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
Background
Determinants of Arterial pCO2
Terms and Assumptions
pCO2: arterial partial pressure of carbon dioxide
k: constant
VCO2: carbon dioxide production (normal = 90-130 L/min/m2)
Measured Using a Metabolic Cart (Which is Capable of Measuring Expired Carbon Dioxide)
VE: minute ventilation (respiratory rate x tidal volume)
Elevated pH Results in Hypoventilation with a Compensatory Increase in pCO2
However, the Degree of Hypoventilation is Limited by the Hypoxic Respiratory Drive to Breathe
The Predicted Compensatory Increase in pCO2 in Response to a Primary Metabolic Alkalosis Obeys the Acid-Base Rules (see Acid-Base Physiology)
Expect an Increase of 7 in pCO2 for Each Increase of 10 in the HCO3
Expected pCO2 = (bicarb x 0.7) + 21 + 1.5
Clinical Pearls
ALL Cases of Subacute or Chronic Hypercapnia are Accompanied by Elevated Serum Bicarbonate (on Serum Chemistry or Arterial Blood Gas)
Presence of Elevated Serum Carbon Dioxide Should Raise the Suspicion for Presence of Either a Primary Metabolic Alkalosis OR a Primary Respiratory Acidosis with Compensatory Metabolic Alkalosis
One Would Order an Arterial Blood Gas to Differentiate These Conditions
Increased Carbon Dioxide Production (VCO2)
Occurs with Overfeeding (Generally with Tube Feedings or Total Parenteral Nutrition)
Increased Carbon Dioxide Production Only Results in Hypercapnia When Alveolar Ventilation (VE) is Inadequate (ie: in the Presence of Significant Lung Disease, Such as Chronic Obstructive Pulmonary Disease, Acute Respiratory Distress Syndrome, etc)
Acute Hypoventilation with Acutely Decreased Minute Ventilation (VE) (see Respiratory Failure)
Chronic Hypoventilation with Chronically Decreased Minute Ventilation (VE) (see Respiratory Failure)
Increased Dead Space Ventilation with Increased VD/VT Ratio
Hypercapnia Only Occurs When the VD/VT Ratio Exceeds 50%
Physiology
Simplified Alveolar Gas Equation (see also Hypoxemia)
Terms and Assumptions
PAO2: alveolar partial pressure of oxygen (PO2 or alveolar oxygen tension)
Respiratory Exchange Ratio: 0.8
Arterial PaCO2 (pCO2) is Assumed to Be Nearly the Same as Alveolar PACO2 in This Equation
FIO2 is Assumed to Be Room Air (21% FIO2)
Altitude is Assumed to Be Sea Level
Inverse Relationship Between Arterial pCO2 and pO2
Terms and Assumptions
A-a Gradient Remains the Same (in this Case, A-a Gradient = 10)
Respiratory Exchange Ratio: 0.8
Increased Carbon Dioxide (CO2) Production Normally Results in a Compensatory Increase in Alveolar Ventilation
At a Constant Alveolar (Minute) Ventilation, Increased Carbon Dioxide (CO2) Production Should Theoretically Increase the pCO2
In a Normal Patient
Increased Carbon Dioxide (CO2) Production Results in an Increase in Alveolar (Minute) Ventilation, Decreasing the pCO2 Back to a Normal Level (i.e. Approximately 40 mm Hg)
In a Patient with Moderate-Severe Lung Disease
Patient May Be Unable to Increase Their Alveolar (Minute) Ventilation to Compensate for the Increased Carbon Dioxide (CO2) Production
Therefor, pCO2 May Increase, Possibly Resulting in Respiratory Failure
Alveolar Ventilation is Inversely (But Not Linearly) Related to pCO2 (at Varying Levels of CO2 Production)
Clinical Examples
In a Patient with Acute/Chronic Hypocapnia: assuming a constant CO2 production (VCO2), a significant increase in minute ventilation (VE) must be present to maintain the low pCO2
Example: DKA patient with pH 7.40 and pCO2 30 must maintain a significanty increased VE to maintain the pCO2 at that level -> despite a normal pH, rapid respiratory failure can occur if, for any reason, patient cannot maintain that high VE
In a Patient with Acute/Chronic Hypercapnia: assuming a constant CO2 production (VCO2), a relatively small decrease in VE can produce a significant increase in pCO2
Example: chronically hypercapnic COPD with pCO2 60 can experience a significant increase in pCO2 with even a small decrease in VE (due to minimal sedation, etc)
Minute Ventilation (VE) is Inversely (But Not Linearly) Related to pCO2 (at Varying VD/VT Ratios)
Terms and Assumptions
Graph Assumes a Constant Carbon Dioxide Production (VCO2) of 200 ml/min
VCO2 = VA x (PaCO2/PB)
VE = VA x 1.21/(1-VD/VT)
Key Points
VD/VT Ratio Determines How Efficiently the Lungs Excrete Carbon Dioxide (CO2) Per Breath (i.e How “Sick” the Lungs Are)
Low VD/VT Ratio = More Efficient Carbon Dioxide (CO2) Excretion Per Breath
High VD/VT Ratio = Less Efficient Carbon Dioxide (CO2) Excretion Per Breath
At a Low VD/VT Ratio (Healthy Lungs), a Relatively Low Minute Ventilation (VE) is Required to Maintain pCO2 Constant at 40 mm Hg
At a High VD/VT Ratio (“Sick Lungs”), a High Minute Ventilation (VE) is Required to Maintain pCO2 Constant at 40 mm Hg
If This Level of Increased Minute Ventilation Cannot Be Maintained, the Patient Will Develop Hypercapnic Respiratory Failure
Impact on Shunt Fraction on Arterial pO2 and pCO2
Key Points
pO2 Decreases Linearly and Inversely with Increasing Shunt Fraction
The Higher the Degree of Shunt, the Lower the pO2
In Contrast, pCO2 Remains Relatively Constant Over a Wide Range of Shunt Fractions
pCO2 Only Increases After the Shunt Fraction Exceeds 50%
For This Reason, Shunt Does Not Typically Result in Hypercapnia
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
