Disorders of Fluid, Electrolyte, & Acid-Base Balance PDF

Disorders of Fluid, Electrolyte, & Acid-Base Balance Chapter 8 Prof. Dr. Mustafa Ghazi Alabbassi 1 Fluids and electrolytes are present in body cells, in the tissue spaces between the cells, and in the blood that fills the vascular compartment. Prof...

Disorders of Fluid, Electrolyte, & Acid-Base Balance Chapter 8 Prof. Dr. Mustafa Ghazi Alabbassi 1 Fluids and electrolytes are present in body cells, in the tissue spaces between the cells, and in the blood that fills the vascular compartment. Prof. Dr. Mustafa Ghazi Alabbassi 2 Body fluids transport gases, nutrients, and wastes; help generate the electrical activity needed to power body functions; take part in the transforming of food into energy; and otherwise maintain the overall function of the body. Prof. Dr. Mustafa Ghazi Alabbassi 3 Introductory Concepts Dissociation of Electrolytes: Electrolytes are substances that dissociate in solution to form charged particles, or ions. For example, a sodium chloride (NaCl) molecule dissociates to form a positively charged Na and a negatively charged Cl ion. Prof. Dr. Mustafa Ghazi Alabbassi 4 Particles that do not dissociate into ions such as glucose and urea are called nonelectrolytes. Positively charged ions are called cations because they are Prof. Dr. Mustafa Ghazi Alabbassi 5 attracted to the cathode of a wet electric cell, and negatively charged ions are called anions because they are attracted to the anode. Prof. Dr. Mustafa Ghazi Alabbassi 6 However, cations and anions may be exchanged for one another, providing they carry the same charge. For example, Prof. Dr. Mustafa Ghazi Alabbassi 7 A positively charged hydrogen ion (H) may be exchanged for a positively charged K and a negatively charged bicarbonate ion (HCO3 ) may be exchanged for a negatively charged chloride ion (Cl). Prof. Dr. Mustafa Ghazi Alabbassi 8 Diffusion: is the movement of charged or uncharged particles along a concentration gradient. Osmosis: Osmosis is the movement of water across a semipermeable membrane (i.e., one that is permeable to water but impermeable to most solutes). Prof. Dr. Mustafa Ghazi Alabbassi 9 Prof. Dr. Mustafa Ghazi Alabbassi 10 Tonicity: refers to the tension or effect that the effective osmotic pressure of a solution with impermeable solutes exerts on cell size because of water movement across the cell membrane. (The ability of extracellular solution to make water move into or out of the cell by osmosis). Prof. Dr. Mustafa Ghazi Alabbassi 11 Prof. Dr. Mustafa Ghazi Alabbassi 12 Compartmental Distribution of Body Fluids Body water, which constitutes a high percentage of body weight, is distributed between the ICF and ECF compartments. Prof. Dr. Mustafa Ghazi Alabbassi 13 In the adult, the fluid in the ICF compartment constitutes approximately 40% of body weight and that in the ECF approximately 20% of body weight. Prof. Dr. Mustafa Ghazi Alabbassi 14 Prof. Dr. Mustafa Ghazi Alabbassi 15  Capillary/Interstitial Fluid Exchange The transfer of water between the vascular and interstitial compartments occurs at the capillary level. There are four main forces that control the movement of water between the capillary and interstitial spaces: Prof. Dr. Mustafa Ghazi Alabbassi 16 (1) The capillary filtration pressure, which pushes water out of the capillary into the interstitial spaces. (2) The capillary colloidal osmotic pressure, which pulls water back into the capillary. Prof. Dr. Mustafa Ghazi Alabbassi 17 (3) The interstitial or tissue hydrostatic pressure, which opposes the movement of water out of the capillary. (4) The interstitial colloidal osmotic pressure, which pulls water out of the capillary into the interstitial spaces. Prof. Dr. Mustafa Ghazi Alabbassi 18 Edema It can be defined as palpable swelling produced by an increase in interstitial fluid volume. Edema does not become evident until the interstitial volume has been increased by 2.5 to 3 L. Prof. Dr. Mustafa Ghazi Alabbassi 19 Prof. Dr. Mustafa Ghazi Alabbassi 20 The physiologic mechanisms that contribute to edema formation include factors that: Prof. Dr. Mustafa Ghazi Alabbassi 21 A. increase the capillary filtration pressure. Due to: (1) Increased arterial pressure. (2) Increase in venous pressure. (3) Capillary distention due to increased vascular volume. Prof. Dr. Mustafa Ghazi Alabbassi 22  Examples on edema caused due to increased capillary pressure: Increase vascular volume(HF, kidney disease, premenstrual sodium retention, pregnancy, environmental heat stress). Venous obstruction(liver disease with portal vein obstruction). Calcium channel blockers(decrease arteriolar resistance). Prof. Dr. Mustafa Ghazi Alabbassi 23 Prof. Dr. Mustafa Ghazi Alabbassi 24 B. Decrease the capillary colloidal osmotic pressure. Edema caused by decreased capillary colloidal osmotic pressure Prof. Dr. Mustafa Ghazi Alabbassi 25 usually is the result of inadequate production or abnormal loss of plasma proteins, mainly albumin. The plasma proteins are synthesized in the liver. Prof. Dr. Mustafa Ghazi Alabbassi 26 This type of edema concerned with liver disease(decrease production of protein) , kidney disease, extensive burns as well as starvation or malnutrition. Prof. Dr. Mustafa Ghazi Alabbassi 27 C. Increase capillary permeability. When the capillary pores become enlarged or the integrity of the capillary wall is damaged, capillary permeability is increased. Prof. Dr. Mustafa Ghazi Alabbassi 28 When this occurs, plasma proteins and other osmotically active particles leak into the interstitial spaces, increasing the tissue colloidal osmotic pressure and thereby contributing to the accumulation of interstitial fluid. Prof. Dr. Mustafa Ghazi Alabbassi 29 Among the conditions that increase capillary permeability are burn injury, capillary congestion, inflammation, and immune responses. Prof. Dr. Mustafa Ghazi Alabbassi 30 D. Obstruction of lymph flow. Edema due to impaired lymph flow is commonly referred to as lymphedema. Prof. Dr. Mustafa Ghazi Alabbassi 31  Note: ( plasma proteins and other large particles that cannot be reabsorbed through the pores in the capillary membrane rely on the lymphatic system for movement back into the circulatory system). Prof. Dr. Mustafa Ghazi Alabbassi 32 Prof. Dr. Mustafa Ghazi Alabbassi 33 Regulation of Water Balance Total body water (TBW) accounts for approximately 60% of body weight. Individual water content varies with the amount of adipose tissue, which is essentially water free (i.e., fat is approximately 10% water composition compared with skeletal muscle, which is 75%). Prof. Dr. Mustafa Ghazi Alabbassi 34 Infants normally have more TBW than older children or adults. TBW constitutes approximately 75% to 80% of body weight in full-term infants and is even greater in premature infants. Prof. Dr. Mustafa Ghazi Alabbassi 35 Gain & Loses of Water Regardless of age, all healthy persons require approximately 100 mL of water per 100 calories metabolized for dissolving and eliminating metabolic wastes. Prof. Dr. Mustafa Ghazi Alabbassi 36 This means that a person who expends 1800 calories for energy requires approximately 1800 mL of water for metabolic purposes. Prof. Dr. Mustafa Ghazi Alabbassi 37 Normally, the largest loss of water occurs through the kidneys, with lesser amounts being lost through the skin, lungs, and gastrointestinal tract. Prof. Dr. Mustafa Ghazi Alabbassi 38 Even when oral or parenteral fluids are withheld, the kidneys continue to produce urine as a means of ridding the body of metabolic wastes. Prof. Dr. Mustafa Ghazi Alabbassi 39 Regulation of Sodium Balance Sodium is the most plentiful electrolyte in the ECF compartment with a concentration ranging from 135 to 145 mEq/L (135 to145 mmol/L). In contrast, only a small amount (10 to 14 mEq/L [10 to 14 mmol/L]) is located in the ICF compartment. Prof. Dr. Mustafa Ghazi Alabbassi 40 Sodium functions mainly in regulating the ECF volume. As the major cation in the ECF compartment, Na and its attendant anions (Cl and HCO3) account for approximately 90% to 95% of the osmotic activity in the ECF. Prof. Dr. Mustafa Ghazi Alabbassi 41 Because sodium is part of the sodium bicarbonate molecule, it is important in regulating acid-base balance, and as a current-carrying ion, it contributes to the function of the nervous system and other excitable tissue. Prof. Dr. Mustafa Ghazi Alabbassi 42 Gain & Losses of Sodium Sodium normally enters the body through the gastrointestinal tract and is eliminated by the kidneys or lost from the gastrointestinal tract or skin. Prof. Dr. Mustafa Ghazi Alabbassi 43 Sodium intake normally is derived from dietary sources. Body needs for sodium usually can be met by as little as 500 mg/day. Prof. Dr. Mustafa Ghazi Alabbassi 44 Regulation of Potassium Balance Potassium balance is strongly influenced by dietary intake and urine output. In healthy persons, potassium balance usually can be maintained by a daily dietary intake of 50 to 100 mEq(Formula: mg= mEq*atomic weight / valence). Prof. Dr. Mustafa Ghazi Alabbassi 45 Additional amounts of potassium are needed during periods of trauma and stress. The kidneys are the main source of potassium loss. Approximately 80% to 90% of potassium losses occur in the urine, with the remainder being lost in stools or sweat. Prof. Dr. Mustafa Ghazi Alabbassi 46  Mechanism of Potassium Regulation Normally, the ECF concentration of potassium is precisely regulated at about 4.2 mEq/L (4.2 mmol/L). The precise control is necessary because many cell functions are sensitive to even small changes in ECF potassium levels. Prof. Dr. Mustafa Ghazi Alabbassi 47 An increase in potassium of as small an amount as 0.3 to 0.4 mEq/L can cause serious cardiac arrhythmias and even death. Prof. Dr. Mustafa Ghazi Alabbassi 48 Serum potassium levels are largely regulated through two mechanisms:(1) renal mechanisms that conserve or eliminate potassium and (2) a transcellular shift between the ICF and ECF compartments. Prof. Dr. Mustafa Ghazi Alabbassi 49  Disorders of Antidiuretic Hormone There are two main physiologic mechanisms that contribute directly to the regulation of body water and indirectly to the regulation of sodium: thirst and ADH. Prof. Dr. Mustafa Ghazi Alabbassi 50 Thirst is primarily a regulator of water intake and ADH a regulator of water output. Both mechanisms respond to changes in ECF osmolality(the concentration of a solution expressed as the total number of solute particles per kilogram) and the effective circulating volume. Prof. Dr. Mustafa Ghazi Alabbassi 51 Prof. Dr. Mustafa Ghazi Alabbassi 52 The reabsorption of water by the kidneys is regulated by ADH, also known as vasopressin. ADH is a small peptide, that is synthesized by cells in the hypothalamus and then transported along a neural pathway (i.e., hypothalamic-hypophysial tract) to the posterior pituitary gland, where it is stored. Prof. Dr. Mustafa Ghazi Alabbassi 53 ADH levels are controlled by ECF volume and osmolality. Osmoreceptors in the hypothalamus sense changes in ECF osmolality and stimulate the production and release of ADH. Prof. Dr. Mustafa Ghazi Alabbassi 54 ADH exerts its effects through three types of vasopressin (V) receptors—V1, V2, and V3 receptors. V1 receptors, which are located in vascular smooth muscle, cause vasoconstriction—hence the name vasopressin. Prof. Dr. Mustafa Ghazi Alabbassi 55 The distal and collecting tabules of the kidney express V2 receptors, which mediate water retention. ADH acts on the luminal membranes of the distal and collecting tubules to increase their permeability to water. Prof. Dr. Mustafa Ghazi Alabbassi 56 The increased water permeability allows water to be reabsorbed from the tubular cells and makes the urine more concentrated or hyperosmotic. Prof. Dr. Mustafa Ghazi Alabbassi 57 V3 receptors are mainly found in the central nervous system (CNS), especially in the anterior pituitary gland, where their stimulation modulates corticotrophin release. Prof. Dr. Mustafa Ghazi Alabbassi 58  The abnormal synthesis and release of ADH occurs in a number of stress situations. Severe pain, nausea, trauma, surgery, certain anesthetic agents, and some narcotics (e.g., morphine and meperidine) increase ADH levels. Among the drugs that affect ADH are nicotine, which stimulates its release, and alcohol, which inhibits it. Prof. Dr. Mustafa Ghazi Alabbassi 59 Two important conditions alter ADH levels: diabetes insipidus and the syndrome of inappropriate secretion of ADH. Prof. Dr. Mustafa Ghazi Alabbassi 60 Diabetes Insipidus(DI) It is caused by a deficiency of or a decreased response to ADH. Persons with DI are unable to concentrate their urine during periods of water restriction and they excrete large volumes of urine, Prof. Dr. Mustafa Ghazi Alabbassi 61 usually 3 to 20 L/day, depending on the degree of ADH deficiency or renal insensitivity to ADH. This large urine output is accompanied by excessive thirst. Prof. Dr. Mustafa Ghazi Alabbassi 62 The danger arises when the condition develops in someone who is unable to communicate the need for water. In such cases, inadequate fluid intake rapidly leads to increased serum osmolality and hypertonic dehydration. Prof. Dr. Mustafa Ghazi Alabbassi 63 There are two types of DI: neurogenic or central DI, which occurs because of a defect in the synthesis or release of ADH, and nephrogenic DI, which occurs because the kidneys do not respond to ADH. Prof. Dr. Mustafa Ghazi Alabbassi 64 The manifestations of DI include complaints of intense thirst, especially with a craving for ice water, and polyuria, the volume of ingested fluids ranging from 2 to 20 L daily with corresponding large urine volumes. Prof. Dr. Mustafa Ghazi Alabbassi 65 DI may present with hypernatremia and dehydration, especially in persons without free access to water, or with damage to the hypothalamic thirst center and altered thirst sensation. Prof. Dr. Mustafa Ghazi Alabbassi 66 The management of central or neurogenic DI depends on the cause and severity of the disorder. Many persons with incomplete neurogenic DI maintain near- normal water balance when permitted to ingest water in response to thirst. Prof. Dr. Mustafa Ghazi Alabbassi 67  Pharmacologic preparations of ADH are available for persons who cannot be managed by conservative measures. The preferred drug for treating chronic DI is desmopressin acetate (DDAVP). It usually is given orally, but is also available in parenteral and nasal forms. Prof. Dr. Mustafa Ghazi Alabbassi 68  The oral antidiabetic agent chlorpropamide may be used to stimulate ADH release in partial neurogenic DI. It usually is reserved for special cases because of its ability to cause hypoglycemia. Prof. Dr. Mustafa Ghazi Alabbassi 69  Both neurogenic and nephrogenic forms of DI respond partially to the thiazide diuretics (e.g., hydrochlorothiazide). Prof. Dr. Mustafa Ghazi Alabbassi 70 Syndrome of Inappropriate Antidiuretic Hormone The syndrome of inappropriate ADH (SIADH) results from a failure of the negative feedback system that regulates the release and inhibition of ADH. Prof. Dr. Mustafa Ghazi Alabbassi 71 In persons with this syndrome, ADH secretion continues even when serum osmolality is decreased, causing marked water retention and dilutional hyponatremia. Prof. Dr. Mustafa Ghazi Alabbassi 72 SIADH may occur as a transient condition, as in a stress situation, or as a chronic condition, resulting from disorders such as lung tumors. Prof. Dr. Mustafa Ghazi Alabbassi 73 Stimuli such as surgery, pain, stress, and temperature changes are capable of stimulating ADH through the CNS. Prof. Dr. Mustafa Ghazi Alabbassi 74  The manifestations of SIADH are: 1. Dilutional hyponatremia. 2. Urine output decreases. 3. Urine osmolality is high and serum osmolality is low. 4. Hematocrit and the serum sodium and BUN levels are all decreased because of the expansion of the ECF volume. Prof. Dr. Mustafa Ghazi Alabbassi 75  The treatment of SIADH depends on its severity. 1. In mild cases, treatment consists of fluid restriction. 2. Diuretics such as mannitol and furosemide (Lasix). Prof. Dr. Mustafa Ghazi Alabbassi 76 3. Lithium and the antibiotic demeclocycline inhibit the action of ADH on the renal collecting ducts. 4. severe water intoxication, a hypertonic (e.g., 3%) sodium chloride solution may be administered intravenously. Prof. Dr. Mustafa Ghazi Alabbassi 77 5. The recently developed antagonists to the antidiuretic action of ADH (e.g., conivaptan) are specific ADH V2 receptor antagonists and result in aquaresis (i.e., the electrolyte-sparing excretion of free water). Prof. Dr. Mustafa Ghazi Alabbassi 78 Hyponatremia Hyponatremia is commonly defined as a serum sodium concentration of less than 135 mEq/L (135 mmol/L). Normal value=135-145 mEq/L. Prof. Dr. Mustafa Ghazi Alabbassi 79 It is one of the most common electrolyte disorders seen in hospitalized patients and is also common in the outpatient population, particularly in the elderly. Prof. Dr. Mustafa Ghazi Alabbassi 80 Hyponatremia can present as a hypotonic or hypertonic state. Prof. Dr. Mustafa Ghazi Alabbassi 81 A. Hypertonic (translocational) hyponatremia results from an osmotic shift of water from the ICF to the ECF, such as occurs with hyperglycemia. Prof. Dr. Mustafa Ghazi Alabbassi 82 In this situation, the sodium in the ECF becomes diluted as water moves out of body cells in response to the osmotic effects of the elevated blood glucose level. Prof. Dr. Mustafa Ghazi Alabbassi 83 B. Hypotonic (dilutional) hyponatremia, the most common type of hyponatremia, is caused by water retention. It can be classified as hypovolemic, euvolemic, or hypervolemic based on accompanying ECF fluid volumes. Prof. Dr. Mustafa Ghazi Alabbassi 84 Diuretic therapy, which affects both sodium and water elimination, can cause either hypovolemic or euvolemic hyponatremia. Prof. Dr. Mustafa Ghazi Alabbassi 85 1. Hypovolemic hypotonic hyponatremia occurs when water and sodium is lost, but the loss of water far exceeds the associated loss of sodium and then only the water is replaced. Prof. Dr. Mustafa Ghazi Alabbassi 86  Causes of hypovolemic hypotonic hyponatremia: 1. Excessive sweating. 2. Loss of sodium from the gastrointestinal tract. 3. decrease in aldosterone levels. Prof. Dr. Mustafa Ghazi Alabbassi 87 2. Euvolemic or normovolemic hypotonic hyponatremia represents retention of water with dilution of sodium while maintaining the ECF volume within a normal range. It is usually the result of SIADH. The hyponatremia becomes exaggerated when electrolyte-free fluids (e.g., 5% glucose in water) are used for intravenous fluid replacement. Prof. Dr. Mustafa Ghazi Alabbassi 88 3. Hypervolemic hypotonic hyponatremia is seen when hyponatremia is accompanied by edema-associated disorders such as decompensated heart failure, advanced liver disease, and renal disease. Prof. Dr. Mustafa Ghazi Alabbassi 89  Manifestations: Muscle cramps, weakness, and fatigue reflect the effects of hyponatremia on skeletal muscle function and are often early signs of hyponatremia. Prof. Dr. Mustafa Ghazi Alabbassi 90  The cells of the brain and nervous system are the most seriously affected by increases in intracellular water. Prof. Dr. Mustafa Ghazi Alabbassi 91 Symptoms include apathy, lethargy, and headache, which can progress to disorientation, confusion, gross motor weakness, and depression of deep tendon reflexes. Prof. Dr. Mustafa Ghazi Alabbassi 92 Diagnosis of hyponatremia is based on laboratory reports of a decreased serum sodium concentration, serum and urine osmolality, and urine sodium concentration. Prof. Dr. Mustafa Ghazi Alabbassi 93 Hypernatremia Hypernatremia implies a serum sodium level above 145 mEq/L (145 mmol/L) and a serum osmolality greater than 295 mOsm/kg. Prof. Dr. Mustafa Ghazi Alabbassi 94 Because sodium is functionally an impermeable solute, it contributes to tonicity and induces movement of water across cell membranes. Prof. Dr. Mustafa Ghazi Alabbassi 95 Hypernatremia is characterized by hypertonicity of extracellular fluids and almost always causes cellular dehydration. Prof. Dr. Mustafa Ghazi Alabbassi 96 Causes of hypernatremia In persons with diabetes insipidus, hypernatremia can develop when thirst is impaired or access to water is impeded. With hypodipsia, or impaired thirst, the need for fluid intake does not activate the thirst response. The therapeutic administration of sodium-containing solutions may also cause hypernatremia. Prof. Dr. Mustafa Ghazi Alabbassi 97 Manifestations of hypernatremia urine output is decreased and urine osmolality increased because of renal water-conserving mechanisms. Body temperature frequently is elevated, and the skin becomes warm and flushed. Prof. Dr. Mustafa Ghazi Alabbassi 98 Hypokalemia Hypokalemia refers to a decrease in serum potassium levels below 3.5 mEq/L (3.5 mmol/L). Prof. Dr. Mustafa Ghazi Alabbassi 99 Causes of hypokalemia: (1) inadequate intake. (2) Excessive gastrointestinal, renal, and skin losses. (3) Redistribution between the ICF and ECF compartments. Prof. Dr. Mustafa Ghazi Alabbassi 100 A wide variety of adrenergic agonist drugs (e.g., decongestants and bronchodilators) shift potassium into cells and cause transient hypokalemia. Prof. Dr. Mustafa Ghazi Alabbassi 101 Insulin also increases the movement of potassium into the cell. Because insulin increases the movement of glucose and potassium into cells, potassium deficit often develops during treatment of diabetic ketoacidosis. Prof. Dr. Mustafa Ghazi Alabbassi 102 The signs and symptoms of potassium deficit seldom develop until serum potassium levels have fallen to less than 3.0 mEq/L (3.0 mmol/L). Prof. Dr. Mustafa Ghazi Alabbassi 103 1. Urine output and plasma osmolality are increased, urine specific gravity is decreased, and complaints of polyuria, nocturia, and thirst are common. Prof. Dr. Mustafa Ghazi Alabbassi 104 2. Metabolic alkalosis and renal chloride wasting are signs of severe hypokalemia. 3. Atony (loss of tone) of the gastrointestinal smooth muscle cause constipation, abdominal distention, and, in severe hypokalemia, paralytic ileus. 4. electrocardiographic (ECG) changes. Prof. Dr. Mustafa Ghazi Alabbassi 105 5. Muscle paralysis with life-threatening respiratory insufficiency can occur with severe hypokalemia. Prof. Dr. Mustafa Ghazi Alabbassi 106 Hyperkalemia Hyperkalemia refers to an increase in serum levels of potassium in excess of 5.0 mEq/L (5.0 mmol/L). It seldom occurs in healthy persons because the body is extremely effective in preventing excess potassium accumulation in the extracellular fluid. Prof. Dr. Mustafa Ghazi Alabbassi 107 The three major causes of potassium excess are: (1) Decreased renal elimination. (2) Movement of potassium from the ICF to ECF compartment. (3) Excessively rapid rate of administration. Prof. Dr. Mustafa Ghazi Alabbassi 108 (4) Chronic kidney disease. (5) Acidosis also increases ECF potassium concentration. (6) A decrease in aldosterone-mediated potassium elimination. Prof. Dr. Mustafa Ghazi Alabbassi 109 (7) Potassium-sparing diuretics can produce hyperkalemia. Prof. Dr. Mustafa Ghazi Alabbassi 110 The signs and symptoms of potassium excess are closely related to a decrease in neuromuscular excitability. There may be complaints of generalized muscle weakness or dyspnea secondary to respiratory muscle weakness. As well as, ECG changes. Prof. Dr. Mustafa Ghazi Alabbassi 111  The management of of hyperkalemia: 1. calcium antagonizes the potassium-induced decrease in membrane excitability, restoring excitability toward normal. Prof. Dr. Mustafa Ghazi Alabbassi 112 2. The redistribution of potassium from the ECF into the ICF compartment can be accomplished by the administration of sodium bicarbonate, B-agonists (e.g., nebulized albuterol), or insulin to rapidly decrease the ECF concentration. 3. Intravenous infusions of insulin and glucose may also be used for this purpose. Prof. Dr. Mustafa Ghazi Alabbassi 113 Metabolic Acidosis It involves a decreased serum HCO3⁻ concentration along with a decrease in pH. In metabolic acidosis, the body compensates for the decrease in pH by increasing the respiratory rate in an effort to decrease PCO2 and H2CO3 levels. Prof. Dr. Mustafa Ghazi Alabbassi 114  Metabolic acidosis can be caused by one or more of the following four mechanisms: (1) Increased production of fixed metabolic acids or ingestion of fixed acids such as salicylic acid. Prof. Dr. Mustafa Ghazi Alabbassi 115 Among the causes of metabolic acidosis are an accumulation of: Prof. Dr. Mustafa Ghazi Alabbassi 116  Lactic Acid Acute lactic acidosis, which is one of the most common types of metabolic acidosis, develops when there is excess production or diminished removal of lactic acid from the blood. Lactic acid is produced by the anaerobic metabolism of glucose. Prof. Dr. Mustafa Ghazi Alabbassi 117 Most cases of lactic acidosis are caused by inadequate oxygen delivery, as in shock or cardiac arrest. Such conditions not only increase lactic acid production, but also tend to impair lactic acid clearance because of poor liver and kidney perfusion. Prof. Dr. Mustafa Ghazi Alabbassi 118 Lactic acidosis can also occur during periods of intense exercise in which the metabolic needs of the exercising muscles outpace their aerobic capacity for production of ATP, causing them to revert to anaerobic metabolism and the production of lactic acid. Prof. Dr. Mustafa Ghazi Alabbassi 119  Ketoacidosis Ketoacids (i.e., acetoacetic and –hydroxybutyric acid), produced in the liver from fatty acids, are the source of fuel for many body tissues. Prof. Dr. Mustafa Ghazi Alabbassi 120 An overproduction of ketoacids occurs when carbohydrate stores are inadequate or when the body cannot use available carbohydrates as a fuel. Under these conditions, fatty acids are mobilized from adipose tissue and delivered to the liver, where they are converted to ketones. Prof. Dr. Mustafa Ghazi Alabbassi 121 Ketoacidosis develops when ketone production by the liver exceeds tissue use. The most common cause of ketoacidosis is uncontrolled diabetes mellitus, Prof. Dr. Mustafa Ghazi Alabbassi 122 in which an insulin deficiency leads to the release of fatty acids from adipose cells with subsequent production of excess ketoacids. Prof. Dr. Mustafa Ghazi Alabbassi 123 Ketoacidosis may also develop as the result of fasting or food deprivation, during which the lack of carbohydrates produces a self-limited state of ketoacidosis. Prof. Dr. Mustafa Ghazi Alabbassi 124  Other causes contribute to chronic metabolic acidosis: (2) Inability of the kidneys to excrete the fixed acids produced by normal metabolic processes. Prof. Dr. Mustafa Ghazi Alabbassi 125 The kidneys normally conserve HCO3⁻ and secrete H⁺ ions into the urine as a means of regulating acid-base balance. Prof. Dr. Mustafa Ghazi Alabbassi 126 In chronic kidney disease, there is loss of both glomerular and tubular function, with retention of nitrogenous wastes and metabolic acids. Prof. Dr. Mustafa Ghazi Alabbassi 127 (3) Excessive loss of bicarbonate via the kidneys or gastrointestinal tract. Severe diarrhea; small- bowel, pancreatic, or biliary fistula drainage. Prof. Dr. Mustafa Ghazi Alabbassi 128 (4) An increased serum Cl⁻ concentration. Hyperchloremic acidosis can occur as the result of abnormal absorption of Cl by the kidneys or as a result of treatment with chloride-containing medications. Prof. Dr. Mustafa Ghazi Alabbassi 129 Hyperchloremic acidosis occurs when Cl⁻ levels are increased. Because Cl⁻ and HCO3⁻ are exchangeable anions. Prof. Dr. Mustafa Ghazi Alabbassi 130 Manifestations Metabolic acidosis is characterized by a decrease in serum pH (7.35). Acidosis typically produces a compensatory increase in respiratory rate with a decrease in PCO2. Prof. Dr. Mustafa Ghazi Alabbassi 131 The signs & symptoms of metabolic acidosis include alterations in cardiovascular, neurologic, and musculoskeletal function resulting from the decreased pH. Prof. Dr. Mustafa Ghazi Alabbassi 132 With diabetic ketoacidosis, which is a common cause of metabolic acidosis, there is an increase in blood and urine glucose and a characteristic smell of ketones to the breath. Prof. Dr. Mustafa Ghazi Alabbassi 133  Treatment of Metabolic Acidosis The use of supplemental sodium bicarbonate (NaHCO3) may be indicated in the treatment. Prof. Dr. Mustafa Ghazi Alabbassi 134 Metabolic Alkalosis Metabolic alkalosis is a systemic disorder caused by an increase in serum pH due to a primary excess in HCO3. Prof. Dr. Mustafa Ghazi Alabbassi 135 Metabolic alkalosis can be caused by: (1) A gain of base via the oral or intravenous route. Oral ingestion of bicarbonate-containing antacids (e.g., Alka-Seltzer) or intravenous infusion of NaHCO3 or base equivalent (e.g., lactate in Ringer lactate, and citrate in blood transfusions). Prof. Dr. Mustafa Ghazi Alabbassi 136 (2) Loss of fixed acids. The loss of fixed acids occurs mainly through the loss of acid from the stomach and through the loss of chloride in the urine. Prof. Dr. Mustafa Ghazi Alabbassi 137 Bulimia nervosa with selfinduced vomiting also is associated with metabolic alkalosis. The loop and thiazide diuretics are commonly associated with metabolic alkalosis, Prof. Dr. Mustafa Ghazi Alabbassi 138 The severity of which varies directly with the degree of diuresis. Prof. Dr. Mustafa Ghazi Alabbassi 139 (3) Maintenance of the increased bicarbonate levels. Many of the conditions that accompany the development of metabolic alkalosis, such as contraction of the ECF volume, hypochloremia, and hypokalemia, also increase reabsorption of HCO3 by the kidney, thereby contributing to its maintenance. Prof. Dr. Mustafa Ghazi Alabbassi 140 Manifestations Metabolic alkalosis is characterized by a serum pH above 7.45. Persons with metabolic alkalosis often are asymptomatic or have signs related to ECF volume depletion or hypokalemia. Prof. Dr. Mustafa Ghazi Alabbassi 141 Neurologic signs and symptoms (e.g., hyperexcitability) occur less frequently with metabolic alkalosis than with other acid-base disorders because HCO3 enters the cerebrospinal fluid (CSF) more slowly than CO2. Prof. Dr. Mustafa Ghazi Alabbassi 142 Metabolic alkalosis also leads to a compensatory hypoventilation with development of various degrees of hypoxemia and respiratory acidosis. Significant morbidity occurs with severe metabolic alkalosis, including respiratory failure, arrhythmias, seizures, and coma. Prof. Dr. Mustafa Ghazi Alabbassi 143  Treatment of Metabolic Alkalosis Potassium chloride is used as a therapy, the Cl⁻ anion replaces the HCO3⁻ anion and the K⁺ corrects the potassium deficit, allowing the kidneys to retain H⁺ while eliminating K⁺. Prof. Dr. Mustafa Ghazi Alabbassi 144 Respiratory Acidosis It is also known as hypercapnia, its characterized by a sustained increase in arterial PCO2, resulting in renal adaptation with amore marked increase in plasma HCO3 & lesser decrease in pH. Prof. Dr. Mustafa Ghazi Alabbassi 145 Causes of Respiratory Acidosis 1. Acute disorder of ventilation. Acute respiratory acidosis can be caused by impaired function of the respiratory center in the medulla (as in narcotic overdose), lung disease, chest injury, weakness of the respiratory muscles, or airway obstruction. Prof. Dr. Mustafa Ghazi Alabbassi 146 2. Chronic disorders of ventilation. Patients with chronic lung disease who receive oxygen therapy at a flow rate that is sufficient to raise theirPO2 to a level that produces a decrease in ventilation. Prof. Dr. Mustafa Ghazi Alabbassi 147 In these persons, the medullary respiratory center has adapted to the elevated levels of CO2 and no longer responds to increases in PCO2. Prof. Dr. Mustafa Ghazi Alabbassi 148 3. Increase carbon dioxide production. Carbon dioxide is a product of the body’s metabolic processes, generating a substantial amount of acid that must be excreted by the lungs or kidney to prevent acidosis. (A carbohydrate-rich diet produces larger amounts of CO2). Prof. Dr. Mustafa Ghazi Alabbassi 149 Manifestations of Respiratory Acidosis Respiratory acidosis is associated with a serum pH below 7.35 and an arterial PCO2 above 50 mm Hg. Elevated levels of CO2 produce vasodilation of cerebral blood vessels, causing headache, blurred vision, irritability, muscle twitching, and psychological disturbances. Prof. Dr. Mustafa Ghazi Alabbassi 150 Treatment The treatment of acute and chronic respiratory acidosis is directed toward improving ventilation. In severe cases, mechanical ventilation may be necessary. Prof. Dr. Mustafa Ghazi Alabbassi 151 Respiratory Alkalosis Respiratory alkalosis is a systemic acid-base disorder characterized by a primary decrease in blood PCO2, also referred to as hypocapnia, which produces an elevation in pH and a subsequent decrease in HCO3. Prof. Dr. Mustafa Ghazi Alabbassi 152  Causes of Respiratory Alkalosis 1. Hyperventilation syndrome, which is characterized by recurring episodes of overbreathing often associated with anxiety. 2. Hypoxemia. Prof. Dr. Mustafa Ghazi Alabbassi 153 Manifestations Respiratory alkalosis manifests with a decrease in PCO2 and a deficit in H2CO3. In respiratory alkalosis, the pH is above 7.45, arterial PCO2 is below 35 mm Hg, and serum HCO3 levels usually are below 24 mEq/L (24 mmol/L). Prof. Dr. Mustafa Ghazi Alabbassi 154 The signs and symptoms of respiratory alkalosis are associated with hyperexcitability of the nervous system and a decrease in cerebral blood flow. Prof. Dr. Mustafa Ghazi Alabbassi 155 The treatment of respiratory alkalosis focuses on measures to correct the underlying cause. Hypoxia may be corrected by administration of supplemental oxygen. Prof. Dr. Mustafa Ghazi Alabbassi 156 Prof. Dr. Mustafa Ghazi Alabbassi 157