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COVID-19: “To PEEP, or not to PEEP”?

COVID-19: Keeping the baby in the bath (Part 4)

To be, or not to be, that is the question.

Hamlet. Act 3, Scene 1

PEEP is positive end expiratory pressure. “To PEEP, or not to PEEP”, and how much, is another area of controversy in the management of COVID-19. Is PEEP dangerous in COVID-19 patients? Is it beneficial? 

The answer is “Yes” – to both questions – just like it is for any other acute respiratory distress syndrome (ARDS) patient…

We suspect that some cases of haemodynamic compromise occurring peri-intubation in patients with COVID-19 result from “too high” PEEP settings. Reasons for this may be that many COVID-19 patients present dehydrated and hypovolaemic, which is understandable if they have been self-isolating while unwell with fevers, sweating, and poor oral intake. If they then also receive induction agents for intubation and analgo-sedation for ongoing mechanical ventilation, they will also venodilate and may have a degree of negative inotropy and blunting of sympathetic responses impairing cardiac and vascular compensation. This combination of hypovolaemia and the circulatory effects of sedative agents puts patients at risk of a precipitous drop in venous return with an abrupt increase in intrathoracic pressures.

Positive pressure ventilation, including PEEP, increases intrathoracic pressure and does so more potently when the lungs are highly compliant (Jardin et al, 1985; Chapin et al, 1979). In poorly compliant lungs, relatively little of the applied PEEP “transmits” to intrathoracic pressure compared with highly compliant lungs. This occurs because there is less over-distention of compliant alveoli, which means there are less lung areas where alveolar pressure exceeds pulmonary venous pressure and results in a lesser increase in pulmonary vascular resistance and right ventricular afterload (Çoruh & Luks, 2014). Furthermore, through similar mechanisms, alveolar distention from high PEEP can worsen hypoxaemia by redirecting blood flow to diseased portions of the lung and by decreasing mixed venous oxygen content due to decreased venous return (and thus cardiac output) (Çoruh & Luks, 2014).  These effects are amplified in patients with co-existent right ventricular dysfunction, as they are less tolerant of the effect of PEEP on right ventricular afterload and right ventricular dilatation can displace the intra-ventricular septum and impair left ventricular function (Jardin et al, 1981). Thus, if one is used to managing patients with poor lung compliance, the profound hemodynamic effects of PEEP in hypoxaemic patients with compliant lungs may be under-estimated and the paradoxical effects of high PEEP worsening oxygenation may be a surprise.

PEEP has benefits too, of course. Unless the patient is at risk of dynamic hyperinflation from a condition like asthma, the use of zero or minimal PEEP is concerning in any intubated, mechanically ventilated patient, especially when the patient is obese. Without PEEP even compliant lungs may become stiffer, and more injured over time. Higher PEEP appears to decrease lung inflammation in ARDS (Tremblay et al, 1997) and is associated with better outcomes in severe ARDS patients (Briel et al, 2010). After a few days of mechanical ventilation, PEEP-induced alveolar recruitment tends to become independent of the underlying cause of ARDS (Thille et al, 2007). Even in patients with normal lungs, PEEP may be required to preserve functional residual capacity and prevent collapse. This is especially so in the obese, where surprisingly high mean PEEPs (e.g. 12 to 18 cmH20) may be required even when the lungs are normal (Erlandsson et al, 2006; Pirrone et al, 2016; Nestler et al, 2017). A key problem with setting PEEP to target “optimal” oxygenation is that increased oxygenation does not correlate with improved alveolar stability, such that lower PEEP may even result in “better oxygenation” but ultimately harm the lung through atelectasis and cyclical opening and collapse of alveoli (Nieman et al, 2019; Schmidt, 2012). Higher PEEP settings may also protect against patient self-inflicted lung injury (P-SILI) in spontaneously breathing patients. 

As always in critical care, we have a tricky balancing act to perform. Although the best way to optimise PEEP to any given patient is controversial, most intensivists would agree that optimisation is necessary – for any mechanically ventilated patient. The ARDSnet Ventilation Strategy provides an evidence-based starting point, but one size is unlikely to fit all. PEEP optimisation involves complex consideration of how to balance optimal oxygenation, optimal lung compliance and recruitment, and the haemodynamic effects of PEEP (Nieman et al, 2019; Schmidt, 2012). The balance of all of these considerations shifts in different patients over time, regardless of the underlying disease. Here, COVID-19 is not an exception, it proves the rule.

Next, we will discuss MacGyverism and “hacking COVID-19”.

Further reading

Please refer to these pages from the LITFL Critical Care Compendium for overviews of the key concepts discussed in this blogpost:

COVID-19: Keeping the baby in the bath series

  1. COVID-19: Keeping the baby in the bath (Introduction)
  2. “Silent hypoxaemia” and COVID-19 intubation
  3. Is COVID-19 ARDS? What about lung compliance?
  4. COVID-19: “To PEEP, or not to PEEP”?
  5. MacGyverism and “hacking COVID-19”
  6. Novel drug therapies and COVID-19 clinical trials
  7. Overcoming uncertainty in the Age of COVID-19

References

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

Jack Iwashyna LITFL

Critical care physician and health services researcher bringing the tools of social science and outcomes research to improve the care of patients with critical illnesses. I practice as an intensivist at the University of Michigan’s and the Ann Arbor VA's Critical Care Medicine units, where we work to bring the latest science and the best of clinical practice to patients  | iwashyna-lab  | @iwashyna |

Intensivist in Wellington, New Zealand. Started out in ED, but now feels physically ill whenever he steps foot on the front line. Clinical researcher, kite-surfer  | @DogICUma |

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