Maybe not. The size of a patient’s tidal volume vs. dead space determines whether the tidal volume is large enough to support life. Just because a patient can speak, doesn’t mean they are breathing well. It could be lifesaving to remember that any patient in respiratory distress may be able to speak, yet still suffer from significant hypoxia and/or hypercarbia. This article discusses:

• definition and types of dead space
• the relationship between tidal volume and anatomic dead space
• the difference of alveolar minute ventilation vs total minute ventilation
• speaking vs breathing

Case

We have all seen this scenario. A patient arrives in the recovery room very sedated, breathing supplemental oxygen by mask spontaneously, but shallowly. The oxygen saturation is 94%. However, end tidal CO2 is in the 70s — clearly bad since that corresponds to a pH of about 7.1. Also, high PaCO2’s themselves are quite sedating, and worsen respiratory depression. You stimulate the patient, encourage deep breathing, and as the CO2 returns toward normal the patient wakes up and takes deeper breaths. Their oxygen saturation was adequate the whole time. What happened? The patient’s tidal volume was about the same as his dead space volume.

What is Dead Space?

Tidal volume is the amount of air that move in and out of the lungs with each respiratory cycle. Not all the air in each breath takes part in gas exchange. The upper and lower parts of the respiratory system that don’t participate in gas exchange are called dead space. There are 3 types of dead space.

• Anatomic: the fixed parts of the respiratory system that are ventilated but not perfused, such as the oropharynx, larynx, trachea and bronchioles. Anatomic dead space is about 1/3 of normal tidal volume in an adult. Anatomic dead space is age dependent. It’s about 2 ml/kg in children and adults and as high as 3 ml/kg in infants.
• Physiologic: alveoli that are ventilated, but not perfused. Physiologic dead space is not fixed but can change as blood flow through capillary beds increases and decreases in certain clinical states. For example, dehydration, heart failure, and pneumonia all increase physiologic dead space, a process called ventilation/perfusion mismatch.
• Equipment: the volume inside the ventilation mask or endotracheal tube, the connecting elbow, and the breathing circuit. This volume becomes significant in small patients or small tidal volumes. Using too small a tidal volume with a high volume mask and/or breathing circuit can hypoventilate a patient.

A more detailed discussion of the 3 types of dead space can be found in these articles:

Anatomic Dead Space Affects Hypoventilation

Ventilation Perfusion Mismatch

Equipment Dead Space Affects Ventilation

Here, we will focus on the effects of anatomic dead space vs. tidal volume. The entire volume of the oropharynx, from nose to larynx, as well as the entire tracheo-bronchial tree down to, but not including, the alveoli, represents anatomic dead space and tidal volume. It is ventilated but doesn’t take part in gas exchange. That can be a significant volume depending on the size of the patient and the size of the tidal volume.

Tidal Volume vs. Anatomic Dead Space

Minute Ventilation

Minute ventilation (MV) is defined as the volume of gas a patient inhales in a minute.  It equals the tidal volume times the respiratory rate.

MV = TV x RR

Minute ventilation is often used as an indirect indicator of adequacy of a patient’s breathing. However, the actual number can be misleading because of the relationship between tidal volume vs. anatomic dead space. to start, a patient can have the numerically same minute ventilation, but significantly different tidal volumes and rates. For example, a 60 kg patient with a normal tidal volume of 500 ml breathing 12 times a minute will have a minute ventilation of 6,000 ml. (see the chart below)

If that patient’s tidal volume drops to 300 ml (shallow) and he’s breathing 20 times a minute (rapid) the minute ventilation is also 6,000 ml. And if he has a 150 ml tidal volume (very shallow) and breathes 40 times a minute (really fast) he still has a 6,000 ml minute ventilation. Despite the same 6,000 ml minute ventilation, the clinical status is very different because of anatomic dead space.

Alveolar Minute Ventilation

Due to anatomic dead space, not all this minute ventilation reaches the alveoli. Instead, we must look at alveolar minute ventilation.  Alveolar minute ventilation equals the alveolar tidal volume (tidal volume minus dead space) times the respiratory rate.

Alveolar MV = (TV – dead space) x RR

Look at this comparison chart, which includes alveolar ventilation.

Assuming a fixed anatomic dead space volume of 150 ml, changing tidal volume while maintaining the same minute ventilation greatly affects alveolar ventilation. In fact, if dead space volume equals tidal volume, there is no alveolar ventilation at all — despite a minute ventilation of 6,000 ml.

Your Patient Can Speak, But Can They Breathe?

Maybe, maybe not. Breathing requires a large enough volume of air to move into the lungs and reach all the way down the bronchial tree to ventilate the alveoli. Speaking, on the other hand, only requires a small amount of air to vibrate the vocal cords inside the larynx, which is at the top of the bronchial tree. The patient’s anatomic dead space becomes a significant determinant of how much tidal volume is enough to ventilate alveoli.

Anatomic dead space is about 1/3 of normal tidal volume. A normal adult tidal volume is about 400-500ml with an anatomic dead space of 150ml. As we have seen, adequate alveolar ventilation requires inhaling and exhaling significantly more than 150ml with each tidal volume. Otherwise, the air simply moves up and down in the bronchial tree but doesn’t reach the alveoli.

Each spoken syllable only requires about 50 ml of air to pass the vocal cords in an adult. Therefore, a patient saying “I can’t breathe” exhales about 150 ml of air out. It doesn’t mean they can inhale enough air back in to ventilate alveoli. As our chart shows, tidal volumes equal to the dead space volume will not ventilate alveoli even if minute ventilation is perfectly normal.

Can Supplemental Oxygen Help?

Look back at our case example. Providing extra oxygen to the patient can delay onset of hypoxia because even with marginal alveolar ventilation, enough oxygen may still reach the alveoli to maintain oxygen saturation for a while. However, for a patient barely moving his dead space gas back and forth, ventilation is poor. As a result, carbon dioxide rises leading to increased PaCO2 and respiratory acidosis. Acute PaCO2 values above 50 mmHg are significant and require treatment, and values above 70 mmHg can be life threatening.

If carbon dioxide rises into the 70–80 mmHg range, it will profoundly sedate the patient. This worsens hypoventilation, and increases carbon dioxide even more. Respiratory acidosis further depresses the patient — respiratory rate slows and the patient can stop breathing. 

It’s important to realize that by providing extra oxygen, a good practice, you delay the onset of hypoxia. But you may also delay the diagnosis of dangerous hypoventilation if you’re not looking for it. 

Increased Work Of Breathing Makes Things Worse

Work of breathing is also key. A patient laboring to breathe uses a lot of oxygen just to breathe — perhaps more than is reaching their alveoli. Patients at this stage often can’t speak complete sentences and pant between words.

As dead space and work of breathing increase, hypoxemia and ultimately hypoxia will increase. Hypercarbia and respiratory acidosis will develop. If patient entrapment, or a disease process, like asthma, pneumonia, or pneumothorax, prevents the patient from adequately inhaling air back in, then cardiopulmonary collapse will eventually occur. It’s possible the patient might be able to speak right up until cardiac arrest.

Size Does Matter: Pediatric Tidal Volume vs. Dead Space

Although infants and toddlers have the same resting tidal volume of about 8ml/kg as an adult, their small size means that tidal volume is extremely tiny. A 2.7-kg infant’s tidal volume is only about 22 ml. Dead space in an infant is higher: 3 ml/kg vs. 2 ml/kg in the adult. A larger dead space means even less of their tidal volume will reach the alveoli. Let’s look at an example.

This tidal volume vs. dead space relationship is especially important in children. Infants or toddlers have a metabolically higher oxygen consumption and CO2 production. They have a higher resting respiratory rate and heart rate to compensate for their small tidal volume and large dead space. Young children are at much higher risk of inadequate alveolar ventilation when injured or ill. In addition, a provider trying to avoid barotrauma could easily deliver a tidal volume smaller than or near dead space volume, leading to hypoxia and hypercarbia.

For a discussion of other reasons infants are at higher risk compared to adults see:

• 10 Common Pediatric Airway Problems—And Their Solutions

Continually Reassess Your Patient

Assess your patient’s ventilation keeping tidal volume vs. dead space volume in mind. We speak on exhalation. Can your patient speak in complete sentences? The more air we can exhale, the more words we can speak without stopping. Is your patient’s voice weak? How loud we are and how far we project our voice depends on how much air was inhaled to begin with. A faint voice implies a low volume of air flow out. Are they breathing fast?

While the ability to talk in the presence of respiratory distress is reassuring, it can unfortunately provide a false sense of security. It’s a sad truth that police restraint of suspects by sitting on their chests has occasionally resulted in deaths from asphyxia — despite the fact the suspect was saying right up until the time of death that they could not breathe .

Each evaluation is a snapshot in time. Status can easily change. Speaking does not equal breathing so don’t be lulled into a false sense of security. If you hear your patient say “I can’t breathe”, take them seriously. When tidal volume and dead space volume are close, alveolar ventilation may well be too low. Always consider anatomic dead space when evaluating your patient’s respiratory status. It could save your patient’s life.