Sasha Rarang, MSN, CCM, RN Purpose Maintain a balance between acids and bases to achieve homeostasis: Homeostasis or State of equilibrium State of equilibrium in body Naturally maintained by adaptive responses Body fluids and electrolytes are maintained within narrow limits Health problems lead to imbalance Diabetes mellitus Vomiting and diarrhea Respiratory conditions Chemotherapy- N/V Water Content of the Body 60% of body weight in adult 45% to 55% in older adults 70% to 80% in infants Varies with gender, body mass, and age Changes in Water Content with Age Compartments Intracellular fluid (ICF) Extracellular fluid (ECF) Intravascular (plasma) Interstitial Transcellular Fluid Compartments of the Body Intracellular Fluid (ICF) Located within cells 42% of body weight Extracellular Fluid (ECF) One third of body weight Between cells (interstitial fluid), lymph, plasma, and transcellular fluid Transcellular Fluid Part of ECF Small but important Approximately 1 L Includes fluid in: Cerebrospinal fluid Gastrointestinal tract Pleural spaces Synovial spaces Peritoneal fluid spaces pH Measure of H+ ion concentration Blood is slightly alkaline at pH 7.35 to 7.45. <7.35 is acidosis. >7.45 is alkalosis. Range of pH Fig. 17-16. The normal range of plasma pH is 7.35 to 7.45. A normal pH is maintained by a ratio of 1 part carbonic acid to 20 parts bicarbonate. Regulators of Acid/Base Metabolic processes produce acids that must be neutralized and excreted. Regulatory mechanisms Buffers Respiratory system Renal system Regulators of Acid/Base Buffers: Act chemically to neutralize acids or change strong acids to weak acids Primary regulators React immediately Cannot maintain pH without adequate respiratory and renal function The buffers in the body include carbonic acid–bicarbonate monohydrogen- dihydrogen phosphate intracellular and plasma protein hemoglobin Electrolytes Substances whose molecules dissociate into ions (charged particles) when placed into water Cat ions: positively charged An ions: negatively charged International standard is millimoles per liter (mmol/L) U.S. uses milliequivalent (mEq) Electrolyte Composition ICF Prevalent cation is K+ (Potasium) Prevalent anion is PO4- (Phosphate) ECF Prevalent cation is Na+ (Sodium) Prevalent anion is Cl- ( Chloride) Mechanisms Controlling Fluid and Electrolyte Movement Diffusion - Movement of molecules from high to low concentration . Occurs in liquids, solids, and gases Membrane separating two areas must be permeable to diffusing substance. Requires no energy Mechanisms Controlling Fluid and Electrolyte Movement Facilitated diffusion Movement of molecules from high to low concentration without energy Uses specific carrier molecules to accelerate diffusion Active Transport Process in which molecules move against concentration gradient Example: sodium–potassium pump External energy required Sodium–Potassium Pump Mechanisms Controlling Fluid and Electrolyte Movement Osmosis Movement of water between two compartments by a membrane permeable to water but not to solute Moves from low solute to high solute concentration Requires no energy Mechanisms Controlling Fluid and Electrolyte Movement Osmotic Pressure Amount of pressure required to stop osmotic flow of water. Determined by concentration of solutes in solution. Hydrostatic Pressure Force within a fluid compartment Major force that pushes water out of vascular system at capillary level Oncotic Pressure Osmotic pressure exerted by colloids in solution (colloidal osmotic pressure) Protein is major colloid Fluid Movement in Capillaries Amount and direction of fluid movement is determined by: Capillary hydrostatic pressure Plasma oncotic pressure Interstitial hydrostatic pressure Interstitial oncotic pressure Fluid Exchange Between Capillary and Tissue Fluid Shifts Plasma to interstitial fluid shift results in : Edema Elevation of hydrostatic pressure Decrease in plasma oncotic pressure Elevation of interstitial oncotic pressure Interstitial fluid to plasma results in: Fluid drawn into plasma space with increase in plasma osmotic or oncotic pressure Compression stockings decrease peripheral edema Fluid Movement between ECF and ICF Water deficit (increased ECF) Associated with symptoms that result from cell shrinkage as water is pulled into vascular system. Water excess (decreased ECF) Develops from gain or retention of excess water. Fluid Spacing First spacing - Normal distribution of fluid in ICF and ECF Second spacing - Abnormal accumulation of interstitial fluid (edema) Third spacing Fluid accumulation in part of body where it is not easily exchanged with ECF. Regulation of Water Balance Hypothalamic Regulation - Osmoreceptors in hypothalamus sense fluid deficit or increase. Stimulates thirst and antidiuretic hormone (ADH) release. Result in increased free water and decreased plasma osmolarity. Pituitary Regulation - Under control of hypothalamus, posterior pituitary releases ADH. Stress, nausea, nicotine, and morphine also stimulate ADH release. Adrenal Cortical Regulation - Releases hormones to regulate water and electrolytes – Glucocorticoids - Cortisol Mineralocorticoids - Aldosterone Factors Affecting Aldosterone Secretion Fluid Regulations Renal/Kidneys Primary organs for regulating fluid and electrolyte balance Adjusting urine volume Selective reabsorption of water and electrolytes Renal tubules are sites of action of ADH and aldosterone Cardiac Regulation Natriuretic peptides are antagonists to the RAAS Produced by cardiomyocytes in response to increased atrial pressure Suppress secretion of aldosterone, renin, and ADH to decrease blood volume and pressure Fluid Regulations Gastrointestinal Regulation Oral intake accounts for most water Small amounts of water are eliminated by gastrointestinal tract in feces. Diarrhea and vomiting can lead to significant fluid and electrolyte loss Insensible Water Loss Invisible vaporization from lungs and skin to regulate body temperature Approximately 600 to 900 ml/day is lost No electrolytes are lost Gerontologic Considerations Structural changes in kidneys decrease ability to conserve water Hormonal changes lead to decrease in ADH and ANP Loss of subcutaneous tissue leads to increased loss of moisture Reduced thirst mechanism results in decreased fluid intake Nurse must assess for these changes and implement treatment accordingly Fluid and Electrolyte Imbalances Common in most patients with illness Directly caused by illness or disease (burns or heart failure) Result of therapeutic measures (IV fluid replacement or diuretics) Regulators of Acid/Base Respiratory system: Eliminates CO2 Respiratory center in medulla controls breathing. Responds within minutes/hours to changes in acid/base. Increased respirations lead to increased CO2 elimination decreased CO2 in blood. Regulators of Acid/Base • When released into circulation, CO2 enters RBCs and combines with H2O to form H2CO3. • This carbonic acid dissociates into hydrogen ions and bicarbonate. • The free hydrogen is buffered by hemoglobin molecules, and the bicarbonate diffuses into the plasma. • In the pulmonary capillaries, this process is reversed, and CO2 is formed and excreted by the lungs. • As a compensatory mechanism, the respiratory system acts on the CO2 + H2O side of the reaction by altering the rate and depth of breathing to “blow off” (through hyperventilation) or “retain” (through hypoventilation) CO2. • If a respiratory problem is the cause of an acid-base imbalance (e.g., respiratory failure), the respiratory system loses its ability to correct a pH alteration. Regulators of Acid/Base Renal system: Eliminates H+ and reabsorbs HCO3 Reabsorption and secretion of electrolytes (e.g., Na+, Cl-) Responds within hours to days. Hyperkalemia results from decreased renal excretion. Na+ may also be retained resulting to water retention, edema, hypertension, and heart failure. Regulators of Acid/Base • The three mechanisms of acid elimination are • secretion of small amounts of free hydrogen into the renal tubule, • combination of H+ with ammonia (NH3) to form ammonium (NH4+), and • excretion of weak acids. • The body depends on the kidneys to excrete a portion of the acid produced by cellular metabolism. • Thus the kidneys normally excrete acidic urine (average pH equals 6). • As a compensatory mechanism, the pH of the urine can decrease to 4 and increase to 8. Alterations in Acid-Base Balance Imbalances occur when compensatory mechanisms fail. Classification of imbalances Respiratory: Affect carbonic acid concentration Metabolic: Affect bicarbonate Respiratory Acidosis Carbonic acid excess caused by Hypoventilation Respiratory failure Compensation Kidneys conserve HCO3- and secrete H+ into urine. Respiratory Acidosis • Hypoventilation results in a buildup of CO2 • carbonic acid accumulates in the blood • Carbonic acid dissociates, liberating H+, and a decrease in pH occurs. • If CO2 is not eliminated from the blood, acidosis results from the accumulation of carbonic acid. • In acute respiratory acidosis, the renal compensatory mechanisms begin to operate within 24 hours. Respiratory Alkalosis Carbonic acid deficit caused by Hyperventilation Hypoxemia from acute pulmonary disorders Metabolic Acidosis Base bicarbonate deficit caused by Ketoacidosis Lactic acid accumulation (shock) Severe diarrhea Kidney disease Metabolic acidosis (base bicarbonate deficit) occurs when an acid other than carbonic acid accumulates in the body, or when bicarbonate is lost from body fluids. Compensatory mechanisms Increased CO2 excretion by lungs Kussmaul respirations (deep and rapid) Kidneys excrete acid Metabolic Alkalosis Base bicarbonate excess caused by Prolonged vomiting or gastric suction Gain of HCO3- Compensatory mechanisms Decreased respiratory rate to increase plasma CO2 Renal excretion of HCO3- Blood Gas Values Arterial blood gas (ABG) values provide information about Acid-base status Underlying cause of imbalance Body’s ability to regulate pH Overall oxygen status Interpretation of ABGs Diagnosis in six steps: Evaluate pH. Analyze PaCO2. Analyze HCO3-. Determine if CO2 or HCO3- matches the alteration. Decide if the body is attempting to compensate. Normal Blood Gas Values Table 17-15. Normal Arterial Blood Gas Values *. Sample ABG Interpretation Table 17-16. Arterial Blood Gas (ABG) Analysis. Acid-Base Mnemonic—ROME Respiratory Opposite Alkalosis↑ pH ↓ PaCO2 Acidosis ↓ pH ↑ PaCO2 Metabolic Equal Acidosis ↓ pH ↓ HCO3 Alkalosis↑ pH ↑ HCO3 Interpretation of ABGs pH 7.18 PaCO2 38 mm Hg PaO2 70 mm Hg HCO3- 15 mEq/L What is this? Metabolic acidosis Interpretation of ABGs pH 7.58 PaCO2 35 mm Hg PaO2 75 mm Hg HCO3- 50 mEq/L What is this? Metabolic alkalosis Question A patient with an acid-base imbalance has an altered potassium level. The nurse recognizes that the potassium level is altered because: 1. Potassium is returned to extracellular fluid when metabolic acidosis is corrected. 2. Hyperkalemia causes an alkalosis that results in potassium being shifted into the cells. 3. Acidosis causes hydrogen ions in the blood to be exchanged for potassium from the cells. 4. In alkalosis, potassium is shifted into extracellular fluid to bind excessive bicarbonate. 47 Answer Answer: 3 Rationale: Changes in pH (hydrogen ion concentration) will affect potassium balance. In acidosis, hydrogen ions accumulate in the intracellular fluid (ICF), and potassium shifts out of the cell to the extracellular fluid to maintain a balance of cations across the cell membrane. In alkalosis, ICF levels of hydrogen diminish, and potassium shifts into the cell. If a deficit of H+ occurs in the extracellular fluid, potassium will shift into the cell. Acidosis is associated with hyperkalemia Alkalosis is associated with hypokalemia. Case Study 1: Jeri Jeri’s been on a 3-day party binge. Friends are unable to awaken her. Assessment reveals level of consciousness difficult to arouse. Respiratory rate 8 Shallow breathing pattern Diminished breath sounds 1. 2. What ABGs do you expect? What is your treatment? 49 Case Study 1: Jeri What ABGs do you expect? Respiratory acidosis reflected by pH <7.35 and PCO2 >45 mm Hg. The HCO3 will be normal (20-30 mEq/L) if her respiratory depression has lasted less than 24 hours; if longer than 24 hours, the HCO3 may be elevated as the result of compensation. The PaO2 may be <80 mm Hg because of respiratory depression leading to hypoxemia. 2. What is your treatment? Determine the cause of the respiratory depression. If induced by opioids or benzodiazepines, treat with appropriate antagonists. If induced by alcohol or other CNS depressants, breathing must be stimulated until the effects of drugs have worn off. Mechanical ventilation may be necessary to increase respiratory rate and depth, increasing oxygenation and promoting excretion of carbon dioxide. Case Study 2: Mayna Presented to the ED after a sexual assault Examination reveals hysteria and emotional distress. Respiratory rate 38 Lungs clear 1. O2 sat 96%What ABGs do you expect? 2. What is your treatment? Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. Case Study 2: Mayna 1. What ABGs do you expect? Respiratory alkalosis indicated by pH >7.45 and PCO2 <35 mm Hg. The HCO3 will be normal (20-30 mEq/L) because compensation will not occur in this acute event. 2. What is your treatment? Relieve her anxiety and coax her to take slow breaths. Carbon dioxide may be administered by mask, or she may be asked to breathe into a paper bag placed over her nose and mouth. Case Study 3: Allen 17 years old History of Feeling bad Fatigue Constant thirst Frequent urination Blood sugar is 484 mg/dL. Respirations are 28 and deep. Breath has a fruity odor. Lungs are clear. 1. 2. What ABGs do you expect? What is your treatment? Case Study 3: Allen What ABGs do you expect? A diabetic ketoacidosis is a metabolic acidosis indicated by a pH <7.35 and a HCO3 <20 mEq/L. The PCO2 will be within the normal range if the acidosis is uncompensated, but will be <35 mm Hg if compensation has occurred. The PaO2 will not be affected. 2. What is your treatment? Administration of insulin to promote normal glucose metabolism and administration of fluids and electrolytes to replace those lost because of the hyperglycemia. Fluid volume deficit Can occur with Abnormal loss of body fluids Diarrhea, hemorrhage, polyuria Inadequate fluid intake Shift of fluid from plasma into interstitial space • Treatment Correct the underlining cause Replace the fluid and electrolyte (LR or NS isotonic solutions) Fluid volume excess May result from excessive intake of fluid Abnormal retention of fluids(heart failure, renal failure) Shift of fluid from interstitial fluid into plasma fluid o Collaborative care o o o ID primary cause Diuretics and fluid restriction Restriction of Na intake Fluid excess may result to ascites or pleural effusion, and paracentesisi or thoracentsis may be necessary. Commonly prescribed crystalloid solutions Dextrose in water 5% isotonic 10% hypertonic Saline 0.45% hypotonic 0.9% isotonic 3.0% hypertonic Dextrose in Saline 5% in 0.225% isotonic 5% in 0.45% hypertonic 5% in 0.9% hypertonic Multiple Electrolyte Solutions Ringer’s solution- isotonic, includes CL, Na, K, Ca Lactated Ringer’s solution- isotonic-Na, K, Cl, Ca, and lactate(the precursor of bicarbonate) CVADs Catheters placed in large blood vessels of people who require frequent access to the vascular system Subclavian vein, jugular vein Three different methods Centrally inserted catheter(by MD) Peripherally inserted central catheter Implanted ports( by MD) CVADs Permit frequent, continuous, rapid, or intermittent administration or monitoring Indicated for patients with limited peripheral vascular access or need for long-term vascular access Centrally Inserted Catheter Inserted into a vein in the neck, chest, or groin with tip resting in the distal end of the superior vena cava Single, double, triple, or quad lumen Nontunneled or tunneled Central .Venous Catheter PICC Central venous catheters inserted into a vein in the arm Single or multilumen, nontunneled For patients who need vascular access for 1 week to 6 months Complications include catheter occlusion and phlebitis. Copyright © 2011, 2007, 2004, 2000, 1996, 1992, 1987, 1983 by Mosby, Inc., an affiliate of Elsevier Inc. PICC Implanted Infusion Ports Central venous catheter connected to an implanted, single or double subcutaneous injection port Port is metal sheath with self-sealing silicone septum. Implanted Infusion Port Implanted Infusion Port Port accessed with special Huber-point needle Advantages Good for long-term therapy Low risk of infection Cosmetic discretion Care requires regular flushing. Complication: (table 17-21 page 330) Cath occlusion(kinked, precipitate build up) Embolism( dislodgment of thrombus, air entry, cath breaking) Cath related infection Cath Migration Nursing Management Inspect catheter and insertion site. Assess pain. Change dressing and clean according to institution policies. Change injection caps. Flushing is important. • Catheter and insertion site assessments include inspection of the site for redness, edema, warmth, drainage, and tenderness or pain. Observation of the catheter for misplacement or slippage is important. • Transparent dressing or gauze may be used. • Discuss cleaning techniques with chlorhexidine-based preparations, povidone-iodine, and isopropyl alcohol • Teach the patient to turn the head to the opposite side of the CVAD insertion site during cap change. • Flushing: Use a normal saline solution in a syringe that has a barrel capacity of 10 mL or more to avoid excess pressure on the catheter. If resistance is felt, force should not be applied. Removing CVADs Should be done according to policy and procedures. Gently withdraw. Apply pressure. Ensure that catheter tip is intact.