Dead space is an often misunderstood and overlooked aspect of veterinary anesthesia patient management. Dead space is always present as a component of the patient’s airway and, to a variable degree, as a component of the anesthetic system. Ignoring dead space increases induced by anesthesia systems or airway adaptors can have a significant clinical impact on very small patients.

There are three different types of dead space; anatomic, alveolar, and equipment/mechanical. Dead space ventilation involves that component of the respiratory gases that does not participate in gas exchange. Increasing the proportion of dead space to alveolar ventilation will lead to retention of carbon dioxide by the patient.  If mechanical dead space volume equals or exceeds alveolar ventilation volume the patient will not be able to clear carbon dioxide at all.

Anatomic dead space is comprised of the upper airway structures that do not participate in gas exchange. This includes the gases in the nasal passages, nasopharynx, larynx, trachea, and in the larger airways. Alveolar dead space represents those alveoli that are ventilated with fresh gas but not perfused by the pulmonary circulation. Together, anatomic and alveolar dead space is referred to as physiologic dead space. Physiologic dead space gases do not participate in CO2 and O2 exchange.

Average tidal volume is 10 to 15 ml/kg ^[1],[2] in the normal unanesthetized patient. Physiologic dead space volume, 3.5 to 5.25 ml/kg, makes up about 35% of this tidal volume ^[3],[4] while the remainder of the tidal volume, 6.5 to 9.75 ml/kg, is the portion of the tidal volume that actually participates in gas exchange (alveolar ventilation volume). During anesthesia, however, patient tidal volume decreases and, to a small degree, alveolar dead space increases. As a result, alveolar ventilation volume is reduced to 3.5 to 5.25 ml/kg (50% of tidal volume^[3]) in a normal anesthetized patient during spontaneous ventilation.

As an example, a 2.0 kg patient would normally have a tidal volume of 20 to 30 ml. Awake, patient physiologic dead space would be 7 to 10.5 ml, leaving 13 to 19.5 ml to participate in alveolar ventilation. Anesthetized, alveolar ventilation drops to 7 to 10.5 ml. Thus, 10.5 ml is the maximum volume of gas available for alveolar ventilation during spontaneous respiration if there is no mechanical dead space associated with the anesthetic system and airway adaptors.

Mechanical or equipment dead space is made up of the endotracheal tube extending beyond the patient’s incisors, patient monitor adaptors (ETCO2, apnea alert, etc.), any adaptors used to facilitate patient/system positioning (right-angle or swivel adaptors used to reduce the risk of tracheal trauma during patient rotation), the volume within a mask, humidification management exchangers (HME), and the “Y” piece (defined as the terminal end of an F circuit or noncircle system and the inhalation/exhalation hose connector in a circle system). 

Exhausted soda lime or malfunctioning one-way valves can also contribute to increasing mechanical dead space. Dead space also increases in a non-rebreathing system when fresh gas flows are inadequate or when certain defects are present in the system (for instance, when the center tube of a Bain system or F circuit is cracked or broken). These dead space contributors can all be controlled through proper system inspection and maintenance.

Mechanical dead space is never zero. As a minimum, the anesthetic system’s contribution to mechanical dead space is the dead space present in the “Y” piece or terminal segment of an F circuit or noncircle system.

The Norman elbow contains the least amount of mechanical dead space of any conventionally used anesthetic system due to the fresh gas inlet tubing being positioned directly at the ET tube adaptor opening. An Ayre T piece, Jackson-Rees modified Ayre T piece, or Bain noncircle system contain 3 to 4 ml of dead space. For our example 2.0 kg patient, a Bain system could reduce its alveolar ventilation volume from 10.5 ml to 6.5 ml.

Modern circle systems have “Y” piece dead space that varies from 8 ml for an adult Y-piece down to 4 ml for a pediatric hose Y-piece. Interestingly, the pediatric F circuits can possess significantly greater terminal dead space (15 ml) than the adult size F circuits (8 ml) offsetting their inherent advantage of reduced system volume.

Endotracheal tube dead space includes any of the tube extending past the patient’s incisors. The ET tube adaptor alone adds about 2 ml of dead space. The added dead space from the ET tube itself extending past the incisors is relatively negligible; a few tenths of an ml per cm excess tube for a 4 or 5 mm OD ET tube. For our 2.0 kg patient on a Bain system, having the ET tube adaptor extending beyond the incisors reduces our alveolar ventilation volume from 6.5 ml to 4.5 ml.

Adult ETCO2 monitor adaptors, apnea alert monitor adaptors, and positional facilitation adaptors can add 7 to 8 ml of dead space each. If our 2.0 kg patient (on Bain system with exposed ET tube adaptor) had one adult ETCO2 adaptor placed between patient endotracheal tube and anesthetic hoses, this would effectively eliminate its alveolar ventilation (4.5 ml – 7 ml = ^-2.5 ml).   

Pediatric ETCO2 adaptors are available for most ETCO2 monitors, and should be a requisite if using an ETCO2 monitor on very small patients. A typical pediatric adaptor reduces dead space volume from 7 ml to 2 ml.  We could add 5 ml to our patient’s alveolar ventilation by using a pediatric rather than adult adaptor giving us, at best, 2.5 ml for alveolar ventilation; better than negative numbers but still far less than normal alveolar ventilation. Add in an apnea alert or a positional adaptor and we again completely eliminate alveolar ventilation during normal spontaneous respiration.

Anesthetic facemasks also contribute mechanical dead space. This effect is exaggerated if the mask is of large volume and, interestingly, if there is a tight seal around the patient’s muzzle. A poor mask seal would reduce this dead space effect but would subject the staff to unwanted waste gas exposure and create more difficulties regulating anesthetic levels.

The consequences of excessive mechanical dead space can be substantial and, potentially, fatal. As dead space volume from any cause increases, effective alveolar ventilation decreases. Therefore, arterial CO2 levels increase. In patients on 100% oxygen there will be negligible effect on arterial oxygen tension. Arterial CO2, however, can reach impressive levels. It is possible to have an ETCO2 > 110 mmHg in patients with a normal pulse oximeter reading ^[5].

• Increased arterial CO2 causes:

  • Respiratory acidosis

  • Sympathetic stimulation

  • Cardiac arrhythmias

    • A mix of sympathetic stimulation and hypoxemic effects

  • Variable peripheral vasoconstriction (sympathetic effect) followed by peripheral vasodilation as a direct effect on peripheral vessels

  • CNS depressant effect and, eventually narcosis

    • PaCO2 levels above 100 mmHg have an anesthetic effect

  • Increased cerebral blood flow and intracranial pressure

  • Tachypnea and an increased work of breathing which can negatively impact a debilitated patient

• Arterial O2 levels may decrease enough to cause hypoxemia, especially in a patient breathing room air

• Inadequate ventilation interferes with adjustments in anesthetic levels

Controlling mechanical dead space is a simple matter.

• Mechanical dead space is most concerning for patients under 6 kg body weight

• Minimize the connectors attached to the endotracheal tube, particularly in small patients.

  • For example, in a 6 kg patient under anesthesia the patient’s alveolar ventilation volume would be 31.5 ml. Using a pediatric F circuit with adult ETCO2 monitor and right angle adaptor (or apnea alert adaptor) would create 30 ml of mechanical dead space; effectively eliminating 95% of normal spontaneous alveolar ventilation.

• Make sure you regularly inspect all anesthetic machines and systems paying particular attention to valve function and inner hose integrity

  • Occluding the inner tube of a Bain system should cause the O2 flow indicator to drop

  • Alternatively, if attached to a Bain block, a filled reservoir bag should empty when the O2 flush valve is pushed

  • Observe proper one way valve function during patient respiration

• Make sure that the ET tube is not excessively long

  • Cut ET tubes to proper length (incisors to thoracic inlet) to help insure proper ET tube positioning

• Select your anesthetic system carefully

  • Dead space associated with the anesthetic system terminal end should be considered in the very small patients where each ml of alveolar ventilation volume is important

  • Do not use a pediatric F circuit as a substitute for conventional pediatric circle hoses or a noncircle system

    • It looks like a Bain system but it is NOT a suitable substitute

• Using no more than one monitor adaptor

  • Make sure it is a pediatric, low volume adaptor for smaller patients to avoid any significant impact on total mechanical dead space

    • In general, the monitor adaptor diameter should be the same as or larger than the patient’s ET tube

    • Apnea alert monitors do NOT normally come with pediatric, low volume adaptors

• Avoid the use of positional (right angle) adaptors in smaller patients

  • They not only increase mechanical dead space but also disturb laminar gas flow increasing the work of breathing

• Avoid maintaining anesthesia with a facemask