Alveolar gas exchange depends not only on ventilation of the alveoli but also on circulation of blood through the alveolar capillaries. In other words it depends both on ventilation and perfusion. This makes sense. You need both oxygen in the alveoli, and adequate blood flow past alveoli to pick up oxygen, other wise oxygen cannot be delivered.When the proper balance is lost between ventilated alveoli and good blood flow through the lungs, ventilation perfusion mismatch is said to exist.
The ventilation/perfusion ratio is often abbreviated V/Q. V/Q mismatch is common and often effects our patient’s ventilation and oxygenation. There are 2 types of mismatch: dead space and shunt.
Shunt is perfusion of poorly ventilated alveoli. Physiologic dead space is ventilation of poor perfused alveoli.
This article will describe how dead space is different from shunt. It will help you understand how you can use these concepts to care for your patient.
One important contributor to ventilation perfusion mismatch is dead space. Dead space is the portion of the respiratory system where tidal volume doesn’t participate in gas exchange: it is ventilated but not perfused. There are three types of dead space: anatomic, physiologic, and that dead space belonging to any airway equipment being used to assist ventilation. They all impact how well a patient ventilates.
Anatomic Dead Space
Anatomic deadspace consists of the 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. It’s called anatomic because it’s fixed by anatomy and doesn’t change.
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 3 ml/kg ideal body weight and is about 2 ml/kg in older children and adults. An adequate tidal volume must include enough volume to also fill the deadspace, otherwise not enough air enters the alveoli and the patient hypoventilates.
A healthy teenage boy weighing 60 kg (132 lb) will have about 360 ml of alveolar ventilation . A healthy infant weighs about 2.7 kg (6 lb) will have about 22 ml alveolar ventilation. In terms of liquid volume, that’s a can of soda vs. abouta tablespoon — an impressive difference. Let’s look at an example of how anatomic deadspace impacts adequacy of breathing.
Anatomic dead space is an important concept in determining if tidal volume is adequate.
Our teenager will have an anatomic dead space of 120ml (2 ml/kg X 60 kg), which means that of his 480 ml breath, roughly 360 reaches the alveoli and 120 doesn’t participate in exchange gas at all. For our baby, the anatomic dead space is 8 (3 X 2.7). So again that’s 14 ml of air reaching the alveoli and 8 ml being effectively wasted.
Let’s say our baby is sick with nausea, vomiting, and a fever of 101F (38C) . She starts to hypoventilate and is now breathingtidal volumes of 10 ml. She’s still moving 10 ml of gas in and out of her mouth and you can feel her breathing and see her chest move, even though it looks shallow. Her dead space is still 8 so now the amount of gas reaching her alveoli is 2 ml (10 ml – 8 ml). That’s not enough.
Remember, 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.
Oxygenation mostly changes PaO2. Ventilation mostly changes PaCO2.
If you’re providing our baby with extra oxygen, she may not become hypoxic right away because enough oxygen will still reach her alveoli to maintain her oxygen saturation for a while. However, she is barely moving her dead space gas back and forth so her ventilation is poor. As a result, her carbon dioxide starts to rise. Hypoventilation leads to increased PaCO2.
Acute values above 50 mmHg are significant and require treatment, values above 70 mmHg can be life-threatening because of respiratory acidosis among other things. Each 10 mmHg change in PCO2 roughly changes your pH by 0.1. So all other things being equal, a PCO2 of 70 is associated with a pH of 7.1.If carbon dioxide rises into the 70–80mmHg range it will also profoundly sedate the patient. This worsens hypoventilation, and increases carbon dioxide even more. Respiratory rate eventually 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. For another clinical explanationof how hypoventilation causes hypoxia and the difference between oxygenation and ventilation click here.
Physiologic Dead Space
A second type of 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.
In physiologic dead space, alveoli are ventilated but not perfused. Physiologic dead space can change as lung perfusion changes.
However, unlike anatomic dead space, which is fixed, physiologic dead space can change from minute to minute with alterationsin cardiac output and pulmonary blood flow. Many things can impair alveolar perfusion and increase physiologic dead space such as:
- cardiovascular shock (blood flow to the lungs is decreased),
- emphysema (lots of enlarged alveoli with less surface area and fewer alveolar capillaries)
- pulmonary embolus (flow is blocked by clot).
Let’s go back to the baby in our clinical scenario. Perhaps the baby is hypoventilating because she is in shock from diarrhea. Now she has two reasons for respiratory failure:
She’s hypoventilating, and barely exceeding her anatomic dead space.
She’s in cardiovascular shock. Hypovolemia and acidosis is decreasing her cardiac output and lung perfusion. Her physiologic dead space has increased and she is not perfusing all of the alveoli that are still getting ventilated. Remember, hypovolemia and shock increases physiologic dead space. And this brings us to the concept of shunt.
Another contributor to ventilation perfusion mismatch is shunt. Shunt is the opposite of dead space and consists of alveoli that are perfused, but not ventilated.
In pulmonary shunt, alveoli are perfused but not ventilated.
Blood flowing past poorly ventilated alveolidoesn’t pick up additional oxygen.This poorly oxygenated blood returns to the heart and mixes with oxygenated blood coming from other areas of the lungs that are ventilated. The mixture lowers the total oxygen content of the arterial blood, producing hypoxemia. The larger the shunt, the lower the oxygen content.
Giving a patient with an intrapulmonary shunt 100% oxygen to breathe won’t increase the PaO2 much, if at all, depending on the size of the shunt because the alveoli that are being ventilated are already filled with oxygen and the blood fromthe non-ventilated alveoli won’t pick up any more.
Common causes of shunt occur in lung tissue disease and include:
- pneumonia and pulmonary edema: some alveoli filled with fluid
- tissue trauma: alveolar wall swelling
- atelectasis: collapse of alveoli from failure to expand, or absorbsion of the air out of the alveoli without replacing it
- mucous plugging: air can’t get into the alveoli
- pulmonary arteriovenous fistulas
You can also havecertain defects in the heart that cause abnormal mixing of oxygenated and un-oxygenated blood, like a right to left shunt, but that’s a different mechanism from pulmonary shunt.
Many types of shunt can be improved with treatment. The most common example of shunt is atelectasis, which is collapse of alveoli. For example, taking deep breaths or sighs easily treats atelectasis, one of the most common day-to-day causes of shunt. We do this naturally several times an hour, often without even being aware of it.In contrast, patients who take very shallow breaths without sighing often develop atelectasis. Factors that can cause atelectasis to develop are:
- painful breathing from surgery or trauma
- depressed levels of consciousness such as from drug, injury, or illness
- the disease process itself
As you can see it’s possible, and quite common, for both deadspace and shunt to be present in the same patient. Looking back at our baby one more time her potential causes of hypoxemia/hypoxiainclude:
- Hypoventilation: tidal volumes close to her anatomic dead space volume producing inadequate alveolar ventilation. If you think about it, this is producing poorly ventilated alveoli which are still being perfused- that’s shunt
- Shock: increasing her physiologic dead space.
- Fever of 101 which will increase her metabolic rate and cause her to need even more oxygen than normal
V/Q mismatchcan lead easily lead to hypoxemia and hypercarbia. When treating hypoxia, it’s important for us to look for both shunt and dead space and treat them.
May The /Force Be With You
Christine Whitten MD,
Author Anyone Can Intubate: a Step by Step Guide, 5th Edition
and
Pediatric Airway Management: A Step by Step Guide
all illustrations copyright Christine Whitten MD
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