Description
- Dead space (VD) describes the lung areas that are ventilated but not perfused. Perioperatively it includes:
- Physiologic dead space: Anatomic and alveolar
- Apparatus dead space: Most concerning for neonates
- Increases in the dead space to alveolar ventilation (VD:VA) ratio result in the retention of carbon dioxide. Thus, any cause of increased VD would require increases in ventilatory support/parameters in order to maintain normocarbia.
- Physiologic dead space (VDtotal) does not participate in carbon dioxide or oxygen exchange. It is composed of 2 different components of lung volume:
- Anatomic (VDanatomic): Upper airway structures that do not contribute to gas exchange; includes air in the nose, pharynx, larynx, trachea, and larger airways. This volume does not reach the alveolar level, will not participate in gas exchange, and is thus "wasted." It is ~1/3rd of the tidal volume, or 2 mL/kg.
- Alveolar (VDalveolar): Ventilated alveoli receiving minimal blood flow; includes zone 1 and nondependent lung areas.
- VDtotal = VDanatomic + VDalveolar
- Apparatus, mechanical, or equipment dead space: Perioperatively, the anesthetic delivery system and monitors can add dead space; it can become significant with pediatric patients. As the volume increases, less fresh gas moves into the patient's alveoli to participate in gas exchange. This also applies to intubated and ventilated patients in the ICU.
- Endotracheal tube or laryngeal mask airway; dead space volume exists in the portion that extends beyond the patient's incisors (can be decreased by cutting the ETT). Of note, however, intubation results in ~1/2 of the anatomical dead space being bypassed (volume of dead space in nasopharynx and mouth).
- Airway adaptors: Straight and elbow can add ~2 mL of dead space
- End-tidal CO2 monitors can add ~8 mL of dead space. The closer the ETCO2 monitor is positioned to the ETT, the less is the amount of dead space.
- Extenders such as corrugated devices
- Face masks
- Humidification management exchangers (HME)
- Y piece: Adults ~8 mL; pediatric ~4 mL
- Malfunctioning one-way valves
- Bain circuit with a cracked or broken center portion
- Exhausted soda lime: Unique in that it normally clears CO2 within the circuit; thus, when it is exhausted, it no longer participates in "ventilation."
- Bohr equation was presented in the beginning of the 20th century. The dead space fraction could be determined by measuring the arterial CO2 (PaCO2) via blood gas measurements and the mean expired CO2 (PeCO2). The end-tidal CO2 (ETCO2) is often substituted for the mean expired CO2 (1).
- Fowler's method—a test for measuring the dead space via nitrogen washout during one or multiple breaths. The patient takes a breath of 100% oxygen and exhales through a one-way valve measuring nitrogen content and volume. It is not commonly used or available perioperatively.
- Breathing efficiency—defined as the volume of fresh gas reaching the alveoli (alveolar tidal volume) divided by the total volume of the gas inhaled per breath (total tidal volume). In normal healthy adults who are breathing spontaneously at rest, it is normally between 60% and 70% (this means that ~30–40% of inhaled fresh gas does not reach the alveoli).
Physiology/Pathophysiology
- Alveolar dead space can be increased in pathological states. Non-perfused, but ventilated, alveoli are defined as lung units with a V/Q ratio of infinity. They include:
- Pulmonary embolus
- Low cardiac output
- Increased alveolar pressure from mechanical ventilation or positive end expiratory pressure (PEEP)
- Chronic obstructive pulmonary disease
- "Shunt dead space" is an erroneous description of right-to-left lung shunt that brings the higher CO2 concentration in venous blood to the arterial side, thereby producing an arterial-to-end-tidal CO2 difference. However, the influence of shunt on dead space is fairly small when shunt values are low; they become significant when the shunt has reached 50%.
- Hypercarbia can potentially have profound effects:
- Directly increases cerebral blood flow and intracranial pressure
- Increases pulmonary arterial pressure
- Sympathetic activation can result in tachycardia, hypertension, or arrhythmias.
- Assessing and measuring VD/VA or dead space will give insight into the matching of ventilation and perfusion and is useful in:
- Evaluating mortality risk in acute respiratory distress syndrome; increases in VD/VA correlate with the severity of lung injury.
- Indicating lung recruitment versus overdistention when PEEP is added or increased to improve oxygenation
- Predicting successful extubation in pediatric and adult patients
- Diagnosing and assessing the severity of pulmonary embolism. The alveolar dead space can increase to excessive amounts (80–90% of the tidal volume in recurrent pulmonary embolism).
- Providing valuable information on the ventilatory support of the critically ill by providing information regarding changes in volume of alveolar dead space (2)
- Breathing pattern: Rapid, shallow breathing, as may be seen from abdominal or thoracic incisional pain, can result in small tidal volumes, and an increased fraction of dead space ventilation (may reach >50%). Continuous epidural anesthesia in the postoperative period may decrease this (as well as atelectasis); the benefits may be pronounced in pulmonary cripples with low reserves.
- Pulmonary embolism: Fat, venous, air, or clot embolic phenomenon may result intraoperatively with sudden pulmonary vascular occlusion. The resultant V/Q mismatch can produce a sudden increase in alveolar dead space and decreased ETCO2 readings (PaCO2 will increase).
- Neonates and infants: Apparatus dead space is more concerning in this patient population. A 5 kg neonate has a dead space of ~10 mL. The addition of apparatus can add several milliliters causing the VD/VA ratio to increase significantly.
- Tracheostomy: Reduces dead space ventilation and improves the efficiency of ventilation. Studies have shown that tracheostomy can reduce VD by 70 mL and reduce the work of breathing by over 30% (3) [C].
- Compensatory breathing techniques: During respiratory distress in the spontaneously ventilating, non-intubated patient, an instinctive unidirectional breathing pattern may develop to avoid rebreathing air in the nose with a high CO2. This consists of inhaling via the nose, and exhaling through the mouth.
