This document discusses the composition and functions of body fluids and electrolytes. It begins by describing the phospholipid bilayer of cell membranes and how it is selectively permeable. It then discusses the different fluid compartments in the body - intracellular fluid, interstitial fluid, plasma. The document covers water balance and distribution across age groups. It also covers electrolytes, osmolality, tonicity, and how fluids move across membranes via diffusion, osmosis, filtration and active transport. The functions of intracellular and extracellular fluids are also summarized.
This document discusses the composition and functions of body fluids and electrolytes. It begins by describing the phospholipid bilayer of cell membranes and how it is selectively permeable. It then discusses the different fluid compartments in the body - intracellular fluid, interstitial fluid, plasma. The document covers water balance and distribution across age groups. It also covers electrolytes, osmolality, tonicity, and how fluids move across membranes via diffusion, osmosis, filtration and active transport. The functions of intracellular and extracellular fluids are also summarized.
This document discusses the composition and functions of body fluids and electrolytes. It begins by describing the phospholipid bilayer of cell membranes and how it is selectively permeable. It then discusses the different fluid compartments in the body - intracellular fluid, interstitial fluid, plasma. The document covers water balance and distribution across age groups. It also covers electrolytes, osmolality, tonicity, and how fluids move across membranes via diffusion, osmosis, filtration and active transport. The functions of intracellular and extracellular fluids are also summarized.
Instructor Phospholipid bilayer Freely permeable to non-polar molecules (CO 2 , O 2 , steroids) Impermeable to large polar and charged molecules (ions, proteins, glucose) Generally permeable to water (though some cells require aquaporins) Approx water content in body Age group 90% Premature infant 70-80% Newborn infant 64% 12 - 24 months 60% Adult 60% fluids 55% fluids Total Body Mass female male 45% solids 40% solids 2/3 Intra- cellular fluid (ICF) 1/3 (ECF) 80% 20% Interstitial fluid Plasma Some fluid is lost from blood in the interstitial tissues, and returned by the lymphatic system (also lymph and other miscellaneous fluids) 5 2/3 (65%) of TBW is intracellular (ICF) 1/3 extracellular water 25 % interstitial fluid (ISF) 5- 8 % in plasma (IVF intravascular fluid) 1- 2 % in transcellular fluids CSF, intraocular fluids, serous membranes, and in GI, respiratory and urinary tracts (third space) Function of ICF & ECF: ICF: is vital to normal cell function, its contain solutes such as oxygen, electrolytes and glucose. It provides a medium to metabolic process.
ECF: it is the transport system that carries nutrients and waste product from the cell.
The proportion of water decreases with aging because fat, age and sex effect of total body water.
Infants have a greater proportion of extracellular fluid than older children and adults.
Because extracellular fluid is more easily lost from the body than intracellular fluid, infants are more at risk of developing dehydration than older children and adults (infants also have a larger surface area to body mass ratio).
Na + Cl - HCO 3 - K + Mg 2+ PO 4 3- +
+
+
+
-
-
-
-
9 Electrolytes charged particles Cations positively charged ions Na + , K + , Ca ++ , H + Anions negatively charged ions Cl - , HCO 3 - , PO 4 3- Non-electrolytes - Uncharged Proteins, urea, glucose, O 2 , CO 2 ICF (mEq/L) ECF (mEq/L) Sodium 20 135-145 Potassium 150 3-5 Chloride --- 98-110 Bicarbonate 10 20-25 Phosphate 110-115 5 Protein 75 10 o Osmolarity = solute/(solute+solvent)
o Osmolality = solute/solvent (275-295 mOsm/L)
o Tonicity = effective osmolality
o Plasma osmolility = 2 x (Na) + (Glucose/18) + (Urea/2.8)
o Plasma tonicity = 2 x (Na) + (Glucose/18) MW (Molecular Weight) = sum of the weights of atoms in a molecule mEq (milliequivalents) = MW (in mg)/ valence mOsm (milliosmoles) = number of particles in a solution
13 Tonicity Isotonic Hypertonic Hypotonic 14 15 Cell in a hypotonic solution 16 Cell in a hypertonic solution Diffusion Osmosis Filtration Active transport
1. Osmosis: Is the movement of water across cell membranes, from the less concentrated solution to more concentrated solution. In other word water move toward higher concentration. Solutes are substance dissolved in liquid. Crystalloid: salts that dissolved readily in to true solution. Colloids: substance such as large protein molecules that do not dissolved in true solution.
Sodium is the major determinant of serum osmolality. 2. Diffusion: Is the continual intermingling of molecules in liquid, gases by random movement of the molecules. 3. Filtration: Is the process where by fluid and solutes moved together across a membrane from one compartment to another. 4. Active transport: substance can move across cell membranes from a less concentrated solution to amore concentrated one by active transport. Sodium and potassium concentrations in extra- and intracellular fluids are nearly opposite This reflects the activity of ATP-dependent sodium-potassium pumps (Na + -K + ATPase) Continuous exchange and mixing of fluid among compartments - regulated by osmotic and hydrostatic pressures
Net leakage of fluid from the blood is picked up by lymphatic vessels and returned to the bloodstream Exchanges between interstitial and intracellular fluids are more complex due to the selective permeability of the cell membranes An increase in ECF solute concentration [NaCl] would cause osmotic and volume changes in the ICF. Which way would water move, into or out of cells? ICF is determined by the ECF solute concentration solute solute solute solute solute solute solute solute solute solute More Solute = Less Water Less Solute = More Water Hypertonic Solution or Hypotonic Solution? solute solute solute H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Which way will Water move? solute solute solute solute solute solute solute solute solute solute H 2 O H 2 O H 2 O H 2 O H 2 O If the oncotic pressure in the interstitium increased, would this promote or inhibit the re-entry of fluid in a capillary bed? H 2 O Daily water intake must equal water output Water Intake Water Output Stimulated by thirst center of hypothalamus Osmoreceptors detect an increase in fluid osmolarity Thirst center inhibited by distension of stomach wall Sensible loss: urine, feces, noticible sweat Insensible loss: respiration and non- noticible sweat Urine output is the primary regulator of water out (ADH from posterior pituitary gland) Water intake: Ingested fluid (60%) and solid food (30%) Metabolic water or water of oxidation (10%) Water output: Urine (60%) and feces (4%) Lost via lungs and skin (28%), sweat (8%) To remain properly hydrated, water intake must equal water output Fluid Gain and Loss Why are you told to drink plenty of fluids when you have a fever? A fever increases water loss (maybe both insensible and sensible) The hypothalamic thirst center is stimulated by: A decline in plasma volume of 10%15% Increases in plasma osmolality of 12% Baroreceptor input, angiotensin II, etc. Feedback signals that inhibit the thirst centers include: Moistening of the mucosa of the mouth and throat Activation of stomach and intestinal stretch receptors Body fluids are: Electrically neutral Osmotically maintained Specific number of particles per volume of fluid Ion transport Water movement Kidney function Water loss (output) exceeds water intake and the body is in negative fluid balance A common sequala to hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, and diuretic abuse Signs and symptoms: dry mouth, thirst, dry flushed skin, and oliguria Prolonged dehydration may lead to weight loss, fever, and mental confusion Other consequences include hypovolemic shock and loss of electrolytes Accumulation of fluid in the interstitial space, leading to tissue swelling, caused by anything that increases fluid flow out of the bloodstream or hinders its return Factors that accelerate fluid loss include: Hypertension, increased capillary permeability, incompetent venous valves, localized blood vessel blockage, congestive heart failure Decreased fluid return usually reflects an imbalance in colloid osmotic pressures across capillary membranes Hypoproteinemia low levels of plasma proteins, may result from protein malnutrition, liver disease, or glomerulonephritis
Fluids are forced out of capillary beds at the arterial ends by blood pressure, but fail to return at the venous ends and interstitium becomes congested with fluid Blocked (or surgically removed) lymph vessels may result in the accumulation of plasma proteins in interstitial fluid Interstitial colloid osmotic pressure increases, fluid leaves blood and moves into tissue Interstitial fluid accumulation could result in a decrease in blood volume, blood pressure, and impaired circulation Kwashiorkor - a form of malnutrition caused by inadequate protein intake and consequent reduced albumin in the blood hypoalbuminemia and reduced plasma oncotic pressure promote the extravasation of fluid from the plasma into the peritoneal cavity Hypertension Polyuria Peripheral edema Wet lung Jugular vein engorgement
Especially when hypo- albuminemia Diminished skin turgor Dry oral mucus membrane Oliguria - <500ml/day - normal: 0.5~1ml/kg/h Tachycardia Hypotension Hypoperfusioncyanosis Altered mental status Thorough history taking: poor intake, GI bleedingetc BUN : Creatinine > 20 : 1 - BUN: hyperalimentation, glucocorticoid therapy, UGI bleeding Increased specific gravity Increased hematocrit Electrolytes imbalance Acid-base disorder CVP Pulse Peripheral Veins Weight Thirst Intake and Output Skin Edema Lab Values Preserve oxygen delivery to tissues Correct hypovolaemia Maintain cardiac output Optimise gas exchange Replace electrolytes & water Maintain urine output
Colloids + RBCs Crystalloids Identify what is the goal Choose fluid which best achieves the goal Methods of estimating basal or maintenance fluid requirements Basal Surface Area Need to know height and weight, requires table, does not allow for deviations from normal activity Basal or Calorie Expenditure Method Requires a table, involves calculations, permits correction for changes in activity or injury, drier Holliday-Segar System Easy to remember, does not require table or difficult calculations, does not allow for deviations from normal activity Isotonic crystalloids - Lactated Ringers, 0.9% NaCl - only 25% remain intravascularly Hypertonic saline solutions - 3% NaCl Hypotonic solutions - D5W, 0.45% NaCl - less than 10% remain intra- vascularly, inadequate for fluid resuscitation Contain high molecular weight substancesdo not readily migrate across capillary walls Preparations - Albumin: 5%, 25% - Dextran - Gelifundol - Haes-steril 10% Solutions Volumes Na + K + Ca 2+ Mg 2+ Cl - HCO 3 - Dextrose mOsm/L ECF 142 4 5 103 27 280-310 Lactated Ringers 130 4 3 109 28 273 0.9% NaCl 154 154 308 0.45% NaCl 77 77 154 D5W D5/0.45% NaCl 77 77 50 406 3% NaCl 513 513 1026 6% Hetastarch 500 154 154 310 5% Albumin 250,500 130- 160 <2.5 130- 160 330 25% Albumin 20,50,100 130- 160 <2.5 130- 160 330 Common parenteral fluid therapy 0.9% Normal Saline
D5W 5 % Dextrose*
D51/4NS 5% Dextrose 0.2% NS
D51/3NS 5% Dextrose 0.3% NS
LR or RL Lactated Ringers Solution
3% N S 3% Normal saline 5 % N S 5% Normal Saline D 10 W Dextrose 10% in water D 20 W Dextrose 20% in Water D5 NS 5%Dextrose,with 0.45% Normal Saline D5NS 5% Dextrose with 0.9% Normal Saline D5LR 5% Dextrose with Lactated Ringers 1/3 N S 0.33% Normal Saline
1/2 N S 0.45% Normal Saline
D 2.5 W Dextrose 2.5% in water Neonates need relatively more fluid intake than older infants and children.
The kidneys in neonates have small immature glomeruli and for this reason the glomerular filtration rate is reduced (about 30ml/min/1.73m2 at birth to 100ml/min/1.73m2 at nine months).
The loops of Henle are short and the distal convoluted tubules are relatively resistant to aldosterone, leading to a limited concentrating ability For oral feeding with standard formula milk, preterm babies may need 200ml/kg per day initially.
Term babies need approximately 150ml/kg per day until fully weaned.
Children and adolescents may drink up to 2-3 litres of fluid per day. Hourly maintenance fluid requirements can be calculated using the following guide:
4ml/kg/hr or 100ml/kg/day for first 10kg body Weight 2ml/kg/hr or 50ml/kg/day for second 10kg body Weight 1ml/kg/hr or 20ml/kg/day for each additional kg body weight
The recommended volume of oral feeds is greater than that calculated using this guide so that adequate calorie and protein intake can be achieved. ElECTROLYTE REQUIREMENTS Na + 3 mEq/100ml Cl - 4 mEq/100ml K + 2 mEq/100ml Definition: Amount of fluid lost before treatment is begun One-time estimate; additional losses after therapy is begun are considered on-going losses Methods: Preillness and current weight change Fluid deficit (L) = Preillness weight (kg) current weight (kg) % Dehydration = (Fluid deficit (L)/Preillness weight (kg))x100 Clinical estimates of weight loss Sodium: usually in pediatrics, losses are gastrointestinal or due to a relatively short period of decreased oral intake approximated by 0.45 NS Potassium: deficit replacement is based on rate of safe replacement and not amount since danger of hyperkalemia is greater than hypokalemia Add 20 mEq potassium/L after UOP is established Potassium infusion rate should not exceed 1 mEq/kg/hour unless in monitored setting Fluid: abnormal losses that occur after the one-time determination of a deficit Diarrhea, vomiting, NG aspirates, polyuria Measured and replaced cc for cc Electrolytes: Consult tables for electrolyte composition of on-going losses GI losses = 0.45 NS Transudates = 0.9 NS Radiant losses = sodium free Maintenance fluid requirements must be modified according to the childs clinical condition.
All types of fluid intake and output must be measured .
If the child is dehydrated or has excessive fluid losses, fluid intake must be increased. For zero fluid balance, fluid losses = fluid intake.
Insensible fluid loss is fluid lost from the body in perspiration and breathing, and is proportional to body surface area (BSA).
It is approximately 300ml/m2/day ,slightly higher in infants and young children, warm temperature, pyrexia, tachypnoea, etc. Using indirect calorimetric measurements, energy expenditure in critically ill children may be as low as 50-60 kcal/kg/day.
Mechanical ventilation decreases the work of breathing as well as evaporative water loss through the respiratory tract and the energy expenditure for thermal regulation.
Warmed humidification of respiratory gases through the ventilator circuit can reduce insensible water losses by as much as one third.
Hence, traditional estimates for maintenance fluid volumes particularly in critically ill children cannot be quantified from these general guidelines. The most potent stimuli for ADH secretion are an increase In serum osmolality, hypovolemia and hypotension. However, multiple nonosmotic stimuli such as pain, drugs and anesthetic agents, stress, and even nausea and vomiting may also result in increased ADH activity.
There will be very little if any excretion of EFW, as ADH limits renal water excretion in this setting, even in the presence of a low plasma osmolality.
As a result, hyponatremia occurs due to a positive balance of EFW in association with an impaired ability to excrete hypotonic urine.
Any exogenous sources of free water, such as the administration of hypotonic IV maintenance fluids, will therefore further exacerbate the fall in plasma sodium (PNa). Recently conducted systematic review of maintenance fluids for hospitalized children revealed that the use of hypotonic fluids remarkably increased the odds of developing hyponatremia by 17 times when compared to isotonic fluids.
Interstitial fluid 10.5 Litres Blood volume 3.5 litres Cells 28 Litres Vasoconstriction & redistribution Interstitial fluid mobilisation Reduced interstitial fluid Intracellular fluid mobilisation Reduced intracellular fluid What are we trying to achieve by giving intravenous fluid ?
Scenario: Acute blood loss
Replacement of RBCs, water and electrolytes - haemostasis
Albumin to Interstitium Vasodilatation loss of SVR
Hypovolaemia Interstitial oedema Interstitial oedema Na + Cl -
water Na + Cl -
water Na + and Cl - Loading Fluid retention Severe interstitial oedema Organ dysfunction What are we trying to achieve by giving intravenous fluid ?
Scenario: Acute inflammation
Blood volume expansion, in the context of vascular dysfunction and leaky capillaries
It is very easy to give salt & water to critically ill patients, and very difficult to remove Urine electrolyte measurement is essential for fluid management in the critically ill Electrolytes are salts, acids, and bases, but electrolyte balance usually refers only to salt balance Salts are important for: Neuromuscular excitability Secretory activity Membrane permeability Controlling fluid movements Salts enter the body by ingestion and are lost via perspiration, feces, and urine Expressed in milliequivalents per liter (mEq/L) - a measure of the number of electrical charges in one liter of solution For monovalent ions, 1 mEq = 1 mOsm For bivalent ions, 1 mEq = 1/2 mOsm no. of electrical charges on one ion mEq/L = (concentration of ion in [mg/L] the atomic weight of ion X For monovalent ions, 1 Eq = 1 mole For divalent ions, 1 Eq = 0.5 mol For trivalent ions, 1 Eq = 0.333 mol The equivalent (Eq or eq) is a measurement unit used in chemistry and the biological sciences - a measure of a substance's ability to combine with other substances - frequently used in the context of normality (GEW/liters of solution) The equivalent is defined as the mass (g) in grams of a substance which will react with 6.022 x 10 23 electrons. The equivalent weight of a substance is equal to the amount in moles divided by the valence. The exchange of interstitial and intracellular fluid is controlled mainly by the presence of the electrolytes sodium and potassium Na + K + Na + K + Na + K + Na + K + Potassium is the chief intracellular cation and sodium the chief extracellular cation Because the osmotic pressure of the interstitial space and the ICF are generally equal, water typically does not enter or leave the cell K + Na + A change in the concentration of either electrolyte will cause water to move into or out of the cell via osmosis A drop in potassium will cause fluid to leave the cell whilst a drop in sodium will cause fluid to enter the cell K + H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O K + K + K + Na + Na + Na + Na + Aldosterone, ANP and ADH regulate sodium levels within the body, whilst aldosterone can be said to regulate potassium K + Na + aldosterone ADH ANP Sodium (Na + ) ions are the important cations in extracellular fluid
Anions which accompany sodium are chloride (Cl - ) and bicarbonate (HCO 3 - )
Considered an indicator of total solute concentration of plasma osmolality Na + HCO 3 - Cl - H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Sodium ions are osmotically important in determining water movements
A discussion of sodium must also include Chlorine Bicarbonate Hydrogen ions
Potassium and calcium serum concentrations are also important electrolytes in the living system H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Click Hypercalcemia - elevated calcium levels
Hyponatremia -- lowered sodium levels Participates in the Na-K pump Assists in maintaining blood volume Assists in nerve transmission & muscle contraction Primary determinant of ECF concentration Controls water distribution throughout the body Primary regulator of ECF volume Regulations: skin, GIT,Aldosterone increases Na retention in the kidney Normal range for blood levels of sodium is app. 137 - 143 meq/liter
Hypernatremia refers to an elevated serum sodium level (145 -150 mEq/liter)
Increased levels of sodium ions are the result of diffusion and osmosis Na + 1) Sodium ions do not cross cell membranes as quickly as water does Na + H 2 O
H 2 O
H 2 O
H 2 O
H 2 O
Na + 2) Cells pump sodium ions out of the cell by using sodium-potassium pumps Na + Na + Na + Na + 3) Increases in extracellular sodium ion levels do not change intracellular sodium ion concentration Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + Na + 1) Water is osmotically drawn out of the cells
Resulting in dehydration
2) Increase in extracellular fluid volume Extracellular fluid volume Intracellular fluid volume In the CNS tight junctions exist between endothelial cells of the capillary walls
These junctions restrict diffusion from capillaries to the interstitium of the brain blood-brain barrier
Increased levels of sodium ions in the blood does not result in increased sodium ions in brain interstitial fluid As the result of an osmotic gradient, water shifts from the interstitium and cells of the brain and enters the capillaries The brain tends to shrink and the capillaries dilate and possibly rupture Result is cerebral hemorrhage, blood clots, and neurological dysfunction H 2 O There is an unknown mechanism that protects the brain from shrinkage
Within about 1 day
Intracellular osmolality of brain cells increases in response to extracellular hyperosmolality Idiogenic osmoles accumulate inside brain cells K + , Mg + from cellular binding sites and amino acids from protein catabolism
These idiogenic osmoles create an osmotic force that draws water back into the brain and protects cells from dehydration H 2 O 1) Water loss
2) Sodium ion overload Most cases are due to water deficit due to loss or inadequate intake
Infants without access to water or increased insensible water loss can be very susceptible to hypernatremia Diabetes insipidus caused by inadequate ADH or renal insensitivity to ADH results in large urinary fluid loss Increased fluid loss also occurs as the result of osmotic diuresis (high solute loads are delivered to the kidney for elimination) Glucose Glucose Glucose diabetes mellitus results in loss of fluids as well by creating an osmotic pull (increased urine solute concentration) on water into the tubules of the kidney Glucose Glucose Glucose Glucose Glucose Glucose Glucose Glucose H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Glucose Glucose Glucose diabetes mellitus results in loss of fluids as well by creating an osmotic pull (increased urine solute concentration) on water into the tubules of the kidney Glucose Glucose Glucose Glucose Glucose Glucose Glucose Glucose H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Glucose Glucose Glucose diabetes mellitus results in loss of fluids as well by creating an osmotic pull (increased urine solute concentration) on water into the tubules of the kidney Glucose Glucose Glucose Glucose Glucose Glucose Glucose Glucose H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Glucose Glucose Glucose diabetes mellitus results in loss of fluids as well by creating an osmotic pull (increased urine solute concentration) on water into the tubules of the kidney Glucose Glucose Glucose Glucose Glucose Glucose Glucose Glucose H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Glucose Glucose Glucose diabetes mellitus results in loss of fluids as well by creating an osmotic pull (increased urine solute concentration) on water into the tubules of the kidney Glucose Glucose Glucose Glucose Glucose Glucose Glucose Glucose H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Glucose Glucose Glucose diabetes mellitus results in loss of fluids as well by creating an osmotic pull (increased urine solute concentration) on water into the tubules of the kidney Glucose Glucose Glucose Glucose Glucose Glucose Glucose Glucose H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Glucose Glucose Glucose diabetes mellitus results in loss of fluids as well by creating an osmotic pull (increased urine solute concentration) on water into the tubules of the kidney Glucose Glucose Glucose Glucose Glucose Glucose Glucose Glucose H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Glucose Glucose Glucose diabetes mellitus results in loss of fluids as well by creating an osmotic pull (increased urine solute concentration) on water into the tubules of the kidney Glucose Glucose Glucose Glucose Glucose Glucose Glucose Glucose H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Glucose Glucose Glucose diabetes mellitus results in loss of fluids as well by creating an osmotic pull (increased urine solute concentration) on water into the tubules of the kidney Glucose Glucose Glucose Glucose Glucose Glucose Glucose Glucose H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Re-animate High protein feedings by a stomach tube create high levels of urea in the glomerular filtrate producing an osmotic gradient the same as glucose does and increased urinary output results Occurs less frequently than water loss
Retention or intake of excess sodium ex: IV infusion of hypertonic sodium ion solutions
Aldosterone promotes sodium and water retention by the kidney High levels of aldosterone may result in mild hypernatremia CAUSE COMMENTS essent i al hyper nat r emi a di sor der i n whi ch t hi r st i s i mpai r ed fever i ncr eased i nsensi bl e fl ui d l oss coma i nadequat e fl ui d i nt ake hot envi r onment , or st r enuous exer ci se sweat , hypot oni c fl ui d l oss vomi t i ng oft en a hypot oni c fl ui d l oss di ar r hea oft en a hypot oni c fl ui d l oss pi t ui t ar y di abet es i nsi pi dus defi ci ency of ADH; excessi ve fl ui d l oss nephr ogeni c di abet es mel l i t us r enal t ubul es i nsensi t i ve t o ADH; excessi ve ur i nar y l oss uncont r ol l ed di abet es mel l i t us gl ucose i n gl omer ul ar fi l t r at e; osmot i c di ur esi s l ar ge amount s of pr ot ei n and ami no aci ds gi ven by nasogast r i c t ube ur ea i s a pr oduct of pr ot ei n met abol i sm; ur ea causes osmot i c di ur esi s excessi ve i nt r avenous i nfusi on of hyper t oni c sodi um sal t sol ut i ons admi ni st r at i on of excessi ve sodi um i ons manni t ol used as di ur et i c manni t ol i n gl omer ul ar fi l t r at e; osmot i c di ur esi s Re-hydration is the primary objective in most cases
Decreases sodium concentrations
A point of concern is when and how rapid the re-hydration occurs After 24 hours the brain has responded by producing idiogenic osmoles to re-hydrate brain cells
If this adaptation has occurred and treatment involves a rapid infusion of dextrose for example:
There is danger of cerebral edema with fluid being drawn into brain tissues Treatment is best handled by giving slow infusions of glucose solutions
This dilutes high plasma sodium ion concentrations Ideally the goal is to avoid overloading with fluid and to remove excess sodium Diuretics can be used to induce sodium and water diuresis However if kidney function is not normal peritoneal dialysis may be required Two pronged approach: 1. Identify and treat the underlying cause.
2 .Correct osmolar imbalance by replacing what was lost (water, hypotonic fluids +/- electrolytes) or ridding the body of excess sodium Hypovolemic: Low total body Na, orthostasis: restore hemodynamics with NS, then change to D5W or NS Hypervolemic: Excess total body Na. Give loop diuretics to increase Na excretion and then replace D5W to correct hypertonicity. Dialyze if kidneys are not working. Euvolemic: Normal total body Na. Give D5W. If the Na has risen over a matter of <12 hours, it can be correctly quickly without consequence. If elevated for longer than 12 hours or if the onset is unclear, decrease Na by no more than 10 mmol/L/day or 0.5 mmol/L/hr. Goal is 145.
One approach: 1. Calculate the total body water (TBW): 0.6 x (wt in kg) 2. Select your fluid and identify the amount of Na in mmol/L D5W 0 NS 34 NS 77 LR 130 NS 154 3--Calculate the effect of 1 L of your selected fluid on serum Na according to this formula: Change in serum Na for 1L of fluid of choice =[IVF Na - serum Na] divided by [TBW + 1] If you are also giving K in your IVF, modify the formula as follows: Change in serum Na for 1L of fluid of choice =[(IVF Na + IVF K) - serum Na] divided by [ TBW + 1] 4-Decide how quickly you want to correct. In cases of prolonged hypernatremia, divide 10 (the desired drop) by the number obtained above to calculate the amount of IVF required over the next 24 hours to decrease the serum Na appropriately. When hypernatremia has been shorter-lived, divide the number necessary to reach 145 by the number of hours over which you want to correct. 5-Account for average obligatory 24 hour water losses (1.5L or so) 6-Convert to mL and divide by 24 to obtain mL/hour Defined as a serum sodium ion level that is lower than normal
Implies an increased ratio of water to sodium in extracellular fluid
Extracellular fluid is more dilute than intracellular fluid
Results in a shift of water into cells Brain cells lose osmoles creating a higher extracellular solute concentration Effect is to protect against cerebral edema by drawing water out of the brain tissue Suppression of thirst
Suppression of ADH secretion
Both favor decreasing water ingestion and increasing urinary output Primarily neurological (net flux of water into the brain) Sodium ion levels of 125 meq / liter are enough to begin the onset of symptoms Sodium ion levels of less than 110 meq / liter bring on seizures and coma Produced by:
1) A loss of sodium ions 2) Water excess
Water excess can be due to: Ingestion Renal retention 1) Isotonic fluid loss 2) Antidiuretic hormone secretion 3) Acute or chronic renal failure 4) Potassium ion loss 5) Diuretic therapy H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Na + Na + Na + H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O H 2 O Na + Na + Na + Na + Na + H 2 O H 2 O H 2 O H 2 O H 2 O 1) Isotonic fluid loss Burns, fever, hemorrhage Indirect cause of hyponatremia Any volume loss stimulates thirst and leads to increased water ingestion Thus isotonic fluid loss can cause hyponatremia not because of sodium loss but because of increased water intake 2) Antidiuretic hormone secretion Enhances water retention
3) Acute or chronic renal failure The kidney fails to excrete water Can lead to hyponatremia 4) Potassium ion loss Potassium ions are the predominant intracellular cations When they are lost they are replaced by diffusion of intracellular potassium into extracellular fluid Electrical balance is maintained by the diffusion of sodium ions into the cells in exchange for potassium ions Thus a loss of extracellular sodium is realized and hyponatremia may ensue K + Na + Na + K + K + K + 1) extracellular potassium loss 2) diffusion of potassium ions into extracellular compartments 3) intracellular electrical balance is maintained by diffusion of sodium ions into cells plasma interstitial fluid cell K + Na + K + K + K + Plasma Interstitial fluid Cell K + K + Na + Na + Click to see animation 5) Diuretic therapy
Common cause of hyponatremia
Loss of sodium and potassium often occurs in addition to fluid loss CAUSE COMMENTS psychogeni c pol ydi psi a excessi ve i ngesti on of water syndrome of i nappropri ate secreti on of ADH ADH causes renal water retenti on Addi son s di sease al dosterone defi ci ency K + l osses from extracel l ul ar fl ui d K + move out of cel l s to repl ace l osses; Na + move i nto cel l s to mai ntai n el ectri cal neutral i ty
Increased Na + Osmoreceptors inhibited
Decreased ADH release Decreased Thirst
Increased urinary H 2 O loss Decreased H 2 O gain Decreased Na + Homeostasis Normal Na + Osmoreceptors stimulated
Increased ADH release Increased Thirst
Additional H 2 O dilutes Na + H 2 O loss concentrates Na + Decreased urinary H 2 O loss Increased H 2 O gain 10 10 60 K + Normal serum potassium level (3-5 meq / liter) As compared to Na + (142 meq / liter) Intracellular levels of potassium (140-150 meq / liter) This high intracellular level is maintained by active transport by the sodium-potassium pump K + Cells pump K + ions in and Na + ions out of the cell by using sodium-potassium pumps Na + Na + Na + Na + K + K + K + K + Hyperkalemia is an elevated serum potassium (K + ) ion level A consequence of hyperkalemia is acidosis an increase in H + ions in body fluids Changes in either K + or H + ion levels causes a compartmental shift of the other K + When hyperkalemia develops potassium ions diffuse into the cell This causes a movement of H + ions out of the cell to maintain a neutral electrical balance As a result the physiological response to hyperkalemia causes acidosis K + K + K + K + K + K + H + H + H + H + H + H + H + H + H + HYPERKALEMIA The reverse occurs as well The body is protected from harmful effects of an increase in extracellular H + ions (acidosis) H + ions inside the cells are tied up by proteins (Pr - ) This causes a shift of potassium ions out of the cells The reverse occurs as well The body is protected from harmful effects of an increase in extracellular H + ions (acidosis) H + ions inside the cells are tied up by proteins (Pr - ) This causes a shift of potassium ions out of the cells H + H + H + H + H + H + H + H + H + K + K + K + K + K + K + ACIDOSIS Summarized: Hyperkalemia causes acidosis Acidosis causes hyperkalemia HYPERKALEMIA H + H + H + H + H + H + H + H + K + K + K + K + K + K + K + K + ACIDOSIS Summarized: Hyperkalemia causes acidosis Acidosis causes hyperkalemia HYPERKALEMIA H + H + H + H + H + H + H + H + K + K + K + K + K + K + K + K + ACIDOSIS Muscle contraction is affected by changes in potassium levels
Hyperkalemia blocks the transmission of nerve impulses along muscle fibers Causes muscle weakness and paralysis Can cause arrhythmia's and heart conduction disturbances 1) Increased input of potassium
2) Impaired excretion of potassium
3) Impaired uptake of potassium by cells A) Intravenous KCl infusion
B) Use of K + containing salt substitutes
C) Hemolysis of RBC during blood transfusions with release of K +
D) Damaged and dying cells release K + Burns, crush injuries, ischemia
E) Increased fragility of RBC Insulin deficiency predisposes an individual to hyperkalemia Cellular uptake of K + ions is enhanced by insulin, aldosterone and epinephrine Provides protection from extracellular K +
overload Insulin K + K + K + K + K + K + Click to view animation Insulin deficiency represents decreased protection if the body is challenged by an excess of K + ions In the absence of aldosterone there is loss of Na + in the urine and renal retention of K + Inherited disorder in which serum K + level rise periodically Caused by a shift of K + from muscle to blood in response to ingestion of potassium or exercise Reasons for the shift are not clear Attacks are characterized by muscle weakness Aldosterone has a primary role in promoting: Conservation of Na + Secretion of K + by the nephrons of the kidney Addisons disease is characterized by aldosterone deficiency Thus the kidney is unable to secrete potassium at a normal rate Kidney loses the ability to secrete K + Diuretic that is antagonistic to the effects of aldosterone Causes some rise in serum K + levels by interfering with K + secretion in the kidneys Increases may not be significant But individuals taking the diuretic are at risk if potassium is administered 1) Counteract effects of K + ions at the level of the cell membrane 2) Promotion of K + ion movements into cells 3) Removal of K + ions from the body Infusion of calcium gluconate or NaCl solutions Immediately counteract the effects of K +
ions on the heart Effective for only 1-2 hours NaHCO 3 also reverses hyperkalemic effects on the heart If acidosis is a factor also raises the pH of body fluids Insulin given with glucose Effective in about 30 minutes Has a duration of action of up to 6 hours
Insulin promotes the shift of K +
ions into cells Glucose prevents insulin- induced hypoglycemia Kayexalate (cation exchange resin) Removes K + ions from the body by exchanging K + for Na +
Exchange time is about 45 minutes Effective for up to 6 hours Peritoneal dialysis or hemodialysis Effectively clears the blood of high K +
levels as well CAUSE COMMENTS hyper kal emi c per i odi c par al ysi s i nher i t ed di sor der i n whi ch t her e ar e sudden shi ft s of cel l ul ar K+ t o ext r acel l ul ar compar t ment s aci dosi s compensat or y shi ft of H+ i nt o cel l s i n exchange for movement of K+ t o ext r acel l ul ar compar t ment s bur ns cel l dest r uct i on wi t h r el ease of K+ t r ansfusi on of bl ood t hat has been st or ed r el ease of K+ fr om hemol yzed r ed bl ood cel l s spi r onol act one di ur et i c t hat i s an al dost er one ant agoni st ; i nt er fer es wi t h r eabsor pt i on of Na+ and secr et i on of K+ t oo r api d i nt r avenous i nfusi on of KCl speci al r i sk of hyper kal emi a i f t hei r i s i mpai r ed r enal secr et i on of K+ use of K+ cont ai ni ng sal t subst i t ut es excessi ve i ngest i on pot assi um sal t s of ant i bi ot i cs addi t i onal sour ce of K+ acut e ol i gur i c r enal fai l ur e i mpai r ed secr et i on of K+ Defined as a serum K + level that is below normal (< 3 meq / liter) Serum concentrations will decrease if: There is an intracellular flux of K + K + ions are lost from the gastrointestinal or urinary tract K + Alkalosis causes and is caused by hypokalemia Alkalosis is defined as a decrease of hydrogen ions or an increase of bicarbonate in extracellular fluids Opposite of acidosis K + H + HCO 3 - Alkalosis elicits a compensatory response causing H + ions to shift from cells to extracellular fluids This corrects the acid-base imbalance HCO 3 - HCO 3 - HCO 3 - HCO 3 - HCO 3 - HCO 3 - H + H + H + H + H + H + H + H + H + ions are exchanged for K +
(potassium moves into cells) Thus serum concentrations of K + are decreased And alkalosis causes hypokalemia HCO 3 - HCO 3 - HCO 3 - HCO 3 - HCO 3 - HCO 3 - H + H + H + H + H + H + H + H + K + K + K + K + K + K + K + K + Conversely when K + ions are lost from the cellular and extracellular compartments Sodium and hydrogen ions enter cells in a ratio of 2:1 as replacement This loss of extracellular H +
causes alkalosis HCO 3 - H + K + HCO 3 - HCO 3 - HCO 3 - HCO 3 - HCO 3 - HCO 3 - H + H + H + H + H + H + Na + K + K + K + K + K + K + K + Na + Na + Na + Na + Na + Na + Kidney function is altered by hypokalemia Na + ions are reabsorbed into the blood when K +
ions are secreted into the urine by kidney tubules K + Tubular lumen K + K + K + K + K + K + Na + Na + Na + Na + Na + Na + Na + Peritubular fluid NORMAL Kidney function is altered by hypokalemia If adequate numbers of K + are not available for this exchange H + ions are secreted instead H + Tubular lumen K + H + K + H + K + H + Na + Na + Na + Na + Na + Na + Na + Peritubular fluid HYPOKALEMIA Hypokalemia promotes renal loss of H + ions and thus results in alkalosis Normal nephron function is to secrete H + and K + in exchange for Na + capillary distal tubule H + K + Na + Blood Urine capillary distal tubule H + K + Na + In Hypokalemia the kidney selectively secretes H + ions in preference to K + ions The loss of H + ions may lead to alkalosis Blood Urine capillary distal tubule H + K + Na + retained K + excreted 1) in alkalosis there is a decrease in extracellular fluid H + 2) the kidney retains hydrogen ions to correct the alkalosis 3) the kidney then eliminates K + ions which can lead to Hypokalemia Blood Urine CAUSE COMMENTS aldosterone excess favors renal Na+ reabsorption and K + secretion diarrhea diarrheal fluid contains high amounts of K +
diuretics in general causes K + loss distal renal tubular acidosis kidney tubule defect in which K + are secreted, and H + are retained by the body hypokalemic periodic paralysis cause unknown; periodic influx of K + into cells Bartters syndrome syndrome in which aldosterone is sometimes elevated; probably a renal tubular defect so that K + are lost
Replacement of K + either by: Oral K + salt supplements Diet Intravenous administration of K + salt solution Diuretic (spinolactone) if renal loss is at work Maximum IV infusion rate: 1 mEq/kg/hr Marked hypokalemia: Monitor serum K closely 0.5-1 mEq/kg/dose given as an infusion of 0.5 mEq/kg/hr for 1-2 hour