Acid-Base Disorders PDF

DISTURBANC ES  ACUTE & CHRONIC METABOLIC ACIDOSIS ACUTE & CHRONIC METABOLIC ALKALOSIS ACUTE & CHRONIC RESPIRATORY ACIDOSIS ACUTE & CHRONIC RESPIRATORY ALKALOSIS MIXED ACID-BASE DISORDERS BLOOD GAS ANALYSIS ACID-BASE BALANCE Maintains the homeostasis regulation of the pH in the extr...

DISTURBANC ES  ACUTE & CHRONIC METABOLIC ACIDOSIS ACUTE & CHRONIC METABOLIC ALKALOSIS ACUTE & CHRONIC RESPIRATORY ACIDOSIS ACUTE & CHRONIC RESPIRATORY ALKALOSIS MIXED ACID-BASE DISORDERS BLOOD GAS ANALYSIS ACID-BASE BALANCE Maintains the homeostasis regulation of the pH in the extracellular compartment between 7.35 – 7.45, with an average of 7.40. Too acidic – body compensates to remove extra acids. Too alkaline, body compensates to remove base excess. The (3) major mechanisms to maintain homeostasis: Buffer system, kidneys, lungs. Importance: variations can significantly affect the organs of the body. Identification of the specific acid–base imbalance is important in identifying the underlying cause of the disorder and determining appropriate treatment. Plasma pH is an indicator of hydrogen ion (H+) concentration. concentration, the more acidic the solution and the lower the pH. H concentration, the more alkaline the solution and the higher the pH. The pH range compatible with life (6.8 to 7.8) represents a 10- fold difference in H+ concentration in plasma. Buffer systems Homeostatic mechanisms keep pH within a normal range (7.35 to 7.45). These mechanisms consist of buffer systems, the kidneys, the lungs Buffers Buffer systems prevent major changes in the pH of body fluids by removing or releasing H+; they can act quickly to prevent excessive changes in H+ concentration. Hydrogen ions are buffered by both intracellular and extracellular buffers Extracellular buffer system The body’s major extracellular buffer system is the bicarbonate–carbonic acid buffer system, which is assessed when arterial blood gases are measured. Less important ECF buffers are inorganic Phosphates & plasma proteins. There are 20 parts of bicarbonate (HCO3 – ) to one part of carbonic acid (H2CO3). (20:1) If this ratio is altered, the pH will change. It is the ratio of HCO3 – to H2CO3 that is important in maintaining pH.  CO2 is a potential acid; when dissolved in water, it becomes carbonic acid (CO2 + H2O = H2CO3). When CO2 is increased, the carbonic acid content is also increased, and vice versa. If either bicarbonate or carbonic acid is increased or decreased so that the 20:1 ratio is no longer maintained, acid–base imbalance results. The kidneys The kidneys regulate the bicarbonate level in the ECF; they can regenerate bicarbonate ions as well as reabsorb them from the renal tubular cells. kidneys excrete hydrogen ions and conserve bicarbonate ions to help restore balance in respiratory and most cases of metabolic acidosis. In respiratory and metabolic alkalosis, the kidneys retain hydrogen ions and excrete bicarbonate ions to help restore balance. The kidneys The kidneys obviously cannot compensate for the metabolic acidosis created by renal failure. Renal compensation for imbalances is relatively slow (a matter of hours or days). The lungs Under the control of the medulla, the lungs control the CO2 and thus the carbonic acid content of the ECF by adjusting ventilation in response to the amount of CO2 in the blood. A rise in the partial pressure of CO2 in arterial blood (PaCO2) is a powerful stimulant to respiration. The lungs In metabolic acidosis, the respiratory rate increases, causing greater elimination of CO2 (to reduce the acid load). In metabolic alkalosis, the respiratory rate decreases, causing CO2 to be retained (to increase the acid load) Intracellular buffers Intracellular buffers include: Proteins organic and inorganic phosphates, in red blood cells, hemoglobin.  Acute & Chronic Metabolic Acidosis (Base bicarbonate deficit) Acute & Chronic Metabolic Acidosis (Base bicarbonate deficit) Metabolic acidosis is a common clinical disturbance characterized by a low pH (increased H+ concentration) and a low plasma bicarbonate concentration. It can be produced by a gain of hydrogen ion or a loss of bicarbonate. It can be divided clinically into two forms, according to the values of the serum anion gap: High & normal anion gap acidosis. The anion gap The anion gap reflects normally unmeasured anions (phosphates, sulfates, and proteins) in plasma. Measuring the anion gap is essential in analyzing acid–base disorders correctly. The anion gap can be calculated by either one of the following equations: Anion gap NA++ K+ - (Cl- + HCO3-) Anion gap Na+ - (Cl- + HCO3- ) Potassium is often omitted from the equation because of its low level in the plasma The normal value: anion gap = 8 to 12 mEq/L (8 to 12 mmol/L) without potassium in the equation. anion gap = 12 to 16 mEq/L (12 to 16 mmol/L) with potassium in the equation. Unmeasured anions in the serum account for less than 16 mEq/L of the anion production. Anion gap greater than 16 mEq (16 mmol/L) suggests excessive accumulation of unmeasured anions. An anion gap occurs because not all electrolytes are measured. More anions are left unmeasured than cations. Pathophysiology Normal anion gap acidosis results from the direct loss of bicarbonate, as in : diarrhea, lower intestinal fistulas, ureterostomies, use of diuretics; early renal insufficiency; excessive administration of chloride; administration of parenteral nutrition without bicarbonate or bicarbonate producing solutes (eg, lactate). Pathophysiology High anion gap acidosis results from excessive accumulation of fixed acid. If increased to 30 mEq/L (30 mmol/L) or more, then a high anion gap metabolic acidosis is present regardless of the values of pH and HCO3 –. High ion gap occurs in: ketoacidosis, lactic acidosis, late phase of salicylate poisoning, uremia, methanol or ethylene glycol toxicity, and ketoacidosis with starvation. The hydrogen is buffered by HCO3 – , causing the bicarbonate concentration to fall. In all of these instances, abnormally high levels of anions flood the system, increasing the anion gap above normal limits. Clinical Manifestations Signs and symptoms of metabolic acidosis vary with the severity of the acidosis but include: headache, confusion, drowsiness, increased respiratory rate and depth, nausea, vomiting. Peripheral vasodilation and decreased cardiac output occur when the pH drops to less than 7. Physical assessment findings include: decreased blood pressure, cold and clammy skin, dysrhythmias, shock. Chronic metabolic acidosis is usually seen with chronic renal failure. Assessment and Diagnostic Findings Expected blood gas changes include a low bicarbonate level (less than 22 mEq/L) and a low pH (less than 7.35) The cardinal feature of metabolic acidosis is a decrease in the serum bicarbonate level. Hyperkalemia may accompany metabolic acidosis as a result of the shift of potassium out of the cells. As the acidosis is corrected, potassium moves back into the cells and hypokalemia may occur. Hyperventilation decreases the CO2 level as a compensatory action. An ECG detects dysrhythmias caused by the increased potassium. Medical Management Treatment is directed at correcting the metabolic imbalance. If the problem results from excessive intake of chloride, treatment is aimed at eliminating the source of the chloride. When necessary, bicarbonate is administered. Although hyperkalemia occurs with acidosis, hypokalemia may occur with reversal of the acidosis and subsequent movement of potassium back into the cells. Thus, serum K level is monitored closely after acidosis is reversed.  In chronic metabolic acidosis, low serum calcium levels are treated before the chronic metabolic acidosis is treated, to avoid tetany resulting from an increase in pH and a decrease in ionized calcium. Alkalizing agents may be administered. Treatment modalities may also include hemodialysis or peritoneal dialysis. ACUTE & CHRONIC METABOLIC ALKALOSIS (BASE BICARBONATE EXCESS) Metabolic alkalosis Is a clinical disturbance characterized by a high pH (decreased H+ concentration) and a high plasma bicarbonate concentration. It can be produced by a gain of bicarbonate or a loss of H+ pH greater than 7.45 Serum HCO3-  wMost common cause - vomiting or gastric suction with loss of hydrogen and chloride ions. Pyloric stenosis, in which only gastric fluid is lost. Gastric fluid has an acid pH (usually 1 to 3), and loss of this highly acidic fluid increases the alkalinity of body fluids Other situations predisposing to metabolic alkalosis include those associated with loss of potassium, such as diuretic therapy that promotes excretion of potassium (e.g., thiazides, furosemide), and excessive adrenocorticoid hormones (as in hyperaldosteronism and Cushing’s syndrome). Other situations predisposing to metabolic alkalosis include Those associated with loss of potassium, such as diuretic therapy that promotes excretion of potassium (e.g., thiazides, furosemide), Excessive adrenocorticoid hormones (as in hyperaldosteronism and Cushing’s syndrome).  Hypokalemia produces alkalosis in two ways: 1. The kidneys conserve potassium, and therefore H excretion increases; Pathophysiology 2. Cellular potassium moves out of the cells into the ECF in an attempt to maintain near-normal serum levels (as potassium ions leave the cells, hydrogen ions must enter to maintain electroneutrality). Excessive alkali ingestion from antacids containing bicarbonate or from use of sodium bicarbonate during cardiopulmonary resuscitation can also cause metabolic alkalosis. Pathophysiology Chronic metabolic alkalosis can occur with: long-term diuretic therapy (thiazides or furosemide), villous adenoma, external drainage of gastric fluids, significant potassium depletion, cystic fibrosis, chronic ingestion of milk and calcium carbonate. Clinical Manifestations Alkalosis is primarily manifested by symptoms related to decreased calcium ionization, such as: tingling of the fingers and toes, dizziness, hypertonic muscles. The ionized fraction of serum calcium decreases in alkalosis as more calcium combines with serum proteins.  Hypocalcemia – predominant - because ionized fraction of calcium influences neuromuscular activity, neuromuscular s/sx also appear. Depressed respiration - as a compensatory action by the lungs. Atrial tachycardia may occur. As the pH increases and hypokalemia develops, ventricular disturbances may occur. Decreased motility and paralytic ileus may also be evident Symptoms of acute metabolic alkalosis are the same as for Acute metabolic alkalosis, and as potassium decreases, frequent premature ventricular contractions or U waves are seen on the ECG. Assessment and Diagnostic Findings Evaluation of arterial blood gases reveals a pH greater than 7.45 and a serum bicarbonate concentration greater than 26 mEq/L. The PaCO2 increases as the lungs attempt to compensate for the excess bicarbonate by retaining CO2. This hypoventilation is more pronounced in semiconscious, unconscious, or debilitated patients than in alert patients. The former may develop marked hypoxemia as a result of hypoventilation. Hypokalemia may accompany metabolic alkalosis. Assessment and Diagnostic Findings Urine chloride levels may help identify the cause of metabolic alkalosis if the patient’s history provides inadequate information. Metabolic alkalosis is the setting in which urine chloride concentration may be a more accurate estimate of fluid volume than the urine sodium concentration. Urine chloride concentrations help to differentiate between vomiting, diuretic therapy, and excessive adrenocorticosteroid secretion as the cause of the metabolic alkalosis. Assessment and Diagnostic Findings Urine chloride concentrations lower than 25 mEq/L, In patients with Vomiting cystic fibrosis, those receiving nutritional repletion, those receiving diuretic therapy, hypovolemia and hypochloremia Assessment and Diagnostic Findings 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. The urine chloride concentration should be less than 15 mEq/L when decreased chloride levels and hypovolemia occur. Medical Management Goal of Treatment of both acute and chronic metabolic alkalosis: Correcting the underlying acid–base disorder. Patient’s fluid I&O must be monitored carefully, (Due to volume depletion from the GI tract.) Sufficient chloride must be supplied for the kidney to absorb sodium with chloride (allowing the excretion of excess bicarbonate). Medical Management Treatment also includes restoring normal fluid volume by administering sodium chloride fluids (because continued volume depletion perpetuates the alkalosis). In patients with hypokalemia, potassium is administered as KCl to replace both K+ and Cl- losses. H2 receptor antagonists, such as cimetidine (Tagamet), reduce the production of gastric HCl, thereby decreasing the metabolic alkalosis associated with gastric suction. Carbonic anhydrase inhibitors are useful in treating metabolic alkalosis in patients who cannot tolerate rapid volume expansion (eg, patients with heart failure). ACUTE & CHRONIC RESPIRATORY ACIDOSIS (CARBONIC ACID EXCESS) Respiratory acidosis is a clinical disorder in which the pH is less than 7.35 and the PaCO2 is greater than 42 mm Hg. It may be either acute or chronic. pH PaC02 - H2 C03 Pathophysiology Respiratory acidosis is always due to inadequate excretion of CO2 with inadequate ventilation, resulting in elevated plasma CO2 concentrations and, consequently, increased levels of carbonic acid. Acute respiratory acidosis occurs in emergency situations, such as: Acute pulmonary edema, Aspiration of a foreign object, Atelectasis, Pneumothorax, Overdose of sedatives, sleep apnea, administration of oxygen to a patient with chronic hypercapnia (excessive CO2 in the blood), severe pneumonia, and acute respiratory distress syndrome Respiratory acidosis can also occur in diseases that impair respiratory muscles, such as: muscular dystrophy, Myasthenia gravis, Guillain-Barré syndrome. Mechanical ventilation may be associated with hypercapnia if the rate of ventilation is inadequate and CO2 retained. Clinical Manifestations Clinical signs in acute and chronic respiratory acidosis vary. Sudden hypercapnia (elevated PaCO2) can cause: increased pulse and respiratory rate, increased blood pressure, mental cloudiness, feeling of fullness in the head. An elevated PaCO2, greater than 60 mm Hg, causes cerebrovascular vasodilation and increased cerebral blood flow. Ventricular fibrillation may be the first sign of respiratory acidosis in anesthetized patients. Clinical Manifestations If respiratory acidosis is severe, intracranial pressure may increase, - papilledema and dilated conjunctival blood vessels. Hyperkalemia due to increased hydrogen concentration more than + the compensatory mechanisms and H moves into cells, causing a shift of potassium out of the cell. Clinical manifestations Chronic respiratory acidosis occurs with pulmonary diseases such a: chronic emphysema and bronchitis, obstructive sleep apnea, obesity. As long as the PaCO2 does not exceed the body’s ability to compensate, the patient will be asymptomatic. If the PaCO2 increases rapidly, cerebral vasodilation will increase the intracranial pressure, and cyanosis and tachypnea will develop. Clinical Manifestations Patients with chronic obstructive pulmonary disease (COPD) who gradually accumulate CO2 over a prolonged period (days to months) may not develop symptoms of hypercapnia because compensatory renal changes have had time to occur. Reminder: If the PaCO2 is chronically higher than 50 mm Hg, the respiratory center becomes relatively insensitive to CO2 as a respiratory stimulant, leaving hypoxemia as the major drive for respiration. Oxygen administration may remove the stimulus of hypoxemia, and the patient develops “carbon dioxide narcosis” unless the situation is quickly reversed. Therefore, oxygen is administered only with extreme caution. Assessment and Diagnostic Findings Arterial blood gas analysis reveals a pH lower than 7.35, a PaCO2 greater than 42 mm Hg, and a variation in the bicarbonate level, depending on the duration of the acute respiratory acidosis. When compensation (renal retention of bicarbonate) has fully occurred, the arterial pH is within the lower limits of normal. Depending on the cause of respiratory acidosis, other diagnostic measures include: monitoring of serum electrolyte levels, chest xray for determining any respiratory disease, drug screen if an overdose is suspected. An ECG to identify any cardiac involvement as a result of COPD may be indicated as well. Medical Management Treatment is directed at improving ventilation; exact measures vary with the cause of inadequate ventilation. Pharmacologic agents are used as indicated. For example: bronchodilators help reduce bronchial spasm, antibiotics are used for respiratory infections, thrombolytics or anticoagulants are used for pulmonary emboli Medical Management Pulmonary hygiene measures are initiated, when necessary, to clear the respiratory tract of mucus and purulent drainage. Adequate hydration (2 to 3 L/day) is indicated to keep the mucous membranes moist and thereby facilitate the removal of secretions. Supplemental oxygen is administered as necessary. Mechanical ventilation, used appropriately, may improve pulmonary ventilation. Inappropriate mechanical ventilation (eg, increased dead space, insufficient rate or volume settings, high fraction of inspired oxygen [FiO2] with excessive CO2 production) may cause such rapid excretion of CO2 that the kidneys are unable to eliminate excess bicarbonate quickly enough to prevent alkalosis and seizures. Medical management the elevated PaCO2 must be decreased slowly. Placing the patient in a semi-Fowler’s position facilitates expansion of the chest wall. Treatment of chronic respiratory acidosis is the same as for acute respiratory acidosis. ACUTE & CHRONIC RESPIRATORY ALKALOSIS (CARBONIC ACID DEFICIT) Respiratory alkalosis is a clinical condition in which the arterial pH is greater than 7.45 and the PaCO2 is less than 38 mm Hg. As with respiratory acidosis, acute and chronic conditions can occur. pH 7.45 PaCO2 than 38mmHg Pathophysiology Respiratory alkalosis is always caused by hyperventilation, which causes excessive “blowing off” of CO2 and, hence, a decrease in the plasma carbonic acid concentration. Causes include: extreme anxiety, hypoxemia, early phase of salicylate intoxication, gram-negative bacteremia, inappropriate ventilator settings that do not match the patient’s requirements. Chronic respiratory alkalosis results from chronic hypocapnia, and decreased serum bicarbonate levels are the consequence. Chronic hepatic insufficiency and cerebral tumors are predisposing factors. Clinical Manifestations Clinical signs consist of: lightheadedness due to vasoconstriction and decreased cerebral blood flow, inability to concentrate, numbness and tingling from decreased calcium ionization, tinnitus, sometimes loss of consciousness. Cardiac effects of respiratory alkalosis include tachycardia and ventricular and atrial dysrhythmias Assessment and Diagnostic Findings Analysis of arterial blood gases assists in the diagnosis of respiratory alkalosis. In the acute state, the pH is elevated above normal as a result of a low PaCO2 and a normal bicarbonate level. (The kidneys cannot alter the bicarbonate level quickly.) In the compensated state, the kidneys have had sufficient time to lower the bicarbonate level to a near-normal level. Assessment and Diagnostic Findings Evaluation of serum electrolytes is indicated to identify any decrease in potassium, as hydrogen is pulled out of the cells in exchange for potassium; decreased calcium, as severe alkalosis inhibits calcium ionization, resulting in carpopedal spasms and tetany; or decreased phosphate due to alkalosis, causing an increased uptake of phosphate by the cells. A toxicology screen should be performed to rule out salicylate intoxication. Patients with chronic respiratory alkalosis are usually asymptomatic, and the diagnostic evaluation and plan of care are the same as for acute respiratory alkalosis. Medical Management Treatment depends on the 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). A sedative may be required to relieve hyperventilation in very anxious patients. Treatment of other causes of respiratory alkalosis is directed at correcting the underlying problem.  MIXED ACID-BASE DISORDERS Patients can simultaneously experience two or more independent acid– base disorders. A normal pH in the presence of changes in the PaCO2 and plasma HCO3 – concentration immediately suggests a mixed disorder. Example: The simultaneous occurrence of metabolic acidosis and respiratory acidosis during respiratory and cardiac arrest. The only mixed disorder that cannot occur is a mixed respiratory acidosis and alkalosis, because it is impossible to have alveolar hypoventilation and hyperventilation at the same time. 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. The kidneys compensate for respiratory disturbances by altering bicarbonate retention and H secretion. Compensation In respiratory acidosis, excess hydrogen is excreted in the urine in exchange for bicarbonate ions. In respiratory alkalosis, the renal excretion of bicarbonate increases, and hydrogen ions are retained. In metabolic acidosis, the compensatory mechanisms increase the ventilation rate and the renal retention of bicarbonate. In metabolic alkalosis, the respiratory system compensates by decreasing ventilation to conserve CO2 and increase the PaCO2. Because the lungs respond to acid–base disorders within minutes, compensation for metabolic imbalances occurs faster than compensation for respiratory imbalances. Blood Gas Analysis Blood gas analysis is to identify the specific acid–base disturbance and the degree of compensation that has occurred. It is based on an arterial blood sample, but if an arterial sample cannot be obtained, a mixed venous sample may be used. Results of arterial blood gas analysis provide information about alveolar ventilation, oxygenation, and acid–base balance. pH 7.54 PaC02 37 mmHg Hc03 31 mEq/L Answer: ______________ pH 7.33 PaC02 45mmHg Hc03 18 mEq/L Answer: ______________ Blood Gas Analysis It is necessary to evaluate the concentrations of serum electrolytes (sodium, potassium, and chloride) and carbon dioxide along with arterial blood gas data, because they are often the first sign of an acid–base disorder. Therefore: Serum electrolytes + ABG data = acid-base disorders Blood Gas Analysis The health history, physical examination, previous blood gas results, serum electrolytes Listed above 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 conditions usually corrects acid-base disorders. END OF TOPIC NEXT TOPIC: PARENTHERAL THERAPY