A maximum strength skeletal muscle contraction can be sustained indefinitely.

Hyperinflation

Hyperinflation is a common pre-existing problem in patients with obstructive lung diseases such as COPD,4 cystic fibrosis,32 bronchiolitis,33 and lymphangioleiomyo matosis.4 The severity of pre-existing hyperinflation commonly worsens in patients experiencing an exacerbation of COPD.34 Hyperinflation can also occur de novo in patients with pneumonia, acute respiratory distress syndrome, and chest trauma.34,35 Hyperinflation has a number of adverse effects on inspiratory muscle function: The inspiratory muscles operate at an unfavorable position ofthe length-tension relationship (Fig. 41-6)36; flattening of the diaphragm reduces the size of the zone of apposition, so that diaphragmatic contraction causes less effective rib cage expansion.4 Hyperinflation has also an adverse effect on the elastic recoil of the thoracic cage.4 This means that the inspiratory muscles must work not only against the elastic recoil of the lungs but also against that of the thoracic cage. The functional consequences of dynamic hyperinflation are probably the main causes of ventilatory failure in patients with COPD.37 Impairment of inspiratory muscle function, however, is less likely in patients with acute respiratory distress syndrome, because they breathe at a low lung volume despite dynamic hyperinflation.35,38

Treatment modalities to optimise cardiopulmonary function

Patients who are critically ill may present with impaired cardiopulmonary physiology secondary to both the underlying pathology and the therapeutic interventions employed to treat them. In their approach to any individual patient, the physiotherapist may use specific treatment techniques targeted at improving ventilation/perfusion (V/Q) disturbances, increasing lung volumes, reducing the work of breathing and removing pulmonary secretions. Physiotherapy treatment modalities may differ depending on the presence of an endotracheal tube, although patient participation with treatment is encouraged and promoted at the earliest point during intubation. Each intervention is rarely used in isolation, but rather as part of an effective treatment plan. Some physiotherapeutic techniques may have short-lived beneficial effects on pulmonary function, and some have no clear evidence to validate their effectiveness (Table 5.1).

Hyperinflation

Hyperinflation refers to an increase in lung volume above that usually seen at rest. As previously discussed, the end-expiratory lung volume coincides with the EEV of the respiratory system in adults and older children with normal lungs. Hyperinflation occurs naturally in two primary settings: (1) in the presence of a significant increase in resistance and (2) in the presence of a significant decrease in elastic recoil. Both of these conditions result in an increase in the time constant of emptying of the respiratory system. If the respiratory rate required to satisfy ventilatory demands does not allow sufficient expiratory time, hyperinflation occurs. Another setting in which hyperinflation may develop is during mechanical ventilation. On theoretical grounds, an expiratory time equal to three times the expiratory time constant allows emptying of 95% of the end-inspiratory volume, whereas an expiratory time equal to five times the expiratory time constant allows emptying of 99% of the volume. In practice, if the expiratory time constant was less than three times the expiratory time constant, hyperinflation (manifested as the development of PEEPi) develops in ventilated infants.13

Hyperinflation does serve a useful purpose. The increase in lung volume is associated with an increase in airway caliber secondary to mechanical interdependence. The increase in lung volume also increases the tissue viscance.16,17 The degree to which resistance and, therefore, the time constant of emptying depends on the balance between these opposing influences. A patient with severe airflow obstruction may have so much expiratory flow limitation that these values are, in fact, flow-limited during tidal breathing at rest. The only way that the expiratory flows can be increased at times of increased ventilatory demand, such as during exercise or febrile illnesses, is to increase lung volume, thus moving tidal breathing to a more advantageous part of the expiratory flow-volume curve. It is not surprising that hyperinflation has been found to be, at least partly, an active phenomenon.18–20 Hyperinflation is achieved by tonic contraction of inspiratory muscles19 and by expiratory “braking” by adduction of the vocal cords.21

The increase in expiratory flows made possible by hyperinflation does come at a cost. Hyperinflation puts the inspiratory muscles at a mechanical disadvantage, placing them at an inefficient part of their length-tension relationships. Under these conditions, the muscle excitation must increase to produce the same external work. This results in an increase in energy consumption and a decrease in efficiency. The work of breathing also increases because although the resistive work decreases and the total resistance is less, the elastic work increases and more than offsets any gain in resistive work. In addition, actively contracting muscles run the risk of limiting their own energy supply by narrowing the feeding arteries. These factors place the inspiratory muscles at risk of developing inspiratory muscle fatigue.

Two compensatory processes have been reported that have the potential to decrease the load on the inspiratory muscles. In patients with severe chronic airflow limitation, end-expiratory lung volume has been reported to increase during exercise, whereas the anteroposterior dimensions of the abdomen decrease because of expiratory recruitment of the abdominal muscles.22 End-expiratory cephalad displacement of the diaphragm, secondary to contraction of abdominal muscles toward the end of expiration,23 aids inspiration in at least two ways: It puts the muscle fibers of the diaphragm on a more favorable part of their length-tension relationship, and it stores elastic and gravitational energy in the abdominal compartment and releases it during the subsequent inspiration, performing inspiratory work and contributing to minute ventilation without increasing the activation of the diaphragm.

The expiratory braking, grunting, achieved by partial glottic adduction, “unloads” the inspiratory muscles by allowing hyperinflation to be maintained with less tonic activation of inspiratory muscles.

Native Lung Hyperinflation

Acute hyperinflation of the native lung leading to respiratory and hemodynamic compromise in the immediate postoperative period has been reported in 15% to 30% of emphysema patients undergoing SLT.111,112 Although risk factors remain poorly defined, the combination of positive-pressure ventilation and significant allograft edema serves to magnify the compliance differential between the two lungs and may predispose to this complication. Acute hyperinflation can be rapidly addressed by initiation of independent lung ventilation, ventilating the native lung with a low respiratory rate and a long expiratory time to facilitate complete emptying. Beyond the perioperative period, some SLT recipients with underlying emphysema demonstrate exaggerated or progressive native lung hyperinflation that more insidiously compromises the function of the allograft. In this setting, surgical volume reduction of the native lung can result in significant functional improvement.113

2. Intrinsic Positive End-Expiratory Pressure

Hyperinflation (overdistention) of the lung occurs in some mechanically ventilated patients because of air trapping. Gas can be trapped within the lung during the expiratory phase because of dynamic airflow limitation (e.g., associated with asthma) or inadequate expiratory time, as might occur when the inspiratory flow is so low that it causes a high inspiratory/expiratory ratio. The hyperinflation that results has been termed auto-PEEP, intrinsic PEEP (PEEPi), or occult PEEP.41,107 The presence of auto-PEEP increases the risk of barotrauma, compromises hemodynamics by reducing venous return, increases the patient's work of breathing, and can result in unilateral lung hyperinflation.28,41,107

The identification of PEEPi is difficult. PEEPi is not reflected in the pressure measured on the manometer of the ventilator at the end of exhalation because at end expiration the exhalation valve is either open to atmospheric pressure (PEEP = 0) or reflects the level of PEEP provided by the ventilator (Fig. 46-8). The presence of PEEPi can be quantitated by occluding the expiratory port of the ventilator circuit at the end of exhalation immediately before the next breath is delivered. The pressure in the lungs and ventilator circuit equilibrates. The level of PEEPi is then displayed on the manometer. Another method to determine whether PEEPi is present, but not to quantitate it, uses evaluation of the expiratory flow waveform. If expiratory flow does not fall to zero before the next inspiration, gas is trapped within the lung, creating PEEPi (Fig. 46-9). When PEEPi is identified using this method, the flow waveform can be monitored while adjusting ventilator parameters to minimize PEEPi.

Hyperinflation

Hyperinflation (frequently observed in obstructive airway diseases) compromises the force-generating capacity of the diaphragm for a variety of reasons: First, the respiratory muscles, like other skeletal muscles, obey the length-tension relationship. At any given level of activation, changes in muscle fiber length alter tension development. This is because the force-tension developed by a muscle depends on the interaction between actin and myosin fibrils (i.e., the number of myosin heads attaching and thus pulling the actin fibrils closer within each sarcomere). The optimal fiber length (Lo) for which tension is maximal is the length at which all myosin heads attach and pull the actin fibrils. Below this length (as with hyperinflation, which shortens the diaphragm), actin-myosin interaction becomes suboptimal, and tension development declines. Second, as lung volume increases, the zone of apposition of the diaphragm decreases in size, and a larger fraction of the rib cage becomes exposed to pleural pressure. Hence, the diaphragm's inspiratory action on the rib cage diminishes. When lung volume approaches total lung capacity, the zone of apposition all but disappears (Figure 6-8), and the diaphragmatic muscle fibers become oriented horizontally internally (see Figure 6-8). The insertional force of the diaphragm is then expiratory, rather than inspiratory, in direction. This observation explains the inspiratory decrease in the transverse diameter of the lower rib cage in subjects with emphysema and severe hyperinflation (Hoover's sign). Third, the resultant flattening of the diaphragm increases its radius of curvature (Rdi) and, according to Laplace's law, Pdi = 2Tdi/Rdi, diminishes its pressure-generating capacity (Pdi) for the same tension development (Tdi).

Physiology: The Ability to Breath: The Load/Capacity Balance

For a human to take a spontaneous breath, the inspiratory muscles must generate sufficient force to overcome the elastance of the lungs and chest wall (lung and chest wall elastic loads), as well as the airway and tissue resistance (resistive load). This requires an adequate output of the centers controlling the muscles, anatomic and functional nerve integrity, unimpaired neuromuscular transmission, an intact chest wall, and adequate muscle strength. This can be schematically represented by considering the ability to take a breath as a balance between inspiratory load and neuromuscular competence (Figure 8-9). Under normal conditions, this system is polarized in favor of neuromuscular competence (i.e., there are reserves that permit considerable increases in load). However, for a human to breathe spontaneously, the inspiratory muscles should be able to sustain the aforementioned load over time as well as adjust the minute ventilation in such a way that there is adequate gas exchange. The ability of the respiratory muscles to sustain this load without the appearance of fatigue is called endurance and is determined by the balance between energy supplies and energy demands (Figure 8-10).

Energy supplies depend on the inspiratory muscle blood flow, the blood substrate (fuel) concentration and arterial oxygen content, the muscle's ability to extract and use energy sources, and the muscle's energy stores. Under normal circumstances, energy supplies are adequate to meet the demands, and a large recruitable reserve exists (see Figure 8-10). Energy demands increase proportionally with the mean pressure developed by the inspiratory muscles per breath (PI) expressed as a fraction of maximum pressure that the respiratory muscles can voluntarily develop (PI/PI,max), the minute ventilation (VE), the inspiratory duty cycle (TI/TTOT), and the mean inspiratory flow rate (VT/TI) and are inversely related to the efficiency of the muscles. Fatigue develops when the mean rate of energy demands exceeds the mean rate of energy supply (i.e., when the balance is polarized in favor of demands).

The product of TI/TTOT and the mean transdiaphragmatic pressure expressed as a fraction of maximal (Pdi/Pdi,max) defines a useful “tension-time index” (TTIdi) that is related to the endurance time (i.e., the time that the diaphragm can sustain the load imposed on it). Whenever TTIdi is smaller than the critical value of 0.15, the load can be sustained indefinitely; but when TTIdi exceeds the critical zone of 0.15–0.18, the load can be sustained only for a limited time period, in other words, the endurance time. This was found to be inversely related to TTIdi. The TTI concept is assumed to be applicable not only to the diaphragm but also to the respiratory muscles as a whole:

Because endurance is determined by the balance between energy supply and demand, TTI of the inspiratory muscles has to be in accordance with the energy balance view. In fact, as Figure 8-4 demonstrates, PI/PI,max and TI/TTOT, which constitute the TTI, are among the determinants of energy demands; an increase in either that will increase the TTI value will also increase the demands. But what determines the ratio PI/PI,max? The nominator, the mean inspiratory pressure developed per breath, is determined by the elastic and resistive loads imposed on the inspiratory muscles. The denominator, the maximum inspiratory pressure, is determined by the neuromuscular competence (i.e., the maximum inspiratory muscle activation that can be voluntarily achieved). It follows, then, that the value of PI/PI,max is determined by the balance between load and competence (see Figure 8-9). But PI /PI,max is also one of the determinants of energy demands (see Figure 8-10); therefore, the two balances (i.e., between load and competence and energy supply and demand) are in essence linked, creating a system (Figure 8-11). Schematically, when the central hinge of the system moves upward, or is at least at the horizontal level, spontaneous ventilation can be sustained indefinitely (see Figure 8-11). The ability of a subject to breathe spontaneously depends on the fine interplay of many different factors. Normally, this interplay moves the central hinge far upward and creates a great ventilatory reserve for the healthy individual. When the central hinge of the system, for whatever reason, moves downward, spontaneous ventilation cannot be sustained, and ventilatory failure ensues.

2 Intrinsic Positive End-Expiratory Pressure

Hyperinflation (overdistention) of the lung occurs in some mechanically ventilated patients because of air trapping. Gas can be trapped within the lung during the expiratory phase because of dynamic airflow limitation (e.g., associated with asthma) or inadequate expiratory time, as may occur when the inspiratory flow is so low that it causes a high inspiratory-to-expiratory (I : E) ratio. The hyperinflation that results has been called auto-PEEP, intrinsic PEEP (PEEPi), or occult PEEP.26,197 The presence of auto-PEEP increases the risk of barotrauma, compromises hemodynamics by reducing venous return, increases the patient's work of breathing, and can result in unilateral lung hyperinflation.26,184,197

Identification of PEEPi is difficult. PEEPi is not reflected in the pressure measured on the manometer of the ventilator at the end of exhalation, because at end expiration, the exhalation valve is open to atmospheric pressure (PEEP = 0 cm H2O) or reflects the level of PEEP provided by the ventilator (Fig. 49-8). PEEPi can be quantitated by occluding the expiratory port of the ventilator circuit at the end of exhalation immediately before the next breath is delivered. The pressure in the lungs and ventilator circuit equilibrates. The level of PEEPi is then displayed on the manometer. Although this approach provides an estimate of the magnitude of gas trapping, it is technically difficult and hard to reproduce. Another method to determine whether PEEPi is present, but not to quantitate it, uses evaluation of the expiratory flow waveform. If expiratory flow does not fall to zero before the next inspiration, gas is trapped within the lung, creating PEEPi (Fig. 49-9). When PEEPi is identified using this method, the flow waveform can be monitored while adjusting ventilator parameters to minimize PEEPi.

Postpneumonectomy Syndrome

Hyperinflation of the remaining lung after pneumonectomy can result in a mediastinal shift toward the operative hemithorax with various degrees of torsion and compression of the mediastinal structures. Central airway compression may occur as the main bronchus is compressed between the vertebral column and pulmonary artery. Fig. 40.6 showsa postpneumonectomy syndrome in a 20-year-old woman who underwent right pneumonectomy for carcinoid 4 years earlier. She developed postpneumonectomy syndrome within 1 year of pneumonectomy and had mediastinal repositioning with breast implants.107 It is not usually an acute event and typically occurs after 6 months postresection. Dyspnea, cough, stridor, and recurrent pneumonia are the common symptoms that are nonspecific and require a high index of suspicion to make the diagnosis. Chest x-ray, CT imaging, or bronchoscopic examination may identify the mediastinal shift and airway compression. Esophageal and pulmonary vein compression have also been described causing dysphagia and dyspnea, respectively.108,109 Surgical prophylaxis or treatment has been successfully achieved by repositioning of the mediastinum with placement of prostheses or by placing a saline-filled breast prosthesis in the empty hemithorax.107

Manual Hyperinflation in Airway Clearance

Manual hyperinflation is one of the chest physiotherapy techniques that is used in intensive care in intubated patients. It involves using an ambu bag in order to produce a slow deep inspiration, inspiratory pause, and unobstructed expiration. The goals of physiotherapy treatment are to remove secretions, resolve atelectasis, and improve ventilation.

Contraindications may include cardiovascular instability, barotraumas, severe bronchospasm, undrained pneumothorax, raised intracranial pressure, and a high level of positive end expiratory pressure >10 cmH2O.

A recent review of the usage of manual hyperinflation in airway clearance remains inconclusive. These techniques, however, have been used widely in intensive care units for many years. Future studies are needed to evaluate the correct dosage, patient position, and level of pressures and volumes.