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Acid-Base Disturbances
Plasma pH is an indicator of hydrogen ion (H+) concentration and measures the acidity or alkalinity of the blood. Homeostatic mechanisms keep pH within a normal range (7.35 to 7.45). These mechanisms consist of buffer systems, the kidneys, and the lungs. The H+ concentration is extremely important: The greater the concentration, the more acidic the solution and the lower the pH. The lower the H+ concentration, the more alkaline the solution and the higher the pH.
- Kidneys a. Selectively retain or reject electrolytes and other substances to maintain normal osmolality and blood volume. Sodium is retained, and potassium is excreted. The kidneys also play an important part in acid- base regulation. The distal tubule has the ability to form ammonia and exchange hydrogen ions (in the form of ammonia) for bicarbonate to maintain the carbonic acid-bicarbonate ratio.
- Lungs a. Selectively retain or reject electrolytes and other substances to maintain normal osmolality and blood volume. Sodium is retained, and potassium is excreted.
- Endocrine glands: a. The adrenal glands influence the retention or excretion of sodium, potassium, and water. These glands secrete aldosterone, a hormone that increases sodium reabsorption from the renal tubules in exchange for potassium, thus maintaining normal sodium concentration. The posterior lobe of the pituitary releases antidiuretic hormone (ADH), which inhibits diuresis by increasing water reabsorption in the distal tubule. Increased concentration of sodium in the ECF stimulates the pituitary to release ADH. This hormone increases water reabsorption to dilute the sodium to the normal concentration level. The parathyroid glands, pea-sized glands embedded in the corners of the thyroid gland, regulate calcium and phosphate balance by means of parathyroid hormone (PTH). When the calcium level is low, PTH secretion is stimulated. This acts on bone to increase the reabsorption of bone salts, releasing large amounts of sodium into the ECF. When the extracellular calcium concentration is too high, PTH secretion is depressed, so almost no bone reabsorption occurs in regulating the body’s fluid composition and volume.
- Potassium is the chief cation of body cells and is concerned with maintaining body fluid composition and electrolyte balance. Potassium participates in carbohydrate utilization and protein synthesis and is critical in regulating nerve conduction and muscle contraction, particularly in the heart.
- Chloride, the major extracellular anion, closely follows sodium metabolism, and changes in the body's acid-base are reflected by changes in the chloride concentration.
- A deficiency of either potassium or chloride will lead to a deficit of the other.
- Acid-base imbalances are normally the result of an excess or a deficit in either base bicarbonate or carbonic acid. Deviations of pH from 7.35 to 7.45 are combated by the buffer system and by the respiratory and renal regulatory mechanisms. Two types of disturbance can affect the acid-base balance: respiratory and metabolic.
- Respiratory disturbances affect the carbonic side of the balance by increasing or decreasing carbonic acid; carbonic acid is produced when carbon dioxide unites with ECF.
- Metabolic disturbances affect the bicarbonate side of the balance. Kidney function controls the bicarbonate concentration by regulating the number of cations (hydrogen, ammonium, and potassium) in exchange for sodium ions to combine with the reabsorbed bicarbonate in the distal tubular lumen. As hydrogen ions are excreted, bicarbonate is generated, maintaining the proper acid-base balance of the blood. Ammonia excretion is increased in response to high acidity; bicarbonate replaces the ammonia.
Metabolic Acidosis
Metabolic acidosis is a common clinical disturbance characterized by a low pH due to an increased H+ concentration and a low plasma bicarbonate concentration. Metabolic acidosis can occur by a gain of hydrogen ions or a loss of bicarbonate ions in the bloodstream. It can be divided clinically into two forms, according to the values of the serum anion gap: high anion gap metabolic acidosis and normal anion gap metabolic acidosis. o The anion gap refers to the difference between the sum of all measured positively charged electrolytes (cations) and the sum of all negatively charged electrolytes (anions) in blood.
o Because the sum of measured cations is typically greater than the sum of measured anions in the bloodstream, there normally exists a disparity with predominance of cations; this is referred to as the anion gap. o The anion gap reflects unmeasured anions (phosphates, sulfates, and proteins) in plasma that replace bicarbonate in metabolic acidosis. o Measuring the anion gap is necessary when analyzing conditions of metabolic acidosis as it can help determine the cause of the acidosis. If potassium is included in the equation, the normal value for the anion gap is 12 to 16 mEq/L (12 to 16 mmol/L). o The unmeasured anions in the serum normally account for less than 16 mEq/L of the anion production. Metabolic acidotic conditions can be differentiated according to the anion gap; there is either a normal anion gap or high anion gap. o A person diagnosed with metabolic acidosis is determined to have normal anion gap metabolic acidosis if the anion gap is within this normal range (8 to 12 mEq/L). o An anion gap greater than 16 mEq (16 mmol/L) suggests excessive accumulation of unmeasured anions and would indicate high anion gap metabolic acidosis. o An anion gap occurs because not all electrolytes are measured. o More anions are left unmeasured than cations.
Pathophysiology
Normal anion gap metabolic acidosis results from the direct loss of bicarbonate, as in: o Diarrhea o Lower intestinal fistulas o Ureterostomies o Use of diuretics o Early renal insufficiency o Excessive administration of chloride o The administration of parenteral nutrition without bicarbonate or bicarbonate-producing solutes (e.g., lactate) High anion gap metabolic acidosis occurs when there is an excessive accumulation of acids. o High anion gap occurs in lactic acidosis, salicylate poisoning (acetylsalicylic acid), renal failure, methanol, ethylene, or propylene glycol toxicity, DKA, and ketoacidosis that occurs with starvation. o The high amount of hydrogen ions due to the acids present are neutralized and buffered by HCO3− causing the bicarbonate concentration to fall and become exhausted. o Other anions in the bloodstream are called upon to neutralize the high acid in the blood. o In all of these instances, abnormally high levels of anions are used to neutralize the H+, which increases the anion gap above normal limits (high anion gap).
Clinical Manifestations
Signs and symptoms of metabolic acidosis vary with the severity of the acidosis but include: o Headache o Confusion (unconsciousness) o Drowsiness o Increased respiratory rate and depth o Nausea o Vomiting o Stupor o Shortness of breath Peripheral vasodilation and decreased cardiac output occur when the pH drops to less than 7. Additional physical assessment findings include: o Decreased blood pressure o Cold and clammy skin o Arrhythmias
o Loss of potassium, such as diuretic therapy that promotes excretion of potassium (e.g., thiazides, furosemide) o ACTH secretion (as in hyperaldosteronism and Cushing’s syndrome) Hypokalemia produces alkalosis in two ways: o (1) when the bloodstream is low in K+, the nephrons reabsorb K+ into the bloodstream and secrete H+ into the tubule fluid which is excreted in the urine. o (2) when the bloodstream is low in K+, intracellular potassium moves out of the cells into the ECF, and as potassium ions leave the cells, hydrogen ions must enter to maintain electroneutrality. Excessive alkali ingestion from antacids containing bicarbonate or from the use of sodium bicarbonate during cardiopulmonary resuscitation can also cause metabolic alkalosis. Chronic metabolic alkalosis can occur with long-term diuretic therapy (thiazides or furosemide), villous adenoma in the GI tract, external drainage of gastric fluids, significant potassium depletion, cystic fibrosis, and the chronic ingestion of milk and calcium carbonate.
Clinical Manifestations
Signs & symptoms include: o Muscular hyperactivity o Tetany o Depressed respiration In alkalosis, H+ ions are decreased in the bloodstream, leaving negatively charged proteins attracting other positive ions. o Calcium (Ca++) ions bind to these proteins. o As calcium ions bind to proteins in the bloodstream, free Ca++ ions decrease in the bloodstream and hypocalcemia develops. Alkalosis is primarily manifested by symptoms related to hypocalcemia, such as tingling of the fingers and toes, dizziness, and tetany (cramping muscles). Because it is the ionized fraction of calcium that is diminished in metabolic alkalosis, neuromuscular symptoms due to hypocalcemia are often the predominant symptoms. In metabolic alkalosis, the lungs attempt to compensate by slowing respiratory rate, which increases CO retention, and in turn increases H+ content of the blood (see carbonic acid equation). If the kidneys are functional, there is increased renal excretion of HCO3− and conservation of H+ in an attempt to reduce the alkalinity of the bloodstream. As the pH of blood increases in metabolic alkalosis, H+ ions are reabsorbed into the bloodstream to neutralize the blood. As the nephrons increase H+ ion reabsorption, they excrete K+, and hypokalemia develops. In hypokalemia a prominent U wave often develops on the ECG and ventricular rhythm disturbances, such as PVCs, may occur. Hypokalemia also can lead to decreased GI motility and paralytic ileus.
Assessment & Diagnostic Findings
In metabolic alkalosis, evaluation of ABGs reveals a pH greater than 7.45 and a serum bicarbonate concentration greater than 26 mEq/L. o The PaCO2 increases as the lungs attempt to compensate for the excess bicarbonate by retaining CO2. o This hypoventilation is more pronounced in patients who are semiconscious, unconscious, or debilitated than in patients who are alert. o Because of hypoventilation the patient may develop hypoxemia. Urine chloride levels may help identify the cause of metabolic alkalosis if the patient’s history provides inadequate information. o Metabolic alkalosis is the setting in which urine chloride concentration may be a more accurate estimate of fluid volume than the urine sodium concentration. o Urine chloride concentrations can help to determine the source of the metabolic alkalosis. o Urine chloride concentrations can be used to differentiate between vomiting, diuretic therapy, and excessive adrenocorticosteroid secretion as the cause of the metabolic alkalosis.
In patients with vomiting or cystic fibrosis, those receiving nutritional repletion, and those receiving diuretic therapy, hypovolemia and hypochloremia produce urine chloride concentrations lower than 25 mEq/L. Signs of hypovolemia are not present, and the urine chloride concentration exceeds 40 mEq/L in patients with mineralocorticoid excess or alkali loading; these patients usually have expanded fluid volume.
Medical Management
Treatment of both acute and chronic metabolic alkalosis is aimed at correcting the underlying acid–base disorder. Because volume depletion is commonly present with GI losses of H+, the patient’s I&O must be monitored carefully. Treatment includes restoring normal fluid volume by administering normal saline because continued volume depletion perpetuates the alkalosis. In patients with hypokalemia, potassium is given as KCl to replace both K+ and Cl− losses. Proton pump inhibitors (e.g., omeprazole) are recommended to reduce the production of gastric hydrogen chloride (HCl). o This decreased HCl will in turn decrease the loss of HCl with gastric suction in metabolic alkalosis. Carbonic anhydrase inhibitors (e.g., acetazolamide) are useful in treating metabolic alkalosis in patients who cannot tolerate rapid volume expansion (e.g., patients with heart failure). o Carbonic anhydrase inhibitors act at the nephron to enhance bicarbonate excretion.
Respiratory Acidosis
Respiratory acidosis is a clinical disorder in which the pH is less than 7.35 and the PaCO2 is greater than 45 mmHg. It may be either acute or chronic.
Pathophysiology
Respiratory acidosis is due to inadequate excretion of CO2 with inadequate ventilation, resulting in elevated plasma CO2 concentrations and, consequently, increased levels of carbonic acid. In addition to an elevated PaCO2, inadequate ventilation usually causes a decrease in PaO2. Acute respiratory acidosis occurs in emergency situations, such as acute pulmonary edema, aspiration of a foreign object, atelectasis, pneumothorax, and overdose of sedatives, as well as in nonemergent situations, such as sleep apnea associated with severe obesity, severe pneumonia, and acute respiratory distress syndrome. Respiratory acidosis commonly occurs in patients with severe chronic obstructive pulmonary disease (COPD) when patients acutely decompensate due to respiratory infection or heart failure. Respiratory acidosis can also occur in diseases that impair respiratory muscle function and cause hypoventilation. o These disorders include severe scoliosis, muscular dystrophy, multiple sclerosis, myasthenia gravis, and Guillain-Barré syndrome.
Clinical Manifestations
Clinical signs in acute and chronic respiratory acidosis vary. o Acute respiratory acidosis can occur due to sudden hypercapnia (elevated PaCO2) that will increase pulse, blood pressure, and respiratory rate. o The patient may complain of confusion, disorientation, or may exhibit diminished level of consciousness. o An elevated PaCO2, greater than 60 mm Hg causes reflexive cerebrovascular vasodilation and increased cerebral blood flow. o Ventricular fibrillation may be the first sign of respiratory acidosis in anesthetized patients. o Weakness o Disorientation o Depressed breathing o Coma
Respiratory alkalosis is caused by: o Hyperventilation, which causes excessive loss or “blowing off” of CO2 and, hence, there is a decrease in the plasma carbonic acid concentration (see carbonic acid equation). Causes include: o Extreme anxiety such as panic disorder o Hypoxemia o Salicylate intoxication o Gram-negative sepsis o Inappropriate ventilator settings Chronic respiratory alkalosis results from chronic hypocapnia which leads to decreased serum H+ ion, resulting in alkalosis. Chronic hepatic insufficiency and cerebral tumors can cause chronic hyperventilation that leads to chronic respiratory alkalosis.
Clinical Manifestations
Clinical signs of respiratory alkalosis consist of: o Lightheadedness and inability to concentrate due to cerebral artery vasoconstriction and decreased cerebral blood flow o Numbness and tingling from decreased calcium ionization in the bloodstream o Tinnitus o Sometimes loss of consciousness o Convulsions o Tetany o Unconsciousness Cardiac effects of respiratory alkalosis include: o Tachycardia o Ventricular and atrial arrhythmias
Assessment & Diagnostic Findings
Analysis of ABGs assists in the diagnosis of both acute and chronic respiratory alkalosis. o In the acute state, the pH is elevated above normal (greater than 7.45) as a result of a low PaCO2 and a normal bicarbonate level. The kidneys take days to compensate for acid–base imbalances. o Therefore, the kidneys cannot alter the bicarbonate level in the bloodstream quickly enough and medical intervention is necessary. In the compensated state of chronic respiratory alkalosis, the kidneys have had sufficient time to lower the bicarbonate level to a near-normal level. Evaluation of serum electrolytes is indicated to identify any decrease in potassium, as hydrogen is pulled out of the cells in exchange for potassium. A decreased calcium level may occur as severe alkalosis inhibits calcium ionization, resulting in carpopedal spasms and tetany. A decreased phosphate level can occur due to alkalosis because there is increased uptake of phosphate by the cells. A toxicology screen should be performed to rule out salicylate intoxication due to aspirin poisoning.
Medical Management
Treatment depends on the exact underlying cause of respiratory alkalosis. If the cause is anxiety, the patient is instructed to breathe more slowly to allow CO2 to accumulate or to breathe into a closed system (such as a paper bag or CO2 rebreather mask). An antianxiety agent may be required to relieve hyperventilation in very anxious patients. Treatment of other causes of respiratory alkalosis is directed at correcting the underlying problem.
Compensation
Generally, the pulmonary and renal systems compensate for each other to return the pH to normal. In a single acid–base disorder, the system not causing the problem tries to compensate by returning the ratio of bicarbonate to carbonic acid to the normal 20:1. The lungs compensate for metabolic disturbances by changing CO2 excretion; hypoventilation accumulates CO2, hyperventilation causes loss of CO2. The kidneys compensate for respiratory disturbances by altering bicarbonate reabsorption and H+ secretion. In respiratory acidosis, excess hydrogen in the blood is excreted in the urine in exchange for bicarbonate ions which are conserved. In respiratory alkalosis, the renal excretion of bicarbonate increases, and hydrogen ions are retained. In metabolic acidosis, the lungs compensate by increasing the ventilation rate and the kidneys retain bicarbonate. In metabolic alkalosis, the respiratory system compensates by decreasing ventilation to conserve CO2 and increase the PaCO2, which in turn increases carbonic acid. Because the lungs respond to acid–base disorders within minutes, compensation for metabolic imbalances occurs faster than renal compensation for respiratory imbalances.
Blood Gas Analysis
Blood gas analysis is often used to identify the specific acid–base disturbance and the degree of compensation that has occurred. The analysis is usually based on an arterial blood sample; however, if an arterial sample cannot be obtained, a mixed venous sample may be used. Results of ABG analysis provide information about alveolar ventilation, oxygenation, and acid–base balance. It is necessary to evaluate the concentrations of serum electrolytes (e.g., sodium, potassium, chloride) along with ABG data because electrolytes are commonly affected by acid–base imbalances. The health history, physical examination, previous blood gas results, and serum electrolytes should always be part of the assessment used to determine the cause of the acid–base disorder. Responding to isolated sets of blood gas results without these data can lead to serious errors in interpretation. Treatment of the underlying condition usually corrects acid–base disorders.
a. Bicarbonate buffer b. Phosphate buffer c. Protein buffer d. All of the above
- Which of the following laboratory results below indicates compensated metabolic alkalosis? a. Low p CO2, normal bicarbonate and, high pH b. Low p CO2, low bicarbonate, low pH c. High p CO2, normal bicarbonate and, low pH d. High pCO2, high bicarbonate and High pH
- The greatest buffering capacity at physiological pH would be provided by a protein rich in which of the following amino acids? a. Lysine b. Histidine c. Aspartic acid d. Leucine
- Which of the following is most appropriate for a female suffering from Insulin dependent diabetes mellitus with a pH of 7.2, HCO3-17 mmol/L and pCO2-20 mm HG? a. Metabolic Acidosis b. Metabolic Alkalosis c. Respiratory Acidosis d. Respiratory Alkalosis
- Causes of metabolic alkalosis include all the following except: a. Mineralocorticoid deficiency b. Hypokalemia c. Thiazide diuretic therapy d. Recurrent vomiting
- Renal Glutaminase activity is increased in: a. Metabolic acidosis b. Respiratory Acidosis c. Both of the above d. None of the above
- Causes of lactic acidosis include all except: a. Acute Myocardial infarction b. Hypoxia c. Circulatory failure d. Infections
- Which out of the following conditions will not cause respiratory alkalosis? a. Fever b. Anxiety c. Laryngeal obstruction d. Salicylate toxicity
- All are true about metabolic alkalosis except one: a. Associated with hyperkalemia b. Associated with decreased ionic calcium concentration c. Can be caused due to Primary hyperaldosteronism d. Can be caused due to Renin secreting tumor
- Choose the incorrect statement out of the followings: a. Deoxy hemoglobin is a weak base b. Oxyhemoglobin is a relatively strong acid c. The buffering capacity of hemoglobin is lesser than plasma protein d. The buffering capacity of Hemoglobin is due to histidine residues
- Carbonic anhydrase is present at all places except: a. Gastric parietal cells b. Red blood cells c. Renal tubular cells
d. Plasma
- All are true for renal handling of acids in metabolic acidosis except: a. Hydrogen ion secretion is increased b. Bicarbonate reabsorption is decreased c. Urinary acidity is increased d. Urinary ammonia is increased.
- Choose the incorrect statement about anion gap out of the followings: a. In lactic acidosis anion gap is increased b. Anion gap is decreased in Hypercalcemia c. Anion gap is decreased in Lithium toxicity d. Anion gap is decreased in ketoacidosis
- Excessive citrate in transfused blood can cause which of the following abnormalities? a. Metabolic alkalosis b. Metabolic acidosis c. Respiratory alkalosis d. Respiratory acidosis
