Last edited: 9/13/2021

1. ACID BASE DISORDERS

Acid Base Disorders and ABG Interpretation | Introduction Medical Editor: Maxine Abigale R. Bunao

OUTLINE
I) INTRODUCTION
II) TYPES OF ACID BASE DISORDERS
III) COMPLICATIONS
IV) COMPENSATION MECHANISMS FOR PRIMARY DISORDERS
V) ABG INTERPRETATION
VI) PRACTICE PROBLEMS
VII) APPENDIX
VIII) REVIEW QUESTIONS
IX) REFRENCES

I) INTRODUCTION
(A) ACIDOSIS (B) ALKALOSIS
Process by which protons are produced in a large amount Process by which protons are produced in a smaller
 ↑proton production or amount that’s present inside amount  ↓proton production
the extracellular fluid (ECF) Effect on the blood  Basic
Effect on the blood  Acidic o By using the formula pH = - log [H+]
o By using the formula pH = - log [H+]  As ↓proton concentration  ↑pH  alkalemia
 As ↑proton concentration  ↓pH  acidemia (alkaline in the blood)
(acidity in the blood) o Normal pH = 7.35 – 7.45
o Normal pH = 7.35 – 7.45 o Level of pH to confer significant acidemia: >7.45
o Level of pH to confer significant acidemia: <7.35
(C) OTHER MOLECULES INFLUENCING THE PH
(1) Henderson-Hasselback Equation (2) Modified Henderson-Hasselback Equation
Our body constantly undergoes metabolism  breaks ● If you want to determine the pH based upon the
down glucose & oxygen  CO2 & water (byproducts of bicarbonate (HCO2- ) & CO2, use this equation:
cellular metabolism) o Equation:
Equation:  pH = pKa + log (HCO3-)
o CO2 + H2O  H2CO3  H+ + HCO3- CO2
o Carbonic anhydrase:  pH = (HCO3-)
 Found in certain cells and membrane borders
pCO2
 Converts the reactants into Carbonic acid
 HCO3-  Uses mEq/L (milliequivalent)
(product)
 CO2  recorded on a pressure, uses mmHg
o Carbonic acid:
 weak acid • pCO2  partial pressure of carbon dioxide
 dissociates into protons and bicarbonate ● Basis of using logic instead of math for distinguishing the
primary disorder
o respiratory disorder OR
o metabolic disorder

II) TYPES OF ACID BASE DISORDERS

(A) RESPIRATORY DISORDER ● Pathophysiology:
Table 2. Respiratory alkalosis formula changes.
(1) Respiratory Acidosis
Formula Changes Interpretation
● Respiratory disorder causes the acidosis (↓pH) pH = (HCO3 )-
[N] (HCO3 ) = ↑ pH
-
↑ alkalinity due to
● Pathophysiology: pCO2 ↓↓↓ pCO2 ↓ pCO2
Table 1. Respiratory acidosis formula changes. Causes
Formula Changes Interpretation o CNS Hyperactivity center in the brain  ↑sending
pH = (HCO3-) [N] (HCO3-) = ↓ pH ↑ acidity due to
signals  ↑RR, consequentially breathes off ↑CO2
pCO2 ↑↑↑ pCO2 ↑ pCO2
 Anxiety
● Causes  Fever
o Depressed respiratory center in the brain (CNS  In pain
depression)  not sending signals  Ingestion of salicylates
o Nerve problem going to the muscles  not sending  Sepsis
signals  ↓ Diaphragmatic contraction o Hypoxemia: blood can’t get to the alveoli  ↓O2 tissue
o Neuromuscular disorder delivery  ↑RR, consequentially breathes off ↑CO2
o Obstructive lung disorders (COPD)
 Pneumonia
 ↓ exhaled CO2 ↑CO2  ↑acidemia
 Pulmonary edema
 Pulmonary embolism, clot
(2) Respiratory Alkalosis

● Respiratory disorder causes the alkalosis (↑pH)

ACID BASE DISORDERS RENAL PATHOLOGY: NOTE #1. 1 of 6

 (B) METABOLIC DISORDER III) COMPLICATIONS
(1) Metabolic Acidosis Organs that need attention
● Pathophysiology: o Heart
o Lungs
o Body ↑ retains H+ protons, not excreting it enough
o CNS
o Body ↑ loses Bicarbonate
(1) Acidosis
Table 3. Metabolic acidosis formula changes.
Table 5. Complications of acidosis.
Formula Changes Interpretation
Organ Effect
pH = (HCO3 ) -
↓ (HCO3 ) = ↓ pH
-
↑ acidity due to ↓
pCO2 [N] pCO2 HCO3- ↑ H+  ↓ contractility of myocardium
↓
● Causes:
↓ SV  ↓ CO  ↓ BP or MAP
RECALL:
Anion Gap (AG) can separate acidosis into two subtypes  Acts on arterial smooth muscle
can measure particular types of organic acids ↓
Formula: ↑ vasodilation: ↑ diameter, ↓ TPR
o Anion Gap = Cations – Anions ↓
o AG = Na+ - (Cl- + HCO3-) ↓ BP (hypotension), sometimes can lead to
o AG = the remaining amount that makes up this gap Heart shock
o <12 = Normal / NAGMA ↓
o >12 = High / AGMA Management: fluids, vasopressors
Note: ↑ Acidosis can be resistant to
Causes of AGMA: MUDPILES vasopressors
o M — Methanol
o U — Uremia (chronic kidney failure) ↑ HR
o D — Diabetic ketoacidosis ↓
o P —Propylene glycol Re-entrant tachycardia  Ventricular
o I — Isoniazid (given for TB regimen tachycardia
o L — Lactic acidosis
Goal: ↑ CO2  breathe it all out
o E — Ethylene glycol
↑ RR  ↑ work of breathing  ↑ fatigue
o S — Salicylates (Aspirin) Lungs
Causes of NAGMA: HARD UP Sequela if not reversed: Respiratory failure
o H — Hyperchloridemia: for patients receiving ↑ Normal Notes: Protons and Potassium go hand in
saline or Hypertonic saline hand
o H — Hyperalimentation: during total parenteral nutrition
(TPN) Metabolic
↑ Protons shift via pump 
o A — Acetazolamide effects
↑ H+ from outside to the inside of the cell
o R — Renal tubular acidosis ↓ Potassium inside = ↑ outside /
o D — Diarrhea (↑ loss of bicarbonate) Hyperkalemia  arrhythmia
o U — Ureteral Diversion: connection between ureter and
a part of the GI tract  ↑ Chloride spill Targets particular hormone produced:
o P — Pancreatic fistula Insulin which works on tissues to perform ↑
metabolic functions = ↓ blood glucose level
(2) Metabolic Alkalosis Pancreas Protons alter insulin function:
● Pathophysiology: ↑ H+  ↓ insulin effects on tissue cells
o ↓ H+ protons concentration ↓
Insulin resistance  ↑ Blood glucose levels
o Body ↑ retains Bicarbonate
↑ Protons
Table 4. Metabolic alkalosis formula changes.
↓
Formula Changes Interpretation CNS ↑ Cerebral volume (cell regulation)
pH = (HCO3-) ↑ (HCO3-) = ↑ pH ↑ alkalinity due to ↓
pCO2 [N] pCO2 ↑ HCO3- Altered mental status / Coma
Causes:
o V — Vomiting  ↑ HCl loss (acid)
o O — Overcorrection of hypercapnia
o M — Mineralocorticoid excess  ↑ aldosterone
o I — Iatrogenic  ↑HCO3- to preserve kidneys for
contrast induced nephropathy, or if (+) kidney failure;
if given NaHCO3- also
o T — Total volume loss: dehydrated, laxative abuse 
↑excrete HCO3- , blood loss, taking diuretics
↑volume loss

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 (2) Alkalosis IV) COMPENSATION MECHANISMS FOR PRIMARY
Table 6. Complications of alkalosis. DISORDERS
Organ Effect
Acute compensation:
N/A on contractility o Buffer system (bicarbonate-carbonic acid buffer
Acts on arterial smooth muscle system) can act on very fast BUT does not produce a
↓ significant change in the pH
↑ Arteriolar vasoconstriction  ↑ diameter,
(A) RESPIRATORY ACIDOSIS
↑ TPR
Heart ↓ ● Main compensation:
↑ BP o Kidneys for when there’s respiratory problem
↑ HR o Problem: Takes time
↓ Table 7. Respiratory acidosis compensations.
Ventricular tachycardia  Ventricular Condition Compensation
fibrillation Sends signals to kidneys but for a
Or SVT When ↑ CO2  LONG time (hours-days)
Goal: ↓ CO2  ↓ ventilation ↓ pH due to ↓
Lungs
↓ RR  ↓ Oxygen in  Hypoxemia (↑H+, ↓ HCO3-) ↑ Urinary excretion protons (H+)
↓ Protons  ↓ shift into the cell ↑ HCO3 reabsorption into the blood

● ↓ potassium leaving the cell = (B) RESPIRATORY ALKALOSIS

Hypokalemia
● ↓ Mg2+ leaving the cell = ● Main compensation:
Hypomagnesemia o Kidneys for when there’s respiratory problem
o Problem: Takes time
↓ Protons + Albumin Table 8. Respiratory alkalosis compensations.
↓ Condition Compensation
free, ionized Ca2+circulating the blood binds Sends signals to kidneys but for a
Pancreas onto the free, negatively charged spaces LONG time (hours-days)
↓ When ↓ CO2 
↓
↓ freely circulating Ca2+ ↑ pH due to
↓ Urinary excretion (H+) = ↑H+in the
(↓H+, ↑ HCO3-)
● Albumin in the blood ↑ negative charges blood
↓ HCO3 reabsorption into the blood
surrounding it = ↑proton binding
● ↑ free. unbound negatively charged (C) METABOLIC ACIDOSIS
spaces  ● Main compensation:
o ↑Ca2+ takes up the free. unbound o Respiratory center and takes a SHORT time to take
negatively charged spaces effect (minutes)
↑ Protons + ↑ neurons firing more than they Table 9. Metabolic acidosis compensations.
should Condition Compensation
CNS ↓ Stimulate CNS to ↑RR
Altered mental status / Coma + Seizures/ When ↓ HCO3
↓
Tetany  ↓ pH due to
↑ breathe off more CO2
(↑H+, ↓ HCO3-)
↓
↓ CO2 in the blood = to ↑ pH

(D) METABOLIC ALKALOSIS

● Main compensation:
o Respiratory center and takes a SHORT time to take
effect (minutes)
Table 10. Metabolic alkalosis compensations.
Condition Compensation
↑ Inhibitory center of CNS to ↓ RR
When ↑ HCO3- ↓
 ↑ pH due to ↓ breathe off more CO2
(↓H+, ↑ HCO3-) ↓
↑ CO2 in the blood = to ↓ pH

ACID BASE DISORDERS RENAL PATHOLOGY: NOTE #1. 3 of 6

 V) ABG INTERPRETATION VI) PRACTICE PROBLEMS
Table 11. Guide for ABG Interpretation. ● Refer to Table 12 in appendix.
Interpretation (use
Parameter
Values modified Henderson-
(Steps)
Hasselback equation)
not automatically normal,
pH = 7.35 –
may be abnormal due to
7.45
compensation which
pH already happened
↓ pH, <7.35 acidosis
↑ pH, >7.45 alkalosis
not automatically normal,
pCO2 [N]: 35-45 may be abnormal due to
(Respiratory mmHg compensation which
vs. already happened
metabolic
↑ pCO2 , ↓ pH = acidosis
disorder)
>45 mmHg
↓ pCO2 , ↑ pH = alkalosis
<35 mmHg
not automatically normal,
[N]: 22-26 may be abnormal due to
mmol/L compensation which
already happened
HCO3-
↓ HCO3- , ↓ pH = acidosis
<22 mmol/L
↑ HCO3-, ↑ pH = alkalosis
>26 mmol/L
If (+) ≤12 NAGMA
Metabolic
acidosis  AGMA  proceed to delta
Anion Gap >12
ratio

Measured AG – (AG or 12)

([N] HCO3- or 24) – Measured HCO3-
Delta Ratio
(± ΔRatio = <1 Pure AGMA
concomitant ΔRatio = 1- Mixed AGMA + NAGMA
disorder) 2
AGMA + Underlying
ΔRatio = >2
metabolic alkalosis
Mnemonic: SMORE
o SM – in metabolic disorders, pH & HCO3- move in the
SAME direction
o OR – in respiratory disorders, pH & HCO3- move in
the OPPOSITE direction

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 VII) APPENDIX

Table 12. Exercise on ABG Interpretation.

pH pCO2 HCO3- Na+ Cl- Interpretation Compensation
● pH & HCO3- move in the SAME direction  ● Lungs ↓ RR to retain CO2 and
SM = metabolic disorder overtime, can rise
● Since pH in the upper limit of normal  ● Refer to pCO2 level which is elevated
metabolic ALKALOSIS (56 mmHg) that it was able to bring
7.44 = ↑ 56 = ↑ pH to the normal range (7.44)
37 ↑ ● Type: FULL Respiratory
Compensation
● Partial compensation means pCO2
is still going up BUT pH is NOT in
normal range!
● pH & HCO3- move in the OPPOSITE direction ● Kidneys
 OR = respiratory disorder o ↑ Urinary excretion protons (H+)
22 = [N] ● Since pH is low = Respiratory ACIDOSIS o ↑ HCO3 reabsorption into the
7.29 = ↓ 58 = ↑ blood
● Refer to HCO3 = NO INCREASE
● Type: NO Metabolic Compensation
● pH & HCO3- move in the SAME direction  ● Lungs
SM = metabolic disorder o ↑ breathe off more CO2
● Since pH is LOW metabolic ACIDOSIS o ↓ CO2 in the blood = to ↑ pH
● Classify if N/AGMA:
o Na+ – (Cl- + HCO3) ● Refer to CO2 = DECREASED
7.32 = ↓ 34 = ↓ o 135 – (109+14) = 12  Normal ● Effect on pH: did it drop enough for
14 = ↓ 135 109 pH to become normal = partial, pH did
o No need for delta ratio because not ↑ AG
not increase
● Metabolic Acidosis NAGMA ● Type: PARTIAL Respiratory
Compensation

● pH & HCO3- move in the SAME direction  ● Lungs

SM = metabolic disorder o ↑ breathe off more CO2
● Since pH is LOW metabolic ACIDOSIS
● Classify if N/AGMA: o ↓ CO2 in the blood = to ↑ pH
o Na+ – (Cl- + HCO3) ● Refer to CO2 = DECREASED
o 140 – (77+10) = 53 ● Effect on pH: did it drop enough for
7.25 = ↓ 25 = ↓ o Since >12, AGMA  proceed to delta pH to become normal = partial, pH did
10 = ↓ 140 77 ratio not increase
● ΔRatio = Measured AG – (12) ● Type: PARTIAL Respiratory
(24) – Measured HCO3- Compensation
● ΔRatio = 53 – 12 / 24 – 10 = 3
o If >2 = AGMA + Underlying metabolic
alkalosis
● pH & HCO3- move in the OPPOSITE direction ● Kidneys
 OR = respiratory disorder o ↑ Urinary excretion protons (H+)
● Since pH is low = Respiratory ACIDOSIS o ↑ HCO3 reabsorption into the blood
7.36 = ↓ 58 = ↑ ● Refer to HCO3 = INCREASED
29 = ↑ ● Effect on pH: Able to keep it on the
normal range (lower limit of normal)
● Type: FULL Metabolic
Compensation
● pH & HCO3- move in the SAME direction  ● Lungs
SM = metabolic disorder o ↑ breathe off more CO2
● Since pH is LOW metabolic ACIDOSIS
● Classify if N/AGMA: o ↓ CO2 in the blood = to ↑ pH
o Na+ – (Cl- + HCO3) ● Refer to CO2 = DECREASED
o 129 – (100 + 11) = 18 ● Effect on pH: : did it drop enough for
7.28 = ↓ 26 = ↓ o Since >12, AGMA  proceed to delta
11 = ↓ 129 100 pH to become normal = partial, pH did
ratio not increase
● ΔRatio = Measured AG – (12) ● Type: PARTIAL Respiratory
(24) – Measured HCO3- Compensation
● ΔRatio = 18 – 12 / 24 – 11 = 0.5
o If <1 = Pure AGMA

Table 13. Abbreviations.

AG Anion Gap NAGMA Normal Anion Gap Metabolic Acidosis
AGMA High Anion Gap Metabolic Acidosis RR Respiratory rate
BP Blood pressure SV Stroke volume
CO Cardiac output TPR Total peripheral resistance
MAP Mean arterial pressure

ACID BASE DISORDERS RENAL PATHOLOGY: NOTE #1. 5 of 6

 VIII) REVIEW QUESTIONS

1) After confirming the patient’s metabolic acidosis,

what is your next step in the ABG interpretation?
a) Proceed to determining its delta ratio
b) Use Na+ – (Cl- + HCO3) to determine whether it is
AGMA or NAGMA
c) If AG is >12, proceed to determine its delta ratio
using the formula given below:
ΔRatio = Measured AG – (12)
(24) – Measured pCO2
d) B & C

Case Vignette:
pH pCO2 HCO3- Na+ Cl-
7.2 50 10 130 100
2) Determine the acid-base disorder:
a) Metabolic acidosis
b) Metabolic alkalosis
c) Respiratory acidosis
d) Respiratory alkalosis
3) Determine the Anion Gap:
a) Not applicable
b) AGMA
c) NAGMA
d) Both
4) Determine the Delta Ratio:
a) Not applicable
b) Pure AGMA
c) Mixed AGMA + NAGMA
d) AGMA + Underlying metabolic alkalosis
5) Determine the compensation:
a) Full respiratory compensation
b) Partial respiratory compensation
c) No respiratory compensation
d) Not enough data

CHECK YOUR ANSWERS

IX) REFRENCES
● Boron WF, Boulpaep EL. Medical Physiology.; 2017.
● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth
Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical; 2018
Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
Pearson; 2020.
● Le T. First Aid for the USMLE Step 1 2020. 30th anniversary
edition: McGraw Hill; 2020.
● Papadakis MA, McPhee SJ, Rabow MW. Current Medical
Diagnosis &amp; Treatment 2018. New York: McGraw-Hill
Education; 2017.
● Sabatine MS. Pocket Medicine: the Massachusetts General
Hospital Handbook of Internal Medicine. Philadelphia: Wolters
Kluwer; 2020.
● Williams DA. Pance Prep Pearls. Middletown, DE: Kindle Direct
Publishing Platform; 2020.

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