Chapter 5: Fluids and Electrolytes, Acids and Bases PDF

Chapter 5 Fluids and Electrolytes, Acids and Bases  Distribution of Body Fluids  Total body water (TBW) Intracellular fluid Extracellular fluid Interstitial fluid Intravascular fluid Lymph, synovial, intestinal, CSF, sweat, urine, ple...

Chapter 5 Fluids and Electrolytes, Acids and Bases  Distribution of Body Fluids  Total body water (TBW) Intracellular fluid Extracellular fluid Interstitial fluid Intravascular fluid Lymph, synovial, intestinal, CSF, sweat, urine, pleural, peritoneal, pericardial, and intraocular fluids  Distribution of Body Fluids (Cont.)  Pediatrics 75 to 80% of body weight Susceptible to significant changes in body fluids Dehydration in newborns  Aging Decreased percent of total body water Decreased free fat mass and decreased muscle mass Renal decline Diminished thirst perception  Water Movement Between Fluid Compartments  Osmolality  Osmotic forces  Aquaporins  Starling forces Net filtration = forces favouring filtration minus forces opposing filtration  Net Filtration  Forces favouring filtration: Capillary hydrostatic pressure (blood pressure) Interstitial oncotic pressure (water-pulling)  Forces favouring reabsorption: Plasma (capillary) oncotic pressure (water-pulling) Interstitial hydrostatic pressure  Edema  Accumulation of fluid within the interstitial spaces  Causes: Increase in capillary hydrostatic pressure Decrease in plasma oncotic pressure Increase in capillary permeability Lymph obstruction (lymphedema)  Localized versus generalized  Pitting edema Edema (Cont.)  Na+ and Cl− Balance  Sodium (Na+) Primary ECF cation Regulates osmotic forces, thus water Roles Neuromuscular irritability, acid–base balance, and cellular chemical reactions and membrane transport  Chloride (Cl−) Primary ECF anion Provides electroneutrality  Na+ and Cl− Balance (Cont.)  Renin-angiotensin-aldosterone system Aldosterone—leads to Na+ and water reabsorption back into the circulation and excretion of potassium (K+) Natriuretic peptides Causes Na+ and water excretion  Water Balance  Antidiuretic hormone (ADH) secretion Increases water reabsorption into the plasma  Thirst perception Osmolality receptors Hyperosmolality and plasma volume depletion Volume receptors Baroreceptors ADH System  Alterations in Na+, Cl−, and Water Balance  Isotonic alterations Total body water change with proportional electrolyte and water change (no change in concentration) Isotonic fluid loss Isotonic fluid excess  Alterations in Na+, Cl–, and Water Balance (Cont.)  Hypertonic alterations Hypernatremia Serum Na+ >145 mmol/L Related to Na+ gain or water loss Water movement from the ICF to the ECF  Intracellular dehydration Manifestations  Clinical – Thirst, weight gain, bounding pulse, and increased blood pressure  Central nervous system – Muscle twitching and hyperreflexia (hyperactive reflexes), confusion, coma, convulsions, and cerebral hemorrhage  Alterations in Na+, Cl–, and Water Balance (Cont.) Hyperchloremia Occurs with hypernatremia or a bicarbonate deficit  Alterations in Na+, Cl–, and Water Balance (Cont.)  Hypotonic alterations Decreased osmolality Hyponatremia or free water excess Hyponatremia decreases the ECF osmotic pressure, and water moves into the cell via osmosis Cells expand  Hyponatremia  Serum Na+ level 5.5 mmol/L  Hyperkalemia is rare because of efficient renal excretion  Caused by increased intake, shift of K+ from ICF into ECF, decreased renal excretion, insulin deficiency, or cellular trauma  Hyperkalemia (Cont.)  Mild attacks Increased neuromuscular irritability Restlessness, intestinal cramping, and diarrhea  Severe attacks Decreases the resting membrane potential Muscle weakness, loss of muscle tone, and paralysis Electrocardiogram (ECG) Changes With Potassium Imbalance  Calcium and Phosphate  Calcium (Ca++) and phosphate (PO43+) concentrations are rigidly controlled by parathyroid hormone (PTH), vitamin D, and calcitonin  Calcium  99% of Ca++ is located in the bone as hydroxyapatite  Necessary for structure of bones and teeth, blood clotting, hormone secretion, cell receptor function, plasma membrane stability, transmission of nerve impulses, muscle contraction  Serum concentration 2.1 to 2.6 mmol/L (adult)  Hypocalcemia  Causes: Inadequate intestinal absorption, deposition of ionized Ca++ into bone or soft tissue, blood administration Decreases in PTH and vitamin D Nutritional deficiencies occur with inadequate sources of dairy products or green, leafy vegetables  Hypocalcemia (Cont.)  Effects: Increased neuromuscular excitability Tingling, muscle spasm (particularly in hands, feet, and facial muscles), intestinal cramping, hyperactive bowel sounds Severe cases show convulsions and tetany Prolonged QT interval, cardiac arrest  Hypercalcemia  Causes: Hyperparathyroidism Bone metastases with Ca++ resorption from breast, prostate, renal, and cervical cancer Sarcoidosis Excess vitamin D Many tumours that produce PTH  Hypercalcemia (Cont.)  Effects: Many nonspecific: fatigue, weakness, lethargy, anorexia, nausea, constipation Impaired renal function, kidney stones Dysrhythmias, bradycardia, cardiac arrest Bone pain, osteoporosis  Phosphate  Like Ca++, most phosphate (PO43+) is also located in the bone.  Provides energy for muscle contraction.  Parathyroid hormone, vitamin D3, and calcitonin act together to control PO43+ absorption and excretion.  Normal value = 0.8 to 1.5 mmol/L (adult).  Hypophosphatemia  Causes: Intestinal malabsorption (vitamin D deficiency, use of magnesium- and aluminum-containing antacids, long-term alcohol abuse) Malabsorption syndromes Respiratory alkalosis Increased renal excretion of PO43+ associated with hyperparathyroidism  Hypophosphatemia (Cont.)  Effects: Reduced capacity for oxygen transport by red blood cells, thus disturbed energy metabolism Leukocyte and platelet dysfunction Deranged nerve and muscle function In severe cases, irritability, confusion, numbness, coma, convulsions, possibly respiratory failure, cardiomyopathies, bone resorption  Hyperphosphatemia  Causes: Acute or chronic kidney failure with significant loss of glomerular filtration Treatment of metastatic tumours with chemotherapy that releases large amounts of PO43+ into serum Long-term use of laxatives or enemas containing phosphates Hypoparathyroidism  Hyperphosphatemia (Cont.)  Effects: Symptoms primarily related to low serum Ca++ levels (caused by high PO43+ levels) similar to the results of hypocalcemia When prolonged, calcification of soft tissues in lungs, kidneys, joints  Magnesium (Mg++)  Intracellular cation  Serum concentration 0.75 to 0.95 mmol/L (adult)  Acts as a cofactor in intracellular enzymatic reactions  Increases neuromuscular excitability  Hypomagnesemia  Causes: Malnutrition Malabsorption syndromes Alcoholism Urinary losses (renal tubular dysfunction, loop diuretics)  Hypomagnesemia (Cont.)  Effects: Behavioural changes Irritability Increased reflexes Muscle cramps Ataxia Nystagmus Tetany Convulsions Tachycardia Hypotension  Hypermagnesemia  Causes: Usually is renal insufficiency or failure Excessive intake of magnesium-containing antacids Adrenal insufficiency  Hypermagnesemia (Cont.)  Effects: Skeletal smooth muscle contraction Excess nerve function Loss of deep tendon reflexes Nausea and vomiting Muscle weakness Hypotension Bradycardia Respiratory distress 1. Which is the initial treatment for hypernatremia? A. Restriction of fluids B. Administration of a diuretic C. Isotonic 0.9% normal saline fluid D. Isotonic salt-free fluid (5% dextrose in water)  Acid–Base Balance  Acid–base balance is carefully regulated to maintain a normal pH via multiple mechanisms.  Hydrogen Ion and pH  Negative logarithm of the H+ concentration  If the H+ are high in number, the pH is low (acidic); if the H+ are low in number, the pH is high (alkaline)  Hydorgen Ion and pH (Cont.)  Acids are formed as end products of protein, carbohydrate, and fat metabolism.  To maintain the body’s normal pH (7.35 to 7.45), the H+ must be neutralized or excreted.  Bones, lungs, and kidneys are the major organs involved in the regulation of acid–base balance.  Buffer Systems  A buffer is a chemical that can bind excessive H+ or OH– without a significant change in pH.  Most important plasma-buffering systems are the carbonic acid–bicarbonate pair.  pH  Body acids exist in two forms: Volatile Carbonic acid (H2CO3) can be eliminated as CO2 gas and water Nonvolatile Sulfuric, phosphoric, and other organic acids Eliminated by the renal tubules with the regulation of bicarbonate (HCO3–)  Carbonic Acid–Bicarbonate Pair  Operates in the lung and the kidney.  Greater the partial pressure of CO2, the more carbonic acid (H2CO3) is formed. At a pH of 7.4, the ratio of bicarbonate to carbonic acid is 20:1. Bicarbonate and carbonic acid can increase or decrease, but the ratio must be maintained.  Carbonic Acid–Bicarbonate Pair (Cont.)  Respiratory system compensates by increasing ventilation to expire CO2 or by decreasing ventilation to retain CO2.  Renal system compensates by producing acidic or alkaline urine.  Other Buffering Systems  Protein buffering (hemoglobin) Proteins have negative charges, so they can serve as buffers for H+  Renal buffering Secretion of H+ in the urine and reabsorption of HCO3–  Acid–Base Imbalances  Normal arterial blood pH 7.35 to 7.45 Obtained by arterial blood gas (ABG) sampling  Acidosis Systemic increase in H+ concentration or decrease in bicarbonate (base)  Alkalosis Systemic decrease in H+ concentration or increase in bicarbonate  Acidosis and Alkalosis  Four categories of acid–base imbalances: Respiratory acidosis—elevation of PaCO2 as a result of ventilation depression Respiratory alkalosis—depression of PaCO2 as a result of alveolar hyperventilation Metabolic acidosis—depression of HCO3– or an increase in noncarbonic acids Metabolic alkalosis—elevation of HCO3– usually caused by an excessive loss of metabolic acids Acidosis and Alkalosis (Cont.)