IV Fluids
- 1. IV Fluids
- 2. Homeostasis • Fluid levels in the body are controlled by homeostatic mechanisms - VOLUME - TONICITY - ELECTROLYTES - WASTE PRODUCTS • In the obese patient there is a lower portion of body water • In children there is a higher portion of total body water
- 3. Body Fluid• Water content of the entire body • The total amount of water in a man of 70 kg is approximately 40 litres, averaging 57 percent of his total body weight. • In a newborn infant, this may be as high as 75 percent of the body weight, but it progressively decreases from birth to old age, most of the decrease occurring during the first 10 years of life. • Also, obesity decreases the percentage of water in the body, sometimes to as low as 45 percent • In diseased states where body water is affected, the compartment or compartments that have changed can give clues to the nature of the problem. Body water is regulated by hormones, including anti-diuretic hormone (ADH), aldosterone and atrial natriuretic peptide. • There are many methods to determine body water. One way to get a simple estimate is by calculation. • Body water is broken down into the following compartments: - Intracellular fluid (2/3 of body water). In a body containing 40 litres of fluid, about 25 litres is intracellular -Extracellular fluid (1/3 of body water). In a 40 litre body, about 15 litres is extracellular, which amounts to 37.5% – Plasma (1/5 of extracellular fluid). Per Guyton's illustration, of the 15 litres of extracellular fluid, plasma volume averages 3 litres. (20%) – Interstitial fluid (4/5 of extracellular fluid) – Transcellular fluid (a.k.a. "third space," normally ignored in calculations) • Contained inside organs, such as the gastrointestinal, cerebrospinal, peritoneal, and ocular fluids.
- 4. Intracellular V Extracellular • 2/3 • intracellular 1/4 intravascular 3/4 interstitial Colloids stay in intravascular space: GOOD FOR EXPANSION OF FLUID VOLUME ***Fluids can move freely between the 2 compartments
- 5. Fluid Comparments ***Na primarily EXTRACELLULAR, K primarily EXTRACELLULAR
- 6. Tonicity ADH 300 mOsmols When tonicity falls below 270mOsmols ADH secretion is switched off ADH reduces the
- 7. ADH / Vasopressin• Neurohypophysial , peptide hormone • Derived from a preprohormone precursor that is synthesised in the hypothalamus and stored in vesicles at the posterior pituitary. • Regulates retention of water; it is released when the body is dehydrated and causes the kidneys to conserve water; concentrating the urine and reducing urine volume. • Vasopressin has two effects by which it contributes to increased urine osmolality (increased concentration) and decreased water excretion: • 1.) Increasing the water permeability of distal tubule and collecting duct cells in the kidney, thus allowing water reabsorption and excretion of more concentrated urine, i.e., antidiuresis. This occurs through insertion of water channels (Aquaporin-2) into the apical membrane of distal tubule and collecting duct epithelial cells. Aquaporins allow water to move down their osmotic gradient and out of the nephron, increasing the amount of water re-absorbed from the filtrate (forming urine) back into the bloodstream. Vasopressin also increases the concentration of calcium in the collecting duct cells, by episodic release from intracellular stores. • 2.) Increasing permeability of the inner medullary portion of the collecting duct to urea by regulating the cell surface expression of urea transporters, which facilitates its reabsorption into the medullary interstitium as it travels down the concentration gradient created by removing water from the connecting tubule, cortical collecting duct, and outer medullary collecting duct. • Vasopressin increases peripheral vascular resistance (vasoconstriction) and thus increases arterial blood pressure. This effect appears small in healthy individuals; however it becomes an important compensatory mechanism for restoring blood pressure in hypovolemic shock such as that which occurs during haemorrhage.
- 8. Volume Renin Angiotensin If the volume drops too low, renin is activated which converts ansiotensinogen to angiotensin I. Ace converts if to angiotensin II. Angiotensin II is a potent vaso-constrictor - bvs constrict, increasingblood pressure. Angiotensin II stimulates the secretion of aldosterone from adrenalcortex => tubules of the kidneys increase the reabsorption of sodium and water into the blood.
- 10. Indications to give Fluid • To replace lost volume • Maintenance of daily requirements • Replace haemoglobin • Replace blood component • Diluent for drugs • Physical effect – promotion of a diuresis *** After surgery, vomiting, diarrhoea, dehydrated, bleeding...
- 11. The things that must be given • Water • Sodium • Potassium Look at U&E’s any abnormalities detected will help you decide if the patient needs extra Na or K supplementation
- 12. Water Prescription • Daily maintenance fluids • Replacement of any remaining defecit • Allowance for predicted excess (insensible) losses - Normal fluid balance for 70-80 year old male ***Insensible losses = respiration and sweating. Fluid given should appear to be more than that lost to allow for these losses
- 13. Maintenance Prescription • Average person requires 2-3 litres/day • Can be calculated by 30mls/kg/day • For thin patients 30mls/kg/day is the best to use • For obese patients, and estimate between 2-3 litres is best In paediatric patients maintenance prescriptions are calculated by weight: -100 mls/kg/day for first 10kg -50mls/kg/day for second 10kgs -20mls/kg/day for the rest
- 14. Prescribing • Generally prescribed at 1.2ml/kg/hr • However some fluids may be given at set rates • EG 70kg patients requires fluids at 84ml/hr totalling 2016ml/day
- 15. Types of Fluids • Saline Sodium Chloride • 5% dextrose • Hartmann’s solution • Colloids – good for expanding the volume Colloids 0.9% NaCl 5% Dextrose Plasma Interstitial Fluid Intracellular Fluid
- 16. Saline NaCl 0.9% • 77 molecules of Na and Cl • Exchange Na for H. Pee the Na out • If you give lots of Na it causes you to keep the fluids and therefore dilutes the volume, leading to a hyponatraemic state. (more sodium you give, the more water you hold onto) • Rapid infusion of NS can cause metabolic acidosis • The solution is 9 grams of sodium chloride (NaCl) dissolved in water, to a total volume of 1000 ml. • It has a slightly higher degree of osmolarity (i.e. more solute per litre) than blood • Uses: hypovolaemia (threatening blood circulation) and maintenance fluids resuscitation
- 17. Saline with KCl • Saline normally has no KCl in it and is available in 500ml or 1000ml bags • Can add in KCl: -500mls NaCl with 20mmol KCl -1000mls NaCl with 40mmol KCl • KCl added in when U&E show hypokalaemia or in maintenance if K is at the lower end of normal, to prevent a hypokalaemia • Saline with KCl cannot be given in resus because K can only be given at a rate of 10mmol/hour
- 18. 5% Dextrose • 50 grams of sugar dissolved in 1000mls water • Kidneys filter glucose out, sugar draws water out with it so the whole volume is lost • Not used for resuscitation
- 19. Hartmann’s Solution Compound Sodium Lactate • Closest to physiological normal. Has a lower Cl content to reduces the likelihood of a hyperchloraemic acidosis • Source of K, only enough for a maintenance dose, not replacement: if U&E show hypokalaemia no point giving it • Less Na. Very similar to GI losses. • Used to replace GI losses, for maintenance, resuscitation
- 20. Sodium and Potassium • Daily requirement Na: 1-2mmol/kg • Daily requirement K: 1mmol/kg • K available in 20mmol aliquots • Maximum rate of infusion is 10mmol/hr • Maximum concentration in any 1 litre is 40mmol • Usual prescription script: -0.5-1l normal saline (75-150mmols Na) -1.5-2l 5% dextrose 60mmol KCl (distributed between these fluids)
- 21. Normal Saline / Hartmann’s • Normal Saline -154mmol Na/l (normal plasma level 135-145) -154mmol Cl/l (normal plasma level 98-108) • Hartmann’s -131mmol Na -111mmol Cl 29mmol lactate -5mmol K -2mmol Ca Large volumes of saline will give considerable excess of chlorine. So using Hartmann’s will incur much less hyperchloraemic acidosis
- 22. GI losses • ALL: Isotonic • Gastric: acid (only if pure gastric losses) • Lower GI: alkaline, small intestine especially • ALL POTASSIUM RICH 10-20 mmol/l
- 23. Assessment of Defecit • Blood loss, vomiting, diarrhoea, diuresis, sweating • Fasting (before admission and during) • Symptoms and signs • Urinalysis: osmolality (>300, decreased Na <10) • Bloods: Urea, Na , haematocrit • Daily weight, any decrease in CVP or increase in pulse P: good estimate of circulating volume • Estimate of insensible losses • Skin turgor, mucous membranes
- 25. Replacement • Estimate % deficit eg mild = 5% • Calculate volume of deficit, = %deficit/100 x weight kg • Eg 0.5 x 70 = 3.5 litres • Tends to slightly overestimate deficit • Replace lost fluids over 1-2 days, this allows you to assess the response of the patient and adjust the regime if necessary
- 26. Insensible (Excess) Losses • Vomiting • NG aspiration • Diarrhoea • Stoma output • Intestinal Fistulae Rich in ions so need careful measured/ estimated
- 27. Gastric and Lower GI Losses • Sodium 80mmol/l • Remaining anoin is H+ • Potassium will be substituted for H+ • Can be replaced as normal saline • May use 1 in 4 bags of 5% dextrose – because of the overload on Na+ ***Be generous with potassium!!! Lower GI Similar approach. Replace some with 1.4% bicarbonate if needed Potassium at 10 to 20 mmol. Over zealous use of N saline may cause hyperchloraemic acidosis look at plasma chlorine replacement ACIDIC ALKALINE
- 28. Monitoring the response • Assess fluid status: thirst, mucous membranes (signs of dehydration), urine output, U&E, oedema, lung fields • Urinalysis: urinary electrolytes (especially is low urine output) • Skin turgor • OBS • Invasive monitoring (if required)
- 29. Fluid replacement water, Na, K. At a safe rate. Consider content carefully
- 30. Common Problems • Hyponatraemia: usually caused by excessive water • Hypokalaemia: usually caused by under- prescription of potassium or excessive losses from the gut. Requires urgent replacement. Max rate 10mmol/hr
- 31. Renal Failure • No safety valve, for excretion of excess fluids • Avoid potassium unless low • Total volume: -yesterday’s urinary output plus measured and insensible losses -WEIGH DAILY -advice from a nephrologist
- 32. Monitoring • Daily U&E • If excess losses, watch for low MG and acid- base balance • If malnourished, watch for low PO4 • Acidosis may be caused by excessive saline • Switch to oral fluids ASAP
- 33. TUTORIAL • When prescribing fluids need to know... weight, fluids since he came in/surgery, losses: blood, vomiting, diarrhoea, insensible. U&Es, BP, pulse, urinary output, renal function, diabetes? Old? CURRENT OBS PMHx: cardiac or renal problems DHx: diuretics etc
- 34. Prescribing fluids • Read full paragraph. • Work out maintenance: 30mls/kg/day • Look at U&E – any hypoNa/K? Yes: what ion? How can you replace it? Saline plus KCl etc No: plain saline or hartmanns Over what time period fluids to be given?
Editor's Notes
- #7: Arginine vasopressin (AVP), also known as vasopressin, argipressin or antidiuretic hormone (ADH), is a neurohypophysial hormone. Vasopressin is a peptide hormone that controls the reabsorption of molecules in the tubules of the kidneys by affecting the tissue's permeability. It also increases peripheral vascular resistance, which in turn increases arterial blood pressure. It plays a key role in homeostasis, and the regulation of water, glucose, and salts in the blood. It is derived from a preprohormone precursor that is synthesized in the hypothalamus and stored in vesicles at the posterior pituitary. Most of it is stored in the posterior pituitary to be released into the bloodstream; however, some AVP is also released directly into the brain, where it plays an important role in social behavior and bonding.
- #8: controls the reabsorption of molecules in the tubules of the kidneys by affecting the tissue's permeability.
- #9: When blood volume is low, juxtaglomerular cells in the kidneys secrete renin directly into circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I.[2] Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin converting enzyme found in the lungs. Angiotensin II is a potent vaso-active peptide which causes blood vessels to constrict, resulting in increased blood pressure. Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of fluid in the body, which also increases blood pressure. If the renin-angiotensin-aldosterone system is too active, blood pressure will be too high. There are many drugs that interrupt different steps in this system to lower blood pressure. These drugs are one of the main ways to control high blood pressure (hypertension), heart failure, kidney failure, and harmful effects of diabetes.[3][4]