外科学-总论英文ppt课件：FLUID-AND-ELECTROLYTE-MANAGEMENT.pptx
FLUID AND ELECTROLYTE MANAGEMENT OF THE SURGICAL PATIENTObjectiveDistribution of water and electrolytes in the bodyMechanism of modulation for water and electrolytes and acid-base balanceDisorder of water and electrolytes and acid-base balancepMechanismpClinical symptoms and signspDiagnosispTreatmentsWater is important for living lifeTransportation of electrolytes,oxygen,nutrients,etcMetabolismWaste elimination etcMultiple water compartmentsMultiple water compartments separated by membranesSubstantial differences in solute composition within the compartmentsBalance is maintained across the membranesThis balance(homeostasis)is sustained by the consumption of energy Intracellular fluid(ICF)Extracellular fluid(ECF)lInterstitial fluidlPlasmaMultiple water compartmentsBody water and solute compositionTotal body water(TBW)constitutes between 50%and 60%of the total body weight in most adults TBW constitutes up to 70%of the total body weight in childrenPercentage of TBW to the body weight40%15%5%15%5%35%MALEFEMALEICFECFINTERSTITIIAL FLUID PLASMA Principal cations&anions in ICF&ECFECFWater and solutes in the plasma Filter across the microvascular membrane interstitial fluidflow through the lymphaticsReturn back to the plasmaECFWater in bone and in dense connective tissue(cartilage and tendons)FixedDoes not readily flowin the interstitium and lymphaticsWater and solutes in circulationDrinking and eatingWater in the GI tract is increased Water and nutrients consumedDistributed in ECF and ICF compartmentsNutrients support metabolismWaste products released from cellsptransported from the ICF to the ECFptransported through the lymphatics to the plasmaWaste excreted primarily through renal functionCO2 exhaled in respiratory gases Water and solutes can be eliminated Water and electrolytes in evacuated stoolWater in respiratory gasesWater and electrolytes in sweatThese three types of excretion are not tightly regulatedRenal function Is critical to the homeostasis of ECF and ICFlModulated by a complex interaction Local regulatory factors To keep the volume of plasmaSystemic hormones (ADH from the hypothalamus and pituitary)To keep the normal osmolality in ICF&ECFOsmolalityA measure of the total number of solutes per mass of water Is clinically measured in units of millimoles per kilogram of water(mmol/kg H2O)Normal osmolality:300 mmol/kg H2O (280310)Principal osmoles in ICF and ECFWater and solutes movementTo keep the body fluid homeostasisTBW moves across cell membranesDistributes between ICF and ECFTo keep the same osmolality in ICF and ECF Cell membranes are readily permeable to waterWater shifts rapidly between ECF and ICF to achieve balance in osmolalityThe majority of solutesDetermine osmolality in the two fluid compartmentsCross the cell membrane only through regulated transport mechanismsPassive transport:concentration gradientActive transport mechanisms lConsume biochemical energylMove electrolytes across the cell membrane Water and solutes movementTo regulates the size of the ICF and ECF by control of the excretion of solutes in urine by control of the osmolality of urine Renal function in water controlRenal function in water controlRenal control of Na+excretion(with Cl-)Determines the size of the ECF compartment If Na+is retained total body Na+mass Expands the size of the ECF compartmentRenal function controls the volume of TBW by producing urine with a range of osmolality from 100 to 1200 mmol/kg H2OTransport enzymes on cell membraneSustain the difference in electrolyte composition between ICF and ECF Actively transport Na+from ICW to ECW in exchange for K+The enzyme Na+,K+-ATPase plays a key role in the active transport Binds 3 Na+in ICF Binds 2 K+in ECF Uses the energy provided by hydrolysis of ATP to ADP 3 Na+out of the cell 2 K+in ECF enter the cell Na+,K+-ATPase activity is a net negative intracellular charge Due to 3 cations out and 2 cations into the cell Na+,K+-ATPase in active transport The Na+,K+-ATPase pump is constantly active Continuously consumes the energy in ATP to ADPSustain the resting membrane potentialInsufficient oxygen is available to sustain aerobic metabolismConsequently,cellular ATP levels fallThe sodium pump function is impairedLead to cell dysfunction and death The intracellular sodium concentration increasesThe resting membrane potential declinesNa+,K+-ATPase Classification of Body Fluid ChangesDisorders in fluid balance in three categories:Disturbances of volumeDisturbances of concentrationDisturbances of compositionVolume ChangesVolume DeficitVolume ExcessVolume DeficitECF deficit is the most common in surgical patientsThe loss of fluid:water and electrolytesIn the same proportion as that in normal ECFCause of volume deficitLoss of gastrointestinal fluidlVomitinglNasogastric suction lDiarrhea lFistula drainageSoft tissue injuresInfectionslIntra-abdominal and retroperitoneal inflammatory processeslPeritonitisIntestinal obstructionBurnsSigns and symptomsModerateSevereCNSSleepinessApathySlow responsesAnorexiaCessation usual activityDecreased tendon reflexesAnesthesia of distal extremitiesStuporComaGastrointestinalProgressive decrease in food consumptionNausea,vomitingRefusal to eatSilent ileus and distentionCardiovascularOrthostatic hypotensionTachycardiaCollapsing pulseCutaneous lividityHypotensionDistant heart soundsCold extremitiesAbsent peripheral pulsesManagement of Volume DeficitFluid administrationEvaluate the degree of dehydrationMild:loss of 1-2%of body weightModerate:loss of 3-5%of body weightSevere:loss of 6-7%of body weightFor example:Moderate:loss of 3-5%of body weight(60Kg)Water loss:5%60=3L=3000mlLoss of 25%of ECFD1:of the volume infusedD2:of the volume infused D3:of the volume infused Management of Volume DeficitVolume excessECF excess is iatrogenic or secondary to renal insufficiencyBoth plasma and interstitial fluid are increasedEdema:all organs and tissuesFor the young:circulatory overloadFor the elder:congestive heart failure with pulmonary edema developsECF excessModerateSevereSubcutaneous edemaGastrointestinalAt Surgery:Edema of stomach,colon,lesser and greater omenta,and small bowel mesenteryCardiovacularElevated venous pressureDistention of peripheral veinsIncreased cardiac outputLoud heart soundsFunctional murmursBounding pulseHigh pulse pressureIncreased pulmonary second soundgallopPulmonary edemaManagement of volume excessTreat the primary diseasesControl the water intakeIncrease the water excretionThe serum Na+:142mEq/L (138 to 145)The serum Na+is responsible for the tonicity of body fluidConcentration changesHyponatremiaSodium loss in ECF:Mild:Na+130-138 mEq/L Moderate:Na+120-130 mEq/LSevere:Na+120 mEq/L.lPatients with mild hyponatremia rarely have signs or symptoms The clinical indications of hyponatremiaDecreased responsivenessSeizuresCatastrophic respiratory arrestSevere hyponatremiaSevere hyponatremia:Na+120 mEq/L.Na+osmolality in ECF and ICF Cells are swellingIntracranial cell swelling Causing headaches and lethargyRapidly progress to coma or have seizuresHyponatremiaSymptoms and signsModerateSevereCNSMuscle twitchingConvulsionsHyperactive tendon reflexesLoss of reflexesIncreased intracranial pressure(compensated)Increased intracranial pressure(decompensated)CardiovascularChanges in blood pressure and pulse secondary to increased intracranial pressureTissue SignsSalivation,lacrimationWatery diarrheaFingerprinting of skinRenal Oliguria progressing to anuriaOliguriaCause of hyponatremiaLoss of GI fluids lVomitinglDiarrhealNasogastric suctionlFistula drainageLoop diuretics and IV infusion of mannitol Excessive infusion of hypotonic solutionsSevere injury or burnsLow sodium in enteral nutritionRenal loss of sodium due to the brain diseaseCause of acute hyponatremiaECF is replaced with either an enterally or IV infused hypotonic fluidIV infusion of 5%dextrose in water rapidly produces hyponatremiaIn the patients with lHemorrhagelAn acute diarrhea lPancreatitis lBurn woundlInflammatory edema has developedHyponatremia exacerbated if blood volume contractedTreatment of acute hyponatremia IV infuse isotonic saline Add hypertonic saline(10%NaCl)to expand a contracted ECF volumeThe rate of infusion of sodium-containing solutions:increasing serum Na+0.25 mEq/L/hrNaCl(g)=(142mmol/L-serumNa+)Kg0.617l0.5(female)Chronic Hyponatremia The syndrome of inappropriate release of antidiuretic hormone(SIADH)Chronic renal disease may have an impaired capacity to retain sodiumManagement for chronic hyponatremiaRapid correction of Na+in patients with chronic hyponatremia can lead a severe,permanent neurologic disorder The rate of sodium infusion 0.25 mEq/L/hrThe rate of increase in serum Na+160 mEq/LCommon cause:water loss For example:1.The water lost after excessive sweating in a hot environment2.Unregulated loss of hypo-osmotic gastrointestinal fluidsNeurologic damage due to contraction of brain cell volumeSever hypernatremiaNa+160 mEq/LAn altered level of consciousness and seizuresComa and intracerebral hemorrhageTreatment of Hypernatremia IV or oral administration of water for hypernatremia secondary to dehydrationIV infusion of isotonic saline solutions due to reduced blood volumes until the contracted ECF has been restoredSerum Na+should be lowered at a rate 5.0 mmol/LK+6 mmol/LIimpair normal depolarization and repolarizationCardiac arrhythmias often prove lethalElectrocardiographic changes K+:6-7 mmol/L:Tall T wavesSymmetrically peaked T waves indicate dangerous hyperkalemiaK+7 mmol/LP-wave amplitudes on the electrocardiogram decreasePR segments increaseThe QRS complex widens.K+8 mmol/L:suddenly lethal arrhythmias ensueAsystoleVentricular fibrillationA wide pulseless idioventricular rhythmECG changes indicating hyperkalemiaCause of hyperkalemiaAn acute renal dysfunction or renal failureSudden release of potassium from ICF can cause hyperkalemia Reperfusion of ischemic skeletal muscle is a clinical syndrome and release of K+.Reperfusion injury occurs at the completion of arterial injury repairTreatment of Acute Hyperkalemia Stop all infusion of potassiumIV infusion of 10%CaCl2 or 10%calcium gluconateIV infusion of NaHCO3Glucose and insulin infusionImmediate hemodialysisPotassium-binding resins into the GI tract with 20%sorbitolPromotion of renal kaliuresis by loop diureticHypokalemia K+3.5 mmol/LSymptoms:fatigue,weakness,and ileusK+2.5 mmol/L:Rhabdomyolysis may occur K+2 mmol/L:Flaccid paralysis with respiratory compromise can occur Cause of HypokalemiaPersistent vomitingDrain large volumes via nasogastric tubesDiarrheaHigh-output entericPancreatic fistulas Patients with congestive heart failure managed with multiple drugsPatients treated with diuretics that excrete urine with an elevated K+Long-term diuretic therapy Treatment of Acute HypokalemiaRequire potassium replacement Potassium infusion 30-40ml/H)KCl 3g per Liter solutionSlow infusion IVMaximal a day:KCl 8gTreatment of Acute HypokalemiaCalciumA critical component of reactions in ICF and ECFAn essential cofactor in the coagulation cascadeParticipates in the regulation of neuronal,myocardial,and renal cellular functionCalcium in ECF is present in three molecular formslprotein-bound calciumldiffusible calcium complex to anions(bicarbonate,phosphate,and acetate)lionized calcium(iCa2+)The biochemically active species is iCa2+MagnesiumMagnesium is an essential cation in ICFSerum Mg2+concentration:1.4 and 2.0 mEq/LSeveral diseases that deplete magnesium have parallel effects on calciumHypercalcemiaserum calcium 2.75 mmol/L Cause of hypercalcemiaPatients with hyperparathyroidism secondary to a parathyroid adenoma Patients with malignancy-related severe hypercalcemiaA renal concentrating defect and leads to polyuria Weakness,stupor,and CNS dysfunctionA renal concentrating defectLeads to polyuria and loss of sodium and waterDehydration Renal lithiasis HypercalcemiaManagement of HypercalcemiaCorrection of the primary problemExcision of the diseased parathyroid tissueSaline infusion to expand ECW A loop diuretic to clear the urinary calciumIsotonic saline infusion is essential Hypercalcemic with renal failure can be managed by hemodialysisBisphosphonates can be managed those related to release of calcium from bone by tumorHypocalcemiaSerum calcium 2 mmol/LAcute hypocalcemia can be a life-threatening eventImpairs transmembrane depolarizationLead to central nervous system dysfunctionMuscle spasms(including tetany),and seizuresPainful muscle spasmsInduce a respiratory alkalosisCardiac dysfunction ECG:a prolonged QT interval leading to heart block or ventricular fibrillationVitamin D metabolic deficitHypoparathyroidismAcute severe pancreatitisRenal failureTumorCause of hypocalcemiaManagement of HypocalcemiaInfusion of 10 mL of a 10%CaCl2 solution 272 mg of calcium=13.6 mmol of Ca2+Infusion of 10 mL of a 10%calcium gluconate 90 mg of calcium=4.5 mmol of Ca2+Hypermagnesemiamost often seen in patients with renal failureexacerbated by the ingestion of magnesium-containing drugs,particularly antacidsMagnesium blocks the shift of calcium into myocardial cellssevere hypermagnesemia show evidence of heart failure.HypomagnesemiaDevelop in patients with chronic diarrhea syndrome prolonged aggressive diuretic therapywith heavy ethanol intake diabetic patients with persistent osmotic diuresislThe magnitude of magnesium deficiency parallels the magnitude of hypocalcemiaCorrection of hypomagnesemia IV infusion of magnesium sulfate(MgSO4)Severe hypomagnesemia(1.0 mEq/L)requires sustained therapy Correction of hypomagnesemia can also reduce the risk for cardiac arrhythmiasACID-BASE BALANCE pH:the negative log of the H+concentrationMaintained in a narrow limitspH:7.357.45Acid:the byproduct of metabolism pNeutralized by buffer systemspExcreted by lung and kidneyBuffer systemsRenal functionRespiratory functionPlay the critical role in acid-base balanceACID-BASE BALANCE Buffer systemsBuffer systems:consisting ofWeak acid or baseSalt of that acid or baseBuffers in ICF and ECFHCOHCO3 3-/H/H2 2COCO3 3H H2 2POPO4 42-2-IMIDAZOLE IMIDAZOLE ON ON PROTEINSPROTEINSECW95%4%1%ICW42%6%52%The bicarbonate buffer system A dominant buffer system in biologic systems Is important in both ICF and ECF Is key to enabling proton transport across cell membranes H+HCO3-=H2O+CO2Renal functionThe renal tubule cells consume biochemical energy and pump protons into urineEnabling net excretion of protons(as NH4+)The renal tubule cells cannot recover the bicarbonate filtered at the glomerulusSo allowing loss of bicarbonate in an alkaline urine.The pulmonary system Increase the loss of CO2 in respiratory gases by increasing alveolar ventilation Decrease the loss of CO2 in respiratory gases by decreasing alveolar ventilation Can consequently reduce the PaCO2 in ECF Timeliness is a critical distinctionTime to correct the proton concentration in ECFThe renal system in hoursthe pulmonary system in minutes A frequent and potentially lethal problem for patientsPatients are acidotic if they h
