ACID – BASE, FLUIDS, AND ELECTROLYTES

EXTRA NOTES:

BASIC

Respiratory: When breathing is inadequate carbon dioxide(respiratory acid) accumulates. The extra CO2 moleculescombine with water to form carbonic acid which contributes to arelative shift towards an acid pH. The treatment, if all else fails,is to lower the PCO2 by breathing for the patient using aventilator or bag and mask.

Metabolic: When normal metabolism is impaired - acid forms,e.g., poor blood supply stops oxidative metabolism and lacticacid forms. This acid is not respiratory so, by definition, it is"metabolic acid." If severe, the patient may be in shock andrequire treatment, possibly by neutralizing this excess acid withbicarbonate, possibly by allowing time for excretion ormetabolism.

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 theODC 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 arrhythmiathreshold)

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 andintracranial 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 ofoxygen

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 inconfusion, muoclonus, asterixis, loss of consciousness and seizures) Onlyseen in acute respiratory alkalosis. Effect last only about 6 hours.

Increased neuromuscular excitability ( resulting in paraesthesias such ascircumoral tingling & numbness; carpopedal spasm) Seen particularly in acuterespiratory 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 enzymesystems to function optimally in the body.4 Normal blood pH ranges from 7.3-7.4.3 Decreased pH is termedacidemia and is caused by an increase in the concentration of hydrogen ions ([H+]). Increased blood pH istermed 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 isthe most important extracellular buffer, while phosphates and proteins contribute mostly to intracellularacid-base balance.2 The bicarbonate system is the only buffer measured for the calculation of acid-basestatus 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 (CO2) or bicarbonate (HCO3

-

) will have on the buffer system and the blood pH. Addition of CO2 to the system will cause the equation toshift to the right, increasing the [H+] and, therefore, lowering the pH. Addition of HCO3

- to the system willcause the equation to shift to the left, lowering the [H+] and increasing the pH. Another way toconceptualize this information is to simply think of CO2 as an acid and HCO3

- as a base. If CO2 is increased itwill 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 functionin ventilation and they are responsible for regulating the amount of CO2 present in plasma. The kidneys areresponsible for controlling the amount of HCO3

- in the blood by resorbing or excreting it in the proximaltubule.1 Abnormalities in acid-base status are classified as to whether the primary abnormality lies with theCO2 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 CO2 or HCO3- with or

without a compensatory response. There are four simple acid-base disorders: respiratory acidosis, metabolicacidosis, respiratory alkalosis and metabolic alkalosis. The primary alterations will be discussed in thissection, compensatory responses will be discussed later.

Acidosis is a physiologic condition that tends to increase the concentration of hydrogen ions, which willdecrease the pH.4 This condition can be respiratory or metabolic in origin. An increase in the concentrationof CO2, expressed as pCO2, is known as respiratory acidosis. Alternatively, a decrease in the [HCO3

-] isknown as metabolic acidosis. Both of these situations cause the buffer equation to shift to the right, causingan 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 Likeacidosis, alkalosis can be respiratory or metabolic in origin. A primary condition that results in decreasedpCO2 is termed respiratory alkalosis and a primary condition that results in increased [HCO3

-] is termedmetabolic 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-basedisorders. Acidemia and alkalemia are alterations in the pH of the blood. Acidosis and alkalosis (respiratoryor metabolic) are the disorders that will cause these pH alterations. Most cases of simple acidosis oralkalosis, such as those described above, will result in acidemia or alkalemia, respectively. However, thereare compensatory mechanisms that the body will employ in an attempt to maintain a normal pH. In thesesituations it is possible to have an acidosis or alkalosis disorder and maintain a normal blood pH. There arealso mixed acid-base disorders in which opposing primary disorders can effectively cancel each other outand produce a normal pH balance.

Etiology

Respiratory acidosis is caused by any condition which increases the pCO2 (hypercapnia).2 While increasedproduction of CO2 (hyperthermia, cardiopulmonary arrest) is a possible cause of hypercapnia, the vastmajority of cases are due to impaired removal of CO2 through the lungs. Hypoventilation, ventilation-perfusion mismatch and impaired alveolar gas exchange can all lead to hypercapnia. Therefore, the broadcategories 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 willlead to hypocapnia, and it can be caused by hypoxemia, pulmonary disease, direct activation of therespiratory center in the brainstem, overzealous mechanical ventilation, or situations causing pain, fear, oranxiety.2

Causes of metabolic alkalosis include loss of acidic chloride-rich fluids from the body and chronicadministration of alkali. In small animal practice, most cases of metabolic alkalosis are caused by vomitingof stomach contents.2 Abomasal reflux of hydrochloric acid (HCl) into the rumen will cause metabolicalkalosis in ruminants.3

There are two types of metabolic acidosis. Both are characterized by a decrease in the [HCO3-] but they

differ in how that decrease occurs. Secretional metabolic acidosis is caused by a direct loss of bicarbonate-rich fluid such as diarrhea or saliva. Titrational metabolic acidosis is caused by the presence of non-CO2

acids that titrate bicarbonate causing a decreased [HCO3-].

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, respectivelyare common causes of titration-type metabolic acidosis.4 In cases of hypovolemic shock, perfusion isdecreased. Anaerobic metabolism is a consequence of decreased perfusion, so lactic acid accumulates. Incases of renal failure, uremic acids will accumulate since the kidneys can not effectively excrete them. Incases 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 fattyacids 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 totalanions in the body must always be equal to the total cations. We regularly measure the most significantions: 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 andthe 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 ordisease and so changes in the anion gap are almost always associated with changes in the unmeasuredanions.

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 increasedloss of bicarbonate by a retaining Cl-. As such, as the [HCO3

-] decreases, the [Cl-] increases and the aniongap remains normal (Figure 2). With titrational metabolic acidosis, the anion gap is increased. Rememberthat 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 metabolicacidosis 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-basedisorder. Overcompensation does not occur. As with the primary disorders, compensation can be metabolicor respiratory in origin.

Respiratory compensation is a rapid process in which ventilation is adjusted to alter the pCO2 in response toa 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 cannever completely regain a normal blood pH. Other factors involved in ventilation control, especially the needfor oxygen, will not allow for full compensation.7

Metabolic compensation is a slower process that occurs in two phases. Intracellular non-bicarbonate buffersare responsible for the first phase, which occurs immediately. The kidneys are responsible for the secondphase, which begins within hours, but takes 2 to 5 days to reach maximal effectiveness. The kidneysachieve compensation by altering net bicarbonate reabsoprtion and net acid excretion into the urine.2 Givenenough time (up to 4 weeks) metabolic compensation may be able to return the blood pH to normal inchronic respiratory disorders.2

Acid-BaseDisturbance

PrimaryDisturbance

CompensatoryResponse

CompensatoryMechanism

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, pCO2,[HCO3

-], and the anion gap. If any of these values are outside of the reference range, an acid-baseabnormality is present.4 The blood gas analysis reports pH, pCO2, [HCO3

-], and pO2. Blood gas analysis iscompleted on whole blood collected in heparin, and the sample should be collected anaerobically andprocessed as soon as possible after collection.4 The serum chemistry profile reports the anion gap and totalCO2 (TCO2). TCO2, not to be confused with pCO2, is another measurement of [HCO3

-] and is often usedsynonomously.

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 requiresanalysis of the pCO2 and HCO3- (TCO2) values. Changes in the HCO3

- value that correspond to the change inpH reflect a primary metabolic disorder while changes in the pCO2 that correspond to the change in pHreflect a primary respiratory disorder. The next step is to determine if there is secondary compensation bythe body to try to correct the primary disturbance. The following algorithm presents this information in theform 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 differentmetabolic 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 mayappear to be overcompensating because the pH is normal or close to normal.4 Since the body does notovercompensate, a mixed disorder should be suspected. A classic example of this type of disorder is avomiting dog who becomes dehydrated. The loss of stomach acid leads to alkalosis while the dehydrationand 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, arespiratory acidosis and metabolic acidosis can occur concurrently in a dog with thoracic trauma that alsohas lactic acidosis due to shock. In this case the pH would be dangerously low. Mixed disorders that have anadditive 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 primarydisease process but there are also clinical signs that can develop as a result of the acid-base disturbanceitself. Most notably, changes in neural function, cardiac output and concentrations of calcium and potassiummay 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 alsocompromised by severe acidosis. Myocardial contractility decreases when the blood pH falls below 7.2 andacidosis may predispose the heart to ventricular arrythmias or ventricular fibrillation.2

Serum ionized calcium concentration can be affected by acid-base abnormalities. Acidosis causesdisplacement of calcium ions from their binding sites on albumin as the binding sites become protonated andan increase in ionized calcium concentration results. Conversely, alkalosis will cause a decrease in ionizedcalcium concentration and may lead to muscle twitching.2

The distribution of potassium ions between the intracellular and the extracellular fluids (and therefore theblood [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+]. Thissituation 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 hyperkalemiacan develop, it is not likely to occur if renal function and urine output are normal. Clinical signs ofhyperkalemia can include muscle weakness and cardiac conduction disturbances.2

Figure 4. Acidosis will cause more potassium ions to be moved extracellularly inexchange for hydrogen ions. Hyperkalemia may result. Courtesy Dr. Perry Bain.

Just as hyperkalemia can accompany acidosis, hypokalemia can accompany alkalosis.3 Hydrogen ions movesout of the cell to increase the [H+] extracellularly, so potassium ions move inside the cell to maintainelectrical 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 tohypokalemia in cases of alkalosis. Courtesy Dr. Perry Bain.

Treatment

Note: Treatment of animals should only be performed by a licensed veterinarian. Veterinariansshould consult the current literature and current pharmacological formularies before initiatingany 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 seriousdisease states, such as severe asthma or moderate pulmonary embolism, respiratory alkalosismay occur. Here hypoxia, due to ventilation perfusion (V/Q) abnormalities, causeshyperventilation (in the spontaneously breathing patient). As V/Q abnormalities have little effecton 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 concentrationof 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 resultsfrom the excessive production of organic acids (usually lactic or pyruvic acid) as a result ofanaerobic metabolism. This may result from local or global tissue hypoxia. Tissue hypoxia mayoccur 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, localhypoperfusion in conditions such as ischaemic bowel or an ischaemic limb may causeacidosis.

Reduced ability to use oxygen as a substrate. In conditions such as severe sepsis andcyanide poisoning anaerobic metabolism occurs as a result of mitochondrial dysfunction.

Another form of metabolic acidosis is diabetic ketoacidosis. Cells are unable to use glucose toproduce energy due to the lack of insulin. Fats form the major source of energy and result in theproduction 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 acidosisoften observed.

b) Ingestion of Acids: this is an uncommon cause of metabolic acidosis and is usually the resultof poisoning with agents such as ethylene glycol (antifreeze) or ammonium chloride.

c) Inadequate Excretion of +: this results from renal tubular dysfunction and usually occurs inconjunction with inadequate reabsorption of bicarbonate. Any form of renal failure may result inmetabolic acidosis. There are also specific disorders of renal hydrogen ion excretion known asthe 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 andH+ excretion are linked, a lack of aldosterone (eg: Addison's disease) tends to result in reducedsodium reabsorption and, therefore, reduced ability to excrete H+ into the tubule resulting inreduced H+ loss. The potassium sparing diuretics may have a similar effect as they act asaldostrone 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 ofbicarbonate resulting in metabolic acidosis. This may be seen in such conditions as Cholera orCrohn's disease.

Acetazolamide, a carbonic anhydrase inhibitor, used in the treatment of acute mountain sicknessand glaucoma, may cause excessive urinary bicarbonate losses. Inhibition of carbonic anhydraseslows the conversion of carbonic acid to CO2 and water in the renal tubule. Thus, more carbonicacid is lost in the urine and bicarbonate is not reabsorbed. The importance of carbonic anhydrasein the reabsorption of bicarbonate was illustrated in Figure 7.

Metabolic Alkalosis

May result from the excessive loss of hydrogen ions, the excessive reabsorption of bicarbonateor the ingestion of alkalis.

a) Excess H+ loss: gastric secretions contain large quantities of hydrogen ions. Loss of gastricsecretions, therefore, results in a metabolic alkalosis. This occurs in prolonged vomiting forexample, pyloric stenosis or anorexia nervosa.

b) Excessive Reabsorption of Bicarbonate: as discussed earlier bicarbonate and chlorideconcentrations are linked. If chloride concentration falls or chloride losses are excessive thenbicarbonate will be reabsorbed to maintain electrical neutrality. Chloride may be lost from thegastro-intestinal tract, therefore, in prolonged vomiting it is not only the loss of hydrogen ionsthat results in the alkalosis but also chloride losses resulting bicarbonate reabsorption. Chloridelosses may also occur in the kidney usually as a result of diuretic drugs. The thiazide and loopdiuretics a common cause of a metabolic alkalosis. These drugs cause increased loss of chloridein the urine resulting in excessive bicarbonate reabsorption.

c) Ingestion of Alkalis: alkaline antacids when taken in excess may result in mild metabolicalkalosis. 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 areinterlinked. As explained earlier, maintenance of pH as near normal is vital, thereforedysfunction in one system will result in compensatory changes in the others. The threemechanisms for compensation mentioned earlier occur at different speeds and remain effectivefor different periods.

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 tochanges in CSF pH. Thus, a change in plasma pH or PaCO2 results in a change inventilation within minutes.

Renal compensation: the kidneys respond to disturbances in acid base balance by alteringthe amount of bicarbonate reabsorbed and hydrogen ions excreted. However, it may takeup 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 notoccur.

Interpretation of Acid Base Disturbances in Blood GasResults

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 obtainmeaningful results from any test it is important that they are interpreted in the light of thepatient'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. Morecomplicated machines will also measure electrolytes and haemoglobin concentration. Most bloodgas machines also give a reading for the base excess and/or standard bicarbonate. These valuesare used to assess the metabolic component of an acid base disturbance and are calculated fromthe measured values outlined above. They are of particular use when the cause of the acid basedisturbance has both metabolic and respiratory components.

The Base Excess: is defined as the amount of acid (in mmol) required to restore 1litre of blood to its normal pH, at a PCO2 of 5.3kPa (40mmHg). During thecalculation any change in pH due to the PCO2 of the sample is eliminated, therefore, thebase excess reflects only the metabolic component of any disturbance of acid basebalance. If there is a metabolic alkalosis then acid would have to be added to return theblood pH to normal, therefore, the base excess will be positive. However, if there is ametabolic acidosis, acid would need to be subtracted to return blood pH to normal,therefore, the base excess is negative.

The Standard Bicarbonate: this is similar to the base excess. It is defined as thecalculated bicarbonate concentration of the sample corrected to a PCO2 of 5.3kPa(40mmHg). Again abnormal values for the standard bicarbonate are only due themetabolic component of an acid base disturbance. A raised standard bicarbonateconcentration indicates a metabolic alkalosis whilst a low value indicates a metabolicacidosis.

The flow chart on the next page indicates how to approach the interpretation of acid basedisturbances. First examine the pH; as discussed earlier a high pH indicates alkalaemia, whilst alow pH acidaemia. Next look at the PCO2 and decide whether it accounts for the change in pH. Ifthe PCO2 does account for the pH then the disturbance is a primary respiratory acid basedisturbance. Now look at the base excess or standard bicarbonate) to assess any metaboliccomponent of the disturbance. Finally, one needs to decide if any compensation for the acid basedisturbance has happened. Compensation has occurred if there is a change in the PCO2 or baseexcess in the opposite direction from that which would be expected from the pH. For example inrespiratory compensation for a metabolic acidosis the PCO2 will be low. A low PCO2 alonecauses an alkalaemia (high pH). The body is therefore using this mechanism to try to bring thelow pH caused by the metabolic acidosis back towards normal.

By now the complexity of acid base disturbance should be clear!! As in many complex conceptsexamples may clarify matters. In the following examples work through the flow charts tointerpret the data.

Example 1: A 70 year old man is admitted to the intensive car unit with acute pancreatitis. He ishypotensive, hypoxic and in acute renal failure. He has a respiratory rate of 50 breaths perminute. 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 doesnot account for the change in pH (a PCO2 of 3.0 would tend to cause alkalaemia). Therefore, thiscannot be a primary respiratory acidosis. The base excess of -21 confirms the diagnosis of asevere metabolic acidosis. The low PCO2 indicates that there is a degree of respiratorycompensation 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 thePCO2. The positive base excess confirms the metabolic alkalosis. The raised PCO2 indicates thatthere 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 mayact as electrolytes under conditions of high temperature or low pressure. Electrolyte solutions canalso result from the dissolution of some biological (e.g., DNA, polypeptides) and syntheticpolymers (e.g., polystyrene sulfonate), termed polyelectrolytes, which contain charged functionalgroup.

Electrolyte solutions are normally formed when a salt is placed into a solvent such as water andthe individual components dissociate due to the thermodynamic interactions between solvent andsolute molecules, in a process called solvation. For example, when table salt, NaCl, is placed inwater, the salt (a solid) dissolves into its component elements, according to the dissociationreaction

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 ofions, or dilute if it has a low concentration. If a high proportion of the solute dissociates to formfree ions, the electrolyte is strong; if most of the solute does not dissociate, the electrolyte isweak. The properties of electrolytes may be exploited using electrolysis to extract constituentelements 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 (HPO4

2−), 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 ofchemical dissociation.

All known higher lifeforms require a subtle and complex electrolyte balance between theintracellular and extracellular milieu. In particular, the maintenance of precise osmotic gradientsof electrolytes is important. Such gradients affect and regulate the hydration of the body, bloodpH, and are critical for nerve and muscle function. Various mechanisms exist in living speciesthat keep the concentrations of different electrolytes under tight control.

Both muscle tissue and neurons are considered electric tissues of the body. Muscles and neuronsare activated by electrolyte activity between the extracellular fluid or interstitial fluid, andintracellular fluid. Electrolytes may enter or leave the cell membrane through specialized proteinstructures embedded in the plasma membrane called ion channels. For example, musclecontraction is dependent upon the presence of calcium (Ca2+), sodium (Na+), and potassium (K+).Without sufficient levels of these key electrolytes, muscle weakness or severe musclecontractions may occur.

Electrolyte balance is maintained by oral, or in emergencies, intravenous (IV) intake ofelectrolyte-containing substances, and is regulated by hormones, generally with the kidneysflushing 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 viablood testing with ion selective electrodes or urinalysis by medical technologists. Theinterpretation of these values is somewhat meaningless without analysis of the clinical historyand is often impossible without parallel measurement of renal function. Electrolytes measuredmost often are sodium and potassium. Chloride levels are rarely measured except for arterialblood gas interpretation since they are inherently linked to sodium levels. One important testconducted on urine is the specific gravity test to determine the occurrence of electrolyteimbalance.

Electrolytes are commonly found in sports drinks. In oral rehydration therapy, electrolyte drinkscontaining sodium and potassium salts replenish the body's water and electrolyte levels afterdehydration caused by exercise, diaphoresis, diarrhea, vomiting, intoxication or starvation.Athletes exercising in extreme conditions (for three or more hours continuously e.g. marathon ortriathlon) 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 electrolytereplacements 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 solidelectrolyte capsule.[3]

Electrochemistry

Main article: electrolysis

When electrodes are placed in an electrolyte and a voltage is applied, the electrolyte will conductelectricity. Lone electrons normally cannot pass through the electrolyte; instead, a chemicalreaction occurs at the cathode consuming electrons from the anode, and another reaction occursat the anode producing electrons to be taken up by the cathode. As a result, a negative chargecloud develops in the electrolyte around the cathode, and a positive charge develops around theanode. The ions in the electrolyte move to neutralize these charges so that the reactions cancontinue and the electrons can keep flowing.

For example, in a solution of ordinary salt (sodium chloride, NaCl) in water, the cathode reactionwill 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 thecathode neutralizing the negative charge of OH− there, and the negatively charged chlorine ionsCl− will react towards the anode neutralizing the positive charge of H+ there. Without the ionsfrom 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 themuch more prevalent salt ions.

In other systems, the electrode reactions can involve the metals of the electrodes as well as theions of the electrolyte.

Electrolytic conductors are used in electronic devices where the chemical reaction at ametal/electrolyte interface yields useful effects.

In batteries, two metals with different electron affinities are used as electrodes; electrons flowfrom one electrode to the other outside of the battery, while inside the battery the circuit isclosed by the electrolyte's ions. Here the electrode reactions convert chemical energy toelectrical energy.

In some fuel cells, a solid electrolyte or proton conductor connects the plates electrically whilekeeping the hydrogen and oxygen fuel gases separated.

In electroplating tanks, the electrolyte simultaneously deposits metal onto the object to beplated, and electrically connects that object in the circuit.

In operation-hours gauges, two thin columns of mercury are separated by a small electrolyte-filled gap, and, as charge is passed through the device, the metal dissolves on one side andplates 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' orinsulating 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 dryelectrolyte.

Hot, softened glass is an electrolytic conductor, and some glass manufacturers keep the glassmolten 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 ionspresent 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 theinteraction 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 toconduct electricity. Electrolytes are present in the human body, and the balance of theelectrolytes 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 forsodium 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 thetotal amount of water in the body and the transmission of sodium into and out of individual cellsalso 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 sodiumtherefore can cause cells to malfunction, and extremes in the blood sodium levels (too much or

too little) can be fatal.

Increased sodium (hypernatremia) in the blood occurs whenever there is excess sodium in relation towater. 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 theamount 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 internationalunits, 135 - 145 millimoles/liter (mmol/L).

Potassium

Potassium is the major positive ion (cation) found inside of cells. The chemical notation forpotassium is K+. The proper level of potassium is essential for normal cell function. Among themany functions of potassium in the body are regulation of the heartbeat and the function of themuscles. 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.

Increased potassium is known as hyperkalemia. Potassium is normally excreted by the kidneys, sodisorders 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 heavysweating, 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 internationalunits, 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 theblood. 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 ofchloride 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 ordecreases in chloride can have deleterious or even fatal consequences:

Increased chloride (hyperchloremia): Elevations in chloride may be seen in diarrhea, certain kidneydiseases, and sometimes in overactivity of the parathyroid glands.

Decreased chloride (hypochloremia): Chloride is normally lost in the urine, sweat, and stomachsecretions. 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 andother fluids in the body. Bicarbonate levels are measured to monitor the acidity of the blood andbody 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- orrepresented 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.