Resident 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:
- Describe the six common acid-base disorders.
- Utilize a step-wise approach to diagnosing common acid-base disorders.
- Solve clinical problems involving acid-base disorders.
References:
- Greenberg, A; et al. Primer on Kidney Disease, 2nd Ed. National Kidney Foundation. San Diego, 1998. (71-97).
- Brenner, B.; et al. Brenner & Rector’s The Kidney, 7th Ed. Saunders, Philadelphia, 2004. (937-941, 944-969, 969-976)
- Hall, P. MKSAP 13. ACP. Philadelphia. 2003. 45-53.
Some “Basic” Definitions and Concepts
- 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
- 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-]
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Attending Physician:
Define the acid-base disorders.
Ask the learners which of the scenarios suggests a given acid-base disorder.
ScenarioAnswer
1. Surgical patient with prolonged NG suction:
2. End stage renal disease patient
3. Patient with early sepsis
4. Patient with respiratory failure
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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
- Does the clinical scenario suggest the possibility of an acid base disorder
- Is there an acid base disorder-(see Steps).
- What is the biggest danger of status asthmaticus?
- What should you have done upon receiving the ABG results?
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.
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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
- What should be done at this point?
- Ask the learner to go through the Steps:
Step I
- Does the clinical scenario suggest a given acid-base disorder?
Step 2 & 3
- 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?
Step 5: Is the compensation appropriate?
- does expected pH = measured pH?
- does expected [HCO3-] = measured [HCO3-]
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?
Step 7: What is the delta-delta? (use only with metabolic acidosis)
- 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, fatembolus, 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.
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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
- Ask the learner to explain potential etiologies of this presentation (Step 1).
- (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
- What is the primary disturbance (Step 4)?
- Is the compensation appropriate (Step 5). In other words, is the change in pCO2 that is measured, appropriate?
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).
- What is the anion gap and how does it modify your acid base diagnosis (Step 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.
- 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-.
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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
- Given the history and presentation, what is the likely diagnosis and what acid-base disturbance would you expect to find (Step 1)?
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)?
4. Is the compensation appropriate (Step 5)?
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)?
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.
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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
- Given the history and clinical presentation, what are some diagnostic considerations?
- What acid base problem would you suspect if the patient had bullumirexia
(Step 1)? .
- 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
- What is the primary is the primary disorder (Step 4)?
- Is compensation appropriate (Step 5)?
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
- What is the anion gap and what process does it indicate (Step 6)?
- What is the delta-delta (Step 7)?
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