Mouth to mouth resuscitation can be historically traced back to the book of Kings in the Old Testament (1). The prophet Elisha, on seeing a little boy who appeared dead, “laid on top of the child, put his mouth to the child’s mouth, his eyes on the child’s eyes, his hands on the child’s hands, and he stretched himself on the child a second time and breathed into his mouth. And he felt the child’s flesh becoming warm…” Parecelsus (Fig 1), the 16th-century Swiss physician and alchemist, attempted ventilation of dead animals and human beings with bellows (2). Vesalius (1514–1564 CE) followed up on this intervention by attempting to ventilate animals through a thoracotomy using bellows. In his ingenious treatise of 1543, titled De Humani Corporis Fabrica (The Structure of the Human Body), he refers to positive pressure ventilation, uncannily similar to the way we practice today. He says, “But that life may be restored to the animal, an opening must be attempted in the trunk of the trachea, into which a tube of reed or cane should be put; you will then blow into this, so that the lung may rise again and take air” (3). However, several centuries passed by before Vesalius’s ingenuity was applied to the practice of medicine.
The earliest mechanical ventilators used negative pressure applied to the chest wall. John Dalziel, a Scottish physician, used a negative pressure tank ventilator, essentially an airtight box that completely surrounded the patient with the head and neck projecting outside. A piston with a one-way valve applied negative and positive pressure alternately to the chest wall to enable air movement during inspiration and expiration.
The early 20th century witnessed a catastrophic spread of poliomyelitis across North America and Europe, leading to widespread loss of lives, including children. Philip Drinker, an industrial engineer, while on a professional visit to the hospital, was moved by the sight of little children suffocating to death. He joined hands with his brother, Cecil, a professor of physiology at Harvard, to develop the tank ventilator, that came to be known later as the “iron lung”. The iron lung was first used in a little girl at the Boston City Children’s Hospital in the late 1940s. The hospital, in sheer desperation, called Phil early one morning as she lay unconscious, gasping for breath. The nurses had placed her inside the tank ventilator but were understandably reluctant to turn it on. Philip Drinker switched on the machine and watched her slowly regain consciousness. When fully awake, all she asked for was an ice cream. He was so touched that he stood there and cried (4).
Although the early tank ventilators (Fig 2) saved many lives, they were beset with problems. Patient access was difficult, and nursing care was cumbersome. It was no easy task for conscious patients to synchronize with the machine (5). Besides, the airway remained unprotected; aspiration and pneumonia turned out to be inevitable consequences.
Cuirass ventilators were an innovation aimed at overcoming the difficulties encountered with tank ventilators. An airtight shell enclosed the chest and abdomen alone, enabling easier patient access (Fig 3). They were smaller, cheaper, and allowed airway management (6). However, the cuirass ventilators delivered lower tidal volumes compared to tank ventilators (7).
Bjørn Ibsen and the dawn of positive pressure ventilation
The resurgence of poliomyelitis that spread like wildfire in the 1950s was an important turning point in the history of mechanical ventilation. Copenhagen’s Blegdam Hospital was overwhelmed with an unprecedented surge of patients with bulbar paralysis and respiratory failure. There were around 50 admissions every day, with mortality close to 80%; all they had to handle this crisis were one tank and six cuirass ventilators. Negative pressure ventilation seemed largely ineffective in offering respiratory support in poliomyelitis.
On 26th August 1952, Bjørn Ibsen (Fig 4) was called in to see 12-year-old Vivi Ebert, as she lay cyanotic, struggling to breathe; one of several children afflicted with bulbar polio. Under Ibsen’s guidance, she underwent a tracheostomy and positive pressure ventilation was performed using a Water’s to-and-fro breathing system. She was difficult to ventilate initially due to secretions and bronchospasm. However, Ibsen did not give up. In his own words, “I gave her 100 mg of pentothal in the hope that I could stop her struggling; her own respiration stopped, and I found that I could now inflate her lungs…”
This event basically changed the way patients with poliomyelitis were managed; the era of positive pressure ventilation in critically ill patients had begun. Manual positive pressure ventilation, by hand bagging, was carried out by medical students and family members (Fig 5). More than 70 patients were manually ventilated at the peak of the polio epidemic at the Blegdam Hospital (8). This single intervention reduced the mortality of acute respiratory failure due to poliomyelitis by 50% (9). It made sense to Ibsen and colleagues to manage patients in need of breathing support in a dedicated area, thus ushering in the era of modern intensive care as we know it today.
The first report of Acute Respiratory Distress Syndrome
On the 12th of August 1967, David Ashbaugh and colleagues reported on a series of 12 patients with acute respiratory failure who presented with acute hypoxia, tachypnea, and poor lung compliance (10). The underlying etiology was severe trauma in seven patients, viral pneumonia in four, and acute pancreatitis in one patient. These patients bore close resemblance to infants with hyaline membrane disease. Unlike other patients with acute respiratory failure, they did not respond to conventional therapies available at that time. The chest radiograph revealed bilateral patchy infiltrates similar to heart failure-related pulmonary edema. Unique microscopic findings were observed in five patients who died early, including hyperemia, dilated capillaries, and patchy alveolar collapse. Extensive interstitial and intra-alveolar edema were noted with macrophage infiltration. The most bewildering finding was the presence of hyaline membranes, akin to infant respiratory distress syndrome. Pressure and volume cycled ventilators were employed to provide mechanical ventilation. Positive end-expiratory pressure of 5–10 cm H2O was used in five patients and resulted in improved oxygenation.
Although the underlying etiology of what they alluded to as “respiratory distress syndrome” perplexed the authors at that time, they had unwittingly stumbled upon what came to be described later as the acute respiratory distress syndrome (ARDS).
The travails that Ashbaugh and colleagues had to endure to get their report published is even more baffling. The New England Journal of Medicine rejected it straightaway citing “inappropriate and potentially dangerous ventilator management” (11). They submitted a revised version to the Journal of the American Medical Association, and later, to the American Journal of Surgery; the editors of these esteemed journals did not deem the report worthy of publication. However, The Lancet readily accepted and published their report. This seminal paper, rejected by leading journals, remains to this day, one of the most cited ever in the history of medicine.
Positive pressure ventilation and PEEP
The increase in the end-expiratory lung volume with improved oxygen saturation was established by Frumin et al. in 1959 (12). They hypothesized that alveolar recruitment and prevention of end-expiratory alveolar collapse resulted in improved oxygenation. By the 1960s, Ashbaugh, Petty, and colleagues had realized the potential of PEEP, which they used to good effect in their case series. They used an Engström anesthesia ventilator with an additional attachment. They immersed the expiratory limb of the breathing circuit under water to a height corresponding to the required level of PEEP (13) (Fig 6). The news of improved oxygenation with this novel PEEP device spread far and wide and would remain the focus of interest for the next several decades.
Henning Pontoppidan established the first Respiratory Intensive Care Unit in the US at the Massachusetts General Hospital in 1961. He hypothesized that the hypoxia observed in acute lung injury may be a consequence of reduced functional residual capacity (FRC); the application of PEEP might alleviate hypoxia by increase in the FRC. The Boston group went on to demonstrate that a stepwise increment in PEEP levels from 5–15 cm H2O led to improved FRC and oxygenation (14). They also observed a steady rise in lung compliance as incremental PEEP led to alveolar recruitment; however, beyond a threshold limit, the compliance decreased, suggesting overdistension.
Lung-protective ventilation: early beginnings
The concept of “lung-protective” ventilation was pioneered in an animal model in the 1970s by Herb Webb and Donald Tierney (15). They reasoned that with extensive lung damage, high ventilating pressures might cause overinflation of the relatively normal lungs leading to injury. When they ventilated anesthetized rats at a peak pressure of 45 cm H2O with no PEEP, the results were catastrophic. According to Tierney, “Within minutes, the rats were cyanotic and appeared moribund; their lungs were very heavy and edematous, with foam in the airways…” (16). Much to their surprise, when a PEEP level of 10 cm H2O was applied, at the same level of inspiratory pressure, the lungs appeared to suffer less damage (Fig 6). Their report did not evoke much interest, probably because such a degree of ventilation pressure-related injury did not seem common in clinical practice. Years later, Tierney, reflecting on their crucial finding, lamented that looking back, it almost seems irresponsible that they did not highlight this important aspect of care in the management of patients with acute respiratory distress syndrome at that time (12).
CT scan of the lungs in critically ill patients was first undertaken in the 1980s, leading to a clearer understanding of the pathophysiology in acute respiratory distress syndrome (17). Pioneered by Rommelsheim et al., Gattinoni and Pesenti followed up with extensive CT-based evaluation of lung involvement in ARDS and established the “baby lung” concept (18). Overdistension of relatively normal lungs leading to injury was firmly ingrained into the paradigm of ventilator-induced lung injury (VILI)
1. Bible Gateway passage: 2 Kings 4:32-35 – New International Version [Internet]. Bible Gateway. [cited 2022 Nov 14]. Available from: https://www.biblegateway.com/passage/?search=2%20Kings%204%3A32-35&version=NIV
2. Asthma History: 1530: The bellows of Paracelsus [Internet]. [cited 2022 Nov 14]. Available from: http://asthmahistory.blogspot.com/2015/08/1530-bellows-of-paracelsus-provide.html
3. De Humani Corporis Fabrica Libri Septem. In: Wikipedia [Internet]. 2022 [cited 2022 Nov 12]. Available from: https://en.wikipedia.org/w/index.php?title=De_Humani_Corporis_Fabrica_Libri_Septem&oldid=1115411754
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18. ARDS: the non-homogeneous lung; facts and hypothesis – ScienceOpen [Internet]. [cited 2022 Nov 12]. Available from: https://www.scienceopen.com/document?vid=6bdb09ff-89e4-4dc4-8c1b-ad58646c489e
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