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ABCs of ABGs: A guide to interpreting acid-base disorders

Article  in  Hospital pharmacy · October 2008

DOI: 10.1310/hpj4310-808


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2 authors:

Kurt A Wargo Robert Centor

Auburn University University of Alabama at Birmingham


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Hospital Pharmacy
Volume 43, Number 10, pp 808–815
2008 Wolters Kluwer Health, Inc.


ABCs of ABGs: A Guide

to Interpreting Acid-Base Disorders
Kurt A. Wargo, PharmD, BCPS,* and Robert M. Centor, MD†

section of the equation will help

Abstract form the basis for the remainder of
Purpose: This objective of this article is to provide a useful resource on the this article. The processes that occur
assessment of arterial blood gasses (ABGs) for clinical pharmacists, phar-
in the body drive this equation
macy residents, and students.
Summary: Acid-base pathophysiology can be separated into metabolic or either to the left or to the right to
respiratory acidosis and alkalosis, as well as those disturbances that are maintain a normal pH. Think in
compensated. This article provides readers with a stepwise approach for terms of the left side of the equation
assessing ABGs, as well as offering actual case examples to familiarize the occurring in the lungs and the right
reader with the concepts of acid-base disorders. By the completion, the side occurring in the kidneys. Any-
reader will have the tools necessary to assess any ABG that may be time hydrogen ions (H+) are lost, the
encountered in clinical practice. equation proceeds to the right. The
Conclusion: Comprehension of acid-base pathophysiology is a compli- lungs retain more carbon dioxide
cated and overwhelming task for novice and experienced clinicians alike. (CO2) in the form of pCO2 (partial
Utilization of the stepwise approach proposed in this article will help clin- pressure of CO2 in the arterial
icians at all levels of training assess and develop treatment options for any
blood) to convert CO2 into carbon-
acid-base disturbance encountered in practice.
ic acid (H2CO3). Carbonic acid is
Key Words—acid-base, acidosis, alkalosis, arterial blood gas then converted to H+ and bicarbon-
ate (HCO3̄), thereby replacing the
Hosp Pharm—2008;43:808–815 lost H+. Likewise, anytime hyper-
ventilation occurs, the lungs are
releasing pCO2, thereby shifting the
equation to the left. The body’s
INTRODUCTION pharmacotherapy of hospitalized compensatory mechanism for this
The memories of pharmacy patients. loss in acid (pCO2) is that the kid-
school that may be conjured by the When discussing any compli- neys hold on to more H+ (or excrete
words acidosis and alkalosis might cated process, it is best to start more HCO3̄), thereby maintaining
very well cause facial flushing, light- from a reference point—one that the pH at a “normal” level. Howev-
headedness, and nausea in the can be referred to whenever confu- er, an important distinction must be
unfortunate individual who hears sion arises. For acid-base distur- made here: pCO2 and HCO3̄ are
them spoken aloud. He or she may bances, that reference point is the excreted independent of one anoth-
also recall having thoughts such as, bicarbonate–carbon dioxide buffer er. If excess pCO2 exists in the body,
“Is this stuff ever going to be use- system, shown in Equation 1.1 it cannot be excreted in the kidneys;
ful?” during efforts to learn the This buffering equation holds rather, it must be exhaled by the
Henderson-Hasselbach equation the basis for all acid-base physiolo- lungs. Similarly, if there is an
and memorize pKas. Although acid- gy within the human body, and dis- increase in H+, the body cannot con-
base pathophysiology seems com-
plex, it contains important concepts Equation 11 CO2 + H2O (water) ↔ H2CO3 ↔ H+ + HCO3̄
that are used daily to optimize the

*Assistant Clinical Professor, Auburn University, Harrison School of Pharmacy, Auburn, Alabama; †Professor and Director, Asso-
ciate Dean, Huntsville Regional Medical Campus, University of Alabama–Birmingham School of Medicine, Huntsville, Alabama;
Corresponding Author: Dr. Kurt A. Wargo, 301 Governors Dr. SW, Department of Internal Medicine, Huntsville, AL 35801-5123;
phone: 256-551-4538; fax: 256-551-4542; e-mail: wargoka@auburn.edu.

808 Volume 43, October 2008

ABCs of ABGs: A Guide to Interpreting Acid-Base Disorders

vert it to pCO2 for excretion in the pCO2 35 to 45 mm Hg. A clinician than metabolic compensation, tak-
lungs; it must be excreted by the must understand that under normal ing minutes to begin and with full
kidneys. physiologic conditions, the human compensation seen in hours.
All acid-base disturbances can body attempts maintenance of One key factor for assessing
be explained using Equation 1. homeostasis by keeping pH and ABG is determination of which pri-
Metabolic acidosis results from pCO2 as close to 7.40 and 40 mm mary acid-base disturbance exists
either an excess in H+ or a deficien- Hg, respectively, as possible. There- and whether compensation has
cy in HCO3̄. On the other hand, fore, any variation from those val- occurred. This is often a daunting
metabolic alkalosis results from an ues should be considered abnormal. task; however, if the clinician uses a
excess in HCO3̄ or a deficiency in Serum HCO3̄ levels, on the other stepwise approach (as outlined in
H+. Respiratory acidosis results hand, may vary from 22 to 28 Figure 1), both simple and complex
from an excess in pCO2, and respi- mEq/L on a daily basis, based on a acid-base disorders can be deter-
ratory alkalosis results from a defi- number of metabolic variables. mined. First, and most importantly,
ciency in pCO2. Primary metabolic In an effort to maintain home- assessment of the patient must be
disorders can be seen as distur- ostasis, the human body must con- completed to determine what is
bances in the serum HCO3̄ level, stantly compensate for either respi- physiologically occurring in the
with compensation occurring via ratory or metabolic changes. For patient at that moment in time.
the respiratory route and reflected example, when undergoing strenu- Assessment of pH points the clini-
in the pCO2 found in the arterial ous exercise, a number of changes cian in the direction of a primary
blood gas (ABG). Similarly, all res- occur within the body. First, as mus- acidosis or alkalosis. Second, assess-
piratory disturbances are reflected cles become deprived of oxygen, ment of pCO2 and HCO3̄ will allow
in the ABG pCO2 level, with com- they begin undergoing anaerobic the clinician to differentiate the pri-
pensation occurring metabolically metabolism. During this process, mary disturbance and whether
as reflected in the serum HCO3̄ muscles produce lactic acid as a compensation has occurred. The
level. If only evaluating the labora- byproduct, thereby creating meta- final step must only be made if a
tory values, it may be unclear at bolic acidosis. In an effort to com- metabolic acidosis is present; that is,
times which disturbance is causing pensate and maintain a normal pH, an anion gap and delta gap must be
the primary problem; thus, patient the respiratory rate increases, caus- calculated to further differentiate
assessment plays a pivotal role in ing ventilation of pCO2 out of the the cause of the disturbance and
diagnosis. The cause of all acid- body and resulting in respiratory better determine treatment options.
base disturbances can be deter- alkalosis. Therefore, if an ABG is
mined by evaluation of electrolyte drawn during exercise activity, low Example
panels, ABGs, and patient assess- HCO3̄ with an increased anion gap, A patient with new-onset,
ment. This article provides a step- as well as a low pCO2, should be community-acquired pneumonia
wise approach to assessing ABGs seen. Although the pH may be has a pH of 7.47, pCO2 of 32 mm
and offers actual case examples to slightly acidic depending on the Hg, and serum HCO3̄ of 28 mEq/L.
familiarize the reader with the con- level of exercise, the respiratory cen- Using the first step in the approach
cepts of acid-base disorders. At the ter will continually compensate to for evaluating ABG (assessment of
completion, the reader will have prevent severe metabolic acidosis. the patient), it is determined that the
the tools necessary for assessing Thus, the topic of compensa- patient has a pulmonary process
any ABG that may be encountered tion is introduced. For any respira- occurring (pneumonia). In addition,
in clinical practice. tory abnormality, the body compen- through assessment of the pH, it is
sates metabolically with changes in evident that this patient has an alka-
STEPWISE APPROACH serum HCO3̄ through renal regula- losis because the pH is greater than
FOR ASSESSING tion. This compensation may take 3 7.40. Next, assessment of both the
ARTERIAL BLOOD GASSES to 5 days to begin, and in some pCO2 and the HCO3̄ (the second
For a clinician to interpret acid- cases, it may take up to a week to step) must be made to determine
base disorders, a basic understand- see the full compensation. Other- which is causing the acid-base
ing of the general concepts is neces- wise, the body compensates for any abnormality. In this case, the pCO2
sary. Many hospital laboratories metabolic disorder through pul- is lower than normal and the HCO3̄
report ranges in normal laboratory monary regulation of pCO2. This is on the high end of normal; this
values, such as pH 7.35 to 7.45 and compensation occurs more rapidly indicates that respiratory alkalosis

Hospital Pharmacy 809

ABCs of ABGs: A Guide to Interpreting Acid-Base Disorders

Evaluate patient
Assess pH
< 7.4 = Acidosis
> 7.4 = Alkalosis

Assess pCO2 Assess HCO3̄

< 40 mm Hg > 40 mm Hg < 22 mEq/L > 28 mEq/L

Respiratory alkalosis Respiratory acidosis Metabolic acidosis Metabolic alkalosis

[Na+] – [Cl¯] – [HCO3̄ ]

If increased AG, calculate delta gap

Observed AG – Expected AG

Add delta gap back to serum HCO3̄ to reveal true HCO3̄

Figure 1. Stepwise approach for assessment of arterial blood gasses. AG = anion gap; Cl¯ = chloride; HCO3̄ = bicarbon-
ate; Na+ = sodium; pCO2 = partial pressure of carbon dioxide in the arterial blood.

is the major driving force for body: metabolic acidosis and alka- mEq/L (136 to 145 mEq/L); potas-
increase in pH. An interesting find- losis, respiratory acidosis and alka- sium (K+) 4.4 mEq/L (3.5 to 5
ing of this ABG is that one may losis, and mixed acid-base distur- mEq/L); chloride (Cl¯) 100 mEq/L
expect a lower HCO3̄ as a compen- bances. All of these disturbances (98 to 106 mEq/L); HCO3̄ 5 mEq/L
satory mechanism for the respirato- can be discovered using the stepwise (22 to 28 mEq/L); serum urea nitro-
ry alkalosis; however, there are 2 approach for assessing ABGs. gen (BUN) 77 mg/dL (10 to 20
possible causes for this higher mg/dL); creatinine 9 mg/dL (0.5 to
HCO3̄. One explanation is that the METABOLIC ACIDOSIS 1.2 mg/dL); glucose 112 mg/dL (70
patient’s kidneys have not had time to 110 mg/dL); lactic acid 178
to compensate for the respiratory Case 12 mg/dL (5 to 20 mg/dL).
alkalosis; the other is that the A 58-year-old woman has a 4- ABG: pH 6.8; pCO2 20 mm Hg;
patient may be volume contracted day history of lethargy, anorexia, partial pressure of oxygen (pO2)
secondary to poor oral intake as a abdominal pain, and nausea. Her 77 mm Hg.
result of pneumonia, and thus, a medical history is positive for type 2
contraction alkalosis may be occur- diabetes, for which she is taking Metabolic acidosis can be
ring. Regardless, treatment of the metformin 500 mg twice daily, and divided into 2 groups: that which is
pneumonia with antimicrobials, as osteoarthritis of the knees, for caused by an increased amount of
well as volume expansion, should which she recently has been started unmeasured anions (increased
resolve the acid-base disturbance. on rofecoxib (unknown dose). The anion gap metabolic acidosis) and
following detail her laboratory that which is caused by a normal
There are 5 acid-base distur- results on admission: anion gap. In the case of an
bances that can occur in the human Electrolytes: sodium (Na+) 140 increased anion gap, several vari-

810 Volume 43, October 2008

ABCs of ABGs: A Guide to Interpreting Acid-Base Disorders

Equation 21,3 Anion gap = [Na+] – [Cl¯] – [HCO3̄] encountered in practice. This type
of lactic acidosis is caused by intra-
venous (IV) infusions of products
Equation 34 Delta gap = Observed anion gap – Expected anion gap containing the excipient propylene
Revealed HCO3̄ = Delta gap + Serum HCO3̄ glycol, such as IV lorazepam and IV
diazepam, and typically occurs after
high doses of continuous infusions.5
ables can lead to an increase in um bicarbonate treatment should Typical presentation is an increased
unmeasured anions. The acronym be administered to correct the acidosis. osmolar gap, an increased anion
KILU—in which K signifies keto- From Case 1, the following can gap, and renal failure.6 Although
acidosis (caused by diabetes, starva- be calculated: propylene glycol can cause either
tion, and chronic alcoholism); I sig- Anion gap lactic acidosis or D-lactic acidosis,
nifies ingestions (typically from sal- = 140 mEq/L – 100 mEq/L – 5 mEq/L the D-isomer is not detected in the
icylates, ethylene glycol, and = 35 mEq/L routine assay; and thus, lactic aci-
methanol); L signifies lactic acido- Expected anion gap dosis may or may not be identified.6
sis; and U signifies uremia—can be = 12 mEq/L In these patients, determination of
used for remembering the potential (No albumin is provided.) the osmolar gap is recommended,
causes of an increase in unmeasured Delta gap and its elevation would indicate the
ions. When faced with a serum elec- = 35 mEq/L – 12 mEq/L presence of D-lactic acid. However,
trolyte panel that reveals a lower- = 23 mEq/L the best option is testing D-lactic
than-normal serum HCO3̄, indicat- Revealed HCO3̄ acid levels if the laboratory has such
ing metabolic acidosis, anion gap = 23 + 5 mEq/L capability.
must be calculated by subtracting = 28 mEq/L
the difference in serum concentra- Based on this case example, the Case 27
tions of the major cation (Na+) and revealed, or adjusted, HCO3̄ A 42-year-old man with human
anions (Cl¯ and HCO3̄). See Equa- excludes either an underlying, nor- immunodeficiency virus (HIV) is
tion 2 for this calculation.1,3 mal gap metabolic acidosis or meta- admitted to the hospital with
Under normal circumstances, bolic alkalosis. The increased anion headache and fever. He is diagnosed
the anion gap is 12 ± 4 mEq/L; gap is secondary to unmeasured with cryptococcal meningitis and
however, negatively charged pro- anions, in this case lactic acid, and initiated on amphotericin B and
teins, specifically albumin, can have secondary to metformin therapy in flucytosine. The patient exhibits a
a significant effect on the anion gap, the setting of acute kidney injury. confused state of mind 1 week later,
such that a 1 g/dL drop in albumin Therefore, if the pH is greater than and the following laboratory values
will lower the anion gap by 2.5 6.9, administration of sodium bicar- are drawn:
mEq/L.1,3 If the albumin of a patient bonate may be inappropriate. How- Electrolytes: Na+ 152 mEq/L;
is known, the normal anion gap can ever, because of the severity of the K 3.4 mEq/L; Cl¯ 120 mEq/L;

be calculated by multiplying the acidosis, the administration would HCO3̄ 20 mEq/L; BUN 32 mg/dL;
serum albumin by 3. This proves be justified. Even though metformin creatinine 1.4 mg/dL; glucose 112
crucial when calculating the delta is an extremely rare cause of lactic mg/dL.
gap, which is the difference between acidosis, particular care should be ABG: pH 7.30; pCO2 36 mm
the observed and the expected taken when using it for patients in Hg; pO2 85 mm Hg.
anion gap (see Equation 3).4 The whom renal blood flow has been Plasma osmolality 315 mOsm/
delta gap is used whenever an altered, such as in those with acute kg (285 to 295 mOsm/kg); urine
increased anion gap is observed to kidney injury, sepsis, contrast stud- osmolality 150 mOsm/kg (500 to
determine what the HCO3̄ level ies, and acutely decompensated 800 mOsm/kg); urine Na+ 25
would be in the absence of unmea- heart failure. More commonly, mEq/L; urine K+ 45 mEq/L; urine
sured anions. That is, the result of nucleoside reverse transcriptase Cl¯ 38 mEq/L; urine pH 6.2.
the delta gap is added back to the inhibitors such as didanosine and
measured HCO3̄, and the result is stavudine, as well as isoniazid, cause Normal anion gap metabolic
the serum HCO3̄ without an anion lactic acidosis. Another type of lac- acidosis is a result of either HCO3̄
gap (see Equation 3). This is espe- tic acidosis, D-lactic acidosis (the D- loss or inadequate buffering.1 The
cially useful in determining if sodi- isomer of lactic acid), is rarely most common cause of HCO3̄ loss

Hospital Pharmacy 811

ABCs of ABGs: A Guide to Interpreting Acid-Base Disorders

is excessive diarrhea, but it can also Equation 41 Urinary anion gap

be seen in proximal (type 2) renal = (Urinary Na+ + Urinary K+) – Urinary Cl–
tubular acidosis (RTA). Because
stool has a basic pH, large-volume
diarrhea can result in a loss of is discovered the patient has a lower Clostridium difficile toxin: neg-
HCO3̄, resulting in normal anion than normal HCO3̄, indicating a ative × 3
gap acidosis. In type 2 RTA, there is metabolic acidosis is present.
a disruption in the proximal reab- According to the approach de- Metabolic alkalosis is charac-
sorption of HCO3̄, resulting in scribed here, because of the pres- terized by a pH greater than 7.40
lower serum HCO3̄ levels. Medica- ence of a metabolic acidosis, the and a HCO3̄ greater than 28
tions such as carbonic anhydrase next step is calculation of anion mEq/L. Causes of metabolic alkalo-
inhibitors and ifosfamide are com- gap. When this is calculated, it is sis can be divided into gastrointesti-
mon iatrogenic causes of type 2 determined that a normal anion gap nal loss of H+, renal loss of H+, intra-
RTA. is present (12 mEq/L). Therefore, it cellular shift of H+, or retention of
Inadequate buffering in normal is evident that the primary acid-base HCO3̄.1 Gastrointestinal loss of H+
anion gap acidosis is a result of disturbance is a normal gap meta- usually is a result of vomiting and
decreased distal H+ secretion by bolic acidosis with respiratory alka- nasogastric (NG) suctioning or
luminal H+-ATPase pumps in the losis compensation. The urine elec- results from antacid use. Renal H+
collecting duct of the kidneys, trolytes demonstrate K+ loss and loss is associated with a number of
defined as distal RTA (type 1).1 This increased pH secondary to mem- conditions, including diseases of
decreased secretion of H+ results in brane permeability. In addition, the mineralocorticoid excess such as
the inability to establish normally urinary anion gap is 32 (see Equa- primary hyperaldosteronism or
acidic urine and, therefore, results in tion 4), indicating very low Cushing disease. The presence of
a urine pH that is typically above amounts of urinary H+.1 The cause hypokalemia in these conditions
5.3. Another mechanism of type 1 of this disturbance is distal RTA acts as a stimulus for H+ secretion
RTA is secondary to increased per- secondary to amphotericin B and HCO3̄ reabsorption. Diuretics
meability of the luminal membrane, nephrotoxicity. also promote renal H+ loss through
resulting in back diffusion of secret- distal secretion. This condition,
ed H+ and distal secretion of K+. METABOLIC ALKALOSIS referred to as contraction alkalosis,
Amphotericin B is an agent that occurs secondary to increased secre-
inserts into the cell membranes and Case 39 tion of aldosterone in response to
creates pores that decrease mem- A 65-year-old man is admitted hypovolemia, increased distal tubule
brane permeability. The net result is to the hospital for abdominal pain flow, and hypokalemia that may
H+ retention and K+ excretion, and diarrhea. He has a history of result from diuretic use. Intracellu-
which results in normal anion gap chronic constipation, for which he lar shift of H+ is a result of
acidosis and hypokalemia.8 takes lactulose. An exploratory hypokalemia caused by the transcel-
In Case 2, the first step in the laparotomy revealed no obstruction lular shift of K+ out of the cell and
approach for evaluation of ABGs 3 weeks before admission. He then H+ into the cell. In addition to
leads the reader to determine that developed pneumonia and received diuretic use, vomiting can also lead
that the patient has a metabolic 5 days of gatifloxacin. He also to a condition of contraction alka-
process occurring with cryptococcal developed large-volume, watery losis in which Na+, Cl¯, and H2O
meningitis and that there is no rea- diarrhea without nausea or vomit- (water) are lost without HCO3–.
son for suspecting a respiratory ing 5 days before admission. The Finally, retention of HCO3̄ as a
problem. In addition to assessing following detail his laboratory result of excessive administration of
the patient, evaluation of the pH results on admission: sodium bicarbonate can also result
reveals the presence of an acidosis. Electrolytes: Na+ 143 mEq/L; in metabolic alkalosis.
Evaluation of the respiratory com- K 3.3 mEq/L; Cl¯ 102 mEq/L;
Because the most common caus-
ponent of the ABG shows that the HCO3̄ 33 mEq/L; BUN 19 mg/dL; es of metabolic alkalosis include
pCO2 is lower than normal, indicat- creatinine 1 mg/dL; glucose 109 vomiting, NG suction, and diuretics,
ing a respiratory alkalosis is present. mg/dL. the usual treatment involves adminis-
Furthermore, when assessing the ABG: pH 7.44; pCO2 42 mm tration of IV fluids containing sodi-
metabolic component of the ABG, it Hg; pO2 53 mm Hg. um chloride (NaCl).1 However, in

812 Volume 43, October 2008

ABCs of ABGs: A Guide to Interpreting Acid-Base Disorders

some cases patients may be resistant ops a urinary tract infection with occurring (respiratory failure), as
to administration of IV NaCl, usu- Pseudomonas aeruginosa and well as a pH that is acidotic.10 Eval-
ally because of edematous states or begins experiencing decreased men- uation of the pCO2 from the time
hypokalemia. In those patients, tal status, a temperature of 103°F, of respiratory failure indicates a
withholding conventional diuretics and a white blood cell count (WBC) respiratory acidosis. Although the
and perhaps administering a car- of 41,000 cells/mm3. At that time, HCO3¯ is not available for assess-
bonic anhydrase inhibitor such as he is on room air and his ABG ment, a change from the normal
acetazolamide is recommended. shows pH 7.43, pCO2 19 mm Hg, values of this measurement is not
In Case 3, the stepwise and pO2 57 mm Hg. Therapy with expected because metabolic com-
approach indicates that the patient gentamicin is started, and the pensation would take several days
currently has a metabolic process patient’s WBC begins to drop and to occur. However, the patient is
occurring (large-volume diarrhea), his mental status improves. Days experiencing acute kidney injury
as well as a pH that indicates alka- later he begins experiencing acute secondary to an elevated gentam-
losis. The second step of the kidney injury secondary to gentam- icin level; therefore, a metabolic
approach leads to the determination icin as evidenced by a serum creati- acidosis may be present. Regard-
that the pCO2 is slightly higher than nine of 4.5 mg/dL and a gentamicin less, through assessment of the
normal, representing a respiratory trough of 6 mg/dL; thus, gentamicin patient, it is evident that a pul-
acidosis. Furthermore, the HCO3̄ is is discontinued. His mental status monary process is occurring; and it
higher than normal, demonstrating begins deteriorating, and he starts going is clear that the patient has a pri-
a metabolic alkalosis. The patient in into respiratory failure. The ABG mary respiratory acidosis with no
this example has a primary meta- reveals pH 7.19, pCO2 57 mm Hg, evidence of metabolic compensa-
bolic alkalosis with respiratory aci- and pO2 59 mm Hg. After 3 days of tion. The authors believe the acute
dosis compensation. It is puzzling, mechanical ventilation, the patient respiratory failure is secondary to a
however, that this patient has large improves and is extubated. rare adverse effect of gentamicin
amounts of diarrhea and an alkalo- therapy known as neuromuscular
sis, a state in which observation of Respiratory acidosis is charac- blockade. After gentamicin is dis-
metabolic acidosis would normally terized by a pH less than 7.40, and continued and mechanical ventila-
be expected. Nevertheless, the etiol- the condition results from retention tion is employed, the patient im-
ogy becomes clear on closer exami- of pCO2; therefore, an elevated proves. Although it is rare, amino-
nation. The metabolic alkalosis pre- pCO2 should be evident. Acutely, glycosides have been associated
sent in this patient is most likely a respiratory acidosis is most com- with neuromuscular blockade, an
result of hypokalemia combined monly associated with severe asth- adverse effect of which all clini-
with lactulose therapy. Lactulose ma exacerbations, pneumonia, pul- cians should be cognizant. This
creates an acidic stool, thereby trap- monary edema, and suppression of condition is more commonly seen
ping ammonium (NH4+) for excre- the respiratory center secondary to with gentamicin and neomycin
tion. Therefore, the patient is losing medications such as opioids, benzo- than with tobramycin and amikacin.
H+ through diarrhea in a way that is diazepines, paralytics, and neuro-
analogous to vomiting or NG suc- muscular blockers.1 Chronic respi- RESPIRATORY ALKALOSIS
tioning. The patient is given IV flu- ratory acidosis is most commonly AND MIXED ACID-BASE DISORDERS
ids; lactulose therapy is discontin- associated with chronic obstructive
ued; and the metabolic alkalosis is pulmonary disease and extreme Case 511
resolved. obesity. Because the kidneys take A 58-year-old schizophrenic
days to compensate through secre- man is brought to the hospital
RESPIRATORY ACIDOSIS tion of H+, acute respiratory acido- because of strange behavior. He is
sis must be treated by removal of completely disoriented and provides
Case 410 the offending agent or by treatment no history. The following laboratory
An 89-year-old man with a his- of the underlying cause. Supplemen- values are collected:
tory of heart failure and chronic tal oxygenation may be required in Electrolytes: Na+ 139 mEq/L;
kidney disease (baseline creatinine severe cases. K 4.7 mEq/L; Cl¯ 90 mEq/L; HCO3¯

1.6 mg/dL) is being treated in the In Case 4, the stepwise 14 mEq/L; BUN 18 mg/dL; creati-
hospital for a left femoral neck frac- approach demonstrates that the nine 1 mg/dL; glucose 100 mg/dL.
ture. While in the hospital, he devel- patient has a pulmonary process ABG: pH 7.49; pCO2 15 mm

Hospital Pharmacy 813

ABCs of ABGs: A Guide to Interpreting Acid-Base Disorders

Hg; pO2 169 mm Hg (2 L nasal losis followed by an increased anion mEq/L; Cl¯ = 115 mEq/L; HCO3̄
oxygen). gap metabolic acidosis. A family = 15 mEq/L; pH = 7.32; pCO2=
member brings in an empty bottle 30 mm Hg.
Respiratory alkalosis is charac- of Alka-Seltzer, which contains 3. A 45-year-old woman in the ICU
terized by a pH greater than 7.40 aspirin and sodium bicarbonate, is intubated after a recent
and hyperventilation resulting in a that was found near the patient’s abdominal surgery. While in the
lower-than-normal pCO2. This is bedside. Thus, the patient is experi- operating room, she received
commonly seen during states of encing respiratory alkalosis and an more than 8 L of fluid and blood
hypoxia, such as in pneumonia, pul- increased anion gap acidosis sec- products, but she has been
monary emboli, heart failure, and ondary to aspirin overdose, and the aggressively diuresed since that
severe anemia.1 Other causes metabolic alkalosis is secondary to time. In the past 3 days she has
include psychogenic hyperventila- excessive HCO3̄ ingestion. generated 7 L of urine output,
tion, pregnancy, hepatic failure, and her BUN and creatinine
salicylate overdose, and cere- CONCLUSION have increased to 40 mg/dL and
brovascular accidents. Treatment Acid-base pathophysiology can 1.5 mg/dL, respectively. This
of respiratory alkalosis should be be complicated and overwhelming morning her ABG shows the fol-
solely aimed at correcting the for both novice and experienced lowing: pH = 7.51; pCO2 =
underlying cause. clinicians. Recalling the 5 major dis- 46 mm Hg; HCO3̄ = 35 mEq/L.
Case 5 is complicated in the orders that can occur and using the 4. In the early morning hours, a 42-
sense that it is a mixed acid-base stepwise approach proposed in this year old man is found down on
disorder. If the stepwise approach is manuscript will help clinicians at all the street; he is unresponsive. He
used, elevation in the patient’s pH levels of training in assessment and is transported via ambulance to
will be observed, indicating alkalo- development of treatment options the ED. The patient is a John Doe
sis. Unfortunately, assessing the for any acid-base disturbance with no known medical history.
patient is difficult because of his encountered in practice. The following laboratory values
current mental status; therefore, are taken: Na+ = 125; Cl¯ = 79;
laboratory values must be relied on TEST YOUR NEW SKILLS K+ = 7.5; HCO3̄ = 3; BUN = 45;
exclusively. The pCO2 is markedly Diagnoses for these cases can be creatinine = 3.2; glucose = 1,500;
decreased, indicating respiratory found on page 818. pH = 6.86; pCO2 = 23. Blood
alkalosis. Furthermore, the HCO3̄ is 1. A 22-year-old man with no med- has large ketones. Urine drug
also markedly decreased, indicating ical history is admitted after screen is positive for cocaine.
metabolic acidosis. After recogniz- being “found down” at a party 5. A 40-year-old man is admitted to
ing metabolic acidosis, the next step where he drank a fifth of the hospital with a 2-day history
is calculation of the anion gap, whiskey in 20 minutes. On of persistent vomiting. The fol-
which in this case is strikingly ele- arrival to the emergency depart- lowing laboratory values are
vated at 35 mEq/L. After an ment (ED), he is neurologically taken: pH = 7.40; pCO2 = 38 mm
increased anion gap is recognized, unresponsive and has the follow- Hg; HCO3̄ = 26 mEq/L; Na+ =
the next step is calculation of the ing laboratory values: pH = 7.23; 149 mEq/L; Cl– = 100 mEq/L;
delta gap (23 mEq/L), which is then pCO2 = 58 mm Hg; HCO3̄ = 24 BUN = 90 mg/dL; creatinine =
added back to the serum HCO3̄ to mEq/L. 7.1 mg/dL.
determine what HCO3̄ would be in 2. A 58-year-old woman has been
the absence of unmeasured anions. hospitalized in the intensive care REFERENCES
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814 Volume 43, October 2008

ABCs of ABGs: A Guide to Interpreting Acid-Base Disorders

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