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Ventilatory Support


Patients who are acutely unwell and in respiratory distress often benefit from respiratory support. The provision of supplemental oxygen via a simple face mask is a generally sensible start. Depending on the clinical progression of individual patients, the flow rate of oxygen delivery can vary between 0 - 15 L/min; the percentage, alternatively known as the fraction of inspired oxygen (FiO2; 0.0 - 1.0) may be targeted by using an appropriate airway equipment.


Choosing the right airway equipment:

A variable performance device, such as a Hudson mask, delivers FiO2 in a way that is dependent on a person’s inspiratory flow rate (IFR). In lay terms, for a Hudson mask that is delivering 50% oxygen at 5L/min from a cylinder, no matter how deeply and quickly you breath in a minute, you will only end up receiving the same amount of oxygen from the cylinder (as stated above). If you were to breath in excess of the supply, you would rebreath the surrounding air that you exhaled. This causes dilution of the inhaled air and subsequently lowers the arterial oxygen saturation. In order to overcome the problem of rebreathing in acute situations such as resuscitation, a “non-rebreather” is used. It contains a reservoir bag that holds approximately up to 1500 ml of fresh oxygen that fills when the IFR of a patient falls below the flow rate of oxygen supply. It is hoped that in doing the patient can inhale fresh oxygen from the reservoir without inhaling room air.


Unlike the above, a fixed performance device enables a constant FiO2 to be delivered irrespective of IFR. It works under a physics principle known as the venturi effect. The theory is that as the fresh 100% oxygen travels through a pinhole of a narrow channel into a much bigger passageway, it creates a negative pressure which “entrains” room air through tiny apertures. As a result, this allows correct dilution of 100% oxygen into the desired FiO2. The venturi masks normally come in different colours that indicate their corresponding FiO2’s (blue = 0.24, white = 0.28, yellow = 0.35, red = 0.40, green = 0.60 etc). This is quite commonly used for patients with acute exacerbations of COPD and other conditions that are prone to hypercapnic respiratory failures. Interestingly, the venturi principle is also applied in the design of oxygen tents and anaesthetics breathing circuits.



Should the above measures fail or the patient's condition deteriorate, the final resort would be to attempt ventilatory support. This could range from backing up a patient’s breathing to taking total control over their ventilation. The basic science and operational principles are explored below.


Basic science

As we inspire, a certain amount of energy which is otherwise known as the work of breathing, is needed to overcome the elastic and non-elastic forces of the chest wall and lungs. The generation of a negative intra-pleural pressure encourages the diffusion of atmospheric air into the respiratory zone, i.e. terminal bronchioles, alveolar ducts and alveoli. The compliance or stretchability of lungs to air, particularly structures in the respiratory zone is a key contributor to gaseous exchange.


Pulmonary compliance

The pressure – volume curve beneath illustrates the four important phases of pulmonary compliance with respect to the gradient of change between lung volume (ΔV) and pressure (ΔP) (ml/cmH2O). A considerably high ΔP is needed to necessitate a small ΔV during the initial phase. Once this is set into motion, the second stage follows. The gradient of change then steepens over time but tails off eventually as the maximal expansion is approached in stage three. Phase four denotes exhalation; this is a similar reverse process of the previous inspiratory phases. In clinical terms, it is therefore unsurprising for atelectasis to occur at a remarkably low pulmonary pressure (phase 1). This causes poor oxygenation, encourages air trapping in the lungs and also metabolic complications. Alternatively, should the pressure (or volume) in the lungs becomes too high (phase 3), the respiratory zones may over distend and potentiate barotrauma (or volutrauma).



The lung volumes and capacities

The volume of air that we normally breathe in and out at rest is the tidal volume (VT = 6 ml/kg). This occurs above the functional residual capacity (FRC = 30 ml/kg) of our normal lungs. During strenuous activity, the accessory muscles contract to increase our inspiratory reserve volume (IRV = 45ml/kg) in addition to normal VT, this supplies additional oxygen for aerobic respiration to our mitochondria. Expiratory reserve volume (ERV = 15ml/kg) is the volume of air that we could forcefully expel beyond vital expiration, used to remove excess carbon dioxide from our body. Finally, vital capacity (VC = VT + IRV + ERV = 60 - 70 ml/kg) denotes the maximum amount of air that an individual can possibly inhale after maximum exhalation.



The clinical significance of FRC

FRC is a rather important factor in the context of acute and critical care medicine. It is the chief oxygen store during apnoea. Preoxygenation with 100% oxygen aims to denitrogenate and enrich the oxygen store within FRC. This is done to extend the “safe period” for performing intubation. The other function of FRC is to oppose the closing capacity (CC; normally 10% of VC) of the lungs. Should this relationship reverse (e.g. supine position, pregnancy, old age, pulmonary oedema or during anaesthesia etc), distal airways would collapse prematurely during exhalation and consequently result in atelectasis, hypoxaemia and ventilation/ perfusion (V/Q) mismatch. The above abnormalities are potentially reversible by the application of positive end-expiratory pressure (PEEP). At therapeutic range, PEEP keeps FRC over CC and ideally places it along the efficient part of the compliance curve (phase 2). It re-opens the collapsed alveoli which then improves oxygenation and V/Q.


Ventilatory support

Potential candidates for receiving ventilatory support may require either non-invasive, invasive mechanical ventilation or both depending on clinical grounds.


Non-invasive ventilation (NIV):

This is deemed suitable for patients who are both conscious and compliant. It is commonly indicated for those who suffer from acute respiratory failure. This includes conditions such as:

  • COPD exacerbation, 
  • asthma, 
  • pneumonia, 
  • cardiogenic pulmonary oedema, 
  • chest wall deformities,
  • various neuromuscular conditions. 


    In order to become eligible for NIV, individual patients must first be haemodynamically stable and free of craniofacial, pharyngeal, oesophageal and gastric trauma (this includes insults following surgery!). They then need to show their ability to keep a clear airway unaided, as well as coughing adequately to clear up secretions in the lungs and throat. Since coughing is not impaired in NIV, patients are less likely to develop ventilator-associated pneumonia (important in the immunocompromised) as opposed to with invasive ventilation. The fact that NIV does not require intubation might also necessitate a smooth weaning process from mechanical ventilation.


    Through a tightly fitted device such as a face mask or hood, positive airway pressure is delivered either constantly or alternately at high-and-low levels in partnership with a patient’s spontaneous breathing cycle. The two major modalities of NIV are described below:


      Continuous positive airway pressure (CPAP; at 5 – 12 cmH20) aims to supersede the intrinsic PEEP, i.e. the inward pressure generated by the elastic and non-elastic forces of the chest wall and the lungs, reducing the work of breathing by respiratory muscles during inspiration. This increases VT and also raises FRC sufficiently to re-open the collapsed alveoli and prevents atelectasis during exhalation. Given that CPAP augments alveolar pressure, it also has a role to counteract with the hydrostatic pressure within the pulmonary vasculature. This mechanism should hopefully relieve cardiogenic pulmonary oedema and improve compliance of the lungs.


        Bi-level positive airway pressure (BIPAP) is another modality of NIV. Although this shares similar features with CPAP, it delivers two levels of positive pressures – inspiratory positive airway pressure and expiratory positive airway pressure (IPAP and EPAP) in synchrony with a patient’s breathing cycle. IPAP which is the higher airway pressure is generated as the patient breathes. As above, it reduces the workload of respiratory muscles and maximizes alveolar ventilation by recruiting the collapsed alveoli. This also favours the removal of carbon dioxide from the respiratory zone. IPAP is returned to EPAP as expiration begins. It then serves as a PEEP to facilitate further gas exchange across the alveoli and improves oxygenation. BIPAP is not only just offered to patients with spontaneous and coordinated breathing, in a critical situation, such as inadequate respiratory drive, its delivery can be timed according to a certain inspiration to expiration (I:E) ratio. The initial I:E ratio is commonly set to 1:2 but it can be further adjusted by experts based on clinical needs.



        Mechanical ventilation

        Further escalation of treatment requires mechanical ventilation. This is an invasive strategy that requires presence of a definitive airway such as an endotracheal tube or tracheostomy. It is mostly indicated for patients:

        • failing to ventilate (not completing full sentences, respiratory rate > 40 / minute, PaCO2 > 8kPa, VC < 10 ml/kg),
        • failing to oxygenate (PaO2 < 8kPa despite FiO2 of 0.6)
        • with specific medical or surgical implications (Guillain-barre syndrome, cardiogenic pulmonary oedema, ARDS, intoxication; trauma to the head, face, thorax or higher spine etc).  


        Mechanical ventilation is generally less tolerable than NIV. Patients may therefore need to be sedated and paralysed with the purpose of preventing them from fighting the ventilators and exacerbating further ventilator-associated complications. The levels of sedation and muscle relaxation can be assessed by various grading systems beyond the scope of this article. As opposed to normal physiological breathing, mechanical ventilation applies intermittent positive pressure ventilation (IPPV) which drives the passage of air down a positive pressure gradient during the phase of inspiration. The following provides a summary of the various modes of IPPV that are available to patients based on their depth of sedation and muscle paralysis:


        Controlled mechanical ventilation (CMV) is suitable for patients who lack a spontaneous breathing effort. Patients who belong to this category are evidently dependent on the mandatory breaths driven by the ventilators. The minute volume, i.e. the product of VT and respiratory rates, is pre-determined but it can always be readjusted based on the clinical progression of a patient. Furthermore, with the intention of safeguarding the lungs during ventilation, either or both of the airway pressure and volume can be limited or controlled to prevent overexpansion of the alveoli, hence to minimize baro- and volu-trauma.


        Synchronized intermittent mandatory ventilation (SIMV) on the other hand is ideal for patients who possess a fair degree of inspiratory effort. By means of a special sensor, SIMV coordinates the patient’s breathing effort and the mandatory breaths from the ventilator. It first ensures that the patient is being sufficiently ventilated according to the preset minute volume and second prevents both breaths from coinciding in order to avoid overexpansion of the respiratory zone.


        It is also feasible for SIMV to work in conjunction with pressure support ventilation (PSV) to facilitate a patient to complete the self-triggered ventilations. Through PSV, a preset positive pressure normally at 5 – 20 cmH20 is delivered to augment and concurrently sustain an individual’s breathing right through the inspiratory phase of the respiratory cycle. The positive pressure of PSV can steadily be reduced as the patient’s breathing stamina grows. The merit of that is it would necessitate a smooth step-down process from the mechanical ventilator so that re-intubation after failed weaning is even less likely.


        Given that the expiration is not supported by IPPV, it remains as a passive event during a patient’s breathing cycle. Should it be clinically indicated, the application of PEEP through CPAP or BIPAP may also be of use to exploit alveolar breathing, facilitate gaseous exchange and reduce the work of breathing.



        Despite being a life-saving treatment, the intended benefits of ventilatory support may deviate unexpectedly causing harm to the patient. Other than ventilator-associated injuries such as pneumothorax, pneumomediastinum and surgical emphysema etc, the positive intra-thoracic pressure that is generated by mechanical ventilation, less so in NIV, can impede venous return and reduce cardiac output. This may also increase intra-cranial pressure.


        Prolonged mechanical ventilation can in addition lead to atrophy of the respiratory muscles. Without a doubt, this increases the likelihood of hospital acquired infections and thus mortality. Patients must therefore be monitored with great vigilance by experienced hospital practitioners, with the effects of ventilatory support and other physiological parameters relating to their clinical conditions also being reviewed on regular basis.



        Ventilatory support is an important means of treatment for patients who are acutely unwell with respiratory distress. Understanding the basic science surrounding lung compliance, volume and capacity is key in determining treatment options beyond the use of a variable or fixed performance oxygen mask. FRC, CC and PEEP are key means of escalating treatment in order to further support and aid respiratory function and drive, albeit it with certain risks and potential complications. Topics recommended for further reading would include other means of optimising ventilation such as the prone position, physiotherapy and the use of nitric oxide, in addition to the theory behind oxygen therapy and its potential toxicity.



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