Episode 6 - Acute Respiratory Failure II: Recognition, Management & Oxygen Therapies
Summary
In this follow-up episode to Episode 1, we discuss clinical pearls in the identification and recognition of acute respiratory failure with a focus on the clinical exam. A key point to bear in mind is that acute respiratory failure may present with evidence of cardiovascular or neurologic end organ dysfunction as manifested by extremes in vital signs (e.g., hypo- or hypertension), confusion due to hypoxic encephalopathy or even stupor in the setting of severe CO2 retention. Institution of immediate lifesaving therapies, typically in the form of oxygen, is mandatory.
The 3 types of O2 delivery systems include low-low, high-flow, and reservoir systems. The final FiO2 inspired by patients is ultimately a function of both the set flow of O2 and our patients’ inspiratory flow rates or demand. A key function of O2 therapy is to not just reverse potentially life-threatening tissue hypoxia through the provision of higher than normal concentrations of oxygen but to decrease the work of breathing. This may be accomplished in a multimodal fashion including modalities such as high-flow nasal cannula (HFNC)
Learning Objectives
#1 – Understand the importance of the primary assessment or ABCDE approach to managing patients with ARF
#2 – Describe the advantages & disadvantages of different modalities for delivering oxygen therapy
#3 – Discuss the optimal oxygen targets in hospitalized patients
Take Home Points
Tachypnea (defined as RR >25 bpm) should alert you to the potential presence of an underlying respiratory condition.
Sign of increased work of breathing on exam include:
sternocleidomastoid phasic contraction
suprasternal retractions
intercostal retractions
tracheal tug
diaphoresis
The finding of paradoxical abdominal breathing is also concerning for acute respiratory failure
Time Stamps
00:12 Introduction
00:33 Objectives
01:04 Recap of Episode 1
02:15 Initial assessment of patients with ARF - Sick versus not sick
05:06 VOMIT mnemonic
07:12 Identifying increased work of breathing
08:15 Paradoxical abdominal breathing
09:35 3 different modalities for delivering oxygen therapy
10:12 Low-flow systems
12:19 High-flow systems
16:10 Reservoir systems
19:28 Necessity to assess response to therapy
21:01 Oxygen targets in hospitalized patients
22:40 Outro
Comparison of Different Oxygen Delivery Systems
Exercise in Determining the Final Oxygen Concentration using a Low-Flow or Mask System
During the show we stated that inspiratory flow rate (normally ~15 - 30 L/min) is a major determinant of the final oxygen concentration in addition to the oxygen flow rate. So imagine that we have a patient in mild acute respiratory distress with an inspiratory flow rate of 20 L/min and we place nasal cannula at a flow of 5 L/min. One way of determining the final FiO2 is as follows:
(5 L/min x 100% = 500 L/min %) + (15 L/min x 21% = 315 L/min %) = 815 L/min % / 20L/min = 41%
Essentially, by summing the product of the inspiratory flow rate provided by the wall oxygen (5L/min) and the patient (10 L/min) with their corresponding FiO2 from the wall (100%) and atmosphere (21%) THEN dividing by the total inspiratory flow rate, we derive the final Fio2 (in this case, 41%).
From this you can deduce that if a patient has a low inspiratory flow rate (let’s say, 10 L/min), then the final FiO2 provided will be HIGHER as more of the flow is being provided in the form of 100% O2. Believe me?
(5 L/min x 100% = 500) + (5 L/min x 21% = 105) = 615 / 10 = 61%
Again, these cases are merely illustrative to demonstrate the relationship between work of breathing and its effect on final oxygen concentration. An inspiratory flow rate of 10L/min is abnormal and the maximum FiO2 normally provide by low flow nasal cannula is ~40%.
Recommended Reading
David T. Neilipovitz. Acute Resuscitation and Crisis Management: Acute Critical Events Simulation (ACES). University of Ottawa Press, 2005.
Tobin MJ. Why Physiology Is Critical to the Practice of Medicine: A 40-year Personal Perspective. Clin Chest Med. 2019 Jun;40(2):243-257.