Physiological Literacy on mechanical ventilation in COVID-19: “Only a small proportion of patients—largely those in a cardiac arrest situation—“require” mechanical ventilation.”

Principles And Practice of Mechanical Ventilation, Third Edition (Tobin, Principles and Practice of Mechanical Ventilation) by Martin J. Tobin.

Last update and review: April 26, 2020.

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Physilogical Literacy on mechanical ventilation and on its use in COVID-19.

Introduction.

Physiological illiteracy and incompetence in the use of mechanical ventilation in COVID-19 patients lead to catastrophic results.

In the New York City area, “mortality for those requiring mechanical ventilation was 88.1%”.

Richardson et al., 2020 (1) on the outcomes of 5700 patients hospitalized in the New York City Area between March 1, 2020, and April 4, 2020:

Mortality for those requiring mechanical ventilation was 88.1%

We need to add that many of those who died in the New York City area were never put on mechanical ventilation. So, it was not the only reason for poor outcomes. But with an almost 90% mortality in those who were put on mechanical ventilation, we can safely say that ventilation was not helpful.

The biggest failure of a health care system.

The biggest failure of a health care system is the inability 1) to recognize highly intelligent medical practitioners among the generally mediocre mass of medical doctors, and 2) to put such highly intelligent medical practitioners in charge of the training and management of the rest of the medical profession.

Pulmonologist Martin J. Tobin.

Martin J. Tobin, MD, seems to be a rare individual to meet the description of a highly intelligent medical practitioner. He wrote two books on mechanical ventilation and intensive care published by McGraw-Hill, Inc, New York, and has more than 40 years of experience in “evaluating patients in outpatient clinics, hospital wards, and intensive care units (ICUs) while concurrently undertaking mechanistic physiologic research in patients and healthy subjects”.

Physilogical Literacy on mechanical ventilation and on its use in COVID-19.

Below, we insert several curated citations form an article by Martin J. Tobin on the use of mechanical ventilation in the treatment of COVID-19 patients (2).

“Only a small proportion of patients—largely those in a cardiac arrest situation—“require” mechanical ventilation.”

“In most instances, mechanical ventilation is instituted preemptively out of fear of an impending catastrophe.”

Only a small proportion of patients—largely those in a cardiac arrest situation—“require” mechanical ventilation. In most instances, mechanical ventilation is instituted preemptively out of fear of an impending catastrophe. These patients are receiving mechanical ventilation and it is impossible to prove that they “required” it when first implemented.

The decision to institute invasive mechanical ventilation (involving an endotracheal tube) is based on physician judgment—clinical gestalt influenced by oxygen saturation, dyspnea, respiratory rate, chest x-ray, and other factors. 10

The dominant respiratory feature of severe COVID-19 is arterial hypoxemia, greatly exceeding abnormalities in pulmonary mechanics.”

“Many patients are intubated (put on mechanical ventilation) early in their course.”

The dominant respiratory feature of severe coronavirus disease 2019 (Covid-19) is arterial hypoxemia, greatly exceeding abnormalities in pulmonary mechanics (decreased compliance). 1-3 Many patients are intubated and placed on mechanical ventilation early in their course.

“Many patients with Covid-19 are intubated because of hypoxemia—yet exhibit little dyspnea or distress.”

Many patients with Covid-19 are intubated because of hypoxemia—yet exhibit little dyspnea or distress. Humans do not typically experience dyspnea until PaO2 falls to 60 mmHg (or much lower). I was once a volunteer in an experiment probing the effect of hypoxemia on breathing pattern; 12 my pulse oximeter displayed a saturation of 80% for over an hour and I was not able to sense differences between saturations of 80% versus 90% (and above). When assessing dyspnea, it is imperative to ask open-ended questions. Leading questions, with the goal of seeking endorsement, can be treacherous.

“Respiratory rates of 25 to 35 breaths per minute should not be viewed as ipso facto (knee jerk) justification for intubation, but rather the expected physiological response to lung inflammation.”

Tachypnea in isolation should rarely constitute the primary reason to intubate (yet it commonly does). 10 Tachypnea is the expected response to lung inflammation that produces stimulation of irritant, stretch, and J receptors. 11 Respiratory rates of 25 to 35 breaths per minute should not be viewed as ipso facto(knee jerk) justification for intubation, but rather the expected physiological response to lung inflammation. It is incorrect to regard tachypnea as a sign of increased work of breathing; instead, work is determined by magnitude of pleural-pressure swings and tidal volume. 9 Palpation of the sternomastoid muscle, and detection of phasic (not tonic) contraction, is the most direct sign on physical examination of increased work of breathing.

Fig. 1.Placement of the index finger (gently, barely touching) on the body of the sternomastoid muscle to judge the presence of phasic contraction and qualitatively determine its magnitude(mild, moderate, marked). Source: Tobin, 2019.
Fig. 1.Placement of the index finger (gently, barely touching) on the body of the sternomastoid muscle to judge the presence of phasic contraction and qualitatively determine its magnitude(mild, moderate, marked). Source: Tobin, 2019.

Hypoxymia in COVID-19 is usually caused by ventilation-perfusion mismatch or intra-pulmonary shunting. The former does not require mechanical ventilation.

Hypoxemia accompanied by a normal alveolar-to-arterial oxygen gradient and increase in PaCO2 signifies hypoventilation. Hypoventilation is uncommon with Covid-19. Instead, hypoxemia with Covid-19 is usually accompanied by an increased alveolar-to-arterial oxygen gradient, signifying either ventilation-perfusion mismatch or intra-pulmonary shunting. 9 (Diffusion problems mainly cause hypoxemia at high altitude.) If a patient’s PaO2 increases with supplemental oxygen, this signifies the presence of ventilation-perfusion mismatch. A satisfactory level of arterial oxygenation can be sustained in these patients without recourse to intubation and mechanical ventilation. If a patient’s PaO2 does not increase with supplemental oxygen, this signifies the presence of an intra-pulmonary shunt; such patients are more likely to progress to earlier invasive ventilator assistance.

“Pulmonary infiltrates on their own are not an indication for mechanical ventilation.”

“It is only when pulmonary infiltrates are accompanied by severely abnormal gas exchange or increased work of breathing that intubation becomes necessary.”

Pulmonary infiltrates are commonly seen with Covid-19. Infiltrates on their own are not an indication for mechanical ventilation. Across four decades, I have been seeing patients with extensive pulmonary infiltrates managed with supplemental oxygen. It is only when pulmonary infiltrates are accompanied by severely abnormal gas exchange or increased work of breathing that intubation becomes necessary.

“Evidence of end-organ damage is difficult to demonstrate in patients with PaO2 above 40 mmHg (equivalent to oxygen saturation of approximately 75%).”

“In critically ill patients, vital organ function becomes impaired only when oxygen delivery decreases to less than 25% of the normal value.”

There is a fear that without mechanical ventilation, Covid-19 will produce organ impairment. Evidence of end-organ damage is difficult to demonstrate in patients with PaO2 above 40 mmHg (equivalent to oxygen saturation of approximately 75%). 10 The amount of oxygen delivered to the tissues is the product of arterial oxygen content and cardiac output. In patients with decreased oxygen delivery, oxygen extraction initially increases and oxygen consumption remains normal. 13 When oxygen delivery decreases below a critical threshold, this extraction mechanism is no longer sufficient and total body oxygen consumption decreases proportionally; metabolism changes from aerobic to anaerobic pathways, and vital-organ function becomes impaired. This critical threshold does not arise in critically ill patients until oxygen delivery decreases to less than 25% of the normal value.

We are highlighting each of the following concise, clear and powerful statements of the pulmonologist Michael J. Tobin.

“Once a patient is placed on a ventilator, the key challenge is to avoid complications. 15”

“Mechanical ventilation (in and of itself) does not produce lung healing—it merely keeps patients alive until their own biological mechanisms are able to outwit the coronavirus.”

“The best way to minimize ventilator-associated complications is to avoid intubation unless it is absolutely necessary. 16,17 “

“The surest way to increase Covid-19 mortality is liberal use of intubation and mechanical ventilation.”

The following passage is technical but concise and is a good place to start for intensive care doctors.

Within 24 hours of instituting mechanical ventilation, physicians need to consciously evaluate patients for weanability. 16,17 This step is especially important during the Covid-19 pandemic in order to free up a ventilator for the next patient. Deliberate use of physiological measurements— weaning predictors, such as frequency-to-tidal volume ratio 18 —alerts a physician that a patient is likely to succeed in weaning before the physician would otherwise think. These tests achieve their greatest impact if performed when a physician thinks that the patient is not yet ready for weaning. Once a patient is ready for a trial of weaning, the most efficient method is to employ a T-tube circuit; 19 flow-by (with PEEP at zero and pressure support at zero) is equally efficient while avoiding environmental contamination. Patients with Covid-19 exhibit severe respiratory failure and differ from the easy-to-wean patients in recent randomized control trials.

It is pivotal that caregivers have the requisite knowledge to interpret arterial oxygenation scientifically, know when to institute mechanical ventilation, and equally know how to remove the ventilator expeditiously to make it available for the next patient.

Martin J. Tobin, MD, Professor, Pulmonary and Critical Care Medicine.
Martin J. Tobin, MD, Professor, Pulmonary and Critical Care Medicine.

How to use this text.

If you are an intensive care doctor, you need to study the work of Michael J. Tobin attentively and to introduce your colleagues to his work. Prepare tests and quizzes that will help you and your colleagues to better assimilate the understanding of the underlying physiology of mechanical ventilation.

If you are a medical practitioner but are not working in intensive care, you may want to make sure that the intensive care doctors of your hospital or the hospitals in your area are physiologically literate and use mechanical ventilation correctly. Recommend the work of Michael J. Tobin to them.

If you are not a medical practitioner, you may want to contact your cost-sharing organization or medical insurance, your health care provider organization, your medical practitioner to inquire about the intensive care practices in the hospital where you or your community members may be treated in case of COVID-19.

If you need help with the above or help with doing your best to avoid a severe course of a possible COVID-19 in you, your community members, or your patients, do not hesitate to contact us.

Selected references:

1. Richardson et al. Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area. JAMA. doi:10.1001/jama.2020.6775
Published online April 22, 2020.

2. Tobin M.J., AJRCCM Articles in Press. Published April 13, 2020, (pre-print).

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