Fluid and Electrolytes Disturbances

60% of body consists of fluid

Intracellular space [2/3]
Extracellular space [1/3]
Electrolytes are active ions: positively and negatively charged
Extracellular Fluid (ECF): 20% of total body weight
Intravascular: Blood plasma
Interstitial fluid
o Between cells
o Cerebrospinal fluid
o Intraocular fluid

Aging and Distribution of Body Fluids

Water is the main component of body mass
Adults: 50% to 60% of total body weight
Newborn: About 80% of total body weight
Childhood: 60% to 65% of total body weight
Further declines with age
Ci fiziologice de eliminare a apei din
organism
Total
25-35 ml/kg/24 2000 ml/24 ore
ore
Rinichi

15-20
ore

ml/kg/24

1000 ml/24 ore

Cutana
t

8 ml/kg/24 ore

500 ml/24 ore

Plmn

7 ml/ kg/24 ore

400 ml/24 ore

Scaun

1-2 ml/kg/24 ore

100 ml/24 ore

Necesar minim lichidian recomandat

greutate (kg)

ml/kg/ora

ml/kg/zi

1-10

120-150

11-20

50-100

> 20

25-40

> 40

25-40

Distributia lichidelor perfuzate

cresterea de volum (V) estimata = V infuzat x V plasmatic normal/ V de distributie
Vi = V estimata x Vd/Vp
Exemplu:
necesar de sol glucoza 5% sau ser fiziologic pentru a creste volemia cu 2 L
G 5% => 2 L x 42 L / 3 L = 28 L
NaCl 0,9% => 2 L x 14 L / 3 L = 9,3 L
Compoziia soluiilor volemice n comparaie cu plasma (mmol/l)
+
+
+
+
Na
Cl
K
Mg
Ca
+
+

Tampon

pH

Plasma (albumina)

140

102

3.7

0.8.

1.2

HCO3 24

7,4

NaCl 0,9 %

154

154

5,7

Sterofundin iso

145

127

4.5

2.5

Acetat 24

5.1-5.9

Ringer lactat

131

109

Lactat 28

6,4

Solutie gelatina
Gelofusin

154

120

7,1-7,7

Solutie gelatina Gelaspan

151

103

Acetat 24

Soluii de amidon Voluven

154

154

Volulyte

137

110

4-7
4

1.5

Acetat 34

4-7

Membrane Permeability
Most cell membranes are relatively highly permeable to water. Membranes are semipermeable to certain anions and cations. Difference in permeability between water and dissolved
solutes
Compoziia ionic a spaiilor hidrice
Plasma
Cationi

Lichid interstiial

Lichid intracelular

Sodiu (mmol/l)

140

145

10

Potasiu (mmol/l)

3,7

3,8

155

Calciu ionizat (mmol/l)

1,2

1,2

<0,01

Magneziu (mmol/l)

0,8

0,8

10

Fosfat (mmol/l)

1,1

1,0

105

Clor (mmol/l)

102

115

Bicarbonat (mmol/l)

28

30

10

Anioni

Diffusion
Due to constant motion of atoms, molecules, ions in solution
Passive process
Moves particles from area of higher concentration to area of lower concentration
Concentration gradient
Water Movement Between ICF and ECF
Osmosis
Flow of fluid across a semi-permeable membrane from a lower solute concentration to a higher
solute concentration
Osmotic pressure determined by:
Number and molecular weights
Permeability of membrane
Electrolyte Balance
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
A change in the concentration of either electrolyte will cause water to move into or out of the cell
via osmosis. A drop in sodium will cause fluid to enter the cell
Plasma osmolality= (2 x Na + G/18 + U/2,8) = 290 mOsm/kg H2O
Tonicity = (2 x Na + G/18 ) = 285 mOsm/kg H2O
Solutions
Hypertonic solution
Hypotonic solution
Isotonic solution
Hyponatremia
Definition:

serum sodium concentration <135 mmol/L

represents a relative excess of water in relation to sodium.

We define mild hyponatraemia as a biochemical finding of a serum sodium concentration

between 130 and 135 mmol/L as measured by ion specific electrode.
We define moderate hyponatraemia as a biochemical finding of a serum sodium concentration
between 125 and 129 mmol/L as measured by ion specific electrode.
We define profound hyponatraemia as a biochemical finding of a serum sodium
concentration<125 mmol/L as measured by ion specific electrode.
We define acute hyponatraemia as hyponatraemia that is documented to exist < 48 h.
We define chronic hyponatraemia as hyponatraemia that is documented to exist for at least 48h.
If the hyponatraemia cannot be classified, we consider it being chronic, unless there is clinical or
anamnestic evidence of the contrary
We define moderately symptomatic hyponatraemia as any biochemical degree of
hyponatraemia in the presence of moderately severe symptoms of hyponatraemia
We define severely symptomatic hyponatraemia as any biochemical degree of hyponatraemia
in the presence of severe symptoms of hyponatraemia
Symptoms
Moderately severe
Nausea without vomiting
Confusion
Headache

Severe
Vomiting
Cardio-respiratory distress
Abnormal and deep somnolence
Seizures
Coma (Glasgow Coma Scale < 8)

Epidemiology:
Hyponatremia is the most common electrolyte disorder
incidence of approximately 1%
surgical ward, approximately 4.4%
30% of patients treated in the intensive care unit
Drugs and conditions associated with acute hyponatraemia
Postoperative phase
Post-resection of the prostate, post-resection of endoscopic uterine surgery
Polydipsia
Exercise
Recent thiazides prescription
3,4-Methyleendioxymethamfetamine (MDMA, XTC)
Colonoscopy preparation
Cyclophosphamide (intravenous)
Oxytocin
Recently started desmopressin therapy

Recently started terlipressin, vasopressin

Types

Hypovolemic hyponatremia
Euvolemic hyponatremia
Hypervolemic hyponatremia
Redistributive hyponatremia
Pseudohyponatremia

Redistributive hyponatremia
Water shifts from the intracellular to the extracellular compartment, with a resultant dilution of
sodium
The TBW and total body sodium are unchanged
this condition occurs with hyperglycemia
administration of mannitol
We recommend excluding hyperglycaemic hyponatraemia by measuring the serum glucose
concentration and correcting the measured serum sodium concentration for the serum glucose
concentration if the latter is increased. (1D)
Hyponatraemia with a measured osmolality <275 mOsm/kg always reflects hypotonic
hyponatraemia. (not graded)
Pseudohyponatremia
The aqueous phase is diluted by excessive solutes (proteins or lipids)
The TBW and total body sodium are unchanged.
hypertriglyceridemia
multiple myeloma
Hypovolemic hyponatremia
develops as sodium and free water are lost and/or replaced by inappropriately hypotonic fluids
Sodium can be lost through renal or non-renal routes
o
o
o
o

Nonrenal loss
GI losses: Vomiting, Diarrhea, fistulas, pancreatitis
Excessive sweating
Third spacing of fluids: ascites, peritonitis, pancreatitis, and burns
Cerebral salt-wasting syndrome: traumatic brain injury, aneurysmal subarachnoid hemorrhage,
and intracranial surgery => Must distinguish from SIADH
Renal Loss: Diuretics

Euvolemic hyponatremia
Normal sodium stores and a total body excess of free water
psychogenic polydipsia, often in psychiatric patients
administration of hypotonic intravenous or irrigation fluids in the immediate postop period
Infants who may have been given inappropriate amounts of free water
bowel preparation before colonoscopy or colorectal surgery
SIADH
SIADH
Caused by various etiologies
CNS disease tumor, infection, CVA, SAH
Pulmonary disease TB, pneumonia, sarcoidosis, PPV
Cancer Lung, pancreas, thymoma, ovary, lymphoma
Drugs NSAIDs, SSRIs, antipsychotics, diuretics, opiates
Surgery - Postoperative
Idiopathic most common
essential criteria
Serum osmolality <275 mOsm/kg
Clinical euvolemia
Absence of adrenal, thyroid, pituitary or renal insufficiency
No recent use of diuretic agents
Urine osmolality greater than 100 mOsm/kg though generally greater than 400-500
mOsm/kg in setting of low serum osmolality (inappropriate)
Urine sodium concentration > 30 mmol/L with normal dietary salt and water intake
Supplemental criteria
Serum uric acid<0.24 mmol/L (<4 mg/dL)
Serum urea<3.6 mmol/L (<21.6 mg/dL)
Failure to correct hyponatraemia after 0.9 % saline infusion
Fractional sodium excretion> 0.5 %
Fractional urea excretion> 55 %
Fractional uric acid excretion> 12 %
Correction of hyponatraemia through fluid restriction
Hypervolemic hyponatremia
Total body sodium increases, and TBW increases to a greater extent
Can be renal or non-renal
acute or chronic renal failure
dysfunctional kidneys are unable to excrete the ingested sodium load
cirrhosis, congestive heart failure, or nephrotic syndrome
Clinical manifestations

Fluid deficit or excess

Altered mental status

Fluid Volume Deficit

Acute weight loss
Weak, rapid, heart rate
Decreased skin turgor
Flattened neck veins
Oliguria
Increased temperature
Concentrated urine
Decreased central venous pressure
Postural hypotension

Fluid Volume Excess

Edema
Other clinical manifestations distended neck veins, crackles, increased blood pressure,
increased weight

Hypervolemia
Hypovolemia.
peripheral and presacral edema
poor skin turgor
pulmonary edema
dry mucous membranes
jugular venous distension
flat neck veins
hypertension
hypotension
decr. hct,
incr. Hct
decr. serum prot
incr. serum prot.
decr. bun/cr
Incr bun/cr ratio >20:1
UNa no help
UNa < 20 meq/l

Cerebral symptoms of hyponatremia

Nausea and vomiting
Headache
Decreased consciousness
o
Lethargy
o
Confusion
o
Coma
Seizures
Muscle weakness, cramps or spasms
Respiratory distress // arrest
Death (5-50%)
Hyponatremia 126-134 mmol/L
Alterations of cognitive function
Gait stability
Falls
Osteoporosis
Fractures and inpatient mortality
Workup for hyponatremia: 3 mandatory lab tests
Serum Osmolality
Urine Osmolality
Urine Sodium Concentration
Additional labs depending on clinical suspicion

TSH, cortisol (Hypothryoidism or Adrenal insufficiency)

Albumin, BNP, triglycerides (psuedohyponatremia, cirrhosis, MM)

We recommend interpreting urine osmolality of a spot urine sample as a first step. (1D)
If urine osmolality < 100 mOsm/kg, we recommend accepting relative excess water
intake as a cause of the hypotonic hyponatraemia. (1D)
If urine osmolality>100 mOsm/kg, we recommend interpreting the urine sodium
concentration on a spot urine sample taken simultaneously with a blood sample. (1D)
If urine sodium concentration < 30 mmol/L, we suggest accepting low effective arterial
volume as a cause of the hypotonic hyponatraemia. (2D)
If urine sodium concentration >30 mmol/L, we suggest assessing extracellular fluid
status and use of diuretics to further differentiate likely causes of the hyponatraemia.(2D)
We suggest against measuring vasopressin for confirming the diagnosis of SIADH. (2D)

Treatment of hyponatremia
Treatment is based on symptoms

Severe symptoms = Hypertonic Saline

Mild or no symptoms = Fluid restriction

Symptomatic
1st step is to calculate the total body water

total body water (TBW) = 0.6 body weight

Sodium deficit = TBW x (desired Na actual Na)

estimate SNa change on the basis of the amount of Na in the infusate

SNa = {[Na + K]inf SNa} (TBW + 1)

IV Fluids
One liter of Lactated Ringer's Solution contains:
o 130 mEq of sodium ion = 130 mmol/L
o 109 mEq of chloride ion = 109 mmol/L
o 28 mEq of lactate = 28 mmol/L
o 4 mEq of potassium ion = 4 mmol/L
o 3 mEq of calcium ion = 1.5 mmol/L
One liter of Normal Saline contains: 154 mEq/L of Na+ and Cl
One liter of 3% saline contains: 514 mEq/L of Na+ and Cl

Hyponatraemia with severe symptoms

First hour management, regardless of whether hyponatraemia is acute or chronic

We recommend prompt intravenous infusion of 150 mL 3 % hypertonic saline or

equivalent over 20 min. (1D)
We suggest checking the serum sodium concentration after 20 min while repeating an
infusion of 150 mL 3 % hypertonic saline or equivalent over the next 20 min.(2D)
We suggest repeating therapeutic recommendations twice or until a target of 5 mmol/L
increase in serum sodium concentration is achieved. (2D)
1. Follow up management in case of improvement of symptoms after a 5 mmol/L increase
in serum sodium concentration in the first hour, regardless of whether hyponatraemia is
acute or
chronic
We recommend stopping the infusion of hypertonic saline. (1D)
We recommend keeping the intravenous line open by infusing the smallest feasible
volume of 0.9 % saline until cause-specific treatment is started. (1D)
We recommend starting a diagnosis specific treatment if available, aiming at least to
stabilize sodium concentration.(1D)
We recommend limiting the increase in serum sodium concentration to a total of 10
mmol/L during the first 24 h and an additional 8 mmol/L during every 24 h thereafter
until the serum sodium concentration reaches 130 mmol/L. (1D)
We suggest checking the serum sodium concentration after 6 and 12 h, and daily
afterwards until the serum sodium concentration has stabilised under stable treatment.
(2D)

2. Follow up management in case of no improvement of symptoms after a 5 mmol/L

increase in serum sodium concentration in the first hour, regardless of whether the
hyponatraemia is acute or chronic
We recommend continuing an intravenous infusion of 3 % hypertonic saline or equivalent
aiming for an additional 1 mmol/L/h increase in serum sodium concentration (1D).
We recommend stopping the infusion of 3 % hypertonic saline or equivalent when the
symptoms improve, the serum sodium concentration increases 10 mmol/L in total or the
serum sodium concentration reaches 130 mmol/L,whichever occurs first (1D).
We recommend additional diagnostic exploration for other causes of the symptoms than
hyponatraemia (1D).
We suggest checking the serum sodium concentration every 4 h as long as an intravenous
infusion of 3 % hypertonic saline or equivalent is continued (2D).

What if the sodium increases too fast?

The dreaded complication of increasing sodium too fast is Central Pontine Myelinolysis
which is a form of osmotic demyelination
Symptoms generally occur 2-6 days after elevation of sodium and usually either
irreversible or only partially reversible
Symptoms include: dysarthria, dysphagia, paraparesis, quadriparesis, lethargy, coma or
even seizures

Hyponatraemia with moderately severe symptoms

We recommend starting prompt diagnostic assessment. (1D)
Stop, if possible, medications and other factors that can contribute to or provoke the
hyponatraemia. (not graded)
We recommend cause-specific treatment. (1D)
We suggest immediate treatment with a single intravenous infusion of 150 mL 3 %
hypertonic saline or equivalent over 20 min. (2D)
We suggest aiming for a 5 mmol/L/24 h increase in serum sodium concentration. (2D)
We suggest limiting the increase in serum sodium concentration to 10 mmol/L in the first
24 h and 8 mmol/L during every 24 h thereafter, until a serum sodium concentration of
130 mmol/L is reached. (2D)
We suggest checking the serum sodium concentration after one, 6 and 12 h. (2D)
We suggest additional diagnostic exploration for other causes of the symptoms if the
symptoms do not improve with an increase in serum sodium concentration. (2D)
We suggest considering to manage the patient as in severely symptomatic hyponatraemia
if the serum sodium concentration further decreases despite treating the underlying
diagnosis. (2D)
Acute hyponatraemia without severe
or moderately severe symptoms
Make sure that the serum sodium concentration has been measured using the same
technique as used for the previous measurement and that no administrative errors in
sample handling have occurred. (not graded)

If possible, stop fluids, medications and other factors that can contribute to or provoke the
hyponatraemia. (not graded)
We recommend starting prompt diagnostic assessment. (1D)
We recommend cause-specific treatment. (1D)
If the acute decrease in serum sodium concentration exceeds 10 mmol/L, we suggest a
single intravenous infusion of 150 mL 3 % hypertonic saline or equivalent over 20 min.
(2D)
We suggest checking the serum sodium concentration after 4 h, using the same technique
as used for the previous measurement. (2D)
Chronic hyponatraemia without severe or moderately severe symptoms
Stop non-essential fluids, medications and other factors that can contribute to or provoke
the hyponatraemia. (not graded)
We recommend cause-specific treatment. (1D)
In mild hyponatraemia, we suggest against treatment with the sole aim of increasing the
serum sodium concentration. (2C)
In moderate or profound hyponatraemia, we recommend avoiding an increase in serum
sodium concentration of >10 mmol/L during the first 24 h and> 8 mmol/L during every 24
h thereafter. (1D)
In moderate or profound hyponatraemia, we suggest checking the serum sodium
concentration every 6 h until the serum sodium concentration has stabilised under stable
treatment. (2D)
In case of unresolved hyponatraemia, reconsider the diagnostic algorithm and ask for
expert advice. (not graded)

SIADH
Water restriction: 0.5-1 liter/day
Demeclocycline: Inhibits the effects of ADH- Onset of action may require up to one week

Vasopressin receptor antagonists= AQUARETICS

o Excretion of electrolyte-free water
o Beneficial impact on serum Na
o Lack of evidence on long term beneficial effects
o Absence of disease-modifying properties
o Risk of overcorrection
o Cost

Practical therapeutic approach to hyponatremia in HF

Establish the diagnosis
Limit Na-free fluid intake
Prescribe iv.loop diuretics saline solution
Prescribe vasopressin receptor antagonist
Institute UF/renal replacement therapy

Practical therapeutic approach to symptomatic hyponatremia in HF

Saline solution - Hypertonic?
No worsening of pulmonary congestion
Increase in urine output
Reduction in serum blood urea nitrogen
No change in HF functional class
Lower readmission rate
Lower hospital mortality
Summary of Hyponatremia
Hyponatremia has variety of causes
Treatment is based on symptoms

Severe symptoms = Hypertonic Saline

Mild or no symptoms = Fluid restriction

Overcorrection, more than 10 mmol increase in 24 hours must be avoided with
monitoring
Serum Osmolality, Urine Osmolality and Urine sodium concentration are initial tests to
order

Hypernatremia

Normal range for blood levels of sodium is: 135 - 145 mmol/liter
Hypernatremia refers to an elevated serum sodium level (145 -150 mmol/liter)

CAUSES OF HYPERNATREMIA
1) Water loss
Insensible and sweat losses
GI losses
Diabetes Insipidus (both central and nephrogenic)
Osmotic diuresis
Hypothalamic lesions which affect thirst function tumors, granulomatous diseases or
vascular disease
2) Sodium ion overload

Pathophysiology
Fluid deprivation in patients who cannot perceive, respond to, or communicate their thirst
Most often affects very old, very young, and cognitively impaired patients
Infants without access to water or increased insensible water loss can be very susceptible
to hypernatremia

CNS reaction to hypernatremia

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 focal intracerebral & subarachnoid hemorrhages,
hemorrhages blood clots, and neurological
dysfunction

Symptoms of hypernatremia
Initial symptoms include lethargy, weakness and irritability
Can progress to twitching, seizures, obtundation or coma
Resulting decrease in brain volume can lead to rupture of cerebral veins leading to
hemorrhage
Severe symptoms usually occur with rapid increase to sodium concentration of 158
mmol/l or more

CNS protective mechanisms

Idiogenic osmoles accumulate inside brain cellsK+, Mg+ from cellular binding sites
and amino acids from protein catabolism
These idiogenic osmoles create an osmotic force that draws water back into the brain and protects
cells from dehydration
If this adaptation has occurred and treatment involves a rapid infusion of dextrose, there is
danger of cerebral edema with fluid being drawn into brain tissues

Pathogenesis of hypernatremia
Normal-Volume Hypernatremia: Conditions associated with a loss of electrolyte
free fluids (loss of pure water)
High-Volume Hypernatremia: Conditions associated with ingestion or
administration of sodium containing hypertonic solutions
Low-Volume Hypernatremia: Conditions associated with the loss of hypotonic
fluids (fluids containing more water than sodium)

Normal-volume hypernatremia= Pure Water Loss

Renal Loss
Central diabetes insipidus: Impairment in urinary concentration due to partial or
complete loss of ADH secretion 2 to CNS pathology

o
o
o
o
o

Idiopathic (?autoimmune)
Neurosurgery or trauma
CNS tumors
Infiltrative disorders (e.g., CNS sarcoidosis)
Others (e.g., hypoxic encephalopathy, bleeding, infection)

Nephrogenic diabetes insipidus: Impairment in urinary concentration due to inability of

collecting duct to respond to ADH

o
o

o
o

Chronic lithium treatment (up to 50%)

Hypocalcaemia
Persistent severe hypokalemia
Hereditary nephrogenic DI (children)
o X-linked: defects in V2 receptor gene
o Autosomal recessive: defects in AQP-2 water channel
Other (e.g., sickle cell Dz, amyloidosis, myeloma)

Diagnosis of hypernatremia
Same labs as workup for hyponatremia: Serum osmolality, urine osmolality and urine
sodium

Urine sodium should be lower than 25 mmol/L if water and volume loss are cause. It can
be greater than 100 mmol/L when hypertonic solutions are infused or ingested
If urine osmolality is lower than serum osmolality then DI is present
Administration of DDAVP will differentiate
Urine osmolality will increase in central DI, no response in nephrogenic DI

Clinical manifestations
o Thirst
o Dry, swollen tongue
o Sticky mucous membranes
o Flushed skin
o Postural hypotension

Low-volume hypernatremia
Treatment
Re-hydration is the primary objective in most cases
Treatment is best handled by giving slow infusions of glucose solutions
If hypotensive: then 5% of total body weight (kg) is needed as isotonic fluids initially
Give free H2O (D5W or p.o. water to correct hypernatremia - only after plasma (and ECF)
volume is re-expanded

Calculation of Free Water Deficit

Free water deficit = TBWnormal - TBWpresent
And, TBWpresent x PNa present = TBWnormal x PNa normal
Or, TBWpresent = TBWnormal x PNa normal/ PNa present

So, free water deficit = TBWnormal (1 - PNa normal/ PNa present)

Treatment of Hypernatremia
First, calculate water deficit

TBW present = current body water assumed to be 50% of body weight in men and 40% in
women
So lets do a sample calculation:

60 kg man with 168 mEq/L

How much water will it take to reduce his sodium to 140 mEq/L
Water deficit = 0.5 x 60 (1-[140/168]) approx 5 L
But how fast should I correct it?
Same as hyponatremia, sodium should not be lowered by more than 10-12 mmol/L in 24
hours
Overcorrection can lead to cerebral edema which can lead to encephalopathy, seizures or
death
So what does that mean for our patient?
The 5 L which will lower the sodium level by 28 should be given over 56-60 hours, or at a
rate of 75-80 mL/hr
Typical fluids given in form of D5 water

High-volume hypernatremia
Treatment
Diuretics
Diuretics:: remove Na+ and water
Replacement of water losses from diuretic
Dialysis if concurrent renal failure

Summary of Hypernatremia
Loss of thirst usually has to occur to produce hypernatremia
Rate of correction same as hyponatremia
D5 water infusion is typically used to lower sodium level
Same diagnostic labs used: Serum osmolality, Urine osmolality and Urine sodium
Beware of overcorrection as cerebral edema may develop

All About Potassium

Major Intracellular electrolyte

98% of the bodys potassium is inside the cells
Influences both skeletal and cardiac muscle activity
Normal serum potassium concentration 3.5 to 5.5 mmol/L.

Hypokalemia

Serum Potassium below 3.5 mmol/L

Causes: diarrhea, diuretics, poor K intake, stress, steroid administration, renal disease
Intracellular movement

o Beta-stimulation
o Alcalosis
o Hypotermia
o Insulin

Clinical manifestations:
o malaise, muscle weakness, fatigue,
o decreased reflexes,
o faint heart sounds,
o hypotension,
o cardiac arrhythmias,
o increased sensitivity to digitalis
o EKG changes

Administering IV Potassium
Should be administered only after adequate urine flow has been established
Decrease in urine volume to less than 20 mL/h for 2 hours is an indication to stop the
potassium infusion
Principii de tratament in hKaliemie
1. Corectarea cauzelor care produc translocare intracelular de potasiu
o 2. nlocuirea deficitului de potasiu
o KCl max 20-40 mmol/l/ora
o KCl max 2,5 mmol/kg /24 ore
o Administrare pe vena central
o Administrare cu pompa de infuzie
o Diluarea soluiei native
o Monitorizare frecvent a kaliemiei
o Corectarea hipomagneziemiei asociate

Hyperkalemia
Serum Potassium greater than 5.5 mEq/L
More dangerous than hypokalemia because cardiac arrest is frequently associated with
high serum K+ levels

Causes:
- Decreased renal potassium excretion as seen with renal failure and oliguria

- High potassium intake

- Hypoaldosteronism

- Shift of potassium out of the cell as seen in acidosis, burns, crush injuries, infections

Medicamente care produc hiperpotasemie

Inhibitori ai
angiotensinei

Anti-inflamatoare
nonsteroidiene

Blocani ai receptorilor pentru angiotensina

Ciclosporina

Betablocante

Tacrolimus

Digital

Pentamidina

Diuretice antialdosteronice

Penicilina potasic

Heparina

Trimetoprim-sulfametoxazol

Succinilcolina

enzimei

de

conversie

ai

Clinical manifestations:
o Skeletal muscle weakness/paralysis
o Irritability
o Abdominal distension
o EKG changes such as peaked T waves, widened QRS complexes
o Heart block

Principii de tratament in HKaliemie

1. Oprirea oricrui aport de potasiu
2. Reversarea efectelor membranare

clorura de calciu 10 % 5-10 ml (3,4-6,8 mmol)

3. Transfer intracelular

glucoza 50 g + insulina 20 U

bicarbonat de sodiu 50-100 mmol

agonisti beta-adrenergici
4. Inlturarea din organism

diuretice de ansa

rini schimbatoare de ioni administrate n clisma sau oral

epurare extrarenal