Journal of Parenteral and Enteral

Nutrition http://pen.sagepub.com/

Simple Acid-Base Tutorial

Phil Ayers and Carman Dixon
JPEN J Parenter Enteral Nutr 2012 36: 18 originally published online 16 December 2011
DOI: 10.1177/0148607111429794

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Tutorial
Simple Acid-Base Tutorial
Phil Ayers, PharmD, BCNSP; and Carman Dixon, PharmD
Financial disclosure: none declared.
The nutrition support practitioner is confronted with numerous
metabolic abnormalities in the daily care of patients. An under-
standing of the basic principles of acid-base balance, along with
the ability to recognize common causes of the various disorders,
enhances the clinicians ability to provide specialized nutrition
support. The basic metabolic and respiratory disorders, along
Preface
I (P.A.) have had the pleasure of precepting pharmacy,
dietary, and medical students as well as residents in the
area of nutrition therapy for more than 20 years. A favor-
ite subject of mine has always been acid-base balance.
Over the period of 1 month on rotation, through lecturing
and practical application, a transformation occurs in
these practitioners. The subject they so dreaded is now
clear, and these young clinicians challenge one another to
ascertain a true understanding of each disorder. Practicing
in the area of nutrition support gives the clinician a
hands-on opportunity to discover how nutrition therapy
influences the various metabolic and respiratory disorders
seen in daily practice.
Acid-base homeostasis requires the lungs, kidneys,
and a complex system of buffers. The maintenance of a
normal pH of 7.357.45 of arterial blood is ideal for opti-
mal organ function. An arterial blood pH <7.35 is deemed
an acidemia, whereas an arterial pH >7.45 is termed an
alkalemia.1-3 Disorders that lower the arterial pH to <7.35
are defined as acidosis, whereas disorders with a pH
>7.45 are termed alkalosis.2 The Henderson-Hasselbalch
equation describes the metabolic and respiratory compo-
nents regulating systemic pH.2
pH = 6.1 + log ([HCO3]/[0.03 pCO2]).
From Mississippi Baptist Medical Center, Jackson, Mississippi.
Received for publication August 19, 2011; accepted for publica-
tion October 18, 2011.
Address correspondence to: Phil Ayers, Mississippi Baptist
Medical Center, 1225 N. State St, Jackson, MS 39202-2002;
e-mail: payers@mbhs.org.
18
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Journal of Parenteral and
Enteral Nutrition
Volume 36 Number 1
January 2012 18-23
2012 American Society for
Parenteral and Enteral Nutrition
10.1177/0148607111429794
http://jpen.sagepub.com
hosted at
http://online.sagepub.com
with common causes, are reviewed in this tutorial. (JPEN J
Parenter Enteral Nutr. 2012;36:18-23)
Keywords:acid-base balance; metabolic; respiratory;
acidosis; alkalosis
The Henderson-Hasselbalch equation demonstrates
that the ratio of bicarbonate and carbon dioxide, not the
absolute values, determines pH.1,2
Lungs
In acid-base balance, the principal function of the lungs
is regulation of the partial pressure of carbon dioxide
(PaCO2). This is commonly seen on laboratory reports as
pCO2 with the normal value of 3545 mm Hg.1-3 The
regulation of carbon dioxide is directly related to the rate
and depth of air movement in the lungs. A normal breath-
ing pattern of a healthy individual is 1418 breaths per
minute.1 Located in the arteries and the medulla are che-
moreceptors that may increase or decrease ventilation in
response to the patients pH, PaO2 (arterial partial pres-
sure of oxygen), and PaCO2.1,2,4 An elevated PaCO2 is
commonly seen with hypoventilation, and hyperventila-
tion is associated with a low PaCO2.1 The other major
function of the lungs is oxygenation of the blood. Oxygen
in the arterial blood is present as PaO2, dissolved oxygen,
and Oxy-Hgb (oxygen bound to hemoglobin).1,2
Kidneys
In acid-base homeostasis, the role of the kidneys is to
maintain the concentration of bicarbonate (HCO3) in
the blood at approximately 24 mEq/L. The kidneys main-
tain acid-base homeostasis through 3 mechanisms1,2,5:
1. Reabsorption of filtered bicarbonate in the proximal
tubule. The process is catalyzed by carbonic anhy-
drase.
2. Titratable acid formation.
3. Excretion of NH4 (ammonium) in the urine.

Acetazolamide is an example of a medication that can
induce a metabolic acidosis by inhibiting carbonic anhy-
drase.3
Blood Gases
Normal blood gas values for arterial and venous blood are
provided in Table 1. Arterial blood gases identify the abil-
ity of the lungs to oxygenate blood, and venous blood
gases determine tissue oxygenation. The oxygen-Hgb dis-
sociation curve shows a sigmoid relationship between the
percentage of available oxygen-binding sites on Hgb that
are occupied and the PaO2. Hgb saturation remains above
90% as long as the PaO2 is >60 mm Hg.1,2 If PaO2 is <60
mm Hg, this may indicate a significant reduction in Hgb
saturation and impaired oxygen delivery to tissues.2
Arterial blood gas (ABG) values normally cited are pH,
PaCO2, PaO2, HCO3, and base excess/deficit.1,2 In inter-
preting ABGs, the pH should be the first value to consider
in the diagnosis of acid-base disorders. A pH of <7.35
represents an acidemia, and values >7.45 are representa-
tive of an alkalemia.1-3 A normal pH can occur in an acid-
base abnormality in mixed acid-base disorders. PaCO2,
commonly noted as pCO2 on laboratory reports, denotes
the ability of the lungs to excrete carbon dioxide. Carbon
dioxide is the acid component of the carbonic acid/bicar-
bonate buffer system.2 PaCO2 may be elevated in respira-
tory acidosis or in a compensated metabolic alkalosis.1-3
Once the pH and PaCO2 are measured, a bicarbonate
level can be calculated.1,2 The bicarbonate level from the
ABG or the serum bicarbonate (total carbon dioxide)
from the blood can be used to assess the acid-base status.
The total carbon dioxide, sometimes seen as CO2 on the
laboratory report, or HCO3 represents the base form of
the carbonic acid/bicarbonate buffer system.1-3 Total car-
bon dioxide may be elevated in a metabolic alkalosis or to
compensate for a respiratory acidosis. The base excess/
deficit is a calculation that provides an estimate of the
metabolic component of the acid base. Base excess is
defined as the amount of H+ required to return the pH of
the blood to 7.4 if the pCO2 were adjusted to normal.6 A
base excess may indicate a metabolic alkalosis, and a base
deficit can occur in a metabolic acidosis.6
Table 1. Reference Blood Gas Values1,2
Arterial Blood Venous Blood
pH 7.40 (7.357.45) 7.36 (7.317.41)
pCO2, mm Hg 40 (3545) 4255
pO2, mm Hg >70 3050
HCO3, mEq/L 24 (2230) 2428
Base excess, mEq/L 3 to +3 3 to +3
O2 saturation >90 6085
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Simple Acid-Base Tutorial / Ayers, Dixon 19
Anion Gap
The anion gap is calculated using the following equation:
Na+ (Cl + HCO3). The normal range for a calculated
anion gap is 816 mEq/L.1,2,7 Clinical laboratories do not
routinely measure anions (negatively charged) such as sul-
fate, pyruvate, lactate, or serum proteins that are negatively
charged. Normally, there are more unmeasured anions
(negatively charged) than cations (positively charged), thus
explaining the positive anion gap.2 In a patient presenting
with a metabolic acidosis, an anion gap should be calcu-
lated. The anion gap is a useful tool in determining the
cause of the acidosis and may assist in treatment. Patients
can present with a normal anion gap or an elevated anion
gap metabolic acidosis.1,2,7 This subject will be addressed in
the discussion of metabolic acidosis.
Acid-Base Principles1-3
A summary of the expected results in the 4 simple acid-
base disorders is demonstrated in Figure 1. In review of
each disorder, you will note a primary occurrence fol-
lowed by a compensatory response. For example, in respi-
ratory alkalosis, the primary issues are an elevated pH and
a decreased pCO2 by the lungs. The kidneys compensate
by excreting bicarbonate to assist in lowering the pH
closer to normal. It is important to remember that the
body never overcompensates, and complete compensa-
tion may not occur. Complete respiratory compensation
requires adequate lung capacity, and complete renal com-
pensation requires adequate volume status and normal
renal function. In the case of the predicted level of com-
pensation not occurring, this could be indicative of an
additional underlying disorder. It is important to remem-
ber that respiratory compensation occurs in a matter of
minutes, whereas renal compensation may require 35
days. Formulas used for estimating the level of compensa-
tion can be found in Table 2. These are estimates only,
and generally changes within 10% of the calculated
values are seen with normal compensation. Changes
greater than 10% of the predicted value may be consistent
with a mixed acid-base disorder.2 The following case stud-
ies provide an example of how to use the compensation
formulas.
Case Study 11-3,8
T.W. is a 65-year-old man with a past medical history
significant for an obstructive lung disease. He is admitted
to the intensive care unit (ICU) with shortness of breath
(SOB) and placed on bilevel positive airway pressure
(BiPAP). ABGs and laboratory on arrival are as follows:
20 Journal of Parenteral and Enteral Nutrition / Vol. 36, No. 1, January 2012

Normal pH
7.35-7.45

Acidosis Alkalosis
pH < 7.35 pH > 7.45

Respiratory Acidosis Metabolic Acidosis Respiratory Alkalosis Metabolic Alkalosis

[pH, pCO2] [pH, HCO3-] [pH, pCO2] [pH,HCO3-]

Pulmonary Compensation: Pulmonary Compensation:

Renal Compensation: Renal Compensation:
Hyperventilation releases Hypoventilation retaining
Kidneys reabsorb HCO3- Kidneys excrete HCO3-
CO2 CO2
[pH, HCO3-] [pH, HCO3-]
[pH, pCO2] [pH, pCO2]

Figure 1. Compensation of simple acid-base disorders.1,2

Table 2. Estimated Level of Compensation in Acid-Base Disorders1,2

Disorder Level of Compensation Formula

Metabolic acidosis PaCO2 = 1.2 (normal HCO3 measured HCO3)

Metabolic alkalosis PaCO2 = 0.6 (measured HCO3 normal HCO3)
Respiratory acidosis (acute) HCO3 = 0.1 (measured PaCO2 normal PaCO2)
Respiratory acidosis (chronic) HCO3 = 0.4 (measured PaCO2 normal PaCO2)
Respiratory alkalosis (acute) HCO3 = 0.2 (normal PaCO2 measured PaCO2)
Respiratory alkalosis (chronic) HCO3 = 0.4 (normal PaCO2 measured PaCO2)
Normal HCO3 = 27 mEq/L; normal PaCO2 = 40.

Sodium 145 (135145 mEq/L) pH 7.38 (7.357.45) Case Study 21-3,8

Potassium 4 (3.55 mEq/L) PCO2 62.9 (3545 mm Hg)
Chloride 104 (98107 mEq/L) pO2 72 (80100 mm Hg) T.W. is a 65-year-old man with a past medical history
CO2 34 (2231 mEq/L) HCO3 36.5 (2430 mEq/L) significant for an obstructive lung disease and small
Serum urea 27 (720 mg/dL) Base excess 10 (+2) bowel obstruction. He is admitted to the ICU with SOB
nitrogen
and placed on BiPAP. ABGs, nasogastric tube to suction,
Creatinine 1.2 (0.71.5 mg/dL)
and laboratory on arrival are as follows:

Sodium 142 (135145 mEq/L) pH 7.43 (7.357.45)

T.W. has a chronic condition; using the equation for
Potassium 4 (3.55 mEq/L) PCO2 62.9 (3545 mm Hg)
respiratory acidosis from Table 2: ( HCO3 = 0.4 Chloride 98 (98107 mEq/L) pO2 72 (80100 mm Hg)
PaCO2). HCO3 = 0.4 (62.9 40) = 9.16. The midrange CO2 42 (2231 mEq/L) HCO3 40.3 (2430 mEq/L)
for HCO3 = 27; therefore, (27 + 9.16 = 36.2). T.W. is Serum urea 27 (720 mg/dL) Base excess 15.2 (+2)
within 10% of the predicted value. This case is then nitrogen
Creatinine 1.2 (0.71.5 mg/dL)
deemed a compensated respiratory acidosis.

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 Simple Acid-Base Tutorial / Ayers, Dixon 21

Table 3. Causes of Metabolic Acidosis1,2,13

Anion Gap NonAnion Gap

Ketoacidosis Hypokalemic
Diabetes mellitus RTA type 1 (distal)
Ethanol RTA type 2 (proximal)
Starvation Diarrhea
Toxic ingestion Fistulous disease
Ethylene glycol Carbonic anhydrase inhibitors
Methanol Hyperkalemic
Salicylates Hypoaldosteronism
Lactic acidosis Hydrochloric acid
Shock RTA type 4
Severe anemia, carbon monoxide poisoning Potassium-sparing diuretics
Seizures Amphotericin B
Liver disease
Medications (ie, metformin, nitroprusside, propofol, intravenous lorazepam)
Rhabdomyolysis
Renal failure
RTA, renal tubular acidosis.

Table 4. Causes of Metabolic Alkalosis1,2,13

Saline Responsive Saline Resistant
(Urine Chloride <10 mEq/L) (Urine Chloride >10 mEq/L) Miscellaneous

Cystic fibrosis Adrenogential syndrome Excessive bicarbonate administration

Gastric fistula Cushing syndrome Hypomagnesemia
Mineralocorticoids Gentamicin Nonparathyroid hypercalcemia
Nasogastric suction Licorice ingestion Penicillin, ticarcillin, carbenicillin
Thiazide and loop diuretics Mineralocorticoids Refeeding syndrome
Villous adenoma Potassium depletion
Volume contraction Primary aldosteronism
Vomiting Renal artery stenosis

T.W. has a chronic condition; using the same equa-
tion for respiratory acidosis from Table 2: ( HCO3 = 0.4
PaCO2). HCO3 = 0.4 (62.9 40) = 9.16. The mid-
range for HCO3 = 27; therefore, (27 + 9.16 = 36.2). T.W.
is not within 10% of the predicted value. This case is then
deemed a respiratory acidosis from obstructive lung dis-
ease and metabolic alkalosis from the nasogastric tube to
suction.
bolic acidosis include a decrease in cardiac output,
hypotension, increase in release of calcium from the
bone, and increase in protein catabolism.9 The treatment
of a metabolic acidosis may include addressing the under-
lying cause, normalization of volume, cardiac output,
oxygenation, and perfusion.1,2,7,9 Alkalinization with bicar-
bonate is reserved for severe cases.

1,2,7
Metabolic Acidosis
Table 3 lists the common causes of metabolic acidosis.
Patients presenting with a metabolic acidosis will have an
arterial pH <7.35 and/or a low bicarbonate level on the
chemistry panel or calculated from the ABGs. In the diag-
nosis of metabolic acidosis, the calculation of an anion
gap is imperative to determine if the acidosis is anion gap
vs nonanion gap in origin.1,2 The lungs provide compen-
sation in patients presenting with a metabolic acidosis.
Lung compensation is initiated within a matter of min-
utes.1,2 Adverse clinical effects associated with a meta-
Metabolic Alkalosis1,2,10
Metabolic alkalosis presents as a pH >7.45 and/or an ele-
vated serum or calculated bicarbonate. Respiratory com-
pensation via hypoventilation may occur, but this is typically
minor. Table 4 reviews the common causes for metabolic
alkalosis. Saline-responsive metabolic alkalosis is more
common than saline resistant.1 The use of thiazide or loop
diuretics may precipitate a contraction of the extracellular
volume and loss of chloride-rich extracellular fluid.
Arteriolar constriction, reduction in coronary blood flow,
hypokalemia, tetany, seizures, and delirium are adverse
consequences seen with severe alkalosis.10 Treatment may

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22 Journal of Parenteral and Enteral Nutrition / Vol. 36, No. 1, January 2012

Table 5. Causes of Respiratory Acidosis1,2,13

Acute Chronic

CNS depression Central sleep apnea

Medications (ie, opioids, propofol, sedatives) Tumor
Head trauma Primary alveolar hypoventilation
CVA Obesity hypoventilation syndrome
Neuromuscular disease Guillain-Barr syndrome Spinal cord injury
Spinal cord injury Diaphragmatic paralysis
Neuromuscular blocking agents Amyotropic lateral sclerosis
Botulism Myasthenia gravis
Acute airway disease Muscular dystrophy
Status asthmaticus Multiple sclerosis
Upper airway obstruction Poliomyelitis
Exacerbation of COPD Hypothyroidism
Parenchymal and vascular disease Kyphoscoliosis
Massive pulmonary emboli COPD
Acute pleural or chest wall disease Severe chronic interstitial lung disease
Pneumothorax
Flail chest
CNS, central nervous system; COPD, chronic obstructive pulmonary disease; CVA, cerebral vascular accident.

Table 6. Causes of Respiratory Alkalosis1,2,13

Pulmonary Central nervous system disorders
Hypoxemia Meningitis, encephalitis
Mechanical ventilation Head trauma, tumors, brainstem lesions
Parenchymal lung disease Anxiety
Pneumonia Miscellaneous
Bronchial asthma Heart failure
Diffuse interstitial fibrosis Pregnancy
Pulmonary embolism Cirrhosis
MedicationSalicylates Sepsis
Nicotine Fever
Xanthine derivatives Pain
Thyrotoxicosis

include volume replacement, correction of potassium and
magnesium deficits, and carbonic anhydrase inhibition
with acetazolamide.1,2,10,11 Treatment of metabolic alkalosis
associated with a primary mineralocorticoid excess includes
the use of spironolactone.1,2
respiratory acidosis.1,12 Treatment may include antidotes
such as flumazenil and naloxone if benzodiazepines or
opioids, respectively, are implicated in the development of
hypoventilation.1,12 Other treatments may include bron-
chodilators, steroids, antibiotics, and ventilator support.
Alkali therapy should be avoided.

Respiratory Acidosis1,2,12
A patient presenting with a respiratory acidosis will have
a low pH and an elevated pCO2 on measurement of
ABGs. Table 5 provides examples of acute and chronic
causes of respiratory acidosis. Hypoventilation is closely
linked with respiratory acidosis. The kidneys begin initia-
tion of compensation within 612 hours and may require
35 days for complete compensation.1,2,12 A greater altera-
tion of pH is seen in acute vs chronic cases of respiratory
acidosis. Anxiety, confusion, personality changes, halluci-
nations, motor disturbances, and dyspnea may be seen in
Respiratory Alkalosis1,2,8
A low pCO2 and elevated pH are seen in patients present-
ing with a respiratory alkalosis. Table 6 references the com-
mon causes of respiratory alkalosis. Anxiety-hyperventilation
syndrome is the most common cause of respiratory alkalo-
sis. Complications related to the disorder include paresthe-
sia, confusion, chest wall tightness, dizziness, muscle
cramps, and tetany. Treatment of respiratory alkalosis
includes rebreathing expired air, supplemental oxygen, or
discontinuation of the offending drug.

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 Simple Acid-Base Tutorial / Ayers, Dixon 23

Case 11-3,10
A 16-year-old girl presents to the emergency department
(ED) with severe gastroenteritis, nausea, and vomiting.
Laboratory and ABGs are ordered:
the 4 basic acid-base disorders builds a foundation for the
practitioner to enhance his or her knowledge. A true
clinical understanding requires utilization of the knowl-
edge and application of the principles.

Sodium 130 (135145 mEq/L) pH 7.47 (7.357.45) Glossary

Potassium 3.2 (3.55 mEq/L) PCO2 46 (3545 mm Hg)
Chloride 86 (98107 mEq/L) pO2 96 (80100 mm Hg) Arterial serum bicarbonate (HCO3): Once the PaCO2
CO2 32 (2231 mEq/L) HCO3 33 (2430 mEq/L) and the pH are measured, the bicarbonate concentration
is calculated.
Disorder: Metabolic alkalosis.
PaCO2 (pCO2) Arterial partial pressure of carbon
1-3,7 dioxide: A measure of the adequacy of the lungs to
Case 2
excrete carbon dioxide, the acid component of the car-
bonic acid/bicarbonate buffer system.
A 67-year-old woman presents to the clinic for a routine
visit. Some laboratory abnormalities are noted, so the PaO2 (pO2) Arterial partial pressure of oxygen: A mea-
physician orders ABGs. sure of the level of oxygenation of arterial blood.
Sodium 135 (135145 mEq/L) pH 7.33 (7.357.45) Venous total carbon dioxide (CO2): Represents the
Potassium 5.2 (3.55 mEq/L) PCO2 33 (3545 mm Hg) base form of the carbonic acid/bicarbonate buffer system.
Chloride 108 (98107 mEq/L) pO2 92 (80100 mm Hg)
CO2 16 (2231 mEq/L) HCO3 18 (2430 mEq/L)
Serum urea 54 (720 mg/dL) Further Reading
nitrogen
Creatinine 1.8 (0.51.5 mg/dL) Ayers P, Warrington L. Diagnosis and treatment of simple acid-base
disorders. Nutr Clin Pract. 2008;23:122-128.
Disorder: Nonanion gap metabolic acidosis. Hall TG. Arterial blood gases and acid base balance. In: Lee M, ed.
Interpreting Laboratory Data. 4th ed. Bethesda, MD: American
Case 31-3,12 Society of Health-System Pharmacists, Inc; 2009:179-189.
Langley G, Canada T, Day L. Acid-base disorders and nutrition support
treatment. Nutr Clin Pract. 2003;18:259-261.
A 27-year-old man with unknown past medical history
arrived to the ED via ambulance. Laboratory and ABGs
on presentation are as follows: References
1. Ayers P, Warrington L. Diagnosis and treatment of simple acid-
Sodium 137 (135145 mEq/L) pH 7.25 (7.357.45) base disorders. Nutr Clin Pract. 2008;23:122-128.
Potassium 4.5 (3.55 mEq/L) PCO2 60 (3545 mm Hg) 2. Hall TG. Arterial blood gases and acid base balance. In: Lee M,
Chloride 100 (98107 mEq/L) pO2 55 (80100 mm Hg) editor. Interpreting Laboratory Data. Bethesda, MD: American
CO2 25 (2231 mEq/L) HCO3 26 (2430 mEq/L) Society of Health-System Pharmacists, Inc; 2004:263-277.
3. Langley G, Canada T, Day L. Acid-base disorders and nutrition
Disorder: Acute respiratory acidosis. support treatment. Nutr Clin Pract. 2003;18:259-261.
4. Kraut JA, Madias NE. Approach to patients with acid-base disor-
ders. Respir Care. 2001;46(4):392-403.
Case 41-3,8 5. Dubose TD. Acidosis and alkalosis. www.accessmedicine.com.
Accessed August 10, 2011.
A 72-year-old man with metastatic colon cancer presents 6. Kellum JA. Determinates of blood pH in health and disease. Crit
to the ED with shortness of breath and the following Care. 2000;4:6-14.
laboratory values and ABGs: 7. Swensen ER. Metabolic acidosis. Respir Care. 2001;46(4):342-353.
8. Foster GT, Vaziri ND, Sasson CS. Respiratory alkalosis. Respir
Care. 2001;46(4):384-391.
Sodium 133 (135145 mEq/L) pH 7.49 (7.357.45)
9. Adrogue HJ, Madias NE. Medical progress: management of life-
Potassium 3.9 (3.55 mEq/L) PCO2 28 (3545 mm Hg) threatening acid-base disorders: first of two parts. N Engl J Med.
Chloride 102 (98107 mEq/L) pO2 52 (80100 mm Hg) 1998;338(1): 26-34.
CO2 22 (2231 mEq/L) HCO3 21 (2430 mEq/L) 10. Khanna A, Kurtzman NA. Metabolic alkalosis. Respir Care.
2001;46(4):354-365.
Disorder: Acute respiratory alkalosis. 11. Adrogue HJ, Madias NE. Medical progress: management of life-
threatening acid-base disorders: second of two parts. N Engl J
Med. 1998;338(2):107-111.
Conclusion 12. Epstein SK, Singh N. Respiratory acidosis. Respir Care. 2001;46(4):
366-383.
A basic understanding of acid-base balance is required to
13. Shannon M. Acid-base, fluid and electrolyte balance. In: Shannon M, ed.
practice in the area of specialized nutrition support. Haddad and Winchesters Clinical Management of Poisoning and Drug
Understanding the basic roles of the lungs, kidneys, and Overdose. 4th ed. Philadelphia, PA: Saunders Elsevier; 2007:208-221.

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