Introduction

Can I be ventilated without anesthesia and intubation?

“However, physiologists realized
that blowing air into the lungs was not as physiological as drawing air into the lungs, which is how we naturally breathe throughout our lives.”

— Jan van Egmond, Clinical physicist & Member of the Exovent Development team

It is not my intention here to provide a comprehensive overview of the history of mechanical ventilation. For that, I refer you to other sources¹². In brief, it has been recognized for centuries that breathing is essential or life, and that life comes to a rapid end if breathing ceases. It was also understood that mouth-to-mouth ventilation could extend life. This led to the idea of creating a mechanical means to sustain breathing. However, physiologists realized
that blowing air into the lungs was not as physiological as drawing air into the lungs, which is how we naturally breathe throughout our lives.

These insights eventually led to a solution that became widely accepted as the standard: the iron lung. In this device, the entire patient, except for their head, was enclosed in a chamber that could be placed under negative pressure. This negative pressure would pull the chest outward during inspiration, mimicking the action of the muscles that expand the ribcage. When the negative pressure was released, the patient could exhale “relaxingly.” This method of ventilation is what we now refer to as Negative Pressure Ventilation (NPV).

As we delve deeper into the material on this website, specific characteristics of the iron lung – and how they differ from current methods of ventilation – will become evident. We will undoubtedly revisit these differences later.

During the 1950s and 1960s, the standard shifted entirely. The world adopted Positive Pressure Ventilation (PPV). Characteristic of PPV is that air is pushed into the lungs under pressure during inspiration and allowed to escape when the airway pressure is reduced. This shift was undoubtedly driven by the life-saving miracle performed by Björn Ibsen in Copenhagen. I cannot narrate this history more compellingly than it has already been described elsewhere³. I encourage you to read that story before continuing.

However, the actual history reveals that the title of that cited story is somewhat misleading. It suggests that positive pressure ventilation was invented as a result of Ibsen’s work. This is not entirely true. What his work did initiate, however, was the further development of ventilation techniques in combination with facilities capable of providing intensive care: the advent of the Intensive Care Unit (ICU), where ventilation plays a central, though not exclusive, role.

A closer look at history shows that Dräger applied for a patent in 1907⁴ for a positive pressure ventilation device called the Pulmotor. By 1913, at least 3,000 of these devices were in use, and by 1944, this number had risen to 12,000. One might wonder whether Ibsen was aware of these developments, and whether he might have chosen the Pulmotor instead of enlisting 1,500 medical students for manual ventilation. Incidentally, in the Netherlands, the successor to the Pulmotor – the Poliomat – was used to ventilate polio patients. René Vercoutre⁵, a Dutch polio patient, lived his life ventilated by a Poliomat until his passing in 2017.

As a clinical physicist in the Department of Anesthesiology at RadboudUMC in Nijmegen, the Netherlands, I became involved around 2005 (or thereabouts) in research on Ventilator – Induced Lung Injury (VILI). The term VILI immediately raises the question: “Does ventilation itself induce lung damage?” Indeed, it is widely acknowledged that mechanical ventilation does more than simply remove carbon dioxide and provide oxygen. Among other things, it is associated with Ventilator-Associated Pneumonia (VAP), a type of pneumonia related to ventilation. VAP is closely linked to atelectasis, the phenomenon where alveoli fill with fluid and no longer contribute to ventilation-perfusion. Open alveoli exchange gases (oxygen and carbon dioxide) with blood flowing from the right heart (perfusion). This oxygenated blood is then distributed throughout the body by the left heart, while carbon dioxide is exhaled through the airways.

Soon after the introduction of PPV, atelectasis emerged as a significant complication. Although one might expect the question to arise, “Could this be related to the transition from NPV to PPV after the polio pandemic?” researchers pointing in that direction (e.g., Grasso⁶, 2008) have been countered with arguments such as, “There is no difference between PPV and NPV” (Loring⁷, 2008; Butler⁸, 2023).

Nonetheless, atelectasis remains the primary adversary associated with mechanical ventilation. If left unresolved, it creates an ideal breeding ground for bacteria and can lead to VAP. For short-term anesthesia, as is common in the operating room, the remedy is to have the patient take deep breaths after waking up to reopen the collapsed alveoli (a process called recruitment). Additionally, a small amount of pressure is maintained in the airways during exhalation (PEEP, Positive End-Expiratory Pressure) to keep the alveoli slightly inflated.

Did atelectasis exist before the introduction of PPV? Yes, it did. Various diseases lead to atelectasis or pulmonary edema. Historically, such conditions were managed using NPV!

Jan van Egmond

References