Physiology of Ventilatory Support

Physiology of Ventilatory Support

Robert M. Kacmarek and Teresa A. Volsko

Mechanical ventilation can be beneficial or detrimental depending on how it is initially applied and modified as the patient’s condition changes. Respiratory therapists (RTs) must be able to anticipate the physiologic effects of mechanical ventilation and respond appropriately when complications arise. This chapter familiarizes the reader with (1) the physiologic effects of mechanical ventilation on lung and cardiovascular function and other body systems, (2) the basic approaches to providing mechanical ventilation, and (3) the complications and hazards of mechanical ventilation. A solid understanding of the normal physiology of breathing is essential for all RTs, especially when working with patients receiving mechanical ventilation. RTs must understand intrathoracic pressure changes associated with spontaneous, negative pressure, and positive pressure breathing. Intrathoracic pressure changes are necessary for ventilation to occur; however, large changes in these pressures may also induce various physiologic changes in other systems.

Pressure and Pressure Gradients

For gas to flow through the airway, a pressure gradient must exist. The airways begin at the mouth and end at the alveoli, so mouth pressure (pressure at the airway opening [Pawo]) and alveolar pressure (Palv) are important in describing gas flow, as are intrapleural pressure (Ppl) and body surface pressure or atmospheric pressure (Pbs). In addition, intraabdominal pressure (Pab) affects the impact of Ppl change on diaphragm movement. Ppl is the pressure in the pleural space, the virtual space between the visceral and parietal pleurae, and is usually negative in relation to Palv. Figure 43-1 shows a graphic model of the respiratory system with these pressures identified as points in space. Mathematical models relating pressure, volume, and flow corresponding to this graphic model are constructed using pressure differences. The various components of the graphic model are defined as everything that exists between these points in space. The respiratory system is everything that exists between the airway opening and the body surface. The associated pressure difference is transrespiratory pressure (Ptr), defined as Pawo − Pbs. The components of transrespiratory pressure correspond to the components of the graphic model. The airways are represented by transairway pressure (Pta), defined as Pawo − Palv. The lungs are represented by the transalveolar pressure: (PL = Palv − Ppl). The chest wall is represented by trans–chest wall pressure: (Ptcw = Ppl − Pbs). If the lungs and chest wall are lumped together, they can be represented by transthoracic pressure: (Ptt = Palv − Pbs).

Another pressure gradient not defined in Figure 43-1 that also affects gas movement is the transdiaphragmatic pressure (Pdi). This pressure gradient is the difference between intraabdominal pressure and pleural pressure and affects diaphragmatic movement: (Ppl − Pab). Once these pressures and pressure gradients are understood, the differences between spontaneous ventilation, positive pressure ventilation (PPV), and negative pressure ventilation (NPV) become evident.

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 (VT) (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.

VT 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:



where Pmusc is muscle pressure (Ptp), 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:



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 (Ppl) during inspiration by exposing the chest to subatmospheric pressure. Negative pressure at the body surface (Pbs) is transmitted first to the pleural space and then to the alveoli (Palv). 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 Palv becomes greater than Pawo, 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:



In this equation, Pvent is the pressure the ventilator develops to overcome the patient’s lung-thorax elastance and airway resistance to deliver the VT. In this case, Pvent 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 Ptp, which allows gas to flow into the lungs. Gas flows into the lungs because pressure at the airway opening (Pawo) is positive, and alveolar pressure (Palv) 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 (Ppl) 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 Pvent not only depends on the patient’s lung mechanics but also on the Pmusc of the patient. If the patient makes no effort, Pvent is responsible for all volume and flow. During volume-controlled ventilation, as muscle effort increases, Pvent decreases, and VT remains constant. During pressure-controlled ventilation, as Pmusc increases, VT increases, and Pvent remains unchanged.

Effects of Mechanical Ventilation on Ventilation

Increased Minute Ventilation

The primary indication for mechanical ventilation is hypercapnic respiratory failure, also known as ventilatory failure. For patients with acute ventilatory failure, the goal of mechanical ventilation is improving alveolar ventilation to compensate for the patient’s inability to maintain normal PaCO2. PaCO2 is inversely related to alveolar ventilation, which is related to minute ventilation. Minute ventilation (image) is the product of tidal volume (VT) and ventilatory rate (f):



Use of a mechanical ventilator usually implies a change in VT, ventilatory rate, or both from preintubation values. A normal spontaneous VT is approximately 5 to 7 ml/kg. The currently accepted VT for mechanical ventilation in acute respiratory failure is 4 to 8 ml/kg for patients with acute respiratory distress syndrome (ARDS) and 6 to 8 ml/kg for patients with normal lungs or with COPD; in some patients, a slightly larger VT (up to 10 ml/kg) may be indicated. These volumes are based on ideal body weight. The mechanical ventilator rate depends on the patient’s status. For postoperative ventilation, a rate of 12 to 20 breaths/min may be adequate. Conditions that necessitate a higher initial rate include ARDS, acutely increased intracranial pressure (ICP) (with caution; see later), and metabolic acidosis. Conditions that may necessitate a lower rate include acute asthma exacerbation, to allow an increased expiratory time to minimize air trapping. When an adequate VT is established, the set rate is adjusted to achieve desired PaCO2. Mechanical ventilation increases minute ventilation by increasing VT, ventilator rate, or both.

Mini Clini

Alveolar, Transpulmonary, and Transalveolar Pressures


Because there is a short end inspiratory pause, it is reasonable to assume that the peak airway pressure in pressure control is equal to the average peak alveolar pressure. The average is used because alveolar units have different time constants and as a result different peak pressure, but when there is end inspiratory equilibration of pressure, the resulting value is the average pressure across all lung units. To be more confident of this value, an additional end inspiratory pause can be added for a single breath to determine better the end inspiratory pause pressure or plateau pressure.

To determine the transpulmonary pressure (Pawo − Ppl) and transalveolar pressure (Palv − Ppl), an estimate of pleural pressure must be made. The ideal method is to measure the esophageal pressure. Although not exactly equal to the pleural pressure, it accurately reflects changes in pleural pressure. Some authors have also recommended evaluation of bladder pressure, which changes in the same manner as esophageal pressure. The reading from the esophageal catheter at the time an end inspiratory pause was applied was 10 cm H2O. The transpulmonary pressure and transalveolar pressure are the same—35 − 10 cm H2O or 25 cm H2O. This is because Mr. Jones was ventilated in pressure control, and there was a short end inspiratory pause, so both peak and plateau pressures were equal. However, if he was ventilated in volume ventilation and the peak airway pressure was 45 cm H2O, while the plateau pressure remained 35 cm H2O when an end inspiratory pause was added, the transalveolar pressure would be the same—35 − 10 cm H2O or 25 cm H2O—but the transpulmonary pressure during peak inspiration would be 45 − 10 cm H2O or 35 cm H2O.

Mr. Jones is receiving lung protective ventilation because his transalveolar pressure is only 25 cm H2O. The high airway pressures are needed because of his stiff chest wall, which minimizes the transmission of pressure across the lung, reducing lung stretch.

Increased Alveolar Ventilation

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



where image 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:



If image decreases or image 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 (image) ratio, effectively increasing physiologic dead space. The increase in P(A − a)O2 often observed with PPV is caused by areas of low image ratio.

PPV decreases the image ratio in the bases and dependent lung zones mainly as a result of ventilation being primarily distributed to nondependent lung zones. The image 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 VT 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 image 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 image 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 VD/VT, 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 image 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 (image) are inadequate to meet the needs of the body. Respiratory acidemia can occur when the VT 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 VT:

Volume lost=Tubing compliance×(Peak pressurePEEP)


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 VD/VT 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 VT 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 VT 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

NaHCO3required=[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.

Effects of Mechanical Ventilation on Oxygenation

Increased Inspired Oxygen

Mechanical ventilators usually deliver an increased fractional inspired oxygen (FiO2) ranging from room air (0.21) to 100% O2 (1.0). As a result, the alveolar partial pressure of oxygen (PaO2) and arterial partial pressure of oxygen (PaO2) may be restored to normal with appropriate management. The effectiveness of increased FiO2 in the management of hypoxemia depends on the cause of hypoxemia. Hypoxemia caused by a decrease in the image ratio or hypoventilation is more responsive to increased FiO2 than hypoxemia caused by a diffusion defect or shunt. Hypoxemia caused by hypoventilation responds well to an increase in FiO2, but alveolar ventilation can be restored only by improved ventilation. Hypoxemia caused by diffusion defect and shunt generally respond better to an increase in PEEP than to an increase in FiO2. The fact that PaO2 responds well to increased FiO2 generally indicates that a low image ratio is the cause of hypoxemia. If the patient is receiving mechanical ventilation and has adequate alveolar ventilation, failure of the PaO2 to respond to increased FiO2 likely means that hypoxemia is due to a diffusion defect or shunt.

Mechanical ventilation increases alveolar ventilation, which increases PaO2 if the underlying problem is hypoventilation. An increase in PaO2 after an increase in FiO2 likely means that the cause of hypoxemia is a low image ratio. In the event that PaO2 is not restored by an increase in FiO2, hypoxemia is probably due to a diffusion defect or shunt.

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; PB 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 (image), 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.

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.

Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on Physiology of Ventilatory Support
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