Ventilators

Pressure support ventilation is similar to non-invasive bilevel positive pressure ventilation, and it is generally used as the weaning mode when working toward extubating a patient. An awake patient with an intrinsic respiratory drive will set the rate (you can set a safety back-up rate if the patient is tenuous). The machine will sense when the patient is trying to take a breath by the negative inspiratory force, and it will trigger a pressure-supported breath. The pressure support is removed when exhaling (it senses this by changing flow rates), but the ventilator keeps a set amount of pressure in the lungs at the end of exhalation to prevent atelectasis (PEEP: positive end-expiratory pressure).  

Parameters:

• Driving Pressure (pressure above the PEEP to deliver)

  • Start at 10 cm H2O

• PEEP

  • Start at 5 cm H2O

• FiO2

Notes: 

• Increasing pressure support (the driving pressure) will increase the amount of volume a patient gets with each breath. If a patient is tachypneic on PSV, it might be because they aren't getting large enough breaths. Increasing the pressure may decrease air hunger. High driving pressures suggest the lung has poor compliance, and this may be injurious to the lung over time. 

As the lungs get sicker, such as progressing toward ARDS, compliance falls. This means that it takes more pressure to get the lung the same amount of volume. (Compliance = Volume / Pressure). Therefore, a patient with worsening pulmonary disease on set PSV will get smaller volumes compared to their healthy state. Diseased lungs have smaller aerated volumes ("baby lung" compared to normal "adult lung"), and ventilating "baby lung" with standard tidal volumes increases the wall strain and pressure and can lead to ventilator-induced lung injury. More on this in the ARDS section... 

Remember, minute ventilation is the product of the tidal volume and the respiratory rate. A patient with progressively worsening lungs and compliance on PSV will become more tachypneic with time to compensate for the dropping volumes. The reverse is true: a patient with improving lungs and compliance will get progressively bigger delivered tidal volumes and slow their respiratory rate. Relating the respiratory rate and tidal volumes on PSV can give one insight into the health and compliance of the patient's lungs. The rapid shallow breathing index (RSBI) does just that. RSBI = frequency of breaths (breaths per minutes) / tidal volume (Liters). A patient with healthy lungs will take infrequent breaths with good tidal volumes, resulting in a low RSBI. A patient with sick lungs will be breathing rapidly and only getting small tidal volumes, resulting in a high RSBI. This is why it was studied as a parameter to help with extubation (a RSBI < 105 is a good prognostic sign for remaining extubated).

Okay, but you've just intubated the patient, and they have no respiratory drive. PSV is not a good choice for them, so you need a different mode... 

The patient declined and got a rapid sequence intubation, so they're paralyzed and sedated. They currently have no respiratory drive. PSV is a bad idea in this situation, since it only supports a patient's breaths, and this patient is not initiating any breaths. You need a ventilator mode that will deliver a desired minute ventilation without needing input from the patient: controlled mechanical ventilation (CMV) fits the bill. This is the mode both Assist Control (AC) as well as Synchronized Intermittent Mandatory Ventilation (SIMV) become when the patient is not initiating breaths.

Basic Parameters: 

• Vidal volume (Vt) OR (less commonly) maximum pressure

  • If using volume-cycled (VC) CMV (meaning you want a desired tidal volume with each breath), set an initial Vt at 6-8 cc/kg of ideal body weight and titrate to prevent barotrauma.

  • If using a pressure-cycled (PC) CMV (meaning you want to set the maximum pressure of each breath), start around 10 cm H2O of driving pressure (Pd) and titrate to ensure volumes are adequate without causing barotrauma. 

• Respiratory rate (RR)

  • Target a minute ventilation (Vm) around 6-8 L/min in healthy individuals. (e.g., a healthy patient set a 500 ml/breath will need a RR set around 12 breaths/min to achieve a Vm of 6 L/min: 6,000 ml/min / 500 ml/breath = 12 breaths/min). 

  • A patient with underlying metabolic acidosis will need a much higher Vm to start, so target around the mid-to-high 20s to match their pre-intubation RR and then get an ABG in 30 minutes to titrate the Vm from there. Rates > 30 can run into auto-peep (where a patient's last breath hasn't been fully expired leading to trapped gas and high pressures) as well as increased dead space (re-breathing un-expired gasses and decreasing the efficacy of each breath). 

• PEEP

  • Set at 5 cm H2O to start, then follow a PEEP ladder or titrate to minimum driving pressure (more on this later in the ARDS section). 

• FiO2

  • Start at 100% and titrate down <50% as quickly as tolerated to keep oxygen saturations (SpO2) > 88%. (This goal can be higher in certain pathologies such as traumatic brain injuries where there are PaO2 targets).  

What happens with CMV when the patient starts to wake up and their respiratory drive picks back up? Well, "we" mostly use AC and SIMV modes. Remember, while these modes become CMV when the patient doesn't have a respiratory drive, they differ when the patient starts to initiate breaths. 

Assist Control will always deliver at least the number of breaths you set the RR to and will always deliver the Vt or maximum pressure you set based on if you are in volume-cycled or pressure-cycled AC respectively. In addition to this mandatory baseline, when the patients begins to breathe on their own, AC will sense the negative inspiratory effort and give the patient a fully supported breath (to the set Vt or pressure) each and every single additional breath. This can be great: that frail old patient with pneumonia and COPD and tiny respiratory accessory muscles needs all the help they can get. If they need to take more breaths than what you've set them at, they will get fully supported each breath, decreasing their respiratory workload and the CO2 generated by their respiratory muscles. 

In an attempt to make this more comfortable for the patient, let's try and synchronize the ventilator's mandatory breaths with the patient's intrinsic respiratory drive. This is what SIMV attempts to do. Just like AC, SIMV will deliver at least the RR you set and ensure the each of those mandatory breaths get the set Vt or Pd. Its algorithm differs in the fact that it tries to synchronize the mandatory breaths up with the patient's breaths. This may make it more comfortable when the patient is starting to wake up and initiate breaths on their own below, or at, the set RR. That sounds nice, and it may be more comfortable, but let's look more into what happens when the patient's start to over-breathe the ventilator. 

AC and SIMV differ a lot when the patient is initiating breaths over the set RR. AC will sense the negative inspiratory effort of an additional breath and give a fully supported (Vt or Pd) breath with each trigger. Again, this can be great if you have a frail patient who needs full metabolic and respiratory support, like those found in the medical intensive care units. But, what happens if they are in the trauma surgical critical care unit and they're a young, agitated traumatic brain injury patient? They will get a supported breath even when breathing 30 times a minute or higher. This can rapidly lead to hyperventilation and hypocapnia, which can cause ischemic damage to the penumbra. Worse, they might not be able to exhale each breath fully and start to stack breaths, leading to auto-peep (where pressure is building up in the lungs with each breath due to the inability to fully exhale a delivered Vt before initiating the next breath) and potentially barotrauma. 

What would SIMV look like in the young TBI patient? Additional breaths are allowed, but they are not supported at all. The patient will only get the Vt that they can pull through the circuit. This prevents the hyperventilation and auto-peep worries with AC, but you can see how this may cause additional workload to the patient. A frail older patient may not be able to get a significant volume from an additional breath on SIMV. This can cause air hunger and a reflexive increase in the RR, but they're too weak to get meaningful Vt through the circuit, so their metabolic demand increases and so will their CO2. This is one reason why MICUs and SICUs often chose AC and SIMV respectively: it's due to different underlying patient populations and their differing ability to wean from the ventilator. 

Now, you can augment SIMV with PSV to decrease the work of breathing the patient has with additional breaths while still trying to gain the synchronized comfort of the modality. This is called SIMV + PS, and each additional breath above the set RR is supported the same way PSV supports each breath. It is important to titrate the pressure support on SIMV + PS to reduce work of breathing and air hunger but to prevent auto-peep and breath stacking. It is not a "set-it-and-forget-it" value. 

Airway Pressure Release Ventilation (APRV) is also a comfortable mode of ventilation, and it can be used as a primary ventilation mode in awake patients with intact respiratory drives, but we'll talk more about it in the ARDS section. 

You're on the international space station (or in a hyperbaric chamber) and only have access to a high-pressure oxygen line. How do you ventilate an incapacitated crew member now?

First, you would step down the high-pressure onboard oxygen system with a regulator. Then, if needed, you would use a venturi valve to entrain some ambient air to dilute the 100% Oxygen down to whatever FiO2 you want to deliver. Then, you would hook up a simple pressure-cycled ventilator. This simple device delivers a set pressure at a set respiratory rate all driven by the input pressure (generally an oxygen tank) and simple valves. These types of devices don't allow you to adjust the flow rate or measure airway pressures, so you definitely need to set the pressure carefully to avoid high peak-airway pressures that could lead to barotrauma and pneumothorax! Have a low threshold for using ultrasound to assess for pneumothorax if the patient is deteriorating (you generally can't auscultate well in these types of environments). 

Your patient is now set up on the ventilator and you've chosen a Volume-Cycled Assist Control mode (VC-AC) because you're worried about work of breathing. Initial settings were as follows:

• Vt: 420 mL

• RR: 14

• PEEP: 5 cm H2O

• FiO2: 100%

An ABG showed a pH of 7.30, a paCO2 of 50, and a paO2 of 450. The SpO2 is 100%. To stop drawing ABGs (which are expensive), you correlate the paCO2 with the end tidal CO2 (EtCO2) which is reading at 56 and note the 6-point delta (normal). You increase the RR to 20 and the EtCO2 comes down to 46, suggesting a PaCO2 of around 40. Over the next few hours, you rapidly wean the FiO2 to 40% and the patient's saturations tolerate that well, remaining well over 88%. 

Why did you make these changes? In standard ventilatory modes we can break down CO2 control and O2 control into different parameters. CO2 diffuses very rapidly across membranes, about 20 times faster than oxygen. This means that CO2 is more dependent on the amount of times gas exchange can occur to reset the gas gradient across the membrane and less dependent on the total surface area available for gas exchange. Thus, CO2 levels classically are taught to be directly linked to total minute ventilation (Vm) and less linked to alveolar recruitment, though both are true. Vm is equal to the product of RR and Vt, so increasing the RR or the Vt can increase the rate of CO2 removal. Since we avoid high tidal volumes nowadays (courtesy of generalized application of the ARDSnet study), the RR is generally used to compensate for high CO2 levels. Remember, the RR can only increase so much, since breath stacking/auto-peep can occur, and high rates can lead to increased dead space. High CO2 levels that cannot be managed with further adjustments in Vt or RR are accepted as unavoidable, termed permissive hypercapnia. Outside of certain pathologies, this is generally well tolerated. 

What about oxygenation? Oxygen is slower to diffuse than CO2, and it takes 1/3-1/2 of the entire pulmonary capillary distance to equilibrate. This rate limitation means that oxygen diffusion becomes more dependent on the total surface area open for gas exchange than CO2: Oxygenation is dependent on the number of recruited alveoli. Recruitment takes pressure over time, not short bursts or "recruitment maneuvers," so alveolar recruitment is proportional to mean airway pressure (MAP). In standard AC and SIMV modes, the majority of the time is spent in exhalation at the pressure level of the set PEEP. Therefore, the PEEP level drives the majority of the MAP. Increasing PEEP will increase the MAP. Increased MAP over time will recruit collapsed alveoli, increasing surface area for oxygen diffusion and improving oxygenation. This principle will become important when talking about PEEP titration later. 

The reason the FiO2 was down-titrated so quickly was to reduce oxygen toxicity. Hyperoxia can cause toxicity through free radicals. Healthy people can get tracheobronchitis and even full-blown ARDS just by being placed on 100% for 24-48 hours. This is why FiO2 is titrated down below 50% (a safe level) as soon as physically possible. When patients get hypoxic on the ventilator, it is reasonable to temporarily increase the FiO2 while you work up the cause and increase the PEEP to slowly re-recruit any collapsed alveoli (assuming right heart failure isn't the cause...). This is why PEEP tables exist, to ensure adequate peep is being used for a given FiO2. 

So, to summarize: 

• CO2 management is dependent mostly on Vm

  • Vm = RR x Vt

  • Increasing RR or Vt will decrease PaCO2

  • Decreasing RR or Vt will increase PaCO2

• O2 management is dependent mostly on MAP and FiO2

  • Increase PEEP to increase MAP

  • Increase FiO2 to increase oxygen concentration

Unfortunately, 5 days later the patient self-extubates, aspirates, and gets immediately reintubated with concern of aspiration pneumonitis. 

Right after the intubation, the ventilator is reading peak inspiratory pressures (PIP) at 30 cm H2O, and you perform a manual inspiratory hold to determine that the plateau pressure (Pplat) is 25. Two days later, after a rocky inflammatory period, the PIP is 35 and the Pplat is 30. What has changed?

First let's learn about peak and plateau pressures. Imagine breathing through a long straw. It takes more pressure than normal to inhale and exhale through the straw because of the flow resistance in the straw. Now, imagine putting a balloon onto the end of the straw and trying to blow up the balloon. Not only do you have to generate enough pressure to overcome the flow resistance in the straw, but you also have to generate enough pressure to overcome the elastic collapsing pressure of the balloon to inflate it. Once you have the balloon inflated to the desired volume, you clamp the inlet and tie it off. As there is no more dynamic flow occurring, the static pressure in the balloon is only counteracting the elastic collapsing pressure of the balloon (ignoring atmospheric pressures) and is related to the balloon's compliance: a thick balloon will require more pressure to inflate to a set volume compared to a thin balloon. 

This "straw and balloon" scenario is analogous to how the ventilator works. At end exhalation, the pressure on the ventilator is the set PEEP. As a breath is initiated, the ventilator pushes air down the circuit and airway into the alveoli to expand them. The peak inspiratory pressure (PIP) is the summation of the pressure needed to overcome airway resistance, the elastic collapsing pressure of the alveoli, and the PEEP. After the dynamic phase of inflation is done, a manual inspiratory hold traps the Vt delivered in the lung and the ventilator can measure the static pressure required to keep the lung inflated, which is the plateau pressure (Pplat). The difference between the plateau pressure and the PEEP is the driving pressure (just like Pd in PSV), which is representative of the strain in the lung caused by the breath to inflate to the desired Vt. High driving pressures translate to large strains and an increased risk for ventilator associated lung injury (try to keep Pd < 15 cm H2O). 

The PIP is calculated automatically by the ventilator for every breath and displayed. A manual inspiratory hold, generally > 3 seconds to allow for complete cessation of flow, is required to find the Pplat. (Pplat can only be calculated on non-spontaneous breaths, since the patient is generating an additional negative inspiratory force when spontaneously breathing). A dry, healthy lung with lots of surfactant and good compliance will have low elastic collapsing pressures (low Pplat). A wet, diseased lung with poor surfactant production will have poor compliance and a high elastic collapsing pressure (a high Pplat). 

A high PIP will indicate one of three things: (1) high airway resistance, (2) poor lung compliance, or (3) both. If a patient has a mucous plug in the endotracheal tube, the PIP may read high. A manual inspiratory hold will show a normal Pplat, cluing you into the fact that the PIP is mostly from flow resistance and not compliance issues. If a patient has developed ARDS and the PIPs are high, a manual inspiratory hold may reveal a high Pplat and a small difference between the PIP and Pplat. This will clue you in to the worsening compliance of the lung relating to the worsening ARDS. A high PIP with a high Pplat and a large delta will be from both airway resistance problems, likely mucous plugs or obstructive lung disease, as well as poor compliance, such as pneumonia or ARDS. The upper limit of Pplat is generally around 30 cm H2O to reduce barotrauma risk, though patients with heavier chest walls may tolerate higher plateau pressures to counteract the heavier chest wall and increased intraabdominal pressures. 

The first, and most important, thing that you need to understand about ARDS is that is not a disease, but a syndrome. That means you have to find and treat the underlying cause while managing ARDS. There are a wide variety of pathologies that can cause ARDS, including pulmonary and non-pulmonary diseases. So, while you're optimizing the ventilator to respond to ARDS, you should be evaluating and treating the underlying cause. 

So, what constitutes acute respiratory distress syndrome?

• Acute onset (<7 days)

• Diffuse bilateral pulmonary infiltrates

• Not exclusively due to heart failure

• PaO2/FiO2 <300 despite a PEEP greater than or equal to 5 cm H2O. 

  • Mild: P/F < 200-300

  • Moderate: P/F < 100-200

  • Severe: P/F < 100

Before you go and diagnose ARDS though, make sure you optimize the ventilator for 12-24 hours to rule out pseudo-ARDS, which is something that meets criteria for ARDS initially but rapidly improves. A good example of this is aspiration pneumonitis. It may meet all the criteria initially, but with good ventilator and critical care, the P/F ratio will rapidly turn around. True ARDS does not rapidly turn around and is associated with a higher mortality rate.

As a healthy adult lung goes into ARDS, previously recruited alveoli get filled up with fluid, causing a local shunt and preventing gas exchange. Hypoxemia ensues due to the worsening shunt. Additionally, surfactant is broken down and dysregulated, leading to alveolar collapse and poor lung compliance. Without surfactant, the collapsed alveoli are very difficult to re-recruit due to surface tension. An adult lung that could easily handle a Vt of 500 mL now only has a small portion that is still ventilated. This is adorably termed "baby lung." If you still attempt to ventilate the "baby lung" with adult lung volumes, you can cause injury to the remaining recruited alveoli. 

It is important to briefly discuss the outcomes of the ARDSnet trial. Patients used to be ventilated with Vt around 12 cc/kg. The ARDSnet trial found a mortality reduction associated with lower tidal volume ventilation (6 cc/kg). This is incredibly important and highlights that ventilator associated lung injury is real. The "baby lung" gets injured with too much pressure or volume, and this begets worsening ARDS. Therefore, it is paramount to reduce trauma to the remaining "baby lung" by limiting the pressure, volumes, and strain delivered to it while waiting for the rest of the lung to re-recruit and recover. 

As ARDS worsens, hypoxemia occurs from progressive shunting and high plateau pressures are caused by worsening compliance. (Additionally, pulmonary arterial pressure will increase due to hydrostatic collapse of capillaries in de-recruited lung segments). How do we treat hypoxemia? That's right, by increasing the mean airway pressure and, if needed, the FiO2. Higher MAPs over time will slowly re-recruit some diseased lung segments. This distributes the delivered Vt over more alveoli, decreasing the overdistension of the "baby lung" and leading to improved compliance. In standard ventilator modes, such as VC-AC or VC-SIMV, PEEP is the main way to increase MAP. PEEP ladders have more meaning now, don't they?

So how does this really work? Our post-aspiration patient is heading into ARDS territory. They were previously on a PEEP of 5 and the nurse increased the FiO2 to 100% as a rescue until you were able to get to bedside. After examining the patient and reviewing the x-ray and labs, you determine the patient is in ARDS (or at least pseudo-ARDS) from aspiration. The saturations are around 90% on these settings. The PIP is 35 cm H2O and Pplat is 30 cm H2O. Remember that the Pd is the difference between the Pplat and the PEEP, so this patient's Pd is 25 cm H2O. That's too high! You first ensure the patient is on appropriate low tidal volume ventilation at 6 cc/kg of ideal body weight. They are. You can now try a PEEP ladder or titrate the PEEP yourself. You chose the latter. 

Remember, the Pplat is near your upper limit (30 cm H2O), but you know that a large part of that is because of the amount of de-recruited lung. You up the PEEP to 10 cm H2O and give it a few minutes. You remeasure the Pplat and it is... 30 cm H2O still. What happened? 

Though you increased the PEEP, which should have increased the Pplat, the Pplat curiously stayed the same. This means you were able to re-recruit some lung! The Vt was distributed to more alveoli, improving compliance and dropping the strain on the, now bigger, "baby lung." The Pd is now 20 cm H2O, down from 25. You try a PEEP of 15 cm H2O now and give it a few more minutes. You remeasure the Pplat and... it is still 30! You have re-recruited even more lung and dropped the Pd to 15. You decide to try again with a PEEP of 20 cm H2O. A few minutes later, the Pplat is now 35 cm H2O. What does this mean?

This means that, at this time, you have recruited as much diseased lung as possible. Further attempts to increase PEEP will only result in increased Pplat without reducing the strain (Pd) on the "baby lung." You reduce the PEEP back down to 15 cm H2O and maintain it there. The sats are up to 94% with a decreased FiO2 to 50%! You are currently preventing volutrauma by limiting Vt to 6 cc/kg, you are limiting barotrauma by limiting Pplat to > 30 cm H2O, you are limiting strain on the recruited lung by limiting Pd to 15 cm H2O, and you're limiting oxygen toxicity by keeping the FiO2 at or less than 50%. Nice job! 

Unfortunately, you are called back to bedside a few hours later because of pressure alarms. The PIPs are high, and after a manual inspiratory hold you determine that the cause is a Pplat of 35 cm H2O. You try titrating around the PEEP again, but you can't seem to improve the Pd at all. What can you do now? This is where dropping tidal volumes and permissive hypercapnia come into play. By dropping the Vt delivered to the poorly compliant lung, the pressures placed on the lung will drop. You try 5 mL/kg, but that only drops the Pplat to 32 cm H2O. You then try 4 mL/kg, and this gets the Pplat to drop to 30 cm H2O again. To compensate some for the lossed Vm, you increase the RR to 28. You tried increasing the RR more, but the patient started to breath-stack. The EtCO2 is reading 70 mm Hg. This patient doesn't have a TBI or right heart failure, so you accept the hypercapnic respiratory acidosis. You did send an ABG just to confirm, and the pH is sitting at 7.10. The patient is hemodynamically tolerating this pH, so you decide not to place them on a sodium bicarb drip at this time to compensate for it (you could, but the kidneys will start to compensate soon). The patient saturation is around 90% still on an FiO2 of 50%, nice job! You recheck your to-do list. You are preventing volutrauma by limiting the Vt to less than 6 cc/kg, you are limiting barotrauma by limiting Pplat to < 30 cm H2O, and you are limiting strain on the recruited "baby lung" by keeping the Pd at or below 15 cm H2O. 

This blurb is meant more to convey the ventilator management of ARDS, so we won't go into all the additional treatment items. Maybe a future post will focus on that...

There are two major problems with conventional (VC-AC and VC-SIMV) ventilator modes in ARDS:

1. The MAP being limited by pressure by the greater time spent in the exhaled part of the respiratory cycle

   • In normal VC-AC, the time spent in exhalation is 2-4 times longer than the time spent in inhalation (an I:E ratio of 1:2-1:4). Therefore, the mean airway pressure is heavily influenced by the pressure in the lungs at end expiration (PEEP). This poses the question: would spending more time in inhalation allow for a higher MAP and more recruitment potential?

2. Often requires deep sedation to be compliant

   • The hypoxemia and (permissive) hypercapnia in ARDS drive a powerful need to hyperventilate, but additional breaths or negative inspiratory effort by the patient can lead to ventilator dyssynchrony, discomfort, anxiety, and ventilator induced lung injury. To improve ventilator synchrony and comfort during such protective and extreme ventilator settings, patients are often heavily sedated, or even paralyzed. Deep sedation and paralysis can lead to delirium and muscle breakdown. This poses the question: is there a more comfortable, lung protective ventilator setting?

Let's design a new ventilator mode and use a healthy patient for a test subject. Instead of spending most of the time in expiration, lets design this mode to spend most of the time in inspiration. This will allow the mean airway pressure to be higher than in a standard mode, allowing for maximum recruitment potential. We'll still have periods where the patient exhales, but they'll be short to prevent collapse of the newly recruited lung segments. (This change by itself is called inverse ratio ventilation). We really want to maximize the MAP without worrying about barotrauma, so let's make it a pressure-cycled mode. This way we can set the maximum airway pressure (Phigh) at a high, but safe, level AND spend most of the time at that pressure. We want to have full control of the time spent at the Phigh, so unlike traditional pressure-cycled modes, we'll make the parameters pressures and times to be at those pressures. Let's start by setting the Phigh to be 30 cm H2O, since we know plateau pressure above that can increase the risk of barotrauma (we'll maybe increase this to 35 cm H2O in morbidly obese patients). 

Let's work on the exhalation phase. Since we want to spend as little time as possible in the exhalation phase, the rate of exhalation should be as fast as possible. This means the pressure of the exhalation phase (Plow) should be set to 0 cm H2O, creating the largest pressure differential and encouraging a rapid exhale. We still want to prevent large tidal volumes, and we don't want the patient to exhale the entire breath and collapse everything that has been recruited (since the Plow is set to 0 cm H2O). Ideally, we would be able to set a Vt or Pd as the parameter that would dictate the time spent exhaled, but since our parameters are static pressures and time, we can't do that. So, for now, we'll have to set the time the ventilator is at the low pressure allowing the patient to exhale (Tlow) and assess if we're meeting our Vt and Pd goals. We can do this by setting it low, around 0.5 seconds and then assessing the ventilator. We'll want to try and keep the exhaled volume of gas < 6 ml/kg and the Pd < 15 cm H2O. A rough surrogate marker for both of those would be the flow rate. When the breath is initially released, the gas flow out of the lungs will rapidly peak, since the pressure difference between the lung and the Plow is at a maximum. As the pressure in the lung drops, the flow rate will slow. Stopping exhalation when the flow is between 50-75% of the peak flow rate will help trap gas in the lung, prevent alveolar collapse, and reduce the total lung strain. Letting the flow rate get below 50% of the peak flow rate will mean too much gas and pressure have left the lung; we won't be meeting our objective of lung protective ventilation. All this means that the Tlow is the parameter we'll have to keep an eye on each time we swing by the ventilator in this new mode. 

We've now set the high pressure we want (Phigh) at a safe value, we've set the low pressure we want (Plow) to maximize the exhalation rate, and we've set the time in expiration (Tlow) to ensure we don't exhale too much. Now we just need to determine how long we need to be at the high pressure (Thigh) to finish defining the mode parameters, and we need to determine if we want the patient to breathe over the vent or not. The first is easier to address. If we want 12 ventilated "breaths" per minute, we will divide 60 seconds by 12 breaths/minute. This would leave us with a combined inspiratory and expiratory cycle time of 5 seconds. If we have the solved the Tlow that works for our patient, we can subtract it from the total respiratory cycle time of 5 seconds. Assuming a Tlow of 0.5 seconds, the time at the high pressure (Thigh) would be 4.5 seconds. This means 90% of the time the patient is in the inspiratory mode and maximizing their mean airway pressure/recruitment potential. 

Only 12 breaths per minute? That's not enough Vm for a sick ARDS patient. You're right. You can drop the Thigh some if you need a few more "breaths" (releases) per minute. Just remember, the more releases per minute, the more time spent in exhalation and the lower the mean airway pressure. So, we'll need to try something else to overcome this problem: let's let the patient ventilate on top of the major releases. 

An awake patient on this new mode won't be able to take large addition breaths at the Phigh we initially set because they're already quite expanded. The additional breath will (and should) only contribute around 25% of the total Vm. (The Vm will be displayed on the ventilator, and we'll be able to compare the Vm allowed by the airway releases per minute and the machine's measured total Vm). Later, as the mode is weaned by deceasing Phigh, they'll be able to take bigger breaths and contribute more to the total Vm. This will make it more comfortable to the patient and allow less sedation. In fact, too much sedation will make this new mode dangerous as they'll get very hypercapnic. This mode will definitely require permissive hypercapnia at the highest settings, but the respiratory acidosis will become unmanageable if the patient isn't contributing to the Vm.

Once the patient is set up and the Phigh, Plow, Tlow, and Thigh set, we'll hopefully start seeing some re-recruitment and improvement in oxygenation. Initially we might see a drop, but we should not be surprised. This is likely due to the hemodynamic effects of such a high thoracic pressure. Prior to switching to this new mode, we'll ensure the patient is euvolemic and that we have pressors ready. If the patient is too dry, the blood pressures will drop due to decreased venous return and the oxygen delivery may suffer until the body adapts. If the patient is too hypervolemic, the increased thoracic pressures my affect the right heart until re-recruitment occurs. As previously collapsed lung segments open, hydrostatically collapsed pulmonary capillaries will open back up and the mPAP pressures will drop. As the re-recruitment occurs, we'll start to see improved oxygenation and be able to wean the FiO2 down. The FiO2 will serve as a metric for re-recruitment and weaning. If you're below 50% FiO2, you're likely able to start dropping the Phigh and stretching the Thigh out some. If the FiO2 requirements increase you've de-recruited and have shown it was too soon for the patient to wean from those current settings. 

So... you've just created Airway Pressure Release Ventilation (APRV). Nice job! Set correctly, this will increase the MAP while still serving as protective again ventilator associated lung injury. Additionally, the patient will be more awake and comfortable. Seems like a win-win-win! We'll need more studies directly comparing ventilator modes to see if it truly is...

This calculator outputs ambient pressure at a given altitude based on the 1962 US Standard Atmosphere. The partial pressure of oxygen in the alveolus uses the simplified alveolar gas equation with a partial pressure of H20 vapor of 47 mm Hg, a PaCO2 of 40, and a RQ of 0.8. This does not account for hypoxic changes in respiratory drive changing PaCO2.

FAA and FAR regulation for commercial aircraft pilots state that supplemental O2 is required for flights > 10,000 ft, 100% O2 is required for flights > 33,000 ft, and positive pressure breathing is required for flights > 40,000 ft. Pressure suits are required for flights > 50,000 ft. 

For more information on O2 systems from the FAA, click HERE.

The current US ISS spacesuit is pressurized to 226 mm Hg (0.3 bar) which is equivalent to 30,000 ft, and therefore require up to a 100% oxygen atmosphere in the suit to maintain PaO2 levels.