Fluid and electrolyte balance

Fluid and electrolyte balance

• 1.
  FLUID AND ELECTROLYTE BALANCE PRESENTER A.Shalini Sampreethi OMFS
• 2.
  CONTENTS  INTRODUCTION  BODYFLUID COMPARTMENTS  SOLUTES  ELECTROLYTE BALANCE  REGULATION OF ELECTROLYTES  I.V.FLUIDS  IMBALANCES  GUIDELINES FOR I.V.FLUIDS  COMPLICATIONS OF I.V. FLUIDS  ACID BASE BALANCE  REFERENCES
• 3.
  INTRODUCTION  The maintenanceof normal volume and normal composition of the fluid is vital to life.  Management of fluids and electrolytes is an integral part of the care of surgical patients.  Many diseases, injuries and operative trauma have a great effect on the physiology of body fluids and electrolytes.  Three types of homeostasis are involved in this maintenance: fluid balance, electrolyte balance, and acid-base balance.
• 4.
  BODY WATER CONTENT Water is the main constituent of the body  Water makes up around two thirds of our total body mass.  Women have 50% of water their total body weight.  Men have 60% of water their total body weight.  Infants have 73% of water.  Total water content declines throughout life, accounting for only about 45% of water present total body weight in old age.
• 5.
  BODY FLUID COMPARTMENTS The total body fluid is mainly distributed between two compartments – extracellular fluid & intracellular fluid.  The extracellular fluid compartment is divided into interstitial fluid and the blood plasma.  There is another small compartment of fluid that is referred to as transcellular fluid. This compartment includes fluid in the synovial, peritoneal, pericardial and intraocular spaces as well as cerebrospinal fluid.  All the transcellular fluids together constitute about 1-2litres.
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  ANATOMY OF BODYFLUIDS
• 7.
   Fluids withinthe body’s total cell population are collectively called the intracellular fluid.  This is about 30-40% body weight.  The fluid of each cell contains its individual mixture of different constituents, but the concentrations of these substances are similar from one cell to another. For this reason, the intracellular fluid of all the different cells together is considered to be one large fluid compartment.  Chemical composition Cations – potassium 125 mEq/liter magnesium 40 mEq/liter Anions - phosphates 150 mEq/liter proteins 40 mEq/liter
• 8.
  EXTRACELLULAR FLUID COMPARTMENT All the fluids outside the cells are collectively called the extracellular fluid.  It constitutes 20% of body weight  The two largest compartments of extracellular fluid are interstitial fluid & plasma which makes up almost ¼ the extracellular fluid. The plasma is the non cellular part of the blood & communicates continuously with the interstitial fluid through the pores of the capillary membranes.  These pores are highly permeable to almost all the solutes in the extracellular fluid except the proteins. Chemical composition Cations – sodium 140 mEq/liter potassium 5mEq/liter calcium 3mEq/liter magnesium 2 mEq/liter anions - chlorides 114mEq/liter bicarbonates 30 mEq/liter
• 9.
  STARLING FORCES The fluidbalance between various compartments is determined by:  Hydrostatic pressure is the mech. pressure in the vascular bed generated by the contraction of the heart.  Osmotic pressure is the driving force that allows water to pass through the semi-permeable membrane to the side with greatest concentration of solutes. Balance between hydrostatic and osmotic forces causing movement out and into the capillaries
• 10.
  FLUID MOVEMENT AMONG COMPARTMENTS Continuous exchange of fluids occur due to hydrostatic and osmotic pressures.  Water moves across compartments due to osmotic gradient.  Solutes distribution depends on molecular size, electrical charge and active transport system.  Plasma acts as link between internal and external environments  Altering the composition and volume of plasma activates the compensatory mechanisms to restore balance.  Water moves across compartments to keep osmolalities of body fluids equal.
• 11.
  SOLUTES: ELECTROLYTES AND NONELECTROLYTES Electrolytes are chemical components that dissociate into ions in water.  Non electrolytes have bonds that prevent them from dissociating in solution. They have no electrical charge. Glucose, lipids, creatinine and urea.  Electrolytes have much greater osmotic power than Non- electrolytes because each electrolyte molecule dissociates into at least two ions.
• 12.
  ELECTROLYTE BALANCE Electrolytes includesalts, acids, and bases, but term electrolyte balance usually refers to the salt balance in the body. Salts provide minerals essential for:  Neuromuscular excitability  Secretory activity  Membrane permeability  Many other cellular functions.  Additionally, salts are important in controlling fluid movements. Salts enter the body by foods and fluids, and small amount of salts are generated during metabolic activity. Salts are lost from the body in sweat, feces, and urine.
• 13.
  SODIUM IN FLUIDAND ELECTROLYTE BALANCE  Balance between sodium input and output is one of the most important functions of the kidneys.  Cellular plasma membranes are relatively impermeable to Na+  The sodium content of the body may change, its concentration in the ECF normally remains stable because of immediate adjustments in water volume.
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  REGULATION OF SODIUMBALANCE  Influence of aldosterone  Cardiovascular baroreceptors  Influence of Anti diuretic harmone  Influence of Atrial natriuretic peptide  Other hormones
• 15.
  ROLE OF ALDOSTERONE Aldosterone is produced by adrenal cortical cells. Most important trigger for aldosterone release is the Renin-Angiotensin mechanism mediated by the juxtaglomerular apparatus of the renal tubules.  High aldosterone concentrations causes Na to be actively reabsorbed in the distal convoluted tubules and collecting ducts.  Inhibition of aldosterone release causes no Na reabsorption.
• 16.
  CARDIOVASCULAR SYSTEM BARORECEPTORS  Bloodvolume is carefully monitered and regulated by baroreceptors in the heart and in the large vessels of the neck and thorax (carotid arteries and aorta) .  As blood volume rises, baroreceptors are stimulated alerts hypothalamus, sympathetic nervous system to reduse the impulses to the kidneys then afferent arterioles of kidney dilate and glomerular filtration rate rises , sodium and water output increase. This is called PRESSURE DIURESIS, reduces blood volume and blood pressure.
• 17.
  ANTI-DIURETIC HORMONE  Amountof water reabsorbed in the collecting ducts of the kidneys is proportional to ADH release.  Osmoreceptors of the hypothalamus sense the ECF solute concentration and trigger or inhibit ADH release from the posterior pituitary.  Decrease in sodium ion concentration, inhibits ADH release, allows more water to be excreted in urine, restoring normal Na levels in the blood. Low ADH levels, most of the water reaching the collecting ducts is allowed to pass through,results in dilute urine and a reduced volume of body fluids.
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  Triggers of ADHrelease :  prolonged fever  excessive sweating  vomiting  diarrhoea  severe blood loss  traumatic burns.
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  ATRIAL NATRIURETIC PEPTIDE Atrial natriuretic peptide is a hormone that is released by certain cells of heart atria when stretched by the effects of elevated blood pressure.  It reduces blood pressure and blood volume by inhibiting events that promote vasoconstriction and Na+ and water retention.
• 20.
  OTHER HORMONES  FemaleSex Hormones – The estrogens are chemically similar to aldosterone, they enhance NaCl reabsorption by the renal tubules.  Progesterone decreases sodium reabsorption by blocking the effect of aldosterone on the renal tubules.  Progesterone has a diuretic like effect and promotes sodium and water loss.  Glucocorticoids – Cortisol and Hydrocortisol, enhances tubular reabsorption of sodium.
• 21.
  REGULATION OF K+BALANCE  Potassium is chief intracellular cation  It is required for neuromuscular functioning , metabolic activities, including protein synthesis.  Potassium excess in ECF decrease their membrane potential, causing depolarization, followed by reduced excitability.  A deficit of K+ in ECF causes hyperpolarization and nonresponsiveness.  The heart is particularly sensitive to K+ levels. Both too much & too little k+ can disrupt electrical conduction in the heart, leading to sudden death.
• 22.
  POTASSIUM REGULATORY SITE INCOLLECTING TUBULES  Potassium balance is maintained chiefly by renal mechanisms.  Renal tubules predictably reabsorb over 90% of the filtered K+  Responsibility for K+ balance falls chiefly on the collecting ducts.  Factors determine the rate and extent of potassium secretion – the plasma potassium ion concentration and aldosterone levels.
• 23.
  REGULATION OF CALCIUMBALANCE  99% of calcium found in bones in the form of calcium phosphate salts.  Ionic calcium in ECF - important for normal blood clotting, cell membrane permeability, and secretory behavior.  Ionic calcium has potent effects on neuromuscular excitability.  Hypocalcemia increases excitability and causes muscle tetany.  Hypercalcemia inhibits neurons and muscle cells and may cause life-threatening cardiac arrhythmias.
• 24.
  HORMONES REGULATING THECALCIUM  Parathyroid hormone  Calcitonin.  Ca2+ homeostasis are exerted by parathyroid hormone (PTH)  Declining plasma levels of Ca2+ stimulate the parathyroid glands to produce PTH. When PTH released effects the:  Bones  kidneys  Small intestine The role of Calcitonin targets bone, where it encourages deposit of calcium salts and inhibits bone resorption.
• 25.
  REGULATION OF MAGNESIUM Second most abundant intracellular cation  It activates coenzymes in carbohydrate and protein metabolism  Magnesium plays role in myocardial functioning, Neurotransmission, and neuromuscular activity.  Half of the magnesium in the body find in the skeleton,remainder is found intracellularly.
• 26.
  REGULATION OF ANIONS Chloride is the major anion accompanying sodium in the ECF  It maintains osmotic pressure of the blood. Blood pH is in normal limits or slightly alkaline, 99% of filtered chloride ions are reabsorbed.  In the PCT, they move passively and simply follow sodium ions out of the filtrate and into the peritubular capillary blood.  Other anions, such as sulfates and nitrates, have definite transport mechanisms and when their concentrations in the filtrate exceed their renal thresholds, excesses spill over into urine.
• 27.
   Fluids infusedintravenously to restore or maintain fluid and electrolyte balance when it is not possible for a patient to do so independently.  Treatment is aimed at correcting the cause of the problem and assisting the body to restore fluid, electrolyte and acid–base balance with the appropriate intervention. IV FLUIDS Classic indications for IV fluid:  maintenance of blood pressure  restoring the ICF volume  replacing ongoing renal or insensible losses when oral intake is inadequate  need for glucose as a fuel for the brain.
• 28.
  CRYSTALLOIDS  A crystalloidis a solution of water containing electrolytes or substances that are easily metabolized such as glucose.  Classified as 2 groups: 1. Replacement solutions 2. Special solutions
• 29.
  REPLACEMENT SOLUTIONS  Usedto replace ECF  These have Na+ same as ECF  To replace blood loss , 3-4 times the volume lost must be administered as only 1/3rd to ¼th remains in ICF after 1hr  In adults 20% blood loss=1000ml loss=3000-4000ml of replacement solution require.  Two solutions used for acute vol. expansion are NS 0.9% and Ringers lactate solution
• 30.
  SPECIAL SOLUTIONS  HalfNS  8.4% bicarbonate sol.  Potassium chloride  Mannitol sol.  5% dextrose
• 31.
  5% DEXTROSE  Dextroseused - dextrose monohydrate  5% dextrose contains 4.5 g/dl of glucose  Is a isotonic solution INDICATIONS : 1. As calorie nutrition 2. Hypertonic dehydration 3. Correction of hypernatremia 4. Emergency fluid to prevent risk of shock 5. To carry drugs
• 32.
  DISADVANTAGES : 1. Cerebraledema 2. Ischemic brain injury 3. Hyponatraemia ADVERSE REACTIONS: 1. pain , burning sensation at infusion site 2. Thrombophlebitis 3. Fever, local tenderness ,abscess , tissue necrosis at injection site
• 33.
  NORMAL SALINE 0.9% Sol.of 0.9%w/v sodium chloride = 9gm of NaCl /lit of water  Contains 154 mmol/L of Na and 154 mmol/lit of Cl  Other NaCl concentrations available are : 1. Half normal saline-0.45% NaCl 2. Quarter NS -0.22% NaCl 3. Dextrose 4% in 0.18% saline
• 34.
  INDICATIONS : 1. Indehydration 2. To maintain daily requirment of salt and water 3. Gastrointestinal losses 4. Perioperative fluid replacement 5. Hypovolemia 6. Vehicle of drugs 7. Hypercalcemia
• 35.
  HYPERTONIC SALINE SOLUTIONS Includes 1.8%,3%,5%,7.5%,10% NaCl solutions INDICATIONS: 1. In hyponatremia states 2. Brain injury 3. Sclerotherapy 4. In hemorrhagic shock, septic shock and major burns 5. Intradermal injections
• 36.
  HARTMANN’S SOLUTION  Alsocalled Sodium Lactate Or Ringers Lactate Sol. CONTENTS: Na+ 130-131mmol/l Cl- 109-111 mmol/l Bicarbonate 29mmol/l K+ 5mmol/l Ca2+ 2 mmol/l Lactate
• 37.
  INDICATIONS: 1. Fluid resuscitation-trauma,surgery ,burns 2. To induce urination in renal failure cases 3. Ideal maintaining fluid during and after surgery 4. Diarrhea induced hypovolemia –in lower GI losses 5. Metabolic acidosis CONTRAINDICATIONS: 1. Hepatic insufficiency 2. Chronic heart failure 3. Addison's disease 4. In upper GI losses
• 38.
  DARROW’S SOL. : 1.Contains sufficient K+ to combat hypokalaemia 2. Safe and convenient method for providing K+ ions 3. Rate of infusion not to exceed 60 drops /min
• 39.
  COLLOIDS  A colloidis a solution containing high molecular weight substances such as proteins or large glucose molecules.  Classification: Natural Albumin Fresh frozen plasma Artificial Gelatin Dextran Hydroxy ethyl starch.
• 40.
  ALBUMIN 1. Albumin isprotein derived from human plasma. 2. Albumin infusion is expensive and should be used for acute volume expansions and not as supplemental source of protein calories. Hydroxyethyl starch - 6% starch and 0.9% sodium chloride. 1. Has no oxygen-carrying capacity 2. It is administered intravenously as a plasma expander. 3. Limitations include acquisition cost, hypersensitivity reactions, and bleeding. 4. Dosing should be reduced in the presence of renal dysfunction.
• 41.
  DEXTRANS: Low-molecular weight& high-molecular weight dextran are polysaccharide plasma expanders .Are used to treat the hypovolemia. FRESH FROZEN PLASMA used in excessive blood loss (surgery or trauma) and to prevent bleeding in presence of abnormal coagulation conditions. Fresh frozen plasma is now rarely used for volume expansion. Risk of anaphylaxis, potential for viral transmission through plasma & increased nosocomial infection rate in the intensive care setting.
• 42.
  WATER DEPLETION ETIOLOGY 1. Difficultyin swallowing due to painful conditions in mouth and pharynx 2. Obstruction in the oesophagus 3. Exhaustion and paresis of pharyngeal muscles 4. vomiting 5. Water unavailability 6. Fever 7. Hyperthyroidism 8. Hyperventilation 9. Diabetes IMBALANCES
• 43.
  CLINICAL FEATURES:  Mild:[1-2 lit ] 1. Weakness and intense thirst 2. Urinary output diminished.  Moderate [ 2-4 lit ] 1. Marked thirst, difficulty in swallowing 2. Dizziness, confusion 3. Oliguria, raised plasma urea and Na+  Severe [ 4- 10 lit ] 1. Confusion, coma, muscle weakness 2. Tachycardia ,low BP
• 44.
  MANAGEMENT: Mild: 2 litof water utilisation by orally /5 % dextrose 2-4 lit infused through IV 6-12 hrs Moderate : 5 % dextrose 2-4 lits infused through IV 24 hrs Severe : 0.9 % saline 1 lit infused through IV -1 hr 5 % dextrose 4 lit infused through IV – 24 hrs 5 % dextrose 2-4 lit IV + oral water 24 -48 hrs
• 45.
  SODIUM DEPLETION ETIOLOGY 1. Obstructionof small intestine 2. Rapid loss of gastric, biliary,pancreatic,and intestinal secretions by antiperistalsis and ejection either by vomiting or aspiration. 3. Severe diarrhea due to dysentry, cholera,ulcerative colitis or psuedomembranous colitis 4. Hypernatremia with elevated K+ is due to adrenocortical insufficiency. 5. Gastric aspiration followed by IV dextrose can cause hyponatremia
• 46.
  CLINICAL FEATURES 1. Sunkeneyes. 2. In infants anterior fontonella is depressed 3. Tongue coated and become dry 4. Skin become dry and wrinkled 5. Peripheral veins contracted and contains dark blood 6. Arterial BP below normal 7. Scanty urine. 8. Normal or slightly low serum Na 9. Low urine output and low urinary Na
• 47.
  MANAGEMENT If plasma Na+levels - 110-120mmol/lit 0.9 % saline IV 1 lit 12 hourly If plasma Na + levels < 110mmol/lit 1.8 % or 3% saline slowly IV to raise plasma Na +
• 48.
  SODIUM EXCESS ETIOLOGY Excess amountof 0.9% saline IV during early post operative period CLINICAL FEATURES: 1. Overloading of circulation 2. Edema of the lungs 3. Slight puffiness of face 4. Causes pitting edema 5. Weight increases 6. In infants – tension at anterior frontonella, increased weight ,increase in no. of urinations, edema occurs. MANAGEMENT 1. Stop infusion 2. Treat pulmonary edema
• 49.
  POTASSIUM DEPLETION  Aftertrauma, there is increased excretion of K+.  Greatest amount of potassium loss occurs in first 24hrs of trauma. [in partial gastrectomy cases it lasts for 3-4 days]  It occurs as two types: 1. Sudden 2. Gradual
• 50.
  SUDDEN HYPOKALEMIA: 1. Prolongedinfusion of saline solution GRADUAL HYPOKALEMIA: 1. It occurs in surgical procedures 2. Diarrhoea from ulcerative colitis 3. Villous tumours of rectum 4. Prolonged gastroduodenal aspiration with replacement with saline sol. 5. Extensive resections for carcinoma of alimentary tract
• 51.
  CLINICAL FEATURES: 1. Slowand slurry speech. 2. Intense drowsiness. 3. Muscular hypotonia. 4. Reflexes are lost. 5. Abdominal distention 6. Weakness of respiratory muscles. 7. ECG shows- prolonged QT interval, depression of ST segment, lowering or inversion of T wave.
• 52.
  PREVENTION : 1. AdditionalKCl 20-60mmol/day 2. Pts on high doses corticosteroids need K+ supplements 3. Pts need 60mmol/day K+ over 24 hrs 4. Monitor K+ levels
• 53.
  HYPERKALAEMIA ETIOLOGY 1. IV fluidshaving K+ 2. Bleeding into soft tissues, hemolysis. 3. Tissue damage. 4. Acidosis,insulin deficiency,aldosterone deficiency. 5. Accute renal failure.
• 54.
  CLINICAL FEATURES: 1. Tinglingaround lips or fingers 2. Bradyarrythmias 3. E.C.G.shows QT intervals,elevation of ST segment and elevation of T wave. 4. Severe muscular weakness with paralysis 5. Loss of tendon jerks 6. Abdominal distension 7. Cardiac arrest if K+ levels exceeds 7 mmol/l
• 55.
  MANAGEMENT: 1. Inject 10-20ml10% Ca gluconate through IV over 10 min 2. Infusion of 50ml 50% glucose IV ,monitor glucose levels and administer insulin if hyperglycemia 3. Infusion 10-20% dextrose 500ml 4-6 hrly. 4. In metabolic acidosis infuse NaHCO3 1.26% 500ml 6-8 hrly
• 56.
  HYPERCALCEMIA ETIOLOGY 1. Hyperparathyroidism 2. Malignancy-lung,renal ,colonic, thyroid 3. Multiple myeloma, thyrotoxicosis 4. Pagets disease 5. Thiazide diuretics
• 57.
  CLINICAL FEATURES: 1. Poluria,polydipsia 2.Lethargy,anorexia,nausea,dyspepsia,peptic ulceration 3. Depression,drowsiness 4. Nephrocalcinosis and renal tubular impairment INVESTIGATIONS: 1. Serological findings shows low plasma phosphate and elevated alkaline phosphatase
• 58.
  MANAGEMENT: 1. Rehydration withnormal saline – 4-6 lit 2. Bisphosphonates - pamidronate 90mg IV over 4 hrs . RAPID THERAPY: Forced diuresis with saline and furesemide Glucocorticosteroid –Predisolone 40 mgs daily Hemodialysis Treat the cause
• 59.
  HYPOCALCEMIA ETIOLOGY : 1. VitaminD Deficiency 2. Chronic Renal Failure 3. Hypo Parathyroidism 4. Acute Pancreatitis
• 60.
  CLINICAL FEATURES : Tetany: 1. Increased excitability of peripheral nerves 2. In children – characteristic feature is carpopedal spasm, convulsions. 3. Metacarpopedal joints are flexed ,interphalangeal joints of fingers and thumb are extended. 4. In adults : tingling of hands ,feet and around mouth Latent tetany: 1. TROUSSEAU’S SIGN 2. CHVOSTEK’S SIGN
• 61.
  Prolonged hypocalcemia: clinical featuresof hypocalcemia 1. Grand mal epilepsy 2. Psychosis 3. Cataracts 4. Calcifications of basal ganglion
• 62.
  MANAGEMENT: Tetany I. Rebreathing expiredair / 5% CO2 in oxygen. II. Inject 20 ml of 10% sol. Ca gluconate slowly into vein. CHRONIC HYPOCALCAEMIA  calcitriol tablets 0.5 – 3 ug / day.  monitor serum Ca level every 3 months.
• 63.
  HYPOPHOSPHATAEMIA ETIOLOGY 1. Hyperparathyroidism 2. Alkalosis 3.Reduced oral absorption in starvation, alcoholism
• 64.
  CLINICAL FEATURES: 1. Normalrange -0.8-1.4mmol/l 2. <0.4 mmol/l cause cell dysfunction and death 3. Muscle weakness and pain, increased plasma creatine kinase 4. Respiratory muscle weakness 5. Cardiac arrythmias 6. Neuroencephalopathy 7. Hemolysis
• 65.
  MANAGEMENT 1. Oral –milk-2 lit/day 2. Oral supplements- phosphate sandoz 3-6 times daily.
• 66.
  ETIOLOGY : 1. Seenin Accute renal failure and chronic renal failure. 2. In states of massive cell necrosis – acute haemolysis ,neoplastic disease treated by chemotherapy CLINICAL FEATURES : 1. Metastatic calcification 2. Secondary stimulation of parathyroid glands 3. Pruritis MANAGEMENT : Oral phosphate binders Dialysis
• 67.
  MAGNESIUM DEPLETION ETIOLOGY : 1.Reducedintake – Because of malnutrition,(sources of magnesium is leafy vegtables,fish,banana,dry fruites,nuts,beans) Mg free IV fluids 2. Alimentary loss - diarrhoea, vomitting, aspiration of GI contents 3. Renal loss – diuretics, chronic alcoholism , ketoacidosis, hyperparathyroidism 4. Miscellaneous - acute pancreatitis
• 68.
  CLINICAL FEATURES: 1. Neuromusculardisturbances – tremors. 2. Depression, confusion, agitation,epileptic fits, hallucinations 3. Gitelman’s syndrome –hypokalaemia and hypomagnesaemia caused by mutation in thiazide sensitive NaCl co-transporter in the distal tubule
• 69.
  MANAGEMENT 1. Amiloride :Given orally. 2. 30-50 mmol MgCl IV in 1 lit of saline or 5% dextrose over 12-24 hrs. 3. 15-20mmol Mg infused daily 4. Monitor Mg levels
• 70.
  POST-OPERATIVE MANAGEMENT OF FLUIDAND ELECTROLYTE BALANCE AVG .PATIENT REQUIRES: 1. 2000-3000ml of water daily 2. 100mmol of Na daily 3. 60mmol of K daily  Requirements are altered by metabolic response to trauma First 24 hrs: Increased secretion of ADH and aldosterone Pt. requires no salt and less water than normal 2 lits of 5 % dextrose to replace abnormal operative loss
• 71.
  Next 24-48hrs period Metabolicresponse to trauma decreases pt. needs 2 lits of 5 % dextrose and 1 lit of isotonic saline / 24 hrs  On 3rd post operative period and thereafter 20 mmol of K+ is added to each lit of IV fluid to make 60 mmol/24 hrs Alternate regime: 3 lit of isotonic sol. – 4.3 % dextrose 0.18% saline daily Add 20mmol of KCl to each lit on 3rd post operative day
• 72.
  RATE OF INFUSION THEHOLLIDAY-SEGAR METHOD For the first 10 kg 4 ml/Kg/hr For the next 10 kg Add 2 ml/Kg/hr For each kg above 20 kg Add 1 ml/Kg/hr For Example: 25 Kg child First 10 Kg : 4 ml/Kg/hr x 10 Kg = 40 ml/hr Next 10 Kg : 2 ml/Kg/hr x 10 Kg= 20 ml/hr Next 5 Kg : 1 ml/Kg/hr x 5 Kg = 5 ml/hr
• 73.
  CONTRAINDICATIONS TO IV THERAPY Failing heart  Pulmonary congestion.  Renal failure  Hepatic failure
• 74.
  GUIDELINES FOR IVTHERAPY  Impossible to measure loss of fluid and electrolytes in admitted pt in dehydrated state 1. Estimation done by detailed history of nature and quantity of fluid loss like in surgical procedure /vomiting 2. Appearance of patient  If large quantities of fluids are necessary: i. Measure central venous pressure ii. Urine output to determine optimum rate and volume of infusion  Replacement started by isotonic 0.9% saline sol.IV  When bulk of loss is made ,maintainance fluid dextrose –saline sol. administered
• 75.
  In cases ofshock: 1. Supplement the vol. of circulating fluid by dextrans or plasma infusion and followed by isotonic saline sol. 2. Fluid loss if rectified then maintenance fluid dextrose –saline sol. advisable Infants: Dehydrated state Fluid required = weight loss (1 gm=1ml)
• 76.
  PRINCIPLES OF INTRAVENOUSTHERAPY  Check all bottles of infusion solution for : (1) A broken vacuum seal. (2) Cloudiness. (3) Precipitation . (4) Foreign contaminants.  Use sterile equipment and wash hands thoroughly.  Disinfect with antiseptic sol. at and around the venipuncture site.  For long term therapy patients: - Change the injection site every 48 to 72 hours - Replace the tubing and solution bottle every 24 hours
• 77.
  Precautions if veinirritation or thrombophlebitis: (a) Plastic catheters likely to cause irritation than stainless steel needles. (b) Use smallest gauge needle or catheter . (c) Use shortest infusion time . (d) Veins of the lower extremities more likely to develop phlebitis (e) less likely to irritate the large veins of the central venous system than the smaller peripheral veins. (f) Aseptic techniques is required to prevent sepsis.
• 78.
  COMPLICATIONS OF IVFLUID THERAPY 1. Dislodgement of the needle or catheter, or puncture of the vein. 2. fluid collects in the surrounding tissue. 3. Slowing or stopping of the intravenous flow 4. Reduced skin temperature in the venipuncture area. …….Restart the intravenous at another site SPEED SHOCK OR CIRCULATORY OVERLOAD 1. when too much fluid or too much medication is administered too rapidly, circulatory overload can result. 2. Patient complaints of headache and chills, a flushed look, irregular pulse, and dyspnea.
• 79.
  SEPSIS AND PYROGENICREACTIONS: 1. Introduction of pyrogenic organisms or their toxins into the bloodstream. 2. Febrile reactions caused by chemicals and certain types of particles. THE REACTION CAN BE LOCALIZED OR SYSTEMIC. 1. Systemic reaction occurs about thirty minutes after start of intravenous infusion. 2. Long-term therapy ,develop sepsis from the growth of microorganisms on the skin after a two to three days of period. 3. Signs include unexpected rise in temperature preceded by chills, nausea, vomiting, backache, and malaise. 4. Using aseptic techniques ,changing the infusion site, bottle, and tubing at least every two to three days on long term intravenous therapy patients.
• 80.
  PHLEBITIS: 1. Irritation orinjury to the vein. 2. Caused by mechanical, chemical, or bacterial irritation. 3. Signs include redness, pain, and swelling at the infusion site , fatigue together with fever and a rapid pulse. 4. Change the needle to another site , warm moist compresses to relieve discomfort and aid healing. Do not rub or massage the affected area.
• 81.
  AIR EMBOLISM: 1. Airgets into circulatory system through the IV administration set. 2. Blocks a vessel & tissues , unable to get oxygen. Nutrients and waste products cannot be removed. 3. Air bubble cuts off cardiac, cerebral, or pulmonary circulation. SYMPTOMS  Fall in blood pressure, tachycardia, or rapid pulse and loss of consciousness. Air embolism - prevented by removing all air from intravenous lines, using venipuncture sites below heart level, and never allowing an intravenous line to run dry before disconnecting or adding another bottle. The larger the embolus, the greater the danger. Death could result.
• 82.
  SOLUTION'S INCOMPATIBILITY: 1. Differaccording to the solution or drug being administered. 2. Effects vary from neutralizing the effects of a drug to causing circulatory collapse. 3. Some solutions, over 10 percent dextrose or potassium chloride, irritating in concentrated doses. Sterile water, saline, or special dilutants are required . 4. Incompatible drugs form a precipitate and cause fever, nausea, vomiting, and intense itching.
• 83.
  ACID –BASE BALANCE 1.ACID - PROTON ( H+) DONOR MOLECULE / ION , LOWERS PH OF SOLUTION Eg: HCl, 2. BASE - MOLECULE / ION THAT ACCEPTS PROTON RAISES PH OF SOLUTION Eg: NH3, OH-
• 84.
   Acidosis andalkalosis are change or tendency to change in the pH of the blood  Acidosis – accumulation of acid or loss of base with fall in pH  Alkalosis –accumulation of base or loss of acid with raise in pH.
• 85.
  THE IMPORTANCE OFCONSTANT PH 1. The ph of arterial blood in health is 7.4 ( range 7.36 to 7.42 ) 2. Functions of many vital proteins of the body strongly dependent on the ph 3. Acidosis – arterial blood ph is < 7.36 & alkalosis - > 7.42
• 86.
  MEASUREMENT OF ACID–BASE DISTURBANCES  Measured in arterial capillary blood  PCO2 –tension or partial pressure of CO2 in the blood  Normal arterial PCO2 -31-42 mm Hg.  PO2 –tension or partial pressure of O2 in the blood. It is 80-110 mmHg.
• 87.
  STANDARD BICARBONATE: It eliminatesrespiratory causes for acid –base imbalance Normal levels -22-25 mmol/l Metabolic causes of acid –base imbalance - changes in Standard bicarbonate levels Respiratory causes – changes in PCO2 and PO2
• 88.
  METABOLIC ALKALOSIS ETIOLOGY: Base excessor deficit of acid other than H2CO3 1. Excessive ingestion of absorbable alkali 2. Repeated vomiting or aspiration 3. Cortisone excess or Cushing’s syndrome COMPENSATION BY: I. Retention of CO2 by lungs II. Excretion of bicarbonate base –alkali urine
• 89.
  CLINICAL FEATURES: I. Seenin Pyloric stenosis by repeated vomiting II. Attenuated by drugs containing Na bicarbonate III. Tetany IV. Hypokalaemia V. Renal epithelial damage VI. Renal insufficiency MANAGEMENT : Cause to be removed and encourage high urine output.
• 90.
  METABOLIC ACIDOSIS Deficit ofbase or excess of any acid other than H2CO3 ETIOLOGY : 1. LOSS OF BASES :Due to sustained diarrhoea ,Ulcerative colitis, gastrocolic fistula. 2. INCREASE IN ACIDS : formation of ketone bodies in diabetes and starvation ,retention of metabolites in renal insufficiency, rapid rise of lactic and pyruvic acid by anaerobic tissue metabolism due to shock,following cardiac arrest,release of clamped aorta in surgery of abdominal aneurysm
• 91.
  CLINICAL FEATURES: In severeacidosis : rapid ,deep, noisy respirations ,urine is strongly acidic,standard bicarbonate level is lowered and base deficit seen MANAGEMENT : Administration of Ringers Lactate sol.or slow infusion of dilute NaHCO3 sol. In dehydration along with acidosis : infusion of NaHCO3 sol. and rapid infusion of isotonic saline sol.to restore ECF
• 92.
  RESPIRATORY ALKALOSIS  PCO2is below normal range  ETIOLOGY : 1. Excessive pulmonary ventilation during surgical procedues 2. Hyperventilation in high altitudes 3. Hyperpyrexia 4. A lesion of hypothalamus During anaesthesia – alkalosis is seen with pallor and fall in BP. Respiratory arrest in severe cases Compensation : Increased Renal excretion of Bicarbonate Management : Infflation with of CO2
• 93.
  RESPIRATORY ACIDOSIS  PCO2is above normal range  Caused by impaired alveolar ventilation  In inadequate ventilation of anaesthetised pt.,effects of muscle relaxants are not fully reversed at the end of anaesthesia  Pre-existing pulmonary disease during surgical practice  Attentuated by abdominal and thoracic incisions MANAGEMENT  Immediate treatment of pulmonary defect  Maintain adequate ventilation  Endotracheal tube & artificial respiration ( Severe Condition)  Avoid over sedation & over usage of muscle relaxants
• 94.
  REFERENCES:  CONCISE MEDICALPHYSIOLOGY – CHAUDHURI  DAVIDSONS’S PRINCIPLES AND PRACTICE OF MEDICINE  BAILEY AND LOVE’S SHORT PRACTICE OF SURGERY – CHARLES AND RUSSELL  ORAL & MAXILLOFACIAL TRAUMA , VOL 1 – RAYMOND FONSECA  TEXTBOOK OF GENERALANESTHESIA BY MILLER