Download Clinical Review of Acid Base Disorders

Clinical Review of Acid
Base Disorders
Parham Eftekhari, D.O., M.Sc.
Assistant Professor of Clinical Medicine
Nova Southeastern University
ACOI Convention 2015
Basic Review of Acid Base
Metabolic acidosis — An acid-base
disturbance initiated by a reduction in plasma [
HCO3- ]
 Metabolic alkalosis — An acid-base
disturbance initiated by an increase in plasma [
HCO3- ]
 Respiratory acidosis — An acid-base
disturbance initiated by an increase in PaCO2
 Respiratory alkalosis — An acid-base
disturbance initiated by a reduction in PaCO2

Clinical Adverse Effects of Severe Acidosis
Impairment of cardiac contractility
 Arteriolar dilatation, venoconstriction
 Attenuation of cardiovascular responsiveness to IV
vasopressor in ICU
 Sensitization to fatal arrhythmias (ventricular fibrillation
and tachycardia).
 Hyperventilation, respiratory muscle fatigue.
 Reductions in cardiac output, arterial BP, and hepatic and
renal blood flow.
 Increased metabolic demands
– Insulin resistance, inhibition of anaerobic glycolysis,
reduction in ATP synthesis, and hyperkalemia

Clinical Adverse Effects of Severe Alkalosis
Decreased myocardial contractility
 Increased arrhythmias
 Decreased cerebral blood flow
 Altered mental status
 Neuromuscular excitability
 Impaired peripheral oxygen unloading

Important Key Points

Metabolic acidosis (Ph < 7.35)
– check anion gap
 Non-anion gap hyperchloremic vs Anion gap

Metabolic alkalosis (Ph >7.45)
– Chloride-sensitive (low urine chloride <10)
 GI losses (vomiting, diuretics common)
– Chloride-resistant (urine chloride >20 )
 Hyperaldosteronism, Cushings, Barters /Gitelmans
Syndrome and severe potassium depletion.
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Mixed acid-base disturbance
Step Wise Approach to Acidosis
Delta Delta Gap
Rastegar, A. J Am Soc Nephrol 18: 2429–2431, 2007
Importance of Osmolar Gap
Osmol Gap= measured osmolality – calculated osmolality
Kraut JA et al. Clin J Am Soc Nephrol 2008; 3:208.

In a patient with a Hyperchloremic NonAnion Gap metabolic acidosis, Calculate Urine
anion gap.

UAG Positive: Think Renal Tubular
Acidosis
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A positive UAG suggests impaired renal distal acidification (renal tubular
acidosis).
UAG Negative: Think GI loss, Diarrhea
– A negative UAG suggests GI loss of bicarbonate (diarrhea)
 Usually less than -10 mmol / L
 “neGUTive” = GUT Loss
Example #1
65 yo female with Diabetes Type 2, HTN
presents to ER with a complaint of severe
vomiting and weakness for 5 days.
 Medication at home includes metformin, hctz.
 Physical examination reveals hypotension,
tachycardia, and diminished skin turgor.
 The laboratory finding include the following:
 Electroyes: Na 140 , K 3.4, Cl 77 HCO3 9,
glucose 220 BUN 60, Cr 2.1, Osmol 314.
 ABG: pH 7.23 , PCO2 22mmHg, PaO2 90

Step Wise Approach

Step 1: Evaluate Acid-Base disturbance. Evaluate ABG.

Step 2: Calculate Anion Gap

Step 3: Calculate Predicted Respiratory Response

Step 4: Calculate Delta [ AG / HCO3 ]

Step 5: Evaluate Potential Cause of High AG acidosis.
Answer
Step 1: Evaluate Acid-Base disturbance.
Acidosis
 Step 2: Anion Gap
Na – [(Cl + HCO3-)] = 134 -(77 + 9) = 54 High
 Step 3: Respiratory Response
–PCO2 = 1.5 × [HCO3-]) + 8 ± 2 = 19-23  Appropriate
–or HCO3 +15 = 24.
 Step 4:Delta AG / HCO3
42/15 = 2.8 high concurrent metabolic alkalosis likely from vomiting
 Step 5: Evaluate High AG acidosis.
Check lactate= 4.8 elevated.
Assessment:
Mixed high anion gap metabolic acidosis with concurrent metabolic
alkalosis likely due to lactic acidosis from Metformin toxicity in
setting of acute renal failure and prolonged vomiting.
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Example #2
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66 year old male with DM2, CAD, and HTN evaluated for 8 day
diarrhea, abd pain, and poor po intake.
Medication include lisinopril 20mg, ASA 81mg, and Metformin.
Physical exam: Volume depleted, dry skin turgor.
Labs: Glucose 128, BUN 21, Creat 1.2, Na 136, Cl 114, C02 13,
albumin 4, and urine PH 6.
Urine Na= 32, Urine K= 21, Urine CL=80.
ABG: 7.27/ C02 28 / 90 po2
Whats the likely Acid-Base disorder?
1) Diarrhea
2) Type 4 RTA
3) Type 1 RTA
4) Metformin
Step Wise Approach

Step 1: Evaluate Acid-Base disturbance. Evaluate ABG.

Step 2: Calculate Anion Gap

Step 3: Calculate Predicted Respiratory Response

Step 4: Calculate Urine Anion Gap

Step 5: Evaluate Potential Cause of High AG acidosis.
Step Wise Approach

Step 1: Evaluate Acid-Base disturbance. Evaluate ABG.
– Metbolic acidosis

Step 2: Calculate Anion Gap
– Normal anion gap / Hyperchloremic
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Step 3: Calculate Predicted Respiratory Response
– PCO2 = 1.5 × [HCO3-]) + 8 ± 2 = 25-29  Appropriate
– or HCO3 +15 = 28.
Step 4: Calculate Urine Anion gap
= 53-80 = - 27 (neGUTive)
Step 5: Evaluate Potential Cause of acidosis.
– Diarrhea
Assessment:
Hyperchloremic NAG acidosis with appropriate
respiratory compensation secondary to diarrhea with negative urine
anion gap and normal lactate.
Example #3
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52 yo homeless alcoholic patient brought in with
profound lethargy, hypoxemia, and in comatose
state.
Physical exam: Lethargic, obtunded, tachycardic,
and tachypnic with minimal urine output.
Labs: Glucose 88, BUN 45, Creat 3.8, Na 138, Cl
98, bicarb 14, plasma osmolality 330. Ethanol level
negative.
ABG: 7.10 / C02 42/ 78 po2
Lactate mildly elevated 2.2 (1.8 upper limit)
Patient was intubated shortly after presentation.
Step Wise Approach

Step 1: Evaluate Acid-Base disturbance. Evaluate ABG.

Step 2: Calculate Anion Gap

Step 3: Calculate Predicted Respiratory Response

Step 4: Calculate Delta [ AG / HCO3 ]

Step 5: Evaluate Potential Cause of High AG acidosis.
Step Wise Approach
Step 1: Evaluate Acid-Base disturbance. Evaluate ABG.
– Life threatening Metbolic acidosis
 Step 2: Calculate Anion Gap
– Elevated at 26
 Step 3: Calculate Predicted Respiratory Response
– PCO2 = 1.5 × [HCO3-]) + 8 ± 2 = 29-31  Poor Resp
Compensation
– or HCO3 +15 = 29.
 Step 4:Delta AG / HCO3
14/10= 1.4 pure metabolic acidosis
 Step 5: : Evaluate Potential Cause of High AG acidosis.
Bc Lactate slightly elevated but very high anion gap, rule out other etiology
such as exogenous toxin / alcohols.
Check Osmol Gap: Measured Osmol (330) – Calculated osmol (297)= 33.
Assessment: Very high anion gap metabolic acidosis with poor respiratory
compensation likely from hypoventilation fatigue r/o toxic alcohol ingestion

CJASN January 2008 vol. 3 no. 1 208-225
Toxic Alcohol Ingestion Review
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Large anion gap without DKA or Lactate or explainable cause of
acidosis, check osmolal gap R/O methanol, ethylene glycol, or
isopropyl alcohol exposure.
The hallmark of isopropyl alcohol metabolism is a marked ketonemia
and ketonuria in the absence of metabolic acidosis.
For isolated ingestions of isopropyl alcohol, there is no role for
antidotal therapy with either fomepizole or ethanol.
Alcohol dehydrogenase (ADH) inhibitor (Fomeprizole
Dialysis if +ingestion and:
– Metabolic acidosis, regardless of drug level
– Elevated serum levels of methanol or ethylene glycol (more than 50
mg/dL), unless arterial pH is above 7.3.
– Evidence of end-organ damage (eg, visual changes, renal failure)
– Activated charcoil or ipecac NO ROLE Rx.
Metabolic Alkalosis
Excessive gastrointestinal hydrogen loss
or
Excessive renal hydrogen loss
When
the etiology of metabolic alkalosis is
not apparent from the history and physical
examination, measurement of the urine
chloride, urine sodium, and urine potassium
can be helpful.
Example #4
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A 40yo thin, female presents to the emergency
room with fatigue, lethargy, dizziness for 3
days.
She denies any pmhx besides anxiety. Denies
vomiting or diarrhea.
Meds at home: alprazolam prn.
Vitals normal.
Exam shows decreased skin turgor.
Labs: Na 131 K 2.4 CL 78 C02 33 BUN 40 Cr
1.6.
ABG: 7.58 / CO2 46 / HCO3 33 /Pao2 90
Example #4

Step 1: Evaluate Acid-Base disturbance.
Evaluate ABG.

Step 2: Calculate Predicted Respiratory
Response

Step 3: What additional labs may be
helpful in diagnosis.
Example #4
Labs: Na 132 K 2.4 CL 78 C02 33 BUN 40 Cr
1.6.
 ABG: 7.58 / CO2 46 / HCO3 33 /Pao2 90
– Metabolic Alkalosis which is compensated
  Urine Cl 8 Na <10 FENa <1%
– Low urine Cl with low Na with normal vitals
without medication or gi loss – suspect
diuretic.
 Diagnosis: diuretic abuse in setting of anxiety
disorder and anorexia nervosa.

Example #5
A 44 yo patient with HTN presents to ER with weakness, headache
and fatigue. He works as a painter but could not go to work
today.
Meds: Aspirin 81 daily, lisinopril 10mg.
Plasma Na 139, Cl 116, HCO3 15, and K of 2.1 Glucose 81
Ethanol level <10. Serum Ketone negative.
ABG: PH 7.31 / C02 30 / HCO3 16 / O2 98
Urine studies: PH 6.5, Na=15, K=20, and CL=10.
 Whats the most likely diagnosis?
1)
2)
3)
4)
Renal Tubular Acidosis (RTA)
Aspirin Toxicity
Alcoholic Ketoacidosis
Isopropyl Alcohol intoxication
Toluene Intoxication
Toluene (methylbenzene, toluol,
phenylmethane) is commonly used as an
industrial solvent for the manufacturing of
paints, chemicals, pharmaceuticals, and
rubber.
 Weakness from hypokalemia and acidosis
(Distal RTA) classic in glue sniffers or
inhalation of paint thinners.

Camara-Lemarroy et al. BMC Emergency
Medicine (2015) 15:19
Definition of RTA
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Renal tubular acidosis (RTA) is applied to a
group of transport defects in:
– the reabsorption of bicarbonate (HCO3-)
– the excretion of hydrogen ion (H+), or both.
The RTA 1 and 2 syndromes are characterized by
a relatively normal GFR and a metabolic acidosis
accompanied by hyperchloremia and a normal
plasma anion gap.
RTA type 4 (Hyperkalemic) can be seen w/ more
advanced CKD.
Ring et al. Clinical Review: Renal Tubular Acidosis
Crit ical Care 2005, 9:573-580
Ammonia Recycling in Acidosis
Rationale for Treating Metabolic
Acidosis
Decreased progression of chronic kidney disease
– Mechanism underlying protective effect of bicarb treatment
unknown, may be related to tubulointerstitial inflammation.
Prevention of bone buffering
– Acidosis enhances osteoclastic activity and inhibits osteoblastic
– Correction acidosis can help diminish stimulus for
hyperparathyroidism
 increased sensitivity of parathyroid gland to calcium.
Improved nutritional status
– Uremic acidosis can increase muscle breakdown and diminish
albumin synthesis
– Muscle wasting and weakness
– Hypercatabolic state, increase cortisol, reduced insulin-like
growth factor.
J Am Soc Nephrol 13: 2186–2188, 2002
Exampe #6
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A 32 yo man with hx of alcoholism + psychiatric
disease brought in to ER disoriented and lethargic.
Denies any meds at home.
Vitals stable, 02 sat 98% 2L NC.
Exam normal.
Labs: Glucose 110 Na 142 K 4.1 HCO3 23 BUN 18 Cr
1.1. Ethanol <10. Serum Ketone+
Urinalysis: No glucosuria, but +4 ketones
ABG: PH 7.4 / Co2 44 / O2 92

Which of the following could account for
these findings?
1)
 2)
 3)
 4)
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Alcoholic Ketoacidosis
Diabetic Ketoacidosis
Isopropyl alcohol intoxication
Toluene
Metabolism of Toxic Alcohols
****The hallmark of isopropyl alcohol metabolism is a marked ketonemia
and ketonuria in the absence of metabolic acidosis.
CJASN January 2008 vol. 3 no. 1 208-225
Review of Toxic Alcohol Ingestion
Kraut, JA et al. CJASN January 2008 vol. 3 no. 1 208-225
Thank You
Main Textbook References

Schrier et al, Metabolic Acidosis
– Kidneyatlas.org online
Brenners and Rectors, The Kidney 14th
edition 2008.
 Comprehensive Clinical Nephrology 4th
edition.
