Pulmonary circulation is composed of the pulmonary circulation from the main pulmonary artery and the smaller bronchial circulation arising from the aorta. The pulmonary circulation dominates, by volume, and serves to deliver the mixed venous blood to the alveolar capillaries to facilitate gas exchange and to act as a large, low-resistance reservoir for the entire cardiac output from the right ventricle. The bronchial circulation serves to provide nutritional support to the airways and their associated pulmonary blood vessels.

Pulmonary Hemodynamics

1. Despite receiving all of the cardiac output from the right ventricle, the pulmonary vasculature maintains a relatively low pulmonary blood pressure. The normal adult mean pulmonary artery pressure (P_PA) is 9 to 16 mm Hg with systolic P_PA of 18 to 25 mm Hg.

2. PVR can change as a result of numerous factors (hypoxia, acidosis, mitral valve stenosis or regurgitation, left ventricular failure, primary pulmonary hypertension, or pulmonary emboli).

Distribution of Perfusion. There is a gradient of distribution of perfusion of the lung that is similar but not identical to the gradient of distribution of ventilation, with increased perfusion of regions in the central and lower regions compared to the upper regions (Fig. 24-8). Gravity, posture, and alveolar pressure will also have effects on the distribution of pulmonary blood flow.

Matching of Ventilation and Perfusion

1. Within certain limits, the lung attempts to match ventilation to perfusion (never ideal because the ventilation and perfusion gradients are not identical) (Fig. 24-9).

2. This matching is closer during spontaneous ventilation than during positive pressure ventilation. With positive pressure ventilation, the effects of alveolar pressure are increased and pulmonary blood flow distribution becomes less homogeneous (concept of perfusion zones of the lung) (Fig. 24-10A,B).

Dead Space

1. Any portion of an inspired breath that does not enter gas exchanging lung units is dead space (V_D). Minute ventilation (V_E) is the sum of alveolar ventilation (V_A) and dead space ventilation (V_D).

2. Dead space can be subdivided into physiologic dead space and apparatus dead space (breathing circuit). Physiologic dead space is further subdivided into airway dead space and alveolar dead space (Fig. 24-11).

3. Airway dead space is relatively constant but does vary directly with lung volume and bronchodilation increases airway dead space. Airway dead space is decreased by endotracheal intubation. For most correctly functioning modern anesthetic apparatus, equipment dead space is not clinically important.

4. A healthy person, breathing spontaneously, will have practically no alveolar dead space.

   1. Tidal volume breathing will usually result in a V_D/V_T ratio of approximately 0.3, entirely due to airway dead space.

   2. Alveolar dead space, however, becomes clinically important during positive pressure ventilation and in any condition of altered hemodynamics. Decreased cardiac output, pulmonary embolism, and changes in posture will all have clinically important effects on alveolar dead space.

Shunt or venous admixture is the portion of the venous blood returned to the heart that passes to the arterial circulation without being exposed to normally ventilated lung units.

1. Shunt may be extrapulmonary (blood does not pass through the lungs, thebesian veins, and bronchial circulation; <1% total pulmonary circulation) or pulmonary (venous blood passing through lung regions with decreased or no alveolar ventilation) (see Fig. 24-11).

2. Shunt and dead space are the extremes of the continuum of ventilation and perfusion matching (Fig. 24-12). Shunt has a large effect on PaO₂ but a limited effect on PaCO₂. Shunt is the commonest cause of hypoxemia during anesthesia (Fig. 24-13).

Alveolar-arterial oxygen difference (A-aD_O2) can be used as a crude monitor of shunt (proportional to shunt but the absolute gradient increases as FIO₂ increases). If FIO₂ and PvO₂ (cardiac output and temperature) remain relatively constant, the trend of the A-aD_O2 is a reasonably reliable monitor of changes in shunt.

Matching of Ventilation and Perfusion

1. Due to the combined effects of the architecture of the lung parenchyma and vasculature and gravity, there is a matching of ventilation and perfusion (V_A/Q) in the lung.

2. Typical resting values in an adult are 4 and 5 L per minute for alveolar ventilation and cardiac output for a V_A/Q ratio of 0.8 (see Fig. 24-11).

3. Positive pressure ventilation, decreased cardiac output, and atelectasis interfere with normal V_A/Q matching.

Hypoxic pulmonary vasoconstriction (HPV) is a unique reflex to try and minimize these perturbations in V_A/Q matching (pulmonary arterioles respond to regional hypoxemia by constricting). The arterioles in essentially all other tissues in the body vasodilate in response to hypoxemia.

1. This reflex will tend to redirect blood flow from poorly or nonventilated lung regions to better ventilated regions.

2. The primary stimulus for HPV is alveolar hypoxia (Fig. 24-14).