Comprehensive Guide to Acid-Base Balance & Blood Gases Interpretation

Acid

Chemical substance that donates protons (H+ ions) in solution. Strong acids readily give up H+.

Base

Chemical substance that accepts protons (H+ ions) in solution. Strong bases readily accept H+.

Buffer

A weak acid plus its conjugate base/salt that resists a change in pH when acid or base is added.

pH

Quantitative expression of acidity; the negative logarithm of hydrogen ion activity: pH = -log H+.

p50

The pO2 at which hemoglobin is 50% saturated with oxygen. It is used to describe hemoglobin-O2 affinity on the dissociation curve.

pCO2

Partial pressure of carbon dioxide. It is the respiratory component used in ABG interpretation.

O2 saturation (sO2)

Ratio/percent of oxygen bound to hemoglobin compared with the total hemoglobin capable of binding oxygen.

Metabolic acidosis

HCO3- decreases, Acidotic: pH < 7.35, Low pH + low HCO3-.

Metabolic alkalosis

HCO3- increases, Alkalotic: pH > 7.45, High pH + high HCO3-.

Respiratory acidosis

pCO2 increases, Acidotic: pH < 7.35, Low pH + high pCO2.

Respiratory alkalosis

pCO2 decreases, Alkalotic: pH > 7.45, High pH + low pCO2.

Bicarbonate-carbonic acid system

The MOST important buffering system, even though its buffering capacity is relatively low.

Hemoglobin buffering

The chloride-shift diagram shows H+ generated from carbonic acid being buffered by hemoglobin inside RBCs.

Bicarbonate-carbonic acid buffering

Core reaction: CO2 + H2O

Chloride shift/Hamburger phenomenon

HCO3- leaves the RBC while Cl- enters to maintain electrical neutrality.

Lungs

Ventilation changes blood pH by controlling removal of CO2.

Kidneys

Regulate acid-base balance by excreting acids or bases and reclaiming HCO3- from glomerular filtrate.

Metabolic acidosis causes

Too much acid or loss of bicarbonate, e.g., overdose on substances that metabolize to acids.

Metabolic alkalosis causes

Too much bicarbonate or loss of acid, e.g., excess sodium bicarbonate administration.

Respiratory acidosis causes

CO2 is not adequately released, e.g., airway obstruction or hypoventilation from drugs.

Respiratory alkalosis causes

Too much CO2 is released, e.g., hyperventilation or anxiety-induced hyperventilation.

HCO3-

23 - 29 mmol/L on the main lecture reference slide

pO2

>80 mmHg on the main lecture reference slide

O2 saturation

>95% on the main lecture reference slide

Base excess

-2 to +2 mEq/L

Total CO2 (TCO2)

22 - 29 mmol/L on the ABG laboratory reference slide

Acidosis

pH < 7.35

Alkalosis

pH > 7.45

Normal pH range

7.35-7.45

Uncompensated

If the OTHER analyte is normal

Partially compensated

If the OTHER analyte is abnormal in the opposite direction

Fully compensated

If pH is normal but pCO2 and HCO3- are both abnormal and oppose each other

Mixed acid-base imbalance

If all three values trend acidotic or all three trend alkalotic

Severe diarrhea

Most likely imbalance: Metabolic acidosis

DKA / ketones

Most likely imbalance: Metabolic acidosis

Renal failure / acid retention

Most likely imbalance: Metabolic acidosis

Methanol or ethylene glycol overdose

Most likely imbalance: Metabolic acidosis

Vomiting or NG suction

Most likely imbalance: Metabolic alkalosis

Excess bicarbonate / antacids

Most likely imbalance: Metabolic alkalosis

COPD / emphysema / hypoventilation

Most likely imbalance: Respiratory acidosis

Sedative drugs that reduce ventilation

Most likely imbalance: Respiratory acidosis

Anxiety hyperventilation

Most likely imbalance: Respiratory alkalosis

High altitude / hypoxemia / pulmonary embolism

Most likely imbalance: Respiratory alkalosis

Fever with increased ventilation

Most likely imbalance: Respiratory alkalosis

Arterial specimen for ABG

Must be clearly identified as arterial vs venous

Patient identifiers

Record two unique identifiers, collection date/time, and collector ID

Patient temperature

Affects instrument calculations

Oxygenation status

Document room air vs supplemental oxygen

Air bubbles / room-air exposure

pO2 falsely increases; pCO2 decreases; ionized Ca decreases; pH increases

Delay / poor transport

O2 decreases; pCO2 increases; pH decreases

Clots / inadequate mixing

Unacceptable specimen; cells are not evenly distributed

Missing patient temperature

Instrument calculations may be inaccurate

Left shift

Hemoglobin has HIGHER O2 affinity

Right shift

Hemoglobin has LOWER O2 affinity

Carbon monoxide poisoning

CO binds hemoglobin to form carboxyhemoglobin (COHb)

Symptoms of carbon monoxide poisoning

Shortness of breath, headache, fatigue, impaired judgment, confusion, fainting, unconsciousness, respiratory failure, and death.

Appearance of blood in carbon monoxide poisoning

Blood may appear cherry red.

Treatment for carbon monoxide poisoning

100% O2; hyperbaric oxygen may be used in extreme cases.

Why blood gases require rapid processing

Blood gases are extremely sensitive to exposure to air and continued cellular metabolism.

Effects of air bubbles on blood gas analysis

Air bubbles can alter pO2, pCO2, pH, and ionized calcium.

Consequences of delay in blood gas analysis

Delay allows in-vitro glycolysis: O2 falls, CO2 rises, and pH falls.

Importance of capping blood gas samples

The sample must remain capped to prevent gas exchange with room air.

Factors preserving true in-vivo gas status

Proper transport, cooling when required, and prompt analysis.

Impact of preanalytical error on ABG interpretation

Preanalytical error can change the apparent diagnosis.

Acidosis and its effect on oxygen affinity

Right shift -> lower affinity -> more O2 released.

Hypercapnia and its effect on oxygen affinity

Right shift -> lower affinity.

Fever and its effect on oxygen affinity

Right shift -> lower affinity.

Alkalosis and its effect on oxygen affinity

Left shift -> higher affinity -> less O2 released.

Low pCO2 and its effect on oxygen affinity

Left shift -> higher affinity.

Low temperature and its effect on oxygen affinity

Left shift -> higher affinity.

Carbon monoxide poisoning effect on oxygen binding

Left shift plus fewer available O2-binding sites -> tissue hypoxia.

Measured blood gas parameters

pH, pCO2, pO2.

Calculated blood gas parameters

HCO3-, Carbonic acid concentration (H2CO3), Total CO2 (TCO2).

Henderson-Hasselbalch equation

pH = pK + log([HCO3-]/[H2CO3]).

Normal bicarbonate-to-dissolved CO2 ratio at pH 7.40

About 20:1.

Base excess reference range

-2 to +2 mEq/L.

Base excess in metabolic acidosis

Base excess < -2 is decreased.

Base excess in metabolic alkalosis

Base excess > +2 is increased.

Mixed disorder causes

Sepsis, overdose, or organ failure are common settings.