Airway, Alveolar, and Intrathoracic Pressure, Volume, and Flow During Spontaneous Ventilation

Spontaneous breathing is normally an autonomic phenomenon. In other words, we do not think about breathing; it is controlled by the autonomic nervous system. Not until our breathing is stressed do we consider the effort to breathe or the energy expended. At end-exhalation, intrapleural pressure is slightly negative. Alveolar, mouth, and body surface pressures are zero. The diaphragm contracts in response to stimulation of the phrenic nerve via the respiratory center in the medulla of the brain. When the diaphragm contracts, it descends into the abdominal cavity, decreasing intrapleural pressure. When intrapleural pressure becomes more negative, alveolar pressure becomes negative as well. The effects of spontaneous breathing on the pressure gradients are shown in Table 43-1. Under normal circumstances, a decrease in intrapleural pressure results in decreased alveolar pressure, increased transairway pressure, and inspiration of the tidal volume (V_T) (Figure 43-2).

At end-inspiration, alveolar pressure returns to zero when the muscles of inspiration stop contracting. Lung recoil causes a sudden increase in alveolar pressure in relation to pressure at the mouth, reversing the transairway pressure gradient, and air flows out of the lungs. Normally, there is a short end expiratory pause before the next inspiration.

V_T and flow during spontaneous ventilation may be described by the equation of motion.1,2 The equation of motion describes the relationship between muscle pressure (analogous to pleural pressure in spontaneous breathing), compliance, resistance, flow, and volume as follows:

Pmusc=Volume/Compliance+(Resistance×Flow)

where P_musc is muscle pressure (P_tp), volume is tidal volume, compliance is lung-thorax compliance, resistance is airway resistance, and flow is gas flow through the airway. When the equation is rearranged, volume inhaled during spontaneous ventilation is proportional to muscle pressure and lung-thorax compliance and inversely related to the product of airway resistance and flow:

Volume=[Pmusc/(Resistance×Flow)]+Compliance

Ventilation (owing to transpulmonary pressure) is the sum of the pressure needed to move gas through the airways (transairway pressure) and the pressure needed to inflate the alveoli (transalveolar pressure):

Transpulmonary pressure=Pta+Palv

Airway, Alveolar, and Intrathoracic Pressure, Volume, and Flow During Negative Pressure Mechanical Ventilation

Mechanical NPV is similar to spontaneous breathing. NPV decreases pleural pressure (P_pl) during inspiration by exposing the chest to subatmospheric pressure. Negative pressure at the body surface (P_bs) is transmitted first to the pleural space and then to the alveoli (P_alv). Because the airway opening remains exposed to atmospheric pressure during NPV, a transairway pressure gradient is created. Gas flows from the relatively high pressure at the airway opening (zero) to the relatively low pressure in the alveoli (negative). As with spontaneous breathing, alveolar expansion during NPV is determined by the magnitude of the transpulmonary pressure gradient. During expiration in both spontaneous breathing and NPV, the lungs and chest wall passively recoil to their resting end expiratory levels. As this recoil occurs, pleural pressure becomes less negative, and alveolar pressure increases above atmospheric pressure (Figure 43-3). This increase in alveolar pressure reverses the transairway pressure gradient. As P_alv becomes greater than P_awo, gas flows from the alveoli to the airway opening. The effects of NPV on the pressure gradients are shown in Table 43-1.

Volume and flow during NPV also are described by the equation of motion except transairway pressure developed by the ventilator fully or partially replaces the patient’s respiratory muscle pressure as follows:

Pmusc+Pvent=Volume/Compliance+(Resistance×Flow)

In this equation, P_vent is the pressure the ventilator develops to overcome the patient’s lung-thorax elastance and airway resistance to deliver the V_T. In this case, P_vent is negative but is the driving force behind decreasing the intrapleural pressure and increasing the transairway and transpulmonary pressures.

Physiologic complications associated with NPV are uncommon because NPV simulates normal spontaneous breathing. The most common problems with NPV are related to interference with caring for the patient caused by the device surrounding the chest (the iron lung or chest cuirass). Supplemental oxygen (O₂) cannot be provided to the patient through the negative pressure ventilator. Depending on patient need, low-flow or high-flow O₂ delivery devices must be used to provide O₂ therapy. Immediate access to patients requiring routine or emergent medical care may be difficult in systems that enclose the entire thorax and lower body, such as the iron lung and Porta-Lung (Respironics Inc, Murrysville, PA). These systems may impede venous return by creating a negative pressure in the abdomen and lower half of the body, which may lead to hypotension, a phenomenon known as “tank shock.” The risk of glottis closure and the development of obstructive sleep apnea have been reported in association with NPV of patients with chronic obstructive pulmonary disease (COPD) and neuromuscular dysfunction.

Airway, Alveolar, and Intrathoracic Pressure, Volume, and Flow During Positive Pressure Mechanical Ventilation

PPV causes air to flow into the lungs because of an increase in airway pressure, not a decrease in pleural pressure as occurs during spontaneous breathing and NPV (Figure 43-4). However, similar to spontaneous breathing and NPV, PPV causes an increase in P_tp, which allows gas to flow into the lungs. Gas flows into the lungs because pressure at the airway opening (P_awo) is positive, and alveolar pressure (P_alv) is initially zero or less positive. Alveolar pressure rapidly increases during the inspiratory phase of PPV. The increased alveolar pressure expands the airways and alveoli. Because alveolar pressure is greater than pleural pressure (P_pl) during PPV, positive pressure is transmitted from the alveoli to the pleural space, causing pleural pressure to increase during inspiration. Depending on the compliance and resistance of the lungs, pleural pressure may markedly exceed atmospheric pressure during a portion of inspiration. These changes in pleural pressure during PPV can lead to significant physiologic changes (see later section). Pressure gradients during PPV are similar to pressure gradients during spontaneous breathing and NPV except that they are created by a positive pressure at the airway opening instead of a negative pressure in the pleural space (see Table 43-1). All pressure gradients change in the same direction as during NPV and spontaneous breathing except the transrespiratory pressure, which changes in the opposite direction.

Similar to spontaneous breathing, the recoil force of the lungs and chest wall, stored as potential energy during the positive pressure breath, causes passive exhalation. As gas flows from the alveoli to the airway opening, alveolar pressure decreases to atmospheric level, while pleural pressure is restored to its normal subatmospheric level (see Figure 43-4).

Volume and flow during PPV are also described by the equation of motion. The magnitude of P_vent not only depends on the patient’s lung mechanics but also on the P_musc of the patient. If the patient makes no effort, P_vent is responsible for all volume and flow. During volume-controlled ventilation, as muscle effort increases, P_vent decreases, and V_T remains constant. During pressure-controlled ventilation, as P_musc increases, V_T increases, and P_vent remains unchanged.

Increased Alveolar Ventilation

Alveolar ventilation () is inversely related to PaCO₂ as defined by the following relationship:

V˙A=(V˙CO2×0.863)/PaCO2

where is carbon dioxide (CO₂) production.²

As alveolar ventilation decreases, PaCO₂ increases. As CO₂ production increases, alveolar ventilation must increase to maintain the same PaCO₂. Mechanical ventilation may be needed in either case. It is more useful to look at this equation solved for PaCO₂ because changes in PaCO₂ usually correlate with the need for mechanical ventilation:

PaCO2=(V˙CO2×0.863)/V˙A

If decreases or increases, PaCO₂ increases, and hypercapnic respiratory failure follows; mechanical ventilation may be indicated in this setting. Because mechanical ventilation increases ventilation, PaCO₂ can be decreased to the desired level depending on the total ventilatory rate.

Decreased Ventilation/Perfusion Ratio

Spontaneous ventilation results in gas distribution mainly to the dependent and peripheral zones of the lungs. PPV tends to reverse this normal pattern of gas distribution, and most of the delivered volume is directed to nondependent lung zones (Figure 43-5). This phenomenon is caused partly by the inactivity of the diaphragm and chest wall during PPV. Although these structures actively facilitate gas movement during spontaneous breathing, inactivity of these structures during PPV impedes ventilation to dependent lung zones. An increase in ventilation to the nondependent zones of the lung, where there is less perfusion, increases the ventilation/perfusion () ratio, effectively increasing physiologic dead space. The increase in P(A − a)O₂ often observed with PPV is caused by areas of low ratio.

PPV decreases the ratio in the bases and dependent lung zones mainly as a result of ventilation being primarily distributed to nondependent lung zones. The ratio is also decreased in nondependent lung zones because of the effect of PPV on perfusion. PPV can compress the pulmonary capillaries. This compression increases pulmonary vascular resistance and decreases perfusion. Minimal blood flow perfuses the areas with the greatest V_T and contributes to a further increase in dead space. Conversely, blood intended for these areas is diverted to regions with lower vascular resistance—generally more dependent lung regions. Pulmonary blood flow during PPV tends to perfuse the least well-ventilated lung regions. This perfusion decreases the ratio in those areas and increases the P(A − a)O₂.

Changes in Alveolar and Arterial Carbon Dioxide

Normal alveolar carbon dioxide tension (PaCO₂) is 40 mm Hg, whereas mixed venous blood typically has a of 45 mm Hg. Under normal circumstances, CO₂ moves out of the blood at the pulmonary capillary interface; the result is a PaCO₂ of 40 mm Hg. In the event of a decrease in alveolar ventilation or an increase in CO₂ production, PaCO₂ increases. Mechanical ventilation can increase minute volume and alveolar ventilation and reduce PaCO₂ and PaCO₂. With an increase in V_D/V_T, PaCO₂ increases if there is no change in minute volume; this may occur when alveolar blood flow is decreased by acute pulmonary embolism, an excessive level of positive end expiratory pressure (PEEP), or advanced dead space–producing disease such as emphysema or pulmonary embolism.

When excessive PEEP is used, blood flow is diverted from ventilated alveoli to hypoventilated alveoli; the result is an increased ratio. In emphysema, formation of bullae is coincident with the destruction of pulmonary capillaries; the result is large areas of poorly perfused but ventilated alveoli. Pulmonary emboli may completely occlude pulmonary vessels; the result is lack of perfusion to alveoli distal to the blockage.

Changes in Acid-Base Balance

Respiratory acidemia, defined by a PaCO₂ greater than 45 to 50 mm Hg and a pH less than 7.35, occurs when minute ventilation and alveolar ventilation per minute () are inadequate to meet the needs of the body. Respiratory acidemia can occur when the V_T is low, even though an accompanying mandatory rate is high.

Volume delivery also decreases if high airway pressures develop secondary to volume loss as a result of ventilator circuit tubing compliance (compressible volume loss). Ventilator circuits may have compliance of 3 ml/cm H₂O, which effectively reduces V_T:

Volume lost=Tubing compliance×(Peak pressure−PEEP)

Tubing compliance was a concern with older ventilators; however, most intensive care unit (ICU) ventilators in use at the present time allow the user to compensate for compressible volume loss as a result of tubing compliance. When activated, the volume set is the volume delivered to the patient. This issue is discussed in more detail later in the chapter.

An increase in V_D/V_T ratio can cause a reduction in alveolar ventilation, even though minute ventilation may be normal or increased. These problems emphasize the importance of proper selection of V_T and mandatory rate. When respiratory acidemia exists, the patient may become restless and anxious, resulting in patient-ventilator asynchrony. A communicative patient may complain of dyspnea. If these symptoms are observed, especially when PaCO₂ is increased, minute ventilation generally should be increased.

Respiratory alkalemia occurs if the minute ventilation is too high. It is recognized when PaCO₂ is less than 35 mm Hg and pH is greater than 7.45. A patient who is dyspneic, anxious, or in pain may develop this condition; the usual manifestations are an increased ventilatory rate or patient-ventilator asynchrony or both. The ventilator can cause respiratory alkalemia secondary to an inappropriately high V_T or rate. Regardless, the result is excessive minute and alveolar ventilation. This condition requires that the RT adjust the ventilator appropriately and address the patient’s pain or anxiety to avoid the systemic effects of a prolonged alkalosis.

Metabolic acidemia in a patient receiving mechanical ventilation is recognized by a normal PaCO₂, with a decreased pH (<7.35), decreased bicarbonate level (<22 mEq/L), and increased base excess (<−2 mEq/L). With metabolic acidemia, the patient tries to compensate by increasing minute ventilation to blow off CO₂ in an effort to increase the pH. The resulting increase in work of breathing (WOB) may lead to ventilatory muscle fatigue and continued respiratory failure. The best therapy for metabolic acidosis is to manage the underlying cause while supporting the patient’s ventilation as needed. Many patients cannot be liberated from mechanical ventilation until the underlying acidosis is controlled.

Bicarbonate has been used as therapy for metabolic acidosis. If it is administered, bicarbonate quickly combines with hydrogen ions and dissociates to form CO₂ and water, a reaction that may increase WOB. Generally, bicarbonate administration is not recommended until acidosis is severe (pH < 7.2). When necessary, bicarbonate is administered according to the following formula:²

NaHCO3−required=[14Body weight(kg)×Base deficit]/2

A temporary measure to compensate partially for metabolic acidosis is to increase minute ventilation during therapy to control the acidosis with the goal of a pH greater than 7.20.

Metabolic alkalemia is defined as a normal PaCO₂ with an elevated pH (>7.45) and an increased bicarbonate level (>26 mEq/L) and base excess (>+2 mEq/L). With metabolic alkalemia, in an effort to compensate for the increased pH, the patient tries to decrease minute ventilation. If weaning is attempted when the patient has a metabolic alkalemia, the patient may continue to hypoventilate, and weaning may fail. As with metabolic acidemia, the underlying cause should be determined and managed. Common causes of metabolic alkalosis include hypochloremia or hypokalemia secondary to gastrointestinal loss, diuretics, or steroid administration. See Chapter 13 for details on acid-base balance.

Alveolar Oxygen and Alveolar Air Equation

Increasing FiO₂ increases PaO₂, according to the alveolar air equation:²

where PaO₂ is the partial pressure of oxygen in the alveoli; FiO₂ is the fractional inspired oxygen; P_B is the barometric pressure in mm Hg; 47 is the partial pressure of water vapor in the alveoli in mm Hg at 37° C; PaCO₂ is the partial pressure of carbon dioxide in arterial blood in mm Hg; and R is the respiratory exchange ratio (), normally 0.8.

When FiO₂ is increased, PaO₂ increases as well, if there is no change in PaCO₂ or the respiratory exchange ratio. PaCO₂ may change with a change in alveolar ventilation or metabolic rate. O₂ consumption and CO₂ production increase with an increase in metabolic rate, such as with fever or overfeeding. If metabolic rate and alveolar ventilation are constant, an increase in FiO₂ results in a proportional increase in PaO₂.

Arterial Oxygenation and Oxygen Content

Mechanical ventilation at FiO₂ of 0.21 may restore arterial oxygenation if the only cause of hypoxemia was hypoventilation. Hypoventilation may be the sole cause with central nervous system depression, apnea, and neuromuscular disease. With other causes of hypoxemia, an increase in FiO₂ is needed to increase arterial O₂ content.

O₂ content is directly related to arterial oxygenation and hemoglobin concentration, defined by the equation for arterial oxygen content (CaO₂):²

CaO2(vol%)=(1.34×Hb×SaO2)+(PaO2×0.003 ml O2/mm Hg)

where 1.34 is a constant for the amount of O₂ carried by each fully saturated gram of hemoglobin (1.34 ml O₂/1 g hemoglobin), Hb is the hemoglobin concentration in g/dl, SaO₂ is the oxygen saturation of hemoglobin, and 0.003 is the amount of O₂ carried in the plasma in ml/mm Hg PaO₂. Under circumstances of normal diffusion, FiO₂, and hemoglobin concentration, the arterial content is normal at approximately 19.8 ml O₂/100 ml blood. As defined by this equation, CaO₂ decreases if hemoglobin concentration, arterial saturation, or PaO₂ decreases.

Decreased Shunt

Mechanical ventilation alone does not decrease shunt. Otherwise, it would be much easier to restore PaO₂ in patients with ARDS. Administration of PEEP with mechanical ventilation or to a spontaneously breathing patient in the form of continuous positive airway pressure (CPAP) helps to maintain open alveoli and stabilize small, collapsed, or fluid-filled alveoli. The results are an increase in alveolar surface area for diffusion and improvement in matching and arterial oxygenation.

PEEP or CPAP should be used judiciously (see later in this chapter and Chapter 44). High pressure can overdistend alveoli and redistribute pulmonary blood flow to capillaries surrounding poorly ventilated alveoli resulting in increased shunt.

Increased Tissue Oxygen Delivery

When a mechanical ventilator is used to improve arterial oxygenation by increasing FiO₂ or PEEP, CaO₂ increases. However, the increase in CaO₂ represents only part of tissue O₂ delivery because O₂ delivery is defined by CaO₂ and cardiac output, as follows:²

DO2(tissue oxygen delivery in ml/min)=CaO2(ml O2/100 ml blood)×Cardiac output(L/min)×10

where 10 is a constant for converting deciliters to milliliters.

Normal tissue O₂ delivery is approximately 990 ml/min because the normal CaO₂ is approximately 20 vol%, and the normal cardiac output is approximately 5 L/min. When PaO₂, CaO₂, and cardiac output are adequate, so is tissue O₂ delivery. When PEEP is needed to improve PaO₂, it must be used cautiously because PEEP increases intrathoracic pressure. When intrathoracic pressure is increased, pleural pressure around the heart also increases, and the increase can affect the mechanical activity of the heart and impede venous return and decrease cardiac output. As discussed in Chapter 44, careful titration of PEEP must include monitoring the cardiovascular status of the patient. Optimal PEEP provides adequate arterial oxygenation and tissue O₂ delivery.

Mini Clini

Oxygen Delivery

 Problem

Oxygen delivery (DO₂) depends on PaO₂, hemoglobin concentration, and cardiac output. The formula for DO₂ is:

DO2=CaO2×Cardiac output(L/min)×10

where CaO₂

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