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In Part 1, we explored a few ways to understand what a patient is experiencing when they say, “I can’t breathe.” There is a dramatic interplay between the chemical feedback to the respiratory centers in the brain stem, the afferent nerves sending sensation messages back to the brain, and the psychological response to those sensations. What we see when we encounter a patient in distress is a combination of the symptom of dyspnea and the patient’s perception of “not getting enough air.”
To truly understand what the patient needs, clinicians must understand how the nervous, cardiovascular, and respiratory systems are related and which one of those is the primary driver of the patient’s distress. Sometimes the window of time to investigate that is narrow as the patient has progressed to respiratory failure. In Part 2, we will lay out the differences in respiratory distress and respiratory failure and improve our thinking about these common and complex cases.
If you recall from Part 1, there is a language barrier between us and the patient. In most cases, they are not medical personnel and have trouble describing what they are experiencing in the terminology we need to identify the biggest problem. Their problem is colored with their psychological/emotional response to the physical/physiological issue. Luckily, we understand their physiological language perfectly fine.
The urge to breathe, or breathlessness, comes from four main stimuli:1-2
- Increased CO2: Anything that causes a ventilatory issue that inhibits gas exchange (specifically the offloading of CO2), e.g. COPD, asthma, ARDS or acute heart failure. There only needs to be an increase of four in the patient’s PaCO2 to trigger respiratory compensation.
- Low O2: This is not generally a primary stimulus to increase minute ventilation until the PO2 falls below 60 (SpO2 ~90). If they are normocapnic, we may not even see an increase in volume or rate until they fall below that threshold because the patient does not perceive “shortness of breath” until their oxygen content drops that far.
- Increased resistance or reduced compliance: This results in an expiratory flow limitation (EFL) where the patient can take air in faster than they can exhale it. This then results in air-trapping and auto-PEEP forcing the patient to breathe faster in an attempt to move air.
- Irritation or inflammation of lung tissue.
Respiratory Distress
Here is how respiratory distress works:
There is a primary chemo-stimulation of the chemoreceptors and respiratory centers in the brain. This can come from a drop in the pH from an increase in hydrogen ions. It can come from an increase in CO2 retention. Or it can come from low oxygen content in the blood.
Once the physiological thresholds for the need for compensation have been met, there is a mechanical response driven by the inspiratory neural drive (IND).2 This is the system that takes feedback from all elements of the respiratory system and takes action to increase rate or volume in an attempt to compensate for the issue.2
At this point “respiratory distress” begins to manifest. The patient is sensing “I am not breathing normally, and it is not getting any better.” This drives a behavioral reaction. This behavioral reaction is due to an interplay between the sympathetic nervous system and the limbic centers in the brain. The end result is a neuro-mechanical dissociation (NMD).2
NMD is what happens when there is an uncoupling of the chemical stimulus and the mechanical respiratory response that is designed to correct it. Neither system is communicating with the other one due to this emotional hijack that the patient is experiencing from not being able to breathe. When there is a respiratory disease present, the physical obstructions impede the patient’s ability to respond to the initial stimulus and the patient’s respirations feel like “not enough air.”
The anxiety, panic, and other affective distress is what we see when we enter their home to begin assessing them. They called 911 because they feel that their life is in danger, or someone else has called 911 because they ignored their symptoms and have progressed to respiratory failure.
The question of distress versus failure is really one of compensation. Respiratory distress means that although they are uncomfortable and exhibiting distressed behavior, they are still moving an adequate amount of volume and oxygen. Once they can no longer manage to do so, they are reaching respiratory failure. The more of the body and muscle fibers that the patient must use in order to get a breath in, the more severe their disease process is and the less time they have to continue to compensate.
Respiratory Failure
Respiratory failure comes in two flavors and is very difficult to tease apart in the prehospital phase of care. This is because clinicians need to know the patient’s pH, PCO2, PO2, and their HC03, all of which require a blood gas for exact measurement.3 What we can see is respiratory effort, exhaled CO2, and SpO2. We make extrapolations from there.
Clinically, Type 1 respiratory failure is also known as hypoxic respiratory failure and manifests as a PO2 < 60 with a normal PCO2. In the absence of shunt physiology these patients typically are ventilating just fine but need some intervention to increase SpO2 and DO2. However, this is more difficult to isolate and treat effectively if there is some shock state present.
In these cases, the hemodynamic situation makes it difficult to deliver oxygen to the tissues, therefore these patients will not respond to increases in Fio2 to correct hypoxia or low SpO2. To get ahead of these situations, the underlying physiological issue must be identified and corrected.
Correcting hypoxia follows a simple set of escalations:4
1.) We increase the concentration of oxygen in the lungs by increasing the Fio2 the patient is inhaling. In so doing we may create enough of a pressure gradient to get more oxygen across the alveolar membrane and into the bloodstream.
2.) When an increase in Fio2 fails to achieve our goals, we can increase the size of the reservoir (lungs), specifically the functional reserve capacity by adding PEEP to recruit more alveoli. By adding more alveolar units to the mix we increase the amount of oxygen in the lungs and thereby improve oxygenation. In the spontaneously breathing patient, we can use CPAP or BiPAP to add PEEP (positive end expiratory pressure).3 When they are not spontaneously breathing, we can still use PEEP, but it requires the use of a PEEP valve on a BVM.
3.) When the patient’s respiratory effort is poor or there is a barrier to oxygen movement across the membranes into the blood stream, we can use positive pressure ventilation to move the oxygen across the alveolar membrane and into the blood stream.
Type 2 respiratory failure is hypercapnic respiratory failure and manifests with a PC02 > 45-50 and pH < 7.35. The patient can also present with a combination of the two.3,5 Operationally, we are looking at mental status and respiratory effort, an inadequacy or loss of either necessitates an escalation in the respiratory support we provide. This could be as simple as addition of noninvasive respiratory support (such as CPAP or BiPAP) or as complicated as intubation and mechanical ventilation.
Management Goals
There are two primary management goals:
- Correct the underlying pathologic process that is causing the issue.
- Focus on the persistent physiological derangement that is amenable to treatment (hypoxia, hypercapnia, etc.).1
If we want to decrease the negative impact of the inspiratory neural drive (IND), we must optimize both the oxygen content and the physical pathways of the respiratory system. To do that to our focus is to reduce the respiratory drive and improve the respiratory mechanics. 2
To address the respiratory drive, oxygen is our primary method. There are some places, mostly in the hospital, that use medications like opioids (PO morphine to be exact) to reduce the patient’s respiratory drive.2 These medications alter the patient’s processing of sensory signals in the brain and reduce the impact of the sympathetic nervous system and limbic areas of the brain. This is not typically something that is done in the prehospital phase of care.
Supplemental oxygen helps to address a couple of issues, more than just meeting basic metabolic demands. Supplemental oxygen can also reduce carotid chemo-receptor stimulation and thereby decrease the patient’s “desire” for “more air.” It can also improve respiratory muscle endurance and buy more time for the patient to continue to compensate on their own.2
To address the respiratory mechanics, bronchodilators have a large role and the benefits compound and complement one another. Bronchodilators increase the diameter of the airways and thereby increase the amount of air flow that can move through them.2,5 This dilation also decreases the time it takes to empty the alveoli in the expiratory phase.2,5 There is a bonus benefit to both of these actions in that the mechanical loading (hyperinflation) is also reduced, making it easier for the patient to “catch their breath.”2,5
Conclusion
Respiratory distress patients present us with a trifecta of issues that span the physical, physiological, and psychological domains. The key to successfully managing these patients is to identify the cause of their dyspnea: e.g. is it chemical feedback that there is too much CO2 or not enough O2? Is there an underlying inspiratory resistance or lack of lung compliance making it difficult to “get enough air?”
The ability to answer those questions can aid the prehospital teams in identifying what the patient actually needs and drive them to relieving their distress. Remembering that the patient’s psychological distress from not being able to breathe normally is coloring the situation to some degree and that it is important to address that panic, anxiety, etc. as well as the respiratory mechanics.
References
- Santus P, Radovanovic D, Saad M, Zilianti C, Coppola S, Chiumello DA, Pecchiari M. Acute dyspnea in the emergency department: a clinical review. Intern Emerg Med. 2023 Aug;18(5):1491-1507. doi: 10.1007/s11739-023-03322-8. Epub 2023 Jun 2. PMID: 37266791; PMCID: PMC10235852.
- O’Donnell DE, Milne KM, James MD, de Torres JP, Neder JA. Dyspnea in COPD: New Mechanistic Insights and Management Implications. Adv Ther. 2020 Jan;37(1):41-60. doi: 10.1007/s12325-019-01128-9. Epub 2019 Oct 30. PMID: 31673990; PMCID: PMC6979461.
- Poddighe D, Van Hollebeke M, Rodrigues A, Hermans G, Testelmans D, Kalkanis A, Clerckx B, Gayan-Ramirez G, Gosselink R, Langer D. Respiratory muscle dysfunction in acute and chronic respiratory failure: how to diagnose and how to treat? Eur Respir Rev. 2024 Dec 4;33(174):240150. doi: 10.1183/16000617.0150-2024. PMID: 39631928; PMCID: PMC11615664.
- Bauer, E. (2016). Ventilator Management: A Pre-Hospital Pespective. Scottsville, KY: FlightBridgeED LLC
- Poddighe D, Van Hollebeke M, Rodrigues A, Hermans G, Testelmans D, Kalkanis A, Clerckx B, Gayan-Ramirez G, Gosselink R, Langer D. Respiratory muscle dysfunction in acute and chronic respiratory failure: how to diagnose and how to treat? Eur Respir Rev. 2024 Dec 4;33(174):240150. doi: 10.1183/16000617.0150-2024. PMID: 39631928; PMCID: PMC11615664.
Cody Winniford is a flight paramedic and base manager in Baltimore, MD. He has a passion for sharing his professional experience in EMS and management. Cody’s clinical and leadership development background spans both military and civilian settings and has served in several capacities as a leader and prehospital clinician. He specializes in air medical and critical care transport, as well as organizational development and leadership development. He is an active speaker on various leadership and clinical topics and is an established and successful educator for prehospital clinicians of all levels. He has a passion for human performance improvement and the mental health and performance aspects of prehospital care.
