Monitoring respiratory muscle function.

Respiratory muscle weakness is often associated with prolonged mechanical ventilation and the cause of failure or delay in weaning. Diaphragmatic strength can be determined non-invasively in mechanically ventilated patients and can be assessed from the twitch gastric, twitch oesophageal and twitch transdiaphragmatic pressures in response to phrenic nerve stimulation (Mills et al 2001). Maximal static inspiratory and expiratory efforts, electromyography of respiratory muscles, respiratory rate, carbon dioxide (CO₂) level, pressure–time product, vital capacity and maximum voluntary ventilation are all variables which reflect respiratory muscle function. Respiratory rate and tidal volume presently remain the most convenient and frequently used indices of respiratory muscle function (e.g. respiratory rate/tidal volume provides a rapid shallow breathing index) (Spicer et al 1997). These measures may be used to assess the readiness of the patient to breathe spontaneously and to be weaned from ventilatory support.

Lung mechanics.

Improvement in lung volume is associated with improvement in the elastic properties of the lung. The relationship between changes in lung volume and transpulmonary pressure is referred to as static lung compliance (l/cmH₂O). Static lung compliance should be measured during ‘cessation of air flow’, when elastic recoil is independent of airway resistance. Dynamic lung compliance can be measured during ‘uninterrupted’ respiration.

The change in lung volume and pressure are measured at end-inspiration (compliance) and end-expiration (auto-peep); this is when airflow ‘momentarily’ ceases during the ‘normal’ respiratory cycle. Most mechanical ventilators in ICU display/calculate dynamic lung compliance, auto-peep as well as airway resistance.

Assessment of work of breathing.

A patient’s work of breathing may be described as the amount of muscle activity required to overcome the elastic (lung tissue, chest wall and abdominal compartment) and resistive (airways, flow rate) elements of the respiratory system. It includes any additional loads imposed by the mode of ventilator support, artificial airways and humidification devices (which may contribute additional resistive work, particularly through a heat and moisture exchange filter as compared with a heated humidifier circuit). The work of breathing of the intubated and mechanically ventilated patient depends on factors that are either patient- or ventilator-related. Patient-related factors include the type of pulmonary disease (airway, lung parenchyma, pleural space), cardiovascular dysfunction, altered respiratory drive (fever, pain, anxiety, delirium, acid–base disturbance), level of spontaneous respiratory activity and level of sedation/paralysis. Ventilator-related issues include the mode of mechanical ventilation, settings and, most importantly, the level of synchrony between ‘man and machine’.

To optimize mechanical ventilation, the mechanical ventilator must promptly respond to the patient’s demand during inspiration and allow an unimpeded expiration. Mechanical ventilation practices vary internationally and hence patient management varies, depending on institutionally driven, airway and ventilator strategies (Esteban et al 2000).

Most modern mechanical ventilators display real-time ventilator waveforms such as pressure, flow and volume across time or as loops (pressure/volume, flow/volume). Waveform/loop monitoring allows the clinician to interpret the interaction between the patient and the mechanical ventilator. Early detection of unto-ward changes in waveforms may allow the clinician to optimize the ventilator settings (by altering PEEP, trigger sensitivity, pressure support) to minimize any disruption to delivered ventilation (tidal volume, minute volume) and reduce work of breathing during physiotherapy treatment. For adequate synchrony between the patient and the mechanical ventilator, the clinician must ensure that the ventilator responds promptly to the patient inspiratory demand (trigger), provides adequate flow requirements during the inspiratory phase, cycles from inspiration to expiration when the patient starts exhalation and allows full and complete exhalation, before the next ventilator breath delivery. Detailed bedside waveform analysis of various patient work of breathing scenarios throughout the respiratory phases and suggestions for patient clinical management are illustrated later in this chapter.

Monitoring oxygenation

Blood gases. Arterial blood gases (partial pressure of oxygen and carbon dioxide, and pH) provide essential information about a patient’s metabolic as well as respiratory status. Continuous measurement of arterial blood gases is possible but this technique is not widely practised because of cost, calibration drift and clot formation (Shapiro et al 1993, Zimmerman & Dellinger 1993). Interpretation of arterial blood gases is discussed in Chapter 3.

Transcutaneous gas measurement. This method of measurement is based on the principle that blood flow and oxygen exchange are dependent on skin temperature (Baumburger & Goodfriend 1951). Transcutaneous electrodes include a heating element to maximize local blood flow. When the skin is heated the capillary blood becomes ‘arterialized’ and the arterialized gases diffuse through the skin to the electrodes (Whitehead et al 1980). More recently, a new sensor (TOSCA monitor) for combined continuous transcutaneous monitoring of arterial oxygen saturation and carbon dioxide tension has been shown to be an accurate and valuable tool for respiratory monitoring (Bernet-Buettiker et al 2005, Senn et al 2005). At present this is used more commonly in neonates.

Oximetry. Non-invasive assessment of oxygen saturation by a pulse oximeter (SpO₂) was introduced clinically in 1975 (Kendrick 2001). Pulse oximetry is now an expected monitoring component for assessment of hypoxaemia. The oxygen saturation of arterial blood [with partial pressure of oxygen (PO₂) of 100 mmHg or 12–13 kPa] is about 97.5% and that of mixed venous blood (with PO₂ of 40 mmHg or 5–5.5 kPa) is about 75% (West 2005). The absorption of light energy by blood varies, depending on the wavelength. Red (660 nm) and infrared (940 nm) light result in the greatest separation between deoxyhaemoglobin and oxyhaemoglobin absorption spectra. Pulse oximetry uses light-emitting diodes set at these wavelengths, and as the emitted light passes through the finger (or earlobe), the light energy is variably absorbed by the arterial and venous blood. The absorption ratio of the red/infrared light by the blood is proportional to the amount of desaturated haemoglobin, and from these data the pulse oximeter calculates and displays the SpO₂ (Kendrick 2001).

The accuracy of commercial pulse oximeters is about ±2% within the clinical oxygen saturation range of 70–100% (Jensen et al 1998). Pulse oximeter readings may be inaccurate in patients with severe or rapid desaturation, hypotension, hypothermia and low perfusion states. A further limitation of oximetry is that it provides information only on oxygen status, and not on ventilation (PaCO₂).

Monitoring carbon dioxide (capnography).

The concentration of carbon dioxide expired during different phases of the respiratory cycle provides information on the effectiveness of alveolar ventilation (Fig. 8.4), not only the end-tidal carbon dioxide value but also tube position and breathing circuit integrity.

Figure 8.4 A typical capnograph showing normal end-tidal carbon dioxide level. (A–B) Dead space (CO₂-free gas); (B–C) mixed dead space and alveolar gas; (C–D) mostly alveolar gas; (D) end-tidal CO₂; (D–E) inhaled gas (CO₂-free gas).

Detailed ‘indications’ for capnography can be found in the American Association for Respiratory Care (AARC) Clinical Practice Guidelines on Capnography/Capnometry during Mechanical Ventilation (AARC 1995).

Non-invasive monitoring

Blood pressure. The use of automated non-invasive blood pressure (NIBP) devices is common. The mean arterial pressure (MAP) most closely approximates capillary perfusion pressure and is thus a useful measurement. NIBP devices can give inaccurate results in patients with arrhythmias, cardiac valvular lesions, where there is improper cuff application and when the blood pressure is low (Box 8.2).

Electrocardiogram. The electrocardiogram provides information on the rate and rhythm of the heart; it also assists in the diagnosis, and identification of the possible site of myocardial infarction. The pathological feature of myocardial infarction is necrosis of myocardial muscle. Absolute evidence of myocardial necrosis is the pathological Q wave. Q waves, ST elevation and T wave inversion are all associated with transmural infarction (involvement of whole thickness of the myocardium). For sub-endocardial infarction (involvement of the inner layer of the myocardium, adjacent to the endocardium), Q waves do not appear and changes are confined to ST segments and T waves. Thus subendocardial infarction may be difficult to differentiate from ischaemia of the myocardium. Interpretation of the electrocardiogram is discussed in Chapter 3.

Thoracic electrical bioimpedance and impedance cardiography. Thoracic electrical bioimpedance (TEB) relies on measurement of bidirectional blood flow within the aorta by a laser Doppler velocimeter and an impedance measurement unit which determines the cross-sectional area of the vessel. TEB allows the clinician to view beat-to-beat cardiac output. (Newman and Callister 1999, Tjin et al 2001) and provides information on haemodynamic indices such as systolic time interval, left cardiac work index and end diastolic index (Belott 1999, Weiss et al 1997).

Non-invasive measurement of stroke volume and cardiac output by impedance cardiography (ICG) has been shown to be accurate and significantly correlated to conventional thermodilution method (see Thermodilution cardiac output, below) (Scherhag et al 2005). ICG measures synchronized pulse changes in TEB via simple surface electrodes together with a conventional electrocardiogram.

Partial CO₂rebreathing cardiac output and NICO. Rather than applying the oxygen Fick method for cardiac output monitoring, the non-invasive CO₂ Fick methods for estimation of cardiac output are receiving increased clinical interest. Adopting the CO₂ version of the Fick equation has the advantage that CO₂ elimination is easier to measure accurately compared with oxygen uptake (Jaffe 1999). The differential Fick partial rebreathing method computes a cardiac output value based on the changes in carbon dioxide elimination and end tidal CO₂ in response to a change in ventilation. The non-invasive cardiac output (NICO system) is the first commercially available cardiac output system making use of the principle of partial rebreathing of CO₂ (Jaffe 1999).

Echocardiography and Doppler. This uses ultrasound to examine the performance of the heart and great vessels. Information from echocardio-graphy can be presented one- (M-mode), two- or three-dimensionally. M-mode is often used in conjunction with a two-dimensional echo to provide a clear illustration of the structures being investigated (Young & Sanderson 1997).

Doppler echocardiography uses ultrasound to measure blood flow velocity and is able to determine pressure gradients, stenotic valve areas, cardiac output, left ventricular contractility, and diastolic function.

Transoesophageal echocardiography can be considered an invasive technique as it involves the introduction of an ultrasound probe (attached to the end of a flexible endoscope) into the oesophagus. This technique avoids image obstructions caused by the lungs and ribs and allows better views of the valves, septa and thoracic aorta.

Urine output. Urine output is an index of renal perfusion and is a guide to adequacy of cardiac output. With normal renal perfusion, the urine output should be at least 0.5 ml/kg/hour.

Invasive monitoring

Arterial pressure. Intra-arterial measurement should normally be considered accurate, but the systolic pressure may be overestimated due to systolic ‘overshoot’ (a property of the fluid-pressure transducer monitoring system). The ‘area’ under the arterial tracing can provide a rough estimate of the cardiac output (Gomersall & Oh 1997).

Central venous pressure. Central venous pressure (CVP) reflects right ventricular filling and is usually monitored by a catheter inserted via the internal jugular or subclavian vein, and less frequently via the femoral vein. A quick way to confirm correct placement of the catheter is observed pressure change with respiration (Gomersall & Oh 1997). As the right ventricular preload is determined by the volume and not the pressure, the absolute value of CVP is less meaningful. A high CVP value, however, may be associated with conditions that cause a rise in the right atrial pressure (for example right heart failure, reduced right ventricular diastolic compliance, hypervolaemia and pulmonary hypertension) (Gray et al 2002), whereas a low CVP value may suggest hypovolaemia. Changes in CVP may provide useful guidance for fluid management in patients: for example, a minimal rise of CVP despite fluid loading may suggest the loading volume is insufficient; but a rise of CVP of more than 9.5 cmH₂O (7 mmHg) may indicate maximal loading. A raised CVP in response to fluid loading is expected to return to its original value within 10 minutes – an indication that the risk of pulmonary oedema is only moderate (Gomersall & Oh 1997) (Box 8.3).

Pulmonary artery catheter (Swan–Ganz). Pulmonary artery catheters are often used in patients with impaired right or left ventricular function, pulmonary hypertension, septic shock and when measurements of cardiac output or mixed venous saturation are indicated. It can also be used to assist in the diagnosis of an intracardiac shunt, such as a ventricular septal defect. Apart from cardiac output, cardiac index and systemic vascular resistance, a pulmonary artery catheter can provide a measure of mean right atrial pressure, systolic and diastolic right ventricular pressure, systolic, diastolic and mean pulmonary artery pressure, and pulmonary artery occlusion pressure.

Pulmonary artery occlusion pressure (PAOP) (previously referred to as pulmonary capillary wedge pressure (PCWP)) provides an estimation of the left atrial pressure (LAP). PAOP is obtained with the balloon at the catheter tip wedged in a pulmonary capillary. PAOP increases in poor left ventricular function, fluid overload and mitral valve disease (and is low in hypovolaemia). A high pulmonary artery pressure (PAP) may indicate high pulmonary vascular resistance.

Thermodilution cardiac output. Non-invasive monitoring of cardiac output has been discussed above. Traditional measurement of cardiac output by the thermodilution method requires the use of a pulmonary artery catheter. Cardiac output can be computed from the decrease in blood temperature in the pulmonary artery after injection of a known volume of cold saline into the right atrium. Computation of cardiac output is based on the principle that the decrease in blood temperature is inversely proportional to the extent of dilution of the cold saline (i.e. the higher the cardiac output the less the change in temperature between injection and measurement points).

Continuous thermodilution is possible by monitors that use infusion of heat from a filament in the right atrium rather than injection of cold saline. The monitor displays cardiac output averaged over the previous 3 to 6 minutes (Boldt et al 1994, Yelderman et al 1992).

The most commonly used method of continuous cardiac output monitoring is by PiCCO^® technology. This technology is less invasive. It requires the insertion of a thermodilution catheter in the femoral or axillary artery and a central venous catheter. (The use of a right heart catheter is not necessary.) This technology is based on the transpulmonary thermodilution technique and arterial pulse contour analysis and provides specific and quantitative parameters including arterial blood pressure, heart rate, cardiac output, global end-diastolic volume [an indicator of cardiac volume, the normal range of global end-diastolic volume index (GEDVI) is 680–800 ml/m²], intrathoracic blood volume [an indicator of thoracic blood volume, the intrathoracic blood volume index (ITBVI) is 850–1000 ml/m²], extravascular lung water [an indicator of pulmonary oedema, extravascular lung water index (EVLWI) is 3.0–7.0 ml/kg], cardiac function index, global ejection fraction, stroke volume, stroke volume variation SVV (an indicator of the potential for a response to intravascular filling, SVV should be less than 10%), pulse pressure variation (also an indicator of the potential for a positive response to intravascular filling) and systemic vascular resistance (an indicator of left ventricular afterload). (Pulsion Medical Systems) (Fig 8.5).

Figure 8.5 PiCCO.

(© Pulsion Medical Systems AG)

Mixed venous oxygen saturation. Normal oxygen saturation in the venous blood is 75% and mixed venous oxygen saturation (SvO₂) reflects the adequacy of tissue perfusion. SvO₂ falls when oxygen demand increases (such as stressful procedures, shivering, nursing care) and/or when oxygen delivery is inadequate (poor cardiac output as a result of heart failure). Increased SvO₂, however, suggests failure of tissue cells to take up or utilize oxygen from the blood. An SvO₂ of 30% or less suggests that oxygen delivery is insufficient to meet tissue oxygen demands and anaerobic metabolism and lactic acidosis will be likely accompaniments in such circumstances.

Level of consciousness

The Glasgow Coma Scale (Chapter 1) is the most common way to objectively index the level of consciousness. Pupil size and level of reactivity to light provides an index of neurological integrity (pupils equal and reactive to light (PERL)). A fixed dilated unilateral pupil indicates pressure on the oculomotor nerve and urgent investigation is necessary. Physiotherapy intervention should be delayed. Fixed dilated pupils indicate severe neurological impairment, which may be made worse by hypoxia or biochemical abnormalities and are often a sign of brainstem death.

Cranial computed tomography scan.

Computed tomography (CT) of the head provides information about the brain and skull. A plain skull radiograph may identify fractures of the skull and CT with contrast is used for investigation of intracranial space-occupying lesions (haemorrhage, tumour or abscess). Cranial CT permits visualization of the following (Kumar 1997):

cerebral oedema

hemispheric shift

hydrocephalus

subdural haematoma

extradural haematoma

intracerebral haematoma

subarachnoid haemorrhage.

Magnetic resonance imaging (MRI) is now more commonly used when scanning neurological patients.

Intracranial pressure.

Intracranial pressure (ICP) is measured by insertion of a catheter through the skull into the lateral ventricle or by means of an extradural or subarachnoid bolt (Turner 2002). ICP is often monitored in patients with head injuries, post-brain surgery and for patients with intracranial and subarachnoid haemorrhage or cerebral oedema. The intraventricular catheter has the advantage of allowing drainage of cerebrospinal fluid when the intracranial pressure is high but because it penetrates the dura, there is a greater accompanying risk of intracranial infection. Any change in the intracranial pressure is dependent upon the relative amounts of blood, brain and CSF within the adult skull. ICP allows determination of global cerebral perfusion pressure (CPP), which relates closely to cerebral blood flow (CBF) (Box 8.4).

Raised PCO₂ results in an increase in cerebral blood flow, which will cause a rise in ICP and a lowering of CPP. Hyperventilation may lower the PCO₂, thus reducing cerebral vasodilatation and CBF, thereby lowering the ICP. Normal ICP is 10–15 mmHg, but baseline levels are often higher in neurosurgical patients. In order to provide adequate perfusion to the brain, it is generally recommended that CPP should be maintained at a level greater than 60 mmHg (Huang et al 2006).

Jugular bulb oxygen saturation.

Jugular bulb oxygen saturation (SjO₂) reflects the adequacy of global cerebral oxygen delivery, although monitoring of SjO₂ is now rarely used in neurosurgical ICU. Monitoring of SjO₂ is based on the principle that cerebral arterial and mixed venous oxygen difference (A–VDO₂) is directly proportional to cerebral metabolic rate (CMRO₂) but inversely proportional to cerebral blood flow (CBF). The normal values of SjO₂ are between 55–71%. Less than 55% indicates an increase in cerebral oxygen extraction, often due to hypotension or systemic hypoxia. Over 70% indicates hyperaemia. The results have to be interpreted along with other information such as ICP (White & Baker 2002).

Measurement and monitoring of cerebral blood flow

Transcranial Doppler. Transcranial Doppler (TCD) is a non-invasive diagnostic tool that uses sound waves to measure the velocity of blood flow in the basal cranial arteries (Miller 2005). Blood flow velocity, however, is variable and dependent on the diameter of the cerebral arteries. Thus a dimensionless variable, the pulsatility index (PI) is used which is derived from the difference between systolic and diastolic flow velocities divided by the mean velocity. PI is a reflection of the cerebrovascular resistance and a high PI is associated with a low cerebral perfusion pressure (CPP) (Lindegaard 1992). A high correlation between PI and ICP (Voulgaris et al 2005) and CPP (Bellner et al 2004) has been reported. PI has a high predictive value for detecting a CPP of less than 70 mmHg (Voulgaris et al 2005).

Bispectral index (electroencephalographic analysis). The bispectral index (BIS) is a parameter that was developed to measure a patient’s level of awareness during sedation (Haug et al 2004) and to determine the probability of recovery of consciousness in patients in coma (Fabregas et al 2004). BIS is derived from an electroencephalogramic parameter, which includes time and frequency domains and higher-order spectral information. With electrode sensors placed on the forehead of the healthiest brain hemisphere, identified by computed tomography scan, a BIS recording can be quantified on a scale from 0 to 10. BIS correlates with clinical signs of hypnosis (Billard et al 1997, Rosow and Manberg 2001) and is reported to be predictive of traumatic brain injury and neurological outcome at discharge (Haug et al 2004).

Hyperinflation techniques.

The ventilated, critically ill patient often has an underlying problem associated with progressive atelectasis and loss of compliance combined with impaired mucociliary clearance. Hyperinflation techniques, manual hyperinflation (MHI) and ventilator hyperinflation (VHI) have been introduced in an effort to improve ventilation and secretion mobilization in a patient whose normal defensive mechanism is lost.

The aims of hyperinflation techniques are to:

improve lung thoracic compliance (by increased tidal volume/inspiratory pressure, altered inspiratory : expiratory ratio or by increased positive end-expiratory pressure)

enhance mobilization of secretions (by increased expiratory flow rate)

reinflate atelectatic areas (increased tidal volume and inspiratory time)

improve gas exchange (increased tidal volume and inspiratory time).

Manual hyperinflation (MHI) is a technique whereby the patient is disconnected from the ventilator and given an altered breathing pattern via a valve circuit and reservoir bag (Fig. 8.6). To reduce the risk of barotrauma, it is recommended that a pressure manometer be incorporated into the circuit so that the peak airway pressure can be monitored during the MHI procedure.

Figure 8.6 An intubated adult receiving manual hyperinflation and chest wall shaking/vibration (note blue pressure manometer, Laerdal MHI circuit with orange spring-loaded PEEP valve)

The ideal pattern includes a slow inspiration, an inspiratory hold and a fast release. This pattern hypothetically has beneficial effects on volume restoration, compliance and removal of secretions. Evidence and rationale for these mechanisms will be discussed below.

Various types of circuits are utilized. Expiratory flow rate and volume produced by the more pliable Mapleson and Magill circuits and the less pliable Air Viva and Laerdal circuits have been compared, both in laboratory and clinical studies (Jones et al 1991, 1992a, 1992b, Maxwell & Ellis 2003, McCarren & Chow 1998, Rusterholz & Ellis 1998). The Mapleson and Magill circuits provide greater tidal volume and faster expiratory flow. When a pressure manometer is not in use, the latter circuits may be safer.

Ventilator hyperinflation (VHI) has been used as an alternative to manual hyperinflation in ventilated patients. The method consists of leaving the patient attached to the ventilator and altering either the volume, pressure or flow/time characteristics of the breath delivered. This method of ventilation has been shown to result in similar levels of secretions removed and improvements in compliance as manual hyperinflation (Berney & Denehy 2002, Savian et al 2005).

Evidence for hyperinflation techniques

Effect on decreased volumes, compliance and oxygenation. As discussed, the critically ill patient may have low lung volumes and decreased lung compliance due to a number of factors. In order to reverse the process of decreased lung compliance, the inspiratory pressure must exceed a critical opening level to expand collapsed alveoli. A pressure of 40 cmH₂O has been stated to be a minimum (Rothen et al 1999); however, other studies have resolved atelectasis using lower pressures (Maa et al 2005).

A slow inspiration procedure used in both MHI and VHI results in laminar flows, which encourage alveoli with prolonged time constants to reinflate. A larger tidal volume and inspiratory plateau promotes release of surfactant, which will reduce the surface tension of alveoli and assist re-expansion. The inspiratory hold also facilitates alveolar expansion via collateral ventilation.

MHI has been demonstrated to result in reversal of atelectasis (Stiller et al 1990), improvement in tidal volumes, improvement in chest radiograph scores (Maa et al 2005), improvements in static and dynamic compliance (Hodgson et al 2000, Jones et al 1992b, Paratz et al 2002, Patman et al 2000) and increased yield of secretions (Choi & Jones 2005, Hodgson et al 2000, Jones 2002).

Effect on mucociliary clearance. The fast release technique during the expiration phase of MHI encourages movement of the secretions in a cephalad direction. Patients on mechanical ventilation are normally sedated, with a consequence of reduced ability to cough. The movement of airway secretions in these patients is impaired and may be improved by an increased expiratory to inspiratory flow ratio (the ‘two-phase gas liquid transport’), which is proposed to occur during MHI or VHI (Savian et al 2005).

Laboratory and clinical studies have demonstrated that manual hyperinflation compared with a control manoeuvre results in higher peak expiratory flows, improved lung/thorax compliance and increased removal of secretions (Jones 2002). It appears that a critical expiratory flow must be reached during manual hyperinflation in order for sputum movement to occur and this is linked to the method of delivery of manual hyperinflation, including the type of circuit employed (Maxwell & Ellis 2003, Savian et al 2005); tidal volume; and rapid release of the valve and bag. Research on MHI to date has not established a link between the flow rates generated and the volume of secretions removed.

Inclusion of a positive end-expiratory pressure (PEEP) valve in the manual hyperinflation circuit has been shown to decrease expiratory flow. When the PEEP exceeds 10 cmH₂O, MHI may be ineffective as a secretion clearance technique (Savian et al 2005).

Laboratory evidence has suggested that MHI may not be effective in mobilization of thin (low viscosity) secretions and an alternative technique such as gravity-assisted drainage may be more effective (Jones 2002).

A further method of hyperinflation that intensivists and some physiotherapists utilize are ‘recruitment manoeuvres’ (Mols et al 2006). Lung-protective strategies using low tidal volume ventilation are beneficial and improve survival in patients with acute respiratory distress syndrome. However, the low tidal volumes can cause tidal alveolar de-recruitment and atelectasis. A recruitment manoeuvre is a sustained increase in airway pressure with the goal to recruit atelectatic lung tissue. A number of methods are used, including increases in positive end-expiratory pressure (PEEP), sustained increased inspiratory pressure (e.g. 40 cmH₂O PEEP for 40 seconds duration), or sigh breaths. Using these techniques, short-term increases in oxygenation and reversal of atelectasis have been reported (Barbas et al 2005).

Precautions for hyperinflation techniques

Haemodynamic instability. Haemodynamic instability is a vague term and can cover a multitude of events. Each intervention will have a different effect depending on the pathophysiology of the patient. The relationship between hyperinflation techniques and the haemodynamic status highlights the need to consider the following factors:

an intervention such as manual hyperinflation or ventilator hyperinflation (which causes an increase in intrathoracic pressure) may lead to a decrease in preload and subsequently cardiac output and blood pressure. This is more likely in a patient who is hypovolaemic, i.e. has a decrease in overall circulating blood volume either absolutely (haemorrhage) or relatively (sepsis, opiates)

if the systemic blood pressure is below normal values and supported by inotropes or vasopressors – hyperinflation techniques could further decrease the blood pressure

a significant drift in the baseline of the arterial blood pressure waveforms before hyperinflation techniques may indicate that the patient may require increased filling (fluids) and may not tolerate hyperinflation techniques.

Undrained pneumothorax. This is usually an absolute contraindication. If an underwater drain is in situ and a large air leak is present, hyperinflation methods may be ineffective and may worsen the air leak. The presence of bullae on a plain chest radiograph may not be an absolute contraindication, but limiting peak inspiratory pressure with the aid of a manometer may ensure safety.

Severe bronchospasm and asthma. If the patient has acute asthma, an increase in positive pressure and tidal volume or the delivery of dry unhumidified gas may further increase intrinsic PEEP and aggravate hyperinflation and bronchospasm, thereby increasing the potential risk of barotrauma.

As a general rule, the manual hyperinflation technique must always be preceded, and followed, by auscultation. Clinicians should always be mindful of pneumothorax as a potential risk of the MHI technique.

High PEEP, nitric oxide, heat and moisture exchanger (HME) and hypoxic pulmonary vasoconstriction (HPV). If the patient is receiving high PEEP (>10 cmH₂O) and/or nitric oxide as a ventilatory adjunct, it is advisable not to disconnect the ventilator circuit for manual hyperinflation techniques. Interruption to high levels of PEEP can cause de-recruitment and atelectrauma, especially in conditions such as ARDS (Mols et al 2006). Interruption of nitric oxide can cause sudden increases in pulmonary artery pressure and severe strain on the right side of the heart as well as potential severe hypoxaemia. Ventilator hyperinflation may be an alternative in these situations, but may dilute the amount of nitric oxide the patient is receiving, unless the patient is on an automated nitric oxide delivery device.

The use of a heat and moisture exchanger (passive humidifier) in the MHI circuit may optimize humidification and reduce airway irritation. Inhaled bronchodilators before, during or after MHI may be useful if severe bronchospasm is present.

Resolution of severe atelectasis as a consequence of MHI may, however, induce sudden hypoxemia. This is because the blood flow diverted from an atelectatic area due to hypoxic pulmonary vasoconstriction (HPV) may not respond efficiently to re-perfuse the newly re-inflated alveoli. Mismatch of ventilation and perfusion thus occur, leading to sudden hypoxaemia. The patient may need to be ventilated at a higher FiO₂ until the pulmonary circulation to the recently re-inflated lung improves.

Percussion and vibration.

Although manual techniques such as percussion of the chest wall and vibration during the expiratory phase are commonly used in intensive care patients, often in conjunction with hyperinflation techniques and positioning, individual studies of their effectiveness in this setting are currently lacking. Vibration has been shown to increase expiratory flow rate (MacLean et al 1989), but there are no clinical studies that demonstrate whether this increases removal of secretions. A series of animal and human studies by Unoki et al (2004) demonstrated that chest wall compression moved secretions in a cephalad direction.

Precautions.

Precautions applied to manual techniques have been discussed in Chapter 5. In intensive care patients, precautions also include decreased platelet levels, skin wounds and chest trauma.

Suction – open/closed.

As critically ill patients are usually intubated, regular pulmonary toilet must be applied. Formerly this was always via the open suction technique: that is disconnection of the endotracheal tube, instillation of a sterile catheter and application of a negative pressure. As the patient did not receive ventilation during this period, an efficient technique in less than 15 seconds was necessary. Most intensive care units now utilize the ‘in-line’ suction technique (closed-suctioning), whereby a sealed catheter is connected to the endotracheal tube and suction is possible without disconnection from the ventilator. This technique has been associated with less risk of desaturation and reduction in lung volume (Cereda et al 2001), fewer arrhythmias, less cardiovascular changes (Lee et al 2001) and less reduction of PEEP (Maggiore et al 2003). However, in pressure-controlled modes of mechanical ventilation, the negative pressure from the suction catheter may trigger ventilator breaths, and the inspiratory flow from the ventilator may force the secretions away from the catheter tip, resulting in fewer secretions being aspirated (Lasocki et al 2006). After suctioning, a lung recruitment technique such as MHI or VHI may be required to minimize the risk of atelectasis induced by the negative pressure suctioning generated by either the open or closed system.

Nasopharyngeal/oropharyngeal suction and mini-tracheotomy.

Nasopharyngeal and oropharyngeal suction have been discussed in detail in Chapter 5. These techniques are often necessary before and during extubation, as well as in attempt to prevent intubation in patients with inefficient coughing efforts or increased secretions.

Minitracheotomy is often utilized in intensive care and is invaluable for patients with secretion retention, weak cough and contraindications to or intolerance of oral/nasopharyngeal airways. However, as only size 10 French gauge suction catheters can be used, this may limit suction effectiveness in some patients. Also a mini-tracheostomy is an uncuffed tube, and hence will not prevent the patient from aspirating oropharyngeal secretions.

Humidification.

Humidification has been discussed in Chapter 5. Humidification is mandatory for patients on mechanical ventilation to reverse some of the adverse effects of intubation such as reduced tracheal mucus velocity and cilial impairment.

A critically ill patient on high concentration of inspired oxygen will also benefit from heated humidification. A heat and moisture exchanger (HME) can be used as an alternative but has been associated with increased circuit dead space and resistance to airflow. It may also be associated with an increased work of breathing in spontaneously breathing patients who are on low levels of respiratory support (Boots et al 2006). The use of HMEs may increase PaCO₂ in patients with acute lung injury/acute respiratory distress syndromes (Moran et al 2006). Nebulization with normal saline via the ventilator circuit has been reported to increase the yield of airway secretions (O’ Riordan et al 2006).

Saline instillation.

Direct instillation of normal saline to the endotracheal tube during or prior to suction in an attempt to decrease viscosity of secretions is a frequently used (and yet sometimes controversial) technique. A number of studies have found that this practice results in decreased SaO₂ and/or mixed venous saturation (Ackerman & Mick 1998), no increase in secretion yield (Lerga et al 1997) and possible dislodgement/dispersion of microorganisms into the lower respiratory tract (Hagler & Traver 1994). Schreuder & Jones (2004), however, demonstrated increased sputum wet weight and stable arterial oxygen saturation following use of saline when it was combined with chest physiotherapy. It is recommended that instillation of saline should be reserved for patients with excessively tenacious secretions. In addition, the clinician should anticipate a short-term drop in arterial saturation that may require a temporary increase in FiO₂.

Gravity-assisted positioning.

Traditional gravity-assisted positions (Chapter 5) are often not utilized in intensive care patients as full positioning is often hindered by cardiovascular instability, equipment and lack of patient cooperation. However, evidence suggests that specifically positioning the patient for the affected lobe results in increased expiratory flow rate, better oxygenation, increased sputum clearance and faster resolution without adverse effects on haemodynamic stability (Berney et al 2004, Krause et al 2000).

Prone positioning.

Specific prone positioning for extended periods of time has been advocated as a method to improve oxygenation and lung mechanics in patients with acute lung injury and acute respiratory distress syndrome. There is strong evidence that this method results in improved lung mechanics and oxygenation due to expansion of the collapsed dorsal regions of the lung (Messerole et al 2002). This technique is most useful if used early in the disease process and may also result in increased secretion clearance due to drainage of the collapsed dorsal regions of the lung. Reduction in carbon dioxide with prone positioning is indicative of improved alveolar ventilation and is predictive of better survival (Gattinoni et al 2003).

Lateral positioning.

The effects of lateral positioning will depend on pathology of the lung, whether unilateral or bilateral and type of ventilation. To maximize alveolar expansion, lung segments to be expanded are often placed in the upper most (non-dependent) lateral position for facilitation of aeration, especially with positive pressure ventilation. However, blood flow will preferentially move to the dependent lung (even more so during positive pressure ventilation); hence, there may be potent effects on gas exchange dependent upon the extent of pulmonary disease (unilateral or bilateral).

In patients with unilateral lung disease, gas exchange may improve by laying the patient on the non-diseased lung (Ibanez et al 1981, Stiller 2000

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