Fluids, Electrolytes, Acid and Base Imbalances - Nursing Lecture PDF

Fluids, Electrolytes, & Acid/Base Imbalances Dorothy Otremba, DNP, APN, FNP-BC DePaul University NSG 422 Section 1.0 Fluids Imbalances Total Body Water (TBW) & Distribution of Fluids ► Varies according to age and fat...

Fluids, Electrolytes, & Acid/Base Imbalances Dorothy Otremba, DNP, APN, FNP-BC DePaul University NSG 422 Section 1.0 Fluids Imbalances Total Body Water (TBW) & Distribution of Fluids ► Varies according to age and fat ► 60% or 42 liters in 70-kg adult male ► 70% for newborn infants ► Three functional compartments ► Divided across two categories ► Intracellular fluid (ICF) ► Extracellular fluid (ECF) Distribution and Composition of Bodily Fluids Photo Credit: HealthJade ► Intracellular fluid (ICF) ► Inside cells ► 63–70% of TBW ► Water, proteins, electrolytes ► Extracellular fluid (ECF) ► Outside cells ► 30–37% of TBW ► Intravascular component: whole blood ► Interstitial component: surrounds cells in tissues ► Transcellular component: fluid in defined spaces Review: Movement of Water Osmosis Water moves from less concentrated to more concentrated areas to equalize concentrations Review: Movement of Molecules Diffusion Molecules move from higher to lower concentrated areas Review: Movement of Molecules Active transport Requires ATP Move molecules too large to diffuse Movement of Body Fluids: Capillary and Interstitial Fluid Exchange ► Colloid Osmotic Pressure ► AKA Oncotic Pressure ► Concentration of proteins ► Hydrostatic Pressure ► Pressure of fluids or their properties when in equilibrium  Movement of Body Fluids: Capillary and Interstitial Fluid Exchange Image Credit: McCance & Huether, 2020 Alterations in Water Movement: Edema ► Accumulation of fluid in the interstitial spaces ► Causes: ► Increased capillary hydrostatic pressure (venous obstruction; sodium retention) ► Decreased plasma oncotic pressure (losses or diminished production of albumin) ► Increased capillary permeability (inflammation and immune response) ► Lymph obstruction (lymphedema) Spacing ► First Spacing ► Normal distribution of fluid ► Second Spacing ► Abnormal accumulation of fluid in the interstitial space ► Third Spacing ► Abnormal accumulation of fluid in trans-compartmental space such as serous cavity (pericardial sac, peritoneal cavity) Lymphedema Generalized Edema Image Credit: Mayo Clinic Image Credit: ScienceMag.org Alterations in Water Movement: Edema Continued ► Assessment ► Treatment ► Daily Weights ► Elevate edematous limbs ► Visual Assessment ► Use compression stockings or devices ► Localized vs Generalized ► Avoid prolonged standing ► Assess for Pitting Edema ► Serum Albumin ► Clinical Manifestations ► Restrict salt intake ► Localized vs. generalized ► Take diuretic agents ► Dependent edema ► Pitting edema ► “Third space” ► Swelling and puffiness ► Tighter-fitting clothes and shoes ► Weight gain Overview of Electrolytes ► Electrolytes dissociate into ions in water ► Cations: positively charged ► Anions: negatively charged ► Electrolytes are in both ECF and ICF compartments but are in different concentrations. ► Some electrolytes are more concentrated in the ICF compartment, as compared with the ECF compartment. ► All electrolytes move across compartments but must be in balance for optimal health.  Overview of Electrolytes Intracellular Extracellular Cation Potassium (K+) Sodium (Na+) Anion Phosphate Chloride (Cl-) Organic Ions Bicarbonate (HCO3-) Normal Electrolyte Values Lab Normal Value Sodium (Na+_ 135-145 mEq/L Chloride (Cl-) 95-105 mEq/L Potassium (K+) 3.5 –5.0 mEq/L Bicarbonate (HCO3-) 22-26 mEq/L (arterial) Total Calcium (Ca+) 8.5 -10.5 mg/dl Ionized Calcium (Ca+) 4.5-5.6 mg/dl Magnesium (Mg2+) 1.3-2.1 mEq/L Phosphorus (PO43–) 2.5-4.5 mg/dl Serum osmolality 280-300 mOsm/kg Sodium ► Is the primary ECF cation. ► Regulates osmotic forces. ► Roles include: ► Neuromuscular irritability, acid-base balance, cellular reactions, and transport of substances ► Is regulated by aldosterone and natriuretic peptides. Sodium Concentration and Water Regulation ► Sodium concentration regulation ► Natriuretic peptides ► Atrial natriuretic peptide ► Brain natriuretic peptide ► Promote sodium and water excretion ► Renin-angiotensin-aldosterone system ► Aldosterone ► Promotes water and sodium reabsorption ► Promote excretion of potassium  Sodium Concentration and Water Regulation Image Credit: McCance & Huether, 2020  Sodium Concentration and Water Regulation Image Credit: McCance & Huether, 2020  Water Balance ► Is regulated by thirst perception and the antidiuretic hormone (ADH) ► ADH ► Thirst perception ► Released from posterior ► Osmolality receptors (osmoreceptors) pituitary ► Stimulated from hyperosmolality, ► Is released when there is an dry mouth, plasma-volume increase in plasma osmolality depletion or decrease in circulating blood volume. ► Increases water intake ► Is also called vasopressin. ► Increases water reabsorption.  Water Regulation Image Credit: McCance & Huether, 2020  Water and Sodium Imbalances – Classifications ► Volume Imbalances ► May be hypervolemia or hypovolemia ► If these occur in equal alterations of sodium and water concentration = called isotonic imbalances ► Osmolar Imbalances ► Unequal Alteration in the concentration between water and sodium or other solutes in ECF ► Osmolality ► Measure of the number of milliosmoles per kilogram of water or the concentration of molecules per weight of water ► Normal Plasma Osmolality : 280-300 mOsm/kg ► Role of Sodium in Osmolality ► Normal: 135–145 mEq/L ► Hyponatremia: below 135 mEq/L ► Hypernatremia: greater than 145 mEq/L Water and Sodium Imbalances – Classifications ► Normal Plasma Osmolality (280-300 mOsm/kg) ► Isotonic ► Solute concentrations (osmolality) = to that of normal cells (ICF) ► Hypertonic ► Solute concentrations (osmolality) > than that of normal cells (ICF) ► Hypotonic ► Solute concentrations (Osmolality) < than that of normal cells (ICF)  Water and Sodium Imbalances – Classifications Image Credit: McCance & Huether, 2020  Classifications of IV Solutions Image Credit: Rosenthal, 2006 Image Credit: Khan Academy Classifications of IV Solutions 3% sodium chloride Hyper 1026 3% NaCl Isotonic Fluid Volume Excess ► Symmetric Increase in extracellular sodium levels and fluid levels ► Clinical manifestations: ► Weight gain ► Distended neck veins ► Blood pressure: Increased ► Pulses: Bounding and Full ► Increased capillary hydrostatic pressure ► Edema ► Pulmonary: crackles, shortness of breath ► Peripheral edema Isotonic Fluid Volume Excess ► Diagnosis ► Decreased hematocrit ► Decreased blood urea nitrogen (BUN) levels ► High cardiac output ► Treatment ► Restrict fluid intake ► Monitor I/Os ► Correct underlying etiology Isotonic Fluid Volume Deficit ► Symmetric depletion of water and electrolytes ► Clinical manifestations ► Thirst ► Decreased urine output ► Weight loss ► Increased hematocrit ► Tachycardia ► Decreased skin turgor ► Flattened neck veins Photo Credit: NEJ: Feyens ► Decreased blood pressure and de Jager, 2011) ► Potentially hypovolemic shock Isotonic Fluid Volume Deficit ► Diagnosis ► Increased hematocrit ► Increased BUN: creatinine ratio ► Increased urine osmolality ► Increased specific gravity ► Treatment ► Correct underlying etiology ► Increased oral fluid ► IV rehydration Age Considerations for Fluid Volume Deficits ► Potential causes of dehydration: ► Infants ► Diarrhea and vomiting ► Older adults ► Smaller fluid reserves ► Reduced ability to conserve water ► Less acute sense of thirst Section 2.0 Electrolyte Imbalances Normal Electrolyte Values Lab Normal Value Sodium (Na+_ 135-145 mEq/L Chloride (Cl-) 95-105 mEq/L Potassium (K+) 3.5 –5.0 mEq/L Bicarbonate (HCO3-) 22-26 mEq/L (arterial) Total Calcium (Ca+) 8.5 -10.5 mg/dl Ionized Calcium (Ca+) 4.5-5.6 mg/dl Magnesium (Mg2+) 1.3-2.1 mEq/L Phosphorus (PO43–) 2.5-4.5 mg/dl Serum osmolality 280-300 mOsm/kg Sodium ► Is the primary ECF cation. ► Regulates osmotic forces. ► Roles include: ► Neuromuscular irritability, acid-base balance, cellular reactions, and transport of substances ► Is regulated by aldosterone and natriuretic peptides. Hypernatremia ► Sodium concentration greater than 145 mEq/L ► Causes ► Increased output or decreased intake of water ► Other etiologies ► Clinical manifestations ► Hyperosmolality ► Increases thirst ► Dry membranes, decreased skin turgor, salivation decreased ► Vital Signs ► *CNS symptoms: headaches, restlessness, agitation ► Serious: seizures, coma Hypernatremia ► Diagnosis ► Increased serum sodium and increased serum osmolality ► Increased urine specific gravity ► Treatment ► Assess and correct underlying etiology ► Decrease serum sodium ► Hypotonic fluids ► Gradual correction if parenteral  Hyponatremia ► Sodium concentration below 135 mEq/L ► low serum Na levels ► Causes ► prolonged vomiting and diarrhea from losing electrolytes ► hypovolemic and hypervolemic states ► Diuretics- loss of electrolytes ► Other diseases and conditions ► Diabetic Ketoacidosis- uncontrolled high amounts of glucose pulls water from inside of cells to outside ► Clinical manifestations ► **Neurological effects: anxiety, lethargy, headaches ► Severe = coma/seisurez hypotonic environment from water moving into cells cellular edema ► GI: nausea/vomiting, abdominal cramps ► MSK: muscle cramps, fatigue Hyponatremia ► Diagnosis ► Decreased serum sodium, chloride levels ► Increased hematocrit (if vol deficient also present) ► Treatment ► Treat underlying etiology ► Mild: oral sodium replacement- ► Moderate: Isotonic IV fluids 0.9 normal saline sodium chloride ► Severe: hypertonic fluids- 3% NaCl ► Rapid administration can lead to central pontine myelinolysis ► breakdown of myelin in the pons center of the brain ► Brain cells can adapt in hypotonic fluid environments Chloride ► Chloride ► Is the primary ECF anion. ► Normal: 95-105 mEq/L ► Provides electroneutrality. ► Follows sodium. ► Component of hydrochloric acid in the stomach ► Essential for carbon dioxide transport in red blood cells Hyperchloremia ► Abnormally high plasma concentration of chloride ions ► Causes ► Metabolic acidosis ► Water loss, dehydration ► Head injury that causes endocrine abnormalities ► Hypernatremia, severe diarrhea, respiratory alkalosis ► Clinical manifestations ► Resemble hypernatremia ► Symptoms related to dehydration Hyperchloremia ► Diagnosis ► Increased serum chloride ► Metabolic acidosis or respiratory alkalosis ► Treatment ► IV hypotonic fluids, lactated Ringer’s, sodium bicarbonate (acid–base imbalances) ► Diuretic therapy (concurrent hypernatremia) ► Restriction of sodium and chloride in diet Hypochloremia ► Abnormally low plasma concentration of chloride ions ► Causes ► Vomiting, diarrhea, nasogastric suctioning ► Alkalosis ► Burns ► Diuretics ► Hormones Hypochloremia ► Clinical manifestations ► Resemble hyponatremia ► Cerebral edema ► Headache, weakness, nausea, tetany ► Diagnosis ► Decreased serum chloride ► Metabolic alkalosis ► Treatment ► Isotonic saline or hypertonic saline ► Replacement with oral sodium chloride Potassium ► Is the major intracellular cation. ► Normal concentration: 3.5–5.0 mEq/L ► Regulates ICF osmolality- ► Is essential for the transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction. ► The sodium-potassium (Na + /K +) pump maintains concentration.  Potassium ► Factors influencing the movement of potassium ► Acid/Base Balance ► Acidosis ► Facilitates movement of k+ out of cell in exchange for h+ (hyperkolemia) ► Alkalosis ► Facilitates movement of k+ into cell in exchange for h+ (hypokolemia) ► Exercise -causes movement of K outside of cell ► Epinephrine ► Facilitates movement of k+ into cell with ATPase pump ► Aldosterone ► Promotes k+ excretion in distal tubule of kidneys ► Insulin- Used for hypokalemia ,lowers potassium levels in the blood ► Facilitates movement of K+ into liver and muscle cells Hyperkalemia ► Abnormally high plasma concentration of potassium ions [ >5 mEq/L] ► Causes ► Over supplementation of K ► Decreased renal excretion or renal failure (associated with metabolic acidosis) ARBS have side effects of Hyperkalemia- Pril, Losartan, Spironolactone ► Shifts from k+ to ECF ► Acidosis- body will try to compensate and move excess H ions out of ECF and into the cell. K is then moved outside of the cell ► Insulin deficiency- won't be able to move K into muscle cells ► Cell hypoxia ► Endocrine abnormalities- low aldosterone level productions ► Aldosterone= retains Na and H20 and moves out K Hyperkalemia ► Clinical manifestations ► Cardiac: ECG changes [PEAKED T Waves], dysrhythmias Increased neuromuscular excitability ► Severe hyperkalemia = cardiac arrest ► Tall T waves ► Neuromuscular ► Initial increased neuromuscular irritability ► More Severe (Prolonged) : muscle weakness, loss of muscle tone, paralysis ► GI: nausea, vomiting, diarrhea , cramps Hyperkalemia Image Credit: Jorge Muniz , 2013 ► Mild Hyperkalemia ► Tingling of lips and fingers, restlessness, intestinal cramping and diarrhea, Peaked T waves on the ECG ► Severe Hyperkalemia ► Muscle weakness, loss of muscle tone, flaccid paralysis, cardiac arrest Hyperkalemia ► Diagnosis ► Increased serum potassium levels ► Peaked T waves in EKG ► Treatment ► Sodium polystyrene sulfonate- cal oxalate exchanges Na or Ca, PO or enema **Do not mix with juice due to high K in oj.** ► Hemodialysis- if there is renal failure ► Change diuretic medication- ► IV calcium gluconate- antagonizes the increased muscular excitability, Stabilizes cardiac potential (short fix) ► IV Insulin helps increase K entry into the cell and Dextrose 50%-  Hypokalemia ► Abnormally low plasma concentration of potassium ions [ 2.1 mg/dL ► Causes ► Renal failure ► Excessive use of magnesium containing medications (Antacids, laxatives) ► Clinical manifestations ► Decreased neuromuscular excitability ► Lethargy, hyporeflexia, confusion, muscle weakness ► Cardiac ► Hypotension ► Cardiac arrest in severe hypermagnesemia ► Diagnosis: increased serum magnesium ► Treatment: cease all magnesium-containing medications Hypomagnesemia ► Abnormally low plasma concentration of magnesium ions < 1.3 mg/dL ► Causes ► Decrease dietary intake/absorption in GI tract ► Other etiologies : diarrhea, malabsorption syndrome, prolonged NG suction, chronic alcoholism ► Clinical manifestations: ► Increased neuromuscular excitability ► + Chvostek and Trousseau ; tetany, paresthesia ► CV: Tachycardia, HTN ► Diagnosis: decreased serum magnesium ► Treatment ► Dietary management ► Magnesium supplements Section 3.0 Acid –Base Imbalances Acid and Base Balance pH—What is it? ► Negative logarithm of the H+ concentration ► Each number represents a factor of 10. ► If the solution moves from a pH of 7 to a pH of 6, then the H+ ions have increased tenfold. ► If H+ is high in number, pH is low (acidic). ► If H+ is low in number, pH is high (alkaline).  Increasing H+ pH scale Decreasing H+ 0 7 14 Very acidic Neutral Very alkaline Acid – Base Balance ► Acids are formed as end-products of protein, carbohydrate, and fat metabolism. ► To maintain the body’s normal pH (7.35-7.45) the H+ must be neutralized by the retention of bicarbonate or excreted. ► Bones, lungs, and kidneys are major organs involved in the regulation of acid-base balance. ► pH below 6.8 = death. ► pH above 7.8 = death.  Photo Credit: Sorenson et al., 2019 Figure 9.2 ► The pH scale and relationship between bicarbonate and carbonic acid. Acid-Base Balance ► Acid-base balance is mainly concerned with two ions: ► Hydrogen (H+) ► Bicarbonate (HCO3–) ► Alterations of hydrogen and bicarbonate concentrations in body fluids are common in disease processes. Acid- Base Balance ► Volatile Acids in the ► Nonvolatile Acids in the body Body ► Sulfuric, phosphoric, and ► Carbonic acid (H2CO3) other metabolic acids ► Can be eliminated as ► Is eliminated by the renal carbon dioxide (CO2) tubules with the regulation gas via the lungs of HCO3– Acid-Base Balance ► Sources of H+ ions ► CO2 diffuses into the bloodstream where the following reaction occurs: ► Regulated by the Lung Regulated by the Kidney ► CO2 + H2O ←→ H2CO3 ←→ HCO3–+ H+ Compensation vs Correction ► Compensation ► Chemical buffers, renal or respiratory function return pH within normal range ► Underlying disease process still present ► Correction ► Condition responsible for imbalance is controlled or no longer present ► pH is within normal range Renal regulation of Acid – Base Balance ► Essential for maintenance of acid–base balance ► Regulate bicarbonate and nonvolatile acids ► Three mechanisms: ► Conservation/Reabsorption of bicarbonate ► Secretion of H+ into urine; ► Synthesis of new bicarbonate ► Others: ► Buffering of H+ with Ammonia and Phosphate ► Renal compensation less effective in presence of kidney disease  Renal Buffering Figure 9.3 ► Conservation of bicarbonate ions. Photo Credit: Sorenson et al., 2019  Renal Buffering Figure 9.4 ► Secretion of H+ in the urine and synthesis of new HCO3–. Photo Credit: Sorenson et al., 2019  Renal Buffering Figure 9.5 ► Excretion of H+ buffered by ammonia. Photo Credit: Sorenson et al., 2019 Buffering Systems ► Protein buffering ► Proteins have negative charges; as a result, they can serve as buffers for H+; mainly intracellular buffer with hemoglobin ► Respiratory and renal buffering ► Respiratory: Acidemia causes increased ventilation; alkalosis slows respirations ► Renal: Secretion of H+ in urine and reabsorption of HCO3–; synthesis of new bicarb, Buffering of h+ with ammonia and phosphate creating monobasic or dibasic phosphate and ammonium ► Cellular ion exchange ► Exchanges of K+ for H+ in acidosis and alkalosis Acid – Base Imbalances ► Normal arterial blood pH ► 7.35 to 7.45 ► Obtained by arterial blood gas (ABG) sampling ► Acidosis ► pH is less than 7.35 ► Systemic increase in H+ concentration ► Alkalosis ► pH is greater than 7.45 ► Systemic decrease in H+ concentration or excess of base Acid – Base Imbalances ► Four categories ► Respiratory acidosis—Elevation of pCO2 as a result of ventilation depression ► Respiratory alkalosis—Depression of pCO2 as a result of hyperventilation ► Metabolic acidosis—Depression of HCO3– or an increase in non0carbonic acids ► Metabolic alkalosis—Elevation of HCO3–, usually as a result of an excessive loss of metabolic acids Acid – Base Imbalances ► Effects of acidosis ► Similar in respiratory and metabolic acidosis ► Effects of alkalosis ► Similar in respiratory and metabolic alkalosis  Effects of Acidosis and Alkalosis on Neuromuscular Function ► Acidosis ► More H+ bind to proteins with fewer sites available for calcium ► Increases level of calcium ► Blocks sodium channels in nerves and muscles ► Decreased neuromuscular activity ► Causes muscle weakness, resp failure, vasodilation, headaches, confusion ► Alkalosis ► Increased neuromuscular activity ► + Chvostek and Trousseau sign ► Hyperactive reflexes ► Tetany ► Laryngospasms CNS Alterations in Acidosis and Alkalosis ► Due to change in pH and changes in cerebral blood flow ► Acidosis ► Vasodilation of cerebral blood vessels ► Increased cerebral blood flow ► Intracranial pressure ► Alkalosis ► Vasoconstriction of cerebral blood vessels ► Decreased blood and O2 delivery to brain Effects of Acidosis and Alkalosis on Perfusion ► Acidosis ► Decrease in cardiac contractility ► Alkalosis ► Increase in contractility up to pH of 7.7 ► Decreased cardiac contractility with pH levels greater than 7.7 Effects of Acidosis and Alkalosis on Electrolyte Levels ► Metabolic acidosis caused by excess of inorganic acids ► Excess H+ enter cells in exchange for movement of K+ out of cells ► Hyperkalemia results ► Metabolic acidosis caused by excess organic acids ► H+ and anion move into the cell ► Respiratory and metabolic alkalosis ► Some H+ move out of cells in exchange for K+ movement into cells ► Hypokalemia results Effects of Acidosis and Alkalosis on Oxygenation Shift to the right Shift to the left Hemoglobin has Hemoglobin has decreased affinity to O2 increased affinity to O2 Result= Increase in ease Result= inhibits of oxyhemoglobin dissociation in the dissociation ->more tissues-> less unloading unloading o2= o2 moves 02= less O2 moves into into the cells the cells Causes: Causes: Acidosis Alkalosis Others: hypercapnia, Others:hypocapnia, hyperthermia hypothermia Laboratory Tests: Arterial Blood Gases (ABGs) ► Most useful test for acid–base assessment ► Measures these values in arterial blood* ► pH (normal: 7.35–7.45) ► PaCO2 (normal: 35–45 mmHg) ► PaO2 (normal: 80–100 mmHg; 60–70 mmHg in newborns) ► HCO3– (normal: 22–26 mEq/L) ► Total CO2 (TCO2) ► Measure of all forms of CO2 in blood Laboratory Tests: Venous Blood Gases ► Same measures as ABGs but in venous blood ► Normal ranges ► pH: 7.3–7.41 ► HCO3–: 21–22 mEq/L ► In cardiovascular collapse venous blood gas values cannot substitute for arterial blood gases Laboratory Tests: Base Excess Test ► Detects excess of base (positive number) or deficit of base (negative number) ► Measure of all bases in blood ► Positive number >2.0 mEq/L ► Metabolic alkalosis or ► Renal compensation for respiratory acidosis ► Negative number < –2.0 mEq/L ► Metabolic acidosis or ► Renal compensation for respiratory alkalosis Laboratory Tests: Anion Gap ► Detects increased amount of anions ► Calculated by subtracting sum of anions Cl– and bicarbonate from concentration of cation Na+ Laboratory Tests: Anion Gap ► Anion gap ► Used cautiously to distinguish different types of metabolic acidosis. ► By rule, anions (–) should equal cations (+). ► Not all normal anions are routinely measured. ► Represents unmeasured negative ions. ► Normal anion gap is 10 to 12 mEq/L. ► Normal anion gap or elevated anion gap with metabolic acidosis may help determine the cause. ► High= net gain of acid (e.g. renal failure, lactic acidosis, DKA) ► Normal= loss of bicarbonate (e.g. diarrhea, renal tubular acidosis) Laboratory Test: Anion Gap Elevated Anion Gap Normal Anion Gap Ketoacidosis Diarrhea Lactic Acidosis (shock, Ileostomy drainage hypoxemia) Intestinal suctioning Decreased rental H+ Early renal failure (loss of excretion in advanced bicarb) renal failure Laboratory Tests: Anion Gap Section 4.0 Acid/Base Imbalance Diagnosis Respiratory Acidosis ► Pathogenesis: ► Occurs with alveolar hypoventilation ► pH is below 7.35. ► CO2 elevated from hypercapnia Respiratory Acidosis ► Causes ► Impaired elimination of CO2 by lungs ► Respiratory diseases or conditions ► Respiratory muscle paralysis ► Disorders of the chest wall (kyphoscoliosis, pickwickian syndrome, flail chest) ► CNS dysfunction ► Depression of the respiratory center (brainstem trauma, oversedation) ► Electrolyte imbalances ► Metabolic conditions Respiratory Acidosis ► Characteristics ► Elevated PaCO2 (hypercapnia) ► Blood pH 26 mEq/L in arterial blood ► Treatment ► Improve alveolar ventilation to elimination of CO2 ► may need mechanical ventilation ► administer IV lactate fluids Respiratory Acidosis Condition PH Level PACO2 Level HCO3 Level Respiratory Acidosis: Uncompensated Initially Normal Resp Acidosis ↓ ↑ Partially Compensated Resp ↓ Acidosis ↑ ↑ Compensated Resp Normal Acidosis ↑ ↑ Respiratory Alkalosis ► Pathogenesis: ► Occurs with hyperventilation and decreased plasma CO2 (hypocapnia) ► pH above 7.45 ► CO2 is decreased below 35 mm Hg  Respiratory Alkalosis ► Causes ► Hyperventilation (excess elimination of CO2) ► CNS dysfunction ► Emotions ► Medication ► Mechanical ventilation ► Early salicylate intoxication ► Anxiety or panic disorder ► High altitudes ► Hypermetabolic states, such as fever, anemia, and thyrotoxicosis Respiratory Alkalosis ► Characteristics ► Increased blood pH ► Decreased pCO2 (hypocapnia) ► Clinical manifestations ► Increased neuromuscular excitability ► Impaired cell oxygenation ► Dizziness, confusion, tingling of extremities (paresthesias), convulsions Respiratory Alkalosis ► Compensation ► Kidneys decrease H+ excretion and bicarbonate absorption ► Renal compensation ► Decreased bicarbonate resorption ► Decreased H+ excretion ► Bicarbonate ► 1. Increased accumulation of fixed acids ► 2. Inability of kidneys to excrete fixed acids ► 3. Excessive loss of bicarb via kidneys or GI tract ► pH drops below 7.35 ► HCO3– drops: less than 22 mEq/L Metabolic Acidosis ► Characteristics ► Decreased blood pH ► Decreased HCO3– ► Initially Normal PaCO2 > then starts decreasing ► Causes ► Lactic acidosis ► Chronic Kidney Disease ► Diabetic ketoacidosis ► Starvation ► GI: Diarrhea, intestinal suctioning, ileostomy drainage  Metabolic Acidosis – Elevated vs Normal Anion Gap Elevated Anion Gap Normal Anion Gap Ketoacidosis Diarrhea Excess in Loss in Lactic Acidosis (shock, Ileostomy drainage Metabolic hypoxemia) Intestinal suctioning Bicarb Acids Decreased rental H+ Early renal failure (loss of excretion in advanced bicarb) renal failure  Metabolic Acidosis ► Clinical manifestations ► Increased rate and/or depth of breathing (Kussmaul Respirations) ► Decreased neuromuscular excitability ► Headache ► Physiological Compensation ► Hyperventilation and renal excretion of excess acid ► Treatment ► Reversal of underlying cause Sodium bicarbonate for life-threatening normal anion gap metabolic acidosis ► Lactate-containing solutions: Lactate converted into bicarbonate in the liver Metabolic Acidosis Condition PH Level PACO2 Level HCO3 Level Metabolic Acidosis: Uncompensated Metabolic Acidosis ↓ Initially Normal ↓ Partially Compensated ↓ Metabolic Acidosis ↓ ↓ Compensated Normal Metabolic Acidosis ↓ ↓ Metabolic Alkalosis ► Pathogenesis: ► Either: ► 1. Gain of excess bicarbonate ► 2. Loss of fixed acids ► pH is elevated above 7.45 ► HCO3– is elevated above 26 mEq/L Metabolic Alkalosis ► Characteristics ► Increased blood pH ► Increased HCO3– ► Initially Normal PaCO2 > then starts increasing ► Causes ► Excessive loss of hydrogen ions ► Excessive intake of base ► Excessive renal retention of bicarbonate ► Prolonged vomiting ► Gastric suctioning ► Excessive bicarbonate intake ► Hyperaldosteronism with hypokalemia ► Diuretic therapy Metabolic Alkalosis ► Clinical manifestations ► Decreased rate and/or depth of breathing ► Increased neuromuscular excitability ► Muscle cramps ► Impaired cell oxygenation ► Compensation: ► Hypoventilation; kidneys conserve H+ and eliminate bicarbonate. ► Treatment ► Reversal of underlying cause ► Correction of any fluid, potassium, or chloride deficits ► Sodium chloride, potassium, chloride IV (chloride replaces HCO3-) Metabolic Alkalosis Condition PH Level PACO2 Level HCO3 Level Metabolic Alkalosis Uncompensated Metabolic Alkalosis ↑ Initially Normal ↑ Partially Compensated ↑ Metabolic Alkalosis ↑ ↑ Compensated Normal Metabolic Alkalosis ↑ ↑ Mixed Acid- Base Imbalances ► Two or more types of acid–base imbalances ► Two conditions that cause acidosis ► Two conditions that cause alkalosis ► One condition that causes acidosis and one that causes alkalosis ► pH may be low, high, or within normal range ► Depends on degree to which conditions alter pH Stepwise Analysis of Acid – Base Imbalances ► Type determined by: ► Patient’s history ► Clinical manifestations ► Lab tests, including arterial or venous blood gas data ► ROME (direction of change of values) ► Respiratory ► Opposite ► Metabolic ► Equal Stepwise Analysis of Acid – Base Imbalances ► Respiratory acid–base imbalances ► pH and PaCO2 move in opposite directions ► Metabolic acid–base imbalances ► pH and HCO3– move in same direction ► Mixed acid–base imbalances Questions??? Practice Questions  Alterations in Water Movement: Edema Question 1 ►A person with heart failure has edema in the lower legs and sacral area. The nurse suspects this condition is due to a(n): 1. Increase in plasma oncotic pressure 2. Decrease in capillary hydrostatic pressure 3. Decrease in lymph obstruction pressure 4. Increase in capillary hydrostatic pressure Alterations in Water Movement: Edema Question 1 ► ANSWER AND RATIONALE: 4. Increase in capillary hydrostatic pressure. Heart failure produces salt and water retention and subsequent volume overload, which increases capillary hydrostatic pressure which leads to edema. ► 1. An increase in plasma oncotic pressure produces movement of fluid from the interstitial space into the vascular space which would decrease edema. ► 2. A reduction in capillary hydrostatic pressure decreases the force for filtration of fluid from the capillary which would decrease edema. ► 3. A decrease in lymph obstruction would not cause edema; an increase in lymph obstruction would lead to edema.  Water Balance Question 2 ►A person reports severe diarrhea for 2 days. The nurse understands this stimulates a(n): 1. Reduction in aldosterone secretion 2. Reduction in renin secretion 3. Increase in antidiuretic hormone secretion 4. Increase in natriuretic peptide secretion Water Balance Question 2 ► ANSWER AND RATIONALE: 3. Increase in antidiuretic hormone secretion. Hypovolemia stimulates volume sensitive receptors and baroreceptors and results in secretion of antidiuretic hormone to increase water reabsorption. ► 1. Volume depletion produces an increase in aldosterone secretion through the activation of the renin angiotensin aldosterone system. ► 2. Volume depletion produces an increase in renin secretion and initiates the renin angiotensin aldosterone system. ► 4. Volume depletion results in reduced secretion of natriuretic peptides. Natriutetic peptides are diuretics which would make more loss of fluid.  Acid/Base Question 3 ►A person arrives in the emergency department after a loss of consciousness and the development of Kussmaul respirations. The individual has a history of diabetes and 2 days of vomiting and diarrhea. The nurse suspects the person has: 1. Respiratory alkalosis 2. Respiratory acidosis 3. Metabolic alkalosis 4. Metabolic acidosis Acid/Base Question 3 ► ANSWER AND RATIONALE: 4. Metabolic acidosis. ► 1. Respiratory alkalosis is produced by alveolar hyperventilation and reduction in carbon dioxide concentration. ► 2. Respiratory acidosis is produced by alveolar hypoventilation and increase in carbon dioxide concentration. ► 3. Metabolic alkalosis is produced by an excess of bicarbonate ion.  Acid/Base Question 4 ►A person with a history of chronic lung disease arrives in the clinic with a 1-week history of a productive cough, hypoventilation, headache, and muscle twitching. The nurse suspects the person is experiencing: 1. Respiratory acidosis 2. Respiratory alkalosis 3. Metabolic acidosis 4. Metabolic alkalosis Acid/Base Question 4 ► ANSWER AND RATIONALE: 1. Respiratory acidosis. Respiratory acidosis is produced by alveolar hypoventilation, which is commonly found in individuals with chronic obstructive pulmonary disease. Headache and muscle twitching are symptoms of elevated carbon dioxide levels produced by hypoventilation. ► 2. Respiratory alkalosis is produced by alveolar hyperventilation and reduction in carbon dioxide concentration. Symptoms of respiratory alkalosis include dizziness, confusion, paresthesia, convulsions, and coma. ► 3. Metabolic acidosis is produced by an increase in noncarbonic acids and/or a decrease in bicarbonate ion. Symptoms of metabolic acidosis include headache, lethargy, Kussmaul respirations, anorexia, nausea and vomiting, dysrhythmias, and coma. ► 4. Metabolic alkalosis is produced by an excess of bicarbonate ion. Symptoms of metabolic alkalosis include muscle weakness, muscle cramps, hyperreflexia, paresthesias, tetany, and seizures.