Chapter 8 Disorders of Fluid, Electrolytes and Acid-Base Balance Summer 2024 PDF

Chapter 8 Disorders of Fluid, Electrolytes and Acid-Base Balance Dr. Kelly Goebel DNP, ACNP-BC Distribution of Body Fluid Water is found in three different fluid compartments: Intracellular fluid (ICF)= 2/3rd Extracellular fluid (ECF)= 1/3rd Diffusion and Osmosis Diffusion: movement...

Chapter 8 Disorders of Fluid, Electrolytes and Acid-Base Balance Dr. Kelly Goebel DNP, ACNP-BC Distribution of Body Fluid Water is found in three different fluid compartments: Intracellular fluid (ICF)= 2/3rd Extracellular fluid (ECF)= 1/3rd Diffusion and Osmosis Diffusion: movement of particles along a concentration gradient. Osmosis: movement of water across a semipermeable membrane. Urine specific gravity compares weight or urine to water- reflects the kidneys’ ability to produce a concentrated or diluted urine based on serum osmolality and the need for water conservation or excretion. Osmolarity & Tonicity Osmolarity Tonicity The number of osmoles of solute per liter of The effect that the osmotic pressure within a solution; dependent on the number of particles solution exerts on cell size because of water across suspended in a solution. the cell membrane. Fluid status maintained by: osmoreceptors, Describes intravenous fluid solutions (three types) sensation of thirst, RAAS, ADH, natriuretic Isotonic: same tonicity as blood; 0.9% NaCl. hormones Cells do not shrink or swell. Hypotonic: less tonicity than blood; 0.45% NaCl. Water moves into the cell and cells swell. Hypertonic: greater tonicity than blood; 3% NaCl. Water is pulled out of the cell and cells shrink. Pathophysiol ogy of F & E Imbalance Edema Palpable swelling produced by expansion of the interstitial fluid volume (can hole 10-30L of fluid) Patho Increase capillary filtration pressure Decrease capillary osmotic pressure Increase capillary permeability** Produce obstruction to lymph flow Localized or generalized Anasarca: generalized body edema Dependent edema Third space (peritoneum, pleural cavity)  Increased Capillary Decreased Colloidal Increased Capillary Obstruction of Pressure Osmotic Pressure Permeability Lymphatic Flow Increased vascular Increased loss of Inflammation Surgical removal of volume (Heart plasma protein Allergic reaction lymph nodes failure, kidney (kidney disease, Tissue injury/burns disease) burn) Decreased production of protein (malnutrition) See next slide- Albumin Albumin Albumin: smallest of plasma proteins Low albumin (hypoalbuminemia) in the bloodstream causes low oncotic pressure-> results in edema Edema due to decreased colloidal osmotic pressure usually result of loss of albumin-> liver failure-> impaired synthesis of albumin Sodium and Water Balance Effective circulating volume is the major regulator Low effective circulating volume-> activates feedback mechanisms that produce an increase in renal sodium and water retention High effective circulating volume-> triggers feedback mechanisms that decrease sodium and water retention Baroreceptors RAAS Thirst-> regulator of water intake (polydipsia vs. hypodipsia) Antidiuretic hormone (ADH)-> regulator of water output (SIADH vs. DI)- we will cover this under endocrine disorders Isotonic Fluid Volume Deficit Decrease in ECF/circulating blood volume Clinical manifestations: Proportionate losses in sodium and water Acute weight loss Etiology: Decreased urine output Increased osmolality and specific gravity Inadequate fluid intake: Therapeutic withholding, unconscious, impaired thirst Thirst Excessive GI loss: V/D, osmotic diuresis, Increased BUN/Creatinine adrenal insufficiency Hypotension, tachycardia, shock Excessive skin loss: Fever, burns Thready pulse Third-space loss: Edema, ascites Sunken eyes Isotonic Fluid Volume Excess Expansion of the ECF compartment with increased Clinical Manifestations: interstitial and vascular volume Acute weight gain Compensatory vs. Pathologic Edema Etiology: Full, bounding pulse Inadequate sodium and water elimination Venous distension Congestive heart failure, renal failure, Pulmonary Edema (SOB, crackles, dyspnea, Cushing disease, liver failure cough) Excessive sodium intake in r/t output Excessive dietary intake Ingestion of sodium containing medications Excessive fluid intake in relation to output Administration of parenteral fluids or blood at an excessive rate Sodium Imbalance Serum osmolality (275-295 mOsm/kg) changes with plasma sodium concentration (135-145 mEq/L) Common electrolyte disorder Hypertonic Age-related events contribute (Translocational) Hypertonic or Hypertonic State Osmotic shift of water from ICF to ECF Ex. Hyperglycemia (serum os > 280)  Hypovolemic: Water + Sodium lost Hypotonic (Dilutional) Hyponatremi a r/t water dilution Hypervolemic: Euvolemic: Edema-associated Retention of water disorders, increased with dilution of ADH sodium Hyponatremia < 135 mEq/L Hypovolemic hypotonic hyponatremia (decreased serum Hypervolemic hyponatremia (decreased serum sodium with sodium with decreased ECF volume) increased ECF volume) Sweating Hyponatremia + edema GI irrigations with distilled water Decompensated CHF Advanced liver disease GI losses Kidney failure Diuretic use Clinical Manifestations largely r/t sodium dilution Normovolemic (Euvolemia) hyponatremia (decreased serum sodium with normal ECF) N/V Retention of water with dilution of sodium (ECF WNL) Serum osmolality decreased Increased ADH levels Cellular swelling-> coma, headache (neuro), abdominal Syndrome of inappropriate antidiuretic cramps hormone (SIADH) Trauma Hypernatremia > 145 mEq/L (Serum osmolality > 295 mOsm/kg) Patho Clinical Manifestations Water lost in excess of sodium Tachycardia Causes cellular dehydration Polydipsia Oliguria Etiology High specific gravity Excessive water loss (diarrhea, sweating, tachypnea, DI) Dry mucous membranes Decreased water intake (inability to swallow, Headache, agitation unresponsive) Seizures, coma Excessive sodium intake (near drowning in salt Weak, thready pulse (vascular depletion) water) Increased BUN/Creat Cerebral edema ensues if water replacement proceeds at a rate that does not allow for excretion or metabolism of accumulated solutes Hyperkalemia Pathophysiology Potassium regulates: Excitability of cardiac, skeletal and muscle Maintains acid-base balance Nerve impulse conduction Potassium regulation 1. Renal mechanisms (aldosterone) 2. Extracellular-Intracellular shifts Hypokalemia < 3.5 mEq/L Decrease in plasma potassium levels Clinical Manifestations Etiology Cardiac arrhythmias Inadequate intake (diet) Muscle cramps, paralysis Excessive renal loss (potassium sparing Confusion diuretics, corticosteroids) Metabolic alkalosis GI loss (V/D, suction) ECG: Depression of ST segment, U wave Transcompartmental Shift Albuterol, administration of insulin for DKA, metabolic/respiratory alkalosis Hyperkalemia > 5.2 mEq/L Increase in plasma levels of potassium Etiology Seldom occurs in healthy people 1. Decreased renal elimination (renal failure, ACE-I) 2. Excessive rapid administration (PO, supplements) 3. Transcellular shift from ICF to ECF (acidosis, crush injuries) Clinical Manifestations Paresthesia Diarrhea ECG: widened QRS complex, peaked T waves Cardiac arrest Metabolic acidosis Mechanisms Regulating Calcium, Phosphorus and Magnesium Balance Vitamin D facilitates the absorption of calcium from the gastrointestinal tract into the bloodstream Parathyroid Hormone (parathyroid disorders covered in endocrine lecture) Calcium and phosphorus are the major mineral contents of bone Ingested in diet, absorbed from intestine, filtered in kidney, eliminated in urine. There is a reciprocal relationship between calcium and phosphate; Increased calcium in the blood: decrease in phosphate Decreased calcium in the blood: increase in phosphate Calcium Imbalances Hypocalcemia < 8.5 mg/dL Hypercalcemia > 10.5 mg/dL Etiology: malabsorption, vitamin D deficiency, Decreased neuromuscular excitability renal failure, transfusion of citrated blood, Etiology: increased bone resorption secondary hypoparathyroidism to neoplasm or immobilization, thiazide Increased neuromuscular excitability diuretics, excessive intake Clinical Manifestations: Clinical manifestations: Laryngeal spasm Muscle weakness, ataxia Tetany Coma, lethargy Ventricular dysrhythmias Hyperreflexia Chvostek’s sign; facial spasm Flank pain/kidney stones Trousseau’s sign; carpal spasm Osteoporosis Bone pain (chronic) N/V Phosphate Imbalances Hypophosphatemia < 2.5 mg/dL Hyperphosphatemia > 4.5 mg/dL Etiology: Decreased absorption, antacid use, Etiology: renal failure, massive trauma, increased renal loss, alcoholism, hypoparathyroidism hyperparathyroidism Clinical Manifestations: Clinical Manifestations: Paresthesia Intentional tremor Tetany Hyporeflexia Cardiac dysrhythmias Seizures Reciprocal calcium change: hypocalcemia Reciprocal calcium change: hypercalcemia Magnesium Imbalances Hypomagnesemia < 1.8 mg/dL Hypermagnesemia > 3.0 mg/dL Etiology: Etiology: renal failure, magnesium Malabsorption/Malnutrition laxatives/antacids, pre-eclampsia Increased renal excretion of magnesium Clinical Manifestations: Chronic alcoholism Hyporeflexia Clinical Manifestations: Severe > 12 Tetany, + Babinski Calcium-channel blocking effects: Nystagmus cardiac arrest Cardiac dysrhythmias Respiratory muscle paralysis  Chapter 8 Acid-Base Imbalances Regulation of pH 1. Chemical buffer systems 2. Respiratory control mechanisms 3. Renal control mechanisms Respiratory Control Mechanisms Chemoreceptors in blood vessels responsive to C02 in blood Increased ventilation decreases PC0₂ Decreased ventilation increases PC0₂ Control of pH is rapid/within minutes and maximal within 12-24 hours Renal Control Mechanisms Excretes H⁺ Reabsorption of HC0₃ Production of new HC0₃ Laboratory Results Base Carbon Bicarbonate Excess/Defici Dioxide Levels t  Arterial Blood Gases The pressure of the gases in the bloodstream Pac02: the pressure of carbon dioxide in arterial blood (35 to 45 mm Hg) HC0₃: the amount of bicarbonate ion in the blood (22-26 mEq/L) pH: 7.35-7.45 (7.40) Don’t forget about the oxygen! Metabolic vs. Respiratory Acid Base Disorders Metabolic disorders produce an alteration in Respiratory disorders involve an alteration in plasma HC0₃ the PC0₂ Metabolic acidosis: elevation in pH Respiratory acidosis: decrease in pH because of decrease in HC0₃ (decrease in ventilation and increase in Metabolic alkalosis: elevation in pH PC0₂) because of increased HC0₃ Respiratory alkalosis: increase in pH (increase in alveolar ventilation and decrease in PC0₂) ACID BASE IMBALANCE When the lungs or kidneys fail to maintain acid-base balance-> Any of the four Acid-Base Imbalances can occur: 1. Respiratory acidosis 2. Respiratory alkalosis 3. Metabolic acidosis 4. Metabolic alkalosis Respiratory Acidosis Accumulation of PC0₂ (hypercapnia) from impaired ventilation (acute or chronic) Etiology: Respiratory/Airway issues Lung disease: COPD, pneumonia Depression of respiratory center: Drug overdose, head injury Airway obstruction: Chest injuries, extreme obesity, paralysis of respiratory muscles Clinical manifestations: Headache (cerebral vasodilation), confusion, stupor/coma Serum pH is < 7.35 Pc02 > 45 mm Hg Respiratory Alkalosis Decrease in PC02 (Hypocapnia) caused by hyperventilation Etiology: Anxiety, hypoxia, pain, fever, salicylate intoxication Clinical manifestations: Dizziness (cerebral vasoconstriction), numbness/tingling of fingers, panic, muscle spasms Serum pH > 7.45 Pc02 < 35 mm Hg Metabolic Acidosis Excess acids OR abnormal loss of bicarbonate Etiology: Lactic acidosis, ketoacidosis, diarrhea, chronic kidney disease Clinical manifestations: Kussmaul breathing (deep rapid respirations- compensatory), coma, dysrhythmias, hypotension Serum pH < 7.35 Serum HC03 < 22 mEq/L Metabolic acidosis causes H+ to enter cells replacing potassium-> causes hyperkalemia Metabolic Alkalosis Primary excess of bicarbonate (HC0₃) Etiology: Excess bicarb ingestion, vomiting of excess gastric acid, gastric suction Clinical manifestations: asymptomatic, volume depletion, confusion, hypotension, decreased rate/depth of respirations (compensatory) Serum pH > 7.45 Serum HC03 >26 mEq/L Metabolic alkalosis causes potassium to enter the cell-> hypokalemia  *Metabolic acidosis causes H+ to enter cells & potassium to exit the cell -> causes hyperkalemia *Metabolic alkalosis causes H+ to exit the cells & potassium to enter the cell-> hypokalemia Abnormality pH PaC0₂ Hc0₃ Respiratory Acidosis ↓ ↑ Normal Respiratory Alkalosis ↑ ↓ Normal Metabolic Acidosis ↓ Normal ↓ Metabolic Alkalosis ↑ Normal ↑