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Description : Overview of Acid-Base Balance

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Published on : Feb 26, 2021 | Views : 3621 | Downloads : 55

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Acid–Base Disorders And Electrolyte Imbalance
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Hydrogen Ion Concentration & pH Arterial [H+] is normally 40 nEq/L Hydrogen ion concentration is more commonly expressed as pH, which is defined as the negative logarithm (base 10) of [H+] Normal arterial pH is therefore –log (40 × 10−9) = 7.40.
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Because the pH scale is logarithmic, a small change in pH represents a much larger change in [H+]: A small reduction in pH from 7.4 to 7.0 represents more than a doubling of H+ concentration, from 40 to 100 nmol/L. Acidaemia is defined as an arterial pH below 7.35. Alkalaemia is defined as an arterial pH above 7.45.
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Henderson–Hasselbalch equation
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Compensatory Mechanisms Physiological responses to changes in [H+] are characterized by three phases: (1) immediate chemical buffering, (2) respiratory compensation (whenever possible) (3) a slower but more effective renal compensatory response that may nearly normalize arterial pH even if the pathological process remains present.
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BODY BUFFERS Physiologically important buffers in humans include: bicarbonate (H2CO3/HCO3−), hemoglobin (HbH/ Hb−), other intracellular proteins (PrH/Pr−), phosphates (H2PO4−/HPO42−), and ammonia (NH3/NH4+).
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- Bicarbonate is the most important buffer in the extracellular fluid compartment (effective against metabolic but not respiratory acid–base disturbances.) - Hemoglobin, though restricted inside red blood cells, also functions as an important buffer in blood. - Phosphate and ammonium ions are important urinary buffers.
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RESPIRATORY COMPENSATION Changes in alveolar ventilation responsible for the respiratory compensation of Paco2 are mediated by chemoreceptors within the brainstem. These receptors respond to changes in cerebrospinal spinal fluid pH. Minute ventilation increases 1–4 L/min for every (acute) 1 mm Hg increase in Paco2. Respiratory compensatory responses are also important in defending against marked changes in pH during metabolic disturbances.
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Renal Compensation During Acidosis (1) increased reabsorption of the filtered HCO3− (2) increased excretion of titratable acids (3) increased production of ammonia. Although these mechanisms are probably activated immediately, their effects are generally not appreciable for 12–24 hr and may not be maximal for up to 5 days.
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Renal Compensation During Alkalosis Tremendous amount of HCO3 − normally filtered and subsequently reabsorbed allows the kidneys to rapidly excrete large amounts of bicarbonate, if necessary. Metabolic alkalosis is commonly associated with increased mineralo-corticoid activity
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RESPIRATORY ACIDOSIS Respiratory acidosis is defined as a primary increase in Paco2. This increase drives the reaction: H2O+CO2 ↔H2CO3 ↔H+ +HCO3− leading to an increase in [H+] and a decrease in arterial pH. [HCO3−] is minimally affected.
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Acute Respiratory Acidosis The compensatory response to acute (6–12 h) elevations in Paco2 is limited. Buffering is primarily provided by hemoglobin and the exchange of extracellular H+ for Na+ and K+ from bone and the intracellular fluid compartment The renal response to retain more bicarbonate is acutely very limited. As a result, plasma [HCO3−] increases only about 1 mEq/L for each 10 mm Hg increase in Paco2 above 40 mm Hg.
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Chronic Respiratory Acidosis “Full” renal compensation characterizes chronic respiratory acidosis. Renal compensation is appreciable only after 12–24 hr and may not peak until 3–5 days. During chronic respiratory acidosis, plasma [HCO3−] increases approximately 4 mEq/L for each 10 mm Hg increase in Paco2 above 40 mm Hg.
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METABOLIC ACIDOSIS Metabolic acidosis is defined as a primary decrease in [HCO3−] Pathological processes can initiate metabolic acidosis by one of three mechanisms: (1) consumption of HCO3− by a strong nonvolatile acid (2) renal or gastrointestinal wasting of bicarbonate (3) rapid dilution of the extracellular fluid compartment with a bicarbonate-free fluid.
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Pulmonary compensatory response in a simple metabolic acidosis characteristically does not reduce Paco2 to a level that completely normalizes pH but can produce marked hyperventilation (Kussmaul’s respiration).
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The Anion Gap Anion gap = major plasma cations − major plasma anions Anion gap =[Na+ ]−([Cl− ]+[HCO 3− ]) The anion gap decreases by 2.5 mEq/L for every 1 g/dL reduction in plasma albumin concentration.
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High Anion Gap Metabolic Acidosis Metabolic acidosis with an increased anion gap is characterized by an increase in relatively strong nonvolatile acids. These acids dissociate into H+ and their respective anions; the H+ consumes HCO3− to produce CO2, whereas their anions (conjugate bases) accumulate and take the place of HCO3− in extracellular fluid (hence the anion gap increases). Nonvolatile acids can be endogenously produced or ingested.
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A. Failure to Excrete Endogenous Nonvolatile Acids Endogenously produced organic acids are normally eliminated by the kidneys in urine. Glomerular filtration rates below 20 mL/min (renal failure) typically result in progressive metabolic acidosis from the accumulation of these acids.
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B. Increased Endogenous Nonvolatile Acid Production Severe tissue hypoxia following hypoxemia, hypoperfusion (ischemia), or an inability to utilize oxygen (cyanide poisoning) can result in lactic acidosis. Decreased utilization of lactate by the liver, and, to a lesser extent by the kidneys, is less commonly responsible for lactic acidosis; causes include hypoperfusion, alcoholism, and liver disease.
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Ketoacidosis: An absolute or relative lack of insulin can result in hyperglycemia and progressive ketoacidosis from the accumulation of β-hydroxybutyric and aceto- acetic acids. Ketoacidosis may also be seen following starvation and alcoholic binges.
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Ingestion of Exogenous Nonvolatile Acids Ingestion of large amounts of salicylates frequently results in metabolic acidosis. Salicylic acid and other acid intermediates rapidly accumulate and produce a high anion gap acidosis. Because salicylates also produce direct respiratory stimulation, most adults develop mixed metabolic acidosis with superimposed respiratory alkalosis. Ingestion of methanol (methyl alcohol) frequently produces acidosis and visual disturbances (retinitis).
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Normal Anion Gap Metabolic Acidosis Metabolic acidosis associated with a normal anion gap is typically characterized by hyperchloremia. Plasma [Cl−] increases to take the place of the HCO3− ions that are lost. Hyperchloremic metabolic acidosis most commonly results from abnormal gastrointestinal or renal losses of HCO3−, or from excessive intravenous administration of 0.9% NaCl solution.
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ANESTHETIC CONSIDERATIONS IN PATIENTS WITH ACIDOSIS Acidemia can potentiate the depressant effects of most sedatives and anesthetic agents on the central nervous and circulatory systems. Because most opioids are weak bases, acidosis can increase the fraction of the drug in the nonionized form and facilitate penetration of the opioid into the brain.
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ANESTHETIC CONSIDERATIONS IN PATIENTS WITH ACIDOSIS Circulatory depressant effects of both volatile and intravenous anesthetics can also be exaggerated. Halothane is more arrhythmogenic in the presence of acidosis. Succinylcholine should generally be avoided in acidotic patients with hyperkalemia to prevent further increases in plasma [K+].
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RESPIRATORY ALKALOSIS Respiratory alkalosis is defined as a primary decrease in Paco2. Mechanism is usually an inappropriate increase in alveolar ventilation relative to CO2 production.
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Metabolic alkalosis Defined as a primary increase in plasma [HCO3−]. Most cases of metabolic alkalosis can be divided into: (1) those associated with NaCl deficiency and extracellular fluid depletion (often described as chloride sensitive) (2) those associated with enhanced mineralocorticoid activity, commonly referred to as chloride-resistant
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ANESTHETIC CONSIDERATIONS IN PATIENTS WITH ALKALEMIA Respiratory alkalosis seems to prolong the duration of opioid-induced respiratory depression; this effect may result from increased protein binding of opioids. Cerebral ischemia can occur from marked reduction in cerebral blood flow during respiratory alkalosis, particularly during hypotension
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Cont.. . The combination of alkalemia and hypokalemia can precipitate severe atrial and ventricular arrhythmias. Potentiation of nondepolarizing neuromuscular blockade is reported with alkalemia, but may be more directly related to concomitant hypokalemia.
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DIAGNOSIS OF ACID-BASE DISORDERS Interpretation of acid–base status from analysis of blood gases requires a systematic approach 1. Examine arterial pH: Is acidemia or alkalemia present? 2. Examine Paco2: Is the change in Paco2 consistent with a respiratory component? 3. If the change in Paco2 does not explain the change in arterial pH, does the change in [HCO3−] indicate a metabolic component? 4. Make a tentative diagnosis. 5. Compare the change in [HCO3−] with the change in Paco2. Does a compensatory response exist?
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Values obtained by routine blood gas measurement include oxygen and carbon dioxide tensions (Po2 and Pco2), pH, [HCO3−], base excess, hemoglobin, and the percentage oxygen saturation of hemoglobin. As a rule, only Po2, Pco2, and pH are measured. Hemoglobin and percentage oxygen saturation are measured with a cooximeter. [HCO3−] is derived using the Henderson–Hasselbalch equation and base excess from the Siggaard–Andersen nomogram. MEASUREMENT OF BLOOD GAS TENSIONS & pH
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Electrolyte Abnormalities: Potassium, Sodium, Calcium,
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Potassium The total body potassium store in a 70-kg person exceeds 3500 mEq, with less than 2% located in extracellular uid. Potassium balance is primarily maintained by oral intake and renal elimination. Extracellular potassium is dependent on multiple factors, including acid-base balance, the activity and sensitivity of insulin, sodium-potassium adenosine triphosphate dependent exchange channels, and blood insulin and catecholamine levels.
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HYPERKALEMIA The most signicant clinical effect of hyperkalemia involves the electrical conduction system of the heart. These changes include gradual prolongation of the PR interval (with eventual loss of the P wave), prolongation of the QRS complex, ST- segment elevation, and peaking of T waves that can ultimately lead to ventricular arrhythmias
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. Cardiac conduction changes usually occur when the plasma potassium concentration exceeds 6.5 mmol/L, but they may develop at lower levels in the setting of acute hyperkalemia. Options for acute management rely on membrane stabilization and intracellular shifting of potassium and include administration of calcium chloride, sodium bicarbonate, and insulin with glucose
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HYPOKALEMIA For every 1-mmol/L decrease in plasma potassium concentration, the total body potassium store decreases by approximately 200 to 300 mmol. Characteristic electrocardiographic changes associated with hypokalemia include gradual prolongation of the QRS interval, with subsequent development of prominent U waves.
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Hypokalemia Hypokalemia is associated with an increased incidence of atrial and ventricular arrhythmias, and low serum potassium has also been associated with worsening outcomes in the setting of acute myocardial infarction. Hypokalemia may be associated with weakness and potentiate the effect of neuromuscular blocking agents.
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Treatment: To treat hypokalemia, the clinician must consider the patient’s total body potassium levels and the chronicity of the hypokalemia. Intravenous potassium replacement should be gradual to avoid acute overcorrection and hyperkalemia. Respiratory and metabolic alkalosis should be avoided because alkalosis will worsen hypokalemia secondary to intracellular shifting.
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Sodium Serum sodium concentration is dependent on the relationship of total body sodium levels and total body water. Therefore the treatment of abnormal serum sodium concentrations must take into account both total body sodium stores and total body water.
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HYPERNATREMIA Hypernatremia is defined as serum sodium concentration of greater than 145 mmol/L and is often associated with a deficiency in total body water. Manifestations of hypernatremia include mental status changes, hyperreflexia, ataxia, and seizures. Free water deficit can be calculated as follows: free water deficit, in liters = (0.6 × weight, in kg) × ([serum sodium/140] − 1).
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Treatment: Free water is administered to correct hypernatremia, although treatment of severe central diabetes insipidus may involve the use of subcutaneously or intravenously administered vasopressin. In the setting of hypervolemic hypernatremia, diuretics may be required to allow for elimination of both water and sodium while free water is administered.
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HYPONATREMIA Hyponatremia is a serum sodium concentration of less than 135 mmol/L. Hyponatremia may present with mental status changes, lethargy, cramps, decreased deep tendon reflexes, and seizures. A serum sodium concentration of less than 120 mmol/L is a potentially life-threatening condition, with associated mortality rates reported to be as high as 50%.
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If the correction of hyponatremia occurs too rapidly, a demyelinating brainstem lesion—central pontine myelinolysis—may cause permanent neurologic damage. In severely symptomatic patients, the recommendation is to correct sodium at a rate of 1 to 2 mmol·L−1·h−1 until the serum sodium concentration reaches 125 to 130 mmol/L. In hypervolemic or euvolemic hyponatremia, hypertonic (2%–3%) saline may be used to treat symptomatic patients or patients who would not tolerate additional intravascular volume. Management:
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Calcium The total serum calcium concentration comprises three fractions: 50% protein-bound calcium, 5% to 10% anion-bound calcium, and 40% to 45% free, or ionized, calcium. Maintenance of a normal serum calcium concentration involves parathyroid hormone and calcitonin, which regulate the release and uptake of calcium and phosphorus by the kidneys, bones, and intestines through negative-feedback regulation.
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HYPERCALCEMIA Common causes of hypercalcemia include hyperparathyroidism and malignancies that increase mobilization of calcium from bone. Symptoms include nausea, polyuria, and dehydration. Electrocardiographic monitoring may demonstrate prolonged PR intervals, wide QRS complexes, and shortened QT intervals as hypercalcemia worsens.
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Avoidance of respiratory alkalosis may be beneficial because alkalosis lowers the plasma potassium concentration, potentially exacerbating cardiac conduction abnormalities. Management of hypercalcemia includes hydration and diuresis to promote renal elimination. In acute toxicity or renal failure, hemodialysis should be considered.
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HYPOCALCEMIA Multiple factors contribute to the development of hypocalcemia: Acquired hypoparathyroidism after neck surgery is a common cause of hypocalcemia because of decreased parathyroid hormone levels. Respiratory or metabolic alkalosis induces hypocalcemia by increasing protein binding to calcium, thereby decreasing the amount of ionized calcium.
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Renal failure decreases the conversion of vitamin D to 1,25-dihydroxyvitamin D, thereby decreasing intestinal and bone absorption while increasing serum phosphate levels; the phosphate then combines with calcium and precipitates as CaPO4 Massive blood transfusion may also result in hypocalcemia secondary to anticoagulants (ethylenediaminetetra-acetic acid in transfused blood, which chelates calcium).
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. Hypocalcemia is often asymptomatic, although severe hypocalcemia may be associated with a prolonged QT interval, bradycardia, peripheral vasodilation, and decreased cardiac contractility, any of which can cause hypotension. Neurologic manifestations of hypocalcemia include perioral numbness, muscle cramps, tetany, hyperreexia, and seizures.
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Management: Several factors guide calcium replacement therapy, including the absolute serum calcium level, the rapidity of the drop in serum calcium concentration, and the underlying disease process. Calcium causes vasoconstriction, and extravascular infiltration may be associated with morbidity. In patients who have no symptoms, observation may be the most appropriate treatment. Calcium chloride contains three times the amount of calcium compared with calcium gluconate.
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Reference: