Respiratory Failure is Defined as the Occurrence of One or Both of the Following
Decreased pO2, as Predicted for the Patient’s Age (Hypoxemia)
Increased pCO2 (Hypercapnia) in the Setting of a Normal Serum Bicarbonate
A Normal Serum Bicarbonate is Specified Here Since a Primary Metabolic Alkalosis (with Increased Serum Bicarbonate) Would Be Expected to Result in a Normal Compensatory Increase in pCO2: this normal compensatory mechanism functions to maintain a normal serum pH and would not be considered “respiratory failure”
Hypoxemia is Defined a Decrease in Hemoglobin Oxygen Saturation (as Assessed by Pulse Oximetry: SaO2 or SpO2) or Decrease in Arterial pO2 (as Assessed by Arterial Blood Gas)
Note that a Patient May Be Hypoxemic, But Not Be Hypoxic
Example
A Young Hypoxemic Patient Can Significantly Increase Their Cardiac Output to Maintain Tissue Oxygen Delivery
Hypercapnia is Defined as Increase in Arterial pCO2 (i.e. Increased Arterial Blood Partial Pressure of Carbon Dioxide) to >40 mm Hg
Acidemia
Definition
Acidemia is Defined as Decrease in Arterial pH < 7.40 (Due to Either Metabolic or Respiratory Acidosis)
Note that a Patient Can Be Acidemic without having a Respiratory Acidosis
Example
Metabolic Acidosis Can Produce Acidemia without the Presence of a Respiratory Acidosis
Alkalemia
Definition Alkalemia is Defined an Increase in Arterial pH to >7.40 (Due to Either Metabolic or Respiratory Alkalosis)
Acidosis
Definition
Acidosis is Defined as the Presence of an Acid-Producing Acid-Base Disturbance (with or without Concomitant Acidemia)
Clinical Scenarios in Which an Acidosis is Present, But in Which the pH is Not Acidemic
Presence of a Metabolic Acidosis May Not Necessarily Result in an Acidemic pH (pH <7.4), Since Respiratory Compensation (Hyperventilation) Occurs, Resulting in an Increase in the Serum pH
Presence of a (Chronic) Respiratory Acidosis May Not Necessarily Result in an Acidemic pH (pH <7.4), Since Metabolic Compensation (Renal Bicarbonate Retention) Generally Occurs Over a Period of Days, Resulting in an Increase in the Serum pH
Alkalosis
Definition
Alkalosis is Defined as the Presence of an Alkali-Producing Acid-Base Disturbance (with or without Concomitant Alkalemia)
Clinical Scenarios in Which an Alkalosis is Present, But in Which the pH is Not Alkalemic
Presence of a Metabolic Alkalosis May Not Necessarily Result in an Alkelemic pH (pH >7.4), Since Respiratory Compensation (Hypoventilation) Occurs Rapidly, Resulting in a Decrease in the Serum pH
Presence of a (Chronic) Respiratory Alkalosis May Not Necessarily Result in an Alkalemic pH (pH >7.4), Since Metabolic Compensation (Renal Bicarbonate Wasting) Generally Occurs Over a Period of Days, Resulting in a Decrease in the Serum pH
Respiratory Acidosis is Defined as a Disorder Which Results in Increase in Arterial pCO2 with an Associated Decrease in Arterial pH
Note that a Patient Can Have a Respiratory Acidosis without Being Significantly Acidemic
Example
Via Normal Compensatory Mechanisms, Chronic Respiratory Acidosis Induces Metabolic (Predominantly Renal) Compensation (with a Increase in Serum Bicarbonate Over Time), Culminating in Minimal Acidemia
Terms
PaO2: arterial pO2 (arterial oxygen tension)
Usually Referred to Simply as pO2
PAO2: alveolar PO2 (alveolar oxygen tension)
SpO2: pulse oximetry, as determined by peripheral pulse oximeter (see Pulse Oximetry)
SaO2: pulse oximetry, as determined by arterial blood gas co-oximeter (see Arterial Blood Gas)
Etiology of Hypercapnia/Respiratory Acidosis (see Hypercapnia)
Normal Compensatory Responses to Respiratory Acidosis
Initial Acute Response to Respiratory Acidosis (Which is Relatively Modest) is Generated by a Variety of pH Buffering Molecules Present in All of the Body Fluid Compartments (i.e. Total Body Buffering)
Reactions with These Molecules Cause the Serum Bicarbonate to Increase within Minutes
The Normal Compensatory Response to Acute Respiratory Acidosis is that for Each 10 mm Hg Increase in pCO2, the Serum Bicarbonate Concentration Increases by about 1 mEq/L (NEJM, 1969) [MEDLINE] (J Am Soc Nephrol, 2010) [MEDLINE]
Chronic Compensation for Respiratory Acidosis (Which is Comparatively Larger) is Mediated Via the Kidney
Renal Compensatory Response Begins Soon After the Onset of Respiratory Acidosis, But Requires 3-5 Days to Complete
Kidney Increases Acid Excretion in the Form of Titratable Acid and Ammonium Ion, Which Generates Additional Bicarbonate
Renal Tubular Bicarbonate Reabsorption is Also Increased, Which Maintains a Higher Serum Bicarbonate Concentration
The Normal Compensatory Response to Chronic Respiratory Acidosis is that for Each 10 mm Hg Increase in pCO2, the Serum Bicarbonate Concentration Increases by about 3.5-5.0 mEq/L
This Eventually Results in a Serum pH Which is Slightly Acidemic (Since Compensation is Incomplete and Corrects the pH Back Toward a Normal pH, But Not Completely Back to a Normal pH)
Note that Since Renal Compensation is Tightly Regulated, Administering Exogenous Bicarbonate in the Setting of Chronic Respiratory Acidosis and Relatively Normal Renal Function Results in Urinary Excretion of the Excess Alkali without a Further Increase in the Serum Bicarbonate Concentration
Later, Acute Hypercapnia Decreases the Respiratory Drive, Leading to Worsening Hypercapnia with Depressed Mental Status (“CO2 Narcosis”)
Normal (Normocapnic) Patients Generally Do Not Develop Altered Mental Status Until the pCO2 Exceeds 75-80 mm Hg
Chronically Hypercapnic Patients Generally Do Not Develop Altered Mental Status Until the pCO2 Exceeds 90-100 mm Hg
These Later Effects are Mediated Via Increased Brain Glutamine, Increased Brain γ-Aminobutyric Acid (GABA), Decreased Brain Glutamate, and Decreased Brain Aspartate
