Beruflich Dokumente
Kultur Dokumente
Age group
Premature infant Newborn infant
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
1/3 (ECF)
80%
20%
Interstitial fluid
female
male
Plasma
2/3
fluids, serous membranes, and in GI, respiratory and urinary tracts (third space)
5
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).
K+
Mg2+ PO43Na+ ClHCO3- - - + + + +
Non-electrolytes - Uncharged
ICF (mEq/L) Sodium 20 Potassium 150 Chloride --Bicarbonate 10 Phosphate 110-115 Protein 75
o Osmolarity
= solute/(solute+solvent)
Tonicity
Isotonic
Hypertonic
Hypotonic
13
14
15
16
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.
2. Diffusion:
3. Filtration:
Is the continual intermingling of molecules in liquid, gases by random movement of the molecules.
Is the process where by fluid and solutes moved together across a membrane from one compartment to another.
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
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?
If the oncotic pressure in the interstitium increased, would this promote or inhibit the re-entry of fluid in a capillary bed?
solute
solute
Water Intake
Stimulated by thirst center of hypothalamus
Water Output
Sensible loss: urine, feces, noticible sweat
Osmoreceptors detect an increase in fluid osmolarity Thirst center inhibited by distension of stomach wall
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%)
Why are you told to drink plenty of fluids when you have a fever? A fever increases water loss (maybe both insensible and sensible)
Feedback signals that inhibit the thirst centers include: Moistening of the mucosa of the mouth and throat Activation of stomach and intestinal stretch receptors
Ion
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
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
Correct hypovolaemia
Maintain cardiac output
Colloids + RBCs
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 intravascularly, inadequate for fluid resuscitation
Contain high molecular weight substancesdo not readily migrate across capillary walls Preparations - Albumin: 5%, 25% - Dextran - Gelifundol - Haes-steril 10%
6% Hetastarch
5% Albumin 25% Albumin
3% Normal saline 5% Normal Saline Dextrose 10% in water Dextrose 20% in Water 5%Dextrose,with 0.45% Normal Saline 5% Dextrose with 0.9% Normal Saline 5% Dextrose with Lactated Ringers
1/3
1/2 D
NS
NS
2.5 W
Neonates
need relatively more fluid intake than older infants and children. 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
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.
babies need approximately 150ml/kg per day until fully weaned. and adolescents may drink up to 2-3 litres of fluid per day.
Term
Children
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.
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
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.
Cells 28
Litres
What are we trying to achieve by giving intravenous fluid ? Scenario: Acute blood loss
Replacement of RBCs, water and electrolytes - haemostasis
Inflammation
Inflammatory cytokines
Neutrophils
Na+ Clwater
Interstitial oedema
Na+ Clwater
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
The equivalent weight of a substance is equal to the amount in moles divided by the valence.
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 1023 electrons.
For
monovalent ions, 1 Eq = 1 mole For divalent ions, 1 Eq = 0.5 mol For trivalent ions, 1 Eq = 0.333 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
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
Na+
K+
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
Aldosterone,
ANP and ADH regulate sodium levels within the body, whilst aldosterone can be said to regulate potassium
ADH
+ Na
ANP
aldosterone
K+
Sodium
Na+
Anions
Cl Considered
HCO3
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
Potassium and calcium serum concentrations are also important electrolytes in the living system
Click
Click
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+
H2O
2) Cells pump sodium ions out of the cell by using sodium-potassium pumps
Na+
Na+
Na+
1) Water is osmotically drawn out of the cells Intracellular fluid volume 2) Increase in extracellular fluid volume
Resulting in dehydration
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
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 2O
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
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
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
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
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
Glucose 2 Glucose
HO
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
CAUSE essent i al hyp er nat r emi a f ever c oma hot envi r onment , 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 , 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; exc essi ve f l ui d l oss r enal t ub ul es i nsensi t i ve t o ADH; 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; 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; 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
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
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][
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
Na+
H2O
H2O H2O Na+
H2O
H2O
H2O
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
Na+
cell
K+
Na+
Na+ Na+
Cell
K+ K+ K+ Na+
K+ K+ K+ Plasma
Interstitial fluid
5) Diuretic therapy
Common cause of hyponatremia Loss of sodium and potassium often occurs in
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 Na+
Osmoreceptors inhibited
10 10 60
+ K
K+
Cells
pump K+ ions in and Na+ ions out of the cell by using sodium-potassium pumps
K+
Hyperkalemia is an elevated serum potassium (K+) ion level A consequence of hyperkalemia is acidosis
an increase in H+ ions in body fluids
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 -)
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 -)
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:
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
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+
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+
Kidney
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
NaHCO3
also reverses hyperkalemic effects on the heart If acidosis is a factor also raises the pH of body fluids
Insulin promotes the shift of K+ ions into cells Glucose prevents insulininduced hypoglycemia
Peritoneal
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 ; 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
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
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-
HCO3HCO3-
K+ K+ H+ H+ H+ H+ K+
K+ K+
HCO3HCO3HCO3-
H+
H+
H+ H+ 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
HCO3HCO3- H+ + H H+HCO 3
HCO33 -
H+
K+
K+ K+ K+
HCO3-
Peritubular fluid
NORMAL
Na+
Tubular lumen
K+
K+ K+ K+
Na+
K+ K+
K+
Na+
Na+ Na+
Na+
Na+
HYPOKALEMIA
Na+
Tubular lumen
H+
K+ H+ K+
Na+
K+ H+
H+
Na+
Na+ Na+
Na+
Na+
Hypokalemia
capillary
Blood Urine
capillary
Blood Urine
K+
Na+
K+
excreted
distal tubule
capillary
Blood Urine
CAUSE
aldosterone excess diarrhea diuretics distal renal tubular acidosis hypokalemic periodic paralysis Bartters 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
+
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