A Great Lecture on Applied Respiratory Physiology
A Great Lecture on Applied Respiratory Physiology
Jon-Emile S. Kenny MD [@heart_lung]
-What is the world record for longest breath hold?
-Why does the diagnosis of brain death require a rise in PaCO2 to at least 60 mmHg?
-What minute ventilation can a human achieve?
-What’s the difference between an elevated PaCO2 in someone who ‘won’t’ versus ‘can’t’ breathe?
I’d like to share a great lecture on applied respiratory physiology by Dr. Scott Aberegg. These 4 mini-lectures can be found at his blog statusiatrogenicus.com, as well as embedded in the text below. The questions above are answered in these lectures, but rather than being posed as simple medical trivia – so often flaunted as teaching – these facts roll down in a roiling river of relevance; a current of respiratory physiology.
Scott begins by explaining his general disdain for equations in clinical medicine – such as the alveolar gas equation – because has anyone ever found a patient with hypoxemia and a normal A-a gradient? In any case, the underlying thesis of the series of talks is to initiate the viewer into how the body ‘defends the CO2.’ Using dive physiology as a jumping-off point, he discusses rise in the partial pressure of carbon dioxide per unit time and how disorders of ventilation lead to acute respiratory acidosis in the hospital.
The illustrative modal verbs ‘can’t’ and ‘won’t’ are used to differentiate peripheral from central impairment in ventilation, respectively. The latter types of respiratory insufficiency – those who ‘won’t’ breathe – cannot defend the carbon dioxide because of central respiratory depression. For example, the patient who has received opiates and benzodiazepines post-operatively. Another possibility is ‘Ondine’s Curse’ rightly described as ‘esoterica’ in the lecture. Regardless of the underlying cause, the important thing to recognize clinically is that these patients have a low minute ventilation. There is a big difference between a patient with a PaCO2 of 60 mmHg breathing at 4 breaths per minute and a patient with the same PaCO2 but breathing at 40 breaths per minute.
Patients who ‘can’t breathe’ have a peripheral cause of respiratory failure. Such patients want to defend the PaCO2 but cannot because of respiratory workload imbalance; these patients are typically – at least initially – breathing very quickly. Here, Scott describes 3 general etiologies that underpin the patient who ‘can’t breathe:’
Weakness
Excessive work load and
Excessive air to be moved
Perhaps the most common type of patient with 1. weakness as a driving force for poor ventilation is the cachectic elderly patient with chronic inflammation, malignancy and/or chronic cardiorespiratory disease such as emphysema. 2. Excessive load can be parsed into inertial loads placed on the respiratory pump [e.g. obesity], elastic loads placed upon the respiratory system [e.g. severe thoracic kyphoscoliosis, subcutaneous emphysema, pulmonary edema] and dynamic loads that increase airway resistance [e.g. status asthmaticus]. Scott rightly points out that ‘anyone with abnormal pulmonary parenchyma on CXR’ has increased elastic load and also discusses laminar versus turbulent flow as drivers of dynamic breathing work. Also revealed is how patients with an increased elastic load breathe in a ‘rapid-shallow’ fashion which can decrease elastic work of breathing but raise dynamic work of breathing.
Lastly, there are 3. those patients who have ‘too much air’ to move. In this situation, those with an increased production of carbon dioxide and/or an increase in dead space fraction must augment minute ventilation to defend the carbon dioxide. Thus, these patients may have full strength and normal respiratory work load, but minute ventilation must rise to meet the aforementioned challenges. Pain, fear, and fever as drivers of carbon dioxide production are often under-estimated in respiratory failure and partially explains our collective experience of observing a patient’s gas exchange improve with a small dose of an opiate or benzodiazepine. Additionally, an acute increase in dead space will increase the required minute ventilation to achieve the same alveolar ventilation. A common clinical example of dead space is pulmonary embolus, though the VQ abnormalities that evolve in pulmonary embolism are likely quite complicated. Finally, rapid-shallow breathing, as described above, may also augment dead space fraction because tidal volume falls relative to the fixed amount of ever-present anatomic dead space.
Accordingly, a prototypical patient who ‘can’t breathe’ would 1. Be frail, cachectic 2. Have pneumonia with superimposed pulmonary edema, emphysema and chest wall edema who is 3. Fearful, febrile, in pain with a rapid-shallow breathing pattern. Helping the patient defend the carbon dioxide requires helping offset the respiratory work with non-invasive or invasive mechanical ventilation with directed treatments at the underlying cause.
For supplementary viewing and reading, a drier, graphical approach to work of breathing can be found here. As well, this discussion of ventilation and high flow oxygen touches on many similar themes above. Lastly, use all of what you have learned above as a prism for viewing this study on breathing work and high flow oxygen, published this month.
Best,