Ventilators have 4 phases of operation:
1. ‘The inspiratory phase’
2. ‘Cycling between the inspiratory (I) and expiratory (E) phase’
3. ‘The expiratory phase’
4. ‘Cycling between the E and I phase’
(Baker, 2016: 117)
The majority of ventilators are set to an I (Inspiratory) to E (Expiratory) ratio of 1:2, i.e. the expiratory phase is twice as long as the inspiratory phase, ‘which mirrors normal breathing’ (Baker, 2016: 108). If required, some ventilators allow this setting to ‘be altered to assist with restrictive lung diseases’ (Baker, 2016: 108). ICU ventilators contain additional settings that alter this ratio, including a ‘respiratory pause’ between the I and E phases ‘to allow distribution of gas within the lungs’ (Baker, 2016: 108).
So, inspiration occurs when air is ‘forced into the lungs’ (Baker, 2016: vi). Expiration, however, occurs when ‘the ventilator stops delivering a positive pressure and the patient breaths out passively, as in normal breathing. This passive expiration (E) is ensured by the elastic recoil of the lungs and the chest wall’ (Baker, 2016: 108). The timing is aided by a ‘pneumatic oscillator’ (Baker, 2016: 22).
The gas is delivered by the ‘patient circuit’, which also ‘evacuate[s] expired CO2’ (Baker, 2016: 109). This is delivered ‘as close as possible to the airway device being used’ by a valve (Baker, 2016: 109). There are also filters to prevent contamination of the ventilator from the patient.
Early ventilators had a ‘lack of interactivity with the patient’s own breathing efforts if there was only partial respiratory failure’ (Baker, 2016: 22) but modern ventilators tend to have different modes to account for this and additional settings beyond a simple tidal volume dial. In particular, ventilators feature a ‘demand valve’ which detects when a patient takes a breath (Baker, 2016: 22). There are also settings for tidal volume and ventilation frequency. These settings will be discussed in upcoming articles.
The Pneupac ParaPac (Smiths Medical)
Read more: What is the relief pressure dial on the ventilator?
The Positives and Negatives
The main positive effect of artificial ventilation is fairly obvious: it assists with the ventilation of a patient who is completely or partially unable to breathe normally. There are however a number of negative effects created by positive pressure ventilation. Related to these is the fact that mechanical ventilation can cause ‘heterogeneity’ of the lungs, meaning that ‘some lung units are prone to overdistension and others are prone to collapse’ (Hess & Kacmarek, 2014: 493). These are part of the reason most ventilators have relief pressure settings. This setting will be discussed in an upcoming article. You can check back here for the link.
Positive pressure ventilation can cause or effect the following:
The following are unavoidable results of ventilator use:
Decreased cardiac output
…Leading to ‘hypotension and potential tissue hypoxia. This effect is greatest with high mean airway pressure, high lung compliance, and low circulating blood volume’ (Hess & Kacmarek, 2014: 513). The high pressure ‘decreases venous return and right heart filling, which may reduce cardiac output’ (Hess & Kacmarek, 2014: 513).
High pressure –> decreased venous return
Low pressure –> increased venous return
This pressure is normally lowest ‘during inhalation’, so venous return would be highest. But with positive pressure ventilation, ‘venous return is greatest during exhalation’ as opposed to inhalation (Hess & Kacmarek, 2014: 513-520).
Renal and gastric effects
Mechanical ventilation reduces urine output due to ‘decreased renal perfusion’ which results from ‘decreased cardiac output’ (Hess & Kacmarek, 2014: 527). Unfortunately this can cause many of the issues common with fluid retention. Similarly, gastric distension can result, along with gastrointestinal bleeding’ (Hess & Kacmarek, 2014: 533).
Increased intracranial pressure
…in head injury patients, due to ‘a decrease in venous return, which increases intracranial blood volume and pressure’ (Hess & Kacmarek, 2014: 540).
Pneumonia may occur, especially due to invasive ventilation which is the form in emergency practice (non-invasive refers to ventilatory support such as CPAP). It ‘results from aspiration of oropharnygeal secretions around the cuff of the endotracheal tube’ (Hess & Kacmarek, 2014: 499).
The following can occur as a result of ventilator settings:
Hyperventilation and hypoventilation
These risk effecting the pH, and causing respiratory alkalosis (Hess & Kacmarek, 2014: 499)
Oxygen Toxicity due to high oxygen levels (Hess, 2014: 506)
A Shunt is usually partly decreased but settings can change this:
A shunt is ‘perfusion (blood flow) without ventilation’, which happens ‘when blood flows from the right heart to the left heart without participating in gas exchange’ (Hess & Kacmarek, 2014: 427). There are two different types of shunts: capillary and anatomic. The first occurs when the alveoli are not ventilated. One example of this is pneumonia (Hess & Kacmarek, 2014: 427). The latter type of shunt occurs when blood flow ‘completely bypasses the lungs’, which can sometimes happen with ‘congenital cardiac defects’ (Hess & Kacmarek, 2014: 427).
Positive Pressure Ventilation’s typical effect is to decrease capillary shunt by improving ‘the distribution of ventilation, particularly by improving the ventilation of previously underventilated areas of the lungs’ (Hess & Kacmarek, 2014: 427-446)
Despite the above improvements, if the settings are not ideal hypoxemia can result. This is the same outcome as a shunt but would in this case be caused by ‘redistribution of pulmonary blood flow to unventilated regions’ due to ‘overdistension of some lung units’ (Hess & Kacmarek, 2014: 324). Positive pressure ventilation can also increase anatomic shunt (Hess & Kacmarek, 2014: 441)
Also due to incorrect settings, the following can occur as a lack of pressure or volume:
Atelectasis occurs when the pressure or volume during or after artificial ventilation isn’t enough to inflate the lungs –> complete or partial collapse.
Atelectasis ‘is larger with obese patients and when a higher fraction of inspired oxygen (FI02) is used […]. During mechanical ventilation […] atelectasis may occur when lungs are underinflated due to low tidal volumes, or when compression occurs (such as patient position or obesity)’ (Open Anesthesia, 2017). If the volume or pressure isn’t enough to ‘prevent the alveoli from collapsing’ (Open Anesthesia, 2017) then regardless of ventilator type (pressure vs volume controlled) atelectasis may result.
The following can occur as a result of apparatus setup:
Dead Space can be increased by mechanical ventilation (Hess & Kacmarek, 2014: 471). It may be ‘reduced by an artificial airway (ETT) but is increased by increasing distance from the end of the ETT to the means of evacuating CO2 in mechanical ventilation’ (Baker, 2016: 111). Size, age, upright postures and neck extension also increase it (Baker, 2016: 111).
The following can occur due to overdistension:
Barotrauma = ‘alveolar rupture due to overdistension’, which can cause numerous problems including pneumothorax (Hess, 2014: 480). Volume generators have a ‘safety valve which activates at a preset pressure’ to avoid barotrauma’ (Baker, 2016: 118). This will be discussed in an upcoming article.
Ventilator-Induced lung injury caused by overdistension. Massively effected by ventilator settings for tidal volume and relief pressure (Hess, 2014: 493)
There are additional risks of positive pressure ventilation, particularly mechanical ventilation. Some of these are related to the use of airway adjuncts. Others are related to the removal of the ventilator. To read more, check out the references below.
Types of Positive Pressure Ventilation
‘A spectrum of modes exist between total artificial ventilation and a patient who is still breathing spontaneously but with reduced efforts’ (Baker, 2016: 105).
There are two main types of ventilators:
– Pressure generated
– Volume generated
Pressure generators ‘provide a constant pressure during the inspiratory phase’ (Baker, 2016: 118). Volume generators release gas once a set volume has been reached. In each one, only the pressure or the volume is a constant. Everything else is relative and will adjust until the preset parameter of volume or pressure has been reached (Baker, 2016; Hess, 2014).
‘The problem of pressure generation is that it cannot guarantee an adequate Vt [volume] in situations where the lung mechanics are abnormal or where a guaranteed Vt is required due to life-threatening hypoxia. They are therefore not suitable for most emergency ventilation, with the notable exception of neonatal and infant ventilation where flow generators are contraindicated due to the fragility of the lung tissue’ (Baker, 2016: 118).
Most ventilators switch from inspiration to expiration by ‘time cycling’ (Baker, 2016: 119). However, this can also be due to volume or pressure cycling. The time cycling ratio is usually 1:2 for I:E, in other words the expiration time is twice as long as the inhalation time. ‘Ventilation modes can best be understood as a spectrum describing the work of breathing done by the ventilator and by the patient’ (Baker, 2016: 122.
The modes are: Controlled Mandatory Ventilation, in which ‘ventilation is provided entirely by the ventilator’ (Baker, 2016: 122), Assisted Controlled Ventilation which is fairly self-explanatory, and Synchronised Mandatory Ventilation, in which ‘the patient’s respiratory efforts in initiating a ventilation are synchronised with ventilations provided automatically by the ventilator.’ This is best used to supplement the patient’s efforts. It’s otherwise known as ‘assist-control’ and is typically found in ICU. (Baker, 2016: 123).
In portable ventilators the modes are:
Intermittent Mandatory Ventilation, Synchronised intermittent mandatory ventilation, and synchronised mandatory minute volume but only the latter two are still in use. The second overcomes the problems of the first, ensuring that breaths are supplemented by the ventilator and that supplemented breaths are activated only when there is a certain trigger e.g. low pressure. There is a modern, more complex version of this now in use in hospitals but this may exist in emergency ventilation practice to assist a patient who is ‘in partial respiratory failure’ (Baker, 2016: 124).
The first two divide minute volume between the ventilator and the second. The latter is based on time, which is compared with a ‘set minute volume. If there is a discrepancy between the actual minute volume and the set delivered minute volume, an automatic ventilation is delivered which corrects the difference’ (Baker, 2016: 124).
Because there is an issue of the ventilator being unable to tell the difference between dead space ventilation and alveolar ventilation, Pneupac have modified the above with a series of Ifs (if the patient takes a breath, if there is no further breath, if the tidal volume is too low, etc) that adjusts settings accordingly (Baker, 2016: 124). There are more modes that exist for ICU ventilators, which tend to be a lot more complex in design (Baker, 2016).
Read about the solution: What is the relief pressure dial on the ventilator?
CPAP is also a form of positive pressure breathing and is designed ‘to improve oxygenation in lungs that may not be exchanging oxygen with the blood adequately’ (Baker, 2016: 126). There is a constant pressure in CPAP, versus ‘different pressures during inspiration and expiration’ in BIPAP’ but both are designed to allow the patient to do all the work of breathing. They merely increase oxygen and make inspiration easier while increasing the work of expiration. ‘Breathing with CPAP has been compared to the sensation of breathing against a very strong wind’ (Baker, 2016: 128). They ‘open up (recruit) alveoli in the lungs that may be non-ventilated.’ (Baker, 2016: 127). Both push back fluid ‘into the circulation via lymphatic drainage of the lung interstitial space’ and increase ‘the diffusion of oxygen into the pulmonary capillaries’ (Baker, 2016: 127).
Positive End Expiratory Ventilation applies ‘a positive pressure to the patient during the expiratory phase’ to ‘increase the functional residual capacity of the lungs and thus the efficiency of oxygenation of the blood’ (Baker, 2016: 126). ‘In order to be able to deliver a set tidal volume against variable lung compliance and airway resistance, resuscitation ventilators should be time-cycled, volume preset flow generators’ (Baker, 2016: 132).
Baker, D.J. 2016. Artificial Ventilation: A Basic Clinical Guide (ebook), Springer International: Switzerland
Hess, D. & Kacmarek, R.M. 2014. Essential of Mechanical Ventilation (ebook), McGraw-Hill Education: New York
Open Anesthesia, 2017. Ventilator Settings: atelecasis, Available Online: https://www.openanesthesia.org/ventilator_settings_atelectasis/ (Accessed 09/11/17)