Understanding Dead Space Volume
Dead space volume is the volume of gas that does NOT participate in gas exchange (e.g., there is no exchange between O2 and CO2). No matter what we do from an anesthesia standpoint there will always be some degree of dead space present in our patients.
Why is this? Alveolar minute ventilation (VA) is the product of respiratory rate and {effective} tidal volume (Vt).
VA = RR x (effective) Vt
Effective tidal volume is equal to the volume of inspired gas minus dead space volume. Dead space volume is the sum of mechanical, anatomical and alveolar dead space.
Mechanical dead space is related to equipment and is the only form of dead space that we can control to some degree. Things that would greatly increase mechanical dead space include using too long of ET tube that extends past the incisor teeth, not using a septum in the Y-piece of the breathing hoses (dual wye circuit), cracked inner tube of a coaxial circuit, malfunctioning or missing one-way valve (most commonly the exhalation one way valve), improper packing of the CO2 absorbent (mainly the Water-To-Fro circuit), utilizing multiple adapters between the endotracheal tube and the breathing hoses (e.g., ETCO2, apnea alert, right angle adapter, etc.).
Basically, mechanical dead space is going to occur where ever there is bi-directional flow of gases (inspired gases and exhaled gases) occurring outside of the patient. This would include anything that adds length between the connector port on the endotracheal tube and the Y-piece of a rebreathing circuit (or the initial connection of a Universal F or non-rebreathing circuit).
As long as the one-way valves are functioning properly, the length of the breathing hoses does NOT contribute to mechanical dead space because there is not bi-directional flow of gases through them. The inspiratory limb only contains the inspired gases, and the expiratory limb only contains the expired gases. The diameter of the breathing hoses will only affect the overall circuit volume....they do not have any bearing on mechanical dead space.
ALL breathing systems will contribute a little to mechanical dead space!
Here are some reported values for what each circuit will contribute to mechanical dead space:
Rebreathing dual wye hose configuration with no septum in Y-piece (22 mm adult hoses): 17 mL
Rebreathing dual wye hose configuration with septum in Y-piece (22 mm adult hoses): 5.4 mL
Rebreathing dual wye hose configuration with 15 mm pediatric hoses: 4 mL
Adult Universal F circuit: 8 mL
Pediatric Universal F circuit: 15 mL
You read that correctly! The pediatric Universal F circuit contributes 15 mL to mechanical dead space. This is why it is hard to justify or recommend the pediatric universal F circuit over the pediatric dual wye hose.
For non-rebreathing circuits the normal amount of mechanical dead space happens right at the connection that attaches to the endotracheal tube. The normal amount of mechanical dead space for the Jackson Rees is 3 mL and the Bain Coaxial is 4 mL.
The length of the corrugated tubing on the Jackson Rees does NOT affect mechanical dead space unless the oxygen flow rate is too low. If the oxygen flow rate is too low, then there is potential for mixing of the inspired and expired gases in which case the entire length of the tubing will contribute to mechanical dead space.
The Bain Coaxial circuit keeps the inspired gases separate from the exhaled gases so the oxygen flow rate will not affect an increase in mechanical dead space. However, if the inner tube of the coaxial circuit is cracked or disconnected from its attachments then the entire length of the Bain circuit will then contribute to mechanical dead space. This is also true for the universal F rebreathing circuit that has a coaxial hose design.
Additional equipment that will contribute to mechanical dead space:
ET tube connector: 2 mL
Right angle adapter: 7.4 mL
ETCO2 adult adapter: 7 mL
ETCO2 pediatric adapter: 2 mL
Heat and moisture exchange (HME) filters: 2.5 to 90 mL depending on manufacturer
Anatomical and alveolar dead space are collectively known as physiologic dead space. Anatomical dead space refers to the conducting airways such as the nose, nasal passage, nasopharynx and trachea. Anatomical dead space is minimized by endotracheal intubation because the conducting airways are bypassed, and the gases have a straight path to the alveoli. If the patient is intubated then the length of the endotracheal tube from the incisor teeth down to where it sits in the distal trachea plus the rest of the conducting airways to the alveoli is classified as anatomical dead space. If any length of the endotracheal tube extends past the incisors out of the mouth, then that is classified as mechanical dead space (confusing, I know!).
Alveolar dead space relates to specific alveoli that are ventilated but not well perfused. This contributes to ventilation/perfusion (V/Q) mismatch. Conditions which can contribute to this include hypoperfusion (severe hypotension or hypovolemia), bradycardia, cardiogenic shock and pulmonary embolism.
Physiologic dead space makes up about 35% of the overall tidal volume. If using a tidal volume of 10-15 mL/kg then 3.5-5.25 mL/kg would be considered physiologic dead space and the rest, 6.5-9.75 mL/kg, would be participating in the actual gas exchange between oxygen and carbon dioxide at the level of the alveoli.
Due to the respiratory depressant effects of most anesthetic agents, a patient is going to have a decreased respiratory rate and a reduced quality of breath (they will not be taking as deep of a breath) so tidal volume will be reduced. Alveolar dead space might increase depending on how much V/Q mismatch is present. Because tidal volume decreases during anesthesia, alveolar minute ventilation (what participates in gas exchange) can be reduced to only 50% of the overall tidal volume that is inspired by the patient.
There is not much we can do to completely prevent physiologic dead space. We can use a balanced anesthesia protocol to help minimize the amount of alveolar dead space that may occur (by keeping perfusion adequate) but we are blinded to its overall effects because there is no way to directly measure or monitor alveolar dead space.
The overall take home message is that any increase in dead space volume (mechanical, anatomical and/or alveolar) will decrease the overall tidal volume that actually participates in gas exchange for the patient. If dead space is excessive it is going to decrease the alveolar minute volume which can lead to a build up of carbon dioxide (hypercapnia). It will also decrease the amount of oxygen and inhalant the patient is receiving with each breath.
Clear as mud, right?