INTRODUCTION

Normal function of body cells depend on regulation of hydrogen ion

concentration within the narrow limits. If H+ ion levels exceeds these normal limits, acid
base imbalances result and are recognized clinically as abnormalities of serum ph.
Because acid-base imbalances may be caused by any disorders of body systems the
nurses along with other health care professionals are responsible for preventing,
detecting, intervening in acid-base imbalances.

REGULATION OF ACID-BASE BALANCE

The symbol ph refers to the negative algorithm of the H+ concentration.

It is used to express the acidity or alkalinity of a solution. A ph of 7.0 is neutral, having an
equal number of acids and bases. An acidic solution has a ph less than 7.0 and an alkaline
solution has a ph greater than 7.0. Because ph is a negative log, a rise in ph reflects a
drop in H+. Conversely a decline in ph indicates an increase in H+. Normal serum ph is
7.35 to 7.45. The function of cellular proteins is seriously impaired if ph falls to 7.2 or
rises to 7.55.

Three physiologic systems act interdependently to maintain a

normal serum ph:-

Modulation of serum ph by buffer systems

Regulation of volatile acids by lungs

Regulation of fixed acids and bicarbonates by he kidneys

Modulation of serum ph by buffer systems

A buffer system consists of a weak acid and a salt of a base. For example,
carbonic acid is a weak acid and sodium bicarbonate, he salt of a base with which H+ can
combine make up the clinically important bicarbonate buffer in the blood. The organic
acids formed during cellular energy metabolism are strong acids that is they readily
contribute free H+ to body fluids, potentially producing large alterations in ph. The ph of
buffered solution tend to remain fairly stable despite the addition of strong acids or bases
because buffer system components combine with added acids or bases to convert them to
weaker forms. Examples of buffering reactions are presented below

Strong acid buffered: HCl + H2C03 /NaHCO3 --- H2CO3 + NaCl

Strong base buffered: NaOH + H2CO3 / NaHCO3 --- NaHCO3 + H20

 Several buffer systems are present in the blood, both within red blood
cells and within plasma. The negative numerous charges on proteins permit the binding
of large quantities of H+ ions. Hemoglobin in the RBCs and albumin in the plasma are
quantitatively the most important blood buffers. Negatively charged ions such as
phosphate within body cells and carbonates within bones, are important intracellular
buffers.

In clinical settings however the bicarbonate buffer is monitored because of its

easy accessibility within the plasma as well as its physiological importance as an
open buffer system. In an open buffer system, the end product of the acid
buffering reactions are continuosly eliminated from the body by the lungs and the
kidneys

Because all the intracellular and extracellular buffer systems operate interdependently, the
status of the bicarbonate buffer is the representative of acid base homeostasis within the
body as a whole. Buffer systems act instantly to minimize the impact of adding strong
acids or bases to body fluids; thus these systems are the bodys first line of defense
against acid-base imbalance. Unlikr the lungs and kidneys, however, buffers donot
actually eliminate acid or base from the body.

Regulation of volatile acids by the lungs

Volatile acids are the acids that can be converted to gases. During normal
ventilation, the lungs exhale large quantities of carbon dioxide. CO2 is continuously
produced by body cells as an end product of complete oxidative metabolism of nutrients
for energy. CO2 whivh diffuses from the body cells into the blood where it may combine
with water to form H2 CO3 then dissociates or seperates into its component ions H+ and
H2CO3- . This hydrolysis reaction which reversible is shown as follows :

H2O + CO2 H2CO3 HCO3- + H+

It is apparent from this equation that caebon dioxide and carbonic acid are directly
related. As serum CO2 levels rises, H+ ion production increases and ph falls. Conversely
lower CO2 levels are consistent with higher ph values. The hydrolysis reaction further
demonstrates that some of the carbon dioxide entering the blood forms the bse HCO3- .
although hydrolysis occurs in he plasma, most takes place in the cytoplasm of the RBCs,
where the enzyme carbonic anhydrase (CA) catalyzes the reaction at much more rapid
rates than in the plasma.
 Figure 1 explains the hydrolysis reactions at he tissue levels. Consistent
with the law of mass action, the rate and direction of this reaction are determined by (1)
the addition of substrate or (2) removal of end product. In the tissues, the addition of CO2
to the blood by metabolizing cells drives hydrolysis in the forward direction, forming H+
and HCO3- in the RBCs. The H+ formed by hydrolysis is buffered by hemoglobin, thjereby
minimizing the changes in the ph of the RBC cytoplasm. The HCO3- formed in the RBCs
diffuses out into the plasma, while the chloride ion moves into to maintain the
electroneutrality. This anion counter transport is known as chloride shift. When
bicarbonate ion dissolved in plasma it combines with hemoglobin . in the lungs, carbon
dioxide diffuses along its concentration gradient into the alveoli from where it is exhaled.
Removal of carbondioxide drives the hydrolysis reaction in reverse.

Regulation of fixed acids and bicarbonate by the kidneys

The three principal buffer systems in the renal tubules are the
bicarbonate, ammonia and phosphate systems. In the bicarbonate buffer, H+ is screted into
the tubular lumen by the tubular cells in the countertransport with sodium. The
combination of H+ with filtered bicarbonate regenerates CO2 in a reversal of the
hydrolysis reaction. This CO2 is reabsorbed into the tubular cells where hydrolysis
proceeds efficiently because of the presence of carbonic anhydrase. The HCO 3 formed is
reabsorbed with sodium into the blood. Thus for every molecule of H+ secreted, a
molecule of HCO3 is returned to blood to restore the components of the plasma
bicarbonate buffer system. The ammonia buffer depends on the generation of ammonia
from amino acids such as glutamine in renal tubular cells. Ammonia diffuses into the
tubular lumen where it combines with the H+ to form ammonium, a large charged particle
that cannot be reabsorbed. Ammonium is excreted in the urine. The phosphate buffer acts
similarly resulting in the formation of weak acids that are excreted in the urine. Sodium
and bicarbonate are reabsorbed.

INTERACTION OF ACID-BASE REGULATORY SYSTEMS

Clinical evaluation of total acid- base homeostasuis is aided by an

understanding of the Henderson-Hasselbalch equation which describes the relationship
among ph, acid(H2CO3) and base(HCO3-) :

ph = pka + log( [HCO3- ] / [H2 CO3] )

In this equation pka is a constant value(6.1). The base component is represented by

serum HCO3- (normal value 24 mEq/L; because carbonic acid levels are negligible, the
acid is represented by dissolved carbon dioxide. Dissolved carbon dioxide is derived
from the measurement of PaCO2, the partial pressure of CO2 in the arterial blood (normal
value 40 mm Hg, multiplied by a unit conversion factor of 0.03 to yield 1.2). when
normal values are substituted, the equation becomes:

7.4 = 6.1 + log [ 24/1.2 ]

This equation reveals that a ratio of 20 parts base to 1 part acid must be
present to yield a normal ph. An increase in the numerator (base) promotes an increase in
blood ph; a decrease in base lowers ph. An increase in denominator (acid) lowers ph ; a
decrease in acid raises ph.

ACID-BASE COMPENSATION

When primary disease processes alter either the acid or base

component of the ratio, the lungs or the kidneys(which ever is unaffected by the
pathological change) act to restore the 20:1 ratio and normalize the ph. This process is
known as acid-bse compensation. When kidney disease impairs excretion of fixed acids,
for example, the respiratory system can increase ventilation to blow off excess acid as
CO2. In respiratory failure, the kidneys can compensate for retention of acid by secreting
H+ and regenerating HCO3-. As stated blood buffers act to modulate ph changes but donot
eliminate acid or base from the body. The lungs or kidneys alter the actual amounts of
acid and base, but regulation by these systems are not fast. The lungs respond within
minutes, but maximal compensation takes upto 24 hours. The kidneys may require upto
72 hours to achieve optimal compensation.

Except in mild, chronic respiratory alkalosis, compensation does

not fully restore normal ph. Respiratory compensation is limited because reducing
ventilation to compensate for a renal deficit of H+ would eventually result in hypoxemia.
Because hypoxemia is a respiratory stimulant, ventilation would again increase.
Similarly, renal compensation for ventilator disorders is potentially limited by many
factors, including renal blood flow, tubular flow rates and saturability of tubular transport
processes.

ANALYSIS OF ARTERIAL BLOOD GASES

The status of acid-base homeostasis may be monitored clinically

through the serial measurement of arterial blood gases(ABGs). Among he parameters
reported are ph, PaCO2, and HCO3- .The different steps involved in the analysis of arterial
blood gases include the following :
Step 1 Classify the ph

Normal : 7.35- 7.45

Acidemia : <7.35

Alkalemia: >7.45

Step 2 Assess PaCO2

Normal : 35-45 mm Hg

Respiratory acidosis : >45 mm Hg

Respiratory alkalosis : <35 mm Hg

Step 3 Assess HCO3

Normal : 22-26 mEq/L

Metabolic acidosis : <22 mEq/L

Metabolic alkalosis : >26 mEq/L

Step 4 Determine presence of compensation

Compensation present : PaCO2 and HCO3- are abnormal in opposite directions; that is, one
is acidotic and the other is alkalotic.

Compensation absent : One component is normal and the other is abnormal.

DISORDERS OF ACID BASE BALANCE

The four general classes of acid-base imbalances are: (1)respiratory acidosis;

(2)respiratory alkalosis; (3)metabolic acidosis; and (4) metabolic alkalosis. These
disorders are not diseases by themselves rather they are clinical syndromes assosciated
with a wide variety of diseases.

Acidosis refers to any pathologic processes that cause a relative

excess of acid in the body. The academia is excess acid in the blood. Alkalosis indicates a
primary condition resulting in excess base in the body and alkalemia refers more
narrowly to elevation of serum ph.
COMPLEX ACID-BASE DISORDERS

Mixed acid-base disorders, in which two primary acid-base

imbalances coexist, are common. In cardiac arrest, for example, lactic acid quickly
accumulates as a result of anaerobic metabolism; the carbonic acid level is elevated
because of respiratory arrest. In COPD, the underlying respiratory acidosis may be
complicated by metabolic alkalosis secondary to diuretic or steroid therapy.

A triple acid-base disorder is present when metabolic acidosis and

metabolic alkalosis coexist with either respiratory acidosis or respiratory alkalosis. As an
example of triple disorder, imbalances caused by ingestion of methanol(an exogenous
toxin that produces metabolic acidosis), vomiting(which produces metabolic alkalosis),
and respiratory arrest from aspiration(which produces respiratory acidosis) may occur
simultaneously.

A complex acid base disorder should be suspected when a clients

PaCO2 value and HCO3 level do not correlate with ph or when ABG evidence of
compensation exceeds predicted levels.

NURSING MANAGEMENT

Assessment

The nurse must be alert for manifestations of acid-base imbalances

in high risk clients. These clients include those who:

Have a known disease of the pulmonary, cardiovascular or renal system

Are in a hypermetabolic state such as with fever, sepsis, burns

Are receiving total parenteral nutrition, or enteral tube feedings high in

carbohydrates.

Are receiving mechanical ventilation.

Have diabetes.

Are vomiting, have diarrhea or have enteric drainage.

Are an older adult

To assess for acid-base imbalances, document the findings of a

comprehensive physical assessment of ventilator status, cardiovascular status, and fluid
electrolyte imbalance as described in the Critical Monitoring feature on Acid-base
imbalances, below. Consider laboratory values, including ABG, electrolyte, blood urea
nitrogen, creatinine, and serum lactate dehydrogenase values.

Nursing diagnoses and interventions

The nursing diagnoses for the condition of acid base imbalance are :-

Impaired gas exchange related to hypoventilation or hyperventilation

Nursing interventions:

Assess the respiratory status of the patient, the respiratory rate, rhythm

Monitor the intake and output

Initiate oxygen therapy according to the condition. Oxygen therapy may be used
cautiously in case of respiratory acidosis (at low rates) to minimize he risk of
worsening the respiratory status of the client via nitrogen wash out and blunting of
the ventilator drive. Where as in respiratory alkalosis, rebreathing of carbon
dioxide (as from breathing into a paper bag or other closed system) provides
prompt relief in anxiety related respiratory alkalosis.

Prepare for mechanical ventilation if needed. It is usually needed in case of

respiratory acidosis and metabolic acidosis.

Monitor airway throughout the care.

Provide meticulous care as if for a patient on mechanical ventilator.

Administer corrective medications according to the underlying cause.

Ineffective tissue perfusion related to fluid losses, altered respiratory pattern,

decreased cardiac output

Assess the respiratory pattern, mental status of the patient, level of consciousness.

Start oxygen therapy as needed.

Correct the underlying causes.

Provide calm environment and prevent risk of injuries.

Risk for injury- dysrhythmias,seizures, coma, fluid electrolyte imbalances like
hypovolemia, hyponatremia, hypokalemia, hypocalcemia, hyperkalemia.

Nursing interventions:

Dysrhythmias

Keep the patient on continuous ECG monitoring and record the changes.

Monitor lab values of serum potassium and observe for the changes.

Administer the medicines as prescribed by the doctor.

Seizure and coma

Assess the level of consciousness of the patient

Correct the underlying causes immediately

Administer oxygen therapy and maintain patent airway.

Replace the lost fluids as immediately as possible.

Fluid and electrolyte imbalances

Assess the patient for signs of dehydration and other manifestations of electrolyte
imbalances like muscle cramps, tetany ,tremors.

Monitor the ECGs for changes.

Monitor lab values of electrolytes.

Correct the fluid and electrolyte imbalances promptly.

Anxiety related to fear of death and disease condition

Nursing interventions

Support the patient and reassure that the distressing features will be relieved soon.

Provide calm and quite environment

Correct the underlying causes.

Monitor the patient and never leave the patient alone.

CONCLUSION

In collaboration with other health care professionals, we nurses can reduce

the clients risk for adverse outcomes resulting from acid-base imbalances. Because the
narrow homeostatic range of serum ph, the client at risk must be carefully monitored to
detect the imbalance as early as possible. Nursing interventions that promote optional
respiratory and renal function are particularly important in the prevention and treatment
of acid base disorders.

BIBLIOGRAPHY

Book

1. Barbara Kozier et al Fundamentals of Nursing , 6th edition, Pearson publications

page no. 1324-1332.

2. Black M Joyce, Hawks Jane Medical Surgical Nursing , 7th edition, Saunders page
no. 247-261.

3. Brenda G Bare Suzanne Smeltzer Medical Surgical Nursing 10th edition Saunders
page no. 231-236

4. Myers Allen Medicine 4th edition Lippincot Williams and Wilkins page no. 363-
368.