The assessment of the respiratory patient may seem, on the face of things, to be rather straightforward. Air should go in and out, oxygen in, CO2 out, right? While this is partially true, the pathophysiology of the respiratory system is a bit more complicated than that. Every system in the body works in synergy to contribute to homeostasis, and metabolic stability. When assessing a respiratory complaint, we have to consider that more than one system is ultimately affected, and it may sometimes be that another system is actually responsible for a respiratory presentation.
For this reason, we should always take a systems based approach to any patient with a respiratory patient. In order to have a functioning respiratory system, one has to have a neurological control of respirations, a working cardiovascular system, unimpeded musculoskeletal function, and unimpaired renal function.
Neurological system: The control of respiration comes from areas of neurons in the brain stem. The major ones are the pontine respiratory group, the apneustic centre, and the pneumotaxic centre. There are actually about four areas of the brainstem that control respiratory drive, but it is not terribly important to fully understand the anatomy in order to grasp the concept: brain stem injury = respiratory impairment. This injury can come in the form of ischemia, trauma, hemorrhage, or elevated ICP (herniation syndrome). In addition, there are stretch receptors in the lungs themselves that stop inhalation at a set point to avoid barotrauma. If there is any neurological impairment that compromises the respiratory centres or peripheral nerves in this system, we can see impaired respiratory function.
The Cardiovascular system: In order for respiration to take place (the exchange or O2/CO2 at the cellular level), the body requires adequate perfusion of the alveolar vasculature, and an adequate exchange of gases between the lungs and the external environment (ventilation). In the event that there is impaired perfusion due to vascular occlusion, as seen in PE, or pulmonary hypertension, as seen in left sided heart failure, or other causative mechanisms, respiration will be compromised. This will present with respiratory distress, even though the primary problem may be cardiovascular rather than respiratory in nature.
The Musculoskeletal system: Factors such as aging, trauma, or neuromuscular diseases can impair chest wall expansion. This results in a decrease in the amount of negative pressure generated during inspiration, and a subsequent drop in minute volume.
The renal system: The kidneys are responsible for a number of functions in the body. Notably, they control acid-base balance, and fluid balance. Impaired GFR and fluid retention can result in fluid overload, and heart failure. As we know this can cause pulmonary edema and respiratory compromise. Acid-base disorders can lead to metabolic acidosis which may present with tachypnea and altered mental status, that can be confused with respiratory distress.
So, we know that the respiratory patient can have many problems contributing to the simple presentation of dyspnea. This makes them a group that needs a thorough history and physical to identify the underlying cause(s) of their condition. Assessment, as with all patients, begins with determining LOA and correcting threats to the ABCs. In a patient who is in respiratory distress, early intervention to A and B are important. Do not be afraid to start supplemental oxygen early. If the patient is already on home oxygen, inquire about recent changes in settings. It may be worthwhile to increase flow by 2-3 additional LPM while you assess them.
History should follow the same general format as for all patients, beginning with the simple question: “Has this happened before?”. If the patient has a history of COPD, CHF, Asthma, or other respiratory condition (I have had a run of Sarcoidosis patients lately), they will usually be able to tell you. A nasal cannula is the common dead giveaway, and it may feel redundant to ask. Next we want to know when the dyspnea started. Was it an hour ago, a day ago, or has this been going on for some time? Gradual onset in a COPD patient is common in the setting of an exacerbation. CHF can worsen slowly as well and is usually accompanied by sleep disturbances, and decrease in activity tolerance. If the onset was sudden, we really want to know what the patient was doing when the dyspnea began. Exertional dyspnea is common in the setting of MI, especially if it does not improve with rest. That being said, the patient may often have exertional dyspnea, so we want to know if it has happened before.
We want to ask about associated symptoms, particularly:
Chest pain. If it is present, we want an OPQRST.
Cough. Is it new. Is it productive.
Nausea. Common in the setting of MI.
Fever or chills (think infection)
Recent travel, hospitalization, or surgery (Among other PE risk factors).
I will only say this once, but it really shouldn't have to be said: AUSCULTATE THIS PATIENT. We want to look for the air entry, areas of diminished entry, and any adventitious sounds. Lung sounds are your friend (see my post on lung sounds).
EVERY patient who is dyspneic should get a 12-lead. ALL OF THEM. It takes 30 seconds, and most doctors will expect one.
Now, I mentioned several systems that may be at play here in my introduction. We want to include them in our assessment too. If the patient is alert, oriented, and denies any head trauma we can safely rule out neurological causes. If we have an altered patient, we need to determine if they are altered because they are hypoxic, or if they may be altered due to trauma, or systemic infection that may be affecting neurological control of respirations. We need to be aware of potential cardiac causes. For this reason we are going to ask about chest pain, look for JVD, look for peripheral edema, and DO A 12-LEAD. If the patient has chest or thorax trauma, we need to consider that this may be affecting the ability to ventilate. This is easy to check, because we can just watch and feel chest expansion. If they have a neuromuscular disorder this should come up in their history. Patients with renal failure will generally have hallmark peripheral edema, crackles on inspiration, JVD, HTN, and may already be on dialysis.
It takes a bit of detective work, and careful observation of the patient and the scene itself, but when we put everything together we can form a clearer picture of what may be the cause of the patient's dyspnea.
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