respiratory acidosis


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Respiratory Acidosis

 

Definition

Respiratory acidosis is a condition in which a build-up of carbon dioxide in the blood produces a shift in the body's pH balance and causes the body's system to become more acidic. This condition is brought about by a problem either involving the lungs and respiratory system or signals from the brain that control breathing.

Description

Respiratory acidosis is an acid imbalance in the body caused by a problem related to breathing. In the lungs, oxygen from inhaled air is exchanged for carbon dioxide from the blood. This process takes place between the alveoli (tiny air pockets in the lungs) and the blood vessels that connect to them. When this exchange of oxygen for carbon dioxide is impaired, the excess carbon dioxide forms an acid in the blood. The condition can be acute with a sudden onset, or it can develop gradually as lung function deteriorates.

Causes and symptoms

Respiratory acidosis can be caused by diseases or conditions that affect the lungs themselves, such as emphysema, chronic bronchitis, asthma, or severe pneumonia. Blockage of the airway due to swelling, a foreign object, or vomit can induce respiratory acidosis. Drugs like anesthetics, sedatives, and narcotics can interfere with breathing by depressing the respiratory center in the brain. Head injuries or brain tumors can also interfere with signals sent by the brain to the lungs. Such neuromuscular diseases as Guillain-Barré syndrome or myasthenia gravis can impair the muscles around the lungs making it more difficult to breathe. Conditions that cause chronic metabolic alkalosis can also trigger respiratory acidosis.
The most notable symptom will be slowed or difficult breathing. Headache, drowsiness, restlessness, tremor, and confusion may also occur. A rapid heart rate, changes in blood pressure, and swelling of blood vessels in the eyes may be noted upon examination. This condition can trigger the body to respond with symptoms of metabolic alkalosis, which may include cyanosis, a bluish or purplish discoloration of the skin due to inadequate oxygen intake. Severe cases of respiratory acidosis can lead to coma and death.

Diagnosis

Respiratory acidosis may be suspected based on symptoms. A blood sample to test for pH and arterial blood gases can be used to confirm the diagnosis. In this type of acidosis, the pH will be below 7.35. The pressure of carbon dioxide in the blood will be high, usually over 45 mmHg.

Treatment

Treatment focuses on correcting the underlying condition that caused the acidosis. In patients with chronic lung diseases, this may include use of a bronchodilator or steroid drugs. Supplemental oxygen supplied through a mask or small tubes inserted into the nostrils may be used in some conditions, however, an oversupply of oxygen in patients with lung disease can make the acidosis worse. Antibiotics may be used to treat infections. If the acidosis is related to an overdose of narcotics, or a drug overdose is suspected, the patient may be given a dose of naloxone, a drug that will block the respiratory-depressing effects of narcotics. Use of mechanical ventilation like a respirator may be necessary. If the respiratory acidosis has triggered the body to compensate by developing metabolic alkalosis, symptoms of that condition may need to be treated as well.

Key terms

pH — A measurement of acid or alkali (base) of a solution based on the amount of hydrogen ions available. Based on a scale of 14, a pH of 7.0 is neutral. A pH below 7.0 is an acid; the lower the number, the stronger the acid. A pH above 7.0 is a base; the higher the number, the stronger the base. Blood pH is slightly alkali with a normal range of 7.36-7.44.

Prognosis

If the underlying condition that caused the respiratory acidosis is treated and corrected, there may be no long term effects. Respiratory acidosis may occur chronically along with the development of lung disease or respiratory failure. In these severe conditions, the patient may require the assistance of a respirator or ventilator. In extreme cases, the patient may experience coma and death.

Prevention

Patients with chronic lung diseases and those who receive sedatives and narcotics need to be monitored closely for development of respiratory acidosis.

Resources

Books

"Fluid, Electrolyte, and Acid-Base Disorders." In Family Medicine Principles and Practices. 5th ed. New York: Springer-Verlag, 1998.

acidosis

 [as″ĭ-do´sis]
1. the accumulation of acid and hydrogen ions or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, resulting in a decrease in pH.
2. a pathologic condition resulting from this process, characterized by increase in hydrogen ion concentration (decrease in pH). The optimal acid-base balance is maintained by chemical buffers, biologic activities of the cells, and effective functioning of the lungs and kidneys. The opposite of acidosis is alkalosis. adj., adj acidot´ic.

Acidosis usually occurs secondary to some underlying disease process; the two major types, distinguished according to cause, are metabolic acidosis and respiratory acidosis (see accompanying table). In mild cases the symptoms may be overlooked; in severe cases symptoms are more obvious and may include muscle twitching, involuntary movement, cardiac arrhythmias, disorientation, and coma.

In general, treatment consists of intravenous or oral administration of sodium bicarbonate or sodium lactate solutions and correction of the underlying cause of the imbalance. Many cases of severe acidosis can be prevented by careful monitoring of patients whose primary illness predisposes them to respiratory problems or metabolic derangements that can cause increased levels of acidity or decreased bicarbonate levels. Such care includes effective teaching of self-care to the diabetic so that the disease remains under control. Patients receiving intravenous therapy, especially those having a fluid deficit, and those with biliary or intestinal intubation should be watched closely for early signs of acidosis. Others predisposed to acidosis are patients with shock, hyperthyroidism, advanced circulatory failure, renal failure, respiratory disorders, or liver disease.
compensated acidosis a condition in which the compensatory mechanisms have returned the pH toward normal.
diabetic acidosis a metabolic acidosis produced by accumulation of ketones in uncontrolled diabetes mellitus.
hypercapnic acidosis respiratory acidosis.
hyperchloremic acidosis renal tubular acidosis.
lactic acidosis a metabolic acidosis occurring as a result of excess lactic acid in the blood, due to conditions causing impaired cell respiration. It occurs most commonly in disorders in which oxygen is inadequately delivered to tissues, such as shock, septicemia, or extreme hypoxemia, but it can also result from exogenous or endogenous metabolic defects. Initially manifesting as hyperventilation, it progresses to mental confusion and coma.
metabolic acidosis any of the types of acidosis resulting from accumulation in the blood of keto acids (derived from fat metabolism) at the expense of bicarbonate; this diminishes the body's ability to neutralize acids. This type is contrasted with respiratory acidosis. It occurs when there is either an acid gain (as in diabetic ketoacidosis, lactic acidosis, poisoning, or failure of the renal tubules to reabsorb bicarbonate) or a bicarbonate loss (as in diarrhea or a gastrointestinal fistula).

The symptoms of metabolic acidosis include weakness, malaise, and headache. As the acid level goes up these symptoms progress to stupor, unconsciousness, coma, and death. The breath may have a fruity odor owing to the presence of acetone, and the patient may experience vomiting and diarrhea. Loss of fluids can deplete body fluid content and aggravate the acidosis. Hyperventilation may occur as a result of stimulation of the hypothalamus. blood gas analysis will reveal a lowered pH and an elevated PaCO2. (See accompanying table.)
Treatment and Patient Care. Treatment of metabolic acidosis is primarily concerned with control of the underlying causes. Diabetic ketoacidosis may be corrected by the administration of insulin and fluids. In acute renal failure the patient requires dialysis, and in chronic uremic acidosis the condition is controlled by restricting sodium intake and buffering with bicarbonate. The patient's vital signs should be checked frequently to assess the progress of compensation. A rising pulse rate and a drop in blood pressure frequently occur as a result of hypovolemia in the diabetic-acidotic patient, and cardiac arrhythmias can be caused by increased calcium levels in the blood. A careful recording of intake and output provides a means of determining the kidneys' ability to regulate the acid-base balance. Safety measures to avoid injury during involuntary muscular contractions should be carried out. (See also convulsions.) Nursing measures to relieve discomfort from vomiting and to avoid the hazards of aspiration of vomitus are required. Education of the patient and family in the prevention of acute episodes of metabolic acidosis, particularly diabetic ketoacidosis, is of primary importance.
renal tubular acidosis (RTA) a metabolic acidosis resulting from impairment of the reabsorption of bicarbonate by the renal tubules, characterized by low plasma bicarbonate and high plasma chloride; the urine is alkaline.
respiratory acidosis acidosis resulting from ventilatory impairment and subsequent retention of carbon dioxide, in contrast to metabolic acidosis. The respiratory system has an important role in maintaining acid-base balance. In response to an increase in the hydrogen ion concentration in body fluids, the respiratory rate increases, causing more carbon dioxide to be released from the lung. When either an acute obstruction of the airways or a chronic condition involving the organs of respiration causes interference with the exhalation of the carbon dioxide produced by metabolic activity, carbon dioxide accumulates in the blood and unites with water to form carbonic acid.

Acute respiratory acidosis occurs when there is a relatively sudden malfunction of respiratory activities, as in upper airway obstruction, acute infections and inflammation of the lung and bronchial tissues, and pulmonary edema. In acute respiratory acidosis the compensatory chemical buffer systems are of limited benefit in restoring the acid-base balance because they depend on normal blood circulation and tissue perfusion for optimal effect. The physiologic regulators, the lungs and kidneys, are of little help because the lungs are malfunctioning and the kidneys require more time to compensate than the acute condition permits.

Chronic respiratory acidosis results from gradual and irreversible loss of ventilatory function, as in chronic obstructive pulmonary disease (COPD). Although the patient in this condition does have an increased retention of CO2, there is time for the kidneys to compensate by retaining bicarbonate and thereby maintaining a pH within tolerable limits. If, however, even a minor respiratory infection develops, the patient is subject to a rapidly developing state of acute acidosis because the lungs cannot be depended upon to remove more than a minimal amount of CO2.
Treatment and Patient Care. The initial treatment for acute respiratory acidosis is to establish an airway immediately and maintain adequate ventilation and hydration. Acute cases may require the use of an endotracheal tube or tracheostomy tube. Some form of intermittent positive pressure breathing is applied through a machine-driven ventilator, essentially to force adequate O2 delivery and concomitant CO2 removal from the lungs, thereby avoiding further rises in CO2 levels to the point that CO2 narcosis will develop. Beyond a certain point the respiratory center may cease responding to the higher CO2 levels, and breathing will stop abruptly. Drugs that further depress the respiratory center (narcotics, hypnotics, and tranquilizers) must be avoided. Patients in the acute stage are watched for cessation of breathing and cardiac arrest. cardiopulmonary resuscitation may be required to revive the patient.

It is recommended that oxygen administration be limited in patients with chronic obstructive pulmonary disease (COPD). In COPD the stimulus to breathe is a hypoxic state, therefore administration of high concentrations of O2 will remove this needed stimulus. The rate of oxygen flow should be closely correlated with blood gas studies. In patients with acute lung diseases the stimulus to breathe is still dependent on CO2 concentrations, so that O2 can be supplied without fear of inhibiting the stimulus to breathe.

Measures that facilitate breathing are essential to patient care during respiratory acidosis. Frequent turning, coughing, and deep breathing exercises to encourage oxygen–carbon dioxide exchange are beneficial, as is suctioning when needed to remove secretions obstructing the airway. postural drainage, unless contraindicated by the patient's condition, may be effective in promoting adequate ventilation.
starvation acidosis a metabolic acidosis due to accumulation of ketones following a severe caloric deficit.

res·pi·ra·to·ry ac·i·do·sis

acidosis caused by retention of carbon dioxide; due to inadequate pulmonary ventilation or hypoventilation, with decrease in blood pH unless compensated by renal retention of bicarbonate.

respiratory acidosis

n.

respiratory acidosis

Metabolism A condition caused by alveolar hypoventilation, tissue accumulation of CO2, and ventilatory failure leading to ↑ PaCO2–ie, hypercapnia; this leads, in turn to ↓ HCO3/PaCO2 and ↓ pH Lab pH < 7.35, HCO3- > 26 mEq/L–if 'compensating', PaCO2 > 45 mm Hg Etiology Hypoventilation due to drugs, CNS depression, heart disease, lung disease–eg, COPD, neuromuscular disease–eg, ALS, diaphragm paralysis, major kyphoscoliosis, Guillain-Barré syndrome, myasthenia gravis, muscular dystrophy, obesity hypoventilation syndrome Clinical Cyanosis, diffuse wheezing, hyperinflation–ie, barrel chest, ↓ breath sounds, hyperresonance on percussion, prolonged expiration; depressed mental status due to ↑ CO2, accompanied by asterixis, myoclonus, seizures, papilledema,  dilated conjunctival or facial blood vessels. See Metabolic acidosis, Metabolic alkalosis, Respiratory alkalosis.

res·pi·ra·to·ry ac·i·do·sis

(res'pir-ă-tōr-ē as'i-dō'sis)
Acidosis caused by retention of carbon dioxide; due to inadequate pulmonary ventilation or hypoventilation, with decrease in blood pH unless compensated by renal retention of bicarbonate.
Synonym(s): hypercapnic acidosis.

res·pi·ra·to·ry ac·i·do·sis

(res'pir-ă-tōr-ē as'i-dō'sis)
Acidosis caused by retention of carbon dioxide.
Synonym(s): hypercapnic acidosis.
References in periodicals archive ?
Specifically, after transport, decreased total WBC, lymphocyte, monocyte, and eosinophil counts; elevated H : L ratio; and a mild respiratory acidosis with an appropriate compensatory metabolic alkalosis, resulting in an unchanged venous blood pH, can be anticipated in Dalmatian pelicans.
Central inhibition of ventilatory drive resulting in respiratory acidosis may be one of the complications of Bonsai and its derivatives.
Of the patients having initially presented with respiratory acidosis in the postoperative course and subsequently developed BE > + 2 mEq/L, the mean BE was 3.1 [+ or -] 1.0 mEq/L (Figure 2).
In mixed metabolic and respiratory acidosis, elevation of blood pH requires simultaneous therapy of respiratory and metabolic components of the acidosis.
Finally, PaC[O.sub.2] is greater than 45 mmHg, leading unexpectedly to the initial diagnosis of respiratory acidosis, meaning that there is no respiratory compensation.
Because the PaC[O.sub.2] follows the state of the pH, respiratory acidosis is present (Thurkauf & Watson, 2014).
Under most conditions enhanced pC[O.sub.2] with the accompanying respiratory acidosis will cause a decrease in plasma lactate concentration (LA) during and after a bout of exercise.
Due to these properties, there maybe a rationale to use heliox in patients with severe pulmonary disease with respiratory failure whose protective mechanical ventilation with low tidal volumes is not feasible due to the development of respiratory acidosis, for example, in acute respiratory distress syndrome (ARDS) or chronic obstructive pulmonary disease (COPD).
Impaired ventilation produces an increase in PaC[O.sub.2] levels, causing the equation to shift to the right and leading to increased carbonic acid and H+ ion concentration in the plasma, lowered pH and respiratory acidosis. Bicarbonate cannot effectively buffer respiratory acidosis because an increase in HC[O.sub.3]- in the presence of increased C[O.sub.2] will only cause the formation of more carbonic acid.
Arterial blood gas data at this time reflect either an uncompensated respiratory acidosis, or a mixed acidosis (acute respiratory acidosis and lactic acidosis).
The progression of metabolic changes after septic shock may lead to hypoxaemia and metabolic acidosis with a high risk of respiratory acidosis, especially in small infants who may become exhausted.
There is significant evidence of benefit with the use of noninvasive ventilation, particularly with respiratory acidosis of pH less than 7.35, PC[O.sub.2] greater than 45, and significant dyspnea, which is easily detected by clinical means, he said.