Shunt is perfusion (blood flow) without ventilation (Figure 1-1). Pulmonary shunt occurs when blood flows from the right heart to the left heart without participating in gas exchange. The result of shunt is hypoxemia. Shunt can be either capillary shunt or anatomic shunt. Capillary shunt results when blood flows past unventilated alveoli. Examples of capillary shunt are atelectasis, pneumonia, pulmonary edema, and acute respiratory distress syndrome (ARDS). Anatomic shunt occurs when blood flows from the right heart to the left heart and completely bypasses the lungs. Normal anatomical shunt occurs due to the Thebesian veins and the bronchial circulation. Abnormal anatomic shunt occurs with congenital cardiac defects. Total shunt is the sum of the capillary and anatomic shunt.
Schematic illustration of anatomic shunt and capillary shunt.
Positive pressure ventilation usually decreases shunt and improves arterial oxygenation. An inspiratory pressure that exceeds the alveolar opening pressure expands a collapsed alveolus, and an expiratory pressure greater than alveolar closing pressure prevents its collapse. By maintaining alveolar recruitment with an adequate expiratory pressure setting, arterial oxygenation is improved. However, if positive pressure ventilation produces overdistention of some lung units, this may result in redistribution of pulmonary blood flow to unventilated regions (Figure 1-2). In this case, positive pressure ventilation paradoxically results in hypoxemia.
Alveolar overdistention, resulting in redistribution of pulmonary blood flow to unventilated units and an increased shunt.
Although positive pressure ventilation may improve capillary shunt, it may worsen anatomic shunt. An increase in alveolar pressure may increase pulmonary vascular resistance, which could result in increased flow through the anatomic shunt, decreased flow through the lungs, and worsening hypoxemia. Thus, mean airway pressure should be kept as low as possible if an anatomic right-to-left shunt is present.
A relative shunt effect can occur with poor distribution of ventilation, such as might result from airway disease. With poor distribution of ventilation, some alveoli are underventilated relative to perfusion (shunt-like effect and low ventilation-perfusion ratio), whereas other alveoli are overventilated (dead space effect and high ventilation-perfusion ratio). Positive pressure ventilation may improve the distribution of ventilation, particularly by improving the ventilation of previously underventilated areas of the lungs.
Ventilation is the movement of gas into and out of the lungs. Tidal volume (VT) is the amount of gas inhaled or exhaled with a single breath and minute ventilation (V̇E) is the volume of gas breathed in 1 minute. Minute ventilation is the product of tidal volume (VT) and respiratory frequency (fb):
Ventilation can be either dead space ventilation (V̇D) or alveolar ventilation (V̇A). Minute ventilation is the sum of dead space ventilation and alveolar ventilation:
Alveolar ventilation participates in gas exchange (Figure 1-3), whereas dead space ventilation does not. In other words, dead space is ventilation without perfusion. Anatomic dead space is the volume of the conducting airways of the lungs, and is about 150 mL in normal adults. Alveolar dead space refers to alveoli that are ventilated but not perfused, and is increased by any condition that decreases pulmonary blood flow. Total physiologic dead space fraction (VD/VT) is normally about one-third of the V̇E. Mechanical dead space refers to the rebreathed volume of the ventilator circuit and acts as an extension of the anatomic dead space. Due to the fixed anatomic dead space, a low tidal volume increases the dead space fraction and decreases alveolar ventilation. An increased dead space fraction will require a greater minute ventilation to maintain alveolar ventilation (and PaCO2).
Schematic illustration of mechanical dead space, anatomic dead space, and alveolar dead space.
Because mechanical ventilators provide a tidal volume and respiratory rate, any desired level of ventilation can be provided. The level of ventilation required depends upon the desired PaCO2, alveolar ventilation, and tissue CO2 production (V̇co2). This is illustrated by the following relationships (note that the factor 0.863 is not used if the measurements are made at the same conditions and using the same units):
A higher V̇E will be required to maintain Paco2 if V̇co2 is increased, such as occurs with fever and sepsis. If dead space is increased, a higher V̇E is required to maintain the same level of V̇A and Paco2. If this level of ventilation is undesirable due to its injurious effects on the lungs and hemodynamics, Paco2 can be allowed to increase (permissive hypercapnia). Mechanical ventilation can produce overdistention of normal alveoli, resulting in alveolar dead space. Mechanical ventilation can also distend airways, increasing anatomic dead space.
Atelectasis is a common complication of mechanical ventilation. This can be the result of preferential ventilation of nondependent lung zones with passive ventilation, the weight of the lungs causing compression of dependent regions or airway obstruction. Breathing 100% oxygen may produce absorption atelectasis, and should be avoided if possible. Use of PEEP to maintain lung volume is effective in preventing atelectasis.
Barotrauma is alveolar rupture due to overdistention. Barotrauma can lead to pulmonary interstitial emphysema, pneumomediastinum, pneumopericardium, subcutaneous emphysema, and pneumothorax (Figure 1-4). Pneumothorax is of greatest clinical concern, because it can progress rapidly to life-threatening tension pneumothorax. Pneumomediastinum and subcutaneous emphysema rarely have major clinical consequences.
Barotrauma-related injuries that can occur as the result of alveolar rupture.
Ventilator-Induced Lung Injury
Alveolar overdistention causes acute lung injury. Alveolar distention is determined by the difference between intra-alveolar pressure and the intrapleural pressure. The peak alveolar pressure (end-inspiratory plateau pressure) should ideally be as low as possible and less than 30 cm H2O. Alveolar distention is also affected by intrapleural pressure. Thus, a stiff chest wall may be protective against alveolar overdistention. Overdistention is minimized by limiting tidal volume (eg, 4-8 mL/kg ideal body weight) and alveolar distending pressure (< 25 cm H2O). Ventilator-induced lung injury can also result from cyclical alveolar collapse during exhalation and re-opening during subsequent inhalation. This injury is ameliorated by the application of PEEP to avoid alveolar derecruitment. Ventilating the lungs in a manner that promotes alveolar overdistention and derecruitment increases inflammation in the lungs (biotrauma). Inflammatory mediators may translocate into the pulmonary circulation, resulting in systemic inflammation. An important characteristic of the lungs of mechanically ventilated patients is heterogeneity; that is, some lung units are prone to overdistention and others are prone to collapse.
Ventilator-associated pneumonia (VAP) can occur during mechanical ventilation; this is more common during invasive ventilation than with noninvasive ventilation. VAP most often results from aspiration of oropharyngeal secretions around the cuff of the endotracheal tube. A number of prevention strategies can be bundled to reduce the risk of VAP.
Hyperventilation and Hypoventilation
Hyperventilation lowers Paco2 and increases arterial pH. This should be avoided because of the injurious effects of alveolar overdistention and an alkalotic pH. Respiratory alkalosis causes hypokalemia, decreased ionized calcium, and increased affinity of hemoglobin for oxygen (left shift of the oxyhemoglobin dissociation curve). Relative hyperventilation can occur when mechanical ventilation is provided for patients with chronic compensated respiratory acidosis; if a normal Paco2 is established in such patients, the result is an elevated pH. Hypercapnia during mechanical ventilation may be less injurious than the traumatic effects of high levels of ventilation to normalize the Paco2. A modest elevation of Paco2 (50-70 mm Hg) may not be injurious and a pH as low as 7.20 is well tolerated by most patients.
A high inspired oxygen concentration is considered toxic. What is less clear is the level of oxygen that is toxic. Oxygen toxicity is probably related to Fio2 as well as the amount of time that the elevated Fio2 is breathed. Although the clinical evidence is weak, it is commonly recommended that an Fio2 greater than 0.6 be avoided, particularly if breathed for a period more than 48 hours. High Fio2 levels can result in a higher than normal PaO2. A high Pao2 may produce an elevation in Paco2 due to the Haldane effect (ie, unloading CO2 from hemoglobin), due to improving blood flow to low-ventilation lung units (ie, relaxing hypoxic pulmonary vasoconstriction), and due to suppression of ventilation (less likely). However, this is usually not an issue during mechanical ventilation because ventilation can be controlled. A high Pao2 can produce retinopathy of prematurity in neonates, but this is not known to occur in adults.