Skip to main content

“Less is More” in mechanical ventilation

Though formed in the late 1960s, the field of intensive care medicine solidified its place in the 1970s. Critical care practitioners were typically young and enthusiastic, but lacked the benefit of guidance from an established scientific literature or the experience of “older mentors,” as simply they did not exist. The rational basis of this new specialty was systems physiology and short-term observation, on which most of its monitoring and interventions are based. Interestingly, not only were the “intensivists” young, but so were the patients, compared to now. Very importantly, we naively assumed uniformity of diseases and disease mechanisms and translated our familiar deep knowledge of normal physiology to the pathologic state.

Energy, enthusiasm and the pioneering attitudes of the young intensivists were associated with a widespread tendency to “exceed” the confines of prior experience. Adverse consequences gradually became evident. This exuberance characterized many elements of practice: in septic patients, if milligrams of corticosteroids are good, grams might be better [1]. In nutrition, if 2000 kcal/day is good, 5000 must be better [2]. The same applies to sedations and fluids administration. In hemodynamics, supra-normal values of oxygen transport must be better [3], etc. Essentially, the intensivists of that era were doing the same things as we are now, but with far greater dosage, extent and intensity. ARDS is one of the best examples of our evolution from “more-to-less,” nurtured by the difficult lessons of our experience (Fig. 1).

Fig. 1
figure1

Examples of habit changes throughout the decades of the intensive care intervention (C.I.: Cardiac Index, PBW: Predicted Body Weight)

Inspired Oxygen Fraction (FiO2)

In the 1970s, when ARDS became the signature challenge of intensive care, the assumed goal was improved O2 delivery and a key risk was considered pulmonary O2 toxicity. Sixty percent FiO2 demarcated the threshold to the danger zone. Accordingly, the first ECMO trial [4] was designed to decrease the risk of high FiO2 while maintaining O2 delivery, regardless of tidal volume and pressures. In subsequent years, when the dominating roles of high tidal volumes and pressures in causing lung damage were recognized, FiO2 receded to the background, largely because of diverted interest. Only three decades later were the potential risks of sustaining high FiO2 re-evaluated [5].

Tidal Volume (TV)

In the 1970s, tidal volumes of 12–15 ml/kg of observed body weight were recommended by the most prestigious groups treating ARDS [6]. This approach stemmed primarily from the assumed need to maintain normal PaCO2 and the observation that higher tidal volumes often produced less atelectasis and better arterial oxygenation in ARDS [7], as already known in the anesthesia practice at that time. It was rather quickly realized, however, that higher pressures and volumes were accompanied by a worrisome incidence of barotrauma [8]. In the late 1970s, we proposed to provide lung rest in severe ARDS by extracorporeal removal of CO2 [9]. Gentler lung ventilation for ARDS was advocated for the clinical setting by Hickling [10], who, following the experience of Perret with severe asthmatics [11], proposed reducing the intensity of conventional mechanical ventilation by allowing PaCO2 to rise. The superiority of gentler lung ventilation in observational and laboratory studies was confirmed a decade later by results from the ARMA trial of the ARDS network (6 vs 12 ml/kg of PBW). This unmitigated success, however, followed several inconclusive randomized studies with less rigorous separation of cohorts and narrower differences between them in the strength of the tested VT variable [12]. This sequence exemplifies the oft-repeated pattern of theory, anatomic knowledge, experiment, and experience leading the way toward down-regulated therapeutic dosing—not dichotomous RCTs conducted in a broadly defined population sample.

Though now widely accepted by the intensive care community, even 6 ml/kg has been reported to be potentially dangerous in a subgroup of severe ARDS patients [13], leading to the current concept of “hyper-protective” ventilation [14]. In some settings, exuberant embracing of ECMO is a reflection of the impetus to “protect the lungs”—“less ventilation is more.” In so doing we now risk yielding to the same simplistic logic of the early 1970s, just with the opposite sign: if less is good, lesser must be better. Unfortunately, extremely low ventilation may be associated with several undesired effects [15].

Positive End Expiratory Pressure (PEEP)

Given the positive effect of PEEP on oxygenation, using high levels of PEEP (even “super PEEP” up to 25 cm H2O) was proposed early on [16]. The importance of the chest wall properties and body position was seldom considered at that time. The price paid to apply high level of PEEP to maintain “acceptable” arterial oxygenation and O2 delivery was not immediately appreciated (and still is not by some clinicians). Indeed, PEEP ranging from 6 cm H2O (prevention of volutrauma) to 15 cm H2O (prevention of “atelectrauma”) led to similar results in three large randomized trials, suggesting that the competing risks of volutrauma and atelectrauma are offsetting across this range of PEEP in an unselected ARDS population [17]. However, at the higher levels of PEEP set after a recruitment maneuver, the risks of volutrauma and hemodynamic compromise appear to exceed the risk of atelectrauma. Indeed, the higher PEEP treatment group experienced significantly higher mortality than did the control [18].

Respiratory rate

Of itself, using higher respiratory frequency has not traditionally been considered a problem, and it is set to maintain the PaCO2 within certain limits. However, caution is advised, especially at high levels of strain and power; in the 1970s, after some preliminary experimental reports, great enthusiasm was generated concerning high-frequency jet ventilation [19] soon abandoned, due to lack of improvement. Two decades later, however, HFOV at mean airway pressures sufficient to provide a lung volume close to total lung capacity was suggested as an ideal form of “open lung” protection (tidal volume of few ml). Results from clinical trials, however, proved discouraging [20]. We believe that the role of respiratory rate in generating VILI merits careful reevaluation, as it is an essential determinant of the mechanical power delivered to the lung [21].

Conclusion

“Less is More” is a theme that characterizes the evolution and painful lessons of intensive care practice. Yet, aggressive interventions are often well justified in the stabilization phase, and it is extremely unlikely that “Lesser is invariably more than Less.”

References

  1. 1.

    Sprung CL, Caralis PV, Marcial EH et al (1984) The effects of high-dose corticosteroids in patients with septic shock. A prospective, controlled study. N Engl J Med 311(18):1137–1143

    Article  CAS  Google Scholar 

  2. 2.

    Dudrick SJ, Ruberg RL (1971) Principles and practice of parenteral nutrition. Gastroenterology 61(6):901–910

    Article  CAS  Google Scholar 

  3. 3.

    Shoemaker WC, Montgomery ES, Kaplan E, Elwyn DH (1973) Physiologic patterns in surviving and nonsurviving shock patients. Use of sequential cardiorespiratory variables in defining criteria for therapeutic goals and early warning of death. Arch Surg 106(5):630–636

    Article  CAS  Google Scholar 

  4. 4.

    Zapol WM, Snider MT, Hill JD et al (1979) Extracorporeal membrane oxygenation in severe acute respiratory failure. A randomized prospective study. JAMA 242(20):2193–2196

    Article  CAS  Google Scholar 

  5. 5.

    Girardis M, Busani S, Damiani E et al (2016) Effect of conservative vs conventional oxygen therapy on mortality among patients in an intensive care unit: the oxygen-ICU randomized clinical trial. JAMA 316(15):1583–1589

    Article  CAS  Google Scholar 

  6. 6.

    Pontoppidan H, Geffin B, Lowenstein E (1972) Acute respiratory failure in the adult. N Engl J Med 287(14):690–698

    Article  CAS  Google Scholar 

  7. 7.

    Suter PM, Fairley HB, Isenberg MD (1978) Effect of tidal volume and positive end-expiratory pressure on compliance during mechanical ventilation. Chest 73(2):158–162

    Article  CAS  Google Scholar 

  8. 8.

    Kumar A, Pontoppidan H, Falke KJ, Wilson RS, Laver MB (1973) Pulmonary barotrauma during mechanical ventilation. Crit Care Med 1(4):181–186

    Article  CAS  Google Scholar 

  9. 9.

    Gattinoni L, Agostoni A, Pesenti A et al (1980) Treatment of acute respiratory failure with low-frequency positive-pressure ventilation and extracorporeal removal of CO2. Lancet 316:292–294

    Article  Google Scholar 

  10. 10.

    Hickling KG, Henderson SJ, Jackson R (1990) Low mortality associated with low volume pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndrome. Intensive Care Med 16(6):372–377

    Article  CAS  Google Scholar 

  11. 11.

    Darioli R, Perret C (1984) Mechanical controlled hypoventilation in status asthmaticus. Am Rev Respir Dis 129(3):385–387

    PubMed  CAS  Google Scholar 

  12. 12.

    Acute Respiratory Distress Syndrome N, Brower RG, Matthay MA et al (2000) Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 342(18):1301–1308

    Article  Google Scholar 

  13. 13.

    Terragni PP, Del Sorbo L, Mascia L et al (2009) Tidal volume lower than 6 ml/kg enhances lung protection: role of extracorporeal carbon dioxide removal. Anesthesiology 111:826–835

    Article  Google Scholar 

  14. 14.

    Combes A, Fanelli V, Pham T, Ranieri VM, European Society of Intensive Care Medicine Trials G (2019) Strategy of ultra-protective lung ventilation with extracorporeal CORfN-OmtsAi. Feasibility and safety of extracorporeal CO2 removal to enhance protective ventilation in acute respiratory distress syndrome: the SUPERNOVA study. Intensive Care Med 45(5):592–600

    Article  Google Scholar 

  15. 15.

    Gattinoni L (2016) Ultra-protective ventilation and hypoxemia. Crit Care 20(1):130

    Article  Google Scholar 

  16. 16.

    Kirby RR, Downs JB, Civetta JM et al (1975) High level positive end expiratory pressure (PEEP) in acute respiratory insufficiency. Chest 67(2):156–163

    Article  CAS  Google Scholar 

  17. 17.

    Walkey AJ, Del Sorbo L, Hodgson CL et al (2017) Higher PEEP versus lower PEEP strategies for patients with acute respiratory distress syndrome. A systematic review and meta-analysis. Ann Am Thorac Soc 14(Supplement_4):S297–S303

    Article  Google Scholar 

  18. 18.

    Writing Group for the Alveolar Recruitment for Acute Respiratory Distress Syndrome Trial I, Cavalcanti AB, Suzumura EA et al (2017) Effect of lung recruitment and titrated positive end-expiratory pressure (PEEP) vs low PEEP on mortality in patients with acute respiratory distress syndrome: a randomized clinical trial. JAMA 318(14):1335–1345

    Article  Google Scholar 

  19. 19.

    Sykes MK (1989) High frequency ventilation. Br J Anaesth 62(5):475–477

    Article  CAS  Google Scholar 

  20. 20.

    Goligher EC, Munshi L, Adhikari NKJ et al (2017) High-frequency oscillation for adult patients with acute respiratory distress syndrome A systematic review and meta-analysis. Ann Am Thorac Soc 14(Supplement_4):S289–S296

    Article  Google Scholar 

  21. 21.

    Gattinoni L, Tonetti T, Cressoni M et al (2016) Ventilator-related causes of lung injury: the mechanical power. Intensive Care Med 42(10):1567–1575

    Article  CAS  Google Scholar 

Download references

Acknowledgements

Open Access funding provided by Projekt DEAL.

Author information

Affiliations

Authors

Corresponding author

Correspondence to Luciano Gattinoni.

Ethics declarations

Conflicts of interest

The authors declare that they have no competing interests.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Gattinoni, L., Quintel, M. & Marini, J.J. “Less is More” in mechanical ventilation. Intensive Care Med 46, 780–782 (2020). https://doi.org/10.1007/s00134-020-05981-z

Download citation