MAP vs. NAP: The Impact of Mechanical Ventilation on Hemodynamics

Editor’s note: This text-based course is an edited transcript of the webinar, MAP vs. NAP: The Impact of Mechanical Ventilation on Hemodynamics, presented by Evan Richards, Advanced Practice Clinical Consultant, BSc, RT. 

It is recommended that you download the course handout to supplement this text format.

Learning Outcomes

After this course, participants will be able to:

• Describe areas of potential physiological interaction with positive pressure ventilation
• Identify the safest of the five techniques for increasing MAP
• Describe the impact of non-invasive ventilation on hemodynamics
• List ventilator strategies that may reduce the negative impact of positive pressure

 The Impact of  Ventilation on Hemodynamics

I always look forward to these sessions. I have done this for 35 years, and not once have I taken for granted the fact that people take time out of their day to learn. I really respect the fact that you are here, and I am going to try to pay you back with something that might be immediately relevant to your clinical practice. The effect of mean airway pressure (MAP) on pulmonary blood flow and systemic blood flow can be observed in various ways. In this discussion, I will address the consequences of MAP, focusing on both its impact and the strategies to mitigate its negative effects. Additionally, I will briefly explore what I consider the most effective approaches to recruiting and stabilizing lungs. Finally, I will share an anecdote about how a trip to the produce section with my wife provided unexpected insights into pulmonary mechanics, and that is how I will conclude today's presentation.

Areas of Potential Physiological Interaction with MEAN Airway Pressure

• Define MAP and NAP
• Methods of increasing MAP
• MAP and pulmonary blood flow
• Address the consequences of MAP
• Best way to recruit and stabilize lungs
• Learning pulmonary mechanics from the produce section of the grocery store

The 60/90 Rule

Before I end, I want to remind you of the 60/90 rule, which I first learned about on NPR. Hearing it was a sobering moment, as I realized I am often the biggest culprit. According to the rule, 60 minutes after a lecture, people forget 90% of what was said—just like that, it is gone. This isn't about placing blame; it is simply human nature. I empathize because I, too, struggle to retain everything shared during a presentation. After each section, I will summarize the key take-home message. That way, you'll have the 10% of what I said that truly matters. This presentation covers a lot of information, and my goal is to ensure you leave with the most important insights.

Updated Definitions

First, let's begin with MAP versus NAP. I will introduce you to these updated definitions, which I coined myself—they may be entirely new to you. MAP emphasizes the word "mean," referring to any potentially counterproductive pressure applied to the airways. I call it "mean" airway pressure because, quite frankly, it is not very nice. In contrast, NAP stands for Nice Airway Pressure. NAP is the lowest amount of pressure possible, tailored to the patient’s specific pathophysiology.

This distinction may seem like a playful alliteration—with all those P's—but it is also a serious concept. Our goal is to apply just the right amount of airway pressure to avoid harm while still effectively ventilating the patient. As we proceed, we will aim to identify the optimal Nice Airway Pressure (NAP) and steer clear of the counterproductive Mean Airway Pressure (MAP).

What Is the Most Dangerous Component of Mechanical Ventilation?

As I prepared for this talk, I asked myself: What is the most dangerous component of mechanical ventilation? Initially, I was convinced the answer had to be volume. After all, volume trauma is a well-documented risk, and its dangers are emphasized frequently. I also recognized the peril of inspiratory time (or "I-time") for patients with air leaks, where prolonged pressures can exacerbate the damage.

Despite my assumptions, my research revealed a surprising consensus: the most dangerous component of mechanical ventilation is not volume, pressure, or time—it is the act of intubation itself. This realization reframed my perspective on ventilator-induced lung injury (VILI). If we aim to prevent such injury, the best strategy is often to avoid intubation altogether. A patient cannot experience ventilator-induced harm without a ventilator in the first place.

Of course, non-invasive ventilation has its own complexities, but the damage associated with mechanical ventilation begins with the endotracheal tube. The moment that the tube is placed, the dynamics between the patient and the ventilator fundamentally change. Intubation inherently increases mean airway pressure and, with it, the risk of elevated intrathoracic pressure. These pressures, regardless of how carefully they are managed, alter the physiology of the lungs.

The most challenging aspect of mechanical ventilation, however, is not just mitigating pressure or volume—it’s achieving effective gas distribution within the alveoli. Positive pressure ventilation can unevenly inflate the lungs, leading to regions of overdistension while others remain under-ventilated. This uneven distribution not only complicates oxygenation but also increases the risk of lung injury over time.

In summary, mechanical ventilation is a powerful tool, but it comes with inherent risks. While volume, pressure, and timing are all critical considerations, the act of intubation itself sets the stage for potential harm. As clinicians, we must remain vigilant in balancing these factors, seeking opportunities to minimize invasive interventions whenever possible.

This is why so many patients sustain harm during mechanical ventilation. In an attempt to ventilate the poorly compliant or collapsed alveoli—the “bad guys”—we often overventilate the healthy ones. This uneven volume distribution increases the risk of stretch injury to the functional alveoli, compounding the damage.

Stretch injury occurs when the alveoli are forced to expand beyond their physiological limits. This can lead to stress fractures in the delicate capillary-alveolar interface, disrupting the integrity of the lung’s microarchitecture. For example, stress fractures in the capillaries allow red blood cells to leak into the air spaces, triggering an inflammatory cascade. This process can progress to conditions like interstitial emphysema, where air infiltrates tissue spaces, exacerbating inflammation and further impairing lung function.

Overinflation can also compress the pulmonary capillary beds, reducing blood flow and impairing gas exchange. Conversely, underinflation may cause capillaries to become extravascular, disrupting the balance needed for effective ventilation and perfusion. Either scenario—overinflation or underinflation—disrupts pulmonary capillary blood flow, further complicating patient management.

In my experience working in an animal lab with Dr. Kurt Albertine at the University of Utah, I observed how sensitive the lungs are to ventilation-perfusion (V/Q) mismatches. The body has mechanisms to detect and respond to suboptimal V/Q matching, but when mechanical ventilation exacerbates these mismatches, the result is often detrimental. It is a delicate balance, and achieving proper ventilation without causing harm remains one of the greatest challenges in respiratory care.

When alveoli are not in contact with open, compliant neighbors, the body naturally redirects blood flow to areas with greater potential for gas exchange, optimizing ventilation-perfusion (V/Q) matching. However, both overinflation and underinflation can disrupt this delicate balance, impairing pulmonary capillary blood flow and creating further complications.

This phenomenon has been vividly demonstrated in research labs, such as Gary Neiman’s lab in Syracuse, New York. Using advanced imaging techniques, they have shown how a conventional ventilator breath can disrupt pulmonary capillary blood flow. These disruptions, visible as interruptions in the "sparkling" patterns of blood flow around the alveoli, illustrate how even a single ventilator breath can interfere with microcirculation. This effect, though unavoidable to some extent, should be minimized to reduce harm.

One critical component of lung function affected by ventilation is surfactant, a substance essential for reducing alveolar surface tension. When ventilation damages the alveolar walls, or when protein-rich edema fluid accumulates, surfactant becomes inactivated. This breakdown in surfactant function leads to further alveolar instability and exacerbates lung injury. In neonates and infants, who often produce surfactant in limited quantities, this disruption can be particularly catastrophic.

Beyond the lungs, mechanical ventilation can have systemic effects. Excessive mean airway pressure compresses the heart, reducing venous return and impairing cardiac output. The relationship is simple: the heart can only pump as much blood as it receives. Elevated pressures can also impact other organs, including the liver, kidneys, and brain, underscoring the far-reaching consequences of improper ventilator management.

The take-home message is clear: ventilation is an incredibly powerful tool, but it must be used judiciously. While it can save lives, mechanical ventilation has the potential to cause significant harm if not carefully managed. By understanding and addressing these risks, we can improve outcomes and minimize injury to our patients.

Least Invasive Method of Ventilating

When placing a patient on a mechanical ventilator, it is important to remember that this is not how we were naturally designed to breathe. This realization led me to reflect: if mechanical ventilation is not natural, how are we meant to breathe? The answer lies in negative pressure ventilation.

Unlike mechanical ventilation, which uses positive pressure to force air into the lungs, our bodies are designed to breathe by creating negative pressure. When we inhale, the diaphragm contracts and drops, while other respiratory muscles activate. This action expands the chest cavity, creating a pressure gradient that draws air into the lungs to equalize thoracic pressure. It is an elegant, efficient system.

Historically, negative-pressure ventilators like the iron lung mimicked this natural process. One well-known example is the iron lung, which was developed in the mid-20th century at Sick Children’s Hospital in Toronto, Canada. These devices encased the patient’s body and created a vacuum that allowed the chest to expand and air to flow into the lungs. They were remarkably effective and far less invasive than modern positive-pressure ventilation.

So why don’t we still use iron lungs if they align more closely with our natural physiology? The simple answer is practicality. Iron lungs are cumbersome, require specialized environments, and lack the versatility of modern ventilators. While they were lifesaving during their time—especially during the polio epidemics—they have been largely replaced by more portable and adaptable technologies.

Still, the principle behind the iron lung serves as a reminder of how our bodies are designed to function. Understanding the natural mechanics of breathing can inform how we approach mechanical ventilation, helping us to minimize harm and support patients in the safest way possible.

A Brief Tribute to the Iron Lung

Managing patients in an iron lung was notoriously challenging, but I want to take a moment to acknowledge the remarkable legacy of Paul Alexander, a man who lived most of his life in an iron lung. Paul passed away on March 11, 2024, at the age of 78. His life was nothing short of extraordinary.

Despite the limitations of living in an iron lung, Paul taught himself to breathe outside the device for up to three hours at a time. His determination and resilience were unmatched. He earned two master’s degrees, authored three books, and became an inspiration to many. Paul often expressed his appreciation for the iron lung, noting that it breathed the way humans are naturally meant to—with negative pressure.

For those unfamiliar with the iron lung, it is a fascinating device. The patient's body is encased inside the cylindrical chamber, with only their head protruding. The design includes portholes for caregivers to access and manipulate the patient as needed, as well as a window to visually monitor the patient. At its core, the iron lung uses a motor-driven piston to create alternating pressure within the chamber. This shift between negative and positive pressure allows the diaphragm to move, mimicking the natural mechanics of breathing.

The Iron Lung and Negative Pressure

Paul’s story is a powerful reminder of the iron lung’s significance in medical history. While it is no longer practical for modern use, the device served as a lifeline for many, enabling a natural form of breathing that aligns with our physiology. It also stands as a testament to human ingenuity and the resilience of the human spirit.

The iron lung even included a mirror so patients could see themselves, a small but meaningful touch for those who spent much of their lives inside the device. For those who relied on it, the iron lung was remarkable—it allowed them to breathe the way nature intended, with negative pressure. While it may seem unimaginable to live in such a device, patients often expressed gratitude for its ability to sustain their lives in a way that mimicked natural respiration.

I once encountered an unexpected illustration of this principle while working in a lab. An engineer had modified a standard laboratory flask by cutting off the bottom, inserting a tube through a cork, and attaching a Y-connector with two balloons. Curious, I commented, “You have reinvented the iron lung.”

The engineer looked puzzled and asked what I meant. I explained that his setup was essentially a negative-pressure breathing model. The rubber glove stretched across the open end of the flask represented a diaphragm. When the glove was pulled downward, the balloons inside inflated, just as the lungs do when the diaphragm contracts to create negative pressure.

When the rubber glove at the base of the flask is pulled downward, it simulates the diaphragm contracting, creating negative pressure inside the flask. This causes air to rush through the tube and inflate the attached balloons, mimicking how the lungs expand during natural breathing. When the glove is pushed back up, the pressure inside the flask increases, forcing air out of the tube, much like the process of exhalation.

Spontaneous vs. Mechanical Breathing

This mechanism mirrors how human beings breathe. Fortunately, our lungs maintain enough functional residual capacity (FRC) to prevent collapse at the end of exhalation, unlike the simulated system. If you have ever experienced having "the wind knocked out of you," you understand how crucial this reserve air is for maintaining breathing stability.

Negative pressure breathing offers significant physiological benefits. During inspiration, it assists venous return by reducing intrathoracic pressure, which facilitates blood flow back to the heart. It also reduces pressure on the pulmonary capillaries, promoting better circulation and gas exchange.

In contrast, positive pressure ventilation increases intrathoracic pressure during inspiration. This has the opposite effect: it restricts venous return, decreases right ventricular output, and makes it more challenging for blood to flow through the lungs. By effectively compressing the heart and pulmonary vessels, positive pressure ventilation can impair pulmonary blood flow and place additional strain on the cardiovascular system.

Despite these physiological drawbacks, positive pressure ventilation is widely used because it is far more practical and adaptable than negative pressure systems like the iron lung. Understanding these differences allows us to better manage ventilation and minimize potential harm to patients. 

This simple experiment highlighted the elegance of natural respiration and served as a hands-on demonstration of the principles behind devices like the iron lung. it is fascinating how even the most basic tools can mirror complex physiological processes and remind us of the ingenuity of early medical devices.

Ventilation and Hemodynamics

• In normal breathing, the negative pressure phase of inspiration: 
  • Assists venous return
  • Alleviates pressure on the pulmonary capillaries
  • Encourages good blood flow
• In PPV, the intrathoracic pressure increases during inspiration, causing:
  • Decreased venous return
  • Decreased right ventricular output
  • Restricted pulmonary blood flow

Let’s take a moment to discuss ventilation and hemodynamics. Hemodynamics, as we know, is the study of blood flow and its properties. Maintaining stable hemodynamics is critical because any disruption can compromise blood flow and, ultimately, organ function. Two key components of hemodynamics are venous return and cardiac output. Venous return refers to the amount of blood returning to the heart, while cardiac output is the volume of blood the heart pumps out. Both of these processes depend on two critical factors: preload and afterload.

Preload

• The amount of blood in the heart just before it contracts
• Depends on how much is coming back (Venous Return)
• Decreased pressure on the heart from MAP
• Reduced preload will tend to decrease cardiac output
• Increased preload is good

When I first started exploring this topic, I realized I needed a better understanding of preload. Like many, I found it a challenging concept at first, so I did some research. Preload is the volume of blood in the heart at the end of diastole, just before the heart contracts. It is directly influenced by venous return—how much blood is flowing back to the heart—and can be reduced by factors that apply pressure to the heart, such as excessive mean airway pressure from mechanical ventilation.

Interestingly, managing preload can significantly impact cardiac output. By optimizing preload—ensuring the heart is not overloaded or underloaded with blood before contraction—you can improve cardiac output. However, cardiac output may suffer when preload is decreased by external pressures, such as those caused by positive pressure ventilation.

When preload is reduced, cardiac output decreases because the heart simply doesnot have enough blood to pump effectively. Factors like excessive mean airway pressure from mechanical ventilation can compress the heart, reducing venous return and subsequently decreasing preload. This disruption impairs the heart’s ability to maintain adequate cardiac output.

Conversely, increased preload is beneficial. It ensures the heart receives more blood, allowing it to send more oxygenated blood to the body. The key takeaway is that reduced preload is generally detrimental, as it leads to reduced cardiac output, while increased preload supports efficient circulation.

For example, turning up the mean airway pressure too high can "squeeze" the heart, particularly the right side, making it harder for blood to return to the heart. Since cardiac output is directly dependent on venous return—essentially, the heart can only pump out as much blood as it receives—disrupting venous return disrupts the entire system.

Preload plays a vital role in maintaining cardiac output. Managing ventilatory pressures to avoid excessive compression of the heart and ensuring adequate venous return are key strategies for optimizing preload and supporting overall cardiovascular function.

Understanding Increased Afterload

• The pressure the heart must overcome to eject blood to the rest of the body
• Increases when blood vessels are compressed or restricted (e.g., excessive MAP)
• Reducing afterload will tend to improve cardiac output
• Increased afterload is bad

Afterload, unlike preload, refers to the resistance the heart must overcome to pump blood into circulation. It is the pressure against which the heart works to eject blood. Increased afterload occurs when blood vessels are compressed or restricted, which can happen with excessive mean airway pressure.

Reducing afterload generally improves cardiac output because it decreases the resistance the heart has to overcome. Here's a simple rule to keep in mind: increased preload is beneficial, but increased afterload is detrimental. Increased preload ensures more blood returns to the heart for pumping, while increased afterload creates more resistance to blood flow out of the heart, reducing efficiency.

Increased afterload can manifest in different ways. On the left side of the heart, it might result from high resistance in the systemic circulation, such as compression of the aorta or other vessels due to elevated mean airway pressure. While a cardiologist might point out that squeezing the heart can improve ejection fraction, the heart still struggles to push blood against narrowed or restricted vessels, which increases afterload.

On the right side of the heart, increased afterload often results from elevated pulmonary vascular resistance. This can happen when alveoli are overinflated, compressing pulmonary capillaries and creating resistance to blood flow. Conversely, underinflation of alveoli can also increase pulmonary vascular resistance, as the body may shut down blood flow to vessels that aren’t in contact with adequately inflated alveoli.

Balancing Pulmonary Vascular Resistance

Both overinflation and underinflation of alveoli can disrupt pulmonary vascular blood flow. Overinflation compresses pulmonary vessels, while underinflation fails to provide adequate contact between blood vessels and open alveoli. As a respiratory therapist, your job is to find the “sweet spot” in ventilation—a balance where alveoli are optimally inflated without overdistension or collapse. This balance ensures maximum surface area for gas exchange, with the greatest number of vessels in contact with open alveoli.

The Goldilocks Approach

The take-home message is that hemodynamics can be compromised by either too much or too little mean airway pressure. As respiratory therapists, we excel at finding this balance because we are attentive and meticulous. Think of it as the "Goldilocks principle": too much or too little of something is not ideal, but when it is just right, the lungs function optimally. By carefully optimizing mean airway pressure, we ensure the best outcomes for our patients, providing stable hemodynamics and efficient gas exchange.

How Is MAP Increased?

To effectively manage mean airway pressure (MAP) during mechanical ventilation, it is essential to understand the various strategies available and their physiological implications. Here are five key methods to increase MAP:

1. Shortening the Rise Time: By accelerating the time it takes to reach peak inspiratory pressure, you can enhance MAP. This rapid attainment of pressure allows for more immediate recruitment of alveoli, improving oxygenation. However, caution is necessary, as overly aggressive rise times may lead to patient discomfort or barotrauma.
2. Increasing Peak Inspiratory Pressure (PIP): Elevating PIP directly raises the pressure delivered to the lungs, thereby increasing MAP. While this can improve oxygenation, it is crucial to monitor for potential lung injury due to higher pressures, especially in patients with compromised lung compliance.
3. Extending Inspiratory Time (I-time): Prolonging the duration of inspiration maintains the lungs at a higher pressure for a longer period, which increases MAP. This strategy can enhance gas exchange but may also reduce the time available for exhalation, potentially leading to air trapping or hyperinflation if not carefully managed.
4. Increasing Respiratory Rate: Raising the number of breaths per minute reduces the time allocated for exhalation. This can elevate MAP by maintaining higher average pressures. However, an excessive respiratory rate may cause incomplete exhalation, resulting in air trapping and increased intrathoracic pressure, which could adversely affect hemodynamics.
5. Raising Positive End-Expiratory Pressure (PEEP): Elevating PEEP prevents alveolar collapse at the end of expiration, thereby increasing MAP. This method is often considered the most effective and safest way to enhance oxygenation, as it promotes alveolar recruitment and improves functional residual capacity. Nonetheless, excessive PEEP can lead to overdistension and impede venous return, so it must be titrated carefully.

A pivotal study by Dr. Marcelo Amato and colleagues (2014) examined the impact of ventilator management strategies on patient outcomes. The study introduced the concept of relative risk of death associated with different ventilatory approaches:

• Raising PIP without Increasing PEEP: This approach was associated with a significant increase in the relative risk of death. Elevating PIP alone can lead to overdistension and ventilator-induced lung injury, especially when PEEP is not adjusted to maintain alveolar stability.
• Raising Both PIP and PEEP: Combining increases in PIP and PEEP showed a moderate improvement in outcomes compared to raising PIP alone. However, in patients with severe illness, this strategy still poses substantial risks. Maintaining an appropriate driving pressure (the difference between PIP and PEEP) was crucial in mitigating potential harm.
• Raising PEEP Alone: This method resulted in the most significant reduction in the relative risk of death. Elevating PEEP alone provided a stable and protective pressure, enhancing alveolar recruitment without the detrimental effects associated with high PIP.

The study underscores the importance of driving pressure as a critical determinant of patient outcomes. Driving pressure, calculated as the difference between PIP and PEEP, reflects the cyclic stress applied to the lungs during ventilation. Maintaining a lower driving pressure has been associated with improved survival in patients with acute respiratory distress syndrome (Amato et al, 2014).

In clinical practice, the goal is to optimize MAP to improve oxygenation while minimizing the risk of ventilator-induced lung injury. Among the strategies discussed, adjusting PEEP is often the most effective and safest method. However, individual patient factors must be considered, and ventilator settings should be tailored to achieve the best possible outcomes.

In summary, while several methods exist to increase MAP, careful consideration of their physiological impacts is essential. Elevating PEEP stands out as a particularly effective strategy, but it should be implemented judiciously within the context of a comprehensive ventilatory management plan.

Impact of MAP on Cerebral Circulation

Positive end-expiratory pressure (PEEP) is a critical component in mechanical ventilation, particularly for patients with acute respiratory distress syndrome (ARDS). By maintaining alveolar recruitment and improving oxygenation, PEEP plays a vital role in patient care. However, its application requires careful consideration due to potential systemic effects, especially concerning cerebral circulation.

Impact on Cerebral Circulation

Elevated PEEP levels can increase intrathoracic pressure, which may impede venous return from the brain, leading to elevated intracranial pressure (ICP). This rise in ICP can reduce cerebral perfusion pressure (CPP), potentially compromising cerebral blood flow and increasing the risk of hypoxic or ischemic injuries. Studies have shown that while moderate PEEP levels may have minimal impact, higher levels can significantly affect ICP and CPP.

Clinical Considerations

In patients with brain injuries or compromised cerebral autoregulation, the application of PEEP necessitates meticulous monitoring. The balance between optimizing oxygenation and maintaining stable cerebral hemodynamics is delicate. Adjustments to PEEP should be individualized, taking into account the patient's respiratory mechanics, intracranial dynamics, and overall clinical status. Continuous monitoring of ICP and CPP is advisable when applying higher levels of PEEP in such patients.

Recommendations for Practice

• Individualized PEEP Titration: Tailor PEEP levels to the patient's specific needs, considering both pulmonary and cerebral parameters.
• Monitoring: Employ invasive monitoring techniques to assess ICP and CPP in patients at risk of cerebral complications.
• Interdisciplinary Approach: Collaborate with neurology and critical care specialists to optimize ventilatory strategies for patients with concurrent respiratory and neurological concerns.

Understanding the nuances between hypoxic and ischemic brain injuries is crucial for accurate diagnosis and treatment.

Hypoxic Brain Injury

This occurs when the brain receives blood that is inadequately oxygenated. Despite sufficient blood flow, the reduced oxygen content leads to cellular dysfunction and damage. Common causes include respiratory failure, carbon monoxide poisoning, and high altitudes. Depending on the duration and severity of oxygen deprivation, symptoms can range from mild cognitive impairments to severe neurological deficits. 

Ischemic Brain Injury

In contrast, ischemic injury arises when there is an obstruction or reduction in blood flow to the brain despite the blood being oxygen-rich. This deprivation prevents brain tissues from receiving necessary oxygen and nutrients, leading to cell death. Causes often include blood clots, strokes, or cardiac arrest. The resulting damage can lead to motor deficits, speech difficulties, and other neurological impairments.  Both types of injuries can result in significant neurological impairments, and their management requires precise monitoring of both oxygenation and perfusion.

Near-Infrared Spectroscopy (NIRS)

NIRS is a non-invasive monitoring technique that offers real-time insights into tissue oxygenation and perfusion. By emitting near-infrared light into tissues and measuring the absorption spectra, NIRS can determine the balance between oxygenated and deoxygenated hemoglobin. This provides continuous data on both oxygen delivery and utilization in specific regions, making it invaluable in settings like cardiac surgery and critical care. 

The NIRS device operates by placing sensors on the skin's surface. A light source emits near-infrared light, which penetrates tissues and is absorbed by hemoglobin. Two detectors measure the intensity of light after it has traversed the tissue:

• Shallow Detector: Captures light that has traveled a shorter path, providing information about superficial tissue layers.
• Deep Detector: Measures light that has penetrated deeper, offering data on underlying tissues and organs.

By analyzing the differential absorption at these depths, NIRS calculates regional oxygen saturation and assesses tissue perfusion. This dual capability distinguishes it from standard pulse oximetry, which primarily measures arterial oxygen saturation without providing direct information on tissue perfusion. 

In clinical practice, NIRS has proven beneficial in various scenarios:

• Cardiac Surgery: Monitoring cerebral oxygenation to prevent neurological complications.
• Neonatal Care: Assessing brain oxygenation in preterm infants to detect and prevent hypoxic-ischemic injuries.
• Critical Care: Evaluating tissue perfusion in patients with circulatory shock or traumatic brain injuries.

By providing continuous, real-time data, NIRS aids clinicians in making informed decisions to optimize patient outcomes. In summary, distinguishing between hypoxic and ischemic brain injuries is essential for targeted therapeutic interventions. Utilizing advanced monitoring tools like NIRS enhances the ability to assess and manage these conditions effectively, ultimately improving patient care.

This device is remarkable because it monitors both oxygen delivery and perfusion simultaneously, providing critical real-time insights into a patient’s condition. Its utility lies not just in what it measures but in how it empowers clinicians to act proactively. Unlike many diagnostic tools—such as X-rays, CT scans, MRIs, or ultrasounds—this device doesn’t simply confirm whether harm has occurred. While these technologies are invaluable for diagnosing existing issues, they are typically reactive, informing clinicians only after an injury or complication has already taken place.

What sets this device apart is its ability to alert clinicians to potential harm before it happens. Rather than waiting for signs of an adverse event to appear, it provides early warnings, enabling timely interventions that can prevent injury altogether. This proactive functionality represents a significant shift in how we approach patient care, moving us closer to truly preventive medicine. By identifying and addressing risks in real-time, clinicians can reduce complications, improve outcomes, and potentially save lives.

The device monitors critical metrics related to organ saturation, such as how well oxygen is reaching the kidneys and brain—two organs particularly vulnerable to oxygen deprivation. These metrics are essential because they reflect how effectively the body is maintaining vital functions. A decline in saturation values signals potential organ dysfunction, allowing clinicians to act immediately, whether by adjusting oxygen delivery, optimizing perfusion, or addressing other underlying issues.

In one instance, a drop in both cerebral and renal saturation levels was identified within a few hours. The clinical team traced the issue to excessive mean airway pressure. They responded by suctioning the patient and switching from a device that utilized higher mean airway pressure to one that used less. This change led to a rapid improvement in oxygenation, preventing brain injury before it occurred. The ability to detect and address such problems early highlights the profound impact of this technology.

What’s remarkable is how this device facilitates real-time monitoring of both cerebral and renal saturations. By providing continuous feedback, it bridges the gap between reactive diagnostics and preventive care, offering precision and foresight that redefine patient safety standards. This capability ensures that clinicians can make informed, timely decisions in critical care settings, where even slight delays can have serious consequences.

The key takeaway here is that mean airway pressure can significantly impact cerebral circulation, making its careful management critical. Another takeaway is more general but equally important: attention to detail matters, whether you’re managing a clinical device or inflating a raft. Small adjustments can have big impacts, and proactive care can make all the difference in patient outcomes.

Consequences of MAP

I have personally experienced lightheadedness when blowing up something for my grandkids, which serves as a reminder to be cautious. Overexertion, even in seemingly simple tasks, can have consequences—similar to the clinical risks associated with excessive mean airway pressure. Understanding this concept is critical because the implications can be significant, as highlighted in a fascinating study.

This study, titled Cardiovascular Effects of HFOV with Optimal Lung Volume Strategy in Term Neonates with ARDS (Acherman, R.J., Siassi, B., deLemos, R., Lewis, A.B., & Ramanathan, R.), examined the cardiovascular effects of high-frequency oscillatory ventilation (HFOV) using optimal lung volume strategies. The collaboration included notable figures in the field: Dr. Reuben Acherman, a cardiologist; Dr. Ramanathan, the inventor of the RAM cannula; and the late Dr. deLemos, known as the "grandfather" of the SensorMedics oscillator. This team was based at LA Children’s Hospital, a hub for groundbreaking pediatric care.

Dr. Acherman, intrigued by the team's approach, visited Dr. deLemos to discuss their use of high mean airway pressures during oscillation. Dr. deLemos explained that using HFOV allowed for higher mean airway pressures with improved safety compared to conventional ventilation methods. The reduced risk of overdistension, as confirmed by X-ray imaging, supported their strategy.

However, Dr. Acherman, ever cautious, expressed concerns about the potential effects of mean airway pressure on the cardiovascular system. He proposed using his ultrasound machine to investigate further. The team welcomed his input, as they had not observed evidence of overdistension on imaging but were open to additional insights. 

The primary challenge with oscillation and jet ventilation lies in their mechanics. Both devices essentially function as CPAP systems with added oscillatory movement, often referred to as “CPAP with a wiggle.” They operate at higher mean airway pressures while maintaining lower peak inspiratory pressures, which can obscure traditional signs of overdistension. For example, on a conventional ventilator, overinflation often causes visible changes like diaphragm flattening or rib expansion on X-rays. These indicators are typically absent in oscillatory ventilation, making it harder to detect underlying issues.

Dr. Acherman became concerned when he observed that patients on these devices, particularly at higher mean airway pressures, were showing signs of systemic cardiovascular stress. Despite interventions to maintain blood pressure and cardiac output, these patients continued to exhibit troubling symptoms. Using his ultrasound machine, Dr. Acherman investigated further and made a critical discovery: many of these patients had a significantly dilated inferior vena cava (IVC), elevated central venous pressure (CVP), and widespread edema.

His findings were striking. While the heart and lungs initially appeared normal on imaging, the inferior vena cava below the diaphragm was dilated, in some cases up to three times its normal size. This indicated that venous return to the heart was being obstructed. Both the superior and inferior vena cava were affected, contributing to increased intracranial pressure, which can have severe neurological consequences. Additionally, the hepatic veins, which drain blood from the liver, were also significantly dilated—approximately three times their normal size. This systemic venous congestion confirmed that elevated mean airway pressure was creating significant hemodynamic strain.

Dr. Acherman concluded that the elevated mean airway pressures were not just ventilating the lungs but also exerting pressure on the heart and pulmonary vasculature. This compression impaired venous return and increased resistance within the pulmonary and systemic circulations. These findings were critical because they highlighted a hidden risk of oscillatory ventilation that could not be readily detected with traditional methods like X-rays.

The study conducted at LA Children’s Hospital brought together several pioneers in neonatal and pediatric care, including Dr. Acherman, Dr. Ramanathan (inventor of the RAM cannula), and the late Dr. deLemos, known as the "grandfather" of the SensorMedics oscillator. Their work illustrated the complex interplay between ventilation strategies and cardiovascular physiology. While HFOV was deemed safer than conventional ventilation in certain cases, Dr. Ackerman’s findings underscored the importance of monitoring not just pulmonary parameters but also cardiovascular effects.

One of the most illustrative demonstrations of HFOV mechanics involved placing a pig or sheep lung inside a sealed bottle. When high mean airway pressures were applied, the lung inflated while maintaining low internal pressures, a feature often touted as an advantage of HFOV. However, Dr. Acherman noted a critical limitation of this model: it did not account for the constraints of an intact thoracic cavity. In a living patient, the rib cage, diaphragm, and surrounding structures limit lung expansion. This restriction is especially pronounced in adults but can also affect pediatric patients. Consequently, the pressures that seemed safe in an isolated lung model could, in practice, result in significant hemodynamic consequences when applied in vivo.

At LA Children’s Hospital, the clinical team observed that patients with high mean airway pressures did not exhibit traditional signs of overdistension, such as diaphragm flattening or rib spacing changes, commonly seen on X-rays. However, the elevated pressures were compressing the heart and pulmonary vasculature, leading to increased CVP, venous congestion, and impaired cardiac function. These effects were subtle yet profound, illustrating the need for advanced diagnostic tools like ultrasound to detect and address such complications.

This study demonstrated the importance of interdisciplinary collaboration in improving patient care. By combining the expertise of cardiologists, neonatologists, and pulmonary specialists, the team was able to identify and mitigate risks associated with HFOV. It also highlighted the need for careful consideration of mean airway pressures, even when using “safer” ventilation strategies. The findings emphasize that while advanced technologies can offer significant benefits, they also require a thorough understanding of their potential systemic impacts.

In clinical practice, this case serves as a reminder to monitor not just respiratory parameters but also the broader physiological effects of ventilation strategies. The insights gained from this study continue to inform how we approach high-frequency ventilation, emphasizing the importance of vigilance, comprehensive assessment, and early intervention to prevent complications.

Consequences of Too Much MAP

Managing mean airway pressure is critical, whether using a conventional ventilator or a high-frequency ventilator because elevated pressures can have serious consequences. The question then becomes: what can be done to address the problem? At Children’s Hospital Los Angeles, under the guidance of Dr. Philippe Friedlich, an experienced neonatologist, the team approached this challenge with innovation and collaboration. Dr. Friedlich and his team worked closely with biomedical technicians to design practical solutions that address real clinical needs, not just theoretical ones.

During a visit to speak with his group, I discussed the process of developing medical devices, emphasizing that they must solve real problems in the ICU, NICU, or PICU. Before my talk, Dr. Friedlich and I discussed a pivotal study conducted at his hospital (Marked Reduction in MAP and OI Using HFJV in Neonates with Severe Refractory Hypoxemic Respiratory Failure). This study focused on addressing mean airway pressure and overdistension in neonates, particularly those who had failed conventional ventilation and were deteriorating on oscillators after missing their ECMO window.

The Problem: Overdistension and Gas Trapping

In these cases, the neonates were experiencing gas trapping and hyperinflation, which contributed to elevated mean airway pressures. These pressures, in turn, exacerbated issues like barotrauma—or as Dr. Friedlich coined it, "mapotrauma." The team hypothesized that gas trapping was the primary cause of the elevated pressures, leading to poor oxygenation and ventilation. They realized that conventional ventilators with a 1:2 inspiratory-to-expiratory (I:E) ratio were not sufficient to alleviate this problem. This led them to revisit high-frequency jet ventilation (HFJV) to explore its potential in these critical cases.

The Solution: Extending Expiratory Time

Using HFJV, the team was able to adjust the I:E ratio to as much as 1:6 or 1:12, significantly increasing the time available for exhalation. This approach helped to minimize gas trapping and, subsequently, reduce mean airway pressure. The goal was to resolve hyperinflation, improve oxygenation, and ultimately stabilize these fragile patients.

The Results: Rapid Improvement

The first ten patients in the study had failed conventional ventilators and oscillators. These neonates were critically ill, with oxygen indexes (OI) averaging 30, indicating severe respiratory failure. Over 50 days, they had been stuck on oscillation without significant improvement. Once switched to HFJV, the results were striking:

• Reduction in Mean Airway Pressure: Within four to five hours of starting HFJV, the mean airway pressure dropped from 14 to below 10 cm H₂O
• Improved Oxygenation: As mean airway pressure decreased, the fraction of inspired oxygen (FiO₂) could be weaned from nearly 90% to below 50%
• Improved Oxygen Index: The OI, which reflects the severity of respiratory failure, fell from 30 to 10 within hours and remained low over the next several days

This rapid improvement allowed the team to extubate the patients and eventually send them home. Of the ten initial patients, nine survived and were discharged. Tragically, one patient suffering from sepsis did not survive. However, the surviving neonates—all with chronic lung disease at the time of intervention—were able to leave the NICU and go home on oxygen.

The Impact: Better Outcomes and Reduced Costs

While some neonates required supplemental oxygen at discharge, Dr. Friedlich emphasized that sending them home was a success. Each day a patient spends in the NICU costs $10,000 to $20,000. By reducing the time spent on mechanical ventilation and in the NICU, the team not only improved patient outcomes but also reduced financial burdens for families and healthcare systems. On average, after the intervention, patients were on mechanical ventilation for just seven more days before being weaned.

Lessons Learned

Dr. Friedlich and his team concluded that lowering mean airway pressure was the key to success. By resolving hyperinflation and gas trapping, they achieved better oxygenation and reduced the risk of complications. The study also highlighted the importance of avoiding hyperinflation in the first place. Prolonged expiratory times, achieved through HFJV, proved to be a critical strategy for minimizing barotrauma and reducing mean airway pressures.

MAP During Noninvasive (NIV) 

Mean airway pressure has long been a focus of discussion in mechanical ventilation, but I had initially thought it wasn’t an issue during noninvasive ventilation (NIV). My reasoning was simple: during NIV, patients typically breathe in a way that mimics natural physiology. Humans are designed to breathe with negative pressure, not positive pressure. Unlike invasive ventilation, which requires mechanical assistance, NIV generally relies on the patient’s normal breathing mechanisms unless supplemental breaths are delivered. Because of this, I assumed mean airway pressure wouldn’t play a significant role in NIV. I was wrong.

Over time, I began to question what might be better for patients: delivering breaths through the nose using noninvasive positive pressure ventilation (NIPPV) or maintaining continuous positive airway pressure (CPAP) through the nose. Which approach was more effective? Was one safer than the other? To answer this question, I turned to a pivotal study by Dr. Haresh Kirpalani, a Canadian physician who researched this topic during his time in Washington, D.C. The study, published in The New England Journal of Medicine in 2013 (A Trial Comparing Noninvasive Ventilation Strategies in Preterm Infants), sought to compare these two strategies in preterm infants.

Key Findings of the Study

Dr. Kirpalani’s study explored whether NIPPV—delivering breaths through the nose—or CPAP—maintaining a continuous positive pressure—offered better outcomes for preterm infants. The findings were intriguing. There was no substantial difference between the two strategies in terms of preventing complications. There was a slight advantage for avoiding breaths through the nose, but the difference was minimal, just a few percentage points. Importantly, the rates of bronchopulmonary dysplasia (BPD) were nearly the same in both groups.

This was surprising to me. BPD, a chronic lung condition, is commonly associated with invasive mechanical ventilation and prolonged exposure to high oxygen concentrations. These preterm infants, however, had never been intubated. How could they develop BPD? This challenged my understanding of the condition and highlighted the complexity of its underlying mechanisms.

Rethinking Assumptions

Dr. Marty Kessler once made a thought-provoking observation about our attachment to terminology in respiratory care. He said, “I think we’re misled by these terms.” Terms like continuous positive airway pressure, high-flow nasal cannula, and noninvasive ventilation create an impression of minimal intervention. They suggest that these methods are inherently safer or less likely to cause harm compared to invasive approaches. Yet, as this study demonstrated, even noninvasive techniques can contribute to conditions like BPD.

The Implications

The findings of this study—and my reflections on it—serve as an important reminder of the nuanced nature of respiratory support. While NIV strategies like NIPPV and CPAP are invaluable tools, they are not without risks. Mean airway pressure, even during noninvasive support, can play a critical role in patient outcomes. it is not just about delivering the right therapy; it is about understanding the potential consequences of each approach and tailoring care to the individual needs of the patient.

Dr. Marty Kessler made an important observation during a conference we attended together. He pointed out that regardless of the terminology we use—whether it is CPAP, high-flow nasal cannula, or noninvasive ventilation—all these techniques share three critical components: pressure, flow, and ventilation. Even in noninvasive strategies, maintaining sufficient pressure and flow is essential to adequately ventilate the patient. Without these, complications can arise.

The Challenge of Maintaining Pressure

Dr. Kessler emphasized that a CPAP level must be sufficient to keep the lung open, even when the patient is not intubated. This principle ties into the concept of lung protection. If the lung collapses, particularly in a surfactant-deficient state, reopening it becomes more challenging and can cause injury. Dr. Jack Emerson, an early pioneer of the iron lung, referred to this phenomenon as “sticky lung syndrome.” He described how surfactant-deficient alveoli tend to stick together when they collapse. Reopening these collapsed alveoli can result in shear stress and lung injury, even with noninvasive techniques.

Dr. Emerson’s insight underscores an important reality: just as patients can experience ventilator-induced lung injury (VILI) with invasive strategies, they can also suffer lung injury from noninvasive methods if pressure and flow are inadequate. Persistent attempts to maintain noninvasive support in a struggling patient can sometimes do more harm than good.

When to Transition to Intubation

One of the key lessons from these discussions is knowing when to transition from noninvasive to invasive ventilation. Dr. Kessler explained that while noninvasive strategies are often preferable, there are cases where intubation and low-pressure, low-volume lung-protective ventilation may be the safer and more effective option. Administering a dose of surfactant in such scenarios can help stabilize the lung, making it easier to extubate the patient later.

A colleague in Canada shared a compelling example of this principle in action. They had a 24-week-old preterm infant who was started on nasal prongs immediately after birth. Initially, the infant responded well and defied the odds, maintaining stability on noninvasive support. However, over time, the team struggled to maintain adequate ventilation. Despite their best efforts—repositioning the prongs, switching systems, and adjusting the patient—they couldn’t achieve stability. After 24 days of noninvasive ventilation, they decided to intubate the infant.

What was striking was the infant’s first chest X-ray post-intubation, which revealed chronic lung disease (CLD). This was surprising, as the patient had never been intubated prior to that point. The cause? Insufficient or unstable mean airway pressure during noninvasive support. The lesson was clear: sufficient mean airway pressure is critical to maintaining functional residual capacity (FRC) and alveolar inflation. Without it, the lung remains unstable, even in a noninvasive strategy.

Noninvasive Ventilation: Not Always "Noninvasive"

Dr. Kessler’s reflections challenge the notion that noninvasive ventilation is entirely “noninvasive.” While it avoids the physical invasiveness of endotracheal intubation, it can still cause harm if mean airway pressure is insufficient to maintain stable lung function. In this way, “noninvasive” can be a misnomer. The absence of an endotracheal tube doesn’t negate the physiological invasiveness of inadequate support.

The take-home message is this: noninvasive strategies are highly effective when applied correctly, but they require careful attention to mean airway pressure. If mean airway pressure is too low or unstable, noninvasive ventilation can fail, leading to lung injury and complications like CLD. Achieving therapeutic outcomes hinges on delivering adequate pressure, flow, and ventilation. Noninvasive may be better in many cases, but it is only truly noninvasive if it provides sufficient support to maintain stable lung function.

Recruitment Maneuvers and Optimal MAP 

Ventilating patients effectively requires an open lung strategy. For noninvasive ventilation to work, the lungs must remain open, which often involves recruitment maneuvers. However, if mean airway pressure is critical and too much or too little can be problematic, the question becomes: how do you optimize it? What is the best way to recruit and stabilize the lungs while avoiding injury?

Learning from a New Perspective

I recently discussed this topic with Dr. Molly, a physician I admire greatly who works at a hospital in Winnipeg, Manitoba. She is not only a colleague but also a friend, and I had the pleasure of having dinner with her during a visit to her hospital. Our conversation drifted to a pivotal moment we shared years earlier at the PAS conference in Washington, D.C., where Molly attended a lecture that left a lasting impression on both of us.

At that conference, Molly was intrigued by an anesthesiologist’s perspective on lung recruitment strategies. She recalled how she had initially planned to challenge the presenter, confident in her own NICU experience. Yet, after hearing his approach, she found herself rethinking some deeply held beliefs. The anesthesiologist argued that many ICU and NICU patients, particularly babies, are recruited improperly. He explained that high-pressure, short-duration breaths, often used in the ICU, can push the lungs into the injury zone, increasing the risk of barotrauma and other complications.

A Different Recruitment Strategy

The anesthesiologist described his approach to recruiting patients during surgery when their lungs had collapsed. Instead of giving a short, high-pressure breath, he advocated for a longer-duration, lower-pressure breath. For example, he would hold a breath 5 to 8 cm above PEEP (and no more than 15 cm in extreme cases) for 20 to 30 seconds. After releasing the pressure for four to five seconds, he would repeat the maneuver two or three times. In nearly all cases, this method restored lung function without causing injury.

Molly relayed this to me with a big smile, admitting she had been skeptical at first. “We cannot give 20- or 30-second breaths in the ICU,” I said. She agreed but suggested we could modify the strategy with one- to three-second breaths at lower pressures. “It’s safer than it sounds,” she explained. “The anesthesiologist emphasized that longer inspiratory times are far less dangerous when pressures are kept low. it is the combination of high pressure and long inspiratory time that increases the risk of injury.”

Optimizing Mean Airway Pressure Safely

Molly explained how her team applies these principles in their unit. After optimizing PEEP to ensure the lungs remain open, they often transition to high-frequency ventilation. This approach allows them to maintain higher mean airway pressures safely, as the oscillatory nature of high-frequency ventilation (CPAP with a wiggle) minimizes the risk of overdistension and injury.

She emphasized the importance of keeping the lungs open while using the gentlest means possible. “The take-home message,” she said, “is to optimize mean airway pressure to open the lungs and keep them open, but to do so gently. Recruitment maneuvers should be tailored to the patient, using lower pressures and longer durations to avoid harm.”

The Future of Recruitment Research

Inspired by these discussions, Molly’s team and others have begun exploring the best ways to recruit and stabilize lungs effectively. Preliminary studies suggest that a longer inspiratory time with lower pressures is more effective and less injurious than shorter, high-pressure recruitment strategies. Additional research is underway to examine whether simply raising PEEP or mean airway pressure alone can achieve the same results or whether recruitment breaths are necessary for optimal outcomes.

The hope is that these studies will provide clear evidence for the safest and most effective recruitment methods, ensuring better outcomes for patients in the ICU, NICU, and PICU. As Molly put it, “We need to find the balance—enough pressure to open the lungs but not so much that we cause harm. And we need to use every tool and strategy at our disposal to get it right.”

This ongoing research represents an exciting opportunity to refine our understanding of lung recruitment and improve how we manage mean airway pressure. I look forward to sharing more about these findings as they develop, but for now, the key takeaway is clear: recruitment and stabilization must be done with care, precision, and a focus on gentle, patient-centered strategies.

MAP vs NAP in the Produce Section

Ventilation, like grocery shopping, requires balance, observation, and attention to detail—at least that is how I see it. My wife, who’s far better at navigating grocery stores, loves to remind me how chaotic I find them. On Mother’s Day, she convinced me to join her on a grocery run. How could I refuse on her special day? Reluctantly, I agreed, thinking I could survive one trip. Little did either of us know how the produce section would ignite my respiratory therapist brain.

When we got to the produce section, I couldn’t help myself. Suddenly, I saw lung dynamics everywhere. “Look at these vegetables,” I exclaimed. “That is a great example of a good distribution of tidal volume. Over there, hyperinflation! And here, underinflation.” My wife, a fellow respiratory therapist, stared at me, baffled. “What are you talking about? We’re here to shop!” But I couldn’t stop. This was too exciting.

I pointed out the divine ripened tomatoes. “These are perfect! They represent optimal lung inflation. See how balanced they are?” Then I held up the heirloom tomatoes and explained how their irregular shapes resembled overinflated alveoli, with their stems acting like pulmonary capillaries. “And look at these habanero peppers,” I continued. “When insufficient PEEP lets the alveoli collapse, they look just like this—uneven and deflated.”

As we moved through the store, I found more metaphors. A broken bag of frozen peas scattered on the floor became pulmonary interstitial emphysema. Clumps of ruptured alveoli spilling into tissue spaces came vividly to life through the imagery of scattered peas. My wife rolled her eyes, begging me to move on. But I was having too much fun.

By the end of the trip, she was regretting bringing me along. “Never again,” she declared, assigning me errands elsewhere in the store whenever we shop together. Despite her exasperation, the trip reminded me of something profound: ventilation, like selecting produce, requires care. Too much pressure, and you risk damage; too little, and the lungs fail to function. Each lung, much like each tomato, has unique needs that must be respected.

The Take-Home Message: Individualized Care

This playful metaphor brings us back to a critical point about ventilation: no two patients are the same. As respiratory therapists, our job is to assess, adapt, and respond to each patient’s unique pathophysiology. My colleague, Marty Kessler, often says, “It is very important to tailor your strategy to the pathophysiology. Choose the right strategy for the right disease.” To that, I would add: “It is equally important to change the strategy as the pathophysiology evolves.”

This is what makes our profession so rewarding and vital. Our expertise lies in our ability to understand pulmonary dynamics and hemodynamics, identify what each patient needs, and continuously adapt. We don’t take a cookie-cutter approach because the same strategy that worked for one patient might fail for another. This adaptability is what makes us the experts in pulmonary care.

Critical Thinking: The Heart of Respiratory Therapy

Our role as RTs demands critical thinking—skills that grow with every shift, patient, and case. Bedside care is dynamic, requiring us to make real-time decisions and adjust as conditions change. Sessions like those offered by Continued are invaluable in honing our knowledge and keeping us at the forefront of respiratory care.

So, the next time you’re in the produce section, maybe you’ll think of tomatoes, peppers, and peas in a new light. More importantly, remember the delicate balance required to ventilate and protect the lungs. By optimizing mean airway pressure—finding that sweet spot between too much and too little—we ensure better outcomes for our patients. And if nothing else, let this story serve as a reminder: never take a respiratory therapist grocery shopping!

Thank you for allowing me to share my thoughts on mean airway pressure, its impact on pulmonary dynamics, and the parallels we can draw from everyday life. It is these connections and insights that make our profession both challenging and deeply rewarding. Now, let’s dive into the questions you have for me.

Questions and Answers

You mentioned in your talk about the importance of PEEP. Why do you think we don’t give enough PEEP, and why is that significant?

that is an excellent question. My colleagues and I use a term we jokingly call “PEEPophobia.” For some reason, many clinicians are more apprehensive about increasing PEEP than they are about mean airway pressure (MAP). I have seen this repeatedly, particularly with high-frequency ventilation. For example, on devices I worked with, we displayed both PEEP and MAP. Over time, we noticed people were much more hesitant to increase PEEP.

Why? It could be that MAP is calculated—it’s an average of several variables and doesn’t have a direct adjustment knob. On the other hand, PEEP is tangible; you turn a knob, and the change is immediate. This directness may make it feel riskier. I’ll admit, I was once “PEEPophobic” myself. But we must overcome that fear. Properly optimizing PEEP is critical for patient care and stability, especially when trying to prevent lung collapse and ensure proper oxygenation.

Regarding noninvasive ventilation (NIV), what adjustments or precautions would you recommend when NIV doesn’t seem to provide sufficient MAP for a patient with hemodynamic concerns?

that is a great question. One key thing to remember is not to assume the pressures displayed on the NIV device are entirely accurate at the patient’s airway. Resistance in the system, such as prongs or mask interfaces, can significantly affect delivered pressure. A doctor once told me about a case where they set a pressure of 6 cmH₂O on a patient, but when the prongs were laid on the bed, the device still displayed 4 cmH₂O—clearly inaccurate.

If a patient is not responding well to NIV, start by ensuring the prongs or mask are positioned correctly. Next, verify that you’re delivering enough pressure to keep the lungs open. I would err on the side of providing slightly more pressure rather than less. Remember, noninvasive systems are prone to under-delivering pressure compared to invasive systems. that is why careful monitoring and adjustments are crucial when managing patients on NIV.

You discussed near-infrared spectroscopy (NIRS) for monitoring cerebral and renal tissue oxygenation. Is this technology frequently used in practice, especially in the pulmonary and RT fields?

Unfortunately, no, it is not as widely used as it should be. Years ago, I worked at a hospital that was an early adopter of this technology, and I saw its benefits firsthand. However, in many newborn intensive care units (NICUs) and pediatric ICUs I visit, I don’t see it being implemented as often. NIRS has immense potential—not only for monitoring but also for preventing injuries by giving clinicians a real-time “heads up” before harm occurs.

Technologies like NIRS and electrical impedance tomography (EIT) could significantly improve decision-making in patient care, but they haven’t fully caught on yet. it is a great question, and I hope to see more widespread adoption of these tools in the future, as they align perfectly with our goal of proactive, rather than reactive, care.

To wrap things up, what’s the overarching takeaway from your presentation on MAP and its role in ventilation?

The key takeaway is this: get the lungs open and keep them open. Optimizing MAP is crucial in achieving this balance. Too much MAP can cause overdistension and injury, while too little leads to alveolar collapse and inadequate oxygenation. We must tailor ventilation strategies to each patient’s unique physiology and needs.

Critical thinking is essential, and we cannot use a one-size-fits-all approach. Every patient’s condition evolves, and we must adapt accordingly. As RTs, our role is to assess, identify the pathophysiology, and apply strategies that maximize outcomes while minimizing risks. With ongoing education and tools like NIRS, EIT, and careful PEEP adjustments, we can elevate our care standards.

References

Acherman, R. J., Siassi, B., deLemos, R., Lewis, A. B., & Ramanathan, R. (n.d.). Cardiovascular effects of HFOV with optimal lung volume strategy in term neonates with ARDS. USC School of Medicine, Division of Neonatology, and Children's Hospital of Los Angeles, Division of Cardiology, Los Angeles.

Amato, M. B. P., Meade, M. O., Slutsky, A. S., Brochard, L., Costa, E. L. V., Schoenfeld, D. A., Stewart, T. E., Briel, M., Talmor, D., Mercat, A., Richard, J. C. M., Carvalho, C. R. R., & Brower, R. G. (2014). Driving pressure and survival in the acute respiratory distress syndrome. New England Journal of Medicine, 372(8), 747-755. https://doi.org/10.1056/NEJMsa1410639.

Friedlich, P., Subramanian, N., & Garg, M. (n.d.). Marked reduction in MAP and OI using HFJV in neonates with severe refractory hypoxemic respiratory failure. Children’s Hospital Los Angeles, Division of Neonatology, Keck School of Medicine, University of Southern California, Los Angeles, CA.

Fu, Z., Costello, M. L., Tsukimoto, K., Prediletto, R., Elliott, A. R., Mathieu-Costello, O., & West, J. B. (1992). High lung volume increases stress failure in pulmonary capillaries. Journal of applied physiology (Bethesda, Md. : 1985), 73(1), 123–133.

Kirpalani, H., Millar, D., Lemyre, B., Yoder, B. A., Chiu, A., & Roberts, R. S., for the NIPPV Study Group. (2013). A trial comparing noninvasive ventilation strategies in preterm infants. New England Journal of Medicine, 369(7), 611-620.