interpretation of the abg

Interpretation of the ABGSapna Shah

August 19, 2021

Objectives

To apply a systematic approach to identifying a patient’s acid‐base disorders

To understand acid‐base physiology

To be able to answer ABIM board‐style questions that address acid‐base disorders

Stepwise Approach: pLACO

p: L: A: C: O:

pH Labs (pH, pCO2) Anion GapCompensationIs there another/third process? Osmolality?

Acidosis: process that tends to lower pH Alkalosis: process that tends to raise pH

Acidosis Respiratory pH ↓ PaCO2 ↑

Acidosis Metabolic pH ↓ PaCO2 ↓

Alkalosis Respiratory pH ↑ PaCO2 ↓

Alkalosis Metabolic pH ↑ PaCO2 ↑

AG = Na+ – (Cl‐ + HCO3‐)

Balance between bases

Blood pH

H2CO3HCO3‐7.35‐7.45Electrically

neutral

Total cations (+)

Total anions (‐)

=

(↑pH) and acids (↓pH)

Blood pH

Total cations (+)

Total anions (‐)=

Na+

Cl‐

HCO3‐

13724

104

mEq

/L

Cation Anion

(3‐11mEq/L)

137 – (104+24) = 9 mEq/L

Anion GapUnmeasured Anions

① Organic Acids② Neg charged plasma proteins

Albumin

So what causes metabolic acidosis?

Metabolic acidosis

H2CO3HCO3‐

Build‐up of acid‐ Produced or ingested in ↑↑↑ amounts ‐ Excessive HCO3

‐ loss → kidneys or GI tract

HCO3‐

↓↓↓ HCO3‐ in the blood

How is metabolic acidosis classified?

Anion Gap

High or Normal

Na+

Cl‐

HCO3‐

mEq

/L

Cation Anion

HCO3‐ + H+ H2CO3Carbonic acid

H2O + CO2

①↑↑ produc on in blood②Acid build‐up③Organic acids accumulated in the blood

Anion Gap

High or Normal

Na+

Cl‐

HCO3‐

mEq

/L

Cation Anion

↑↑ produc on in blood ① Lactic acidosis

‐ Decreased O2 delivery to tissues

‐ ↑↑ anaerobic metabolism and build‐up of lactic acid

‐ Uncontrolled diabetes mellitus ② Diabetic ketoacidosis

‐ Lack of insulin forces cells to use fat for energy instead of glucose

‐ Fats ‐ → ketoacids ‐ (acetoacetic acid) (β‐hydroxybutyric acid)

Anion Gap

High or Normal

Na+

Cl‐

HCO3‐

mEq

/L

Cation Anion

Acid build‐up① Inability of the kidneys to excrete, even when produced in normal amounts

‐ Chronic renal failure ‐ Organic acids, like uric

acid or sulfur containing amino acids, accumulate

Anion Gap

High or Normal

Na+

Cl‐

HCO3‐

mEq

/L

Cation Anion

Organic acid ingestions ①Oxalic acid (Ethylene glycol)② Formic acid (Methanol)③ Hippuric acid (Paint, Glue)

(H+)

H+ + HCO3‐** Plasma maintains electron neutrality **‐ For each new negatively charged anion there is one less bicarbonate ion

Organic acids are not part of AG equation, thus the AG will be high

Na+

Cl‐

HCO3‐

Cation Anion

Anion Gap

High or Normal

↓↓HCO3‐ offset by Cl‐ ions AG normal ‐ Severe diarrhea

* HCO3‐ rich intestinal/pancreatic sections aren’t reabsorbed

‐ Type 2 RTA * PCT unable to reabsorb HCO3‐* In response kidneys reabsorb more Cl‐ions ‐> hyperchloremic metabolic acidosis

How does the body compensate?

Mechanism to keep pH in balance

Moving H+ from blood into cells ‐ Cells exchange H+ for K+‐ Helps with acidosis, but also causes

hyperkalemia‐ With organic acids (lactic acid,

ketoacids) H+ enters with the organic anion and is not exchanged with K+


Respiratory system

carotid artery, aortic archChemoreceptors

↓pHBrainstem

↑Respiratory rate and depth of breathing

CO2 moves out of the body

So what causes metabolic alkalosis?

T

Metabolic alkalosis

Loss of H+ Gain of HC03‐

Gastrointestinal tract‐ Vomiting ‐ Gastric secretions are acidic (H+) Kidneys

‐ Too much aldosterone

Urine Blood

KidneysIncreased reabsorption of HCO3

‐

Stimulated by volume contraction of excessive loss of extracellular fluid Loop diuretics, thiazide diuretics, severe dehydration

Hypokalemia

H2O retention

Renin‐angiotensin‐aldosterone


Moving H+ from cells into blood‐ Cells exchange H+ for K+‐ Helps with alkalosis, but also causes

hypokalemia


Respiratory system

carotid artery, aortic archChemoreceptors

↑pHBrainstem

↓Respiratory rate and depth of breathing

CO2 moves into the body

A vomiting, ill‐appearing patient with alcohol use disorder has laboratory results showing:

Na: 137 pH: 7.40 K: 3.8 pCO2: 41Cl: 90 pO2: 85 HCO3: 22

P: pHL: Labs (pH, pCO2)A: Anion GapC: Compensation O: Is there another process? Osmolality?

Winter’s Formula: Expected pCO2 = 1.5 (HCO3) + 8 +/‐ 2

Delta Gap: ‐ Difference between pts AG and normal AG ‐ This amount is considered an HCO3

‐ equivalent‐ For every unit rise in AG, the HCO3

‐ should lower by 1‐ If HCO3

‐ is higher than expected, there is metabolic alkalosis

So what causes respiratory acidosis?

Normal respiratory physiology


H2O + CO2

pCO2 kept in a narrow range to maintain pHLungs maintain ventilation rate needed to remove CO2

Respiratory acidosis

Normal mechanism of ventilation is disturbed Minute ventilation is inadequate to balance pH

Brainstem Respiratory centers

‐ Stroke, medication overdose‐ Respiratory centers slow their rate

of firing, breathing slows

Neuromuscular disorder

Myasthenia gravis → nerves don’t s mulate muscleTrauma, obesity → diaphragm/chest muscles don’t

work correctly

Airway obstruction

Object in bronchus prevents lung from ventilating

Impaired gas exchange

Impaired gas exchange between alveoli and capillaries

Alveoli are damaged (COPD) Fluid in alveoli (pneumonia) Fluid between alveoli and capillary walls (pulm edema)

Lungs can’t efficiently remove CO2

Respiratory acidosis

CO2 accumulates in the blood

pCO2 rises (usually >45)pH falls (usually <7.35)


Excess CO2 diffuses across cell membranes, especially into RBCs, binds water and forms carbonic acid, which then diffuse to HCO3

‐ and H+

Acute phase


H2O + CO2

Escapes into circulation

Remains intracellular

‐ Limited intracellular buffers for H+

‐ Thus minimal CO2 moves into cells ‐ Generate 1mEq HCO3

‐ for every 10mmHg increase in pCO2


Chronic phase (3‐5d)

Sense pH too low

Cells in PCT start generating and reabsorbing more HCO3

‐ in the blood stream

Generate 4mEq HCO3‐ for every 10mmHg

increase in pCO2

Much more substantial increase in pH

So what causes respiratory alkalosis?

Respiratory alkalosis

Normal mechanism of ventilation is disturbed Minute ventilation is higher than needed to balance pH

Brainstem Respiratory centers

↑ chemoreceptor firing

‐ Hypoxia‐ Pneumonia‐ Pulmonary embolism‐ High altitude

Abnormal response:Normal response:‐ Anxiety/panic attack‐ Sepsis‐ Salicylate overdose

Lungs removes too much CO2

Respiratory alkalosis

pCO2 falls (usually <35)pH rises (usually >7.45)


Acidic molecules in cells, especially RBCs, release H+ where they bind to HCO3

‐ in order to carbonic acid, which then diffuse to H2O and CO2

Acute phase


H2O + CO2

Moves extracellular

‐ Limited intracellular acidic molecules compared to serum HCO3

‐

‐ Thus minimal H+ move out of cells ‐ Decrease 2mEq HCO3

‐ for every 10mmHg decrease in pCO2

↓ levels as it binds H


Chronic phase (3‐5d)

Sense pH too high

Cells in PCT excrete more HCO3‐

Decrease 5mEq HCO3‐ for every 10mmHg

decrease in pCO2

Much more substantial decrease in pH

What’s the difference between an ABG/VBG?

ABG pH = VBG pH + 0.04ABG pCO2 = VBG pCO2 – 4

*ABG better for septic shock

*Need ABG to assess OXYGENATION

So, lets apply these concepts in practice..

Stepwise Approach: pLACO

p: L: A: C: O:

pH Labs (pH, pCO2) Anion GapCompensationIs there another/third process? Osmolality?

Acidosis: process that tends to lower pH Alkalosis: process that tends to raise pH

Acidosis Respiratory pH ↓ PaCO2 ↑

Acidosis Metabolic pH ↓ PaCO2 ↓

Alkalosis Respiratory pH ↑ PaCO2 ↓

Alkalosis Metabolic pH ↑ PaCO2 ↑

AG = Na+ – (Cl‐ + HCO3‐)

A woman with CKD stage 4 is admitted to the hospital with protracted vomiting. The following laboratory data are obtained::

Na: 145 pH: 7.40 K: 4 pCO2: 42Cl: 100 pO2: 92 HCO3: 25


A young man is admitted to the hospital with protracted vomiting. The following laboratory data are obtained:

Na: 146 pH: 7.51 K: 2.8 pCO2: 50Cl: 92 pO2: 96HCO3: 38


A patient presents complaining of a tight feeling in their chest, shortness of breath and some tingling in their fingers and around their mouth. Na: 144 pH: 7.49 K: 4 pCO2: 27Cl: 108 pO2: 99HCO3: 24


Resources

• https://www.merckmanuals.com/professional/endocrine‐and‐metabolic‐disorders/acid‐base‐regulation‐and‐disorders

• https://www.thoracic.org/professionals/clinical‐resources/critical‐care/clinical‐education/abgs.php

interpretation of the abg

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