Dead Space

Supervising Professor: Nasreen Kader

Names Yousif Hussin Mardan

Taha Mahmoud Marhun

Mohammed Naif Hezan

Introduction
Dead space of the respiratory system refers to the space in which oxygen (O2) and carbon dioxide
(CO2) gasses are not exchanged across the alveolar membrane in the respiratory tract. Anatomic
dead space specifically refers to the volume of air located in the segments of the respiratory tract
that are responsible for conducting air to the alveoli and respiratory bronchioles but do not take
part in the process of gas exchange itself. These segments of the respiratory tract include the
upper airways, trachea, bronchi, and terminal bronchioles. Alveolar dead space, on the other
hand, refers to the volume of air in alveoli that are ventilated but not perfused, and thus gas
exchange does not take place.[1][2][3]
Physiologic dead space (VDphys) is the sum of the anatomic (VDana) and alveolar (VDalv) dead
space.
VDphys = VDana + VDalv (L)
Dead space ventilation (VD) is then calculated by multiplying VDphys by respiratory rate (RR).
VD = VDphys x RR (L/min)
Total ventilation (VE) is, therefore, the sum of alveolar ventilation (Valv) and VD.
VE = Valv + VD (L/min)
Enghoff's equation compiles these variables with PaCO2, tidal volume (TV), and expired CO2
(PECO2). It is then implied that VDphys/VT is representative of the portion of a tidal volume that
does not participate in gas exchange.
VDphys/VT = (PaCO2 - PECO2)/PaCO2
Dead space has particular significance in the concept of ventilation (V) and perfusion (Q) in the
lung, represented by the V/Q ratio. Alveoli with no perfusion have a V/Q of infinity (Q=0),
whereas alveoli with no ventilation have a V/Q of 0 (V=0). Therefore, in situations (i.e., V/Q
=infinity) in which the alveoli are ventilated but not perfused, gas exchange cannot occur, such as
when pulmonary embolism increases alveolar dead space.

Structure and Function

The function of a seemingly wasteful design for ventilation that includes dead space is as
follows:
 Carbon dioxide is retained, resulting in a bicarbonate-buffered blood and
interstitium.
 Inspired air is raised or lowered to body temperature, increasing the affinity of
hemoglobin for O2 and improving O2 uptake.
 Particulate matter is trapped in the mucus that lines the conducting airways,
allowing it to be removed by mucociliary transport.
 Inspired air is humidified, thus improving the quality of airway mucus.
Physiologic Variants
Alveolar dead space typically is negligible in a healthy individual. Anatomic, and
therefore physiological, dead space normally is estimated at 2mL/kg of body weight and
comprises 1/3 of the TV in a healthy adult patient; it is even higher in pediatric patients.
Effectively, 1/3 of a TV of inhaled air is rebreathed due to dead space. At the end of
expiration, the dead volume consists of a gas mixture high in CO2 and low in O2
compared to ambient air.
End-expiratory dead volume: 5-6% CO2, 15-16% O2; Ambient air: 0.04% CO2, 21% O2
Numerous physiologic factors can influence dead space:
 Respiratory Cycle: Inhalation leads to increases in bronchial diameter and length,
effectively increasing the anatomic dead space. Likewise, exhalation decreases
the amount of anatomic dead space by "deflating" the bronchial tree.
 Positioning: Dead space decreases with the supine position and increases during a
sitting position. The upright position allows a mismatched ratio of ventilation (V)
and perfusion (Q) to occur, in which the apices of the lungs can not be as well
perfused as ventilated (due to gravity's greater effect on blood than air), so wasted
ventilation occurs and effectively increases dead space volume.
 Sleep: Anatomic dead space is believed to decrease during sleep and be the
primary physiologic cause of observed decreases in tidal volume, minute
ventilation, and respiratory rate during sleep.
 Maxilla: Variation also can occur in patients with maxillary defects or those who
have undergone maxillectomy procedures. These patients have an increased
anatomic dead space due to communication between the nasal and oral cavities,
which can ultimately affect respiratory function.

Surgical Considerations
In patients with disease-free lungs who are undergoing general anesthesia for procedures
non-affective of the thoracic cavity or diaphragm, dead space and compliance of the
lungs has enabled physicians to tailor patients' PEEP to optimal levels, with the reasoning
that the point of minimum dead space with maximum compliance represents the point at
which the maximum amount of alveoli are opened for ventilation. Increasing VD,
however, can signify that alveoli may be over-distending from overly-aggressive
ventilation parameters. Lung recruitment maneuvers in adjunct to PEEP in mechanical
ventilation has been shown to significantly increase functional residual capacity,
compliance, and PaO2 with decreases in dead space compared to PEEP alone.[4][5][6]
Clinical Significance
Dead space can be affected by various clinical scenarios:
 Lung Disease: Emphysema destroys alveolar tissue and leads to air trapping and
decreased diffusion surface area, thereby increasing dead space volume. Acute
Respiratory Distress Syndrome (ARDS) creates disturbances in the pulmonary
microvasculature, theoretically increasing dead space. However, it is poorly understood if
these portions of the lung are ventilated sufficiently to be considered dead space.
VDphys/VT measured by Enghoff's equation increases in ARDS, however, due to the
ratio being reflective of any changes in V/Q which occur in pulmonary shunting
mechanisms (perfusion without ventilation).
 V/Q Mismatch/Decreased Perfusion: Perfusion to the alveoli is decreased in clinical
scenarios such as pulmonary embolism and hypotension, increasing the V/Q ratio and
creating dead space ventilation.
 Mechanical Ventilation: Tubing from the ventilator increases dead space volume by
adding volume to the effective space not participating in a gas exchange.
 PEEP: Excessive PEEP can over-distend alveoli and result in lung barotrauma, increasing
the dead space volume.
 Hypoxia: Bronchoconstriction and vasoconstriction from hypoxia decrease dead space
volume.
 Anesthesia: Bronchodilation from anesthetic gases increases dead space volume.
Estimation of the dead space can be of significant value in clinical situations for diagnostic,
prognostic, and therapeutic value. Dead space is an integral part of volume capnography, which
measures expired CO2 and dead space (VDphys/VT) on a breath-by-breath basis for
efficient monitoring of patient ventilation. Despite that the VDphys/VT ratio measured by
Enghoff's equation is adversely affected by pulmonary shunting in ARDS, VDphys/VT has been
shown to be a significant predictor of mortality during early-phase acute respiratory distress
syndrome (ARDS), and increases in the VDphys/VT ratio correlated with poorer patient
outcomes. Measurement of this dead space provides a quantifiable indicator of overall lung
function for physicians to assess throughout the course of ARDS patients' hospital course. PEEP,
an integral part of ARDS ventilation management, can be titrated to a patient's specific need
based off of capnography and dead space monitoring, but this finding has not been consistently
shown in multiple studies.
Physicians with patients suspected of pulmonary embolism can use dead space and capnography
findings to exclude the diagnosis with elevated D-dimer, a sensitive but not specific test for an
embolism. Furthermore, capnography can be used for periodic monitoring of thrombolysis
treatment in pulmonary embolism by trending changes in dead space measurements. Dead space
and capnography can prove to be useful tools, minimizing unnecessary tests by ruling out
pulmonary embolism with simple capnography measurements.
Clearance of the anatomic dead space is believed to play a significant role in the use of nasal high
flow cannulas. It is believed that high nasal flow allows dead space to be cleared more rapidly
and subsequently decreasing the portion of dead space that is rebreathed, increasing alveolar
ventilation.
References

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the mechanically ventilated patient. Minerva Anestesiol. 2006
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