HARLEY L.

DELA CRUZ RN MAN Instructor

• Phospholipid bilayer • Freely permeable to non-polar molecules (CO2, O2, steroids)

• Impermeable to large polar and charged molecules (ions, proteins, glucose)

• Generally permeable to water (though some cells require aquaporins)

Age group
Premature infant Newborn infant

Approx water content in body 90%
70-80%

24-12 months
Adult

64%
60%

45% solids 40% solids • Some fluid is lost from blood in the interstitial tissues. and returned by the lymphatic system 2/3 Intracellular fluid (ICF) 55% fluids 60% fluids (also lymph and other miscellaneous fluids) 1/3 (ECF) 80% 20% Interstitial fluid female male Plasma Total Body Mass .

2/3 (65%) of TBW is intracellular (ICF) 1/3 extracellular water • 25 % interstitial fluid (ISF) • 5. respiratory and urinary tracts (third space) 5 .8 % in plasma (IVF intravascular fluid) • 1.2 % in transcellular fluids – CSF. intraocular fluids. serous membranes. and in GI.

its contain solutes such as oxygen. It provides a medium to metabolic process. . electrolytes and glucose.  ECF: it is the transport system that carries nutrients and waste product from the cell.Function of ICF & ECF:  ICF: is vital to normal cell function.

 Infants have a greater proportion of extracellular fluid than older children and adults. infants are more at risk of developing dehydration than older children and adults (infants also have a larger surface area to body mass ratio).  . age and sex effect of total body water. Because extracellular fluid is more easily lost from the body than intracellular fluid. The proportion of water decreases with aging because fat.

.K+ Mg2+ PO43Na+ ClHCO3.+ + + + ..

. urea. HCO3. H+ Anions – negatively charged ions Cl-. PO43- Non-electrolytes . Ca++. O2.Electrolytes – charged particles Cations – positively charged ions Na+.Uncharged Proteins. glucose. K+ . CO2 9 .

ICF (mEq/L) Sodium 20 Potassium 150 Chloride --Bicarbonate 10 Phosphate 110-115 Protein 75 ECF (mEq/L) 135-145 3-5 98-110 20-25 5 10 .

8) o Plasma tonicity = 2 x (Na) + (Glucose/18) .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.

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 .

Tonicity Isotonic Hypertonic Hypotonic 13 .

14 .

Cell in a hypotonic solution 15 .

Cell in a hypertonic solution 16 .

 Diffusion  Osmosis  Filtration  Active transport .

Osmosis:  Is the movement of water across cell membranes.1. from the less concentrated solution to more concentrated solution. In other word water move toward higher concentration. .

• Colloids: substance such as large protein molecules that do not dissolved in true solution.• Solutes are substance dissolved in liquid.  Sodium is the major determinant of serum osmolality. • Crystalloid: salts that dissolved readily in to true solution. .

Diffusion:  3. 4.2. Is the process where by fluid and solutes moved together across a membrane from one compartment to another. Active transport: • substance can move across cell membranes from a less concentrated solution to amore concentrated one by active transport. . gases by random movement of the molecules. Filtration: • Is the continual intermingling of molecules in liquid.

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) .

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 . Continuous exchange and mixing of fluid among compartments .

ICF is determined by the ECF solute concentration 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? Hypertonic Solution or Hypotonic Solution? solute H2O H2O H2O solute H2O H2O H2O H2O H2O H2O H2O solute H2O H2O H2O H2O H2O solute H2O solute H2O solute solute H2O solute solute solute solute H2O solute H2O solute Less Soluteway = More Water Solute = Less Water Which will Water More move? .

would this promote or inhibit the re-entry of fluid in a capillary bed? solute H2O solute H2O solute H2O solute H2O solute solute solute H2O solute H2O solute solute .If the oncotic pressure in the interstitium increased.

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noticible sweat • Osmoreceptors detect an increase in fluid osmolarity • Thirst center inhibited by distension of stomach wall • Insensible loss: respiration and nonnoticible sweat • Urine output is the primary regulator of water out (ADH from posterior pituitary gland) .• Daily water intake must equal water output Water Intake • Stimulated by thirst center of hypothalamus Water Output • Sensible loss: urine. feces.

water intake must equal water output 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%).To remain properly hydrated. sweat (8%) .

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) .

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 . angiotensin II.The hypothalamic thirst center is stimulated by: •A decline in plasma volume of 10%–15% •Increases in plasma osmolality of 1–2% • Baroreceptor input.

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Body fluids are: • Electrically neutral • Osmotically maintained • Specific number of particles per volume of fluid .

 Ion transport  Water movement  Kidney function .

and mental confusion  Other consequences include hypovolemic shock and loss of electrolytes . thirst. severe burns. and oliguria  Prolonged dehydration may lead to weight loss. prolonged vomiting or diarrhea. and diuretic abuse  Signs and symptoms: dry mouth. fever. Water loss (output) exceeds water intake and the body is in negative fluid balance  A common sequala to hemorrhage. profuse sweating. water deprivation. dry flushed skin.

congestive heart failure . localized blood vessel blockage. 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.Accumulation of fluid in the interstitial space.

liver disease. may result from protein malnutrition. or glomerulonephritis Fluids are forced out of capillary beds at the arterial ends by blood pressure.Decreased fluid return usually reflects an imbalance in colloid osmotic pressures across capillary membranes Hypoproteinemia – low levels of plasma proteins. but fail to return at the venous ends and interstitium becomes congested with fluid .

fluid leaves blood and moves into tissue Interstitial fluid accumulation could result in a decrease in blood volume.Blocked (or surgically removed) lymph vessels may result in the accumulation of plasma proteins in interstitial fluid Interstitial colloid osmotic pressure increases. and impaired circulation . blood pressure.

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 hypoalbuminemia .

normal: 0.<500ml/day .5~1ml/kg/h Tachycardia Hypotension Hypoperfusioncyanosis Altered mental status .       Diminished skin turgor Dry oral mucus membrane Oliguria .

glucocorticoid therapy. GI bleeding…etc BUN : Creatinine > 20 : 1 . UGI bleeding Increased specific gravity Increased hematocrit Electrolytes imbalance Acid-base disorder .      Thorough history taking: poor intake.BUN↑: hyperalimentation.

 CVP  Pulse  Peripheral Veins  Weight  Thirst  Intake and Output  Skin  Edema  Lab Values .

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Preserve oxygen delivery to tissues • Correct hypovolaemia • Maintain cardiac output Colloids + RBCs • Optimise gas exchange • Replace electrolytes & water • Maintain urine output Identify what is the goal Choose fluid which best achieves the goal Crystalloids .

“drier” • Holliday-Segar System  Easy to remember. does not allow for deviations from normal activity . does not allow for deviations from normal activity • Basal or Calorie Expenditure Method  Requires a table. does not require table or difficult calculations. involves calculations. permits correction for changes in activity or injury. requires table.Methods of estimating basal or maintenance fluid requirements • Basal Surface Area  Need to know height and weight.

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3% NaCl Hypotonic solutions .45% NaCl .D5W.Lactated Ringer’s.less than 10% remain intravascularly.9% NaCl .   Isotonic crystalloids . inadequate for fluid resuscitation .only 25% remain intravascularly Hypertonic saline solutions . 0. 0.

Dextran .Gelifundol .  Contain high molecular weight substancesdo not readily migrate across capillary walls Preparations .Haes-steril 10% . 25% .Albumin: 5%.

500 20.9% NaCl 0.45% NaCl 3% NaCl 77 513 500 250.100 154 130160 130160 <2.50.5 <2.Common parenteral fluid therapy Solutions ECF Lactated Ringer’s 0.45% NaCl D5W D5/0.5 77 513 154 130160 130160 50 406 1026 310 330 330 Volumes Na+ 142 130 154 77 K+ 4 4 Ca2+ 5 3 Mg2+ Cl103 109 154 77 HCO327 28 Dextrose mOsm/L 280-310 273 308 154 6% Hetastarch 5% Albumin 25% Albumin .

9%  D5W  D51/4NS  D51/3NS  LR Normal Saline 5 % Dextrose* 5% Dextrose 0.3% NS or RL Lactated Ringers Solution .2% NS 5% Dextrose 0. 0.

9% Normal Saline 5% Dextrose with Lactated Ringers .       3% N S 5%NS D 10 W D 20 W D5 ½ NS D5NS D5LR 3% Normal saline 5% Normal Saline Dextrose 10% in water Dextrose 20% in Water 5%Dextrose.45% Normal Saline 5% Dextrose with 0.with 0.

33% Normal Saline 0. 1/3  1/2 D NS NS 0.5 W .45% Normal Saline Dextrose 2.5% in water 2.

73m2 at nine months). Neonates need relatively more fluid intake than older infants and children.  The  The loops of Henle are short and the distal convoluted tubules are relatively resistant to aldosterone. leading to a limited concentrating ability . 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.

and adolescents may drink up to 2-3 litres of fluid per day. For oral feeding with standard formula milk.  Term  Children . babies need approximately 150ml/kg per day until fully weaned. preterm babies may need 200ml/kg per day initially.

. 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

45 NS  Transudates = 0. polyuria • Measured and replaced cc for cc Electrolytes: • Consult tables for electrolyte composition of on-going losses  GI losses = 0. vomiting.Fluid: abnormal losses that occur after the one-time determination of a deficit • Diarrhea.9 NS  Radiant losses = sodium free . NG aspirates.

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and is proportional to body surface area (BSA). fluid intake must be increased.     . Maintenance fluid requirements must be modified according to the child’s clinical condition. pyrexia. Insensible fluid loss is fluid lost from the body in perspiration and breathing. If the child is dehydrated or has excessive fluid losses. fluid losses = fluid intake. tachypnoea. warm temperature.slightly higher in infants and young children. It is approximately 300ml/m2/day . All types of fluid intake and output must be measured . etc. For zero fluid balance.

Hence.  . traditional estimates for maintenance fluid volumes particularly in critically ill children cannot be quantified from these general guidelines.   Warmed humidification of respiratory gases through the ventilator circuit can reduce insensible water losses by as much as one third. 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. Using indirect calorimetric measurements.

hypovolemia and hypotension. As a result. The most potent stimuli for ADH secretion are an increase In serum osmolality. such as the administration of hypotonic IV maintenance fluids. as ADH limits renal water excretion in this setting. multiple nonosmotic stimuli such as pain. . However.    Any exogenous sources of free water. will therefore further exacerbate the fall in plasma sodium (PNa). hyponatremia occurs due to a positive balance of EFW in association with an impaired ability to excrete hypotonic urine. There will be very little if any excretion of EFW. and even nausea and vomiting may also result in increased ADH activity. even in the presence of a low plasma osmolality. stress. drugs and anesthetic agents.

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. .

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5 Litres Blood volume 3.Cells 28 Litres Interstitial fluid 10.5 litres .

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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.haemostasis . water and electrolytes .

‘Inflammation’ .

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Inflammatory cytokines Neutrophils .

Systemic capillary leak .

Na+ ClAlbumin to Interstitium Vasodilatation loss of SVR .Leak of Water.

Interstitial oedema Hypovolaemia .

Na+ Clwater Interstitial oedema .

Na+ Clwater .

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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 .

and very difficult to remove Urine electrolyte measurement is essential for fluid management in the critically ill .It is very easy to give salt & water to critically ill patients.

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Electrolytes are salts. 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 bases. acids. and urine .

of electrica charges on one X ion For monovalent ions. 1 mEq = 1 mOsm  For bivalent ions.a measure of the number of electrical charges in one liter of solution mEq/L = (concentration of ion in [mg/L] the atomic weight of ion  no. Expressed in milliequivalents per liter (mEq/L) . 1 mEq = 1/2 mOsm .

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 6.5 mol  For trivalent ions. 1 Eq = 0. 1 Eq = 1 mole  For divalent ions. 1 Eq = 0.  For monovalent ions.a measure of a substance's ability to combine with other substances .The equivalent weight of a substance is equal to the amount in moles divided by the valence.022 x 1023 electrons. The equivalent (Eq or eq) is a measurement unit used in chemistry and the biological sciences .333 mol .

 The exchange of interstitial and intracellular fluid is controlled mainly by the presence of the electrolytes sodium and potassium + Na + K + Na + Na K+ Na+ K+ + K .

water typically does not enter or leave the cell 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.

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 H2O Na+ H2O Na+ Na+ K+ H2O H2O K+ K+ H2O H2O Na+ H2O K+ H2O .

ANP and ADH regulate sodium levels within the body. whilst aldosterone can be said to regulate potassium ADH + Na ANP aldosterone K+ . Aldosterone.

 Sodium (Na+) ions are the important cations in extracellular fluid Na+  Anions which accompany sodium are chloride (Cl-) and bicarbonate (HCO3-) Cl Considered HCO3 - an indicator of total solute concentration of plasma osmolality .

Sodium ions are osmotically important in determining water movements A discussion of sodium must also include • Chlorine • Bicarbonate • Hydrogen ions H2O H2O H2O H2O H2O H2O H2O H2O H2O H2O H2O H O H2O 2 H O H2O 2 Potassium and calcium serum concentrations are also important electrolytes in the living system .

elevated potassium levels Hypokalemia ---.elevated sodium levels Hyponatremia -.lowered sodium levels Hyperkalemia -.lowered calcium levels Click .elevated calcium levels Hypokalcemia -.Hypernatremia .lowered potassium levels Click Hypercalcemia .

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 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 refers to an elevated serum sodium level (145 -150 mEq/liter) levels of sodium ions are the result of diffusion and osmosis

 Hypernatremia

 Increased

Na+

1) Sodium ions do not cross cell membranes as quickly as water does
H2O H2O H2O Na+ Na+ H2O

H2O

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 Intracellular fluid volume 2) Increase in extracellular fluid volume • Resulting in dehydration Extracellular fluid volume .

 In the CNS tight junctions exist between endothelial cells of the capillary walls junctions restrict diffusion from capillaries to the interstitium of the brain • blood-brain barrier  These  Increased levels of sodium ions in the blood does not result in increased sodium ions in brain interstitial fluid .

and neurological dysfunction H 2O . blood clots. 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. As the result of an osmotic gradient.

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 H 2O draws water back into the brain and protects cells from dehydration .

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)

 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

H2O H2O Glucose H2O H2O
Glucose

H2O
Glucose Glucose Glucose 2 Glucose

HO

H2O H2O
Glucose

2 Glucose
Glucose

HO

H 2O Glucose

H2O

H2O

 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 H2O H2O Glucose H2O H2O Glucose H2O Glucose Glucose Glucose 2 Glucose HO H2O H2O Glucose 2 Glucose Glucose HO H 2O Glucose H2O H2O .

 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 H2O H2O H2O H2O Glucose Glucose H2O Glucose Glucose Glucose 2 Glucose HO H2O H2O Glucose 2 Glucose Glucose HO H 2O Glucose H2O H2O .

 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 H2O H2O H2O H2O Glucose Glucose H2O Glucose Glucose Glucose 2 Glucose HO H2O H2O Glucose 2 Glucose Glucose HO H 2O Glucose H2O H2O .

 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 H2O H2O H2O Glucose Glucose H2O H2O Glucose Glucose Glucose 2 Glucose HO Glucose H2O Glucose 2 Glucose HO H2O H2O H2O Glucose H2O .

 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 2O H2O H Glucose Glucose Glucose 2 Glucose Glucose H2O H2O H2O Glucose HO H2O H2O Glucose 2 Glucose Glucose HO H 2O Glucose H2O H2O .

 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 H2O H2O Glucose Glucose H2O Glucose H2O Glucose H2O Glucose H2O H2O Glucose Glucose 2 Glucose HO H2O H2O Glucose H 2O Glucose H2O .

 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 H2O H2O Glucose HGlucose Glucose 2O H2O H2O Glucose H2Glucose O Glucose H2O H2O Glucose H2Glucose O H 2O Glucose Glucose H2O H2O .

 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 H2O H2O Glucose HGlucose Glucose 2O H2O H2O Glucose H2Glucose O Glucose H2O H2O Glucose H2Glucose O H 2O Glucose Glucose H2O H2O 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 .

exc essi ve ur i nar y l oss g l uc ose i n g l omer ul ar f i l t r at e. osmot i c d i ur esi s ur ea i s a p r od uc t of p r ot ei n met ab ol i sm. hyp ot oni c f l ui d l oss of t en a hyp ot oni c f l ui d l oss of t en a hyp ot oni c f l ui d l oss d ef i c i enc y of ADH. osmot i c d i ur esi s nep hr og eni c d i ab et es mel l i t us unc ont r ol l ed d i ab et es mel l i t us l ar g e amount s of p r ot ei n and ami no ac i d s g i ven b y nasog ast r i c t ub e exc essi ve i nt r avenous i nf usi on of hyp er t oni c sod i um sal t sol ut i ons manni t ol used as d i ur et i c . or st r enuous exer c i se vomi t i ng d i ar r hea p i t ui t ar y d i ab et es i nsi p i d us COMMENTS d i sor d er i n w hi c h t hi r st i s i mp ai r ed i nc r eased i nsensi b l e f l ui d l oss i nad eq uat e f l ui d i nt ak e sw eat . ur ea c auses osmot i c d i ur esi s ad mi ni st r at i on of exc essi ve sod i um i ons manni t ol i n g l omer ul ar f i l t r at e. exc essi ve f l ui d l oss r enal t ub ul es i nsensi t i ve t o ADH.CAUSE essent i al hyp er nat r emi a f ever c oma hot envi r onment .

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. hypotonic fluids +/electrolytes) or ridding the body of excess sodium .Correct osmolar imbalance by replacing what was lost (water. 2 .

Dialyze if kidneys are not working. Hypovolemic: Low total body Na. Give D5W. orthostasis: restore hemodynamics with NS. then change to D5W or ½ NS  Hypervolemic: Excess total body Na. . Give loop diuretics to increase Na excretion and then replace D5W to correct hypertonicity.  Euvolemic: Normal total body Na.

 If elevated for longer than 12 hours or if the onset is unclear. it can be correctly quickly without consequence.5 mmol/L/hr. If the Na has risen over a matter of <12 hours. decrease Na by no more than 10 mmol/L/day or 0. . Goal is 145.

6 x (wt in kg) 2. Select your fluid and identify the amount of Na in mmol/L D5W 0 ¼ NS 34 ½ NS 77 LR 130 NS 154 . Calculate the total body water (TBW): 0.One approach: 1.

serum Na] divided by [TBW + 1] If you are also giving K in your IVF.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 . 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][ .

5L or so) 6-Convert to mL and divide by 24 to obtain mL/hour . In cases of prolonged hypernatremia. divide the number necessary to reach 145 by the number of hours over which you want to correct. 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.4-Decide how quickly you want to correct. 5-Account for average obligatory 24 hour water losses (1. When hypernatremia has been shorter-lived.

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 H2O Na+ H2O Na+ H2O H2O Na+ H2O Na+ H2O H2O H2O H2O H2O H2O Na+ Na+ H2O H2O Na+ H2O H2O H2O Na+ H2O H2O H2O .

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+ 3) intracellular electrical balance is maintained by diffusion of sodium ions into cells 1) extracellular potassium loss Na+ cell K+ Na+ 2) diffusion of potassium ions into extracellular compartments K+ K+ interstitial fluid plasma .

Na+ Na+ Cell K+ K+ K+ Na+ Click to see animation K+ K+ K+ Plasma Interstitial fluid .

5) Diuretic therapy • Common cause of hyponatremia • Loss of sodium and potassium often occurs in addition to fluid loss .

CAUSE psychogenic polydipsia syndrome of inappropriate secretion of ADH Addison’s disease COMMENTS excessive ingestion of water ADH causes renal water retention aldosterone deficiency K + losses from extracellular K + move out of cells to replace fluid losses. Na+ move into cells to maintain electrical neutrality .

Osmoreceptors stimulated Increased ADH release Increased Thirst Decreased urinary H2O loss Increased H2O gain Increased Na+ Homeostasis Normal Na+ Decreased Na+ Additional H2O dilutes Na+ H2O loss concentrates Na+ Osmoreceptors inhibited Decreased ADH release Decreased Thirst Increased urinary H2O loss Decreased H2O gain .

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+ 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 K+ K+ Na+ Na+ Na+ Na+ 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 H+ K+ K+ K+ K+ K+ + H+ K HYPERKALEMIA H+ H+ H+ H+ H+ H+ H+ .

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 K+ K+ K+ K+ K+ H+ K+ H+ H+ H+ H+ H+ H+ + H+ H ACIDOSIS .

Summarized: • Hyperkalemia causes acidosis • Acidosis causes hyperkalemia HYPERKALEMIA H+ H+ H+ H+ H+ K+ K+ ACIDOSIS K+ K+ K+ H+ H+ H+ K+ K+ K+ .

Summarized: • Hyperkalemia causes acidosis • Acidosis causes hyperkalemia HYPERKALEMIA H+ H+ H+ H+ H+ K+ K+ ACIDOSIS K+ K+ K+ H+ H+ H+ K+ K+ K+ .

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. ischemia E) Increased fragility of RBC . crush injuries.

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 Addison’s 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 .

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 1) .

Infusion of calcium gluconate or NaCl solutions • Immediately counteract the effects of K+ ions on the heart • Effective for only 1-2 hours .

NaHCO3 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 insulininduced 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 .

int er fer es w it h r eabsor pt ion of Na+ and sec r et ion of K + spec ial r isk of hyper k alemia if t heir is impair ed r enal sec r et ion of K + exc essive ingest ion addit ional sour c e of K + impair ed sec r et ion of K + ac idosis bur ns t r ansfusion of blood t hat has been st or ed spir onolac t one t oo r apid int r avenous infusion of K Cl use of K + c ont aining salt subst it ut es pot assium salt s of ant ibiot ic s ac ut e oligur ic r enal failur e .CAUSE hyper k alemic per iodic par alysis COMMENTS inher it ed disor der in w hic h t her e ar e sudden shift s of c ellular K + t o ext r ac ellular c ompar t ment s c ompensat or y shift of H+ int o c ells in exc hange for movement of K + t o ext r ac ellular c ompar t ment s c ell dest r uc t ion w it h r elease of K + r elease of K + fr om hemolyzed r ed blood c ells diur et ic t hat is an aldost er one ant agonist .

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 + H HCO3 K+ .

Alkalosis elicits a compensatory response causing H+ ions to shift from cells to extracellular fluids HCO3• This corrects the acid-base imbalance H+ HCO3- HCO3H+ H+ H+ HCO3HCO3- H+ H+ H+ H+ HCO3- .

H+ ions are exchanged for K+ (potassium moves into cells) • Thus serum concentrations of K+ are decreased  And alkalosis causes hypokalemia HCO3HCO3- K+ K+ H+ H+ H+ H+ K+ K+ K+ HCO3HCO3HCO3- H+ H+ H+ H+ K+ K+ K+ HCO3- .

H+ + H H+HCO 3 HCO33 - H+ K+ K+ K+ K+ HCO3- .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 Na+ K+ K+ Na+ Na+ K+ K+ Na+ Na+ Na+ H+ HCO3H+ Na+ H+ HCO HCO3HCO3.

Kidney function is altered by hypokalemia • Na+ ions are reabsorbed into the blood when K+ ions are secreted into the urine by kidney tubules Peritubular fluid NORMAL Na+ Tubular lumen K+ K+ K+ K+ Na+ K+ K+ K+ Na+ Na+ Na+ Na+ Na+ .

Kidney function is altered by hypokalemia • If adequate numbers of K+ are not available for this exchange  H+ ions are secreted instead Peritubular fluid HYPOKALEMIA Na+ Tubular lumen H+ K+ H+ K+ Na+ K+ H+ H+ Na+ Na+ Na+ Na+ Na+ .

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+ H+ K+ Na+ distal tubule capillary Blood Urine .

In Hypokalemia the kidney selectively secretes H+ ions in preference to K+ ions The loss of H+ ions may lead to alkalosis H+ K+ Na+ distal tubule capillary Blood Urine .

1) in alkalosis there is a decrease in extracellular fluid H+ 3) the kidney then eliminates K+ ions which can lead to Hypokalemia H+ retained K+ Na+ K+ excreted distal tubule capillary 2) the kidney retains hydrogen ions to correct the alkalosis Blood Urine .

CAUSE aldosterone excess diarrhea diuretics distal renal tubular acidosis hypokalemic periodic paralysis Bartter’s syndrome COMMENTS favors renal Na+ reabsorption and K secretion + diarrheal fluid contains high amounts of K in general causes K + loss kidney tubule defect in which K + are secreted. and H+ are retained by the body + cause unknown. periodic influx of K into cells 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 .

5-1 mEq/kg/dose given as an infusion of 0.5 mEq/kg/hr for 1-2 hour .Maximum IV infusion rate: 1 mEq/kg/hr Marked hypokalemia: Monitor serum K closely 0.