Respiratory acidosis causes

It might be acceptable to administer sodium bicarbonate to improve plasma pH based on anecdotal evidence, if it caused no harmful effects. Unfortunately this is not the case. The production of carbon dioxide and accompanying respiratory acidosis causes a more profoimd depression in... 

Respiratory acidosis results when decreased respiration raises the concentration of C02 in the blood. Asthma, pneumonia, emphysema, or inhaling smoke can all cause respiratory acidosis. So can any condition that reduces a person s ability to breathe. Respiratory acidosis is usually treated with a mechanical ventilator, to assist the victim s breathing. The improved exhalation increases the excretion of C02 and raises blood pH. In many cases of asthma, chemicals can facilitate respiration by opening constricted bronchial passages. 

Respiratory acidosis is caused by respiratory insufficiency resulting in an increased arterial C02 concentration. The compensation for respiratory acidosis (if present for prolonged periods) is an increase in serum HC03 . 

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... 

Respiratory alkalosis is characterized by an increased arterial pH, a primary decrease in the arterial PaC02 and, when present for sufficient time, a compensatory fall in the HCOf concentration. Respiratory alkalosis represents hyperventilation and is remarkably common. The most common etiologies of respiratory acidosis are listed in Table 25-7 and range from benign (anxiety) to life-threatening (pulmonary embolism). Some causes of hyperventilation and respiratory acidosis are remarkably common (hypoxemia or anemia). 

It is imperative to identify serious causes of respiratory alkalosis and institute effective treatment. In spontaneously breathing patients, respiratory alkalosis is typically only mild or moderate in severity and no specific therapy is indicated. Severe alkalosis generally represents respiratory acidosis imposed on metabolic alkalosis and may improve with sedation. Patients receiving mechanical ventilation are treated with reduced minute ventilation achieved by decreasing the respiratory rate and/or tidal volume. If the alkalosis persists in the ventilated patient, high-level sedation or paralysis is effective. 

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. 

Respiratory acidosis Acidosis caused by retention of carbon dioxide due to a respiratory abnormality (e.g., chronic obstructive lung disease). 

Like ketoacidosis, respiratory acidosis can also upset the acid-base balance in the body. Respiratory acidosis occurs when the lungs cannot remove enough carbon dioxide from the body. This may be due to severe lung diseases such as chronic asthma, emphysema, or bronchitis, or it could be caused by mechanical restrictions to the emptying of the lung due to scoliosis (curvature of the spine) or severe obesity. 

Acidosis occurs during cardiac arrest because of decreased blood flow and inadequate ventilation. Chest compressions generate only about 20% to 30% of normal cardiac output, leading to inadequate organ perfusion, tissue hypoxia, and metabolic acidosis. Furthermore, the lack of ventilation causes retention of carbon dioxide, leading to respiratory acidosis. The combined acidosis reduces myocardial contractility and may cause arrhythmias because of a lower fibrillation threshold. 

Respiratory acid-base disorders are caused by altered alveolar ventilation producing changes in arterial carbon dioxide tension (PaC02). Respiratory acidosis is characterized by increased PaC02, whereas respiratory alkalosis is characterized by decreased PaC02. 

The partial pressure of CO is important in connection with a number of physiological problems. For example, respiratory acidosis is the result of an abnormally high p... CO . The value of arterial pC O varies directly with changes in the metabolic production of CO and indirectly with the amounl of alveolar ventilation. The problem is more commonly ihe result of decreased alveolar ventilation caused by abnormally low CO excretion by the lungs (alveolar /ivpoveniilulion). 

Acetazolamide can cause a metabolic acidosis in 50% of elderly patients (SEDA-11,199) occasionally (particularly if salicylates are being given or renal function is poor) the acidosis can be severe. It does this by inhibiting renal bicarbonate reabsorption. This effect is of particular use in treating patients with chronic respiratory acidosis with superimposed metabolic alkalosis. Life-threatening metabolic acidosis is rarely observed in the absence of renal insufficiency and/or diabetes mellitus. In three patients with central nervous system pathology alone conventional doses of acetazolamide resulted in severe metabolic acidosis (34). After withdrawal it took up to 48 hours for the metabolic acidosis and accompanying hyperventilation to resolve. 

If the salicylate level continues to rise, the respiratory centers become depressed, the PC02 level becomes elevated, and the blood pH becomes more acidic, causing respiratory acidosis. Dehydration, reduced bicarbonate levels, and the accumulation of salicylic acid, salicyluric acid resulting from metabolism of aspirin, and lactic and pyruvic acid resulting from deranged carbohydrate metabolism may cause metabolic acidosis. 

Inhalation of small amounts of mustard gas produees nasal diseharge, sneezing, epistaxis, and coughing within 12 to 24 h of exposure. Higher concentrations or longer exposures can cause pulmonary damage, hypoxia, and respiratory acidosis. Seizures may be seen with extremely acute, high doses (Sidell et al, 1997). 

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. 

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. 

These disorders are classified according to their cause and the direction of the pH change into respiratory acidosis, metabolic acidosis, respiratory alkalosis, or metabolic alkalosis. Any derangement of acid-base balance elicits... 

The answer is e. (Murray, pp 298-307. Scriver, pp 1471-1488. Sack, pp 217-218. Wilson, pp 361-384.) In the presence of insulin deficiency, a shift to fatty acid oxidation produces the ketones such as acetoacetate that cause metabolic acidosis. The pH and bicarbonate are low, and there is frequently some respiratory compensation (hyperventilation with deep breaths) to lower the PCO2, as in choice e. A low pH with high PCO2 would represent respiratory acidosis (choices a and b—the low-normal bicarbonate values in these choices indicate partial compensation). Choice d represents respiratory alkalosis as would occur with anxious hyperventilation (high pH and low Peep, partial compensation with high bicarbonate). Choice c illustrates normal values. 

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