CASE
A 62-year old male is admitted through the Emergency Department (ED) with a fifty-hour history of worsening sore throat, cough, and increased work of breathing.
RESULTS
(WOB) Samples have been collected for Covid-19 and an arterial blood gas was drawn with the following results:
EVALUATION
Although somewhat lethargic, the patient is awake and cooperative. Based upon the signs of impending respiratory collapse, the options of intubation and mechanical ventilation vs. a trial using positive end-expiratory pressure via silicon elastomer mask were discussed. It was agreed to proceed with the less invasive CPAP trial.
INITIAL TREATMENT
After providing detailed instructions to the patient, 10cmH20 of CPAP (FI02 = .40) was administered via the mask secured in place by a standard anesthesia harness. The respiratory frequency dropped from 48/minute to 39/minute. The patient indicated his WOB felt improved. After 20 minutes, a repeat ABG was drawn with the following results:
DISCUSSION
This patient presented in early respiratory failure apparently due to COVID-19 infection. (Lab findings returned positive for the virus.) Although intubation and mechanical ventilation would happen often in a variety of clinical settings, the option of using CPAP via tight-fitting face mask yielded significant improvement in not only oxygenation status but improved the efficiency of the patient’s own ventilatory status.
This report is simply intended to remind practitioners that therapeutic end-pressure does not have to be administered via an artificial airway in conjunction with unnecessary augmented tidal ventilation.
All practitioners making these decisions should pay careful attention to the patient’s LOC and especially their ability to protect their airway. These patients require careful monitoring, preferably in a critical care setting.
A 69-year old male is brought into your department in acute respiratory distress. He is breathing 56 times per minute, using all of his accessory muscles of respiration. His skin is cold and moist. His BP is 188/110, with sinus tachycardia at a rate of 152/minute. His S02 = 70% per pulse-oximeter. He has bilateral inspiratory crackles in all lung fields and his wife states he has been “battling heart failure” for several years.
As we all know, tissue damage from hypoxic ischemic injury during a heart attack leads to ongoing problems, like congestive heart failure. Once heart muscle is damaged, neighboring healthy tissue will become damaged too, due to the “bystander effect.” This can turn what might be relatively minor heart damage into major, life-threatening damage. So the question becomes: is it possible to stop this “bystander effect” in its tracks?
Are your patients following a low-dose aspirin regimen thinking it will reduce their risk of stroke, heart attack or heart disease? According to researchers and the 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease, they should stop immediately. Three recent studies have found that aspirin therapy may not be benefiting them. And, in some cases, it could be doing harm.
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