Attending Version
“Perturbations in pH: Evaluation of Acid Base Disorders”
Module
created by Dr. George D. Comerci, Jr.
Disorders involving abnormalities of acid base balance are very common in hospitalized
patients and often provide clues to underlying pathology. This goal of this short module
is to provide an overview of an approach to these disorders. It is not intended to be an
exhaustive treatise on acid-base metabolism, but an introduction to the management of
these problems. This module is case-based, and designed to allow the attending to pick
the cases most suited to the team’s needs.
Objectives:
At the end of this module the learner will be able to:
1. Describe the six common acid-base disorders.
2. Utilize a step-wise approach to diagnosing common acid-base disorders.
3. Solve clinical problems involving acid-base disorders.
References:
1. Greenberg, A; et al. Primer on Kidney Disease, 2nd Ed. National Kidney
Foundation. San Diego, 1998. (71-97).
2. Brenner, B.; et al. Brenner & Rector’s The Kidney, 7th Ed. Saunders,
Philadelphia, 2004. (937-941, 944-969, 969-976)
3. Hall, P. MKSAP 13. ACP. Philadelphia. 2003. 45-53.
Some “Basic” Definitions and Concepts
1.
2.
3.
4.
5.
6.
7.
Acidosis is a process whereby the unopposed accumulation of protons
[H+] results in a state of acidemia.
Alkalosis is a process whereby the unopposed loss of protons [H+] results
in a state of alkalemia.
Respiratory processes result from accumulation or loss of CO2.
Metabolic processes result from the accumulation or loss of non-volatile
acids.
Simple disorders involve one perturbance in acid-base, whereas mixed
disorders are due to two or more simultaneous disorders.
Anion Gap: the concentration of unmeasured anions (proteinate,
phosphates, sulfates, and organic acids):AG = [Na+] – ([Cl-] + [HCO3-]):
normal = 6-13
H2O + CO2
[HCO3-] + [H+]
“Basic” Approach to Acid-Base Disorders
1.
2.
3.
4.
5.
6.
7.
*
Does the patient’s history or exam suggest a possible acid-base problem?
Obtain venous blood sample for: CO2 (HCO3-), [Cl-], [K+].*
Obtain an ABG for: pH, PCO2, pO2 and [HCO3-].
Determine the primary disturbance.
Determine whether compensation is appropriate.
Calculate the AG.
If a gap, metabolic acidosis, calculate the delta-delta to detect “hidden
disorders.
With regard to a venous sample CO2 is the same as [HCO3-]
******************************
Attending Physician:
Define the acid-base disorders.
Ask the learners which of the scenarios suggests a given acid-base disorder.
Scenario
1.
2.
3.
4.
Surgical patient with prolonged NG suction:
End stage renal disease patient
Patient with early sepsis
Patient with respiratory failure
********************************
Answer
Metabolic Alkalosis
Metabolic Acidosis
Respiratory Alkalosis
Respiratory Acidosis
Case #1: “When is normal, not normal”
Objective-To consider the clinical scenario when interpreting the lab data
You are called to evaluate an asthmatic patient who “doesn’t look good” on 4E.The
patient is a 21 y/o student who was admitted with a severe asthma exacerbation. This is
his 2nd day on round the clock nebs. His sats are stable on 92% nasal O2, does not seem
to be working hard to breath, he has diffusely decreased breath sounds but he is moving
air in all fields, albeit with diffuse expiratory and inspiratory wheezes. You order an
ABG and a chem. 10. The electrolytes are normal as is the Ca++ and Phos and the AG.
The ABG reveals a pH of 7.42, pO2 = 75, pCO2 = 40 and a [HCO-3] of 25.
You order another neb and return to the ER to evaluate your next admission. Two hours
later, you are called back to 4E as the patient has coded. What went wrong?
Attending Physician
1. Does the clinical scenario suggest the possibility of an acid base disorder? (yes,
respiratory alkalosis)
2. Is there an acid base disorder-(see Steps). (no)
3. What is the biggest danger of status asthmaticus? (respiratory fatigue)
4. What should you have done upon receiving the ABG results? (consider
transfering the patient as he made need mechanical ventilation).
Teaching Point: Patients with status asthmaticus are always tachypneic and usually
demonstrate a respiratory alkalosis due to the hyperventilation that accompanies this
problem. When the patient with status asthmaticus has a “normal ABG” this in fact is an
indication of respiratory fatigue and impending respiratory failure. The patient, at this
point, should be considered a candidate for mechanical ventilation or at the very least,
transfer to the MICU for aggressive treatment and monitoring. Thus, normal is not
always normal and the ABG must be interpreted with the clinical scenario in mind.
********************************
Case #2: Too much of a good thing
Case objective: To recognize respiratory acidosis
Mr. Bond, James Bond, is admitted to the Burn and Trauma service after having suffered
a gunshot wound to the proximal femur. He has returned for reconstructive surgery and
is doing quite well. He is placed on morphine PCA. You are called to evaluate Mr. Bond
later on that evening because the nurse found him unresponsive, hypotensive and with a
“sat” of 77%.
Attending Physician
1.
What should be done at this point?
Attend to ABCs
 Assure airway patency
 Ambu bag support with 100%O2
 Saline Bolus
2.
Ask the learner to go through the Steps:
Step I
a. Does the clinical scenario suggest a given acid-base disorder? (yes,
this appears to be an rather acute cardio pulmonary or CNS event
which would suggest that a metabolic and/or respiratory acidosis will
be found)
Step 2 & 3
b. Obtain a venous sample and arterial sample for appropriate lab studies
The patient responds to the interventions with an O2 sat of 94% and a systolic BP of
99mmHg. You send a chem. 7, CBC, ABG and a “tox screen- (he may have been
poisoned by a rival spy!). You stop the PCA and administer .4mg of Narcan IV and Mr.
Bond wakes up and requests, “a Martini, shaken, not stirred”. The lab values drawn by
the nurse earlier are as follows:
CBC = nl
Chem 7: Na=140, K=4, Cl=100, HCO3=29
ABG: pH = 7.10, pCO2 = 80, pO2 = 56
3.
Ask the learner to continue with the Steps:
Step 4: What is the primary disturbance? (respiratory acidosis)
Step 5: Is the compensation appropriate?
 does expected pH = measure pH? (yes)
 does expected [HCO3-] = measured [HCO3-] (yes)
In a simple respiratory acidosis;
Expected pH = 7.40 – [(measured pC02-normal pCO2) x .008]
pH = 7.40-[(80-40) x .008]
pH = 7.40-.32
pH = 7.08 (which is almost the same as measured)
The CO2 or [HCO3-] increase 1 point for each 10-point rise in pC02, thus,
CO2 or [HCO3-] = 25 + 4
CO2 or [HCO3-] = 29
Step 6: What is the anion gap? (11, which is normal)
Step 7: What is the delta-delta? (use only with metabolic acidosis)
3.
Ask what mechanisms are responsible for respiratory acidosis.
(examples?)
Teaching Point: Always attend to ABCs first prior to entering diagnostic mode. The
learner should also be asked to describe the differential diagnosis of the patient’s
presentation: (MI, arrhythmia, PE, fat embolus, CVA, etc).
Respiratory Acidosis (Case 2)
Hypercapnia develops, most commonly from decreased alveolar ventilation, this being
the most common mechanism underlying hypercapnia that occurs in our patients. This
could result from CNS depression (drugs), neuromuscular impairment (fatigue,
myasthenia gravis) or a mechanical disorder causing ventilatory restriction
(pneumothorax). Other causes include frank airway obstruction (aspiration of a foreign
body) or disordered diffusion of CO2 from the blood through the pulmonary parenchyma
into the alveolus (instl lung disease, emphysema due to loss of parenchyma, etc.). Even
mild hypercapnia must be evaluated and monitored very closely as it is often the
harbinger of deteriorating physiologic homeostasis.
********************************
Case #3: A Case of Turista
Objective: Identify a case of metabolic acidosis
Mr. N.B. Forrest, a 36 y/o diabetic is admitted to the ER with a six-day history of nausea,
and diarrhea after a trip to Mexico. He has eaten and drank little in the past two days. He
was previously well aside from his DM that is well controlled with metformin, his only
medication. He appears dehydrated and complains of fatigue and weakness. His vitals
are all normal except for mild tachypnea at a rate of 24. His physical examination is
unremarkable aside from evidence of dehydration.
Attending Physician
1. Ask the learner to explain potential etiologies of this presentation (Step 1).
 DKA
 Metabolic acidosis due to diarrhea and resultant loss of HCO3 Metabolic acidosis from metformin
 Metabolic alkalosis due to protracted vomiting
2. (Step 2-3)- Ask the learner what laboratory studies should be ordered.
The laboratory values are as follows:
CBC c Diff: nl.
Chem 7: Na = 146, Cl = 102, K = 5, CO2 = 12, BUN = 84, Creat. = 3.4
AG = 32
ABG = pH = 7.24, pCO2 = 14, pO2 = 70, HCO3 = 12
U/A = trace ketones, high spec gravity
Serum lactate = pending
3. What is the primary disturbance (Step 4)? (metabolic acidosis-low pH, HCO3)
4. Is the compensation appropriate (Step 5). In other words, is the change in pCO2
that is measured, appropriate? (Yes)
Change in pCO2 = [(1.5) HCO3] + 8
Change in pCO2 = [(1.5) 12] + 8
Change in pCO2 = 26
Normal pCO2 = 40
Measured pCO2 = 14 (a change of 26, thus appropriate compensation is
noted and there is not an additional acid base disturbance).
5. What is the anion gap and how does it modify your acid base diagnosis (Step 6)?
(anion gap, metabolic acidosis)
6. What is the delta-delta (used only with metabolic acidosis to detect the presence
of an additional acid-base disorder).
Delta-delta = change in anion gap / change in HCO3
32 (measured AG) – 14(nl AG) / 25(nl HCO3) – 12(observed HCO3)
18 / 12 = 1.5
A delta-delta of 1–2, suggests that there is only one organic acid
contributing to the process. A delta-delta < 1 suggest that the acidosis is
more severe than expected, a delta-delta > 2 suggests that there is also a
superimposed metabolic alkalosis.
7. What is the differential diagnosis of an anion gap acidosis?
M= methanol
U = uremia
D = Diabetic/alcoholic ketoacidosis
D = Drugs (metformin,
P = paraldehyde (an old fashioned drug used for EtOH withdrawal)
I = infection( i.e. sepsis)
L = lactate (i.e. from bowel ischemia)
E = ethylene glycol
S = salicylates
Teaching Note: This patient has a lactic acidosis due to metformin. Metformin rarely
causes this disorder unless there is a concomitant problem, such as renal insufficiency. In
this case, the patient probably developed the pre-renal azotemia, which led to a cascade
of events.
Metabolic Acidosis (Cases 3 and 5)
Metabolic Acidosis is a condition characterized by one of the following mechanisms:
consumption of plasma HCO3-, loss of HCO3- from the GI tracts or kidneys, or when
the kidneys fail to regenerate HCO3-. The principle of electroneutrality notes, quite
simply, that the number of (+) charges has to equal the number of (-) charges. The anion
gap is the difference between unmeasured cations (UC) and unmeasured anions (UA):
UC = primarily Ca++, Mg++
UA = albumin, phosphate, sulfates and organic anions
Thus…
(Na+) + (K+) + (UC+) = (Cl-) + (HCO3-) + UA
AG = UA – AC
In the case of gap acidoses (Table 2), the added anion is usually an organic acid (ie
lactate). The HCO3- is consumed by lactic acid’s proton (H+) and is proportionally
decreased as the lactate (UA) increases, thus the decrease in the HCO3 and rise in AG.
Note that normal AG of 10-11 [+/-] 2 can be affected by negatively charged albumin.
For every 1-point fall in albumin, the normal AG drops by 4. Also, the effect of
unmeasured cations (i.e., paraproteins of myeloma), can, likewise, decrease the AG.
The non-anion gap acidoses (Table 3), or hyperchloremic metabolic acidoses, do not
affect the gap due to the fact the loss of HCO3- is associated with a 1 to 1 increase in Cl-.
*******************************
Case #4 “When suction sucks”
Case Objectives: Metabolic Alkalosis
John LeGrange is a 25 y/o man who you are asked to see for severe weakness. He was
admitted for a SBO and had 4 days of NG suction. He is now passing stool.
He is otherwise healthy and takes no medicines, uses no drugs and works at a Circle K.
His initial evaluation reveals him to be somewhat hypotensive (86mmHg in the standing
position/ pulse = 119) and with very dry mucous membranes. His physical examination
is normal.
Attending Physician
1. Given the history and presentation, what is the likely diagnosis and what acidbase disturbance would you expect to find (Step 1)?
(This patient is probably dehydrated and has developed a significant metabolic
alkalosis due to loss of gastric HCL).
2. What lab work would the learner like to order (Step 2and 3)?
U/A = nl, but concentrated
CBC c Diff = nl
Chem 7: NA = 131, k = 3.1, Cl = 87, CO2 = 34
ABG: pH = 7.48, pO2 = 70, pCO2 = 48, HCO3 = 35
3. What is the primary disorder (Step 4)? (metabolic alkalosis-high pH, low HCO3)
4. Is the compensation appropriate (Step 5)? (Yes)
For every 1 mEq increase in the HCO3, the pCO2 increases by .7mmHg
The HCO3 has increased by 10:[35(measured HCO3 – 25(nl HCO3)]
The pCO2 should increase by 7:[40(nl pCO2) = 7(.7 x increase in HCO3)]
The measure pCO2 = 48 which is very close to calculate rise, thus there is
Probably no hidden disorder
5. What is the anion gap (Step 6)?
131 – ( 87 + 34) = 10. The anion gap is normal
6. What is the delta-delta(Step 7)?
(not calculated, as is only used in metabolic acidosis)
Metabolic Alkalosis:
The kidneys are responsible for maintenance of HCO3- levels in the plasma. The
kidneys generate HCO3- to titrate accumulation of acid in the plasma and retain acid/
excrete HCO3- when the plasma HCO3- is too high. Common causes of a non-gap
acidosis include the loss of acid via the kidneys or via loss of stomach HCL.
Volume /(chloride-responsive) vs. Non-volume /(chloride-resistant)
Normally, the kidneys would respond to this by expanding the volume and secreting
HCO3-. Often the conditions resulting in metabolic acidosis are associated with a
contracted plasma volume and despite the apparent hyperchloremia, a total body deficit
of NaCl. The kidneys first responsibility is to preserve volume, thus, diminished HCO3
excretion is a result of the kidney’s attempt to preserve volume. Once the volume is
restored with saline solutions, bicarbonaturia results. This is called chloride or volume
responsive metabolic alkalosis and urine electrolytes demonstrate a Cl- < 15.
The chloride resistant forms of metabolic alkalosis are often associated with endocrine
conditions causing total body K+ deficits (primary hyperaldosteronism, Cushings).
Usually, total body sodium is normal or high. The kidney, is avidly resorbing K +, must
generate a [H+] in exchange. The K+ is absorbed with the HCO3 generated from the
production of H +: remember: [H2O + CO2
H+ HCO3-]. In this case, the
urinary Cl- is > 20mEq.
********************************
Case # 5: When thin is too thin
Objectives: To identify a case of non-anion gap metabolic acidosis.
Cindy Chio is a 25 y/o ballet dancer who is referred to you by her family physician for
unrelenting fatigue. She has been very healthy, and denies any symptoms of any kind.
She is preparing for a major audition in LA and has been working hard to prepare for it.
She has been amenorrheic for six months, has no symptoms of thyroid disease or
diabetes. She uses no alcohol, drugs or tobacco. She denies meds of any kind.
Her physical exam is remarkable for normal vital signs. You are impressed by her very
thin build and calculate a BMI of 18. Her examination is totally normal.
Attending Physician
1. Given the history and clinical presentation, what are some diagnostic
considerations?
(anorexia nervosa, bullumirexia, HIV, endocrinopathy, cancer, etc.).
2. What acid base problem would you suspect if the patient had bullumirexia
(Step 1)? (metabolic acidosis).
3. What would be appropriate lab test to order (Step 2-3)?
(Chem 7, TFTS, CBC, HIV, urine pregnancy test, stool test for laxatives and an
ABG after you see the Chem 7)
The test results are as follows:
CBC, TFTs = nl, stool test for laxative +
Glucose = nl
Urine pregnancy test and HIV test = negative
Na = 139, K = 3.5, Cl = 114 CO2 = 10, BUN/CREAT = nl
ABG: pH = 7.28, pCO2 = 17, HCO3 = 11, pO2 = 70
4. What is the primary is the primary disorder (Step 4)? (metabolic acidosis low pH
5. Is compensation appropriate (Step 5)? (yes)
Change in pCO2 = (1.5) HCO3 + 8
Change in pCO2 = (1.5)(10) + 8
Change in pCO2 = 23
Expected pCO2 = 40 (nl pCO2) – 23 (change in pCO2)
Expected pCO2 = 17. This approximates the measured pCO2 closely,
thus there is unlikely to be a hidden disorder
6. What is the anion gap and what process does it indicate (Step 6)?
(The anion gap is 15, which is normal, indicating that this is a non-gap,
hyperchloremic acidosis).
7. What is the delta-delta (Step 7)? (not used as this is a non-gap acidosis)
Normal metabolism of an average protein diet results in the production of approximately
1 mEq/kg of H + ion. The kidney is responsible for, not only “off-loading acid”, but for
regenerating HCO3- lost in the titration of these H+ ions. It is obvious, than, that loss of
renal function, by any means, results in inability to carry out this function. Chloride
replaces the lost HCO3-, thus, the hyperchloremia that occurs. The hyperchloremic
acidoses occur via three mechanisms: excess loss of HCO3 through the GIT, loss of
HCO3 through the kidney (proximal RTA) or inability to secrete H+ (distal RTA).
Rarely, this can occur by acid loading with NH3Cl or by means of hyperalimentation.
The next step in this case (and indeed that of all hyperchloremic acidoses, is to determine
if the kidneys are appropriately secreting acid. This is done either by the urine dipstick
or, more accurately, by inference from the Urine Anion Gap (UAG).
UAG = ( Na + K) – (Cl + HCO3).
A value of 0 to –50 suggests that the kidneys are appropriately secreting acid. This is the
most common situation with excessive losses of HCO3 in the stool, as is occurring in this
patient who is abusing laxatives. This can also be seen in proximal RTA, the discussion
of which is beyond the intent of this module.
Post Module Evaluation
Please place completed evaluation in an interdepartmental mail envelope and address to
Dr. Wendy Gerstein, Department of Medicine, VAMC (111).
1) Topic of module:__________________________
2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)
3) Were there any obvious errors, confusing data, or omissions? Please list/comment
below:
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
4) Was the attending involved in the teaching of this module? Yes/no (please circle).
5) Please provide any further comments/feedback about this module, or the inpatient
curriculum in general:
6) Please circle one:
Attending
Resident (R2/R3)
Intern
Medical student