ACID – BASE BALANCE

1
Introduction
q Nearly all biochemical reactions in the body depend on the
maintenance of a physiological hydrogen ion concentration.
q Abnormal hydrogen ion concentrations are associated with
widespread organ dysfunction.
q Disorders of this regulation—usually referred to as acid–base
balance.
q Changes in ventilation and perfusion, infusion of electrolyte-
containing solutions, are common during anesthesia and can
rapidly alter acid–base balance.
üAcid : molecule that release H+ in a solution
üBase : molecule that can accept H+
üAcidosis : excess addition of H+ to solution
üAlkalosis : excess removal of H+ from solution
üAcid-base disorders are changes in arterial PCO2,
serum HCO3− and serum pH.

3
 What is the acid base balance
• Acid-base balance is defined by the concentration of
hydrogen ions.
• In order to achieve homeostasis, there must be a balance
between the intake or production of hydrogen ions and
the net removal of hydrogen ions from the body.

4
 An Acid
• Molecules containing hydrogen atoms that can release hydrogen
ions in solutions are referred to as an acid.

• An example of an acid is hydrochloric acid (HCL)

5
 A Base
• A base is an ion that can accept a hydrogen ion.

• An example of a base is is the bicarbonate ion. ( HCO3)

6
 Acid Base balance
• Hydrogen ion is the most reactive cations in the body fluids
• A great number of cell functions, enzymes, receptors, ion channels
and transporters are pH sensitive.
• Normal pH of body fluids
– Usually maintained within 7.35 - 7.45
– Values outside the range 7.0 – 7.8 are lethal

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8
 Source of H+ ion
• Most hydrogen ions originate from cellular metabolism

• The human body normally produces a large amount of H+ ion as a

result of
– Metabolic processes
– Ingested acids
– Product of fat, sugar & amino acid metabolism

• Maintaining pH homeostasis is the major physiologic function of

organ system

9
 Cont’d..
q The body produces volatile and non volatile acids
– Sulfuric acid
• Oxidation of sulfur containing amino acid-Cystein
– Phosphoric acid
• Oxidation of Phospholipids and phosphoproteins
– Hydrochloric acid
• Conversion of ingested ammonium chloride to urea
– Lactic acid
• Anaerobic glucose metabolism. It can be converted to CO2
• Other fixed acids ingested accidentally

10
 How is Acid-Base balance measured

• Hydrogen ion concentration is expressed on a logarithm scale using pH

units (part/percentage hydrogen).

11
 pH

• Body systems carefully control pH of the body within the range of

7.35-7.45
• A low pH corresponds to a high hydrogen ion concentration
• The term “Acidosis” refers to the addition of excess hydrogen ions
and the body has a pH that falls below 7.35

12
 pH cont’d..

• A high pH corresponds to a low hydrogen concentration

• The term “Alkalosis” refers to excess removal of hydrogen ions from

the body and has a pH that rises above 7.45

13
How the Body defends against fluctuations in pH

Three Systems in the body:

[Link] in the blood
[Link] through the lungs
[Link] by the kidneys

14
 Buffers in the Blood
• A buffer is defined as a substance within a solution that
can prevent extreme changes in pH.
• A buffer system is composed of a base molecule and its
weak conjugate acid.
• Buffers are substances that neutralize acids or bases
• Bicarbonate which is a base and carbonic acid in the body
fluids protect the body against changes in acidity
• These buffer systems serve as a first line of defense
against changes in the acid-base balance
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 Respiration through the lungs
• Carbon Dioxide which is formed during cellular metabolism forms
carbonic acid in the blood decreasing the pH

• When the pH drops respiration rate increases this hyperventilation

increases the amount of CO2 exhaled thereby lowering the carbonic
acid concentration and restoring homeostasis

16
 Excretion by the Kidneys
• Renal mechanism is the 3rd line of defence in acid base balance.
• The kidneys play the primary role in maintaining long term control
of Acid-Base balance

• The kidney participate by conservation of HCO3 and excretion of

acid.

• The kidneys adjust the body’s Acid-Base balance

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 The Importance of the Body’s Buffering Systems
• Can be quickly realized if one considers the low concentration of
hydrogen ions in the body fluids and the relatively large amounts of
acids produced by the body each day

• Example: 80 milliequvilalants of hydrogen is either ingested or

produced each day by metabolism.

• Whereas the hydrogen ion concentration of the body fluids

normally is only about .0004meq/L or (40neq/l)

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 Acid-Base Balance
• Normal pH
7.35 – 7.45
• Alkalosis or alkalemia – arterial blood pH rises above 7.45
• Acidosis or acidemia – arterial pH drops below 7.35 (physiological
acidosis)

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 Sources of Hydrogen Ions
• Most hydrogen ions originate from cellular metabolism

q Breakdown of phosphorus-containing proteins releases phosphoric

acid into the ECF

q Anaerobic respiration of glucose produces lactic acid

q Fat metabolism yields organic acids and ketone bodie

q Transporting carbon dioxide as bicarbonate releases hydrogen ions

20
 Hydrogen Ion Regulation
qConcentration of hydrogen ions is regulated sequentially by :

üChemical buffer systems – act within seconds

üThe respiratory center in the brain stem – acts within 1-3 minutes

üRenal mechanisms – require hours to days to effect pH changes

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 Physiological Buffer Systems
The respiratory system regulation of acid-base balance is a
physiological buffering system

There is a reversible equilibrium between:

ØDissolved carbon dioxide and water
ØCarbonic acid and the hydrogen and bicarbonate ions

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3¯

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 Physiological Buffer Systems
§ During carbon dioxide unloading, hydrogen ions are incorporated
into water

§ When hypercapnia or rising plasma H+ occurs :

§ Deeper and more rapid breathing expels more carbon dioxide
§ Hydrogen ion concentration is reduced

§ Alkalosis causes slower, more shallow breathing, causing H+ to

increase

§ Respiratory system impairment causes acid-base imbalance

(respiratory acidosis or respiratory alkalosis)

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 Renal Mechanisms of Acid-Base Balance
§ Chemical buffers can tie up excess acids or bases, but they cannot eliminate
them from the body

§ The lungs can eliminate carbonic acid (volatile acid) by eliminating carbon
dioxide

§ Only the kidneys can rid the body of metabolic acids (phosphoric, uric, and
lactic acids and ketones) and prevent metabolic acidosis

§ The ultimate acid-base regulatory organs are the kidneys

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The Basic Relationship between PCO2
and Plasma pH

25
 Renal Mechanisms of Acid-Base Balance
qThe most important renal mechanisms for regulating acid-base
balance are:
q Conserving (reabsorbing) or generating new bicarbonate ions
q Excreting bicarbonate ions

qLosing a bicarbonate ion is the same as gaining a hydrogen ion

(the blood becomes acidic);
qreabsorbing a bicarbonate ion is the same as losing a hydrogen ion
(the blood becomes alkaline)

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 Respiratory Acidosis and Alkalosis
qResult from failure of the respiratory system to
balance pH

qPCO2 is the single most important indicator of respiratory inadequacy

qPCO2 levels
• Normal PCO2 fluctuates between 35 and 45mm Hg
• Values above 45 mm Hg signal respiratory acidosis
• Values below 35 mm Hg indicate respiratory alkalosis

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 Respiratory Acidosis and Alkalosis
• Respiratory acidosis is the most common cause of acid-base
imbalance
• Occurs when a person breathes shallowly,
• or gas exchange is hampered by diseases such as pneumonia,
cystic fibrosis, or emphysema

• Respiratory alkalosis is a common result of hyperventilation

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 Metabolic Acidosis
qAll pH imbalances except those caused by abnormal blood carbon dioxide
levels

qMetabolic acid-base imbalance – bicarbonate ion levels above or below normal

(22-26 mEq/L)

qMetabolic acidosis is the second most common cause of acid-base imbalance

üTypical causes are ingestion of too much alcohol and excessive loss of
bicarbonateions
üOther causes include accumulation of lactic acid, shock, ketosis in diabetic
crisis, starvation, and kidney failure

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 Metabolic Alkalosis
qRising blood pH and bicarbonate levels indicate metabolic alkalosis

qTypical causes are:

• Vomiting of the acid contents of the stomach
• Intake of excess base (e.g., from antacids)
• Constipation, in which excessive bicarbonate is reabsorbed

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 Respiratory and Renal Compensations

qAcid-base imbalance due to inadequacy of a

physiological buffer system is compensated for
by the other system

§ The respiratory system will attempt to correct metabolic acid-

base imbalances
§ The kidneys will work to correct imbalances
caused by respiratory disease

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 Respiratory Compensation
• Metabolic acidosis has low pH:
• Bicarbonate level is low
• Pco2 is falling below normal to correct the imbalance
• The rate and depth of breathing are
elevated

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Respiratory Compensation
• Metabolic alkalosis has high pH:
• High levels of bicarbonate
• Correction is revealed by:
– Rising PCO2
– Compensation exhibits slow, shallow breathing, allowing
carbon dioxide to accumulate in the blood

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Renal Compensation
• To correct respiratory acid-base imbalance, renal mechanisms are
stepped up
• Respiratory Acidosis has low pH
§ Has high PCO2 (the cause of acidosis)
§ In respiratory acidosis, the respiratory rate is often depressed and
is the immediatecause of the acidosis
• High bicarbonate levels indicate the kidneys are retaining
bicarbonate to offset the acidosis

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Renal Compensation
• Respiratory Alkalosis has high pH
• Low PCO2 (the cause of the alkalosis)
• Low bicarbonate levels
üThe kidneys eliminate bicarbonate from the body by failing to
reclaim it or by actively secreting it

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Developmental Aspects
ü Water content of the body is greatest at birth (70-80%) and declines until
adulthood, when it is about 58%

ü At puberty, sexual differences in body water content arise as males develop

greater muscle mass

ü Homeostatic mechanisms slow down with age

ü Elders may be unresponsive to thirst clues and are at risk of dehydration

ü The very young and the very old are the most frequent victims of fluid, acid-
base, and electrolyte imbalances

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4-Step approach to blood gas interpretation
1. Determine the pH or H+ concentration.
2. Determine the respiratory component.
3. Determine the metabolic component.
4. Determine the primary disturbance and whether there is any metabolic or
respiratory compensation.

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 1. The pH or H+ concentration
§ pH > 7.44  Alkalosis
§ pH < 7.36  Acidosis

40
2. The respiratory component
• PaCO2:
– > 5.6 kPa (45 mmHg)  Respiratory acidosis
– < 5.0 kPa (35 mmHg)  Respiratory alkalosis

41
3. The metabolic component
-
üHCO3 :

ü> 26 mmols / L  (metabolic alkalosis)

ü< 22 mmols / L  (metabolic acidosis)

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 4. Combine information from 1, 2 and 3 and determine:

üWhere is the primary disturbance ?

üIs there any metabolic or respiratory compensation ?

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Summary of changes

Acid-base disorder pH PaCO2 HCO3-

Respiratory acidosis   …..
Metabolic acidosis  ….. 
Respiratory alkalosis   ….
Metabolic alkalosis  ….. 
…/Normal

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 Anesthetic consideration in patient with acidosis
ü Acidemia can potentiate the depressant effects of most sedatives and
anesthetic agents on the central nervous and circulatory systems.
ü Most opioids are weak bases, acidosis can increase the fraction of the
drug in the non-ionized form and facilitate opioid penetration into the brain,
potentiating its sedative effect.
ü The circulatory depressant effects of both volatile and intravenous
anesthetics can also be exaggerated.
ü Halothane is more arrhythmogenic in the presence of acidosis.
ü Succinylcholine should generally be avoided in acidotic patients with
hyperkalemia to prevent further increases in plasma [K+].
Anesthetic consideration for patient with alkalosis

ü Cerebral ischemia can occur from a marked reduction in cerebral

blood flow during respiratory alkalosis, particularly during
hypotension.
ü The combination of alkalemia and hypokalemia can precipitate
severe cardiac arrhythmias.
ü Reports of the effects of alkalemia on neuromuscular blockers are
inconsistent.
Common Electrolyte Disturbance &
their mgt and anesthesia
consideration
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
Normal range b/n ECF- ISF- ICF-mEq/L
mEq/L mEq/L

Sodium 135-145 140 142 10

Potassium 3.5-5.5 4.5 4 150
Calcium 4.5-5.5 5 5 1
Magnesium 1.7-2.5 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.
q 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
ü Nausea, vomiting,
üvisual disturbances,
ü depressed level of consciousness,
ü agitation, confusion, coma,
üseizures, muscle cramps,
üweakness, 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 0.5 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
Con`t
q patients are sensitive to:
ü the vasodilating and negative inotropic effects of the volatile
anesthetics,
übarbiturates, and agents associated with histamine release
(morphine, meperidine,curare, atracurium).
q 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 sign of hypernatremia is lethargy or mental
status changes, which can proceed to coma and convulsions

• shock, peripheral edema

• 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 .
Con`t
• 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.
con`t
• 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
Con`t

• 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
qHypokalemia 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
Con`t

• 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

§ Dextrose-containing solutions should generally be avoided because the

resulting hyperglycemia and secondary insulin secretion may actually
lower plasma [K+] even further.
 Anesthetic Considerations
• 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
Ø Increased potassium intake
Ø Extracellular translocation(acidmia)
Ø Adminstretion of sux for burned patients
Ø Hypoaldosteronisim
Ø Drugs that may limit potasium excretion (NSAIDs,potasium
sparing diuretics such as triamterene)
Ø Acute or chronic renal failure
Clinical manifestation
qCVS
• 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
con`t
Treatment
qThe 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
q The normal plasma calcium concentration is 4.5 -5.5 MEq/L
qcalcium 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
Ø essentially involves diuresis and administration of
normal saline to dilute plasma calcium.
Ø 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 ECG 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
qplasma 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
Clinical Presentation of hypocalcemia
v The hallmark sign of acute hypocalcemia is tetany due neuromuscular
irritability .
v Neurologic: tetany, anxiety, memory loss, confusion, hallucinations, tonic
clonic seizures and parkinsonism
Ø +ve Chvostek’s and/or Trousseau’s sign
ü Hypotension,
ü decreased myocardial contractility,
ü prolonged QT interval
ü Bradycardia
ü laryngeal spasm
ü Myopathy , muscle cramps
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
Con`t

• 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
Con`t
• 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
• [Link]
[Link]
• [Link] January 15, 2004
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