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Physiology of positive-pressure ventilation 

Physiology of positive-pressure ventilation
Chapter:
Physiology of positive-pressure ventilation
Author(s):

Göran Hedenstierna

and Hans Ulrich Rothen

DOI:
10.1093/med/9780199600830.003.0088
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date: 24 October 2020

Key points

  • Positive-pressure ventilation (PPV) compared with spontaneous breathing increases airway and alveolar pressures.

  • It also distributes ventilation preferentially to non-dependent, possibly less perfused lung regions.

  • PPV squeezes blood flow to regions with lower alveolar pressure, possibly less or not at all ventilated regions.

  • It impedes venous return to the right heart that may lower cardiac output.

  • PPV elevates systemic capillary pressure that promotes vascular leakage, at the same time abdominal lymph drainage may be impeded, all-in-all promoting oedema formation.

Introduction

Ventilatory support can be provided by different techniques, the dominating one being positive pressure ventilation (PPV), with the breath forced into the lungs via the airways by increasing airway pressure. The force applied to the respiratory system (lung and chest wall) is the upper airway pressure (PAW) minus the pressure surrounding the body, normally atmospheric pressure (PB). This pressure difference can be partitioned into PAW minus pleural pressure (and its substitute, oesophageal pressure, PES) for expanding the lung and the pressure required to expand the chest wall (ribcage and the diaphragm), PES minus PB. In principle, these pressures generate the volume changes also during a spontaneous breath.

Respiratory muscle tone

Although pressure differences over the respiratory system may be similar during spontaneous breathing (SB) and PPV, the effects on the ventilation distribution and lung perfusion are different. In addition, with PPV there is frequently a fall in respiratory muscle tone, either by the deliberate use of muscle relaxants, anaesthetics, or sedatives or by reduced consciousness of the patient. This causes a lowering of the resting lung volume (FRC) [1]‌, which has an additional and substantial effect on respiratory and circulatory mechanics.

With SB, the major respiratory muscle is the diaphragm and when it contracts the dome is flattened and the thoracic cavity will be increased. In the supine position, the tensing of the diaphragm will mainly shorten the dorsal fibres, which are the ones that are most elongated because they have been pushed cranially by the abdominal organs. In addition, the distribution of muscle fibres in the diaphragm may vary with more fibres in the dorsal part studied by Decramer et al. in dogs [2]‌. Moreover, dependent lung regions (dorsal in supine position) are located on the lower, steeper part and non-dependent regions are located higher up on the upper, flatter part of the pressure–volume curve. An inspiration is assumed to cause similar change in the transpulmonary pressure along the whole pleural space, causing larger volume change for dependent than non-dependent lung regions.

Ventilation distribution

With mechanical ventilation, the distribution of the breath may be different from that by spontaneous breathing. The reason is two-fold. First, the lung volume is reduced because of loss of respiratory muscle tone as discussed in ‘Respiratory Muscle Tone’, and this promotes airway closure that occurs primarily in more dependent lung regions [3]‌. The closure prevents at least the initial inspiration to go to the dependent regions, but during the succeeding inflations, the airways may open up so that some ventilation goes to lower lung (dorsal regions in the supine subject). If airways are continuously closed, which is also possible in a healthy lung when breathing at low lung volume, atelectasis will eventually develop because of gas absorption behind the continuously closed airways. The time it takes until collapse occurs depends on the inspired oxygen concentration, from a few minutes with 100% oxygen to a few hours with air [4]. The other reason for a different distribution of the breath is that the diaphragm is no longer acting as an active muscle, but just as a passive membrane separating abdominal content from the thoracic cavity. Since the abdominal pressure increases down from anterior to posterior in the gravitational orientation, more pressure is needed to move the dependent part of the diaphragm and the abdominal content than the non-dependent region of the diaphragm. Volume expansion of the thoracic cavity will thus be facilitated in the upper regions [5].

The smaller lung volume that is frequently seen in the mechanically-ventilated subject increases airway resistance and the difference will be larger between the dependent, narrower, and upper, non-dependent, less narrowed airways [6]‌. This adds to the shift in ventilation to upper lung regions.

Pulmonary circulation

The pulmonary circulation is a low pressure system and is, therefore, susceptible to increased intrathoracic pressure. The lower the vascular pressure is, the larger is the difference in perfusion to upper and lower lung units [7]‌. With increase in vascular pressure as, for example, during physical exercise, perfusion of the lung will be more homogeneous. If alveolar pressure is increased, as during a mechanical breath, it may exceed that of the surrounding capillaries, compressing them so that the alveolus is non-perfused. This is possible, even likely, in the non-dependent lung regions where perfusion pressure is the lowest. Due to hydrostatic forces vascular pressure increases down the lung by approximately 1 cm H2O (0.7 mmHg) per cm distance so there may be a pressure difference between top and bottom of the lung by 11–12 mmHg. A mechanical breath will thus force the blood flow towards dependent regions, whereas ventilation is forced towards non-dependent regions. The ventilation/perfusion ratio (V/Q) departs from an ideal ratio of 1 to well above 1 (‘high V/Q’) in non-dependent regions (a dead space like effect) to a ratio well below 1 (‘low V/Q’) in dependent lung regions causing a shunt-like effect [8] (Fig. 88.1).

Fig. 88.1 Atelectasis (left panel) and distributions of ventilation and blood flow in an anaesthetized and mechanically-ventilated (ZEEP) subject (right panel). Note the atelectasis and absence of ventilation in the bottom of the lungs, causing shunt (QS), the poor ventilation in a zone above the atelectasis, causing low V/Q, and the preferential ventilation of the upper half of the lung, well in excess of perfusion, causing high V/Q and adding to dead space as measured by CO2 technique. Compare also with the schematic drawing of ventilation and perfusion distributions in awake, upright man in the insert (upper right).

Fig. 88.1 Atelectasis (left panel) and distributions of ventilation and blood flow in an anaesthetized and mechanically-ventilated (ZEEP) subject (right panel). Note the atelectasis and absence of ventilation in the bottom of the lungs, causing shunt (QS), the poor ventilation in a zone above the atelectasis, causing low V/Q, and the preferential ventilation of the upper half of the lung, well in excess of perfusion, causing high V/Q and adding to dead space as measured by CO2 technique. Compare also with the schematic drawing of ventilation and perfusion distributions in awake, upright man in the insert (upper right).

Data from Tokics L et al., ‘V/Q distribution and correlation to atelectasis in anaesthetized paralyzed humans’, Journal of Applied Physiology, 1996, 81(4), pp. 1822–33.

The spontaneous breath may more easily recruit collapsed lung tissue in the dependent regions because of larger tidal swing of the diaphragm in the dorsal part than in the mechanically-ventilated subject, where the diaphragm moves more in the non-dependent regions, as mentioned in ‘Ventilation Distribution’. A prerequisite for such beneficial effects is that the spontaneous breath is large enough to overcome the forces that keep collapsed alveoli together (e.g. surface tension [9]‌). This should reduce shunting and improve oxygenation of blood. However, even without recruitment of collapsed lung by the spontaneous breath a beneficial effect can still be seen. This is because the spontaneous breath attracts blood flow to ventilated regions from collapsed areas, whereas the mechanical breath squeezes blood away from the ventilated region to atelectatic and consolidated regions [10,11].

Systemic circulation

PPV may impede return of venous blood to the thorax and the right heart [12]. With high enough pressure, stroke volume and also heart rate can be reduced to zero. A hypovolaemic subject will be more susceptible to a decrease in cardiac output when intrathoracic pressure is elevated as during mechanical ventilation [12].

Impeded venous return raises venous pressure that is causing an increase in systemic capillary pressure with increased capillary leakage and possible oedema formation in peripheral organs. Lymph vessels will take care of an increased capillary leakage and there is also a return of fluid in the distal end of the capillary back to the venous system. However, in the abdomen lymph flow may be impeded because the thoracic duct is the main channel for the abdominal lymph return. It passes through the thorax and with an elevated intrathoracic pressure as during mechanical ventilation, the thoracic duct may be compressed and lymph flow impeded [13]. Thus, there may be a double cause of abdominal oedema formation in the mechanically-ventilated subject—increased capillary leakage and impeded lymph drainage.

PPV may also impede drainage of the lung tissue and increase lung fluid. PPV with positive end-expiratory pressure (PEEP), has been shown to impede lung lymph flow [14] and this can be one of several mechanisms behind the fluid accumulation. However, conflicting results have also been reported [15].

How to reduce negative effects of positive pressure ventilation?

What then can be done to counter the negative effects of mechanical ventilation? First, an increase in lung volume by recruitment of the collapsed lung, the application of appropriate PEEP to keep the aerated lung open, and to prevent cyclic airway closure should redirect ventilation to more dependent lung regions. Secondly, maintaining normo- or even hypervolaemia should make the pulmonary circulation less vulnerable to increased airway and alveolar pressures, and result in a better match of ventilation and perfusion. Thirdly, maintenance of any respiratory muscle tone or mimicking spontaneous breaths in addition to the mechanical breaths may improve matching of ventilation and blood flow, facilitate venous return and decrease systemic organ oedema formation (keeping in mind respiratory muscle fatigue and even overexpansion of lung if uncontrolled).

Different forms of positive pressure ventilation

A short note will also be made on different forms of PPV. Different inspiratory flow patterns can be used to fine-tune the ventilator settings, but with limited effects on respiratory function [16]. A combination of slow mechanical respiratory rates, e.g. 8 breaths/min, on top of which the patient can breathe spontaneously (airway pressure release ventilation (APRV), or bi-level positive airway pressure, (BiPAP)) appears also to improve gas exchange [17,18]. Applying a cuirass around the chest enables negative pressure selectively over the thorax. This will be as close to a spontaneous breath as possible and it will cause an improvement of blood flow to the lung [19]. This is different from negative pressure ventilation with a patient in a tank just keeping the head outside the tank. With this technique the whole body is exposed to the same pressure variation and there will be no favourable return of venous blood to the heart.

The spontaneously breathing subject changes both respiration rate and size of the tidal volume, and will intermittently also take deep breaths, which may even mimic a recruitment manoeuvre. In conventional mechanical ventilation, respiratory rate and tidal volume are kept constant with a monotonous ventilatory pattern. If anything, this will promote successive deterioration of surfactant function and also promote alveolar collapse. One can speculate on other negative effects on vascular pressures and perfusion distribution. There are reports showing that the gas exchange is improved if the ventilatory pattern is varying in a random fashion [20].

Conclusion

To summarize, positive pressure ventilation differs from spontaneous breathing by exposing the lung to higher pressures, impairing matching of ventilation and blood flow, and impeding cardiac output. At the same time, PPV may be a life-saving treatment, but not necessarily the optimum technique for ventilatory support.

References

1. Wahba RWM. (1991). Perioperative functional residual capacity. Canadian Journal of Anaesthesia, 38, 384–400.Find this resource:

2. Decramer M, De Troyer A, Kelly S, and Macklem PT (1984). Mechanical arrangement of costal and crural diaphragms in dogs. Journal of Applied Physiology, 56, 1484–90.Find this resource:

3. Milic-Emili J, Torchio R, and D‘Angelo E (2007). Closing volume: a reappraisal (1967–2007). European Journal of Applied Physiology, 99, 567–83.Find this resource:

4. Hedenstierna G and Edmark L (2010). Mechanisms of atelectasis in the peri-operative period. Best Practice & Research, Clinical Anaesthesiology, 24, 157–69.Find this resource:

5. Froese AB and Bryan AC (1974). Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology, 41, 242–55.Find this resource:

6. West JB. (1989). Mechanics of breathing. In: West JB (ed.) Best and Taylor´s Physiological Basis of Medical Practice, pp. 560–78. Baltimore, MD: Williams and Wilkins.Find this resource:

7. West JB, Dollery CT, and Naimark A (1964). Distribution of blood flow in isolated lung: relation to vasculkar and alveolar pressures. Journal of Applied Physiology, 19, 713–24.Find this resource:

8. Tokics L, Hedenstierna G, Svensson L, et al. (1996). V/Q distribution and correlation to atelectasis in anesthetized paralyzed humans. Journal of Applied Physiology, 81, 1822–33.Find this resource:

9. Rothen HU, Neumann P, Berglund JE, et al (1999). Dynamics of re-expansion of atelectasis during general anaesthesia. British Journal of Anaesthesia, 82, 551–6.Find this resource:

10. Carvalho AR, Spieth PM, Pelosi P, et al. (2009). Pressure support ventilation and biphasic positive airway pressure improve oxygenation by redistribution of pulmonary blood flow. Anesthesia and Analgesia, 109, 856–65.Find this resource:

11. Vimlati L, Kawati R, Hedenstierna G, Larsson A, and Lichtwarck-Aschoff M (2011). Spontaneous breathing improves shunt fraction and oxygenation in comparison with controlled ventilation at a similar amount of lung collapse. Anesthesia and Analgesia, 113, 1089–95.Find this resource:

12. Pinsky MR. (2007). Heart–lung interactions. Current Opinions in Critical Care, 13, 528–31.Find this resource:

13. Lattuada M and Hedenstierna G. (2006). Abdominal lymph flow in an endotoxin sepsis model: Influence of spontaneous breathing and mechanical ventilation. Critical Care Medicine, 34, 2792–8.Find this resource:

14. Frostell C, Blomqvist H, Hedenstierna G, Halbig I, and Pieper R (1987). Thoracic and abdominal lymph drainage in relation to mechanical ventilation and PEEP. Acta Anaesthesiologica Scandinavica, 31, 405–11.Find this resource:

15. García-Delgado M, Touma-Fernández A, Chamorro-Marín V, Ruiz-Aguilar A, Aguilar-Alonso E, and Fernández-Mondéjar E (2010). Alveolar fluid clearance in healthy pigs and influence of positive end-expiratory pressure. Critical Care, 14R36.Find this resource:

16. Jansson L and Jonson B (1972). A theoretical study on flow patterns of ventilators. Scandinavian Journal of Respiratory Diseases, 53, 237–46.Find this resource:

17. Putensen C, Zech S, Wrigge H, et al. (2001). Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury. American Journal of Respiratory and Critical Care Medicine, 164, 43–9.Find this resource:

18. Wrigge H, Zinserling J, Neumann P, et al. (2003). Spontaneous breathing improves lung aeration in oleic acid-induced lung injury. Anesthesiology, 99, 376–84.Find this resource:

19. Schiavina M, Fabiani A, and Gunella G. (1994). External negative pressure ventilation techniques. Monaldi Archives for Chest Diseases, 49, 516–21.Find this resource:

20. Spieth PM, Carvalho AR, Guldner A, et al. (2011). Pressure support improves oxygenation and lung protection compared to pressure-controlled ventilation and is further improved by random variation of pressure support. Critical Care Medicine, 39, 746–55.Find this resource: