Respiratory Failure: Type 1 or Type 2?

To recap the last blog post about oxygen saturations versus PaO2:

  • Respiration is the process of gas exchange, both at the alveoli to blood interface and blood to cellular tissue interface
  • Oxygen has to bind to haemoglobin in order to be effectively transported around the body, but must dissociate from the haemoglobin prior to be taken up by the cells
  • The amount of haemoglobin in the body that has oxygen attached is measured via oxygen saturations while the amount of oxygen freely floating in the blood unattached to haemoglobin is measured via PaO2
  • When we experience a failure to oxygenate, we have a problem with our oxygen
  • A decrease in oxygen saturations below 90% will cause the body to increase it’s ventilatory effort as a compensatory mechanism
  • A failure to oxygenate is known as type 1 respiratory failure, defined as a decreased PaO2 with a normal carbon dioxide level

In this blog post, we are going to discuss type 1 and type 2 respiratory failure in detail and explore which pathophysiological respiratory conditions lead to which type of failure.

Type 1 Respiratory Failure

This occurs when there is an issue with gas exchange between the alveoli in the lungs and the blood flowing through the pulmonary vasculature. This results in a  failure to oxygenate and is defined as a PaO2 of < 50 mmHg on room air, where normal PaO2 levels range between 80 – 100 mmHg. Patients in type 1 respiratory failure will often have a normal carbon dioxide level between 35 – 45 mmHg, or a low carbon dioxide level due to the compensatory hyperventilation that occurs when PaO2 falls below 60 mmHg.

In the last blog post about oxygen saturations versus PaO2, it was mentioned that oxygen is a terrible swimmer that struggles to move through fluid filled areas. For this reason, issues with gas exchange usually involve the pathophysiological build up of fluid within the alveoli. Oxygen is also not very strong and struggles to push through thick surfaces. This means that issues with gas exchange can also occur when there is collapse of the alveoli that results in less air entry into the affected alveoli and a thickening of these alveoli walls.

A failure to oxygenate causes a decrease in oxygen saturations and PaO2
Oxygen is 1 word
Therefore, a failure to oxygenate is type 1 respiratory failure

Conditions that cause issues with gas exchange and can eventually lead to type 1 respiratory failure include:

  • Atelectasis
    • The collapse of alveoli sacs resulting in a thickening of the alveoli walls and reduction of air entry
    • This makes it harder for oxygen enter the alveoli and to move through the alveoli wall into the bloodstream when participating in gas exchangeatelectasis
  • Acute pulmonary oedema (APO)
    • The collection of excess fluid that has moved from the pulmonary vasculature into the alveoli sacs
    • This makes it harder for oxygen to swim through the fluid to get to the edge of the alveoli in order to participate in gas exchangeapo
  • Pneumonia
    • The inflammation of alveoli sacs and consolidation of purulent material within these alveoli sacs secondary to an infection that may be bacterial, viral or fungal in nature
    • The consolidation of purulent material makes it harder for oxygen to swim through the fluid to get to the edge of the alveoli in order to participate in gas exchange, while the inflammation of the alveoli sacs makes it harder for oxygen to move through the alveoli wall into the bloodstream when participating in gas exchangepneumonia
  • Pulmonary embolism
    • The blockage of blood flowing through a particular section of the pulmonary vasculature due to a clot
    • This prevents blood from flowing past the alveoli affected by this blockage thereby preventing the oxygen within the affected alveoli sacs to participate in gas exchangepe

Type 2 Respiratory Failure

This occurs when there is an issue with the physical movement of air in and out of the lungs. This results in a failure to ventilate and is defined as a carbon dioxide level > 50 mmHg with a pH < 7.35, where normal carbon dioxide levels range between 35 – 45 mmHg and normal pH levels range between 7.35 – 7.45. Patients in type 2 respiratory failure will often have a low PaO2 on room air due to the eventual inability to physically move sufficient air into the alveoli to participate in gas exchange.

In the blog post about the importance of counting respiratory rate, it was mentioned that the build up of carbon dioxide in a person with normal respiratory mechanics was what stimulated the respiratory centre in the brain to take a breath. For this reason, any condition that causes a build up of carbon dioxide in the body should result in the compensatory act of an increased respiratory rate and/or and increased work of breathing. This may include causative factors such as a reduction in lung volume capacity or an airway obstruction. The respiratory muscles are not built to sustain the increased work of breathing and respiratory rate seen in compensation, similar to how our muscles ache when we do a new workout at the gym, and will eventually have to rest. This is known as decompensation and results in a reduction in ventilation, a rise of carbon dioxide, a drop in pH and drop in PaO2 as there is now minimal to no air entry into the alveoli to participate in gas exchange. A high enough rise in carbon dioxide and subsequent drop in pH also results in an unconscious patient.

A failure to ventilate causes an increase in carbon dioxide levels
Carbon dioxide is 2 words
Therefore, a failure to ventilate is type 2 respiratory failure

Conditions that cause issues with ventilation and can eventually lead to type 2 respiratory failure include:

  • Reduction in lung volume capacity
    • Pneumothorax
      • The collection of air within the pleural space, which causes the affected lung to collapse due to the build up of pressure
      • If the pneumothorax is severe enough, it can result in the build up of enough pressure to not only fully collapse the affected lung, but to compress the heart to the point of where it cannot pump blood out into the aorta thereby leading to a cardiac arrestpneumo
    • Pleural effusion
      • The collection of excess fluid within the pleural space, which causes basal collapse of the affected lung
      • This is different from APO where the fluid is inside the alveoli
      • A pleural effusion follows the same concept of a pneumothorax, but with fluid instead of air599_Pleural_Effusion
  • Airway obstruction
    • Asthma
      • A respiratory condition that results in the narrowing of the airways within the respiratory system secondary to spasming and increased mucous production that results in an increase in airway resistance
      • As the diameter of the airways are naturally smaller during exhalation compared to inhalation, this is especially problematic when trying to breathe out
      • The turbulent flow of air trying to force it’s way out of the narrow airway results in the classical wheezing sound often associated with asthma15-asthma-schematic
    • Anaphylaxis
      • An acute allergic reaction that makes the body become hypersensitive thereby causing various life threatening responses
      • In the respiratory system, anaphylaxis can cause a complete closing of the airway, similar to the mechanics observed in asthma
  • Apnoea (temporary cessation of breathing)
    • Over sedation
      • The accumulation of opioids within the body interfering with the body’s ability to recognise that it has to take a breath
      • Due to this reduction in respiratory drive, there is an increased level of carbon dioxide within the body resulting in a decreased level of consciousness
    • Obstructive sleep apnoea
      • The partial or full closure of the airway when it relaxes during sleep
      • A partial closing results in a snoring sound while a full closing will usually startle the patient away when the carbon dioxide levels build up and PaO2 levels decrease

Think about the respiratory conditions that can lead to type 2 respiratory failure (a failure to ventilate). If I asked you to choose one, only one, thing that you could do if presented with a patient experiencing this condition…what would you choose?

Pneumothorax…chest drain?

Pleural effusion…chest drain?

Asthma…Salbutamol puffer?

Anaphylaxis…Adrenaline/Epipen?

Over sedation…Naloxone?

Obstructive sleep apnoea…Continuous positive airway pressure (CPAP)?

Notice how none of those answers had anything to do with oxygen? Because type 2 respiratory failure is not fixed with oxygen, it is fixed by fixing the problem! With that being said, if a failure to ventilate is left untreated for too long, it will result in a failure to oxygenate as well. Likewise, if a failure to oxygenate is left untreated for too long, it will result in a failure to ventilate as well. Oxygenation and ventilation are independent of each other, yet co-dependent! Therefore, in any situation where there are low oxygen saturations…there is an oxygenation problem. This is true whether it is purely a patient in type 1 respiratory failure, or a patient that as completely decompensated in type 2 respiratory failure. And the fix for low oxygen? Give more oxygen! If you fix what needs to be fixed, the lungs will eventually return to their once happy state of functioning…
LUNGS

If you remember only one thing from this blog post, make it this:

  • If you are using terminologies like increased respiratory rate, increased work of breathing, respiratory fatigue, altered breathing pattern, decreased air entry…you are describing a problem with ventilation! So fix the ventilation problem!
  • If you are using terminologies like low oxygen saturations and low PaO2…you are describing a problem with oxygenation! So give them more oxygen!

Does the information in this post align with what you see in the practical setting with the deteriorating patient? What are your experiences with patients experiencing type 1 or type 2 respiratory failure? Which type of respiratory failure do you tend to see more often in the clinical setting? Do you think there is anything you might be able to do to pick up on changes in the deteriorating patient quicker? Please feel free to leave your comments or questions in the section below…

References

  • Darovic, G. O., & Zbilut, J. P. (2002). Pulmonary anatomy and physiology. In G. B. Darovic (Ed.), Hemodynamic monitoring: Invasive and noninvasive clinical application (3rd ed., pp 9-42). Philadelphia: Saunders Elsevier.
  • Pooler, C. (2009). Disorders of ventilation and gas exchange. In C. M. Porth & G. Matfin (Eds.), Pathophysiology: Concepts of altered health states (8th ed., pp. 701-738). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.

  • Porth, C. M., & Litwack, K. (2009). Structure and function of the respiratory system. In C. M. Porth & G. Matfin (Eds.), Pathophysiology: Concepts of altered health states (8th ed., pp. 640-669). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.

  • Roussos, C., & Koutsoukou, A. (2003). Respiratory failure. European Respiratory Journal, 22(47), 3s-14s. doi: 10.1183/09031936.03.00038503

Acknowledgements

Simon Plapp – ICU Education Consultant, Western Private

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