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Fluids & Electrolytes

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  • 1. Prof. M.C.Bansal. MBBS;MS. FICOG. MICOG. Founder Principal & Controller, Jhalawar Medical college , Jalawar. Ex.Principal&Controller; Mahatma Gandhi Medical College,sitapura , Jaipur.
  • 2.  Total body water is 60% in male, 50% in female i.e. 30 litres  Inraceullar fluid (ICF) –20 litres water (2/3).  Extracellular fluid (ICF)– 10 litres water (1/3). >Plasma –2.2 litres (1/4). > Interstitial fluid – 7.5 litres (3/4). EcF volume and Osmalality regulation is controlled by 3 hormones –aldosterone, ADH Atrial natriuretic hormoneION ICF ECF Sodium 10mml/L 140mml/L Potassium 150mml/L 4.5mml/L Chloride Traces 105mml/L
  • 3.  It is decrease in whole body fluid volume which includes both exta and intracellular fluid loss.  Extracellular fluid loss is more important and has to be assessed .  This fluid loss may be : >Isotonic –Water and salt loss leading to Hypovolaemia. > Hypotonic – only water loss with minimal electrolyte loss; leading to dehydration.
  • 4.  Isotonic Volume Depletion Occurs due to diarrhea, vomiting and excess dieresis. > Fluid loss is only of ECF compartment and so immediate reduction in intravascular volume results leading to hypovolaemia and fall in BP. > decreased Tissue perfusion. features  Dry tongue , rapid pulse, cold clammy skin , sunken eyes , decreased BP, oliguria , raised blood urea and decreased urinary sodium. Hypovolaemia –Mild (<2l), Moderate (2-3L) ; severe ( > 3l ) fluid loss.
  • 5.  Hypotonic Fluid loss  > i.e. only water loss , occurs due to decreased intake of water and diabetes insipidus . > It causes dehydration and appropriate and decrease in total body water in all fluid compartments ( 2/3rd ICF , 1/3rd ECF ). >As ECF loss is less ---intravascular fluids loss is also less hence Fall in BP is also less . Features  severe thirst , confusion, convulsions( due to hypernatraemia ), BP relatively normal . Dehydration : mild (weight loss 5%), moderate (10%) , severe (15% ).
  • 6.  Evaluation is done by estimation of serum Na+, urinary Na+ and blood urea .  Isotonic volume depletion is corrected by o.9% normal saline infusion ,  Pure water depletion is corrected by more water in take / IV 5% dextrose infusion .  Monitoring fluid therapy by skin and tongue examination, weight gain pulse, BP, urine output , CVP and PCWP.
  • 7.  Water & Salt excess occurs in CCF , Cirrhosis, nephrotic syndrome , hypoproteinaemia, renal failure , excessive saline infusion.  Water Intoxication  TCRE, excess infusion of 5% dextrose only, SIADH secretion, Psychogenic polydypsia. It is managed by stopping fluid infusion or procedure (TCRE), fluid restriction and treating the cause.
  • 8.  Excessive amount of intravenous dextrose(5%).  Bowel Wash by plane water in place of normal saline.  In TCRE (TUR in urology ) hydro dissection in tumour surgery , when excessive fluid Plane water or glycine is used for uterine distension.  In syndrome of inappropriate Anti diuretic hormone secretion which is commonly associated with lobar pneumonia, empyema , oat cell carcinoma and head injury .
  • 9.  Drowsiness , weakness.  Convulsions , coma.  Nausea and vomiting.  Passage of dilute urine.  Distended neck veins.  Gain in body weight .  Circulatory over load –tachycardia, pulmonary edema, hypertension and pedal edema.  Bilateral basal crepitations , ascites.  Raised CVP, PCWP.
  • 10.  Investigations >Haematocrit and sodium level (will show fall in level) > Low Potassium and Low blood urea.ECG< X-ray Chest. Treatment >Water and salt restriction and observation . > Monitoring in ICU. > Management of fluid and electrolyte balance as per serum electrolyte reports. > Infusion of( ½) hypotonic saline. Administration of diuretics and hypertonic saline should be avoided as it may de arrange serum electrolytes which may lead to neuronal demylation and FATL OUTCOME.
  • 11.  ECF Loss > Here only ECF loss occurs , ICF remains Normal. > It is seen in diarrhoea , vomiting, intestinal obstruction / fistula. > Normal Saline infusion = to calculated ECF loss. ECF excess  Only ECF Excess ,ICF remains normal. It occurs when excessive infusion of saline with impaired excretion as in renal diseases. Raised JVP , cardiac failure and peripheral edema. Treatment is fluid restriction and diuretics like frusamide.
  • 12.  Definition  > Serum Sodium level is < 130mEq/L > Severe degree hyponatraemia, when serum sodium level < 100 mEq/L in acute type and in chronic type serum sodium level <115 is taken as reference value. < May be due to water over loading (dilution) or sodium loss.
  • 13.  Acute—presents as neurological manifestations.  Chronic – cause pontine myelonlysis , presents as behavioral changes , weakness and central nerve palsies. Other types may be  (a) hypervolaemic Hyponatraemia –Rapid absorption of fluid occurs leading to dilution and decreased Na+ concentration. Decreased osmalality results in migration of ECF in to ICF compartment and hence patient develops cerebral and pulmonary edema ., causing convulsions and respiratory symptoms. -Urinary Na+ conc. Is 15 mmol/L. -fluid restriction ,hypertonic saline (double strength) infusion and loop diuratics like frusamide injection are the main lines of management. - Monitoring is done by Serum Na= estimation and its correction till it reaches above the level of 125mmol/L . - correction should be slow and gradual at the rate of 2mEq/L /Hr and up to 20 mEq/L in 24 hours. Serum Na+ estimation should be done at 4 hourly interval . - Rapid correction may lead to irreversible myelinlysis of pontine . - Over correction should always be avoided.
  • 14. (b) Hypovolumaemic hyponatraemia – - Hypovolaemic as in dirrhoea and vomiting , hyponatraemic as urinary Na= level is < 20mmol/L. - Due to forced diuresis and renal causes water is lost and urinary Na+ level is more than 20mmol/L. - It may be due to over correction of hypovolaemia by only dextrose / hypotonic fluid. - condition is treated by using Isotonic fluid(normal saline ) therapy.
  • 15. (c) Normovolaemic Hyponatraemia— - It may be due to renal failure or Syndrome of inappropriate ADH secretion - Mild cases fluid restriction (1 litre /day ) will raise the Na+ level . - In severe cases Vasopressin antagonist ( Demeclocyclin) will increase the diluting ability of kidney . And Na+ level will improve.
  • 16. ( d) Pseudo-hyponatraemia – - Plasma osmalality is mainly achieved by Na+ but small portion of it i.e. 25% is due to other solutes like glucose , proteins, urea and lipids which do not move out easily from vascular compartment, in IC / EC Spaces. - When concentration of this substances increase , the Na+ level will fall causing Pseudo hyponatraemia. Correction of increased element will correct the Na+ level. Causes  - Intestinal obstruction, -intestinal fistula, -gastric outlet obstruction with excess of vomiting , -prolonged Ryle’s tube aspiration, -Severe diarrhoea due viral cause –in colitis and cororectal polyposis, -SIADH, -Immediate after surgery / trauma Na+ depletion occurs . -stroke etc.
  • 17.  Dry coated tongue.  Sunken eyes.  Dry wrinkled skin.  Hypotension .  Dark scanty urine .  Irritability, disorientation , neurological manifestations.  Convulsions.  In chronic Hyponatraemia– hypothermia, reduced tendon reflexes, pseudobulbar palsy.
  • 18.  Serum electrolytes --- Low serum Na= Level.  Urinary Na+ level low,  Sodium deficit = ( 125- present Na+ ) X body weight in Kg X 0.6.
  • 19.  In acute cases --IV infusion of normal saline to achieve slow and gradual correction of serum Na+ level at the rate of 2mEq/L / hr. Maximum 20mEq/L in 24 hrs. monitor Na= Level at 4 hrs interval.  In chronic Case--< 1mEq/L/Hr and should not exceed > 10mEq/l in 24 hrs.  Hypertonic saline 1.6 % or 3% can be used in acute severe cases with caution of too early and rapid correction is associated with myelinlysis of pontine.  Cause is also treated simultaneously. Type of Saline fluid NaCl content 0,9% normal saline /L 154mEq/L 3% hypertonic Saline 500 mEq/L
  • 20.  Serum Na+ level >150mEq/L., is taken as hypernatraemia.  Causes >Renal Dysfunction. >Cardiac Failure. >Drug induced like NSAID , Corticosteroids. >Excess infusion of hypertonic saline /intra amniotic hypertonic saline previously used for mid trimester MTP. > excess of normal saline infusion causes overloading in circulating salt and water. It is due to when water deficit present in initial stage..
  • 21. (A) Euvolaemic ( pure water loss ): - It is due to decreased water intake as in coma, bedridden people , post operative patients when iv therapy has been stoped but pt does not take reqired amount of water, patient in high fever leading to external loss of water. It can also occur in diabetes incipidus / chronic renal failure as renal loss of only water. ( B ) -Hypovolaemic: -( Among loss of water and Na= but water is more lost than Na+.) as in cases of vomiting ,diarrhoea , more undue sweating ( extra renal ) , osmotic diuresis by high concentration glucose/ mannitol infusion (renal ). ( C ) Hyper volaemic : - (Both water and Na+ gain But Na= gain is more than water.) as seen in more salt intake, excess steroids , Na HCo3/ hyper tonic saline infusion ( salt gain )
  • 22.  Pitting edema.  Puffiness of face .  Increased urination .  Often dilated jugular vein.  Features of pulmonary Edema.
  • 23. Investigations >Serum Electrolytes. > Plasma and Urinary osmolality. > Renal Function Test. > Haematocrit. Treatment >Restriction of saline , Na+. > Correction should be slow and gradual – Initial infusion of normal saline ,then infusion of ½ strength (0.4.5% ) saline later with 5% dextrose ; otherwise cerebral edema and hyperglycaemia can develop. > oral / nasogastric administration of water / other fluids as condition improves.
  • 24.  Serum Potassium level < 3.5 mEq/L is leveled as hypokalaemia.( normal range –4.0 to 4.5 mEq /L) 1.Sudden onset  It occurs in diabetic coma cases treated with insulin and saline infusion ; as insulin causes influx of K+ in the cells and saline (containing NO K+) dilutes its concentration in serum. 2. Gradual onset  Diarrhoea of any cause, ulcerative colitis, gastric aspiration / vomiting, After trauma or surgery , duodenal fistula/ileostomy , insulin therapy , poisoning , beta blockers , prolong diuretic therapy etc.
  • 25.  Slurred speech.  Muscular hypotonia (physical sign).  Depressed reflexes.  Paralytic Ileus.  Weakness of respiratory muscles.  Cardiac arrhythmias.  Inability to produce concentrated urine.  Nocturia and polyuria.
  • 26.  ECG– shows prolonged QT interval, depression of ST segment , inversion of T wave and prominent U wave.  Often hypokalaemia is associated with alkalosis.  Serum potassium < 3.5 mEq/L.  Treatment  > oral potassium 2gm ;6hrly , 15 ml K Cl syrup(2ommol of K) > Iv K CL 40mmol?L in5% dextrose / normal saline slowly , often under ECG monitoring . Maximum dose / hr is 20 mmol . >Hypocalaemic alkalosis if present should be treated carefully by iv Potassium .
  • 27.  Normal serum K+ level ranges from 4.0 to 4.5 mEq/L  Hyperkalaemia menifests when serum K+ exceeds 6.0 mEq/L
  • 28. Causes  Renal Failure.  Rapid infusion of potassium.  Transfusion of stored blood –K+ diffuse out of stored RBC.  Diabetic Ketoacidosis .  Adrenal Insufficiency.  Potassium sparing drugs like diuretic therapy (spironolactone), beta blockers , cyclosperine .  Massive tissue destruction ,burns , trauma, tumor necrosis, crush injury –intra cellular K+ is released in blood.  In vitro haemolysis, thrombocytosis , torniquet application exercise cause pseudo hyperkalaemia.  Familial hyperkalaemic periodic paralysis. Note Hyperkalaemia is dangerous state can result in cardiac arrest.
  • 29. (A) Investigations > High serum potassium level. > Peak T wave on ECG. ( B ) Treatment > IV infusion of 50 ml of 50% glucose with 10 units of soluble insulin , slowly . >Infusion of 10% cal gloconate IV ( cardio protection) > CaCl2 is given Iv in severe cases as calcium in this form is immediately released without hepatic metabolism. > Dieresis using Frusemide –causes K+ excretion. > Haemolysis / dialisis when required. > continuous ECG monitoring , > Salbutamol / Albuterol nebulisation > IV Sodium bicarbonate –shifts K+ in to cells – 50- 100 ml slowly over 10 minutes in 7.5% concentration .
  • 30.  It is rare: serum magnesium level > 2.5mEq/L(normal level is 1.5- 2.5mEq/L ).  Intracellular magnesium is more 26mEq/L ( 2nd more higher element).  Mg is mainly deposited in bones.  It is a co- factor for many enzymes necessary for phosphorylation of glucose in cell and ATP utilization in muscle fibers.  Daily dietary of Mg is 0.4 gram.  It is reabsorbed well in proximal renal tubules.
  • 31.  Advanced renal failure, patient treated with Mg containing antacids.  Diabetic ketoacidosis .  Over dose of Mg SO4 in treatment of PIH / Eclampsia. Clinical features > Loss of tendon reflex. > Flaccid quadriplegia. >Neuromuscular depression. > Respiratory depression– muscle paralysis. > Hypotension. > renal out put decreased ; oligourea and anurea. Monitoring  urine out put should not go down < 3o ml in one hour. Knee jerk, planter reflex should not depress. Keep watch on respiration Rate. Serum Mg estimation . Management  next dose to be given after checking , respiratory rate, urinary output and reflexes . - I V inj. Ca gluconate / CaCl2 in 10% concentration, 10-20 ml slowly over 20-30 minutes.
  • 32.  Serum MG < 1.5mEq/L Causes  Malnutrition , chronic alcoholism, large GI fluid loss; patient on parenteral fluid therapy for along time. Clinical Features  hyper reflexia, muscle spasm , parasthesia , tetany, it mimics hypo calcaemia associated with hypokalaemia. Treatment  2 gm ( 16mEq /L ) of MgSO4 given IV slowly in 10 minutes. Later maintenance dose of 1mEq /kg / day is infused as slow IV drip.
  • 33.  Normal pH( - log of H+ ) is 7.36 – 7.44  When H+ increases pH decrases. Factors which Control pH .> Buffer System – Bicarbonate Buffer Protein Buffer Phosphate Buffer > Renal Control Of pH > Respiratory Control of pH
  • 34.  Acid – is a substance that dissociates Waterto release hydrogen Ion .  Base – is a substance that takes hydrogen Ion  Buffer – is combination of weak acid and conjugate base.  These buffers maintain the H+ concentration in blood with in a fine limit / range .  Buffers are 1. Intra cellular . 2. Extracellular.
  • 35.  Extra Cellular Buffer – Bicarbonate / Carbonic acid , phosphate buffer and Plasma Protein buffer arte extracellular natural buffers .Bicarbonate / carbonic Acid buffer is most important as carbonic acid level in blood is regulated by lungs which removes excess of Co2 gas. , while bicarbonate pare is contrilled by Kidney.  Intra Cellular Buffer – Haemoglobin and other protein inside cell are playing major role of intra cellular Buffer.  Acidosis---When pH of blood is < 7.35 .  Alkalosis ---- when pH is more > 7.45 .
  • 36.  H+ (nmol/L ) = K x H2Co3m mol /L _____________ HCO3m mol/L or K x d PCO2 __________ HCO3 m mol/L Here K is coefficien a constant factor =800( for H2 CO3 / HCO3 buffer ) Carbonic acid (H2CO3) is solubility coefficient of CO2 in blood (d) multiplied by partial pressure of CO2 (pCO2) d is 0.03ml/mmHg / ml blood . pCO2 is 40 mmHg . H2CO3 = d pCO2 = 0.03 x 40 ==1.2ml . Normal blood Bicarbonate (HCO3) level is 24 m mol /L So H+ is 800 x 1.2 devided by 24 = 40m mol / L
  • 37.  It is used to find out pH of blood using Logrithm .  Negetive log of K (800 for carbonic buffer ) is called as pKa . It is 6.1 for H2CO3 / HCO# buffer system.  pH = pKa + log HCO3 / H2CO3 means 6,1 + log 24 devided by 1.2 = 6.1 + log 20 = 6.1 + 1.3 = 7.4
  • 38.  Primary base excess . E.g. HCO3 . A standard bicarbonate above 27m mol /L. Causes 1. Repeated vomiting as in pyloric stenosis . Here hypokalaemic alkalosis develop due to loss of K+ and acid in vomit . 2. Excess alkali intake e.g. antacid . 3. Cortisol excess due to over ingestion /injection or cushing’ syndrome. Clinical Features 1.Chine strokes breathing in period of apnoea of 5-30 seconds. 2.Tetany due to alkalosis ---latent tetany revealed by Trousseau’s sign .
  • 39. Investigations  Serum electrolytes. Arterial blood gas analysis. Treatment Normal saline or double strength saline IV with slow IV infusion of KCl 40 m mom/L under ECG monitoring . pH < 7.7 causes life threatening alkalosis and requires rapid correction by infusing dilute HCl acid or Ammonium chloride with careful monitoring
  • 40.  Arterial PCO2 is below normal(45mmHg).  Causes  1. Hyperventilation during anaesthesia, severe pain , hyper pyrexia , head injury . 2. High altitude. 3. encephalitis , hypothalamic tumors , salicylates over dose / poisoning , Liver cirrhosis. 4. Hysteria.
  • 41.  Clinical Features and Management 1. Headache , tingling , circum oral anaesthesia ,tightness in chest ,tetany and Arrhythmias are the features. 2.Low PaCO2 , low HCO3, High alkaline Ph . 3. It can be acute or chronic. 4. It is managed by O2 therapy , treating the cause and tab Aceozolamide in high altitude. 5. respiratory depression is treated by CO2.
  • 42. Acidosis 1. Metabolic . 2. Respiratory,
  • 43. - It is state of excess acid / base deficit .  A standard Bicarbonate below 21 m mol /L.  Causes  a. Diabetic Ketoacidosis. b. Starvation. c. Hypoxia—CO2 accumulation. d. Renal efficiency . e. cardiac arrest ---Hypoxia. f. Excessive exercise --- Lactic acid over production . g. Intestinal strengulation , here anion gap is increased.
  • 44.  Loss of base causing metabolic acidosis a, Diarrhoea. b, Ulcerative Colitis . c, Gastrocolic Fistula . d, Intestinal Fistula . e, Uretero-sigmoidostomy done for urinary diversion --- results in Hyperchoraemic – Hypokalaemic acidosis , anion gap is normal
  • 45.  Clinical Features  a, Rapid, deep, noisy breathing – air hunger; known as KUssMaul’s Breathing. Cold clammy skin , Tachycardia, right heart strain , altered level of consciousness. Cardiac Arrhythmia , hypotension . Anorexia, vomiting , muscle weakness. Ph < 7.2 A dangeorus and life threatening level. capillary stassis. Strongly acidic Urine. Low standard HCO3. Base deficit. Evaluation --. Do Arterial blood gas analysis. , showing Low HCO3 level . Low Ph , anion Gap , Urinary anion Gap which is zero or positive , Note __ U A G become negative in metabolic acidosis due to GI cause as there is increased NH4Cl excretion . If it is due to renal orgion UAG will be positive .
  • 46.  Treatment  > correction oh hypoxia. > 50M ML OF 8,4 % Sodium bicarbonate iv infusion – NAHCO3 requirement in m Eq/L = Body weight in Kg X base deficit X 0.3 >Correction of Electrolytes. > Specific Treatment for acidosis depends on .Type A (Shock , Respiratory , CO/ Cynide Poisoning , Anaemia ) . Type B ( Diabetic , hepatic , toxins / drugs .) It needs only careful use of NaHCO3 in severe cases. Dicholoroacetate therapy will stimulate Pyruvate Dehydrogenase enzymes to reduce Lactate. > Specific treatment is needed to start in cases of diabetic Ketoacidosis , Alcoholic acidosis , Salicylates poisoning and Renal cause . Astrup Formula Total base deficit / exceesve = Base deficit / excess X Body Wt In KG X 0.3
  • 47.  It is feature of respiratory insufficiency to breath out CO2 as in respiratory failure ; resulting in High PCO2 and fall in pH.  Causes > During or after anasthesia . > Chronic Bronchitis , obstructive lung disease, Emphysema. > diseases of Thoracic cage. > Upper abdominal surgery / disease3 decreasing abdomino –thoracic respiration . > Respiratory air ways obstruction . > Myesthenia Gravis, > Poliomyelits causing paralysis of respiratory muscles to variable extend. > Stroke, infection , obesity, Hypoventilation.
  • 48.  Clinical Features  > Dyspnoea, confusion , psychosis , Hallucinations , sleep disturbances, tremors , jerks and personality changes . > CNS changes are more common and severe in Respiratory acidosis than in metabolic acidosis . As in respiratory acidosis lipid soluble C)2 crosses brain barrier easily than HCO3.
  • 49.  Treatment > O2 Therapy ; ventilator support . > O2 therapy should not be used in chronic hypercapnoea unless it is realy indicated as Hypoxia induced respiratory stimulation may be decreased as more CO2 is washed out at faster rate. > Alkali therapy is also not started unless pH is < 7.15. 0r there is severe bronchospasm .
  • 50.  It is a calculated estimation of the undetermined or unmeasured ANIONS in blood .  ANION GAP = ( Na+ + K+ ) – ( HCO3- + Cl - ). e.g. Total ANION – total Cation in blood Normal anion gap is 10-16m mol /L. Important unmeasured are +ve charged proteins , phosphate , sulphate and organic acids . Important unmeasured Cations –Ve charged CA and Mg. Albumin is main component of Anion Gap . When albumin level in blood decreases by 1 gm / dl –anion gap decreases by 2m Eq /L .
  • 51. Increased Anion Gap Is seen In Normal Anion Gap Is seen in Metabolic acidosis due to Ketoacidosis. Diuarrhoea. Lactic acidosis. GIT Fistula . Poisoning ( CO / salicylates/ cynide Hyper chloraemic acidosis . Renal Failure
  • 52. FLUID THERAPY
  • 53.  Osmolality of a solution is assessed by the amount of solute dissolved in a solvent like water measured in weight (Kg).  Osmolality of a solution is assessed by amount of solute dissolved in solvent like water measured in volume (litre) .  Normal plasma is 285 mOsm / Kg (275 -295 ).
  • 54. * Plasma Crystalliod osmolality --2 Methods  a. Osmolality of plasma = 0.54/1.86 X 1o rase to power 3 mOsmol / Kg. It is based on the fact that solution of 1mOsmol/ Kg freezes at -1.86 degree Centigrade ; where as plasma freezes at -0.54 degree Centigrade . b . Osmolality of plasma= 2X(Na) +( Glucose mg%/18) + ( Blood urea mg % /6) It is based on the concentration of major solutes ( Na , glucose and urea) in plasma. Na+ contributes maximum in plasma osmolality. *Colloidal Osmotic Pressure  It is difference in plasma osmotic pressure and interstitial fluid pressure = 25 mmHg. This is mainly due to concentration of Albumin in plasma. Plasma proteins do not go out of capillary wall and do not enter in interstitial compartment.
  • 55.  Indications  > For rapid restoration of fluid and electrolite deficit as in dehydration as in cases of diarrhoa, vomiting , burns, Haemorrhagic shock and sepsis. > Total parentral nutrition. > anaphylaxis, cardiac arrest , hypoxia. > Post operative period . > for maintenance , replacement of loss or as a special fluid. Advantage Controlled , accurate , adjustable, rapid , predictable and specfic in terms of solutes and solvent as per need of clinical situation.
  • 56.  Needs Hospitalisation : costaly ; needs to practice universal aseptic measures.  Fluid over load; pulmonary edema; cardiac failure .  Infection , thrombophlebitis , haematoma;cellulitis ion local area.  Pyogenic infection , air embolism , bacteraemia .  Discomfort , poor acceptance by patient and relatives.
  • 57.  Daily requirement  > Na –100mEq ; K– 60mEq ; Ca – 5mEQ ; Mg 1mEq.  Crystalloid Solutions(fluids) . Name of fluid NA + mEq/L K+ mEq/l Cl- mEQ /L Lactate (HCO3)mEq /L Ca+ mEq/L Normal Saline 154 - - - - Ringer lactate 130 4 109 28 3 Dextrose Saline 5% dextrose Isolyte P Isolyte G Isolyte M
  • 58.  Colloids are large molecules which shift the fluid (solvent/ Water ) from interstitial compartment to intravascular compartment., used as plasma volume expanders. name Na K Cl Ca bicarbo nate Molecula r size Remar ks
  • 59.  Isolyte G  Isolyte P  Islyte M  NS  RL½ NS  Hypertonic saline  GDW 5%  GDW10%  GDW 40%  Fructodex  Lomodex  Hamaccoele  Invertase