common electrolyte disturbance

their management and anesthesia

consideration

BY HELINA GETACHEW
 outline

Objective
Introduction
Electrolyte composition
Sodium imbalance
Potassium imbalance
Calcium imbalance
Magnesium imbalance
Summary
Reference
 Objective

At the end of this session you will be able to

1. Explain the function of different electrolyte

2. Define different disorder of electrolyte

3. explain the cause and treatment of common

electrolyte disorders

4. explain Anesthetic consideration of electrolyte

disorders
 Introduction

Fluid balance is a daily balance between the amount of

water gained and the amount of water lost to
environment.

Electrolyte balance is a balance among the electrolyte in

the body or the ion gain each day equals the ion loss

Water is the major component of all fluid compartments

within the body. Total-body water represents
approximately 60% of the body's total weight in an
average adult.
 Introduction cont…..

Total-body water is separated into two basic

components, the intracellular and extracellular
compartments.

 The major components of the extracellular

compartment are the plasma volume and the
interstitial fluid
 Electrolyte composition in body fluids

ECF-mEq/L ISF-mEq/L ICF-mEq/L

Sodium 140 142 10

Potassium 4.5 4 150
Calcium 5 5 1
Magnesium 2 2 40
 sodium

 Sodium is the most abundant positive ion of the

ECF compartment and is critical in determining
the extracellular and intracellular osmolality.
FUNCTIONS
It maintains arterial blood pressure
Extracellular fluid volume maintenance
Increases cell excitability and action potential
generation
 Hyponatremia

 Hyponatremia : a plasma sodium concentration

<135 mEq/L
 Causes
 excessive loss of sodium from excessive sweating,
vomiting, diarrhea, burns, and the administration of
diuretics
 Mineralocorticoid deficiency
 Third-spacing
 Congestive heart failure
 signs and symptoms


Nausea, vomiting,
 visual disturbances,
 depressed level of consciousness,
 agitation, confusion, coma,
 seizures, muscle cramps,
 weakness, or myoclonus
 Treatment of Hyponatremia

 correcting the underlying disorder as well as the

plasma [Na+].

Isotonic saline is generally the treatment of choice.

water restriction, in a case of water overload

improving cardiac output in patients with heart

failure.
 CONT…

 Cerebral edema occurs at or below a serum level of

123 mEq/L, and cardiac symptoms occur at 100
mEq/L

The optimal rate of correction appears to be 0.6 to

1 mmol/L/hour until the sodium concentration is
125 mEq/L, and then correction proceeds at a
slower rate.
 CONT…

One
 half the deficit can be administered over the first 8 hours and the
next half over 1 to 3 days

A loop diuretic may be

 added to facilitate free water excretion.

.

 CONT…

Hypertonic saline should be used only in cases of

severe hyponatremia with neurologic symptoms
Sodium concentration should be monitored every 1
to 2 hours during rapid correction
 Anesthetic Considerations
 Plasma [Na+] should be corrected above 130
mEq/L for all elective procedures, even in the
absence of symptoms.

Lower concentrations may result in significant

cerebral edema that can be manifested
intraoperatively as a decrease in minimum alveolar
concentration or postoperatively as agitation,
confusion
patients are sensitive to:
 the vasodilating and negative inotropic effects of the volatile
anesthetics,
 barbiturates, and
 agents associated with histamine release (morphine,
meperidine,curare, atracurium).
 So, dosage decrement is essential
are particularly sensitive to sympathetic blockade from
spinal or epidural anesthesia.
ketamine may be the induction agent of choice for general
anesthesia; etomidate may be a suitable alternative.
 Hypernatremia

 It is defined as an increase in extracellular sodium

concentration >145meq/l.
major causes
o excessive loss of water
o inadequate intake of water
o a lack of ADH
o excessive intake of sodium
o Administration of hypertonic saline, Na HCO3
 Sign and symptoms

The most common objective sign of hypernatremia

is lethargy or mental status changes, which can
proceed to coma and convulsions

 shock, peripheral edema, myoclonus,

ascites, muscular tremor,
 muscular rigidity, hyperactive reflexes,
pleural effusion,
 expanded intravascular fluid volume.
 Anesthetic Considerations

Hypernatremia clinical significance is more closely

related to the associated fluid deficits

 there is impaired gas exchange due to:

 pulmonary interstitial edema, alveolar edema, or large
collections of pleural or ascitic fluid as a result of increases
in extracellular volume .
 Hypervolemia should generally be corrected preoperatively
with
 administration of diuretics and hypotonic crystalloid solutions
to remove excess sodium

Hypernatremia increases MAC for inhalation

anesthetics possibly because of enhanced sodium
conductance during depolarization of excitatory
membranes.
 Anesthetic Considerations

Decreases in the volume of distribution for drugs

necessitate dose reductions for most iv agents

Elective surgery should be postponed in patients

with significant hypernatremia (> 150 mEq/L)
until the cause is established and fluid deficits are
corrected
Hypernatremic patients with increased total body
sodium should be treated with a loop diuretic along
with intravenous 5% dextrose in water
 POTASSIUM

 it is the principal intracellular cation, with more

than 98% of the body's potassium found within the
intracellular water.
 In the resting state, cell membrane conductance is
higher for potassium than sodium.
 Functions

Used for electrophysical cellular integrity

Maintains resting membrane potential
 generates action potential
Excitation of cardiac tissue
 Hypokalemia

plasma [K+] <3.5 mEq/L may occur because of an

absolute deficiency or redistribution into the
intracellular space.

Hypokalemia in the range of 2 to 2.5 mEq/L is

likely to cause muscular weakness, arrhythmias,
and electrocardiographic abnormalities.
 most common causes

 reduced intake,
potassium shifts from the extracellular to the
intracellular fluid Caused by:
o excess insulin (exogenous or endogenous)
o beta-adrenoceptor agonists (such as endogenous
catecholamines or exogenous salbutamol)
o acute rise in plasma pH
Vomiting – this is not caused by a loss of K+ in the
vomit; rather, loss of H+ and water lead to metabolic
alkalosis and increased aldosterone
excessive renal losses of potassium (with excess of
mineralocorticoids or diuretics)
gastrointestinal losses
 Clinical Manifestations

 Hypokalemia can produce widespread organ

dysfunction.
o Cardiovascular effects are most prominent and
include;
an abnormal ECG, arrhythmias, decreased
cardiac contractility, and a labile arterial blood
pressure due to autonomic dysfunction.
Skeletal muscle weakness
Tetany
ECG manifestations are primarily due to delayed
ventricular repolarization and include:
 T-wave flattening and inversion, an increasingly prominent
U wave, ST-segment depression, increased P-wave
amplitude, and prolongation of the P–R interval
 Increased myocardial cell automaticity and
delayed repolarization promote both atrial and
ventricular arrhythmias
Electrocardiographic effects of hypokalemia.
 Treatment of Hypokalemia

 depends on the presence and severity of any

associated organ dysfunction
Oral replacement with potassium chloride solutions
is generally safest (60–80 mEq/d).
 Replacement of the potassium deficit usually requires several
days.
Peripheral potassium chloride intravenous
replacement should not exceed 8 mEq/h because of
the irritative effect of potassium on peripheral veins.
 Anesthetic Considerations

The decision to proceed with elective surgery is

often arbitrarily based on lower limits somewhere
between 3 and 3.5 mEq/L

The decision, however, should also be based on the

rate at which the hypokalemia developed as well as
the presence or absence of secondary organ
dysfunction.
 Anesthetic Considerations

 intraoperative potassium should be given if atrial

or ventricular arrhythmias develop.
 Faster intravenous replacement (10–20 mEq/h)
requires a central venous catheter and close
monitoring of the ECG.
The intraoperative management of hypokalemia
requires vigilant ECG monitoring
 Anesthetic Considerations
Dextrose-containing solutions should generally be
avoided because the resulting hyperglycemia and
secondary insulin secretion may actually lower plasma
[K+] even further.
Glucose-free intravenous solutions should be used
hyperventilation avoided to prevent further decreases in
plasma [K+]
Increased sensitivity to neuromuscular blocking agents .
 Dosages of NMBAs should therefore be reduced 25–50%, and a
nerve stimulator should be used to follow the degree of paralysis and
the adequacy of reversal.
 Hyperkalemia

 >5.5 mEq/L may occur in various disease states,

in response to drugs that diminish renal potassium
excretion, or after sudden transcellular shifts of
potassium from the intracellular to the ECF.
 causes

Increased potassium intake

Extracellular translocation(acidmia)
Adminstretion of sux for paraplegic or burned
patients
Hypoaldosteronisim
Drugs that may limit potasium excretion
(NSAIDs,potasium sparing diuretics such as
triamterene)
 Acute or chronic renal failure
 Clinical manifestation

 CVS
Earliest change( 6 to 7 mEq/L) may present with peaked
T waves and shortened QT interval
8-10mEq/L widened QRS complex and eventual loss
of P wave
>10mEq/L VF
Neuromuscular – weakness, paralysis ,paresthesia
respiratory arrest
 Treatment

 The management is directed to antagonize effect of

potassium on the heart facilitating movement of
potassium into the cell from the plasma

Calcium gluconate 10% IV(0.5ml/kg to maximum

20ml)given over 5 min because it redistributes
potassium from the plasma into cells
 Cont…

Glucose 50(5-1gm/kg)plus insulin 20unit(3u/kg) as

single IV bolus dose

Sodium bicarbonate 1.5-2mmol/kg IV over 5min

Hyperventilation of the lung

Furosemide promotes kaliuresis in a dose-depending

fashion
 Anesthetic Considerations

Elective surgery should not be undertaken in

patients with hyperkalemia
Anesthetic management of hyperkalemic is
directed at both lowering the plasma potassium
concentration and preventing any further
increases.
The ECG should be carefully monitored
Succinylcholine is contraindicated, as is the use of
any potassium-containing intravenous solutions
such as lactated Ringer's injection.
 Anesthetic Considerations

 The avoidance of metabolic or respiratory acidosis

is critical
 Ventilation should be controlled under general anesthesia;
mild hyperventilation may even be desirable
Drugs such as calcium, glucose, and insulin must
readily be available.
neuromuscular function should be monitored
closely, as hyperkalemia can accentuate the effects
of NMBAs.
 CALCIUM

 The normal plasma calcium concentration

is 4.5 -5.5 MEq/L
calcium exists in three forms:
o bound to plasma proteins (primarily albumin) and
not filtered by glomerular capillaries (40%);
o ionized, physiologically active, filtered at the
glomerular membrane, and maintained at a
concentration of 2.0 to 2.5 mEq/L (50%); and
o nonionized and chelated with phosphate, sulfate, and
citrate (10%).
 Function

 mediates muscle contraction

mediates exocrine, endocrine secretion
cell growth; and
 transport and secretion of fluids and electrolytes
 Hypercalcemia

 hypercalcemia is when the calcium level is

>5.5MEq/L
Manifestations
 central nervous system (e.g., mental status

changes),
 the gastrointestinal tract (e.g., vomiting),
 the kidneys (e.g., polyuria, renal calculi,
oliguric renal failure), and
 the heart (e.g., cardiac conduction
disturbances).
 causes of Hypercalcemia

 malignancy, or parathyroid hormone adenoma.

 Treatment
 essentially involves diuresis and administration of
normal saline to dilute plasma calcium.
 Additional therapies include , calcitonin,
ambulation, and treatment of the underlying
condition.
 Anesthetic Considerations

 maintenance of hydration and urine output

with sodium-containing fluids.
Rehydrate with NS and IV lasix which inhibits
Na -Ca symport which increases calciuria
Avoid hypoventiletion so as to avoid
respiratory acidosis which may cause
conversion of plasma protein bounded calcium
into free and ionized calcium
Restriction of calcium containing solution
 Anesthetic Considerations

o Monitoring the patient by means of

electrocardiograms is useful to detect cardiac
conduction abnormalities with shortened PR or QT
intervals, with or without widening of the QRS
complex.
o Patients who have muscle weakness should receive
decreased doses of nondepolarizing muscle
relaxants
 Hypocalcemia

 plasma concentration less than 4.5 mEq/L

Cause
Vitamin D deficiency
Nutritional
Malabsorption
Postsurgical (gastrectomy,
a low albumin level, such as in critically ill patients with
severe sepsis, burns, or acute renal failure and
 in patients after extensive transfusions
 signs and symptoms

 mental status changes

tetany
positive Chvostek and Trousseau signs,
laryngospasm,
hypotension, and dysrhythmias.

ECG: prolongation of the QT interval or even

heart block in severe cases
 Treatment of Hypocalcemia

 involves intravenous infusion of 10% calcium

chloride (1.36 mEq/mL) or calcium gluconate
(0.45 mEq/mL).
 Anesthetic Considerations

In the OR, hypocalcemia is most commonly caused by

acute hyperventilation or the infusion of citrated blood
in excess of 1.5 mL/kg/min.
Hypocalcemia should be corrected preoperatively.
 Alkalosis should be avoided to prevent further
decreases in [Ca2+].
Potentiation of the negative inotropic effects of
barbiturates and volatile anesthetics should be expected
Responses to NMBAs are inconsistent and require close
monitoring with a nerve stimulator
 MAGNESIUM

Magnesium is the fourth most important cation in

the body and the second most important
intracellular cation.
Plasma [Mg2+] is closely regulated between 1.7
and 2.1 mEq/L
 Functions

 activates approximately 300 enzyme systems,

including many involved in energy metabolism

 is an essential regulator of calcium access into the

cell and of the actions of calcium within the cell

anticonvulsant activity of magnesium is related to

its powerful cerebral vasodilator action that
reverses cerebral vasospasm,
 Hypomagnesaemia

Magnessium <1,7 Meq/L

Slight hypomagnesemia occurs in athletes, in
hypermetabolic states such as pregnancy

Magnesium stores can become depleted in patients

undergoing prolonged diuretic therapy or patients
with chronic diarrhea.
 Hypomagnesaemia

Chronic alcohol ingestion leads to significant loss

of magnesium
Manifestations include :
 central nervous system irritability with seizures and
hyperreflexia and skeletal muscle spasm.
 Treatment includes:
o magnesium sulfate (1 to 2 mEq/kg), which should be
administered over 8 to 12 hours with careful
measurement and assessment of electrolyte levels
 Hypomagnesaemia

For acute arrhythmias, magnesium can be

administrated in a dose of 8 to 12 mmol/L (200 to
300 mg) intravenously over 1 to 5 minutes with
close monitoring of blood pressure and heart rate.
 Anesthetic Considerations

 Isolated hypomagnesemia should be corrected

prior to elective procedures because of its potential
for causing cardiac arrhythmias.

Respiratory muscle power is impaired by

hypomagnesaemia, which may have important
clinical consequences for anesthesia and critical
care
coexistent electrolyte disturbances such as
 hypokalemia, hypophosphatemia, and hypocalcemia are often
present and should be corrected prior to surgery
 Hypermagnesemia

Hypermagnesemia (>2.5 mEq/L)

Because elimination is directly related to the
glomerular filtration rate, patients with kidney failure
are at increased risk of developing hypermagnesemia.
Signs and symptoms
 Hyporeflexia, sedation, and skeletal muscle weakness
 Vasodilation, bradycardia, and myocardial depression can lead
to hypotension at levels > 10 mmol/dL (> 24 mg/dL).
 ECG signs are inconsistent but often include prolongation of
the P–R interval and widening of the QRS complex. Marked
hypermagnesemia can lead to respiratory arrest.
 Treatment of Hypermagnesemia

All sources of magnesium intake (most often antacids)

should be stopped.
Intravenous calcium (1 g calcium gluconate) can
temporarily antagonize most of the effects of
hypermagnesemia.
A loop diuretic along with an infusion of ½-normal
saline in 5% dextrose enhances urinary magnesium
excretion.
Definitive therapy involves dialysis.
Temporary reversal of the effects of magnesium can be
managed with calcium
 Anesthetic Considerations

Hypermagnesemia requires close monitoring of

the ECG, blood pressure, and neuromuscular
function

In the peripheral nervous system, magnesium

interferes with the release of neurotransmitters at
all synaptic junctions and potentiates the action
of local anesthetics
 Dosages of NMBAs should be reduced by 25–50%.

 A urinary catheter is required when diuretic and saline

infusions are used to enhance magnesium excretion

 Potentiation of the vasodilating and negative inotropic

properties of anesthetics should be expected
 Summary

Potassium is the most important determinant of intracellular osmotic

pressure, whereas sodium is the most important determinant of extracellular
osmotic pressure.

Serious manifestations of hyponatremia are generally associated with plasma

sodium concentrations < 123 mEq/L.

The major hazard of increases in extracellular volume is impaired gas

exchange due to pulmonary interstitial edema, alveolar edema, or large
collections of pleural or ascitic fluid.

Intravenous replacement of potassium chloride should usually be reserved for

patients with or at risk for serious cardiac manifestations or muscle weakness.
 Summery

Symptomatic hypercalcemia requires rapid treatment.

The most effective initial treatment is rehydration.
Symptomatic hypocalcemia is a medical emergency and
should be treated immediately with intravenous calcium
chloride (3–5 mL of a 10% solution) or calcium gluconate
(10–20 mL of a 10% solution)..
Marked hypermagnesemia can lead to respiratory arrest.
Isolated hypomagnesemia should be corrected prior to
elective procedures because of its potential for causing
cardiac arrhythmias.
 Reference

Ronald D. Miller M.D.2005 Miller's Anesthesia, 6th

ed
G. Edward Morgan, Jr., Maged S. Mikhail, Michael
J. Murray Clinical Anesthesiology, 4th Editio
http://www.preservearticles.com/201105317358/w
hat-is-the-importance-of-chlorine-in-human-
body.html
http://www.mgwater.com/bicarb.shtml January
15, 2004
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