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Osmolality Goldman

Osmolality Goldman. A mole of a substance is the mol wt of that substance in grams E.g. the mol wt of NaCl is 23+35.5= 58.5 Therefore 1mole NaCl = 58.5 g. 1 millimole is 1/1000 of a mole Therefore 1millimole of NaCl is 58.5 mg.

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Osmolality Goldman

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  1. Osmolality Goldman A mole of a substance is the mol wt of that substance in grams E.g. the mol wt of NaCl is 23+35.5= 58.5 Therefore 1mole NaCl = 58.5 g. 1 millimole is 1/1000 of a mole Therefore 1millimole of NaCl is 58.5 mg. The weight of a salt in mg can be converted into millimoles by dividing the weight in mg by the mol.wt e.g 1g (1000mg) NaCl = 17.1 millimoles Mol wt of NaCl =58.5 Therefore 1000/58.5= 17.1 Mol wt of glucose C6H12O6 = 12x6 +1x12 +16x6 = 72+12+96=180 Osmolality – a Molal solution contains a gram mol wt of the substance dissolved in 1000g of the solvent (A Molar solution contains a gram mol wt of the substance dissolved in 1 Liter of solvent) It is determined by measuring the depression of the freezing point of a solution, compared to water,using an osmometer and expressing the value in *C below 0*C The value can also be expressed in milliosmoles ,using the factor 1000Osm=186*C or 1*C=538mOsm The normal range of serum osmolality is 275-290mOsm/kg of serum

  2. NORMAL BODY COMP WashMan Total Body Water- Water makes up 60% of body wt in males (42l in 70kg male) 50% in females 80% in newborns 2/3 is ICF – Intracellular Fluid ( 40%-28L in 70kg male) 1/3 is ECF-Extracellular (20% body wt-14I) of which1/4 is Intravascular (plasma 5% body wt-3.5L) and 3/4 Interstitial(10.5L) Total body water is controlled by ADH SODIUM-85-90% is in ECF Change in serum Na (i.e. Intravascular Na) indicates disturbed water homeostasis and ICF volume Change in sodium content ( total body Na) are manifest as ECF expansion (edema) or contraction Osmolality or tonicity is the solute or particle concentration of a fluid. Solutes that are restricted to the ICF ( K & organic phosphate esters) or ECF(Na & accompanying anions) determine the effective tonicity or osmolality Rule of thumb -Extracellular osmolality = 2x serum Na + 10 Normal body fluid vol and osmolality is maintained by kidneys despite wide variations in salt and water intake

  3. NORMAL ELECTROLYTE COMP OF IV &IC mmol/L Schwartz

  4. GI –NORMAL VALUES Condon /ACS Manual

  5. ELECTROLYTES/DAY Wash Man • Na- usually 50-150mmols provided. Renal excretion can fall to < 5mmols/d in absence of intake • K –usually 20-60 mmols when renal function normal Rule of thumb - Na/K 1mmol/kg/day • CHO- 100-150 g in the form of dextrose to minimise- protein catabolism& ketoacidosis • 2-3 l of 1/2N Dextrose Saline (90-125ml/hr) with 20mmols K/ l

  6. MAINTAINENCE THERAPY Wash Man 500ml - min amount of water req to excrete daily solute load Solute load of 600mOsm is produced daily by the body. Healthy people can concentrate urine to a max of 1200mOsm/L • +500ml - insensible loss thru skin, lungs & feces • -300ml- water prod from endogenous met Min water required/day=1000-300ml =700ml Rule of thumb (ROT)- 30 ml/kg/d normal water reqd Normally 2-3l water/day to prod 1-1.5L urine Check daily weight

  7. COMP OF COMMONLY USED IV FLUIDS Condon

  8. ABNORMAL FLUID & ELECTROLYTE LOSSES Wash Manual • INSENSIBLE WATER • GI • RENAL • RAPID INTERNAL SHIFTS • BLOOD

  9. INSENSIBLE WATER LOSSWash Manual From skin and lungs –very variable Inc with inc resp rate,ambient temp and humidity. Inc by 100-150 ml/*C>37* body temp(2ml/kg/*C) • Sweating- variable 100-2000ml/hr dep on physical activity and ambient temp Replacement with 5% dextrose or ¼ NS

  10. RENAL LOSSES Wash Manual • Na losses significant in diuretic phase of ATN, diuretic use,GI losses and catabolic states • Na retention sig in postop state, dehydration, steroid use • K loss sig in diuretic use, steroid use, GI losses esp diarrhoea, ( intracellular shift with Beta agonists like salbutamol) • K retention sig in high output renal failure, post trauma, blood transfusion

  11. RAPID INTERNAL FLUID SHIFTS Wash Man • Occurs with peritonitis, burns, intestinal obstruction, sepsis, crush injury • Need to replace sequestered fluid with normal saline

  12. RENAL FUNCTION Condon Assessed by Urine sp.gr, pH & osmolality of 1st voided urine in the morning- • sp.gr should be or > 1.016 and pH 5.8 or lower • and urine osmolality should be 850mOsmol/Kg water and ratio of urine to serum osmolality should be at least 3

  13. ANION GAP • Determination of the anion gap is useful in assessing the etiology of metabolic acidosis. Mmol Na = mmol Cl- + mmol HCO3- + Metabolic acidosis can be divided into 2 groups 1- with inc Cl ( as in diarrhoea with loss of HCO3) 2 with inc of unknown anion as in renal failure where there is inc sulphate and phosphate, Diabetes ketoacidosis where there is increased ketocacids, Salicylate poisoning where there is inc salicylate Lactic acidosis where there is inc lactic acid Na+140mmol / l= Cl 100mmol + HCO3 10mmol + ?

  14. HYPONATREMIA ACS Caused by • replacing body loss by water alone or 5% dextrose eg diarrhoea • Head injury with inappropriate secretion of ADH • Renal disease with inappropriate loss of Na in the urine • Starvation where there is breakdown of muscle with production of salt free water • Diuretic use especially thiazides Pseudohyponatremia- The serum Na is falsely low because of • High serum lipids or protein – Na falls but osmolality stays the same • If plasma glucose is > 20mmol/L,make a correction • Blood is drawn from an arm with a dextrose drip The decreased serum Na causes a fall in the osmolallity of extracelluar comp and there is movement of water intracellularly causing swelling of cells. This can cause brain edema with inc intracranial pressure This causes edema, inc in weight, confusion, apathy, weakness, nausea and vomiting. If not corrected the water excess will progress to muscle twitching, convulsions, stupor and even death as serum Na falls < 120mmol/l

  15. HYPONATREMIA - TREATMENT • Dont base treatment on serum Na conc alone • Correct the underlying cause if possible • With urine omolality and sodium conc it is possible to come to a diagnosis

  16. HYPERNATREMIA Much rarer. Caused by • Fever in septic patients • Tube feeding when not diluted with adequate water • Renal disease with loss of solute poor water as in high output renal failure where there is dec tubular response to ADH • Tracheostomy patients • Nonketotic hyperosmolar dehydration in diabetics secondary to severe dehydration caused by diuresis and glcosuria • Clinical manifestations is caused by intracellular dehydration. Pt is thirsty, irritable, restless,disoriented eventually leading to coma,convulsions, and even death as serum Na rises to 160mmol/l • Brain dehydration leads to dec intracranial pressure causing headache, and when severe can lead to dilatation of intracerebral vessels and eventual tear/ rupture- cerebral hg is frequent finding in pts dying of hypernatremia • Treatment is giving adequate volumes of water by mouth or as IV 5% dextrose. Correction takes 1-2 days

  17. HYPOKALEMIA The kidney does not conserve K like Na There is a constant urinary loss of 40-60 mmol K / day Normal serum K of 4mmol/l is needed for proper function of muscle- skeletal, cardiac and smooth Skeletal- muscle weakness, paresthesia, flaccid paralysis when K<3 Cardiac- hypotension, bradycardia, arrythmias, ECG- flat / inverted T waves, prominent U waves, dep S-T segment Smooth- decreased intestinal motlity, paralytic ileus, abd distention Hypokalemic periodic paralysis- after exercise, heavy CHO meal A deficit of 4-5mmol/l /kg exists for each 1mmol decrease in serum K Only an emergency when K<2 Can be corrected over 1-2 days If oral is tolerated this is safest – diet rich in fruits. Check if renal function is normal IV K should not exceed 20mmol/hr in thru a peripheral line at a concentration not greater than 40mmol/L of normal or ½ normal saline with ecg monitering

  18. HYPERKALEMIA ACS/WASH MAN/Currentdiag07 Usually ass with renal impairment Caused by • Metabolic acidosis • Overaggressive K replacement • Transcellular shift- tumour lysis, rhabdomyolysis • Pseudohyperkalemia- due to lysis of RBCs during venepuncture / transport Affects cardiac function- bradycardia, hypotension, vent fibrillation, cardiac arrest as K reaches 7mmol/l ECG changes- peaked T waves, prolonged PR interval and widening of QRS complex, loss of P waves, Emergency which needs rapid treatment- Stop all K Give IV cal gluconate-10ml of 10% soln over 2 min. Immediate, effect lasts1hr 50ml of 50% dextrose + 10 units insulin over 30min K will drop by1mmol/l in 15min and effect lasts sev hrs HCO3- 3 ampoules in 1litre 5%dextrose if pt not overhydrated Frusemide Salbutamol nebuliser-beta2 agonist therapy. Lowers K by 1mmol in 30min and lasts3 hrs Cation exchange resins- retention enema- 50gm in150 ml tapwater or 50gm in 100ml of 20% sorbitol orally. Lowers K by 1mol in 1hr and lasts 6hrs

  19. Anion Gap ACS • In any biological system in which ions are present , electrical neutrality is maintained by the total # of cations with the total # of anions • This principal is utilised clinically in patients with suspected acid base disorders by measuring the serum sodium, chloride and bicarbonate concentrations. • Normally the extracellular conc of Na+ = the extracellular conc of Cl- + HCO3- + a constant designated as delta Mmol Na = mmol Cl- + mmol HCO3- + Where delta = 8 +/- 4 mmol/l

  20. ACID BASE BALANCE ACS • Enormous amount of acid is produced everyday from daily metabolism • Oxidation of CHO and fats produce 15,000-20,000 mmols of volatile acid as CO2 • Breakdown of sulphur containing aminoacids and incomplete oxidation of CHO & fats produce 60-70 mmols of fixed acid • Normally this H+ produced does not change in extracellular pH from its normal value of 7.4(+/-0.2) because of intracellular buffers, pulmonary and renal mechanisms • Intracellular buffers are phosphates and proteins • Extracellular buffers are haemoglobin, proteins and the bicarbonate- carbonic acid system

  21. ACID BASE BALANCE ACS • Normally the body keeps the ph at 7.4 by maintaining the bicarbonate(HCO3) to carbonic acid (H2CO3) ratio at 20 to 1 HCO3 = 20 H2CO3 1 Increase in the ratio will produce alkalosis ( inc pH) and decrease will produce acidosis ( dec pH) Carbonic acid behaves as an acid or as the neutral gas carbon dioxide and is expressed by the following equation: CO2+H2O<->H2CO3 <-> H++HCO3- Where formation of carbonic acid from carbon dioxide or reversion of carbonic acid to water and carbon dioxide will depend on the acid-base status

  22. ACID BASE BALANCE H++HCO3- <->H2CO3 <-> CO2+H2O When acid is added to the system bicarbonate conc will decrease with a corresponding drop in the HCO3/H2CO3 ratio <20/1 To combat this ventilation is increased and the newly formed carbonic acid is quickly converted to CO2 and blown off by the lungs, thereby reestablishing the ratio. If alkali is added to the system the HCO3 increases and the reverse occurs and CO2( and hence carbonid acid) is retained by the lungs through a decrease in ventilation and an increased excretion of HCO3 by the kidneys

  23. ACID BASE BALANCE-ACIDOSIS ACS Respiratory Acidosis- When normal resp is depressed as in airway obstruction, hypoventilation, pneumonia, pneumothorax, asthma, heavy sedation, emphysema, pleural effusion CO2 is retained increasing Pco2 > 45mmHg, pH decreases. The kidney attempts to compensate by increasing HCO3 absorption and H+ excretion Patient needs ventilatory assistance- intubation and ventilation to blow off the CO2

  24. Metabolic Acidosis Metabolic Acidosis- Here there is a deficit of HCO3 due to excessive acid production eg diabetes with excessive ketone formation or • renal disease ( inadequate excretion of inorganic acids like phosphate and sulphate) or • when there excessive loss of bicarbonate as in diarrhoea, pancreatic or enterocutaneous fistula or • Lactic acidosis secondary to shock when anaerobic glycolysis results in accumulation of lactic acid Acidosis is dangerous as it • decreases myocardial contractility causes a reduction in cardiac output, • decreases responsiveness of peripheral vessels to circulating cathecholamines causing hypotension and • increases refractoriness of the fibrillating heart to defibrillation making cardiac resuscitation difficult

  25. ACID BASE BALANCE-ALKALOSIS Alkalosis is better tolerated than acidosis and is fact the most common acid base abnormality seen in the early postop period. This is due to post traumatic aldosteronism stimulated by volume reduction causing retention of Na and HCO3 and secretion of K, hyperventilation secondary to pain and anxiety and nasogastric suction causing loss of acid. Respiratory Alkalosis- Secondary to hyperventilation usually abates when pain and anxiety subsides. When secondary to hypoxemia it may need ventilatory support. It results in hypokalemia as extracellular K moves intracellularly. Hypocapnea results in cerebral vasoconstriction Metabolic Alkalosis – results from nasogastric suction with loss of H+.( hypocholeremic, hypokalemic alkalosis) As a result of hypovolemia the kidney reabsorbs Na exchanging it for K and H – thus resulting in acid urine – paradoxical aciduria

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