The SLP and The Respiratory System: A Love Story

In case you missed it, here are the links to part one (The Respiratory System) and part two (Respiratory Disease) of this blog series. If you like it- please share the love!

The final part in my series on the respiratory system ends where you may have wanted it to begin (sorrynotsorry): Our scope of practice and how we can help with respiratory disease. Breathing affects swallowing. Swallowing affects breathing. The two are inseparable like those two love birds on the park bench that are putting on a show for the whole neighborhood when their apartment would have been just fine. When things are going great, that love flourishes as a healthy system. But when one goes down it could pull the other down with it until they’re both on the ground like Steve Urkel unable to get up (that one’s for all the 90’s kids out there). But there’s always the heroic SLP with the symbolic helping hand, ready to pull ‘em up and make sure they don’t fall down again.

Make Me One with Everything

It is fair to say that the oropharyngeal swallow is “connected” to the respiratory system. We can even say that the respiratory system is the foundation of the oropharyngeal swallow (in theory and literally as it sits right on top of it). But what is most accurate is that the oropharyngeal swallow and its anatomy actually is the respiratory system- interwoven within it making the two one seamless path. You can of course separate the two using reductive science but I think that does healthcare and, more specifically, patient care a disservice. By thinking of it all as one system it becomes clearer why you have spent your time reading 3 blogs about the respiratory system (you’re welcome :). To understand the swallow, we must also understand the status, capabilities, and weaknesses of the respiratory system. Because they’re essentially inseparable from one another.

The Respiratory Rate

An enormously important indicator of respiratory health, and thus dysphagia, is the respiratory rate (RR), or breaths per min. This measurement tells us a couple of things.

#1 Their medical stability for PO trials.

#2 Their ability to coordinate breathing and swallowing and, ultimately, the likelihood of inhaling food, liquid, saliva, or medications from the upper airway.

Increased RR, or tachypnea (anything above 20), has a number of causes. Some aren’t pathological (i.e. exercise) and some are ephemeral (i.e. psychological distress- like a bad reaction to seeing PDA on a park bench). But what we are most concerned about is the pathological kind caused by respiratory disease. Tachypnea is both a sign that the patient is more likely to aspirate (things really get hairy after a RR 30) and that the aspirate may be extra harmful to the patient (because the lungs are already trying to fight off a disease process), ultimately increasing the likelihood of aspiration pneumonia. The takeaway? Respiratory disease leads to aspiration leads to respiratory disease leads to aspiration leads to respiratory disease… bringing each other down together like two toddlers in a bounce house.

SpO2, SaO2, FiO2, and SLPO2

No, you’re right- there’s no such thing as SLPO2. Now that I know you’re paying attention we can move forward. SpO2, or pulse oximetry, is a cheap and simple way to monitor a patient’s oxygenation. The SLP can measure this quickly and easily using a small device called a pulse oximeter, which is placed over the finger, toe, or earlobe in order to examine the number of hemaglobin carrying oxygen vs those not carrying oxygen (normal is 90-100%). While it provides cheap and easy access to important information about the patient’s oxygen levels, it does come at the expense of accuracy which can change depending on the device used and factors that have to do with the device’s contact with the patient (e.g. Skin pigmentation, thickness, temperature, and fingernail polish). SaO2 on the other hand, which is acquired through an arterial blood gas (ABG) test is much more accurate and should always be used to get the true measurement of the patient’s respiratory status. No access to ABG? Then make sure your patient is saturating at least 94% or above on the pulse oximeter to make room for any error, as anything below this could be a true measure of less than 90%.

If a patient’s oxygen levels are low (hypoxemia) we need to be extra vigilant in determining if they are safe for PO intake. Hypoxemia increases the risk of all-cause mortality in the critically ill so this is not something to be ignored. Looking at the FiO2 (the amount of oxygen in the air being delivered to the patient) will tell you how much supplemental oxygen is needed (room air is 21% so anything above this is supplemental) in order to maintain healthy oxygenation. FiO2 is delivered through a number of airflow devices, many of which are discussed in my previous blog on respiratory support. The more air being delivered to the patient per minute means more opportunity for a higher FiO2, but you can also have a high air flow with a relatively low FiO2 if the patient simple needs the air pressure to keep the airways open for adequate ventilation (e.g. biPAP or CPAP).

In any case, the important takeaway here is to know what FiO2 the patient is on (anything over 50 or 60% and the patient may be considered unstable) and the flow rate (there is no cutoff here, but higher pressures (~40 LPM) may increase the likelihood of aspiration from increased pressure with PO intake (like a tornado in your throat sending the food where the air goes). But don’t stop there. Understand why they are requiring these levels of support. That’s where the money is. Also ask: What’s the underlining diagnosis and prognosis? What was the patient on yesterday, today, and how about tomorrow? Are they expected to get better or worse? Talk to the interdisciplinary team to understand the patient’s trajectory and whether or not they are stable enough for PO intake. Teamwork can make the dream work for our patients who have been dreaming of fried chicken for the last week (or month).

So, how can we help?

After you’ve decided that the patient is stable enough for PO, there are some management strategies that may improve their likelihood for success. I think it goes without saying (but I’ll say it anyway) that we need to be extra conservative with these patients. That means maybe starting with an instrumental study vs a clinical swallow evaluation. Sounds backwards, I know, but even a small amount of aspiration in these patients can send them into a downwards spiral. Further, a longer study may be beneficial to allow for a more accurate look at the patient’s natural response to a full meal which may show fatigue-related respiratory deficits (e.g. tachypnea, increased work of breathing, etc.) that would have been missed otherwise.

In order to manage these potential deficits, patients may require cueing for slow pacing, 6 smaller meals instead of 3 large ones, and training on breathing strategies to utilize in-between bites such as pursed-lip breathing (respiratory therapy can help with this). A modified texture may also be beneficial to…

1. Make the work of eating easier to reduce the fatigue factor

2. Decrease the opportunity for residue build up in the throat that may be inhaled (e.g. from tachypnea or from high pressure respiratory support).

Always keep your eye on the vitals and monitor overt signs of aspiration (as well as the “covert” ones hidden in the chart via CXR, lab work, etc.) over time in order to make sure the patient stays stable.

Respiratory muscle strength training (RMST) is a useful tool for those with respiratory deficiency for several reasons (breathing, speaking, coughing, and swallowing) however benefits may be small and research is mixed. Most importantly though, make sure your patient is stable first. RMST can have a deleterious impact if we overwork the muscles especially if a patient is still recovering from critical illness. This deleterious impact applies to any form of rehab we do on our most fragile patients, as it can result in fatigue, which may reverse some of the functional gains the patient has made in their recovery. My motto? Move, but move slowly.

The Takeaway

The takeaway I hope you have gotten from this 3-part blog series is that in order to understand the complexity of the respiratory system, we have to understand:

1. Normal function

2. How that function can be disrupted

3. How our interventions can further alter the patient’s outcomes.

Breathing affects swallowing affects breathing affects swallowing, right? This is not only to make sure we are being cautious, but to demonstrate that there are countless ways we can help our patients with respiratory deficiency. But we can only do this if we understand the risks and benefits of what it is we are doing. This way we can make an accurately weighted decision based on the interdisciplinary team and the patient’s goals.

What’s next?

Nothing is Black and White

Healthcare is a myriad of rainbow colored possibilities with every decision carrying a range of probabilities that can be tweaked slightly here and there, but always at the expense of some other factor. For example, starting a PO diet can both decrease reliance on a feeding tube (which carries its own risk of aspiration pneumonia) AND can increase the risk at the same time if the patient has severe dysphagia. In the next couple of years I am hoping my research team has completed its aspiration pneumonia calculator in order to understand the patient’s risk profile and to find creative ways to manage that risk, but in the meantime we have to use our knowledge of the risk factors to make a subjective judgment on the overall risk of a patient. In my next blog I will be doing a case study that examines this very process so you have something to work with in the meantime. Although this is the end of the respiratory series, the end of the learning process is nowhere in sight. I hope you continue to join me as I leap into another rabbit hole and try to figure out how to best care for our patients.

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