Ventilation

Inspired gas flows into the lungs influenced by pulmonary compliance and airway resistance. Gravity, interacting with posture, and regional alveolar time constants for filling and emptying of lung regions, interacting with the frequency of respiration, are the other two major factors determining the distribution of within the lungs. The right lung is larger than the left lung, receiving approximately 52% to 53% of a tidal breath in the supine position, during both spontaneous breathing and with mechanical ventilation. These percentages change under the influence of gravity with change in posture. Anesthesia, paralysis, and mechanical ventilation introduce further changes.

At functional reserve capacity, in each slice of lung, from nondependent (apex in sitting position, anterior lung in supine, up lung in lateral decubitus position) to most dependent portion, the alveolar volume decreases. Basal alveoli are one quarter the volume of apical alveoli at end expiration. This puts the basal alveolar characteristics on a steeper portion of their pressure-volume (P-V) curve (Figure 29-1); although the basal alveoli are smaller than apical alveoli at functional reserve capacity, the basal alveoli expand more than do the apical alveoli during inspiration. Therefore, in an awake, spontaneously breathing patient, in all positions, ventilation per unit of lung volume is smallest at the highest portion (e.g., the apex in an upright patient) and increases with vertical distance down the lung.

In the supine patient, general anesthesia with paralysis and mechanical ventilation decreases the difference between the ventilation of the dependent and nondependent alveoli, causing nearly uniform distribution of ventilation throughout the lung. This is attributed to a decreased functional reserve capacity, shifting alveolar characteristics downward on their P-V curves (see Figure 29-1). When the patient is in the lateral decubitus position, anesthesia reverses the distribution of ventilation so that the nondependent (upper) part of the lung receives more ventilation than does the dependent (lower) part of the lung. This arrangement holds for both spontaneous and mechanical ventilation and is clinically significant because the dependent lung has greater perfusion, which causes increased / mismatch. The change in distribution of to lung regions in the lateral decubitus position is attributed to (1) decreased functional reserve capacity, causing a shift along the P-V curve (which can be partially reversed by positive end-expiratory pressure); (2) more compression of the dependent lung by the mediastinum and abdominal contents; and (3) increased compliance of the nondependent hemithorax.

The time constant for filling and emptying of a lung region is determined by the product of compliance and resistance of the region. If respiratory frequency is such that complete emptying of a region does not occur before the next inspiratory effort is applied, gas trapping will occur. This is a concern when obstructive airways disease is present. Incomplete filling or emptying of lung regions may also increase / mismatching. Anesthesia may reverse bronchoconstriction and favorably impact this factor.

Pulmonary blood flow

The two major determinants of distribution of pulmonary blood flow () within the lung are (1) gravity and (2) hypoxic pulmonary vasoconstriction (HPV). Pulmonary artery pressure (PPA) decreases by 1 mm Hg or 1.35 cm H₂O for every cm of vertical distance up the lung. Because the pulmonary circulation is a low-pressure system, this causes significant differences in between the lower and higher regions of the lung, with greater going to the lower lung regions. The actual to an alveolus also depends on the alveolar pressure (PALV), which opposes the PPA and pulmonary venous pressure (PPV). This interaction is summarized in Figure 29-2. All of these relationships are dynamic, varying throughout the cardiac and respiratory cycles. There are four defined zones of blood flow in the lung. In zone 1, at the apex of an upright lung, PALV is greater than PPA, preventing any blood flow and thereby creating alveolar dead space. Zone 1 is negligible in healthy lungs. In zone 2, PPA is greater than PALV, which is greater than PPV, so that depends only on PPA minus PALV. In zone 3, PPA is greater than PPV, which is greater than PALV, and is a function of PPA minus PPV independent of PALV. In zone 4 flow is determined by the difference between PPA and PISF. In general, decreases in PPA (e.g., hemorrhagic shock) will increase the size of the upper zones (1 and 2) at the expense of the lower zones (2 and 3), whereas increases in PPA have the opposite effect. Increases in PALV (e.g., with positive end-expiratory pressure) may recruit alveoli from lower zones into higher zones (i.e., increase the volumes of zones 1 and 2).

HPV is a local response of pulmonary arterial smooth muscle to a decreased regional alveolar PO₂. It acts to decrease to underventilated regions of lung and maintain normal /. HPV is effective only when there is a significant section of normally ventilated and oxygenated lung to which flow can be diverted (e.g., one-lung ventilation during thoracic operations). Intravenously administered anesthetic agents do not inhibit HPV, whereas the inhaled anesthetic agents and potent vasodilators do. Therapeutically inhaled NO is a unique pulmonary-specific vasodilator that may attenuate HPV and often improves oxygenation because it is delivered only to alveoli that are already being ventilated.

Ventilation/perfusion ratio

Both and increase toward the dependent part of the lung, but at different rates (Figure 29-3). Therefore, / is greater than 1 at the top, / equals 1.0 at the third rib in upright lungs, and / is less than 1 below the third rib. / is, of course, also affected by the factors that affect or separately.

Dead space

Dead space (VD) is the volume of a breath that does not participate in gas exchange, VT is the total tidal volume, and VD/VT is the fraction of the tidal volume composed of dead space volume. Anatomic dead space, VD(AN), is that volume of gas that ventilates only the conducting airways. Alveolar dead space, VD(ALV), is that volume of gas not taking part in effective gas exchange at the alveolar level, that is, ventilated but unperfused alveoli. Total (or physiologic) VD equals VD(AN) plus VD(ALV). Normally, the ratio of the physiologic dead space to the tidal volume (VD/VT) equals one third, and VD(AN) equals 0.5 mL/kg of body weight. In awake, healthy, supine patients, the VD(ALV) is negligible. One mechanism contributing to this is a bronchiolar constrictive reflex that constricts airways to alveoli that are unperfused.

VD/VT may be measured by the Bohr method, based on the fact that all expired CO₂ comes from perfused alveoli and none from dead space:

< ?xml:namespace prefix = "mml" />VD/VT=PACO2–mixed expired PCO2PACO2

Clinically, we assume that arterial PCO₂ equals alveolar PCO₂. Mixed expired PCO₂ is the average PCO₂ in an expired gas sample; this is not the same as end-tidal PCO₂.

Factors affecting dead space and dead space/tidal volume

VD and VD/VT are affected by / and the anatomy of the conducting airways. Decreased PPA (e.g., hemorrhage, drug effects) causes increased VD(ALV) owing to an increase in zone 1.

Loss of perfusion to ventilated alveoli despite normal or high PPAS causes increased VD(ALV) and, therefore, an increase in VD/VT. These conditions may result from pulmonary emboli (including venous air embolism), pulmonary arterial thrombosis, surgical manipulation of the pulmonary arterial tree, or emphysema with loss of alveolar septa and vasculature.

Increased airway pressure (e.g., positive-pressure ventilation) causes increased VD(AN) from radial traction on conducting airways by surrounding lung parenchyma and increased VD(ALV) from increased zone 1. When the patient’s neck is extended and jaw is protruded, the VD(AN) increases twofold, compared with a flexed neck and depressed chin. Compared with supine posture, erect posture causes increased VD(ALV) because decreased perfusion to the uppermost alveoli causes an increased volume of zone 1.

The dead space of anesthesia apparatus increases the VD/VT ratio from the normal 0.3 to values of 0.4 to 0.5 with tracheal intubation and Y-piece connectors or 0.64 with facemask ventilation. Tracheostomy or intubation decreases the VD(AN) by roughly half unless anesthesia apparatus is added to the breathing circuit.

General anesthesia, with spontaneous or controlled ventilation, increases VD and VD/VT. The etiology is multifactorial and incompletely understood; it may be partially due to moderate pulmonary hypotension, loss of skeletal muscle tone, or loss of bronchoconstrictor tone. Rapid short inspirations increase VD by ventilating a greater fraction of noncompliant and badly perfused alveoli, as compared with slower deeper inspirations.

Increasing age increases both anatomic and alveolar dead space due to decreased elasticity of lung tissues. Additionally, closing volume and closing capacity increase with aging.

Shunt

Shunt (S) is that portion of blood flow that does not participate in gas exchange. S/T is that fraction of pulmonary blood flow (total cardiac output) that is shunt. There are anatomic contributions to shunt from thebesian veins, bronchial veins, and any other anatomic right-to left shunt paths directly emptying into the left side of the heart beyond the lungs. These shunts may deflect up to 5% to 7% of T. / mismatching may contribute about a further 1% to 3% such that total shunt may be 6% to 10% of cardiac output in normal lungs (Box 29-1). S/T may be estimated using the Fick principle embodied in the shunt equation:

Q˙S/Q˙T=Cc’O2– CaO2Cc’O2–Cv_O2

where CC”O₂ is end-capillary O₂ content, CaO₂ is arterial O₂ content, and CO₂ is mixed venous O₂ content.

Acknowledgment

The author wishes to thank Michael E. Johnson, MD, PhD, for his work in previous editions.