Download ACID – BASE, FLUIDS, AND ELECTROLYTES EXTRA NOTES

ACID – BASE, FLUIDS, AND ELECTROLYTES
EXTRA NOTES:
 BASIC

Respiratory: When breathing is inadequate carbon dioxide
(respiratory acid) accumulates. The extra CO2 molecules
combine with water to form carbonic acid which contributes to a
relative shift towards an acid pH. The treatment, if all else fails,
is to lower the PCO2 by breathing for the patient using a
ventilator or bag and mask.
Metabolic: When normal metabolism is impaired - acid forms,
e.g., poor blood supply stops oxidative metabolism and lactic
acid forms. This acid is not respiratory so, by definition, it is
"metabolic acid." If severe, the patient may be in shock and
require treatment, possibly by neutralizing this excess acid with
bicarbonate, possibly by allowing time for excretion or
metabolism.
Acidosis is excessive blood acidity caused by an overabundance of acid in the blood
or a loss of bicarbonate from the blood (metabolic acidosis), or by a buildup of
carbon dioxide in the blood that results from poor lung function or slow breathing
(respiratory acidosis).

Blood acidity increases when people ingest substances that contain or
produce acid or when the lungs do not expel enough carbon dioxide.

People with metabolic acidosis have nausea, vomiting, and fatigue and may
breathe faster and deeper than normal.

People with respiratory acidosis have headache and confusion, and breathing
may appear shallow, slow or both.

Tests on blood samples show there is too much acid.

Doctors treat the cause of the acidosis.
If an increase in acid overwhelms the body's pH buffering systems, the blood will
become acidic. As blood pH drops, the parts of the brain that regulate breathing
are stimulated to produce faster and deeper breathing. Breathing faster and
deeper increases the amount of carbon dioxide exhaled.
The kidneys also try to compensate by excreting more acid in the urine. However,
both mechanisms can be overwhelmed if the body continues to produce too much
acid, leading to severe acidosis and eventually coma.
Causes
Metabolic acidosis develops when the amount of acid in the body is increased
through ingestion of a substance that is, or can be broken down (metabolized) to,
an acid—such as wood alcohol (methanol), antifreeze (ethylene glycol), or large
doses of aspirin SOME TRADE NAMES
BAYER
( acetylsalicylic acid SOME TRADE NAMES
SEE ASPIRIN
). Metabolic acidosis can also occur as a result of abnormal metabolism. The body
produces excess acid in the advanced stages of shock and in poorly controlled type
1 diabetes mellitus. Even the production of normal amounts of acid may lead to
acidosis when the kidneys are not functioning normally and are therefore not able
to excrete sufficient amounts of acid in the urine.
Major Causes of Metabolic
Acidosis and Metabolic
Alkalosis
Metabolic acidosis

Diabetic
ketoacidosis (buildup of
ketones)

Drugs and
substances such as
acetazolamide SOME TRADE
NAMES
DIAMOX
, alcohol, aspirin SOME
TRADE NAMES
BAYER
, iron

Lactic acidosis
(buildup of lactic acid as
occurs in shock)

Loss of bases, such
as bicarbonate, through the
digestive tract from
diarrhea, an ileostomy, or a
colostomy

Kidney failure

Poisons such as
carbon monoxide, cyanide,
ethylene glycol, methanol,

Renal tubular
acidosis (a form of kidney
malfunction)
Metabolic alkalosis

Loss of acid from
vomiting or drainage of the
stomach

Overactive adrenal
gland (Cushing's syndrome)

Use of diuretics
(thiazides, furosemide SOME
TRADE NAMES
LASIX
, ethacrynic acid SOME
TRADE NAMES
EDECRIN
)
Respiratory acidosis develops when the lungs do not expel carbon dioxide
adequately, a problem that can occur in diseases that severely affect the lungs
(such as emphysema, chronic bronchitis, severe pneumonia, pulmonary edema, and
asthma). Respiratory acidosis can also develop when diseases of the brain or of the
nerves or muscles of the chest impair breathing. In addition, people can develop
respiratory acidosis when their breathing is slowed due to oversedation from
opioids (narcotics) or strong drugs that induce sleep (sedatives).
Major Causes of Respiratory
Acidosis and Alkalosis
Respiratory acidosis

Lung disorders,
such as emphysema, chronic
bronchitis, severe asthma,
pneumonia, or pulmonary
edema

Sleep-disordered
breathing

Diseases of the
nerves or muscles of the
chest that impair breathing,
such as Guillain-Barré
syndrome or amyotrophic
lateral sclerosis

Overdose of drugs
such as alcohol, opioids, and
strong sedatives
Respiratory alkalosis


Anxiety
Aspirin SOME
TRADE NAMES
BAYER
overdose (early stages)

Fever

Low levels of
oxygen in the blood

Pain
Symptoms
People with mild metabolic acidosis may have no symptoms but usually experience
nausea, vomiting, and fatigue. Breathing becomes deeper and slightly faster (as the
body tries to correct the acidosis by expelling more carbon dioxide). As the
acidosis worsens, people begin to feel extremely weak and drowsy and may feel
confused and increasingly nauseated. Eventually, blood pressure can fall, leading to
shock, coma, and death.
The first symptoms of respiratory acidosis may be headache and drowsiness.
Drowsiness may progress to stupor and coma. Stupor and coma can develop within
moments if breathing stops or is severely impaired, or over hours if breathing is
less dramatically impaired.
Diagnosis
The diagnosis of acidosis generally requires the measurement of blood pH in a
sample of arterial blood, usually taken from the radial artery in the wrist. Arterial
blood is used because venous blood contains high levels of bicarbonate and thus is
generally not as accurate a measure of the body's pH status.
To learn more about the cause of the acidosis, doctors also measure the levels of
carbon dioxide and bicarbonate in the blood. Additional blood tests may be done to
help determine the cause.
Treatment
The treatment of metabolic acidosis depends primarily on the cause. For instance,
treatment may be needed to control diabetes with insulin SOME TRADE NAMES
HUMULINNOVOLIN
or to remove the toxic substance from the blood in cases of poisoning.
The treatment of respiratory acidosis aims at improving the function of the lungs.
Drugs that open the airways (bronchodilators, such as albuterol SOME TRADE
NAMES
PROVENTIL-HFAVENTOLIN HFA
) may help people who have lung diseases such as asthma and emphysema. People
who have severely impaired breathing or lung function, for whatever reason, may
need mechanical ventilation to aid breathing (see Respiratory Failure and Acute
Respiratory Distress Syndrome: Acute Respiratory Distress Syndrome (ARDS)).
Acidosis may also be treated directly. If the acidosis is mild, the administration of
intravenous fluids may be all that is needed. Rarely, when acidosis is very severe,
bicarbonate may be given intravenously. However, bicarbonate provides only
temporary relief and may cause harm—for instance, by overloading the body with
sodium and water.
Alkalosis is excessive blood alkalinity caused by an overabundance of bicarbonate in
the blood or a loss of acid from the blood (metabolic alkalosis), or by a low level of
carbon dioxide in the blood that results from rapid or deep breathing (respiratory
alkalosis).

People may have irritability, muscle twitching, or muscle cramps, or even
muscle spasms.

Blood is tested to diagnose alkalosis.

Metabolic alkalosis is treated by replacing water and electrolytes.

Respiratory alkalosis is treated by slowing breathing.
Metabolic alkalosis develops when the body loses too much acid or gains too much
base. For example, stomach acid is lost during periods of prolonged vomiting or
when stomach acids are suctioned with a stomach tube (as is sometimes done in
hospitals). In rare cases, metabolic alkalosis develops in a person who has ingested
too much base from substances such as baking soda (bicarbonate of soda). In
addition, metabolic alkalosis can develop when excessive loss of sodium or
potassium affects the kidneys' ability to control the blood's acid-base balance. For
instance, loss of potassium sufficient to cause metabolic alkalosis may result from
an overactive adrenal gland or the use of diuretics.
Respiratory alkalosis develops when rapid, deep breathing (hyperventilation) causes
too much carbon dioxide to be expelled from the bloodstream. The most common
cause of hyperventilation, and thus respiratory alkalosis, is anxiety. Other causes
of hyperventilation and consequent respiratory alkalosis include pain, low levels of
oxygen in the blood, fever, and aspirin SOME TRADE NAMES
BAYER
overdose (which can also cause metabolic acidosis—see Acid-Base Balance:
Acidosis).
Symptoms and Diagnosis
Alkalosis may cause irritability, muscle twitching, muscle cramps, or no symptoms
at all. If the alkalosis is severe, prolonged contraction and spasms of muscles
(tetany) can develop.
A sample of blood usually taken from an artery shows that the blood is alkaline.
Treatment
Doctors usually treat metabolic alkalosis by replacing water and electrolytes
(sodium and potassium) while treating the cause. Occasionally, when metabolic
alkalosis is very severe, dilute acid is given intravenously.
With respiratory alkalosis, usually the only treatment needed is slowing down the
rate of breathing. When respiratory alkalosis is caused by anxiety, a conscious
effort to slow breathing may make the condition disappear. If pain is causing the
person to breathe rapidly, relieving the pain usually suffices. Breathing into a paper
(not a plastic) bag may help raise the carbon dioxide level in the blood as the
person breathes carbon dioxide back in after breathing it out.
Respiratory Effects
 Hyperventilation ( Kussmaul respirations)
 Shift of oxyhaemoglobin dissociation curve to the right
 Decreases 2,3 DPG levels in red cells, which opposes the effect above. (shifts the
ODC back to the left) This effect occurs after 6 hours of acidemia.
Cardiovascular Effects
 Depression of myocardial contractility (this effect predominates at pH < 7.2 )
 Sympathetic over-activity ( tachycardia, vasoconstriction, decreased arrhythmia
threshold)
 Resistance to the effects of catecholamines (occur when acidemia very severe)
 Peripheral arteriolar vasodilatation
 Venoconstriction of peripheral veins
 Vasoconstriction of pulmonary arteries
 Effects of hyperkalemia on heart
Central Nervous System Effects
 Cerebral vasodilatation leads to an increase in cerebral blood flow and
intracranial pressure (occur in acute respiratory acidosis)
 Very high pCo2 levels will cause central depression
Other Effects
 Increased bone resorption (chronic metabolic acidosis only)
 Shift of K+ out of cells causing hyperkalemia (an effect seen particularly in
metabolic acidosis and only when caused by non organic acids)
 Increase in extracellular phosphate concentration
Respiratory Effects
 Shift of oxyhaemoglobin dissociation curve to the left (impaired unloading of
oxygen
 The above effect is however balanced by an increase in 2,3 DPG levels in RBCs.
 Inhibition of respiratory drive via the central & peripheral chemoreceptors
Cardiovascular Effects
 Depression of myocardial contractility
 Arrhythmias
Central Nervous System Effects
 Cerebral vasoconstriction leads to a decrease in cerebral blood flow (result in
confusion, muoclonus, asterixis, loss of consciousness and seizures) Only
seen in acute respiratory alkalosis. Effect last only about 6 hours.
 Increased neuromuscular excitability ( resulting in paraesthesias such as
circumoral tingling & numbness; carpopedal spasm) Seen particularly in acute
respiratory alkalosis.
Other Effects
 Causes shift of hydrogen ions into cells, leading to hypokalemia.
Acid-base balance is critical for maintaining the narrow pH range that is required for various enzyme
systems to function optimally in the body.4 Normal blood pH ranges from 7.3-7.4.3 Decreased pH is termed
acidemia and is caused by an increase in the concentration of hydrogen ions ([H+]). Increased blood pH is
termed alkalemia and is caused by a decrease in the [H+].
The buffer systems that maintain this pH balance are bicarbonate, phosphates, and proteins. 4 Bicarbonate is
the most important extracellular buffer, while phosphates and proteins contribute mostly to intracellular
acid-base balance.2 The bicarbonate system is the only buffer measured for the calculation of acid-base
status in patients and is represented by the equilibrium equation: CO2 + H2O <—> H2CO3 <—> H+ + HCO3-.
This equation allows one to visualize what effects the addition of carbon dioxide (CO 2) or bicarbonate (HCO3) will have on the buffer system and the blood pH. Addition of CO2 to the system will cause the equation to
shift to the right, increasing the [H+] and, therefore, lowering the pH. Addition of HCO3- to the system will
cause the equation to shift to the left, lowering the [H+] and increasing the pH. Another way to
conceptualize this information is to simply think of CO2 as an acid and HCO3- as a base. If CO2 is increased it
will tend to cause acidemia. If HCO3- is increased, then alkalemia is the expected result.
In addition to buffers, the lungs and kidneys play a major role in acid-base homeostasis.1 The lungs function
in ventilation and they are responsible for regulating the amount of CO2 present in plasma. The kidneys are
responsible for controlling the amount of HCO3- in the blood by resorbing or excreting it in the proximal
tubule.1 Abnormalities in acid-base status are classified as to whether the primary abnormality lies with the
CO2 concentration or the HCO3- concentration ([HCO3-]). If CO2 is primarily affected, then a respiratory
disturbance is present. If HCO3- is primarily affected, then a metabolic disturbance is present.
Simple Acid-Base Disorders
Simple acid-base disorders are those that are confined to one primary alteration in CO 2 or HCO3- with or
without a compensatory response. There are four simple acid-base disorders: respiratory acidosis, metabolic
acidosis, respiratory alkalosis and metabolic alkalosis. The primary alterations will be discussed in this
section, compensatory responses will be discussed later.
Acidosis is a physiologic condition that tends to increase the concentration of hydrogen ions, which will
decrease the pH.4 This condition can be respiratory or metabolic in origin. An increase in the concentration
of CO2, expressed as pCO2, is known as respiratory acidosis. Alternatively, a decrease in the [HCO3-] is
known as metabolic acidosis. Both of these situations cause the buffer equation to shift to the right, causing
an increased [H+] and a decreased pH.
Acid-base Disorder
[H+]
pH
Primary Disturbance
Respiratory Acidosis
Increased Decreased Increased pCO2
Metabolic Acidosis
Increased Decreased Decreased [HCO3-]
Alkalosis is a physiologic condition that tends to decrease the [H+], which will increase the pH.4 Like
acidosis, alkalosis can be respiratory or metabolic in origin. A primary condition that results in decreased
pCO2 is termed respiratory alkalosis and a primary condition that results in increased [HCO3-] is termed
metabolic alkalosis. Both situations shift the bicarbonate equation to the left, resulting in a decreased [H+]
and an increased pH.
Acid-base Disorder
[H+]
pH
Primary Disturbance
Respiratory Alkalosis
Decreased Increased Decreased pCO2
Metabolic Alkalosis
Decreased Increased Increased [HCO3-]
An important distinction needs to be made at this point with respect to certain definitions in acid-base
disorders. Acidemia and alkalemia are alterations in the pH of the blood. Acidosis and alkalosis (respiratory
or metabolic) are the disorders that will cause these pH alterations. Most cases of simple acidosis or
alkalosis, such as those described above, will result in acidemia or alkalemia, respectively. However, there
are compensatory mechanisms that the body will employ in an attempt to maintain a normal pH. In these
situations it is possible to have an acidosis or alkalosis disorder and maintain a normal blood pH. There are
also mixed acid-base disorders in which opposing primary disorders can effectively cancel each other out
and produce a normal pH balance.
Etiology
Respiratory acidosis is caused by any condition which increases the pCO2 (hypercapnia).2 While increased
production of CO2 (hyperthermia, cardiopulmonary arrest) is a possible cause of hypercapnia, the vast
majority of cases are due to impaired removal of CO2 through the lungs. Hypoventilation, ventilationperfusion mismatch and impaired alveolar gas exchange can all lead to hypercapnia. Therefore, the broad
categories of disease which can lead to respiratory acidosis include: respiratory center depression,
neuromuscular disease, restrictive extrapulmonary disease, intrinsic pulmonary and small airway disease,
large airway obstruction, and increased CO2 production with impaired alveolar ventilation.2
Respiratory alkalosis is caused by conditions that will decrease the pCO2 (hypocapnia).2 Hyperventilation will
lead to hypocapnia, and it can be caused by hypoxemia, pulmonary disease, direct activation of the
respiratory center in the brainstem, overzealous mechanical ventilation, or situations causing pain, fear, or
anxiety.2
Causes of metabolic alkalosis include loss of acidic chloride-rich fluids from the body and chronic
administration of alkali. In small animal practice, most cases of metabolic alkalosis are caused by vomiting
of stomach contents.2 Abomasal reflux of hydrochloric acid (HCl) into the rumen will cause metabolic
alkalosis in ruminants.3
There are two types of metabolic acidosis. Both are characterized by a decrease in the [HCO 3-] but they
differ in how that decrease occurs. Secretional metabolic acidosis is caused by a direct loss of bicarbonaterich fluid such as diarrhea or saliva. Titrational metabolic acidosis is caused by the presence of non-CO2
acids that titrate bicarbonate causing a decreased [HCO 3-].
Titration-type metabolic acidosis is the result of increased endogenous or exogenous acids in the plasma. 4
Exogenous acids include ethylene glycol metabolites and salicylate. Endogenous acids include lactic acid,
uremic acids, and ketones. It follows then that shock, renal failure, and diabetic ketoacidosis, respectively
are common causes of titration-type metabolic acidosis.4 In cases of hypovolemic shock, perfusion is
decreased. Anaerobic metabolism is a consequence of decreased perfusion, so lactic acid accumulates. In
cases of renal failure, uremic acids will accumulate since the kidneys can not effectively excrete them. In
cases of undiagnosed or uncontrolled diabetes mellitus, cells cannot utilize glucose due to a lack of insulin.
Therefore, the body must metabolize its adipose tissue. Ketones are the byproduct of oxidation of free fatty
acids by the liver.2
Secretional and titrational metabolic acidosis can be differentiated by their effects on the anion gap (AG).
The anion gap is a calculated value based on the principle of electroneutrality which states that the total
anions in the body must always be equal to the total cations. We regularly measure the most significant
ions: Na+, K+, Cl- and HCO3-. The ions we do not regularly measure are referred to as unmeasured ions.
There are unmeasured cations (Ca+2, Mg+2, and gammaglobulins) and unmeasured anions (albumin,
phosphates, sulfates, and organic acids). The unmeasured anions outnumber the unmeasured cations and
the difference is the anion gap (Figure 1). The anion gap is easily calculated from the ions we do measure:
AG = (Na+ + K+) – (Cl- + HCO3-).4 Unmeasured cations do not undergo significant changes in health or
disease and so changes in the anion gap are almost always associated with changes in the unmeasured
anions.
Figure 1. Normal anion gap. Courtesy Dr. Perry Bain.
With secretion-type metabolic acidosis, the anion gap is normal.4 The body compensates for the increased
loss of bicarbonate by a retaining Cl-. As such, as the [HCO3-] decreases, the [Cl-] increases and the anion
gap remains normal (Figure 2). With titrational metabolic acidosis, the anion gap is increased. Remember
that titration type metabolic acidosis is associated with increased levels of exogenous or endogenous acids.
Since HCO3- is consumed to buffer these organic acids and there is no effect on the [Cl-], the anion gap
increases (Figure 3). The anion gap is therefore very useful in determining a possible etiology for metabolic
acidosis that can be confirmed based on history and clinical signs.
Figure 2. A normal anion gap in secretion acidosis. Courtesy Dr. Perry Bain.
Figure 3. Increased anion gap in titration acidosis. Courtesy Dr. Perry Bain.
Compensation
Compensation is the process whereby the body attempts to restore the normal blood pH during an acid-base
disorder. Overcompensation does not occur. As with the primary disorders, compensation can be metabolic
or respiratory in origin.
Respiratory compensation is a rapid process in which ventilation is adjusted to alter the pCO 2 in response to
a primary alteration in the [HCO3-]. Increased HCO3- levels will stimulate hypoventilation and a subsequent
rise in pCO2. Decreased HCO3- levels will produce the opposite effect. Respiratory compensation begins
within seconds and can reach maximum effectiveness within 12-24 hours.2 Respiratory compensation can
never completely regain a normal blood pH. Other factors involved in ventilation control, especially the need
for oxygen, will not allow for full compensation.7
Metabolic compensation is a slower process that occurs in two phases. Intracellular non-bicarbonate buffers
are responsible for the first phase, which occurs immediately. The kidneys are responsible for the second
phase, which begins within hours, but takes 2 to 5 days to reach maximal effectiveness. The kidneys
achieve compensation by altering net bicarbonate reabsoprtion and net acid excretion into the urine.2 Given
enough time (up to 4 weeks) metabolic compensation may be able to return the blood pH to normal in
chronic respiratory disorders.2
Acid-Base
Disturbance
Primary
Disturbance
Compensatory
Response
Compensatory
Mechanism
Respiratory acidosis
Increased pCO2
Increase [HCO3-]
Acidic urine
Respiratory alkalosis
Decreased pCO2
Decreased [HCO3-]
Alkaline urine
-
Metabolic acidosis
Decreased [HCO3 ]
Decrease pCO2
Hyperventilation
Metabolic alkalosis
Increased [HCO3-]
Increased pCO2
Hypoventilation
Diagnosis
The values that need to be examined to determine if there is an acid-base imbalance are: blood pH, pCO 2,
[HCO3-], and the anion gap. If any of these values are outside of the reference range, an acid-base
abnormality is present.4 The blood gas analysis reports pH, pCO2, [HCO3-], and pO2. Blood gas analysis is
completed on whole blood collected in heparin, and the sample should be collected anaerobically and
processed as soon as possible after collection.4 The serum chemistry profile reports the anion gap and total
CO2 (TCO2). TCO2, not to be confused with pCO2, is another measurement of [HCO3-] and is often used
synonomously.
Most simple acid-base disorders are associated with a change in pH. Once acidemia or alkalemia is detected,
the next step is to determine if the primary cause is respiratory or metabolic in nature. This requires
analysis of the pCO2 and HCO3- (TCO2) values. Changes in the HCO3- value that correspond to the change in
pH reflect a primary metabolic disorder while changes in the pCO2 that correspond to the change in pH
reflect a primary respiratory disorder. The next step is to determine if there is secondary compensation by
the body to try to correct the primary disturbance. The following algorithm presents this information in the
form of a flow chart, courtesy of Dr. Bruce LeRoy.
Mixed acid-base disorders are more difficult to diagnose and are discussed in the next section.
Mixed acid-base disorders
A mixed acid-base disorder is one in which two different primary conditions are acting at the same time.
Mixed disorders can be a combination of metabolic and respiratory disorders or a combination of different
metabolic disorders. The separate processes may have either a neutralizing or additive effect on the pH.
First, there are mixed disorders which have a neutralizing effect on pH.2 In these cases, the body may
appear to be overcompensating because the pH is normal or close to normal.4 Since the body does not
overcompensate, a mixed disorder should be suspected. A classic example of this type of disorder is a
vomiting dog who becomes dehydrated. The loss of stomach acid leads to alkalosis while the dehydration
and subsequent lactic acid buildup leads to acidosis.
Second, it is possible to have mixed disorders which have an additive effect on pH. 2 For example, a
respiratory acidosis and metabolic acidosis can occur concurrently in a dog with thoracic trauma that also
has lactic acidosis due to shock. In this case the pH would be dangerously low. Mixed disorders that have an
additive effective on the pH will always have an abnormal pH.2
Clinical Implications
Many of the clinical signs observed in animals with acid-base disturbances are the result of the primary
disease process but there are also clinical signs that can develop as a result of the acid-base disturbance
itself. Most notably, changes in neural function, cardiac output and concentrations of calcium and potassium
may all occur as a direct result of acid-base abnormalities.
Severe acidosis will impair the ability of the brain to regulate its volume, resulting in obtundation and coma.
Severe metabolic alkalosis can induce agitation, disorientation, stupor and coma. Cardiac output is also
compromised by severe acidosis. Myocardial contractility decreases when the blood pH falls below 7.2 and
acidosis may predispose the heart to ventricular arrythmias or ventricular fibrillation. 2
Serum ionized calcium concentration can be affected by acid-base abnormalities. Acidosis causes
displacement of calcium ions from their binding sites on albumin as the binding sites become protonated and
an increase in ionized calcium concentration results. Conversely, alkalosis will cause a decrease in ionized
calcium concentration and may lead to muscle twitching.2
The distribution of potassium ions between the intracellular and the extracellular fluids (and therefore the
blood [K+]) may be affected by acid-base disorders as well. As the blood [H+] rises in cases of acidosis,
more H+ ions are pumped intracellularly in exchange for K+ ions that are pumped extracellularly (Figure 4).
This exchange of ions is necessary to maintain electrical neutrality. The result is a rise in serum [K +]. This
situation has only been observed in cases of titration-type metabolic acidosis caused by non-organic
(mineral) acids like hydrochloric acid and secretion-type metabolic acidosis.2,5 Even though hyperkalemia
can develop, it is not likely to occur if renal function and urine output are normal. Clinical signs of
hyperkalemia can include muscle weakness and cardiac conduction disturbances. 2
Figure 4. Acidosis will cause more potassium ions to be moved extracellularly in
exchange for hydrogen ions. Hyperkalemia may result. Courtesy Dr. Perry Bain.
Just as hyperkalemia can accompany acidosis, hypokalemia can accompany alkalosis. 3 Hydrogen ions moves
out of the cell to increase the [H+] extracellularly, so potassium ions move inside the cell to maintain
electrical neutrality (Figure 5). Clinical signs of hypokalemia can include muscle weakness, polyuria,
polydipsia, impaired urinary concentrating ability, and cardiac arrhythmias.2
Figure 5. The exchange of potassium and hydrogen ions that can lead to
hypokalemia in cases of alkalosis. Courtesy Dr. Perry Bain.
Treatment
Note: Treatment of animals should only be performed by a licensed veterinarian. Veterinarians
should consult the current literature and current pharmacological formularies before initiating
any treatment protocol.
Treatment of respiratory acidosis and respiratory alkalosis is aimed at correcting
hypercapnia and hypocapnia, respectively.2 Therefore, causes of hypoventilation
and hyperventilation need to be investigated in order to determine the underlying
cause of hypercapnia and hypocapnia, respectively.
Treatment of metabolic alkalosis is aimed at replacing the chloride deficit in cases
where vomiting of stomach contents or diuretic administration is the underlying
cause.2 However, potassium and sodium deficits are likely to be present also, so
these must be addressed simultaneously. Therefore, the treatment of choice for
the correction of metabolic alkalosis in dogs and cats is intravenous administration
of a sodium chloride (NaCl) solution with added potassium chloride (KCl). If ongoing
gastric losses are present, H2-blocking agents can be useful to decrease gastric
acid secretion. In cases where a gastric foreign body is causing vomiting, definitive
treatment consists of surgical removal of the foreign body.2
Treatment of metabolic acidosis is dependent upon the underlying etiology. Fluid
therapy to correct dehydration and electrolyte disturbances, if present, is
warranted. However, specific treatments will vary for ethylene glycol intoxication,
lactic acidosis, renal failure, and diabetic ketoacidosis
Respiratory Alkalosis
Results from the excessive excretion of CO2, and occurs when the PaCO2 is less than 4.5kPa
(34mmHg). This is commonly seen in hyperventilation due to anxiety states. In more serious
disease states, such as severe asthma or moderate pulmonary embolism, respiratory alkalosis
may occur. Here hypoxia, due to ventilation perfusion (V/Q) abnormalities, causes
hyperventilation (in the spontaneously breathing patient). As V/Q abnormalities have little effect
on the excretion of CO2 the patients tend to have a low arterial partial pressure of oxygen (PaO2)
and low PaCO2.
Metabolic Acidosis
May result from either an excess of acid or reduced buffering capacity due to a low concentration
of bicarbonate. Excess acid may occur due increased production of organic acids or, more rarely,
ingestion of acidic compounds.
a) Excess H+ Production: this is perhaps the commonest cause of metabolic acidosis and results
from the excessive production of organic acids (usually lactic or pyruvic acid) as a result of
anaerobic metabolism. This may result from local or global tissue hypoxia. Tissue hypoxia may
occur in the following situations:



Reduced arterial oxygen content: for example anaemia or reduced PaO2.
Hypoperfusion: this may be local or global. Any cause of reduced cardiac output may
result in metabolic acidosis (eg: hypovolaemia, cardiogenic shock etc). Similarly, local
hypoperfusion in conditions such as ischaemic bowel or an ischaemic limb may cause
acidosis.
Reduced ability to use oxygen as a substrate. In conditions such as severe sepsis and
cyanide poisoning anaerobic metabolism occurs as a result of mitochondrial dysfunction.
Another form of metabolic acidosis is diabetic ketoacidosis. Cells are unable to use glucose to
produce energy due to the lack of insulin. Fats form the major source of energy and result in the
production of ketone bodies (aceto- acetate and 3-hydroxybutyrate) from acetyl coenzyme A.
Hydrogen ions are released during the production of ketones resulting in the metabolic acidosis
often observed.
b) Ingestion of Acids: this is an uncommon cause of metabolic acidosis and is usually the result
of poisoning with agents such as ethylene glycol (antifreeze) or ammonium chloride.
c) Inadequate Excretion of +: this results from renal tubular dysfunction and usually occurs in
conjunction with inadequate reabsorption of bicarbonate. Any form of renal failure may result in
metabolic acidosis. There are also specific disorders of renal hydrogen ion excretion known as
the renal tubular acidoses.
Some endocrine disturbance may also result in inadequate H+ excretion e.g. hypoaldosteronism.
Aldosterone regulates sodium reabsorption in the distal renal tubule. As sodium reabsorption and
H+ excretion are linked, a lack of aldosterone (eg: Addison's disease) tends to result in reduced
sodium reabsorption and, therefore, reduced ability to excrete H+ into the tubule resulting in
reduced H+ loss. The potassium sparing diuretics may have a similar effect as they act as
aldostrone antagonists.
d) Excessive Loss of Bicarbonate: gastro- intestinal secretions are high in sodium bicarbonate.
The loss of small bowel contents or excessive diarrhoea results in the loss of large amounts of
bicarbonate resulting in metabolic acidosis. This may be seen in such conditions as Cholera or
Crohn's disease.
Acetazolamide, a carbonic anhydrase inhibitor, used in the treatment of acute mountain sickness
and glaucoma, may cause excessive urinary bicarbonate losses. Inhibition of carbonic anhydrase
slows the conversion of carbonic acid to CO2 and water in the renal tubule. Thus, more carbonic
acid is lost in the urine and bicarbonate is not reabsorbed. The importance of carbonic anhydrase
in the reabsorption of bicarbonate was illustrated in Figure 7.
Metabolic Alkalosis
May result from the excessive loss of hydrogen ions, the excessive reabsorption of bicarbonate
or the ingestion of alkalis.
a) Excess H+ loss: gastric secretions contain large quantities of hydrogen ions. Loss of gastric
secretions, therefore, results in a metabolic alkalosis. This occurs in prolonged vomiting for
example, pyloric stenosis or anorexia nervosa.
b) Excessive Reabsorption of Bicarbonate: as discussed earlier bicarbonate and chloride
concentrations are linked. If chloride concentration falls or chloride losses are excessive then
bicarbonate will be reabsorbed to maintain electrical neutrality. Chloride may be lost from the
gastro-intestinal tract, therefore, in prolonged vomiting it is not only the loss of hydrogen ions
that results in the alkalosis but also chloride losses resulting bicarbonate reabsorption. Chloride
losses may also occur in the kidney usually as a result of diuretic drugs. The thiazide and loop
diuretics a common cause of a metabolic alkalosis. These drugs cause increased loss of chloride
in the urine resulting in excessive bicarbonate reabsorption.
c) Ingestion of Alkalis: alkaline antacids when taken in excess may result in mild metabolic
alkalosis. This is an uncommon cause of metabolic alkalosis.
Compensation
From earlier in the article it should be clear that the systems controlling acid base balance are
interlinked. As explained earlier, maintenance of pH as near normal is vital, therefore
dysfunction in one system will result in compensatory changes in the others. The three
mechanisms for compensation mentioned earlier occur at different speeds and remain effective
for different periods.
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Rapid chemical buffering: this occurs almost instantly but buffers are rapidly exhausted,
requiring the elimination of hydrogen ions to remain effective.
Respiratory compensation: the respiratory centre in the brainstem responds rapidly to
changes in CSF pH. Thus, a change in plasma pH or PaCO2 results in a change in
ventilation within minutes.
Renal compensation: the kidneys respond to disturbances in acid base balance by altering
the amount of bicarbonate reabsorbed and hydrogen ions excreted. However, it may take
up to 2 days for bicarbonate concentration to reach a new equilibrium.
These compensatory mechanisms are efficient and often return the plasma pH to near normal.
However, it is uncommon for complete compensation to occur and over compensation does not
occur.
Interpretation of Acid Base Disturbances in Blood Gas
Results
Blood gas analysis is available in the vast majority of acute hospitals in the developed world.
Increasingly blood gas machines are available for use in developing countries. In order to obtain
meaningful results from any test it is important that they are interpreted in the light of the
patient's condition. This requires knowledge of the patient's history and examination findings.
The simplest blood gas machines measure the pH, PCO2 and PO2 of the sample. More
complicated machines will also measure electrolytes and haemoglobin concentration. Most blood
gas machines also give a reading for the base excess and/or standard bicarbonate. These values
are used to assess the metabolic component of an acid base disturbance and are calculated from
the measured values outlined above. They are of particular use when the cause of the acid base
disturbance has both metabolic and respiratory components.

The Base Excess: is defined as the amount of acid (in mmol) required to restore 1
litre of blood to its normal pH, at a PCO2 of 5.3kPa (40mmHg). During the
calculation any change in pH due to the PCO2 of the sample is eliminated, therefore, the
base excess reflects only the metabolic component of any disturbance of acid base
balance. If there is a metabolic alkalosis then acid would have to be added to return the
blood pH to normal, therefore, the base excess will be positive. However, if there is a
metabolic acidosis, acid would need to be subtracted to return blood pH to normal,
therefore, the base excess is negative.
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The Standard Bicarbonate: this is similar to the base excess. It is defined as the
calculated bicarbonate concentration of the sample corrected to a PCO2 of 5.3kPa
(40mmHg). Again abnormal values for the standard bicarbonate are only due the
metabolic component of an acid base disturbance. A raised standard bicarbonate
concentration indicates a metabolic alkalosis whilst a low value indicates a metabolic
acidosis.
The flow chart on the next page indicates how to approach the interpretation of acid base
disturbances. First examine the pH; as discussed earlier a high pH indicates alkalaemia, whilst a
low pH acidaemia. Next look at the PCO2 and decide whether it accounts for the change in pH. If
the PCO2 does account for the pH then the disturbance is a primary respiratory acid base
disturbance. Now look at the base excess or standard bicarbonate) to assess any metabolic
component of the disturbance. Finally, one needs to decide if any compensation for the acid base
disturbance has happened. Compensation has occurred if there is a change in the PCO2 or base
excess in the opposite direction from that which would be expected from the pH. For example in
respiratory compensation for a metabolic acidosis the PCO2 will be low. A low PCO2 alone
causes an alkalaemia (high pH). The body is therefore using this mechanism to try to bring the
low pH caused by the metabolic acidosis back towards normal.
By now the complexity of acid base disturbance should be clear!! As in many complex concepts
examples may clarify matters. In the following examples work through the flow charts to
interpret the data.
Example 1: A 70 year old man is admitted to the intensive car unit with acute pancreatitis. He is
hypotensive, hypoxic and in acute renal failure. He has a respiratory rate of 50 breaths per
minute. The following blood gas results are obtained:
pH 7.1
PCO2 3.0kPa (22mmHg)
BE -21.0mmol
From the flow charts: firstly, he has a severe acidaemia (pH 7.1). The PCO2 is low, which does
not account for the change in pH (a PCO2 of 3.0 would tend to cause alkalaemia). Therefore, this
cannot be a primary respiratory acidosis. The base excess of -21 confirms the diagnosis of a
severe metabolic acidosis. The low PCO2 indicates that there is a degree of respiratory
compensation due to hyperventilation. These results were to be expected given the history.
Example 2: A 6 week old male child is admitted with a few days history of projectile vomiting.
The following blood gases are obtained:
pH 7.50
PCO2 6.5kPa (48mmHg)
BE +11.0mmol
The history points to pyloric stenosis. There is an alkalaemia, which is not explained by the
PCO2. The positive base excess confirms the metabolic alkalosis. The raised PCO2 indicates that
there is some respiratory compensation
Problems With Electrolyte Balance
The level of any electrolyte in the blood can become too high or too low. The main electrolytes
in the blood are sodium, potassium, calcium, magnesium, chloride, phosphate, and carbonate.
Most commonly, problems occur when the level of sodium, potassium, or calcium is abnormal.
Often, electrolyte levels change when water levels in the body change.
Doctors refer to a low electrolyte level with the prefix "hypo-" and to a high level with the prefix
"hyper-." The prefix is combined with the scientific name of the electrolyte. For example, a low
level of potassium is called hypokalemia, and a high level of sodium is called hypernatremia.
Older people are more likely to develop abnormalities in electrolyte levels for the same reasons
that they are more likely to become dehydrated or overhydrated. The main reason is that as the
body ages, the kidneys function less well. The use of certain drugs, including diuretics and
some laxatives, can increase the risk of developing electrolyte abnormalities. Problems with
walking can increase the risk of developing electrolyte abnormalities because getting fluids and
food may be difficult. Many chronic disorders (such as Paget's disease) and any disorder that
causes fever, vomiting, or diarrhea can result in electrolyte abnormalities.
Electrolyte abnormalities can be diagnosed by measuring electrolyte levels in a sample of blood
or urine. Other tests may be needed to determine the cause of the abnormalities.
To treat a low level of some electrolytes, such as sodium or potassium, doctors usually advise
eating foods rich in the electrolyte or taking supplements. If the level is very low, the electrolyte
may be given through a tube inserted in a vein (intravenously). If the level is high, treatment
consists of consuming more fluids. Sometimes fluids must be given intravenously. Sometimes
treatment is more complex because the disorder causing the electrolyte abnormality must be
treated.
Sodium
Hyponatremia: A low sodium level (hyponatremia) may result from not consuming enough
sodium in the diet, excreting too much (in sweat or urine), or being overhydrated. The sodium
level may decrease when a person drinks a lot of water without consuming enough salt (sodium
chloride), typically during hot weather when a person also sweats more. The sodium level may
decrease when large amounts of fluids that do not contain enough sodium are given
intravenously. Diuretics help the kidneys excrete excess sodium and excess water. However,
diuretics may cause the kidneys to excrete more sodium than water, resulting in a low sodium
level.
A low sodium level (and overhydration) can result when the body produces too much antidiuretic
hormone, which signals the kidneys to retain water. Overproduction of this hormone can be
caused by disorders such as pneumonia and stroke and by drugs, including anticonvulsants
(such as carbamazepine) and a type of antidepressant called selective serotonin reuptake
inhibitors (SSRIs—such as sertraline). Other disorders that can cause a low sodium level
include poorly controlled diabetes, heart failure, liver failure, and kidney disorders.
Having a low sodium level can cause confusion, drowsiness, muscle weakness, and seizures. A
rapid fall in the sodium level often causes more severe symptoms than a slow fall. A low sodium
level is restored to a normal level by gradually and steadily giving sodium and water
intravenously.
Hypernatremia: A high sodium level (hypernatremia) is usually caused by dehydration or
use of diuretics. (Diuretics may also cause the kidneys to excrete more water than sodium.)
Typically, thirst is the first symptom. A person with a high sodium level may become weak and
feel sluggish. A very high sodium level can cause confusion, paralysis, coma, and seizures. If
the sodium level is slightly high, it can be lowered by drinking fluids.
If the sodium level is very high, fluids are given intravenously. Once the body's fluids are
replaced, the high level of sodium returns to a normal level.
Potassium
Hypokalemia: A low potassium level (hypokalemia) is often caused by use of a diuretic.
Many diuretics cause the kidneys to excrete more potassium (as well as more water) in urine. A
low potassium level can also result from having diarrhea or vomiting for a long time.
A slight decrease in the potassium level rarely produces symptoms. If the potassium level
remains low for a long time, the body tends to produce less insulin. As a result, the level of
sugar in the blood may increase. If the potassium level becomes very low, fatigue, confusion,
and muscle weakness and cramps typically occur. A very low potassium level can cause
paralysis and abnormal heart rhythms (arrhythmias). For people who take digoxin (used to treat
heart failure), abnormal heart rhythms tend to develop when the potassium level is even
moderately low.
Treatment involves taking potassium supplements by mouth as a tablet or liquid or eating foods
rich in potassium. People who are taking a diuretic that causes potassium to be excreted are
sometimes also given another type of diuretic, which reduces the amount of potassium excreted
(potassium-sparing diuretic).
Hyperkalemia: A high potassium level (hyperkalemia) is much more dangerous than a low
potassium level. Most commonly, the cause is kidney failure or use of drugs that reduce the
amount of potassium excreted by the kidneys. These drugs include the diuretic spironolactone
and angiotensin-converting enzyme (ACE) inhibitors (used to lower blood pressure). When a
person who takes one of these drugs also eats potassium-rich foods or takes a potassium
supplement, the kidneys cannot always excrete the potassium. In such cases, the potassium
level in the blood can increase rapidly.
The first symptom of a high potassium level may be an abnormal heart rhythm. When doctors
suspect a high potassium level, electrocardiography (ECG) may help with the diagnosis. This
procedure can detect changes in the heart's rhythm that occur when the potassium level is high.
People with a high potassium level must stop eating potassium-rich foods and stop taking
potassium supplements. They may be given drugs that cause the body to excrete excess
potassium, such as diuretics. If the potassium level is very high or is increasing, treatment must
be started immediately. If the heart rhythm is abnormal, calcium is given intravenously. This
treatment helps protect the heart. Then diuretics or drugs that prevent potassium from being
absorbed are given to reduce the amount of potassium in the body. These drugs may be given
intravenously, taken by mouth, or given as enemas.
Calcium
Hypocalcemia: A low calcium level (hypocalcemia) can result when a disorder such as a
widespread infection in blood and other tissues (sepsis) develops suddenly. A low calcium level
can also result when the body produces less parathyroid hormone, as may occur if the
parathyroid glands are removed or damaged during neck surgery. A low level can also result
from a deficiency of vitamin D. Vitamin D helps the body absorb calcium from foods. People
may develop a vitamin D deficiency when they do not eat enough foods that contain vitamin D
or when they do not spend much time outside. (Vitamin D is formed when the skin is exposed to
direct sunlight.) Certain drugs, such as the anticonvulsants phenytoin and phenobarbital, can
interfere with the processing of vitamin D, resulting in a deficiency of vitamin D. Several
disorders, such as an underactive thyroid gland (hypothyroidism) and pancreatitis, can result in
a low calcium level.
A low calcium level makes a person weak and causes numbness in the hands or feet. It can
cause confusion or seizures. Treatment involves taking calcium supplements by mouth. If a
disorder is the cause, it should be treated.
Hypercalcemia: A high calcium level (hypercalcemia) can result when bone is broken down
and releases calcium into the bloodstream. Calcium may be released when cancer spreads to
the bone or when Paget's disease (a bone disorder) becomes so severe that it makes a person
unable to move around. Normally, parathyroid hormone helps the body control the level of
calcium in blood. An abnormally high level of parathyroid hormone can result in a high calcium
level. Usually, the cause is production of an excessive amount of hormone by a tumor in the
parathyroid gland. But some cancers, including certain lung cancers, can also produce
parathyroid hormone. A high calcium level can also result when the level of thyroid hormone is
abnormally high.
A slight increase in the calcium level may not cause any symptoms. A very high level can result
in dehydration because it causes the kidneys to excrete more water. A very high level can also
cause loss of appetite, nausea, vomiting, and confusion. A person may even go into a coma and
die.
If the calcium level is very high, rapid treatment is needed. Giving fluids intravenously helps.
Often, drugs such as calcitonin and bisphosphonates must be given intravenously for short
periods of time. These drugs decrease the amount of bone being broken down and thus the
amount of calcium released into the bloodstream. Other treatments may be needed, depending
on the cause of the high calcium level. When the cause is cancer or Paget's disease,
bisphosphonates are often taken by mouth indefinitely. When the cause is a tumor in the
parathyroid gland, surgery to remove the tumor or part of the parathyroid gland may be done.
Principle
Electrolytes commonly exist as solutions of acids, bases or salts. Furthermore, some gases may
act as electrolytes under conditions of high temperature or low pressure. Electrolyte solutions can
also result from the dissolution of some biological (e.g., DNA, polypeptides) and synthetic
polymers (e.g., polystyrene sulfonate), termed polyelectrolytes, which contain charged functional
group.
Electrolyte solutions are normally formed when a salt is placed into a solvent such as water and
the individual components dissociate due to the thermodynamic interactions between solvent and
solute molecules, in a process called solvation. For example, when table salt, NaCl, is placed in
water, the salt (a solid) dissolves into its component elements, according to the dissociation
reaction
NaCl(s) → Na+(aq) + Cl−(aq)
It is also possible for substances to react with water when they are added to it, producing ions,
e.g., carbon dioxide gas dissolves in water to produce a solution which contains hydronium,
carbonate, and hydrogen carbonate ions.
Note that molten salts can be electrolytes as well. For instance, when sodium chloride is molten,
the liquid conducts electricity.
An electrolyte in a solution may be described as concentrated if it has a high concentration of
ions, or dilute if it has a low concentration. If a high proportion of the solute dissociates to form
free ions, the electrolyte is strong; if most of the solute does not dissociate, the electrolyte is
weak. The properties of electrolytes may be exploited using electrolysis to extract constituent
elements and compounds contained within the solution.
Physiological importance
In physiology, the primary ions of electrolytes are sodium(Na+), potassium (K+), calcium (Ca2+),
magnesium (Mg2+), chloride (Cl−), hydrogen phosphate (HPO42−), and hydrogen carbonate
(HCO3−). The electric charge symbols of plus (+) and minus (−) indicate that the substance in
question is ionic in nature and has an imbalanced distribution of electrons, which is the result of
chemical dissociation.
All known higher lifeforms require a subtle and complex electrolyte balance between the
intracellular and extracellular milieu. In particular, the maintenance of precise osmotic gradients
of electrolytes is important. Such gradients affect and regulate the hydration of the body, blood
pH, and are critical for nerve and muscle function. Various mechanisms exist in living species
that keep the concentrations of different electrolytes under tight control.
Both muscle tissue and neurons are considered electric tissues of the body. Muscles and neurons
are activated by electrolyte activity between the extracellular fluid or interstitial fluid, and
intracellular fluid. Electrolytes may enter or leave the cell membrane through specialized protein
structures embedded in the plasma membrane called ion channels. For example, muscle
contraction is dependent upon the presence of calcium (Ca2+), sodium (Na+), and potassium (K+).
Without sufficient levels of these key electrolytes, muscle weakness or severe muscle
contractions may occur.
Electrolyte balance is maintained by oral, or in emergencies, intravenous (IV) intake of
electrolyte-containing substances, and is regulated by hormones, generally with the kidneys
flushing out excess levels. In humans, electrolyte homeostasis is regulated by hormones such as
antidiuretic hormone, aldosterone and parathyroid hormone. Serious electrolyte disturbances,
such as dehydration and overhydration, may lead to cardiac and neurological complications and,
unless they are rapidly resolved, will result in a medical emergency.
[edit] Measurement
Measurement of electrolytes is a commonly performed diagnostic procedure, performed via
blood testing with ion selective electrodes or urinalysis by medical technologists. The
interpretation of these values is somewhat meaningless without analysis of the clinical history
and is often impossible without parallel measurement of renal function. Electrolytes measured
most often are sodium and potassium. Chloride levels are rarely measured except for arterial
blood gas interpretation since they are inherently linked to sodium levels. One important test
conducted on urine is the specific gravity test to determine the occurrence of electrolyte
imbalance.
Electrolytes are commonly found in sports drinks. In oral rehydration therapy, electrolyte drinks
containing sodium and potassium salts replenish the body's water and electrolyte levels after
dehydration caused by exercise, diaphoresis, diarrhea, vomiting, intoxication or starvation.
Athletes exercising in extreme conditions (for three or more hours continuously e.g. marathon or
triathlon) who do not consume electrolytes risk dehydration (or hyponatremia)[1].
A simple electrolyte drink can be home-made by using the correct proportions of water, sugar,
salt, salt substitute for potassium, and baking soda.[2] However, effective electrolyte
replacements should include all electrolytes required by the body, including sodium chloride,
potassium, magnesium, and calcium that can be either obtained in a sports drink or a solid
electrolyte capsule.[3]
Electrochemistry
Main article: electrolysis
When electrodes are placed in an electrolyte and a voltage is applied, the electrolyte will conduct
electricity. Lone electrons normally cannot pass through the electrolyte; instead, a chemical
reaction occurs at the cathode consuming electrons from the anode, and another reaction occurs
at the anode producing electrons to be taken up by the cathode. As a result, a negative charge
cloud develops in the electrolyte around the cathode, and a positive charge develops around the
anode. The ions in the electrolyte move to neutralize these charges so that the reactions can
continue and the electrons can keep flowing.
For example, in a solution of ordinary salt (sodium chloride, NaCl) in water, the cathode reaction
will be
2H2O + 2e− → 2OH− + H2
and hydrogen gas will bubble up; the anode reaction is
2H2O → O2 + 4H+ + 4e−
and oxygen gas will be liberated. The positively charged sodium ions Na+ will react towards the
cathode neutralizing the negative charge of OH− there, and the negatively charged chlorine ions
Cl− will react towards the anode neutralizing the positive charge of H+ there. Without the ions
from the electrolyte, the charges around the electrode would slow down continued electron flow;
diffusion of H+ and OH− through water to the other electrode takes longer than movement of the
much more prevalent salt ions.
In other systems, the electrode reactions can involve the metals of the electrodes as well as the
ions of the electrolyte.
Electrolytic conductors are used in electronic devices where the chemical reaction at a
metal/electrolyte interface yields useful effects.
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In batteries, two metals with different electron affinities are used as electrodes; electrons flow
from one electrode to the other outside of the battery, while inside the battery the circuit is
closed by the electrolyte's ions. Here the electrode reactions convert chemical energy to
electrical energy.
In some fuel cells, a solid electrolyte or proton conductor connects the plates electrically while
keeping the hydrogen and oxygen fuel gases separated.
In electroplating tanks, the electrolyte simultaneously deposits metal onto the object to be
plated, and electrically connects that object in the circuit.
In operation-hours gauges, two thin columns of mercury are separated by a small electrolytefilled gap, and, as charge is passed through the device, the metal dissolves on one side and
plates out on the other, causing the visible gap to slowly move along.
In electrolytic capacitors the chemical effect is used to produce an extremely thin 'dielectric' or
insulating coating, while the electrolyte layer behaves as one capacitor plate.
In some hygrometers the humidity of air is sensed by measuring the conductivity of a nearly dry
electrolyte.
Hot, softened glass is an electrolytic conductor, and some glass manufacturers keep the glass
molten by passing a large current through it.
Certain substances that are called electrolytes produce ions when they dissolve in solution. Because
these ions are free to move in solution, the solution conducts electricity. Ions can be produced in
solution in either of two ways. Electrolytes can be either ionic compounds (i.e. sodium hydroxide,
potassium nitrate) that dissolve in water, giving solutions of ions, or they may be covalent compounds
that react with water and form ions in solution as a result.
1. When an ionic substance such as NaCl dissolves in H2O, the water then separates the ions
present in the NaCl crystal lattice. This process, known as dissociation, is shown below:
Na+Cl-(s) --> Na+(aq) + Cl-(aq)
2. When a polar covalent substance such as HCl dissolves in water, ions are created by the
interaction between HCl and H2O molecules. This process, known as ionization is shown below:
HCl(g) + H 2O(l) --> H3O+(aq) + Cl-(aq)
When the boiling and freezing points of solutions of electrolytes are seen, it's found that they don't
follow the simple relationship t=k*m. The boiling points are higher, and the freezing points are lower,
than what is expected.
Non-Electrolytes
Nonelectrolytes are compounds that don't ionize when they dissolve in water.
Nonelectrolytes are limited to covalent compounds. Many compounds of
carbon such as mathane CH4, benzene C6H6, ethanol C2H5OH, ether (C2H5)2O,
and formaldehyde CH2O, are nonelectrolytes. A few inorganic compounds such
as nitrous oxide N2O, phosphine PH3, and nitrogen(III) chloride NCl3, are
nonelectrolytes.
What are electrolytes?
Chemically, electrolytes are substances that become ions in solution and acquire the capacity to
conduct electricity. Electrolytes are present in the human body, and the balance of the
electrolytes in our bodies is essential for normal function of our cells and our organs.
Common electrolytes that are measured by doctors with blood testing include sodium, potassium,
chloride, and bicarbonate. The functions and normal range values for these electrolytes are
described below.
Sodium
Sodium is the major positive ion (cation) in fluid outside of cells. The chemical notation for
sodium is Na+. When combined with chloride, the resulting substance is table salt. Excess
sodium (such as that obtained from dietary sources) is excreted in the urine. Sodium regulates the
total amount of water in the body and the transmission of sodium into and out of individual cells
also plays a role in critical body functions. Many processes in the body, especially in the brain,
nervous system, and muscles, require electrical signals for communication. The movement of
sodium is critical in generation of these electrical signals. Too much or too little sodium
therefore can cause cells to malfunction, and extremes in the blood sodium levels (too much or
too little) can be fatal.
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Increased sodium (hypernatremia) in the blood occurs whenever there is excess sodium in relation to
water. There are numerous causes of hypernatremia; these may include kidney disease, too little water
intake, and loss of water due to diarrhea and/or vomiting.
A decreased concentration of sodium (hyponatremia) occurs whenever there is a relative increase in the
amount of body water relative to sodium. This happens with some diseases of the liver and kidney, in
patients with congestive heart failure, in burn victims, and in numerous other conditions.
A Normal blood sodium level is 135 - 145 milliEquivalents/liter (mEq/L), or in international
units, 135 - 145 millimoles/liter (mmol/L).
Potassium
Potassium is the major positive ion (cation) found inside of cells. The chemical notation for
potassium is K+. The proper level of potassium is essential for normal cell function. Among the
many functions of potassium in the body are regulation of the heartbeat and the function of the
muscles. A seriously abnormal increase in potassium (hyperkalemia) or decrease in potassium
(hypokalemia) can profoundly affect the nervous system and increases the chance of irregular
heartbeats (arrhythmias), which, when extreme, can be fatal.
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Increased potassium is known as hyperkalemia. Potassium is normally excreted by the kidneys, so
disorders that decrease the function of the kidneys can result in hyperkalemia. Certain medications may also
predispose an individual to hyperkalemia.
Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive loss due to heavy
sweating, vomiting, or diarrhea, eating disorders, certain medications, or other causes.
The normal blood potassium level is 3.5 - 5.0 milliEquivalents/liter (mEq/L), or in international
units, 3.5 - 5.0 millimoles/liter (mmol/L).
Chloride
Chloride is the major anion (negatively charged ion) found in the fluid outside of cells and in the
blood. An anion is the negatively charged part of certain substances such as table salt (sodium
chloride or NaCl) when dissolved in liquid. Sea water has almost the same concentration of
chloride ion as human body fluids. Chloride also plays a role in helping the body maintain a
normal balance of fluids.
The balance of chloride ion (Cl-) is closely regulated by the body. Significant increases or
decreases in chloride can have deleterious or even fatal consequences:

Increased chloride (hyperchloremia): Elevations in chloride may be seen in diarrhea, certain kidney
diseases, and sometimes in overactivity of the parathyroid glands.
 Decreased chloride (hypochloremia): Chloride is normally lost in the urine, sweat, and stomach
secretions. Excessive loss can occur from heavy sweating, vomiting, and adrenal gland and kidney disease.
The normal serum range for chloride is 98 - 108 mmol/L.
Bicarbonate
The bicarbonate ion acts as a buffer to maintain the normal levels of acidity (pH) in blood and
other fluids in the body. Bicarbonate levels are measured to monitor the acidity of the blood and
body fluids. The acidity is affected by foods or medications that we ingest and the function of the
kidneys and lungs. The chemical notation for bicarbonate on most lab reports is HCO3- or
represented as the concentration of carbon dioxide (CO2). The normal serum range for
bicarbonate is 22-30 mmol/L.
The bicarbonate test is usually performed along with tests for other blood electrolytes.
Disruptions in the normal bicarbonate level may be due to diseases that interfere with
respiratory function, kidney diseases, metabolic conditions, or other causes.