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Indications for mechanical ventilation 

Indications for mechanical ventilation
Chapter:
Indications for mechanical ventilation
Author(s):

Neil R. MacIntyre

DOI:
10.1093/med/9780199600830.003.0091
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date: 26 November 2020

Key points

  • Mechanical ventilation can be life-sustaining, but is associated with significant risk.

  • Mechanical ventilation with a guaranteed rate/tidal volume is indicated when the patient’s ventilatory control system is unreliable.

  • Mechanical ventilation with appropriate muscle unloading is indicated when a mechanical load–metabolic demand imbalance exists.

  • Mechanical ventilation with end-expiratory pressure is indicated when alveolar patency is compromised.

  • Mechanical ventilation with low level inspiratory pressure is indicated if an artificial airway imposes an uncomfortable muscle load.

Introduction

Mechanical ventilation is the process of using positive pressure devices to provide O2 and CO2 transport between the environment and the pulmonary capillary bed. The desired effect of mechanical ventilation is to maintain adequate levels of PO2 and PCO2 in arterial blood, while also unloading the inspiratory muscles. At the same time, this process should be done in a manner that avoids injury to the lungs and other organ systems. Ventilator-induced lung injury [1]‌, infection [2], and the need for potentially harmful sedatives/neuromuscular blockers [3], all underscore the need to assure that initiation of mechanical ventilatory support is worth these risks.

The basic components of a mechanical ventilatory support system are:

  • An artificial airway (or sometimes a mask) that provides the interface between the mechanical ventilator and the patients airways.

  • A source of oxygen enriched positive pressure breaths delivered either in accordance with a set timer or in response to a patient effort.

  • The capability to maintain an end expiratory positive pressure.

These features are designed to address the following clinical problems that constitute the ‘indications’ for providing mechanical ventilatory support:

  • The need for providing a reliable number of breaths in patients without an appropriate spontaneous ventilatory controller.

  • The need for unloading fatigued or impaired ventilatory muscles that are incapable of providing adequate tidal breaths.

  • The need for maintaining alveolar patency in patients with inflamed or flooded lung units.

  • The need to support an artificial airway in a patient who cannot maintain and/or protect the natural airway.

In a large survey of over 5000 mechanically-ventilated patients in 361 ICUs worldwide [4]‌, the vast majority required mechanical ventilation because of either acute cardio-pulmonary failure (68%) or acute on chronic cardio-pulmonary failure (13%)—the second and third indications 2 and 3 in the list above. The remainder (the first and fourth indications in the list above) were patients requiring mechanical ventilation for largely neuromuscular issues.

The remainder of this chapter will review the underlying pathophysiology of these indications and clinical signs/thresholds that usually trigger institution of mechanical ventilatory support. There will also be brief discussions on how modern systems are designed to address these indications.

Controller failure

The ventilatory control system is centered in the brain stem and consists of an intrinsic ventilator pattern generator with three types of inputs [5]‌. One input is a series of afferent nerves from mechanoreceptors in the lung and chest wall. These sense respiratory system stretch, irritants, and ventilatory muscle loads. A second set of inputs arise from central and peripheral chemo receptors sensing pH, PCO2, and PO2. A final input involves cortical signals designed to modulate the respiratory pattern for voluntary activities. The purpose of the control system is to provide an adequate level of ventilation to effect CO2 and O2 transport, while minimizing the mechanical loads on the ventilatory muscles. The normal resting ventilatory pattern of 10–12 breaths/min, tidal volumes of 5–7 mL/kg, and inspiratory:expiratory timing of 1:2–1:3 is a consequence of this control system strategy [6].

This system can be compromised with any central nervous system (CNS) injury, but especially those that affect brain stem function. In addition to CNS injury, general anaesthesia and a variety of drugs, especially sedatives and opioid analgesics can also affect this function. At its extreme, ventilatory controller failure results in a respiratory arrest. Damage to efferent nerves, primarily the phrenic nerve, will compromise the controller’s ability to provide adequate inspiratory muscle stimulation.

Although some CNS injuries can produce inappropriate hyperventilation, the consequence of most diseases/drugs affecting the ventilatory control system is usually inadequate ventilation resulting in a respiratory acidosis (hypercarbic respiratory failure). The pH threshold from a respiratory acidosis that requires intervening with mechanical ventilatory support depends on the clinical situation. In the absence of significant cardiac dysrhythmias, pressor-dependent hypotension, or elevated intracranial pressure, pH values as low as 7.15 (or perhaps lower) have been shown in clinical trials to not cause harm [7]‌. However, the initiation of mechanical ventilatory support for hypoventilation and respiratory acidosis from CNS causes is usually driven by the clinical judgment that the ventilatory drive is unreliable for maintaining a safe level of ventilation for an extended period.

If mechanical ventilation is required for an impaired ventilatory controller, the mechanical ventilation strategy must assure that an adequate minute ventilation is delivered. This often requires clinician set ventilator breath rates, and either set tidal volumes or pressure targeted feedback mechanisms to assure adequate tidal volumes. Alarm systems that are properly set are critical.

Abnormal ventilatory control systems may also create inappropriate flow demands and breath timing patterns. These can be especially challenging to clinicians trying to minimize sedation while providing assisted breaths that can synchronize with these patient demands [8]‌.

Demand/capability imbalances

The mechanical loads on the ventilatory muscles are primarily those imposed by the minute ventilation demands, airway resistance, and the compliance/elastance of the respiratory system [9]‌. Minute ventilation demands are driven by metabolic demands (i.e. oxygen consumption (VO2) and carbon dioxide production (VCO2)) and the amount of minute ventilation that is wasted (dead space ventilation or VD). Airway resistance is due to both patient airway geometry and the artificial airway properties. Compliance/elastance properties are driven by both parenchymal lung abnormalities, as well as chest wall abnormalities (e.g. tight surgical bandages, abdominal compartment syndrome, anasarca, ascites, and obesity). Imposed loads from the ventilator itself (artificial airway resistance and patient ventilator dys-synchrony) can also exist [10]. The presence of intrinsic positive end expiratory pressure (PEEP) can add to inspiratory muscle loads required to initiate a breath.

The capability of the patient’s ventilatory system is composed of the inspiratory muscle’s strength and endurance properties. These can be affected by metabolic abnormalities, systemic inflammation, nutritional factors, electrolyte factors, and drugs. The resting position of the diaphragm is particularly important as it is the major muscle of inspiration. If the diaphragm is flattened from lung hyperinflation, bullous disease and/or intrinsic PEEP, inspiratory muscle capabilities are greatly diminished.

Ventilatory muscle failure and resulting inadequate ventilation occurs when the demands outstrip the capabilities (Fig. 91.1). Clinically, this is often manifest initially by rapid-shallow breathing (a muscle ‘protective’ response driven by the ventilatory control center) [11]. As overloaded muscles continue to work, muscle damage occurs, hypoventilation worsens, and a respiratory acidosis develops (hypercarbic respiratory failure). At its extreme, ventilatory muscle failure produces a respiratory arrest.

Fig. 91.1 Conceptual relationship between ventilatory muscle demands (left side of balance) and capabilities (right side of balance). As demands overwhelm capabilities, the balance shifts to the left and indications for mechanical ventilatory support increases.

Fig. 91.1 Conceptual relationship between ventilatory muscle demands (left side of balance) and capabilities (right side of balance). As demands overwhelm capabilities, the balance shifts to the left and indications for mechanical ventilatory support increases.

Reproduced with permission of MacIntyre NR, ‘Respiratory factors in weaning from mechanical ventilatory support’, Respiratory Care, 40, pp. 244–8, © The Journal Respiratory Care Company 1995.

Because gas exchange may be adequate in the face of progressive ventilatory muscle overload for a prolonged period, the clinical decision to initiate mechanical ventilatory support for demand/capability imbalances is best driven by mechanical assessments. Importantly, this is not so much by an assessment of mechanical loads (e.g. work of breathing or pressure time product which may be elevated several fold in patients requiring mechanical ventilation), but rather by an assessment of muscle load tolerance. Conceptually, this can be expressed using a transdiaphragmatic pressure referenced to muscle strength to calculate a pressure time index (PTI) (12):

PTI = ( P Dtidal / P Dmax ) × ( T i / T tot )
[eqn 1]

where PDtidal is the transdiaphragmatic pressure change during inspiration, PDmax is the maximal voluntary transdiaphragmatic pressure, and Ti/Ttot is the fraction of the ventilator cycle spent in inspiration. A PTI value greater than 0.15 is associated with impending inspiratory muscle failure.

Clinically, load intolerance is associated with diaphoresis, accessory muscle use, abdominal paradox, inability to speak short phrases, and tachycardia [11,13,14]. The decision to institute mechanical ventilation in this setting is usually based on clinical judgment that load intolerance is becoming life threatening. Objective measurements or laboratory values can support the decision to initiate mechanical ventilatory support under these circumstances but these rarely provide definitive information that would override the clinical assessment.

Mechanical ventilation strategies in the setting of demand/capability imbalances focus on both improving muscle capabilities and reducing muscle loads. This involves proper unloading of ventilatory muscles with positive pressure breaths. Support strategies, however, must not totally unload ventilatory muscles as this can produce muscle atrophy [15]. In practice, this means a mechanical ventilation strategy focused on patient-triggered assisted modes of ventilation titrated to comfort. This requires skill in assuring appropriate triggering of breaths (including the use of circuit PEEP in the setting of intrinsic PEEP), proper flow synchrony such that ventilator flow matches patient demand, and proper breath cycling to coincide with neural cycling [8,10]. It also requires the proper setting of the respiratory rate and I:E ratio to assure adequate lung emptying is occurring, and intrinsic PEEP is minimized. Importantly, placement of an endotracheal tube is not always required for this support. In patients with load/capability imbalances, but with good airway protection capabilities, non-invasive (mask) ventilation may avoid endotracheal intubation, most notably in the COPD population with an acute exacerbation.

Maintaining alveolar patency

Many lung diseases affecting lung parenchyma can cause alveoli to flood and/or collapse. Inhalation injuries, infections, systemic inflammation (e.g. sepsis, pancreatitis), blunt chest trauma, aspiration, congestive heart failure, and fluid overload all can contribute. The predominant clinical manifestation of loss of alveolar patency is ventilation perfusion mismatching, producing shunts and hypoxaemia (hypoxaemic respiratory failure). If severe enough, the resulting compliance/elastance loads from alveolar instability can also contribute to ventilatory muscles overload and hypercarbic respiratory failure.

Provided that other components of oxygen delivery (i.e. cardiac output and haemoglobin concentration) and tissue oxygen extraction are adequate, arterial PO2 values above 55 mmHg are generally adequate to assure tissue oxygen delivery. Clinical clues that oxygen delivery is inadequate and in need of therapy include altered mental status, cardiac dysrhythmias, and other organ dysfunction. Objective data suggesting impaired tissue oxygenation includes the development of a metabolic (lactic) acidosis.

Support of patients with compromised alveolar function involves the judicious use of PEEP to stabilize alveoli along with administration of supplemental oxygen [16]. If a tolerable load/capability balance exists (e.g. patients with some forms of cardiogenic pulmonary oedema), continuous positive airway pressure (CPAP), through either a mask or an endotracheal tube, may be all that is required to accomplish this. However, concomitant ventilatory support is often as needed as well. Under these conditions it is important to remember that PEEP is a two-edged sword. While, on one hand, the expiratory pressure can help maintain alveolar patency during exhalation, it will add to the total interthoracic pressure and could increase the risk of overdistention injury, especially when coupled with an excessive tidal volume [16,17,18]. Balancing PEEP and FiO2 to provide proper oxygenation in the setting of alveolar injury is clearly a major clinical challenge and, as described elsewhere in this book, various imaging, mechanical, and gas exchange methodologies have been proposed.

Support for an artificial airway

Airway function can be compromised from a variety of different disease states [19]. CNS abnormalities (e.g. CNS injury, tumours, drugs) can result in a failure to maintain appropriate muscle tone for airway patency, and loss of cough and/or other airway defence reflexes. Clinical consequences can include the inability to ventilate due to airway compromise and aspiration of posterior pharyngeal material. Airway function can also be compromised by structural injuries to the pharynx, larynx, and major airways.

Clinically, loss of airway patency is manifest by a high work of breathing, inadequate ventilation, and sometimes stridor. Inadequate airway protection is manifest by weak or absent cough (especially when being suctioned), a need for frequent suctioning (e.g. more than every 2 hours), and clinical aspiration [19].

Although a mask system with constant positive airway pressure can often alleviate airway compromise from some structural abnormalities (e.g. obstructive sleep apnoea), compromised airway function, and/or inability to protect the airway often requires placement of an artificial airway (endotracheal tube or tracheostomy). In a large survey of over 5000 patients receiving mechanical ventilation [4]‌, 89% had an oral tracheal tube, 4% had a nasal tracheal tube, and 4.9% had a facial mask. A tracheostomy was present in 2% of the patients. Interestingly, 85 patients with COPD received non-invasive ventilation (NIV) in this survey of whom 22% subsequently required tracheal intubation. One-hundred-and-forty-eight patients with other forms of respiratory failure received NIV and 36.5% subsequently required tracheal intubation.

Unless a need for positive pressure ventilation is required many patients can tolerate an artificial airway for isolated airway issues reasonably well (especially a tracheostomy). However, endotracheal tubes in particular can impose a significant resistive load on inspiratory muscles, especially if narrow (i.e. less than 7 mm internal diameter) and/or partially occluded with secretions [20]. Endotracheal tubes can also be uncomfortable, and require sedation and/or analgesics to assure tolerance. Under these conditions, some mechanically-ventilatory support may be needed to allow patients to tolerate the artificial airway. Often this is a low level of pressure, targeted ventilation (e.g. inspiratory pressure support of 5–10 cmH2O) with optional back-up rates and PEEP. Some devices offer an automatic tube or airway compensation feedback mechanism that delivers inspiratory pressure support in a pattern designed to specifically unload the calculated resistance loads of the artificial airway. While theoretically appealing, this feedback capability has not as yet been shown to improve clinical outcomes.

Conclusion

Mechanical ventilation is a commonly-used modality in ICUs worldwide. Conceptually, mechanical ventilation is indicated when the patient’s ability to ventilate the lung and/or effect gas transport across the alveolar capillary interface is compromised to a point that harm is imminent. In practice, this means addressing one or more of three fundamental pathophysiological processes—loss of proper ventilatory control, ventilatory muscle demand–capability imbalances, and/or loss of alveolar patency. A fourth general indication involves providing a positive pressure assistance to allow tolerance of an artificial airway in the patient unable to maintain a patent, protected airway.

Although some hard and fast thresholds for initiating mechanical ventilation exist (e.g. respiratory arrest, refractory hypoxaemia, severe acidosis from ventilatory muscle failure, inability to protect the airway), the decision to initiate mechanical ventilation usually involves an integrated assessment of the patient. This assessment should include mental status, airway protection capabilities, ventilatory muscle load tolerance, spontaneous ventilatory pattern, and signs of organ dysfunction from either acidosis, and/or hypoxaemia. This involves a high level of clinical expertise. Providing mechanical ventilatory assistance can be life sustaining; however, it is associated with significant risk and must be applied only when indications justify the risk.

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