Anatomic Dead Space Affects Hypoventilation

Understanding anatomic dead space is important to recognizing subtle hypoventilation. Hypoventilation from sedation, pain medications, anesthesia in the immediate postoperative period is common. The most obvious sign is slowing of the rate of breathing. A more subtle sign is that tidal volume becomes shallower. Having a tidal volume close to, or smaller than the patient’s dead space can lead to significant hypercarbia, hypoxia, and respiratory failure. This article discusses the concept of dead space and it’s clinical use in recognizing hypoventilation and preventing hypoxia and hypercarbia.

What Is Dead Space?

Dead space is the portion of the respiratory system where tidal volume doesn’t participate in gas exchange. There are three types of dead space: anatomic, physiologic, and the dead space belonging to any airway equipment being used to assist ventilation.

Types of Dead Space

Anatomic Dead Space

Anatomic dead space consists of the fixed parts of the respiratory tract that are ventilated but not perfused. It consists of conducting airways such as the trachea, bronchi, and bronchioles —structures that don’t have alveoli. Since it is not perfused, oxygen can’t be absorbed and carbon dioxide cannot be eliminated— that air here is wasted breath. It’s called anatomic because it’s fixed by anatomy and doesn’t change.

Illustration showing a cross section of a baby's airway airway next to a trachea to demonstrate the concept of anatomic dead space

Physiologic Dead Space

Physiologic dead space, consists of alveoli that are ventilated but lack capillary blood flow to pick up oxygen and drop off carbon dioxide. In other words, they are not perfused .  Unlike anatomic dead space, which is fixed, physiologic dead space can change from minute to minute with changes in cardiac output and pulmonary blood flow. Decreased cardiac output or lung perfusion increases dead space and makes ventilation less efficient.

This illustration defines the concept of physiologic dead space

In physiologic dead space, alveoli are ventilated but not perfused. Physiologic dead space can change as lung perfusion changes.

Equipment Dead Space

Equipment dead space includes the mask, the part of the endotracheal tube outside the patient’s mouth, even the elbow on the endotracheal tube connecting it to the ventilation bag. Your manually administered breath must include enough volume to cover this equipment dead space to ensure that you give an adequate tidal volume.

Illustration of a child's head with a mask attached to an airway elbow demonstrating the concept of equipment dead space

All 3 types of dead space impact how well a patient ventilates. However, here we will concentrate on how failure to take anatomic dead space into account can lead to significant hypoventilation and, potentially, hypoxia.

How Can Anatomic Dead Space Cause Hypoventilation and Hypoxia?

It’s not intuitively obvious how a fixed quantity like anatomic dead space can cause hypoventilation. About a third of each normal breath we take is anatomic dead space, which means that a third of each breath is essentially wasted. Dead space is age dependent. It’s highest in the infant at 3ml/kg ideal body weight and is about 2ml/kg in older children and adults. If anatomic dead space is fixed, and doesn’t change from breath to breath, how can it effect ventilation?

Illustration comparing dead space and tidal volume in a teenager vs a healthy infant

Anatomic dead space is an important concept in determining if tidal volume is adequate.

An adequate tidal volume must always include enough volume to also fill the dead space, in addition to filling the lungs — otherwise not enough air enters the alveoli and the patient hypoventilates.

Let’s look at a common example of how anatomic dead space impacts adequacy of breathing: the healthy patient who does well intraoperatively, arrives in PACU apparently stable, but who then suffers respiratory failure within the first 30 minutes of arrival.

Clinical Case

A healthy, 31 y.o. man just underwent an appendectomy under general anesthesia. He weighs 90 kg, is 6 ft 1 inches tall and is quite muscular. His normal tidal volume would be about 7ml/kg X 90 kg = 630 ml. His anatomic dead space is about 2ml/kg X 90 kg or 180 ml. The difference, 630ml-180ml = 450 ml, represents the amount of air actually reaching his lungs. The amount in his anatomic dead space is wasted, since that space is not perfused.

As sometimes happens, our patient suffers severe emergence delirium on wake up from anesthesia. The entire surgical team struggles to hold him on the OR table to keep him from injuring himself, or others. The anesthesia provider quickly gives some additional IV fentanyl to treat possible pain and to sedate him.

He quiets down and the team transfers him to the recovery room. Once there his oxygen saturation is 100%, his pulse is 80, his blood pressure is 130/80, and his respiratory rate is 10. He is wearing an oxygen mask and receiving 8 liter per minute of supplemental oxygen. The team is grateful that the patient is now sound asleep. The advice given to his RN is to let him sleep undisturbed to avoid possible recurrence of his agitated wake up.

So now our patient is in a quiet space, comfortable, without stimulation, and deeply sedated from residual anesthesia as well as the additional opioid. While he’s breathing 10 times a minute, no one notices that he’s breathing very shallowly. His chest is moving and the RN can feel air moving in and out of the patient’s mouth, but his tidal volume is only about 200 ml. His anatomic dead space of 180 ml has not changed. So now the amount of air reaching his lungs is only 20ml. Because he is breathing supplemental oxygen, this 20ml is mostly oxygen so his saturation remains above 95%. However, he is hypoventilating badly.

Oxygenation and ventilation are different. Ventilation exchanges air between the lungs and the atmosphere so that oxygen can be absorbed and carbon dioxide can be eliminated. Oxygenation is simply the addition of oxygen to the body. If you breathe a high concentration of oxygen, but don’t increase or decrease your respiratory rate, your arterial oxygen content (PaO2) will greatly increase, but your PaCO2 won’t change.

If you are providing your patient extra oxygen, he may not become hypoxic right away because enough oxygen will still reach the alveoli to maintain the oxygen saturation for a while. However, he is barely moving his dead space gas back and forth so his ventilation is poor. As a result, his carbon dioxide starts to rise. Hypoventilation leads to increased PaCO2 and respiratory acidosis. For an adult, typical PaCO2 rise is 13 mmHg for the first minute and then 3 mmHg for each minute thereafter (1).

Hypercarbia Can Be Dangerous

Acute values of PACO2 above 50 mmHg are significant and require treatment. 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 remember that a patient can have a normal oxygen saturation, and even a normal arterial oxygen concentration, and still be in respiratory distress or failure because of hypoventilation and a rising CO2. In the above example our treated patient’s O2 saturation would be 100%, but with a PaCO2 of 80 mmHg, the pH would be about 7, a dangerous and potentially life-threatening respiratory acidosis. Don’t be lulled into missing a patient’s tenuous status just because the oxygen saturation looks good.

If this degree of hypoventilation continues, the patient will eventually become hypoxic.

How Does Hypoventilation Cause Hypoxemia?

I’m going to use the Alveolar Gas Equation, but bare with me, this will be quick and painless. Hypoventilation is a common cause of too little oxygen in the blood. When breathing room air, CO2 takes up space in the alveoli, leaving less room for oxygen. Let’s see how big an effect this is. The concentration of oxygen in the alveoli can be calculated using the Alveolar Gas Equation:

PAO2 = FiO2 (PB – PH2O) – PACO2/ R

Where: PAO2 = partial pressure of oxygen in the alveoli

FiO2 = concentration of inspired oxygen

PB = the barometric pressure where the patient is breathing

PH2O = the partial pressure of water in the air (usually 47 mmHg)

PACO2 = alveolar carbon dioxide tension

R = respiratory quotient, a constant usually assumed to be 0.8

Let’s say that our postoperative patient were breathing room air, has an alveolar PACO2 of 80 mmHg, or twice normal. That carbon dioxide takes up space and leaves less room for oxygen.

Using the Alveolar Gas Equation, that PAO2 calculation is:

PAO2 = 0.21 (760 – 47) – 80/0.8 = 49 mmHg

Normal PAO2 is about 100 mmHg, so this is quite hypoxic, especially since the alveolar PAO2 is always a little higher than the arterial PaO2. If it weren’t, oxygen would not flow out of the alveoli into the blood — it would stay in the alveoli.

Now let’s treat this patient with 50% oxygen (roughly the 6 Liter flow through the green face mask that we were giving him) and see what happens:

PAO2 = 0.5 (760 – 47) – 80/0.8 = 256 mmHg

That’s a five-fold increase in alveolar oxygen without changing ventilation at all. Putting the patient on oxygen will buy you time for treatment. If this is a quickly reversible process, such as a narcotic overdose, you may not need to intubate. However, if this is not quickly reversible, then oxygen protects brain and heart while you manually ventilate or intubate.

Early Recognition & Treatment of Hypoventilation Can Prevent Respiratory Failure

We all know to look for signs of airway obstruction, such as stridor, a rocking chest wall motion, or tensing of the accessory neck muscles of respiration. But it’s also important to evaluate adequacy of ventilation. By this I mean not just rate of respiration; you should also assess size of tidal volume. Feel the amount of air being exhaled in order to judge how big the tidal volume is.

Measuring end tidal CO2 (ETCO2)  is rapidly becoming more readily available in the PACU, emergency departments and on the ward. ETCO2 can allow you to directly monitor ventilation and spot trends, such as a rising ETCO2 — something that previously required blood gas sampling.

Don’t wait for hypoxia to develop. When you believe ventilation may be inadequate, then stimulate your patient to breath more deeply. Of ten stimulation is all that’s required. If hypoventilation continues, alert the rest of your team. Prepare for additional intervention, such as assisted ventilation or even opioid reversal. Early recognition and treatment of hypoventilation can prevent respiratory failure. Be on the alert, especially if you’re patient is sleeping peacefully.

To read more about dead space as it relates to ventilation/perfusion mismatch click here.

To read more about Equipment Dead Space click here.

May The Force Be With You

Christine Whitten MD
Author Anyone Can Intubate, A Step By Step Guide
Pediatric Airway Management: A Step by Step Guide

(1) Stock MC1, Schisler JQ, McSweeney TD. The PaCO2 rate of rise in anesthetized patients with airway obstruction. J Clin Anesth. 1989;1(5):328-32.

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