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Joseph Toscano, MD, FCUCM
Though periodically there are calls to add new data points as “the next vital sign”, we still need to pay attention to the traditional ones. Among these, respiratory rate (RR) has always seemed to be the least regarded. Other vital signs can be obtained with the push of a button, and we consider the values we see displayed to be highly accurate. Though wearable devices to measure RR are being used by some high-tech sports enthusiasts, in most medical practices, RR remains an old school assessment. We were classically taught to count respirations for 30 seconds and double the value. At least one study1 found that even this can miss occasional crucial abnormalities. Counting for longer is always going to be more accurate. Of course, counting for 60 seconds will give you the exact number of breaths per minute, and counting for 120 seconds and dividing by 2 may be a better overall evaluation1, but who has even 30 seconds these days? The other seemingly obvious issue with RR is that we feel like we should get a general sense of the normality or abnormality of it as part of our gestalt of the patient – if patients look to be in respiratory distress, their RRs will be high. If they appear to have agonal respirations, RR will be low. But another study2 showed that even some subjective assessments may be flawed.
It is indeed the case that discrete RR numbers are essential parts of some asthma scores, the qSOFA criteria, CURB-65 scores and other clinically useful indicators. But how important are actual RR numbers in everyday Urgent Care practice, particularly when patients either look good overall or have no respiratory complaints?
Consider the following case report:
A 28-year-old male presents to Urgent Care with blurry vision for the past day or so. He denies any trauma to the eyes or chemical or other exposure. He reports no prior eye disease. He does not wear contact lenses or eyeglasses. He has no headache and has had no recent illness, though he does note a lot of stress at work. He has had no drainage from the eyes. On physical exam, he is afebrile with a temperature (T) of 98.2, pulse (P) is 68, blood pressure (BP) 118/68, and RR is documented as 20. Pulse oximetry is 100% on room air. Visual acuity is 20/20 bilaterally. Looking back in the record, his visual acuity was 20/15 when measured at a prior visit a few years ago. Eye exam shows PERRL, EOMI, clear conjunctivae and sclerae, and no abnormal fluorescein uptake. Slit-lamp exam shows normal cornea and anterior chamber and iris. Direct funduscopy does not appear abnormal. The optic discs are sharp, vessels appear normal, and there are no hemorrhages or other retinal abnormalities. The clinician recommends routine referral to an optometrist or ophthalmologist. The patient returns the next day with worsening vision but no other symptoms. At intake, vital signs include T 98.0, P 64, BP 116/72, and RR is recorded as 24. Pulse oximetry is 99% on room air. He is in no distress, and the exam is unchanged except that visual acuity is now measured at 20/30 bilaterally. The prior recommendation to see a specialist is encouraged. The following day, the patient presents with further worsening vision, now with headache and lightheadedness as well. He says that he has an eye appointment the following day but does not feel like he can make it that long. He denies, as he had before, other symptoms of fever, dyspnea, or chest pain. Vital signs include T 98.2, P 68, BP 122/78, and RR is recorded as 28 with room air pulse oximetry of 100%. External eye exam is normal but visual acuity is now 20/50 in both eyes. The clinician decides to recount the respirations and though the patient does not seem to be in any distress, the RR is indeed 28 per minute and lungs are clear to auscultation. The patient is referred to the emergency department for evaluation.
Apart from blurry vision, what about this patient’s presentation was abnormal from the start? Why would a respiratory rate be elevated even when the patient has no shortness of breath or other respiratory complaint?
As mentioned, with respiratory complaints, our expectation is that RR matches the overall clinical scenario, whether in response to hypoxemia or hypercarbia, or to abnormal airway resistance, alveolar compliance, or respiratory muscular issues. When the patient looks to be breathing abnormally, they usually are. But when they seem to be in no distress, they may still be tachypneic when you count out their RR, and that may need to be addressed.
This patient in the scenario was referred and examined by an emergency physician and an ophthalmologist. He was found to have inflammatory changes of the optic nerves bilaterally, an anion-gap metabolic acidosis and an osmol gap that led to testing, which eventually confirmed methanol poisoning. He made a full recovery.
Take home points:
We should train staff and ourselves to count RR with proper technique. A longer count is always going to be a better assessment. Normal RRs comprise a range which varies by patient age, and these are hard to memorize. EMRs often flag abnormal values for age, but having a chart or other reference is also helpful to be able to tell how far out of range any patient’s values are.
Error is inherent in all data collection, and patient condition can change over time but never ignore an abnormal RR recorded in the chart. If the value recorded by someone else does not make sense to you based on the patient’s present appearance, recheck the RR yourself. Conversely, if a normal RR has been recorded previously in the visit, but you think that is incorrect, recount and use the most current value to make decisions. Try to clinically reconcile inconsistencies over time. Did the patient’s status change?
Someone with a low O2 saturation will usually have an abnormal RR, but O2 sat can also be completely normal in someone with a truly abnormal RR. Pulse ox saturations indicate only part of a patient’s respiratory status.
As we learned from our patient here, an elevated RR with clear lungs and no respiratory complaint, sometimes referred to as “quiet tachypnea”, can indicate metabolic acidosis. Think about DKA or other metabolic or toxic conditions as a cause. In infants, consider inborn errors of metabolism or congenital heart disease.
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