and CNS depressants. 

The hemolytic anemia caused in pregnant rabbits by diflunisal was severe enough to explain the concomitant axial skeletal malformations (Clark et ah, 1984). Acetazolamide-induced fetal malformations in mice are apparently related to maternal hypercapnia (Weaver and Scott, 1984a, b) and hypokalemia (Ellison and Maren, 1972). The increased resorption rate induced in rabbits by the antibiotic norfloxacin depends on exposure of the maternal gastrointestinal tract (Clark et ah,... 

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. 

Acute abdominal conditions Narcotics may obscure diagnosis or clinical course. Do not give SR morphine to patients with Gl obstruction, particularly paralytic ileus, as there is a risk of the product remaining in the stomach for an extended period and the subsequent release of a bolus of morphine when normal gut motility is restored. Special risk patients Exercise caution in elderly and debilitated patients and in those suffering from conditions accompanied by hypoxia or hypercapnia when even moderate therapeutic doses may dangerously decrease pulmonary ventilation. Also exercise caution in patients sensitive to CNS depressants, including those with cardiovascular disease myxedema convulsive disorders increased ocular pressure acute alcoholism delirium tremens cerebral arteriosclerosis ulcerative... 

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