This is the first of a series of posts on the National Continued Competency Requirements (NCCR), each covering a core competency for prehospital providers.
Ventilation with a BVM is arguably one of the most important skills of any prehospital provider. In cases where the patient is not apneic, it is critical that the provider is able to identify when ventilation is appropriate. In EMT class, students are often given the guideline that a respiratory rate less than 8 or greater than 24 requires assisted ventilations with a BVM. While this is perhaps a reasonable guideline, it is only a half-truth. Patients in even mild respiratory distress can have respiratory rates exceeding 24 breaths/min, but obviously do not require assisted ventilations, while a patient with a respiratory rate of 10 breaths/min may require assistance with a BVM. The decision to ventilate a patient should be based on the adequacy of breathing, not the respiratory rate alone.
The key to determining if breathing is adequate or not is the patient’s minute ventilation (MV), or minute volume of respiration, which is their tidal volume (Vt) multiplied by their respiratory rate (or frequency), f.
MV = Vt * f
The average tidal volume, or volume per breath, in a healthy adult is around 500mL, which is the size of a 16.9 oz bottle of water[i]. (This may also be estimated as 4-8 mL per kilogram of body mass). Using the formula above, we can determine the average minute volume to be somewhere between 6,000mL (12 breaths/min) and 9,000mL (18 breaths/min). In other words, a healthy, average-sized adult breathes at a rate of 6-9 liters per minute.
If you’ve ever wondered what constitutes “high flow” vs. “low flow” oxygen, this is it. High flow oxygen refers to administering oxygen at a flow rate greater than the patient’s own rate, while low flow is the opposite. For a 70 kg adult with a respiratory rate of 12 breaths/min, 8 liters per minute might just count as “high flow” oxygen. So why do EMT instructors make their students repeat “high flow oxygen at 15 L/min via NRB” ad nauseam?
Consider the average 70 kg adult with a textbook tidal volume of 500mL and a respiratory rate of 18 breaths/min. Their minute volume is (500 * 18 = 9,000 mL/min = 9 L/min). If their respiratory rate increases to 24 breaths/min, their minute volume is now 12,000 mL/min, or 12 L/min. At 30 breaths/min, which is not uncommon, this becomes 15,000 mL/min, or 15 L/min. Administering oxygen at a rate of 15 L/min ensures that they are getting 100% oxygen with each breath. On the other hand, if her breathing becomes shallower as the rate increases, this can cause a plateauing of minute volume (250 mL/breath x 30 breaths/min = 7.5 L/min).
Therefore, a determination of whether or not a patient’s breathing is adequate must be made based on an assessment of both tidal volume and respiratory rate. Assisting ventilations is required any time the patient’s own ventilations are insufficient, which can be due to an inadequate tidal volume, an inadequate rate, or both. If the patient is determined to be breathing adequately, positive pressure ventilation is not required, but you should continue to determine if other interventions are appropriate.
A naive interpretation of the relationship between tidal volume and respiratory rate might suggest that there are an infinite number of combinations that result in the same minute volume. While mathematically correct, this interpretation ignores the presence of anatomic dead space that is present in the airways. Anatomic dead space refers to the parts of the airway that cannot exchange gasses. Since gas exchange occurs in the alveoli, the anatomic dead space is the volume of the conducting airways (nose and mouth down to the terminal bronchioles). This dead space is around 150 mL on average (West, 1962) but can be larger due to devices like advanced airway adjuncts and SCUBA gear, which physically extend the airway.
When dead space is accounted for in the minute ventilation, we can determine the amount of air that moves through the alveoli each minute. This is called the alveolar ventilation (Va) and is calculated by subtracting the dead space from the tidal volume, then multiplying by respiratory rate (Levitzky, 2013).
Va = (Vt – Vd) * f
This metric is more relevant to our assessment than minute volume, as it reflects the actual amount of air available for gas exchange. As tidal volume decreases, an increase in rate alone will not be sufficient; these patients require supplemental volume. Consider our prototype adult (70 kg, Vt = 500mL, f=16) whose tidal volume starts to fall. Initially, her alveolar ventilation is 5.6 L/min. When the tidal volume is cut in half (250mL), the alveolar ventilation falls to below a third of what it was originally.
Normal: (500 mL/breath – 150 mL/breath) * 16 breaths/min = 5.6 L/min
Hypoventilation: (250 mL/breath – 150 mL/breath) * 16 breaths/min = 1.6 L/min
Increasing her respirations to around 22 breaths/min would maintain her minute volume, but her alveolar ventilation would only rise to 2.2 L/min. To return to her initial Va of 5.6 L/min, this patient would have to breathe at around 100 breaths/min. This is obviously problematic. Instead, increasing the depth of ventilation, either with a BVM or through increased work of breathing, is a better way to increase overall ventilation. If your patient has an excessively high respiratory rate (> 30), intervention is necessary to prevent deterioration in their condition.
As you can see, management of a patient’s ventilations requires careful attention to both rate and depth of ventilation. Assisting ventilations should generally be done at a rate of 10-12 breaths/min (one breath every 5-6 seconds), while delivering enough air to see the chest rise and fall (Weiss, 2008).
When discussing alveolar gas exchange, alveolar ventilation (Va) is only one half of the picture. The other half comes from alveolar perfusion, which provides the red blood cells that transport oxygen and carbon dioxide throughout the rest of the body. When alveoli are not perfused, perhaps due to a blockage in the pulmonary vasculature (i.e., pulmonary embolism), this creates alveolar dead space. You may also hear the term physiologic dead space, which refers to the sum of anatomic and alveolar dead spaces. Since this post focuses on ventilation, I’ll assume alveolar perfusion is within normal limits here, and cover V/Q ratios in a separate post.
Effects of Ventilation on Cardiac Output
Exceeding these parameters can result in a decreased cardiac output, which is obviously undesirable. As a refresher, cardiac output is comparable to minute ventilation, as it is a function of heart rate and stroke volume. Stroke volume, of course, is the amount of blood ejected from the left ventricle with each contraction. As you inhale, your diaphragm contracts and accessory muscles lift the chest wall up and out, causing a larger cavity. In turn, this creates negative pressure that draws air into the lungs and allows venous blood to return to the right side of the heart.
Positive pressure ventilation (PPV), as the name implies, relies on positive pressure to force air into the chest cavity. In this instance, there is little or no cooperation from the diaphragm and accessory muscles, resulting in air being forced into a fixed-size cavity. (While the chest wall certainly expands to accommodate this increased volume of air, it is doing so reluctantly.) This positive pressure also obstructs the venous return to the heart, and decreases cardiac output.
Respiratory conditions, like many other conditions, can be described in a spectrum ranging from mild distress to respiratory failure. Likewise, episodes can be acute, chronic, or chronic with acute exacerbation. While many of our respiratory patients require only comfort care, it is important to closely monitor your patient for signs of impending respiratory failure. Respiratory failure is characterized by inadequate oxygenation or inadequate alveolar ventilation. The hallmark sign of respiratory failure is deterioration in mental status. This is often accompanied by, or preceded by, a decrease in SpO2, cyanosis, accessory muscle use, grunting, and nasal flaring. Respiratory failure can be further classified by whether or not hypercapnia (elevated levels of carbon dioxide) is present. These patients are severely ill and will likely die without intervention. Once a patient is in respiratory failure, assisting ventilations with a BVM is the best treatment option. Again, this should be done at a rate of 10-12 per minute.
Using a BVM is simple enough in theory, but numerous studies have shown that we’re just not that good at it. In fact, the AHA recommends against using a BVM in cardiac arrest when there is only one rescuer (mouth-to-mask is better). BVM ventilation is most effective when two trained rescuers are available: one to maintain the airway and mask seal and a second provider to ventilate the patient.
Since cardiac output is reduced during CPR (around 25-33% of normal), gas exchange is also reduced. Therefore, the AHA recommends tidal volumes of 500-600 mL (6-7 mL/kg), which is enough to produce visible chest rise. Be sure to avoid overzealous ventilation, as it can lead to gastric inflation as well as a reduction in cardiac output (Link MS, 2015).
Continuous Positive Airway Pressure (CPAP)
Patients in impending respiratory failure – exhibiting signs of inadequate oxygenation, but not a change in mental status – can sometimes be managed successfully with Continuous Positive Airway Pressure (CPAP). As the name implies, CPAP works to keep the airways open with positive pressure. (It also increases the A-a gradient, which I’ll cover in the post about ventilation-perfusion ratios.) This is primarily a problem during exhalation in which the small, flexible bronchioles are squeezed shut by the positive intrathoracic pressure surrounding them. By supporting these narrow airways and increasing the A-a gradient, oxygenation is improved and carbon dioxide can exit the body more easily.
The primary advantage of CPAP is mitigating respiratory failure and avoiding unnecessary intubation. Since CPAP does not ventilate the patient, the patient must be alert, able to obey commands, and have a respiratory rate greater than 8 breaths/min. As discussed above, positive airway pressure can impede cardiac function, so CPAP is contraindicated in hypotensive (SBP < 90 mmHg) patients or those with a suspected or known pneumothorax.
Recognition of respiratory failure is critical for any level of prehospital provider. As the patient begins to experience signs of inadequate oxygenation – cyanosis, decreased SpO2, and accessory muscle use, etc. – the provider should consider interventions to increase alveolar ventilation. CPAP and assisting ventilations with a BVM are basic interventions available to most prehospital providers. CPAP is indicated when the patient is inadequately oxygenated (SpO2 < 90% despite high-flow oxygen), but not yet in respiratory failure. Once the patient’s mental status or respiratory effort begins to deteriorate, immediate ventilation with a BVM is indicated. Ventilation should be performed at a rate of 10-12 breaths/min in most cases. Whenever possible, ventilation should be performed with a basic airway adjunct in place (OPA or NPA).
Levitzky, M. (2013, Jul 15). Alveolar Ventilation. Retrieved Oct 20, 2016, from LSUHSC School of Medicine – Dept. of Physiology: https://www.medschool.lsuhsc.edu/physiology/courses_respiratory_mgl2.aspx
Office of Academic Computing. (1995). Dead Space. Retrieved 10 18, 2016, from Johns Hopkins University School of Medicine: http://oac.med.jhmi.edu/res_phys/Encyclopedia/DeadSpace/DeadSpace.HTML
Weiss, A. L. (2008). Focus On – Bag-Valve Mask Ventilation. ACEP News.
West, J. (1962, Nov). Regional differences in gas exchange in the lung of erect man. Journal of Applied Physiology, 17(6), pp. 893-898.
Link MS, Berkow LC, Kudenchuk PJ, Halperin HR, Hess EP, Moitra VK, Neumar RW, O’Neil BJ, Paxton JH, Silvers SM, White RD, Yannopoulos D, Donnino MW. Part 7: adult advanced cardiovascular life support: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015;132:S444–S464.