High Velocity Therapy Used to Avoid NIV and Reverse Acute Carbon Dioxide Retention in a COPD Exacerbation

Patient reading

Marcia Jeffers, RRT • Kale Spivey, RRT-NPS • Terrell Ashe, RRT-NPS • Sheldon Spivey, RRT • Rose Dennis, RRT
Athens Regional Medical Center (Athens, Georgia)

Vapotherm does not practice medicine or provide medical services or advice. Vapotherm’s high velocity therapy is a tool for treating respiratory distress. Although individual results may vary, Vapotherm believes this case study is an example of the clinical benefit Vapotherm’s high velocity therapy can have in an emergency department setting.

Patient History and Presentation

A 60 year-old female with a history of end-stage COPD, having been intubated within the last month for a similar exacerbation, arrived by ambulance to our Emergency Department. The chief complaint was severe difficulty breathing which came on gradually. Initial assessment noted tachypnea with nasal flaring and purse lipped breathing, as well as bilateral wheezing and wet cough.

This patient is well known to our staff with multiple prior admissions. Eighteen days prior, this patient presented with a similar exacerbation, wherein she was intubated and admitted to the ICU with a three day length of stay. Based on history, it was anticipated that this patient would be intubated and admitted to the ICU.

Treatment and Response

Non-Invasive ventilation was ordered but never initiated; high velocity therapy was started (Precision Flow, Vapotherm, Exeter, NH: Adult cannula with 4.8mm O.D.) at 25 L/min with a 60% oxygen blend and the patient immediately and markedly began to improve. Arterial blood gas analyses (ABGs) were made immediate after the initiation of high velocity therapy, and again 44 minutes thereafter; data are reported below. Following the initiation of high velocity therapy respiratory rate dropped precipitously and the patient demonstrated a reduction in dyspnea. In the time between ABGs, and despite the drop in respiratory rate, PaCO2 was reduced and pH increases markedly. Arterial oxygen tension dropped in conjunction with the decrease in respiratory rate, but hemoglobin oxygen saturation was maintained. The patient was admitted to the medical floor and discharged the following day.


In conjunction with the mechanistic evidence that high velocity therapy provides ventilation support by way of dead space purge, high velocity therapy resulted in a reduced minute ventilation by way of a reduction in respiratory rate. The blow-off of CO2 from the anatomical dead space improved arterial CO2, and corresponding pH, despite the drop in rate. The improvement in pH stabilized hemoglobin saturation in the face of a reduced arterial oxygen tension (Bohr effect) that was associated with the drop in minute ventilation. The arterial CO2 was reduced to 53 mmHg, which is normal for a compensated COPD patient (HCO3 = 33 mEq/L), and so much of the ventilation work was seen as a reduced respiratory rate. This reduced work of breathing likely averted respiratory muscle fatigue.


The application of high velocity therapy resulted in rapid improvement that is believed to have averted the use of mechanical ventilation and ICU admission. Note that this patient returned twelve days later with an identical presentation, and was again successfully treated with high velocity therapy.

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