2012-Fluid and Electrolytes

8/12/2019 2012-Fluid and Electrolytes

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HARLEY L. DELA CRUZ RN MANInstructor



• Phospholipid bilayer

• Freely permeable to non-polarmolecules (CO 2, O 2, steroids)

• Impermeable to large polar andcharged molecules (ions,

proteins, glucose)

• Generally permeable to water (though somecells require aquaporins)



Approx watercontent 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

2/3Intra-

cellularfluid(ICF)

1/3(ECF)

80%

20%

Interstitialfluid

Plasma

• Some fluid is lost from blood in theinterstitial tissues, and returned by the

lymphatic system

(also lymph and othermiscellaneous 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, respiratoryand urinary tracts (third space)



Function of ICF & ECF: ICF: is vital to normal cell function, its containsolutes such as oxygen, electrolytes andglucose. It provides a medium to metabolicprocess.

ECF: it is the transport system that carriesnutrients 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 fluidthan older children and adults.

Because extracellular fluid is more easily lost fromthe body than intracellular fluid, infants are more atrisk of developing dehydration than older children and

adults (infants also have a larger surface area to body

mass ratio).



Na+

Cl-

HCO3-

K+

Mg2+

PO43-

+ + + + - - - -



9

Electrolytes – charged particlesCations – positively charged ionsNa +, K+ , Ca ++ , H +

Anions – negatively charged ionsCl-, HCO 3

- , PO 43-

Non-electrolytes - Uncharged

Proteins, urea, glucose, O 2, CO 2



ICF (mEq/L) ECF (mEq/L) Sodium 20 135-145Potassium 150 3-5

Chloride --- 98-110Bicarbonate 10 20-25Phosphate 110-115 5Protein 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 ofatoms in a molecule

mEq (milliequivalents) = MW (in mg)/ valence

mOsm (milliosmoles) = number of particles in asolution



13

Tonicity

Isotonic

Hypertonic

Hypotonic



14



15

Cell in ahypotonic

solution



16

Cell in ahypertonicsolution



DiffusionOsmosisFiltration

Active transport



1. Osmosis : Is the movement of water across cellmembranes, from the less concentratedsolution to more concentrated solution. In otherword 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 serumosmolality.



2. Diffusio n: Is the continual intermingling of molecules inliquid, gases by random movement of themolecules.

3. Filtr atio n :• Is the process where by fluid and solutes moved

together across a membrane from one compartment toanother.

4. A ct ive t ransp or t :• substance can move across cell membranes

from a less concentrated solution to amoreconcentrated one by active transport.



Sodium and potassium concentrations in extra- andintracellular fluids are nearly opposite

This reflects the activity of ATP-dependent sodium-potassium pumps (Na +-K + ATPase)



Continuous exchange and mixing of fluid amongcompartments - regulated by osmotic and hydrostaticpressures

Net leakage of fluid from the blood is picked up by lymphaticvessels and returned to the bloodstream

Exchanges between interstitial and intracellular fluids aremore complex due to the selective permeability of the cellmembranes



An increase in ECF solute concentration [NaCl] would cause osmotic andvolume changes in the ICF. Which way would water move, into or out of cells?

ICF is determined by the ECF solute concentration

solutesolute

solutesolute

solutesolute

solute

solute

solutesolute

More Solute = Less WaterLess Solute = More Water

Hypertonic Solution orHypotonic Solution?

solute

solute

solute

H2OH2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O H2O

H2O

H2O

H2O

H2O

H2O

Which way will Water move?



solutesolute

solutesolute

solutesolute

solute

solute

solutesolute

H2OH2O

H2O

H2O

H2O

If the oncotic pressure in the interstitium increased, would this promote orinhibit the re-entry of fluid in a capillary bed?

H2O



• Daily water intake must equal water output

Water Intake Water Output

• Stimulated by thirstcenter ofhypothalamus

• Osmoreceptorsdetect an increasein fluid osmolarity

• Thirst center inhibited bydistension of stomach wall

• Sensible loss: urine,feces, noticible sweat

• Insensible loss:respiration and non-noticible sweat

• Urine output is the primary regulator ofwater out (ADH from posterior pituitarygland)



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 1 – 2%•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 transportWater movementKidney function



Water loss (output) exceeds water intake and thebody is in negative fluid balance

A common sequala to hemorrhage, severe burns,prolonged vomiting or diarrhea, profuse sweating,water deprivation, and diuretic abuseSigns and symptoms: dry mouth, thirst, dry flushedskin, and oliguriaProlonged dehydration may lead to weight loss,fever, and mental confusion

Other consequences include hypovolemic shock andloss of electrolytes



Accumulation of fluid in the interstitial space, leading to

tissue swelling, caused by anything that increases fluidflow out of the bloodstream or hinders its return

Factors that accelerate fluid loss include:Hypertension, increased capillary permeability, incompetent venousvalves, localized blood vessel blockage, congestive heart failure



Decreased fluid return usually reflects an imbalance in colloidosmotic pressures across capillary membranes

Hypoproteinemia – low levels of plasma proteins, may result from proteinmalnutrition, 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 resultin the accumulation of plasma proteins in interstitial fluid

Interstitial colloid osmotic pressure increases,fluid leaves blood and moves into tissueInterstitial fluid accumulation could result in adecrease in blood volume, blood pressure, andimpaired circulation



Kwashiorkor - a form of malnutrition caused by inadequate proteinintake and consequent reduced albumin in the blood

hypoalbuminemia and reduced plasma oncotic pressure promote theextravasation 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 Hypoperfusion cyanosis Altered mental status



Thorough history taking: poor intake, GIbleeding…etc

BUN : Creatinine > 20 : 1- BUN↑: hyperalimentation, glucocorticoid

therapy, UGI bleeding Increased specific gravity Increased hematocrit Electrolytes imbalance Acid-base disorder



CVPPulsePeripheral VeinsWeightThirstIntake and OutputSkinEdemaLab 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 maintenancefluid requirements• Basal Surface Area

Need to know height and weight, requires table, does not allowfor deviations from normal activity

• Basal or Calorie Expenditure MethodRequires a table, involves calculations, permits correction forchanges in activity or injury, “drier”

• Holliday-Segar SystemEasy to remember, does not require table or difficultcalculations, does not allow for deviations from normal activity



Isotonic crystalloids- Lactated Ringer’s, 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 fluidresuscitation



Contain high molecular weightsubstances do not readily migrate acrosscapillary walls

Preparations- Albumin: 5%, 25%

- Dextran- Gelifundol- Haes-steril 10%

Common parenteral fluid therapy



Solutions Volumes Na + K+ Ca 2+ Mg 2+ Cl - HCO 3- Dextrose mOsm/L

ECF 142 4 5 103 27 280-310

LactatedRinger’s 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



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 saline5 % N S 5% Normal Saline D 10 W Dextrose 10% in waterD 20 W Dextrose 20% in WaterD5 ½ 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 olderinfants and children.

The kidneys in neonates have small immatureglomeruli and for this reason the glomerular filtrationrate is reduced (about 30ml/min/1.73m2 at birth to100ml/min/1.73m2 at nine months).

The loops of Henle are short and the distalconvoluted tubules are relatively resistant toaldosterone, leading to a limited concentrating ability



For oral feeding with standard formula milk,preterm babies may need 200ml/kg per dayinitially.

Term babies need approximately 150ml/kg perday until fully weaned.

Children and adolescents may drink up to 2-3litres of fluid per day.



Hourly maintenance fluid requirements can becalculated using the following guide:

4ml/kg/hr or 100ml/kg/day for first 10kg body Weight2ml/kg/hr or 50ml/kg/day for second 10kg body Weight1ml/kg/hr or 20ml/kg/day for each additional kg bodyweight

The recommended volume of oral feeds is greater thanthat calculated using this guide so that adequatecalorie and protein intake can be achieved.

ElECTROLYTE REQUIREMENTS



ElECTROLYTE REQUIREMENTS

Na + 3 mEq/100ml

Cl- 4 mEq/100mlK+ 2 mEq/100ml

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Definition: Amount of fluid lost before treatment isbegunOne-time estimate; additional losses after therapy isbegun 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 aregastrointestinal or due to a relatively short period ofdecreased oral intake• approximated by 0.45 NS

Potassium: deficit replacement is based on rate ofsafe replacement and not amount since danger ofhyperkalemia is greater than hypokalemia• Add 20 mEq potassium/L after UOP is established

• Potassium infusion rate should not exceed 1 mEq/kg/hourunless in monitored setting



Fluid: abnormal losses that occur after theone-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

lossesGI losses = 0.45 NSTransudates = 0.9 NSRadiant losses = sodium free



Maintenance fluid requirements must be modified according to thechild ’s 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 andbreathing, and is proportional to body surface area (BSA).

It is approximately 300ml/m2/day ,slightly higher in infants andyoung children, warm temperature, pyrexia, tachypnoea, etc.

Using indirect calorimetric measurements, energyexpenditure in critically ill children may be as low as



50-60 kcal/kg/day.

Mechanical ventilation decreases the work of breathingas well as evaporative water loss through therespiratory tract and the energy expenditure forthermal regulation.

Warmed humidification of respiratory gases throughthe ventilator circuit can reduce insensible water lossesby as much as one third.

Hence, traditional estimates for maintenance fluid

volumes particularly in critically ill children cannot bequantified from these general guidelines.

The most potent stimuli for ADH secretion are an increase In serumosmolality, 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 renalwater excretion in this setting, even in the presence of a low plasmaosmolality.

As a result, hyponatremia occurs due to a positive balance of EFW inassociation 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 thefall in plasma sodium (PNa).

Recently conducted systematic review ofmaintenance fluids for hospitalized children



maintenance fluids for hospitalized childrenrevealed that the use of hypotonic fluidsremarkably increased the odds of developinghyponatremia by 17 times when comparedto isotonic fluids.





Interstitial fluid 10.5 Litres

Blood volume 3.5 litres

Cells 28 Litres




Interstitial fluid

mobilisation



Reducedinterstitial fluid



Intracellular fluidmobilisation



Reduced intracellular fluid



What are we trying to achieve by givingintravenous fluid ?

Scenario: Acute blood loss

Replacement of RBCs, water andelectrolytes - haemostasis




‘ Inflammation’







Inflammatory

cytokines

Neutrophils



Systemic

capillary leak



Leak of Water, Na + Cl - Albumin to Interstitium

Vasodilatation loss of SVR



Hypovolaemia

Interstitialoedema



Interstitialoedema

Na + Cl -

water



Na + Cl -

water



Na + and Cl - Loading

Fluid retention

Severe interstitial oedema

Organ dysfunction



What are we trying to achieve by givingintravenous fluid ?

Scenario: Acute inflammation

Blood volume expansion, in the context ofvascular dysfunction and leaky capillaries



It is very easy to give salt & w ater to cr i t ic al ly i l lpa t ients , and very d i ff icul t to remo ve

Urine elec t ro ly te m easur ement i s essent ial for f lu id

m anagem ent in the cr i t ical ly i l l





Electrolytes are salts, acids, and bases, but

electrolyte balance usually refers only to saltbalanceSalts are important for:• Neuromuscular excitability• Secretory activity• Membrane permeability• Controlling fluid movementsSalts enter the body by ingestion and are lost viaperspiration, feces, and urine

Expressed in milliequivalents per liter (mEq/L)



Expressed in milliequivalents per liter (mEq/L)- a measure of the number of electrical charges inone liter of solution

For monovalent ions, 1 mEq = 1 mOsm

For bivalent ions, 1 mEq = 1/2 mOsm

no. of electrcharges on oion

mEq/L = (concentration of ion in [mg/L]

the atomic weight of ionX

The equivalent weight of a substance is equal to the amountin moles divided by the valence.



For monovalent ions, 1 Eq = 1 moleFor 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 withother substances - frequently used in the context of normality (GEW/litersof solution)

The equivalent is defined as the mass (g) in grams of a substance which

will react with 6.022 x 1023

electrons.

The exchange of interstitial and intracellular fluid is



gcontrolled mainly by the presence of the electrolytessodium 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 interstitialspace and the ICF are generally equal, watertypically 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 leavethe cell whilst a drop in sodium will cause fluidto enter the cell

K+

H2OH2O

H2O H2O

H2OH2O

H2O H2OK+

K+

K+

Na +

Na +

Na +

Na +

Aldosterone, ANP and ADH regulate sodium



levels within the body, whilst aldosterone canbe said to regulate potassium

K+

Na+

aldosterone

ADH

ANP



Sodium (Na +) ions are the important cations inextracellular 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 -

Sodium ions are osmoticallyimportant in determining water



H2OH2O

H2OH2OH2O

H2O

p gmovements

A discussion of sodium must alsoinclude• Chlorine

• Bicarbonate• Hydrogen ions

Potassium and calcium serum

concentrations are also importantelectrolytes in the living system

H2O

H2O

H2O

H2O

H

H2OH2O

H2OH2O

Hypernatremia - elevated sodium levels



ClickHypercalcemia - elevated calcium levels

Hypokalcemia -- lowered calcium levels

ClickHyperkalemia -- elevated potassium levels

Hypokalemia ---- lowered potassium levels

Hyponatremia -- lowered sodium levels




Participates in the Na-K pumpAssists in maintaining blood volume




Assists in maintaining blood volume

Assists in nerve transmission & muscle contractionPrimary determinant of ECF concentrationControls water distribution throughout the bodyPrimary regulator of ECF volumeRegulations: skin, GIT,Aldosterone increases Na retentionin the kidney

Normal range for blood levels of sodium is app. 137



- 143 meq/liter

Hypernatremia refers to an elevated serum sodiumlevel (145 -150 mEq/liter)

Increased levels of sodium ions are the result ofdiffusion and osmosis

Na +

1) Sodium ions do not cross cell membranes as



quickly as water does

Na +

H2O

H2O H2O

H2O

H2O

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 +

) ll d f h ll



1) Water is osmotically drawn out of the cells

• Resulting in dehydration

2) Increase in extracellular fluid volume

Extracellular

fluidvolume

Intracellularfluid

volume

In the CNS tight junctions exist between



endothelial cells of the capillary walls

These junctions restrict diffusion fromcapillaries to the interstitium of the brain• blood-brain barrier

Increased levels of sodium ions in theblood does not result in increased sodium

ions in brain interstitial fluid



As the result of an osmotic gradient, watershifts from the interstitium and cells of thebrain 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

H2O



There is an unknown mechanism thatprotects the brain from shrinkage

Within about 1 day

• Intracellular osmolality of brain cells increases inresponse to extracellular hyperosmolality

• Idiogenic osmoles accumulate inside brain cells



Idiogenic osmoles accumulate inside brain cells

K+

, Mg+

from cellular binding sites and amino acids fromprotein catabolism

• These idiogenic osmoles create an osmotic force thatdraws water back into the brain and protects cells

from dehydration

H2O

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 orincreased insensible water loss canbe very susceptible to hypernatremia

Diabetes insipidus caused by inadequate ADH orrenal 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 tothe kidney for elimination)

diabetes mellitus results in loss of fluids as well bycreating an osmotic pull (increased urine solute



Glucose

Glucose

Glucose

creating an osmotic pull (increased urine solute

concentration) on water into the tubules of thekidney

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O

diabetes mellitus results in loss of fluids aswell by creating an osmotic pull (increased



Glucose

Glucose

Glucose

well by creating an osmotic pull (increasedurine solute concentration) on water into thetubules of the kidney

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O




Glucose

Glucose

Glucose


Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O




Glucose

Glucose

Glucose


Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O

diabetes mellitus results in loss of fluids as



Glucose

Glucose

Glucose

well by creating an osmotic pull(increased urine solute concentration) onwater into the tubules of the kidney

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2O

H2OH2O

H2O H2O

H2O

H2O

H2OH2O

diabetes mellitus results in loss of fluids aswell by creating an osmotic pull



Glucose

Glucose

Glucose

well by creating an osmotic pull

(increased urine solute concentration) onwater into the tubules of the kidney

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2O H2O

H2O

H2O

H2OH2O




Glucose

Glucose

Glucose


Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O




Glucose

Glucose

Glucose

well by creating an osmotic pull (increasedurine solute concentration) on water intothe tubules of the kidney

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O




Glucose

Glucose

Glucose

well by creating an osmotic pull (increasedurine solute concentration) on water intothe tubules of the kidney

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O

Re-animate

High protein feedings by a stomach tube create high



levels of urea in the glomerular filtrate producing anosmotic gradient the same as glucose does andincreased 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 waterretention by the kidney• High levels of aldosterone may result in mild

hypernatremia

CAUSE COMMENTS

essent ial hyper nat r emia disor der in w hic h t hir st i s impai r ed

fever inc r eased insensib le f luid loss

c oma inadequat e f luid int ak e

hot environment, or str enuous sweat , hypotonic fluid loss



hot environment, or s tr enuousexerc ise

sweat , hypotonic f luid loss

vomi t ing of t en a hypot onic f luid l oss

d iar r hea of t en a hypot onic f luid l oss

p i t ui t ar y d iabet es insip idus def ic ienc y of ADH; exc essive f luidloss

nephr ogenic d iabet es mel l i t us r enal tubules insensi t ive to ADH;

excessive uri nary lossunc ont r ol led d iabet es mel l i t us g luc ose in g lomer ular fi l t r at e;

osmot ic d iures i s

larg e amounts of pr otein and aminoacids given by nasogastr ic t ube

urea i s a product of pro te inmetabolism; urea c auses osmoticd iures i s

excessive intr avenous infusion of

hypertonic sodium sal t solut ions

administr at ion of excessive sodium

ions

manni t ol used as d iur et ic manni t ol in g lomer ular f i l t r at e;osmot ic d iures i s



Re-hydration is the primary objective in most cases

• Decreases sodium concentrations

A point of concern is whenand how rapid there-hydration occurs

After 24 hours the brain has responded by



producing idiogenic osmoles to re-hydrate braincells

If this adaptation has occurred and treatmentinvolves a rapid infusion of dextrose forexample:• There is danger of cerebral

edema with fluid beingdrawn into brain tissues

Treatment is best handled by giving slow



infusions of glucose solutions

• This dilutes high plasmasodium ion concentrations

Ideally the goal is to avoid overloading with fluidand to remove excess sodiumDiuretics can be used to induce sodium and water



Diuretics can be used to induce sodium and waterdiuresis• 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 replacingwhat was lost (water, hypotonic fluids +/-electrolytes) or ridding the body of excesssodium

Hypovolemic:



Low total body Na, orthostasis: restore hemodynamicswith NS, then change to D5W or ½ NSHypervolemic:

Excess total body Na. Give loop diuretics to increase Naexcretion 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 withoutconsequence.If elevated for longer than 12 hours or if theonset is unclear, decrease Na by no more than10 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 inkg)

2. Select your fluid and identify the amount of Na inmmol/L

D5W 0¼ NS 34½ NS 77LR 130NS 154



4-Decide how quickly you want to correct.

In cases of prolonged hypernatremia, divide 10 (thedesired 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 thenumber necessary to reach 145 by the number of hoursover 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 ionlevel that is lower than normal



level that is lower than normal

Implies an increased ratio ofwater to sodium in extracellularfluid

• Extracellular fluid is more dilutethan intracellular fluid

• Results in a shift of water into cells

Brain cells lose osmoles creating a higherextracellular solute concentrationEffect is to protect against cerebral edema by



Effect is to protect against cerebral edema bydrawing water out of the brain tissue



Suppression of thirst

Suppression of ADH secretion

• Both favor decreasing wateringestion and increasingurinary output

Primarily neurological (net flux of water intothe brain)



)Sodium ion levels of 125 meq / liter areenough to begin the onset of symptomsSodium 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:IngestionRenal retention

1) Isotonic fluid loss2) Antidiuretic hormone secretion



)3) Acute or chronic renal failure4) Potassium ion loss5) Diuretic therapy

H2O

H2O

H2OH2O

H2O

H2O

Na +

Na +

Na+

H2O

H2OH2O

H2O

H2O

H2O

H2O

H2ONa +

Na +

Na +

Na +

Na +

H2O

H2O

H2O

H2O

H2O

1) Isotonic fluid loss• Burns, fever, hemorrhage



• Indirect cause of hyponatremia• Any volume loss stimulates thirst and leads to

increased water ingestionThus isotonic fluid loss can cause hyponatremia not

because of sodium loss but because of increased waterintake

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 potassiumions

• Thus a loss of extracellular sodium is realized andhyponatremia may ensue

Na +

K+

1) extracellularpotassium loss3) intracellular electrical balance

is maintained by diffusion ofsodium ions into cells



K+

Na +

K+

K+

2) diffusion of potassium

ions into extracellularcompartments

plasmainterstitial fluid

cell



5) Diuretic therapy



• Common cause of hyponatremia

• Loss of sodium and potassium often occurs inaddition to fluid loss

CAUSE COMMENTSpsychogenic polydipsia excessive ingestion of water



syndrome of inappropriatesecre tion of ADH

ADH causes renal wate rretention

Addiso n’ s d ise ase aldosterone deficiency

K+ losses from extracellularfluid

K+ move out of cells to replacelosses; Na + move into cel ls tomaintain electrical neutrality



10



10

60



K+

Normal serum potassium level (3-5 meq /liter)• As compared to Na + (142 meq / liter)






• As compared to Na + (142 meq / liter)Intracellular levels of potassium (140-150meq / 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 thecell by using sodium-potassium pumps

K+



Na +

Na +

Na +

Na+

K+

K+

K+

K+

Hyperkalemia is an elevated serum potassium

(K+) ion level



(K ) ion level A consequence of hyperkalemia is acidosis• an increase in H+ ions in body fluidsChanges in either K + or H + ion levels causes a

compartmental shift of the other

K+

When hyperkalemia develops potassium ionsdiffuse into the cell• This causes a movement of H+ ions out of the cell to



• This causes a movement of H ions out of the cell tomaintain a neutral electrical balance

As a result the physiological response tohyperkalemia causes acidosis

K+

K+

K+

K+

K+

K+H+

H+

H+

H+

H+H+

H+H+

H+

HYPERKALEMIA

The reverse occurs as wellThe body is protected from harmful effects ofan increase in extracellular H + ions (acidosis)

H+ i i id th ll ti d b t i



• H+ ions inside the cells are tied up by proteins(Pr -)

This causes a shift of potassium ions out ofthe cells

The reverse occurs as wellThe body is protected from harmful effects ofan increase in extracellular H + ions (acidosis)• H+ ions inside the cells are tied up by proteins ( Pr -)



H ions inside the cells are tied up by proteins ( Pr )This causes a shift of potassium ions out ofthe cells

H+

H+

H+

H+

H+

H+H+

H+

H+

K+

K+K+

K+K+

K+

ACIDOSIS

Summarized:• Hyperkalemia causes acidosis• Acidosis causes hyperkalemia



• 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

A id i h k l i



• 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 bychanges in potassium levels



changes in potassium levels

Hyperkalemia blocks thetransmission of nerve impulses alongmuscle fibers• Causes muscle weakness and paralysisCan cause arrhythmia's and heartconduction 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 transfusionswith 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 hyperkalemiaC ll l t k f K + i i h d



individual to hyperkalemiaCellular uptake of K + ions is enhancedby insulin, aldosterone and epinephrine • Provides protection from extracellular K+

overloadInsulin

K+

K+

K+

K+K+

K+

Click to viewanimation

Insulin deficiency represents decreased

protection if the body is challenged byf +



protection if the body is challenged byan excess of K + ionsIn the absence of aldosterone there isloss of Na + in the urine and renalretention of K +

Inherited disorder in which serum K + levelrise periodically• Caused by a shift of K+ from muscle to blood



• Caused by a shift of K from muscle to bloodin response to ingestion of potassium orexercise

• Reasons for the shift arenot clear Attacks are characterizedby muscle weakness

Aldosterone has a primary role in promoting:• Conservation of Na +

• Secretion of K+

by the nephrons of the kidneyAddi ’ di i h t i d b



y p y Addison’s disease is characterized byaldosterone deficiency• Thus the kidney is unable

to secrete potassium at anormal rate

Kidney loses the ability to secrete K +



Diuretic that is antagonistic to the effects

of aldosteroneC i i K+ l l b



o a doste o e• Causes some rise in serum K+ levels byinterfering with K+ secretion in the kidneys

Increases may not be significant• But individuals taking the

diuretic are at risk ifpotassium is administered

1) Counteract effects of K + ions at thelevel of the cell membrane

2) Promotion of K+

ion movements intocells



2) Promotion of K ion movements intocells3) Removal of K + ions from the body

Infusion of calcium gluconate or NaClsolutions• Immediately counteract the effects of K+



yions on the heart

• Effective for only 1-2 hours

NaHCO 3 also reverses hyperkalemiceffects on the heart

If acidosis is a factor also raises the pHf b d fl id



pof body fluids

Insulin given with glucose• Effective in about 30 minutes• Has a duration of action of up to



p6 hours

Insulin promotes the shift of K+

ions into cellsGlucose 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



Exchange time is about 45 minutesEffective for up to6 hours

Peritoneal dialysis or hemodialysisEffectively clears the blood of high K + levels as well



CAUSE COMMENTS

hyper k al emic p er iodic p ar alysi s i nher it ed disor der i n w hi ch t her e ar e suddenshifts of cellular K+ to extr acellular compartments

ac idosis c ompensator y shif t of H+ into c ells in exc hangefor movement of K+ to extr acellular compartments

bur ns c ell dest r uc t ion w ith r elease of K+



tr ansfusion of blood that has beenstored

release of K+ from hemolyzed r ed blood c ells

spir onolac tone diur et ic t hat is an aldost er one ant agonist ;interf eres wit h reabsorpt ion of Na+ andsecret ion of K+

too rap id in t ravenous in fus ion of KCl spec ia l r i sk of hyperka lemia i f the i r i simpaired renal secret ion of K+

use of K+ cont a in ing sa lt subst i t ut e s excess iv e i nges t ion

pot assium salt s of ant ibiot ic s addi t ional sour c e of K+

ac ut e oligur ic r enal failur e impair ed sec r et ion of K+

Defined as a serum K + level that is belownormal (< 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 byhypokalemia Alkalosis is defined as a decrease of



hydrogen ions or an increase ofbicarbonate in extracellular fluids

• Opposite of acidosis

K+

H+

HCO 3-

Alkalosis elicits a compensatory responsecausing H + ions to shift from cells toextracellular fluids• This corrects the acid-base

i b l

HCO 3



imbalance

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

HCO 3



hypokalemia

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 thecellular and extracellular compartments• Sodium and hydrogen ions enter cells

in a ratio of 2:1 as replacementThis loss of extracellular H +

HCO 3-

HCO

H+



causes alkalosisHCO 3

-

H+

K+ HCO 3-

HCO 3-

HCO 3-

HCO 3-

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 exchangeH+ 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 + ionsand thus results in alkalosis



Normal nephron functionis to secrete H + and K + inexchange for Na +

H+

K+



capillary

distal tubule

Na +

Blood

Urine

H+

K+

In Hypokalemia the kidneyselectively secretesH+ ions in preferenceto K + ions

The loss of H + ionsmay lead to alkalosis



capillary

distal tubule

Na +

Blood

Urine

H+

K+

retained

1) in alkalosis there is adecrease in extracellularfluid H +

3) the kidney theneliminates K + ionswhich can lead toHypokalemia



capillary

distal tubule

Na + K+excreted

2) the kidney retains

hydrogen ions tocorrect the alkalosis

Blood

Urine

CAUSE COMMENTS

aldosterone excess favors renal Na+ reabsorption and K+

secretiondiarrhea diarrheal fluid contains high amounts of K+



gdiuretics in general causes K+ lossdistal renal tubularacidosis

kidney tubule defect in which K+ are secreted, and H+ aretained by the body

hypokalemic periodicparalysis

cause unknown; periodic influx of K+ into cells

Bartter’s syndrome syndrome in which aldosterone is sometimesprobably 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

2012-Fluid and Electrolytes

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Transcript of 2012-Fluid and Electrolytes