Acid-Base Imbalances

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Chapter: Anatomy and Physiology for Health Professionals: Fluid, Electrolyte, and Acid Base Balance

The pH of arterial blood is usually between 7.35 and 7.45. Abnormal values below 7.35 produce acidosis, whereas values above 7.45 produce alkalosis.

Acid-Base Imbalances

The pH of arterial blood is usually between 7.35 and 7.45. Abnormal values below 7.35 produce acidosis, whereas values above 7.45 produce alkalosis. Shifts in pH can be life threatening. Survival may be impos-sible if blood pH is below 6.8 or above 8.0 for more than a few hours (FIGURE 23-7 ). The partial pressure of carbon dioxide (Pco2) is the most important indica tor of normal respiratory function. Normal levels are between 35 and 45 mm Hg. Dangerous acidosis and alkalosis conditions may be linked to cardiovascu-lar, respiratory, urinary, digestive, or nervous system abnormalities. To correctly diagnose these conditions, most blood tests include screenings of pH and buffer system function. Blood pH, Pco 2, and bicarbonate ion levels are measured. Additional tests include measur-ing the anion gap and using nomograms or diagnostic charts to plot test results. These steps help to correctly identify the condition, its severity, its causes, and whether it is compensated or uncompensated.

Respiratory Acidosis

The two major types of acidosis are respiratory acido-sis and metabolic acidosis. Respiratory acidosis may be caused by increased carbon dioxide concentration as well as carbonic acid or respiratory acid and may result in the following conditions:

Injury to the brain stem’s respiratory center, decreasing breathing

Obstruction of air passages and interference with air movement into alveoli

Diseases decreasing gas exchange, such as ­pneumonia, or reducing respiratory membrane surface area, such as emphysema; also linked to cystic fibrosis

Respiratory acidosis is generally indicated by a Pco2 that is above 45 mm Hg, known as hyper-capnia, and lowered blood pH. It is usually caused by hypoventilation­, which is an abnormally low ­respiratory rate. When the Pco2 rises in the extra-cellular fluid compartment, hydrogen and bicar-bonate ion concentrations also rise. This occurs as carbonic acid forms and dissociates. When buffer systems cannot keep up, the pH falls rapidly. Just a few minutes of hypoventilation may result in acido-sis. The pH of the extracellular fluid may reduce to as low as 7.0.

When the body’s chemical and physiological buffers return pH to normal, the acidosis is compen-sated. This is normally accomplished by chemorecep-tors that stimulate an increase in breathing rate. In uncompensated acidosis, the pH continues to drop, and the patient can become comatose and eventu-ally die. Acute respiratory acidosis develops when the decline in pH is severe. It is an especially dangerous condition when the patient’s tissues generate large amounts of carbon dioxide or when normal respira-tory activity is not possible. Therefore, for victims of cardiac arrest or drowning, reversing acute respira-tory acidosis is the major goal. As a result, cardio-pulmonary resuscitation, first aid, and lifesaving courses teach Airway, Breathing, and Circulation as the “ABCs” of emergency care.

Chronic respiratory acidosis occurs because normal respiratory function is compromised but compensatory mechanisms have not completely failed. In a patient with central nervous system damage, normal respiratory compensation may not occur even when stimulated by chemoreceptors. People whose respiratory centers are desensitized by ­barbiturates or alcohol may also be unable to achieve normal respiratory compensation. These individuals often develop acidosis because of chronic hypoventilation. Other factors, such as congestive heart failure, emphysema, pneumonia, pneumothorax, and respiratory muscle paralysis, can influence the development of chronic respira-tory acidosis.

When normal pulmonary responses are disabled, the kidneys increase hydrogen ion secretion into the tubular fluid, slowing the rate of pH change. Unfor-tunately, the kidneys are not able to return pH to nor-mal levels on their own. The underlying circulatory or respiratory problems must be corrected. Breath-ing efficiency may be temporarily improved with bronchodilators or mechanical devices providing air that is under positive pressure. Artificial respiration or mechanical ventilation are required once breath-ing has ceased. If the respiratory acidosis was not severe or prolonged, normal pH can still be restored. Respiratory acidosis treatment is made more difficult because the condition also causes metabolic acidosis as lactic acid is generated in tissues that do not have sufficient oxygen. The effects of respiratory acidosis and the compensation for the condition are shown in FIGURE 23-8.

Respiratory Alkalosis

Respiratory alkalosis is a less common condition that results from excessive carbon dioxide and car-bonic acid loss. Called hypocapnia, this ­condition is signified­ by a Pco2 < 35 mm Hg, with raised blood pH. A temporary hypocapnia can be produced by hyperventilation, often in response to anxiety, pain, fever, or poisoning due to salicylates. Hyper-ventilation depletes carbon dioxide and increases body fluid pH to as high as 8.0. Fortunately, respi-ratory alkalosis is usually self-corrected, because chemoreceptor­ stimulation stops and the urge to breathe reduces. Carbon dioxide levels then return to normal.

Hyperventilation often results from pain or other physical stressors and extreme anxiety or other psychological stressors. It gradually elevates the pH of the cerebrospinal fluid, affecting central nervous system function. There are initial tingling sensations in the lips, hands, and feet. The individual may be light-headed and lose consciousness if the condition continues. Because unconsciousness stops percep-tion of causative psychological stimuli, breathing rate declines and the condition is self-corrected. The effects of respiratory alkalosis and compensation for the condition are shown in FIGURE 23-9.

Hyperventilation is easily treated by having the patient rebreathe air that has been exhaled into a small paper bag. Rising Pco2 in the bag results in similar rises in the arterial and alveolar carbon ­dioxide concentrations. The pH is then restored to normal levels. Rare situations that may involve respiratory alkalosis include high altitudes that cause hyperventilation, use of mechanical respira-tors, and those with brain stem injuries that cause them to be unable to respond to changes in plasma carbon dioxide concentrations.

Metabolic Acidosis

Metabolic acidosis is the second most common type of acid-base imbalance. Metabolic imbalances such as this are indicated by bicarbonate levels below or above the normal range, which is 22–26 mEq/L. Metabolic­ acidosis may be caused by accumulation of ­nonrespiratory acids or loss of bases, such as in the following conditions:

Lactic acidosis, which can develop after strenuous exercise or prolonged tissue hypoxia, known as oxygen starvation, as active cells rely on anaerobic respiration.

Diabetes mellitus, which converts some fatty acids into ketone bodies such as acetoacetic acid, beta-hydroxybutyric acid, and acetone, causing ketonuria or ketoacidosis. This conversion of some fatty acids into ketone bodies also occurs during starvation.

Overconsumption of alcohol, which is metabolized to acetic acid.

Vomiting over a long period of time causes the stomach to continue to generate stomach acids to replace those that are lost. As a result, the bicarbonate concentration of the blood continues to rise.

Prolonged diarrhea, which is more common in infants, causing excessive loss of bicarbonate ions.

Kidney disease that reduces glomerular filtration and causes uremic acidosis; this is a less common condition. It may occur from glomerulonephritis and use of diuretics. When the reabsorption of sodium ions stops, secretion of hydrogen ions also stops.

Diagnosis and treatment of metabolic acidosis is based on the cause. Although it can be easily linked to lactic acidosis after extreme physical activity, there may be many more complicated causative factors. The body generally compensates for metabolic ­acidosis via the lungs and kidneys. The lungs eliminate carbon dioxide molecules formed by the interaction of hydro-gen ions with bicarbonate ions. The kidneys excrete additional hydrogen ions into the urine while gen-erating bicarbonate ions, which are released into the extracellular fluid.

Metabolic and respiratory acidosis are often linked because oxygen-starved tissues generate lactic acid in massive amounts and because sus-tained hypoventilation results in decreased arterial ­partial pressure of oxygen. Examples include near-­ drownings, in which there is high Pco2 and low par-tial pressure of oxygen in the body fluids. Lactic acid dominates the muscles because of the attempts of the drowning person to stay above water. Dissociation of lactic acids releases lactate and hydrogen ions. Emergency treatment is vital, including artificial or mechanical respiratory assistance and intravenous administration of an isotonic solution. This solution contains sodium bicarbonate, sodium gluconate, or sodium lactate.

Metabolic Alkalosis

Metabolic alkalosis results from excessive loss of hydrogen ions or gain of bases or bicarbonate ions. It is much less common than metabolic acidosis. In metabolic alkalosis, there is in an increase in blood pH, called alkalemia, after gastric drainage or lavage, use of certain diuretics, overuse of antacids, or pro-longed vomiting. Loss of acidic gastric juice leaves body fluids more basic. A condition called alkaline tide may occur, caused by many bicarbonate ions moving into the extracellular fluid. This movement is related to secretion of hydrochloric acid from the gastric mucosa. Temporary elevation of bicar-bonate ions in the extracellular fluid occurs during eating, but serious metabolic alkalosis may occur because of repeated vomiting as the stomach gen-erates more stomach acids to replace those regur-gitated. This means bicarbonate ion concentrations in the extracellular fluid rise continually. Metabolic alkalosis may also develop from taking excessive quantities of antacids.

Symptoms include decreased breathing rate and depth and increased blood carbon dioxide. The com-pensatory factors for metabolic alkalosis include reduced breathing rate, with a loss of bicarbonate ions in the urine. For mild cases, treatment usually is focused on controlling vomiting or treating other causative factors. Solutions that may be administered include sodium chloride or potassium chloride. Acute metabolic alkalosis is treated with ammonium chloride. As the ammonium ions are metabolized in the liver, hydrogen ions are liberated, which ­basically means hydrochloric acid is generated in greater quantities. As it diffuses into the bloodstream, the pH falls to normal levels. The effects of respiratory and metabolic acidosis and alkalosis are described in TABLE 23-4.

Compensations for Imbalances

If the lung or kidney buffer systems become insuffi-cient, the acid-base balance is disrupted. As a result, the undisturbed system tries to compensate. The respiratory system is responsible for compensation of metabolic acid-base imbalances and works rela-tively quickly. The urinary system, although slower, is responsible for compensation of respiratory-­related acid-base imbalances. The ways these systems com-pensate are reflected in changes in the Pco2 and ­concentrations of bicarbonate ions. A patient can have a serious medical condition and still show a normal pH because of how these systems compensate.

Respiratory Compensation

When the respiratory system compensates for a meta-bolic acid-base imbalance, respiratory rate and depth change. They are usually elevated in metabolic acido-sis. This is because high hydrogen ion levels stimulate the respiratory centers. Blood pH is below 7.35, and bicarbonate ion levels are below 22 mEq/L. The Pco2 falls below 35 mm Hg as carbon dioxide is removed and excess acid leaves the blood. In respiratory aci-dosis, respiratory rate is often depressed, which is the immediate cause of the acidosis. This is not true for conditions of gas exchange impairment, such as pneumonia or emphysema.

For metabolic alkalosis, respiratory compensa-tion involves slow and shallow breathing. This allows carbon dioxide to accumulate in the blood. Evidence of this compensation includes a pH above 7.45 at first, and sometimes longer; bicarbonate levels over 26 mEq/L; and a Pco2 above 45 mm Hg.

Urinary Compensation

The kidneys speed up compensatory actions when an acid-base imbalance is of respiratory cause. Acidosis is shown when a person is hyperventilating. Although the kidneys are compensating, the levels of the Pco2, as well as bicarbonate ions, are high. The raised Pco2 causes the acidosis. The increasing bicarbonate ion level shows the kidneys are retaining bicarbonate to compensate for the acidosis.

Oppositely, an individual who has respiratory alkalosis compensated for by the kidneys has a high blood pH and a low Pco2. As the kidneys eliminate more bicarbonate by not reclaiming it or by secreting it, its levels begin to fall. However, the kidneys cannot compensate for either alkalosis or acidosis if the con-dition is linked to a renal problem.

1. Explain the terms acidosis and alkalosis.

2. What is “normal pH,” and what levels signify acidic or alkaline pH levels?

3. Why can prolonged vomiting produce metabolic alkalosis?

4. What effect does a decrease in the pH of body fluids have on the respiratory rate?

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