1.

ACID-BASE IMBALANCES

 Acid-base balance occurs through control of hydrogen ion (H+) production and
elimination.
 Plasma pH – is an indicator of hydrogen ion (H+) concentration.
 The level of free hydrogen ions, formed from acids, must be rigidly controlled for proper
function. Even small changes in the free hydrogen ion level or pH of the body fluids can
cause major problems in function.
 Keeping the pH within the normal range involves balancing acids and bases in body
fluids.
 Normal pH ranges from 7.35 to 7.45  controlled by the homeostatic mechanisms.

These Mechanisms Consist of:

 Buffer systems
 The kidneys
 The lungs

 The hydrogen ion concentration is extremely important:

 The greater the concentration, the more acidic the solution and the lower the pH.
 The lower the H+ concentration, the more alkaline the solution and the higher the
pH.

 Keeping the pH of the blood within the normal range is important because changes from
normal interfere with many normal physiologic functions. These changes include:
 Changing the shape and reducing the function of hormones and enzymes
 Changing the distribution of other electrolytes, causing fluid and electrolyte
imbalances
 Changing excitable membranes, making the heart, nerves, muscles, and the GI
tract either less or more active than normal
 Decreasing the effectiveness of many drugs
 Fortunately, the body has many mechanisms to ensure minimal changes in
free hydrogen ion level.

ACID-BASE CHEMISTRY

ACIDS are substances that release hydrogen ions when dissolved in water (H2O). An acid in
solution  increases the amount of free hydrogen ions in that solution.
 A strong acid such as hydrochloric acid (HCL) – separates completely in water and
readily releases all of its hydrogen ions.
 A weak acid such as acetic acid (CH3COOH) – does not completely separate in water; it
releases only some of its hydrogen ions.

BASES

A base is a substance that binds free hydrogen ions in solution. Bases are “hydrogen acceptors”
that reduce the amount of free hydrogen ions in solution.
 Strong bases include sodium hydroxide (NaOH) and ammonia (NH3) – bind hydrogen
ions easily.
 Weak bases such as aluminum hydroxide (AlOH3) and bicarbonate (HCO3) – bind
hydrogen ions less readily.
 Although bicarbonate is a weak base, bicarbonate ions in the body prevent
major changes in body fluid pH.
ACID-BASE REGULATORY MECHANISMS

BUFFER SYSTEMS

 Buffer systems are the first line of defense and prevent major changes in the pH of body
fluids by removing or releasing H+  they can act quickly to prevent excessive changes
in H+ concentration.
 Hydrogen ions are buffered by both intracellular and extracellular buffers.
 Bicarbonate-carbonic acid buffer system – is the body’s major extracellular buffer
system which is assessed when arterial blood gasses are measured.
 Normally, there are 20 parts of bicarbonate (HCO3) to one part of carbonic acid
(H2CO3)  if this ratio is altered, the pH will change.
 If either bicarbonate or carbonic acid is increased or decreased so that the 20:1
ratio is no longer maintained  results in an acid-base imbalance.

 Less important buffer systems in the ECF include the inorganic phosphates and the
plasma proteins.
 Intracellular buffers include proteins, organic and inorganic phosphates, and in red blood
cells, haemoglobin.

RESPIRATORY ACID-BASE CONTROL MECHANISMS

 When chemical buffers alone cannot prevent changes in blood pH, the respiratory system
is the second line of defense against changes.
 Breathing controls the amount of free hydrogen ions by controlling the amount of carbon
dioxide (CO2) in arterial blood.
 The lungs, under the control of the medulla, control the CO2 and thus the carbonic acid
content of the ECF  by adjusting ventilation in response to the amount of CO2 in the
blood.
 A rise in the partial pressure of CO2 in arterial blood (PaCO2) is a powerful stimulant
of respiration.
 The partial pressure of oxygen in arterial blood (PaO2)  also influences respiration.
However, its effect is not as marked as that produced by the PaCO2.
 In metabolic acidosis  the respiratory rate increases, causing greater
elimination of CO2 (to reduce the acid load).
 In metabolic alkalosis  the respiratory rate decreases, causing CO2 retention
(to increase the acid load).
 Hyperventilation  increase in rate and depth of breathing  decreased CO2.
 Hypoventilation  decrease in rate and depth of breathing  increased CO2.

RENAL ACID-BASE CONROL MECHANISMS

 The kidneys are the third line of defense against wide changes in body fluid pH.
 Renal mechanisms are stronger for regulating acid-base balance but take longer than
chemical and respiratory mechanisms to completely respond  they take 24 to 48 hours
to respond.
 The kidney movement of bicarbonate is the first renal control mechanism.
 Much of the bicarbonate made in other body areas is excreted in the urine.
 When blood hydrogen ion levels are low, the bicarbonate remains in the urine and
is excreted.
 When hydrogen ion excess occurs, the kidney tubules also can make additional
bicarbonate that will be reabsorbed.
 Formation of acids is the second renal control mechanisms. It occurs through the
phosphate-buffering system inside the cells of the kidney tubules.
 Once the hydrogen ion is in the urine, it binds to phosphate ions  forming an
acid, H2PO4  which is excreted in the urine.
  Formation of ammonium is the third renal control mechanisms.
 Ammonia (NH3) – which is formed during normal protein breakdown
converted into ammonium (NH+4).
 The ammonia is secreted into the urine, where it can combine with hydrogen ions
to form ammonium.
 The ammonium “traps” the hydrogen ions and then allows them to be excreted in
the urine  the result is a loss of hydrogen ions and an increase in blood pH.

COMPENSATION

 In the process of compensation – the body adapts to attempt to correct changes in blood
pH. The ability of the body to adapt to change.
 A pH below 6.9 or above 7.8 – is always fatal.
 The normal pH range for human ECF is 7.35 to 7.45.
 Both the kidneys and the lungs can compensate for acid-base imbalances, but they are not
equal in their compensatory responses.
 The respiratory system is much more sensitive to acid-base changes and can begin
compensation efforts within seconds to minutes after a change in pHhowever; these
efforts are limited and can be overwhelmed easily.
 The renal compensatory mechanisms are much more powerful and result in rapid changes
in ECF composition  however; these more powerful mechanisms are not fully triggered
unless the acid-base imbalance continues for several hours to several days.
 Respiratory compensation occurs through the lungs, usually correct for acid-base
imbalances from metabolic problems.
 To bring the pH level to normal  breathing is triggered in response to increased
CO2 levels  both the rate and depth of respiration is increase  these
respiratory efforts cause the blood to lose CO2 with each exhalation  so ECF
levels of CO2 and free hydrogen ions gradually decrease.
 When the lungs can fully compensate  the pH returns to normal.

 Renal compensation results when a healthy kidney works to correct for changes in the
blood pH that occur when the respiratory system is either overwhelmed or is not healthy.
 For example: A person with COPD, the respiratory system cannot exchange
gasses adequately  CO2 is retained continually and the blood pH falls (become
acidic).
 To oppose the process, the kidney excretes more hydrogen ions and increases the
reabsorption of bicarbonate back in the blood  as a result, the blood pH remains
either within or closer to the normal range.
 When these backup mechanisms are completely effective  acid-base problems
are fully compensated  and the pH of the blood returns to normal even though
the levels of oxygen and bicarbonate are abnormal.
 Sometimes, the respiratory problem causing the acid-base imbalance is so severe
that the kidney actions can only partially compensate  the pH is not quite
normal.
 Partial compensation is helpful because it prevents the acid-base
imbalance from becoming severe or life-threatening.
ACID-BASE IMBALANCES

Acid-base imbalances are changes in the blood hydrogen ion level or pH  these changes are
caused by problems with the acid-base regulatory mechanisms of the body or by exposure to
dangerous conditions.

 Acidosis – reflects an imbalance in which the blood pH is below normal.

 Alkalosis – reflects an imbalance in which the blood pH is above normal.

 Acid-base imbalances impair the function of many organs and can be life-threatening.

ACIDOSIS

Pathophysiology:

 In acidosis  the acid-base balance of the blood and other ECF is upset by an excess of
hydrogen ion (H+).
 This problem is reflected as an arterial blood pH below 7.35.

 Acidosis is not a disease; it is a condition caused by a disorder or pathologic processes.

 Acidosis can be caused by metabolic problems, respiratory problems, or both.
 Patients at greater risk for acute acidosis are those with problems that impair
breathing.
 Older adults with chronic health problems are at a greater risk for developing
acidosis.

 Acidosis can result from an actual or relative increase in the amount or strength of acids.
 An actual acid excess result in acidosis by either overproducing acids (and
release of hydrogen ions) or undereliminating normally produced acids (retention
of hydrogen ions).
 Examples of problems that actually increase acid production are: diabetic
ketoacidosis and seizures.
 Examples of problems that actually decrease acid elimination are:
respiratory impairment and renal impairment.

 In relative acidosis – the amount or strength of acids does not increase, instead,
the amount or strength (or both) of the bases decreases (to create a base deficit)
 which makes the fluid relatively acidic than basic  caused by either
overeliminating bases (bicarbonate ions [HCO-3]) or overproducing bases.
 Examples of problems that underproduce bases are: pancreatitis and
dehydration.
 A condition that overeliminates bases is: diarrhea.

 Regardless of its origin, acidosis causes major changes in body function.

 The main problems are related to the fact that hydrogen ions are positively charged ions
 an increase in H+ creates imbalances of other positively charged electrolytes,
especially potassium.
 These electrolyte imbalances then disrupt the functions of the nerves, cardiac
muscle and skeletal muscle.
 The early manifestations of acidosis first appear in the: musculoskeletal, cardiac,
respiratory, and central nervous systems.
 Even slight increases in blood hydrogen ion levels reduce the activity of many hormones
and enzymes  leading to death.
 Many drugs are less effective during acidosis.

 Acidosis can be caused by metabolic problems, respiratory problems, or combined

metabolic and respiratory problems.
 1.1. Metabolic Acidosis

 Four processes can result in metabolic acidosis:

1. Overproduction of hydrogen ions – can occur with excessive breakdown of fatty
acids, anaerobic (lactic acidosis), and excessive intake of acids.
 Excessive breakdown of fatty acids occurs with diabetic ketoacidosis or
starvation.
= When glucose is not available for fuel  the body breaks down fats (lipids)
 the products of excessive fatty acids breakdown  are strong acids
(ketoacids)  which release large amounts of hydrogen ions.

 Lactic acidosis occurs when cells are forced to use glucose without adequate
oxygen (anaerobic metabolism)  as a result; glucose is incompletely broken
down  and forms lactic acid.
= Lactic acid leaves the cell, enters blood, and releases hydrogen ions 
causing acidosis.
= Lactic acidosis occurs whenever the body has too little oxygen such as
during heavy exercise, seizure activity, fever and reduced oxygen intake.

 Excessive intake of acids floods the body with hydrogen ions.

= Agents that cause acidosis when ingested in excess include: alcoholic
beverages, methyl alcohol, and acetylsalicylic acid (aspirin).

2. Underelimination of hydrogen ions – leads to acidosis when hydrogen ions are

produced at the normal rate but are not removed at the same rate they produced.
 Most hydrogen ion loss occurs through the lungs and the kidneys.
= Kidney failure causes acidosis when the kidney tubules cannot secrete
hydrogen ions into the urine  as a result; too many hydrogen ions are
retained.

3. Underproduction of bicarbonate ions (base deficit) – leads to acidosis when

hydrogen ion production and removal are normal but too few bicarbonate ions are
present to balance the hydrogen ion.
 Such base deficits occur when bicarbonate ions are not produced at the normal
rate  because bicarbonate is made in the kidneys and in the pancreas, renal
failure and impaired liver or pancreatic function  can cause base-deficit
acidosis.

4. Overelimination of bicarbonate ions (base-deficit) – leads to acidosis when

hydrogen ion production and removal are normal but too many bicarbonate ions have
been lost.
 One cause of base-deficit acidosis is diarrhea.

1.2. RESPIRATORY ACIDOSIS

Respiratory acidosis – results any area of the respiratory function is impaired  reducing the
exchange of oxygen (O2) and carbon dioxide (CO2)  causing CO2 retention – because any
increase in CO2 levels causes the same increase in hydrogen ion levels, CO2 retention  leads
to acidosis.

 Unlike metabolic acidosis, respiratory acidosis results from only one mechanism –
retention of CO2 causing increased production of free hydrogen ions.
 Respiratory acidosis is caused by four types of problems:
 1. Respiratory depression – caused by reduced function of the brainstem neurons that
trigger breathing movements  resulting in a reduced rate and depth of breathing 
leading to poor gas exchange and retention of carbon dioxide.

 Respiration can be depressed also by anesthetic drugs (especially opioids) and

poisons such as methyl alcohol, pesticides, and botulinus toxin.
 Physical depression of respiration occurs when neurons are damaged or destroyed
by trauma or when problems in other areas of the brain increases the ICP 
causing edema which presses on the respiratory center located in the brainstem.
= Problems causing cerebral edema and respiratory depression include: brain
tumors, cerebral aneurysm, stroke, and overhydration.

2. Inadequate chest expansion – reduces gas exchange and leads to acidosis.

 Chest expansion can be restricted by skeletal muscle trauma or deformities,
respiratory muscle weakness, or external constriction.
= Respiratory muscle weakness – caused by electrolyte imbalances, fatigue,
muscle dystrophy, muscle damage or breakdown  reduces chest movement.
= External conditions such as body casts, tight scar tissue around the chest,
obesity and ascitis  can restrict chest movement and gas exchange.

3. Airway obstruction – prevents air movement into and out from the lungs  leading
to poor gas exchange, CO2 retention and acidosis.
 The upper airway can be obstructed externally by clothing, neck edema, and
local lymph node enlargement.
 Internal obstruction of the upper airway can be caused by aspiration of foreign
objects, bronchoconstriction, mucus and edema.

4. Reduced alveolar-capillary diffusion – causes poor gas exchange  leading to CO2

retention and acidosis.
 Disorders that reduce diffusion include: pneumonia, pneumonitis,
tuberculosis, emphysema, acute respiratory distress syndrome, chest trauma,
pulmonary emboli, pulmonary edema and drowning.

Combined Metabolic and Respiratory Acidosis

 Metabolic and respiratory acidosis can occur at the same time.

 Uncorrected acute respiratory acidosis always leads to poor oxygenation and lactic
acidosis.
 Combined acidosis is more severe than either metabolic acidosis or respiratory acidosis
alone.
 Cardiac arrest – is an example of problem leading to combined metabolic and respiratory
acidosis.

Clinical Manifestations:

 Manifestations of acidosis are similar whether the cause is metabolic or respiratory.

 These are changes in the excitable membranes of neurons, skeletal muscle and gastric
smooth muscle.

 Central Nervous System (CNS) Changes – include depression of CNS function.

 Problems may range from lethargy to confusion – especially in older patients.
 Stuporous and unresponsive – as acidosis worsens.
= Assess the patient’s mental status.
  Neuromuscular Changes – with acidosis include:
 Reduced muscle tone and deep tendon reflexes (hyporeflexia) – the cause
of these changes are high blood levels of potassium (hyperkalemia) along
with acidosis.
 Skeletal muscle weakness – is bilateral from acidosis.
 Flaccid paralysis – which may progress.

 Cardiovascular Changes – are first seen wild acidosis and are more severe as the
condition worsens.
 Early changes include: increased heart rate and cardiac output.
 With worsening acidosis or with acidosis and hyperkalemia: decreased
heart rate, tall and peaked T waves, widened QRS complexes.
 Thready peripheral pulses – may be hard to find and are easily blocked
 Hypotension – may occur as a result of vasodilation.

 Respiratory Changes – may cause the acidosis and can be caused by the
acidosis.
 Kussmaul respiration – breaths are deep and rapid and not under voluntary
control (in metabolic acidosis with respiratory compensation).
 Shallow and rapid respiration – if acidosis is caused by respiratory
problems breathing efforts are reduced.
 Muscle weakness makes this problem worse.

 Skin Changes – occur with metabolic and respiratory acidosis.

 Skin and mucous membranes warm, dry and pink – caused by vasodilation
due to metabolic acidosis.
 Pale to cyanotic and dry skin – in respiratory acidosis.

Psychosocial Assessment:

 It is vital to complete a psychosocial assessment because behavioural changes may be the

first manifestations of acidosis.
= Observe and document patient’s behaviour by description (objectively) rather than by
interpretation (subjectively).
Ex: you should state that “the patient does not recognize close family members” rather
than “the patient is confused”.

= Ask family members if the patient’s behaviour is typical for him or her, and establish a
baseline for comparison with later assessment findings.

Laboratory Assessment:

 Arterial blood pH is less than 7.35  indicate acidosis.

 Other laboratory data: ABG and blood levels of electrolytes
 Metabolic acidosis
= The pH is low (<7.35) – it is low because the buffering and respiratory
compensation are not adequate to keep the amount of free hydrogen ions
at a normal level.
= The bicarbonate level is low (<21 mEq/L) – it is low because (1)
bicarbonate has been lost  causing a base-deficit acidosis
(2) Bicarbonate production is inadequate  causing a base-deficit
acidosis or (3) bicarbonate may be bound to other substances.
= The partial pressure of arterial oxygen (Pao2) is normal – because gas
exchange is adequate.
= The partial pressure of arterial carbon dioxide (Paco2) is normal or even
slightly decreased – because gas exchange is adequate and CO2 retention
is not a factor.
  High serum potassium level – in acidosis as the body attempts to maintain
electroneutrality during buffering causing hyperkalemia.
 Respiratory acidosis – is reflected by several changes in ABG values.
= The pH is low (<7.35) – lowered by the increased amount of free
hydrogen ions in the blood because the buffering and renal compensation
are not adequate to keep the amount of free hydrogen ions at a normal
level.
= The partial pressure of arterial oxygen (Pao2) is low and the partial
pressure of arterial carbon dioxide (Paco2) is high – because the
pulmonary problem impairs gas exchange  causing poor oxygenation
and CO2 retention.
= The serum bicarbonate level is variable.
- A patient with rapid onset of respiratory acidosis often has a
normal bicarbonate level because the kidney compensation has not
started.
- When respiratory acidosis persists for 24 hours or longer  kidney
compensation increases the levels of bicarbonate.
- Chronic respiratory acidosis is indicated by an elevated bicarbonate
level and increased Paco2.
 Serum potassium levels are elevated in acute respiratory acidosis.
= They are normal or low in chronic respiratory acidosis when renal
compensation is present.

Common Nursing Diagnoses and Collaborative Problems:

Nursing diagnoses that may apply to patients with acidosis include:

 Deficient Fluid Volume related to dehydration
 Decreased Cardiac Output related to poor cardiac contractility and decreased vascular
volume
 Risk for Falls related to skeletal muscle weakness
 Impaired Memory related to fluid and electrolyte imbalances
 Ineffective Breathing Pattern related to reduced gas exchange
 Fatigue related to inadequate tissue oxygenation

Interventions:

 Interventions for acidosis focus on correcting the underlying problem and monitoring for
changes.
 To ensure appropriate interventions, the specific type of acidosis must first be identified.

Metabolic Acidosis

 Interventions for metabolic acidosis include hydration and drugs or treatments to control
the problems causing the acidosis.
Example: if the acidosis is a result of diabetic acidosis – insulin is given to
correct the hyperglycemia and stop the production of ketone bodies.

 Rehydration and antidiarrheal drugs – are given if acidosis is a result of

prolonged diarrhea.
 Bicarbonate is administered only if serum bicarbonate levels
are low.

Interventions for Patients with Metabolic Acidosis:

 Monitor ABG levels for decreasing pH levels, as appropriate.

 Maintain patent IV access.
 MIO
  Monitor determinants of tissue oxygen delivery (ex: PaO2, SaO2 and
haemoglobin levels and cardiac output), if available.
 Monitor loss of bicarbonate through GI tract (ex: diarrhea, pancreatic fistula,
small bowel fistula, and ileal conduit), as possible.
 Administer fluids as prescribed.
 Administer insulin and fluid hydration (Isotonic and hypotonic) for diabetic
ketoacidosis, causing metabolic acidosis, as appropriate.
 Prepare patient for dialysis (ex: assist with catheter placement for dialysis), as
appropriate.
 Institute seizure precaution.

Respiratory Acidosis

 Interventions are aim to maintain a patent airway and enhance gas exchange.
 These include drug therapy, oxygen therapy, pulmonary hygiene (positioning and
breathing techniques), ventilator support and prevention of complications.

 Drug therapy includes agents that increase the diameter of upper and lower airways and
to thin pulmonary secretions.
 The major categories of drugs useful for respiratory problems that lead to acidosis
include:
 Bronchodilators
 Anti-inflammatories
 Mucolytics

 Oxygen therapy – helps promote gas exchange for patient with respiratory acidosis.
 Use caution when giving oxygen to patients with COPD and CO2 retention as
evidenced by a high PaCO2 level  the only breathing trigger for these patients
is a decreased arterial oxygen level.
 Giving too much oxygen to these patient decreases their respiratory drive
 may lead to respiratory arrest.

 Pulmonary hygiene – promotes gas exchange with the use of positioning techniques to
enhance the removal of lung secretions and specific breathing techniques to keep alveoli
inflated.
 Help the patient assume an upright position (mid- to high-Fowler’s position) – to
increase lung expansion.
 Increasing fluid intake – may reduce the thickness of lung secretions and assist in
their removal.

 Ventilation support – with mechanical ventilation may be needed for patients who
cannot keep their oxygen saturation at 90% or who have respiratory muscle fatigue.

 Preventing complications – is a major nursing responsibility.

 Monitor breathing status and intervene when changes occur are critical in
preventing complications.
 For patients with chronic respiratory acidosis:
 Assess breathing status at least every 2 hours.
 Listen to breath sounds and assess how easily air moves into and out of the
lungs.
 Check for any muscle retractions, the use of accessory muscles (especially
the neck muscles [sternocleidomastoids]) and whether breathing produces
a sound (like a grunt or a wheeze).
 Assess the color of the nail beds and oral membranes for cyanosis (a late
finding).
ALKALOSIS

Pathophysiology:

 In patient with alkalosis, the acid-base balance of the blood is disturbed and has an excess
of bases, especially bicarbonate (HCO3).
 Alkalosis is a decreased in free hydrogen ion level of the blood and is reflected by an
arterial blood pH above 7.45.
 Like acidosis, alkalosis is not a disease but, rather, a manifestation of a problem 
caused by metabolic problems, respiratory problems, or both.

Common Causes of Alkalosis

Metabolic Alkalosis
 Increased of base components
 Oral ingestion of bases – Antacids; Milk-alkali syndrome
 Parenteral base administration – Blood transfusion; Sodium bicarbonate; Total
parenteral nutrition

 Decrease of acid components

 Prolonged vomiting
 Nasogastric suctioning
 Hypercortisolism
 Hyperaldosteronism
 Thiazide diuretics

Respiratory Alkalosis
 Excessive loss of carbon dioxide
 Hyperventilation – Fear, anxiety; mechanical ventilation; salicylate toxicity
 Hypoxemia-stimulated hyperventilation – High altitude; shock; Early-stage acute
pulmonary problems
 Alkalosis can result from an actual or relative increase in the amount or strength (or both)
of bases.

 In an actual base excess  alkalosis occurs when base (usually bicarbonate) is either
overproduced or undereliminated.
 In relative alkalosis  the actual amount or strength of bases does not increase, instead,
the amount or strength (or both) of the acids decrease  creating an acid deficit 
making the blood more basic than acidic.

 A relative base-excess alkalosis (acid deficit) results from an overelimination or

underproduction of acids.
 The problems of alkalosis are serious and potentially life-threatening.
 Treatment is aimed at correcting the cause of alkalosis after identifying whether it
is respiratory or metabolic in origin.
 Whether metabolic, respiratory, or both, alkalosis affects specific functions.
 The pathologic effects are caused by the electrolyte imbalances that occur in
response to decreased blood cation levels.
 Most problems of alkalosis are related to increased stimulation of the nervous,
neuromuscular and cardiac systems.

Metabolic Alkalosis – is caused by conditions that create the acid-base imbalance through either
an increase of bases (base excess) or a decrease in acids (acid deficit).
 Base excesses – are caused by excessive intake of bicarbonates, carbonates, acetates, and
citrates.
 Excessive use of oral antacids containing sodium bicarbonate or calcium
carbonate can also cause metabolic alkalosis.
  Other base excesses can occur during medical treatments such as citrate excesses
during massive blood transfusions and IV sodium bicarbonate given to correct
acidosis.

 Acid Deficits – can be caused by disease processes or medical treatment.

 Disorders include prolonged vomiting, excess cortisol, and hyperaldosteronism.
 Medical treatments that promote acid loss causing metabolic alkalosis include
thiazide diuretics and prolonged nasogastric suctioning.

Respiratory Alkalosis – is usually caused by an excessive loss of CO2 through hyperventilation

(rapid respirations).
 Patients may hyperventilate in response to anxiety, fear, or improper setting on
mechanical ventilators.
 Hyperventilation can also result from direct stimulation of central respiratory centers
because of fever, central nervous system lesions and salicylates.

Assessment

 Manifestations are the same for metabolic and respiratory alkalosis.

 Many symptoms are the result of the low calcium levels (hypocalcemia) and potassium
levels (hypokalemia).
 These problems change the function of the nervous, neuromuscular, cardiac and
respiratory systems.

 Central Nervous System (CNS) System – are caused by over-excitement of the nervous
systems.
 Dizziness, agitation, confusion and hypereflexia  may progress to seizure
activity.
 Tingling or numbness (paresthesia) around the mouth and in the toes.
 Positive Chvostek’s and Trousseau’s signs other indicators of alkalosis with
hypocalcemia

 Neuromuscular Changes – are related to the hypocalcemia and hypokalemia that occur
with alkalosis
 Hypocalcemia increases nervous system activity  causing muscle cramps,
twitches, and “charley horses”.
 Deep tendon reflexes are hyperactive
 Tetany (continuous contractions) of muscle groups  painful and indicates a
rapidly worsening condition.
 Skeletal muscle weakness – as a result of nerve overstimulation, but they become
weaker because of hypokalemia.
 Decrease handgrip strength
 The patient may be unable to stand or walk.

 Cardiovascular Changes – occur because alkalosis increases myocardial irritability,

especially when accompanied hypokalemia.
 Increase heart rate and a thready pulse
 Severe hypotension – when hypovolemia (decreased blood volume) is present.
 Increased digitalis toxicity – the hypokalemia increases myocardial sensitivity to
digoxin.

 Respiratory Changes
 Increased rate and depth of breathing – are the main causes of respiratory
alkalosis.
 Respiratory efforts become less effective as the skeletal muscle of respiration
weakens in metabolic alkalosis.
Laboratory Assessment:

 Arterial blood pH greater than 7.45 – confirms alkalosis, but this test alone does not
identify its cause because the manifestations of metabolic and respiratory alkalosis are
similar.
 Arterial blood gas (ABG) values and specific serum electrolyte levels – are critical to
obtain these additional laboratory data.

Interventions:

 Interventions are planned to prevent further losses of hydrogen, potassium, calcium and
chloride ions.
 To restore fluid balance
 To monitor changes.
 Drug therapy – are prescribed to resolve the causes of alkalosis and to restore
normal fluid, electrolyte and acid-base balance.
 Fluid and electrolyte replacement given orally or parenterally – for
metabolic alkalosis caused by diuretic therapy.
 Antiemetic drugs – for vomiting.
= Carefully monitor the patient’s progress, and adjust fluid and electrolyte
therapy.
= Monitor serum electrolyte values daily until they return to normal or
near normal.

Normal Values for Arterial Blood

Parameter Arterial Blood

pH 7.35 – 7.45
PaCO2 35 – 45 mm Hg
PaO2* 80 – 100 mm Hg
HCOз 21 – 28 mEq/L
Base excess/deficit +- 5 mEq/L
Oxygen saturation >90 – 95%

Acid-Base Disorders and Compensation

Disorder Initial Event Compensation
↓ pH, ↑ or normal HCOз, ↑ ↑ Renal acid excretion and
Respiratory acidosis PaCO2 ↑serum HCOз
↑ pH, ↓ or normal HCOз, ↓ ↓ Renal acid excretion and ↓
Respiratory alkalosis PaCO2 serum HCOз
 ↓ pH, ↓ HCOз, ↓ or normal Hyperventilation with
Metabolic acidosis PaCO2 resulting ↓ PaCO2 (conserves
HCOз)
↑pH, ↑ HCOз, ↑ or normal Hypoventilation with
Metabolic alkalosis PaCO2 resulting ↑ PaCO2

To determine if compensation has begun:

 Compensated = pH is normal; PaCO2 and HCOз is abnormal.
 Partially-compensated = pH, PaCO2 and HCOз are all abnormal.
Uncompensated = pH is abnormal; either of PaCO2 and HCOз is normal