Topics For The Day Fluid And Electrolytes & Renal Disorders

Topics for the DayFluid and Electrolytes& Renal Disorders Fluids and Electrolytes: review ofnormal physiology * Fluid imbalances * Electrolyte Disturbances * Beginning acidacid-base imbalance * Renal Disorders Fluid Types *Electrolytes Solutes that form ions (electricalcharge) Cation ( ) Anion ((-) Major body electrolytes: Na , K , Ca , Mg ClCl-, HCO3-, HPO4--,--, SO4-Fluid & Electrolytes Fluid: Water Electrolytes: ions dissolved in water Sodium, potassium, bicarbonate, etc. Also used medically for non ions (glucose) Osmolarity – osmols/kgosmols/kg solvent Osmolality – osmols/literosmols/liter solution In clinical practice are usedinterchangeablyElectrolyte Distribution Major ICF ions K HPO4-- Major ECF ions NA CLCL-, HCO3- Intravascular (IVF) vs Interstitial (ISF) Similar electrolytes, but IVF has proteins1

Mechanisms Controlling Fluidand Electrolyte Movement Diffusion Selective Permeability Facilitated diffusion Active transport Osmosis 2*Na BUN Glucose/18 Hydrostatic pressure Oncotic pressureCells are selectively permeableSodium is the largest Determinantof Osmolality Na : 135 – 145 mEq/LmEq/L Ca : 8.5 – 10.5 mEq/LmEq/L K : 3.5 – 5 mEq/LmEq/L Osmolality Osmolality 2*(Na ) 2*(135 - 145mEq/L)mEq/L) Normal (Isotonic) 280 – 300 Low (hypotonic) 280 High (hypertonic) 3002

Fluid Exchange Between Capillaryand Tissue: Sum of PressuresFluid Shifts Plasma to interstitial fluid shiftresults in edema Elevation of hydrostatic pressure Decrease in plasma oncotic pressure Elevation of interstitial oncotic pressureFig. 17-8Fluid Movement betweenECF and ICFFluid Spacing Water deficit (increased ECF) First spacing: Normal distribution of Associated with symptoms that resultfrom cell shrinkage as water is pulledinto vascular system Water excess (decreased ECF) ECF) Develops from gain or retention ofexcess waterRegulation of Water Balance Hypothalamic regulation Pituitary regulation Adrenal cortical regulation Renal regulation Cardiac regulation Gastrointestinal regulation Insensible water lossfluid in ICF and ECF Second spacing: Abnormalaccumulation of interstitial fluid(edema) (edema) Third spacing: Fluid accumulation inpart of body where it is not easilyexchanged with ECF (e.g. ascites) ascites) F&E BalanceReninEpinephrineAngiotensin IAngiotensin IIAtria (ANP) Ventricles (BNP) Endothelium (CNP) Aldosterone3

Fluid Status Indicators Physical exam Mucous membranes Turgor Output (volume) (volume) Specific Gravity* Blood Hematocrit PlasmaF&E Balance Urine 1.003: less conc 1.030: more conc Electrolytes Fluids Normal Contracted Expanded Electrolytes (Sodium!!!) Isotonic Hypertonic Hypotonic BUNExtracellular Fluid Deficit Causes Inadequate intake, diuresis, excesssweating, burns, diarrhea, vomiting,hemorrhage Treatment Stop underlying disorder Replace fluids appropriately Treat complicationsD5WHypotonicVolume Deficit½ NS½ NS(0.45%) CrystalloidsIsotonicNS (0.9%) Lactated RingerHypertonicPlasmalyteIV Fluids3% SalineAlbuminD5W in ½ NSDextranD10WColloidsFFP Isotonic Deficit Electrolyte drinks Isotonic saline (0.9%) injection Hypertonic Deficit Drinking Water Hypotonic saline (0.45%) injection, D5W Hypotonic Deficit Isotonic Saline Hypertonic saline (3%)PRBCs4

Extracellular Fluid Excess Causes The Three failures: heart, liver, kidney Treatment Remove fluid -- -- ? Treat underlying disorderElectrolyte Disorders: Signs &Symptoms (most common*) ElectrolyteExcessDeficitSodium (Na) HypernatremiaThirstCNS deteriorationIncreased interstitial fluidHyponatremiaCNS deteriorationPotassium (K) HyperkalemiaVentricular fibrillationECG changesCNS changesWeaknessHypokalemiaBradycardiaECG changesCNS changesFatigueElectrolyte Normal Values(memorize!!!!!) Sodium 135 – 145 Potassium 3.5 – 5 Chloride 106 – 106 Calcium 9 – 11 BUN 10 – 20 Creatinine 0.7 – 1.2 CO2 (really bicarb)bicarb) 22 – 26 Magnesium: 1.5 – 2.5Electrolyte DisordersSigns and SymptomsElectrolyteExcessDeficitCalcium (Ca) HypercalcemiaThirstCNS deteriorationIncreased interstitial fluidHypocalcemiaTetanyChvostek’s, Trousseau’ssignsMuscle twitchingCNS changesECG changesMagnesium (Mg) HypermagnesemiaLoss of deep tendon reflexes(DTRs) Depression of CNSDepression of neuromuscularfunctionHypomagnesemiaHyperactive DTRsCNS changesHypernatremiaHypernatremia Treatment Manifestations Treat underlying cause If oral fluids cannot be ingested, IV Thirst, lethargy, agitation, seizures, andcoma Impaired LOC Produced by clinical states Central or nephrogenic diabetesinsipidussolution of 5% dextrose in water orhypotonic saline Diuretics if necessary Reduce levels gradually to avoidcerebral edema5

HyponatremiaTreatment Results from loss of sodiumsodium-containing Oral NaCl If caused by water excessfluids Sweat, diarrhea, emesis, etc. Or from water excess Inefficient kidneys Drowning, excessive intake Manifestations Confusion, nausea, vomiting, seizures, andcoma Fluid restriction is needed If Severe symptoms (seizures) (seizures) Give small amount of IV hypertonicsaline solution (3% NaCl) NaCl) If Abnormal fluid loss Fluid replacement with sodiumsodiumcontaining solutionHyperkalemiaHyperkalemia High serum potassium caused by Manifestations Massive intake Impaired renal excretion Shift from ICF to ECF (acidosis) (acidosis) Drugs Weak or paralyzed skeletal muscles Ventricular fibrillation or cardiacstandstill Abdominal cramping or diarrhea Common in massive cell destruction Burn, crush injury, or tumor lysis False High: hemolysis of sampleTreatment Emergency: Calcium Gluconate IV Stop K intake Force K from ECF to ICF IV insulin Sodium bicarbonate Increase elimination of K (diuretics,dialysis, Kayexalate) Kayexalate) 6

HypokalemiaHypokalemia Low serum potassium caused byK Abnormal losses ofvia the kidneysor gastrointestinal tract Magnesium deficiency Metabolic alkalosis Manifestations Most serious are cardiac Skeletal muscle weakness Weakness of respiratory muscles Decreased gastrointestinal motilityHypokalemiaCalcium KCl supplements orally or IV Should not exceed 10 to 20 mEq/hr Obtained from ingested foods More than 99% combined with No Pee no Kay!!!!!!!!!!!!!!!!!!!!!!!!!phosphorus and concentrated inskeletal system Inverse relationship with phosphorusCalciumCalcium Bones are readily available store Blocks sodium transport and Functions To prevent hyperkalemia and cardiacarreststabilizes cell membrane Ionized form is biologically active Bound to albumin in blood Bound to phosphate in bone/teeth Calcified deposits Otherwise Otherwise Transmission of nerve impulses Myocardial contractions Blood clotting Formation of teeth and bone Muscle contractions7

CalciumHypercalcemia Balance controlled by High serum calcium levels caused by Parathyroid hormone Calcitonin Vitamin D/Intake Bone used as reservoir Hyperparathyroidism (two thirds ofcases) cases) Malignancy (parathyroid tumor) tumor) Vitamin D overdose Prolonged immobilizationHypercalcemiaTreatment Manifestations Excretion of Ca with loop diuretic Hydration with isotonic saline Decreased memory Confusion Disorientation Fatigue Constipationinfusion Synthetic calcitonin MobilizationHypocalcemiaHypocalcemia Low serum Ca levels caused by Manifestations Decreased production of PTH Acute pancreatitis Multiple blood transfusions Alkalosis Decreased intake Weakness/Tetany Positive Trousseau’Trousseau’s orChvostek’Chvostek’s sign Laryngeal stridor Dysphagia Tingling around themouth or in the extremities8

TreatmentPhosphate Treat cause Oral or IV calcium supplements Primary anion in ICF Essential to function of muscle, red Not IM to avoid local reactions Treat pain and anxiety to preventhyperventilationhyperventilation-induced respiratoryalkalosisblood cells, and nervous system Deposited with calcium for bone andtooth structurePhosphateHyperphosphatemia Involved in acid–acid–base buffering High serum PO43 caused bysystem, ATP production, and cellularuptake of glucose Maintenance requires adequate renalfunctioning Essential to muscle, RBCs, andnervous system function Acute or chronic renal failure Chemotherapy Excessive ingestion of phosphate orvitamin D Manifestations Calcified deposition: joints, arteries,skin, kidneys, and corneas Neuromuscular irritability and tetanyHyperphosphatemiaHypophosphatemia Management Low serum PO43 caused by Identify and treat underlying cause Restrict foods and fluids containingPO43 Adequate hydration and correction ofhypocalcemic conditions Malnourishment/malabsorption Alcohol withdrawal Use of phosphatephosphate-binding antacids During parenteral nutrition withinadequate replacement9

HypophosphatemiaHypophosphatemia Manifestations Management CNS depression Confusion Muscle weakness and pain Dysrhythmias Cardiomyopathy Oral supplementation Ingestion of foods high in PO43 IV administration of sodium orpotassium phosphateMagnesiumMagnesium 50% to 60% contained in bone Coenzyme in metabolism of protein Acts directly on myoneural junction Important for normal cardiacand carbohydrates Factors that regulate calcium balanceappear to influence emia High serum Mg caused by Manifestations Increased intake or ingestion ofproducts containing magnesium whenrenal insufficiency or failure is present Lethargy or drowsiness Nausea/vomiting Impaired reflexes*** Respiratory and cardiac arrest10

HypermagnesemiaHypomagnesemia Management Low serum Mg caused by Prevention Emergency treatment IV CaCl or calcium gluconate Fluids to promote urinary excretion Prolonged fasting or starvation Chronic alcoholism Fluid loss from gastrointestinal tract Prolonged parenteral nutrition withoutsupplementation DiureticsHypomagnesemiaHypomagnesemia Manifestations Management Confusion Hyperactive deep tendon reflexes Tremors Seizures Cardiac dysrhythmias Oral supplements (MgO, MgSO4) Increase dietary intake Parenteral IV or IM magnesium whensevereElemenary Acid-Base balanceMetabolic Panel and acid-base Buffer systems “CO2”CO2” on a BMP means bicarb!!!!!! normal 22 – 26 22 ? 26 ? Carbonic Acid Bicarbonate Metabolic: bicarb low metabolic acidosis high metabolic alkalosis Respiratory: carbon dioxide11

Metabolic Acidosis ManifestatMetabolic Alkalosis Manifestat Acidosis causes HYPERKALEMIA!!! Neuro:Neuro: Drowsiness, Confusion, H/A, Alkalosis causes HYPOKALEMIA!!! Neuro:Neuro: Dizziness, Irritability,coma CV: BP, dysrhythmia (K ), dilation GI: NVD, abd pain Resp: increased resp (comp) (comp) MEMORIZE Arterial pH, PaCO2,HCO3-!!!!!!!Nervous, Confusion CV: HR, dysrhythmia (K ) (K ) GI: NV, anorexia Neuromuscular: Tetany, tremor,paresthesia, seizures Resp: decreased resp (comp) (comp) Interpretation of ABGs Diagnosis in six steps Evaluate pH Analyze PaCO2 Analyze HCO3 Determine if Balanced or Unbalanced Determine if CO2 or HCO3 matchesthe alteration Decide if the body is attempting tocompensateInterpretation of ABGInterpretation of ABGs1.2.3.4.5. pH 7.36 PaCO2 67 mm Hg PaO2 47 mm Hg HCO3 37 mEq/L What is this?pH over balancePaCO2 “respiratory”respiratory” balanceHC03HC03- “metabolic”metabolic” balanceIf all three normal balancedMatch direction. e.g., if pH and PaCO2are both acidotic,acidotic, then primaryrespiratory acidosis6. If other is opposite, then partialcompensation; if pH normal, then fullycompensated.12

Interpretation of ABGsInterpretation of ABGs pH 7.18 PaCO2 38 mm Hg PaO2 70 mm Hg HCO3 15 mEq/L What is this? pH 7.60 PaCO2 30 mm Hg PaO2 60 mm Hg HCO3 22 mEq/L What is this?Interpretation of ABGsInterpretation of ABGs pH 7.58 PaCO2 35 mm Hg PaO2 75 mm Hg HCO3 50 mEq/L What is this? pH 7.28 PaCO2 28 mm Hg PaO2 70 mm Hg HCO3 18 mEq/L What is this ?D5WPutting it all togetherHypotonic½ NS½ NS(0.45%) Always pay attention to Patient history Vital signs Symptoms and physical exam findings Lab ValuesCrystalloidsNS (0.9%) Lactated RingerHypertonicPlasmalyteFluids3% SalineAlbumin Always ask: What is causing this abnormal finding? What can be done to fix it?IsotonicD5W in ½ NSDextranD10WColloidsFFPPRBCs13