How to Interpret Respiratory Failure 🫁

First lets understand Oxygenation and Ventilation

The status of a patient’s respiratory function is one of the essential things an ABG can give you information on. A key concept to keep in mind is the difference between oxygenation and ventilation. First a reminder: diffusion speed relies on several factors, the 2 most important factors here are diffusion gradient and membrane permeability.

Oxygenation refers to diffusion of O2 across the alveolar membrane so that arterial blood is sufficiently saturated to maintain appropriate delivery of oxygen to the body. In both type 1 and type 2 respiratory failure oxygenation is impaired (O2 is low). Oxygenation depends on 2 main factors:

1. Membrane permeability - aka. the ability of the alveoli to facilitate diffusion. This is governed by healthy alveoli function. This impacts O2 far more than CO2 because CO2 is much more soluble than O2. This means CO2 can diffuse even across damaged or malfunctioning alveoli. A problem with the alveoli microscopic function to diffuse oxygen is what causes type 1 respiratory failure. The high solubility of CO2 is why type 1 respiratory failure has a normal CO2 (it can diffuse even across damaged alveoli e.g. alveoli with thickened walls due to mucous in pneumonia). This is a slight over simplification (for example a PE causes shunting which is a surface area issue as oppose to membrane permeability issue) but it is enough knowledge to start interpreting blood gas results accurately - ultimately if the alveoli aren’t working it’s type 1 failure.

2. Concentration gradient - The concentration gradient O2 is diffusing down. This is governed by Ventilation. Ventilation refers to the literal act of moving air in and out of the lungs and the main function of this is to maintain the concentration gradients which O2 and CO2 diffuse down (O2 into the blood, CO2 out of the blood). This impacts both CO2 and O2. If a patient is not breathing/ventilating then there will be high alveolar CO2 levels, this reduces alveolar CO2 concentration gradients and CO2 can no longer diffuse out of the blood leading to high blood levels of CO2. Ventilation failure causes type 2 respiratory failure and this is why CO2 levels rise in type 2 respiratory failure.

Types of Respiratory failure

By definition in respiratory failure O2 is low in both types. The reason why O2 is low (membrane permeability vs concentration gradient) impacts what type of respiratory failure is present as we will now discuss. There are two types of respiratory failure, defined by if CO2 levels:

1. Type 1 Respiratory Failure (low O2, low/normal CO2): A failure to adequately oxygenate arterial blood, but ventilation is normal. Type respiratory 1 failure is characterised by low PaO₂ but the PaCO2 is not raised. - this is due to failure of the alveoli to appropriately facilitate diffusion of O2. CO2 is largely unaffected because of its high permeability/solubility. Some key examples include pneumonia, pulmonary embolism, or acute respiratory distress syndrome (ARDS). These pathologies reduce available surface area for diffusion and increase diffusion distance e.g. by lining alveoli with consolidation.

2. Type 2 Respiratory Failure (low O2, high CO2): This is identified by both low pO₂ AND high pCO₂. This is caused by pathologies which restrict ventilation. Causes include neuromuscular disorders (due to paralysis of the diaphragm), sedative overdose (due to reduced respiratory drive), chest wall deformities (such as flail chest). No breathing -> CO2 isn’t removed from lungs -> CO2 concentration in the lungs increases -> no longer a concentration gradient for CO2 to move out of the blood -> hypercapnia (-> badness). That’s why in type 2 failure (poor ventilation) the CO2 also rises. It’s worth noting severe forms of pathologies that cause type 1 failure can also cause type 2 failure e.g. severe COPD can restrict chest expansion and therefore ventilation - causing CO2 retention.

In general type 1 is considered a problem with the microscopic exchange function of the lung tissue (oxygenation) where as type 2 is considered a problem with lung ventilation.

Note PaO2 and PaCO2 refer to partial pressure of oxygen and CO2 respectively in arterial blood.

How to Interpret Acid-Base Balance 🧪

Step 1

Assess the pH and decided if there’s an acidaemia (pH <7.35) or alkalaemia (pH >7.45)… or neither.

Step 2

Assess pCO₂ (the respiratory component) and HCO₃ (the metabolic component) levels.

• Respiratory - CO2 is the respiratory component of your blood gas. CO2 in the blood is converted into an acid (carbonic acid), so the higher the CO2, the more acid there is in the blood and therefore the lower the pH.

• Metabolic - HCO3 is the metabolic component of your blood gad. Bicarbonate (HCO3) is alkaline. The higher the bicarbonate the more alkaline (higher) the pH is.

• In other words, bicarbonate is proportional to pH (if there’s more HCO3 then pH rises) where as CO2 is inversely proportional to pH (if there’s more CO2 then pH reduces).

Step 3

To work out which of respiratory or metabolic is causing the acid-base disturbance simply look which of CO2 or HCO3 is “pulling” the pH in the deranged direction e.g. if the pH is low (acidic) two things could cause this, a low HCO3 (metabolic) or a high CO2 (respiratory) - look to see which of these is derange in this direction and you have your answer as to respiratory vs metabolic. If one of them is deranged but in the opposite direction to the pH disturbance then it would suggest partial compensation which we will go over in the next section.

Examples

Lets work through the examples.

1. pH < 7.35 indicates acidosis

   • if HCO3 is low its metabolic

     • Metabolic Acidosis: This is due to a decrease in HCO3 (or an increase in acid production). Causes include renal tubular acidosis (loss of bicarb), severe diarrhoea (loss of bicarbonate), lactic acidosis (increase in metabolic acids), diabetic ketoacidosis (increase in metabolic acids). In the case of metabolic acid production HCO3 on your gas would still fall as it acts as a buffer so is “used up”.

   • if CO2 is high its respiratory

     • Respiratory Acidosis: This occurs when CO₂ is increased due to hypoventilation. Remember CO2 turns into carbonic acid, so more CO2 means more acid and lower pH. Causes include severe COPD, obstructive sleep apnoea,, or airway obstruction.

   • If HCO3 is low AND CO2 is high it’s mixed acidosis

2. pH > 7.45 indicates alkalosis

   • if HCO3 is high its metabolic

     • Metabolic Alkalosis: This results from an increase in HCO3, often due to vomiting or diuretic use.

   • if CO2 is low it’s respiratory

     • Respiratory Alkalosis: This happens when CO₂ is decreased, usually from hyperventilation. Causes include anxiety, pain, or altitude sickness.

   • if HCO3 is high AND CO2 is low it’s mixed alkalosis

How to Interpret Acid-Base Compensation ⚠️

Acidosis vs Acidaemia

Before diving into this topic It’s worth noting the difference between acidosis/alkalosis and academia/alkalaemia:

• Acidaemia and alkalaemia refer to only the pH of the blood (aemia = blood), whereas acidosis and alkalosis refer to the an underlying process of either producing or decreasing H+ ions and therefore changing a pH.

• Why is this important you may ask…?

  • The body has a huge number of acid and base producing processes but as we know the homeostatic mechanisms of HCO3 and CO2 along with other buffers help to keep pH in the 7.35 - 7.45 range. As a result of buffers you can have an acid producing process going (an acidosis) without any pH imbalance (no academia). This is important because an acidosis indicates a process that can kill you, even if there isn’t an acidaemia (eg because of compensation).

  • Let’s look at an example - Sepsis typically results in increased production of lactic acid -ie lactic acidosis - that unchecked would cause an acidaemia. This is for a few reasons including impaired microvascular circulation, microcirculatory shunting, increased rates of glycolysis and impaired intracellular respiration. The resulting acidaemia can be completely buffered by the respiratory CO2 system (e.g. a raised respiratory rate in sepsis blowing off extra CO2). In this example we can see there is both an acidosis (lactic acid from sepsis) and a compensatory alkalosis (reduced CO2 from breathing faster). If you did a gas the pH would probably be normal due to appropriate (ie full) compensation. In this scenario, a normal pH doesn’t exclude the presence of an underlying acidosis that is indicating that the pH is critically unwell. It’s an important distinction.

  • Acidaemia is just a description of the blood pH and can be compensated for, the acidosis is the pathological process underlying it - remember it’s the acidosis that kills you.

Compensated vs Uncompensated Acid-Base imbalances

This is the concept that if the pH is outside normal range the body will try to compensate for this. In general this is done through excretion / production of HCO3 via the kidneys or retention / expiration of CO2 via the lungs.

Remember more CO2 (acid) decreases pH, more HCO3 (base) increased pH.

Lets work through some examples.

1. pH < 7.35 indicates acidosis

   • if HCO3 is low it’s Metabolic Acidosis

     • If there was an uncompensated metabolic acidosis then CO2 would be normal. If there was compensation it would occur through hyperventilation (this lowers pCO₂ therefore lowering the acidic CO2 levels). The gas would therefore show a LOW pCO2 in compensated metabolic acidosis.

   • if CO2 is high it’s Respiratory Acidosis

     • If there was an uncompensated respiratory acidosis then HCO3 would be normal. If there was compensation it would occur via kidneys retaining bicarbonate (HCO₃⁻). HCO3 is alkaline so would increase the pH in an attempt to restore normal pH.

2. pH > 7.45 indicates alkalosis

   • if HCO3 is high so it’s Metabolic Alkalosis:

     • If there was an uncompensated metabolic alkalosis then CO2 would be normal. If there was compensation it would occur through hypoventilation of the lungs, thus increasing the levels of acidic CO2 in an attempt to reduce pH.

   • if CO2 is low so it’s Respiratory Alkalosis:

     • If there was an uncompensated respiratory alkalosis then HCO3 would be normal. If there was compensation it would occur via kidneys excreting more bicarbonate (HCO₃⁻). HCO3 is “alkaline” so secreting it would decrease the pH in attempt to restore homeostasis.

Of note, if there is a pH imbalance by definition the compensation is only “partial” - for full compensation the pH must be normal (this is why the concept of acidosis vs acidemia is important - in full compensation you can have normal pH even with an underlying pathological acidotic or alkalotic process occurring).

How to Interpret the Remaining Blood Gas ✅

Electrolytes (Na, K, Cl)

Derangements in each can have their own significant and adverse effects. A gas is the fastest way to obtain these electrolyte levels, and although a formal is often required to verify levels you can start urgent treatment based on a gas if it fits the clinical picture. Potassium derangement is especially important - if you have a patient having runs of arrhythmias or ECG changes and a deranged potassium on the gas it’s reasonable to treat. Be aware that issues with sampling can throw off blood gas results so if you have a result that doesn’t fit with the clinical picture and your patient is otherwise stable, it’s perfectly reasonable to rush the formal U&Es and wait the 15-20 minutes to get a more accurate result.

Glucose

A common cause of reduced GCS is low blood glucose (<4), and people often say to D in A-E stands for “don’t ever forget glucose”. If it’s low be sure to replace with oral or IV glucose as appropriate. If you’re in a bind and have an unconscious, hypoglycaemic patient with no vascular access and oral glucose isn’t a viable route, you can use IM glucagon but be aware it’s only a temporising measure because it’ll only work once.

Lactate

Elevated lactate (>2 mmol/L) suggests tissue hypoxia or metabolic disturbances, which can result from sepsis, shock, or excessive muscle activity (eg seizures)..

Base Excess (BE)

This one always confuses people but it pretty much does what is says on the tin - how much excess base (bicarbonate) is there in the blood. Normal BE is between -2 and +2 mmol/L.

1. A positive (>+2) excess of base means…well there’s excess base so things are more alkalaemic (ie metabolic alkalosis)

2. A negative (<-2) excess of base means there isn’t…excess…base, eg there’s less base than normal which indicates the blood will be more academic (ie metabolic acidosis).

Written by: Dr Benjamin Armstrong

Sense checked by: Dr Rishil Patel

Please email oscesense@outlook.com if you find any errors or have queries