Airway & Respiratory, Patient Care

In-Depth Overview of Mechanical Ventilation

Issue 3 and Volume 40.

Learning Objectives

  • Learn the anatomy and physiology of normal respiration.
  • Understand the types of breaths that can be given to patients via mechanical ventilators.
  • Identify the standard settings and modes of mechanical ventilators and understand what they do.

Key Terms

  • Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS): A disease process with high mortality and morbidity affecting mainly mechanically ventilated patients. The constellation of symptoms for this disease process is hypoxia, diffuse pulmonary congestion, and diffuse inflammatory changes at the cellular level of the alveoli. ALI is the less severe of the two, with ARDS representing severe organ failure.
  • Compliance: A term used to describe how easily the lungs can inflate and stretch during inflation.
  • Pressure-limited ventilation: A form of mechanical ventilation where a ventilator uses the pressure exerted against the lungs to control the respiratory cycle.
  • Ventilation: The process by which gas moves in and out of the lungs. Although not completely accurate, ventilation is often used interchangeably with respiration, which is the process of cells exchanging materials for homeostasis (when O2 and CO2 are exchanged in the lung’s alveolar capillary beds).
  • Volume-limited ventilation: A form of mechanical ventilation where a ventilator uses the volume of air forced into the lung to control the respiratory cycle.
  • Mechanical ventilation, also known as positive pressure ventilation (PPV) is a mainstay of intensive and critical care medicine. Providers looking to further their career into flight and intensive/critical care transport must have a concrete understanding of these concepts. This article will serve to examine some of the finer details of PPV in the critically ill patient.

Anatomy & Physiology

The anatomy of the chest is fairly straightforward. The chest is the most superior cavity of a person’s trunk and is housed by the 12 ribs. The chest is separated from the abdominal cavity via the diaphragm—a large, powerful muscle that’s the driving force behind ventilation. Within the chest lie the thoracic organs (heart and two lungs) and the great vessels (aorta, vena cava, and pulmonary arteries and veins).

Each lung, when fully expanded, fills its respective side of the chest. The only remaining space is mostly occupied by the heart and great vessels. The space in between the chest wall and the lungs is known as the pleural space, and is lined by two membranes. The visceral pleura is the membrane that covers each lung and the parietal pleura lines the chest wall.

These two membranes separate and provide friction-reducing lubrication between the lung parenchyma and chest wall. When the lungs are deflated at the end of exhalation, the pleural space is basically empty and the pressure inside the thorax is essentially equal to that of the atmospheric pressure outside of the body.

The diaphragm is unique as far as skeletal muscles go. It’s a dome-like structure shaped like a doughnut with a thin but incredibly strong disk of connective tissue in the middle known as the “central tendon.” It’s anchored to ribs 6–12, the xyphoid process, and vertebrae T12, L1 and L2. At rest, the diaphragm is located just inside the rib cage—its location moves during inspiration.

Inspiration begins with the intercostal muscles stabilizing the placement of the lower rib cage. You can think of this process as the rib cage bracing itself and giving the diaphragm something sturdy to hold on to. As the diaphragm contracts, it begins to flatten out around the central tendon and dive inferiorly toward the abdominal cavity. (See Figure 1 below.) This contraction pushes the abdominal contents down into the pelvis and creates a larger thoracic cavity relative to its size when the diaphragm is relaxed. This causes a vacuum to form in the chest, by which the pressure inside the chest is less than that of the outside atmospheric pressure. The negative pressure inside the chest causes the outside air to rush in and expand the lungs. This phenomenon is collectively known as negative pressure ventilation (NPV).

Once air is in the lungs, it travels down to the alveoli and gas exchange occurs at the alveolar capillary beds.

Expiration—the complete opposite of inspiration—is a passive process in healthy people. As the diaphragm relaxes, it retreats back inside the rib cage to its resting location. This, combined with the elasticity of the lungs and the outside atmospheric pressure, expels most of the inhaled air from the lungs with the exception of a minimal amount of residual air known as the “functional residual capacity.”

When ventilation and perfusion are adequate enough to maintain homeostasis, we refer to this as “ventilation/perfusion matching” or “V/Q match” for short. When this isn’t occurring because of some pathologic process such as respiratory failure or pulmonary embolism, it’s referred to as a “V/Q mismatch.”

Figure 1: Cycle of breathing, inspiration and expiration

Introduction to PPV

As the name implies, PPV is achieved in the opposite manor of the normal physiologic process of ventilation. PPV occurs when air outside of the chest is forced into the lungs, overcoming atmospheric pressure and the elasticity of the deflated lungs.

As with any invasive maneuver, care, caution and expertise need to be exercised when considering initiating PPV, or caring for a patient being mechanically ventilated prior to your arrival. The decision to initiate PPV isn’t one to be taken lightly, especially when it involves emergent intubation. 

Although the benefits of PPV greatly outweigh the risks, in most cases, the associated risks are significant. Despite the fact the decision to initiate PPV should be immediate and based on sound clinical judgment, aggressively protecting a spontaneously patent and breathing airway is always paramount.

There are two general ways to administer PPV to a patient: noninvasive positive pressure ventilation (NPPV) and invasive positive pressure ventilation (IPPV). The main difference is that NPPV is generally achieved by way of a face mask, similar to current prehospital application of continuous positive airway pressure (CPAP). NPPV is generally reserved for patients in respiratory failure secondary to heart failure or a reactive airway pathology (i.e., chronic obstructive pulmonary disease) and should be used as an initial management of respiratory failure if it’s feasible. (For more on NPPV, read “Noninvasive Positive Pressure Ventilation: Changing the respiratory distress prehospital paradigm of ventilation & intubation” in the November issue.)

Alternately, IPPV is applied to an intubated patient. A simple way to remember this is “NPPV = non-intubated PPV” and “IPPV = intubated PPV.” In fact, many newer ventilator models simply ask, “Is the patient intubated?” rather than having the operator select “IPPV” or “NPPV,” as some ventilator settings and modes are only possible with intubated patients.  Intubation of dyspneic patients should be reserved for patients in obvious, intractable respiratory failure, or for those who’ve failed NPPV trials.

Patients with altered mental status, fulminant secretions, hyperemesis, copious/thick facial hair, or other conditions that prevent the mask from sealing wouldn’t be candidates for NPPV.

Note that the patient doesn’t need to be intubated with an endotracheal tube. IPPV, while not optimal, can be successfully achieved via supraglottic or emergency adjunct airways.

Types of Breath Delivery

The provider needs to decide what type of breath to deliver to the patient. Does the patient need a volume-limited breath or a pressure-limited breath?

In volume-limited ventilation (VLV), breaths are given to achieve a certain volume of air delivered to the lungs. VLV breaths are exclusively for intubated patients. The force associated with each breath is variable based on the patient’s compliance and pulmonary status.

Pressure-limited breaths are given in pressure-limited ventilation (PLV) in an attempt to deliver a breath at a certain amount of force for a specific length of time. The volume of air delivered during each breath is variable-based on the health and compliance of the lungs. For patients ventilated via noninvasive means, the patient is going to always receive PLV. However, depending on the type of ventilator support needed, intubated patients can receive both PLV and VLV.

In previous generations, a provider would also have to decide whether or not to allow a patient to trigger his or her own breath. Nearly all ventilators now allow patients to take their own breaths in synchrony with or in addition to the ventilator-triggered breaths. If a patient has a condition where they shouldn’t be allowed to “over-breathe” the ventilator and trigger his or her own breaths, the patient needs to be pharmacologically treated with sedative drugs and possibly paralytics to prevent a respiratory drive.

Unfavorable outcomes associated with a PPV setting that prevents a patient from over-breathing the ventilator include: barotrauma, increased intracranial/intrathoracic/intraabdominal pressures, and risk for acute lung injuries.

Types of Support & Settings

With IPPV, there are a few settings that are standard on all ventilators and are used in treating all patients. These settings are parameters that guide the ventilator in conjunction with the mode of ventilation to achieve a certain outcome.

The first setting to consider is respiratory rate (RR). The RR will either be the actual number of breaths delivered or the minimum number of breaths delivered if the patient is initiating his or her own breaths.

The RR is measured in breaths per minute and is based on the patient’s clinical needs. For instance, if the patient is retaining carbon dioxide (CO2), the RR would be increased to blow off a greater amount of CO2.

The next setting to be determined is the tidal volume (VT). The VT is the actual amount of air that will be delivered in each breath, and is measured as a volume in milliliters. VT is set using a formula that takes into account the patient’s ideal body weight (IBW) in kilograms. Depending on the patient’s clinical status, the VT is determined based on this equation: 5–8 mL x IBW kg = VT mL/kg. Patients who are suffering from or are at risk for acute lung injury and acute respiratory distress syndrome (ARDS) are typically ventilated at 5–6 mL/kg, and non-ARDS patients at a volume of approximately 8 mL/kg. Any VT > 8 mL/kg can dramatically increase a patient’s risk for barotrauma and mortality due to the development of ARDS.1 VT is only set in modes that are specific to VLV.

The product of the RR and VT is known as the minute ventilation (MV). The MV is the total volume of air inspired by the patient per minute. While the provider will set both of these criteria (RR and VT) independently of one another, they’re in essence really just setting a minimum MV.

The provider should next consider the percent of oxygen (O2) to be delivered with each breath, otherwise known as the fraction of inspired oxygen (FiO2). The goal in titrating FiO2 is maintaining a SpO2 > 93% while utilizing FiO2 as close to room air (21%) as possible.

Oxygen toxicity is a very real concern in mechanically ventilated patients. The damage caused from oxygen toxicity can include delayed healing due to oxidation injury and an increased risk of airway/lung injury.2

Now we move on to the next setting, positive end-expiratory pressure (PEEP). You can think of PEEP as the amount of residual pressure left in the lungs at the end of expiration that’s needed to keep alveoli from collapsing. Intrinsic or physiologic PEEP is the amount of PEEP a healthy person normally maintains during each breath. The normal physiologic PEEP is measured at approximately 5 cmH2O. When a patient is intubated, however, they lose the ability to maintain this. Therefore, PEEP has to be applied by the ventilator, and 5 cmH2O is generally the starting point. If a patient is having difficulty oxygenating, a PEEP of as much as 20 cmH2O can be utilized. Keep in mind though, higher levels of PEEP can lead to acute lung injury, decrease cardiac pre-load (increased intrathoracic pressure), increase barotrauma (increased airway pressures), and increase intracranial pressure from a decrease in cerebral venous return (increased intrathoracic pressure).3

Lastly, if the patient requires PLV instead of VLV, the provider will need to set the inspiratory pressure and the inspiratory to expiratory time ratio (I:E).

Inspiratory pressure is the amount of pressure applied on top of the already existing PEEP, forming the peak inspiratory pressure (PIP)—the highest amount of pressure exerted on the lungs during PPV. This total pressure (the PIP) will then force air into the lungs during inspiration. The I:E ratio is the amount of time allotted for inspiration and expiration during each breath.

In the modes that utilize PLV, the VT is variable based on the PIP and inspiratory time. Generally, the higher these two values go, the larger the VT.

However, this is also dependent on the compliance of the lungs. If the lungs are stiff from disease or the small airways are reactive, the PIP will be reached sooner with less air flow, causing the breath to occur without meeting an adequate VT. VT in PLV can be thought of as a goal or target that you’re using the pressure settings to reach; in VLV, the inverse is true.

Modes of Ventilation

Modes of ventilation can be basically thought of as a program that specifically tells the ventilator how to use all of the settings.

There are specific criteria and disease processes that determine the utilization of certain modes. The sidebar “VLV and PLV Modes” explains the more commonly seen modes in prehospital and critical care medicine. It’s important to understand that most of the modes are very similar between VLV and PLV. Generally, the large differentiating factor between each group of modes has to deal with how the inspiratory phase of the breath is terminated: Is the breath terminated after the set VT is reached (VLV), or is the breath terminated once the set inspiratory pressure and inspiratory time are reached (PLV)?

Conclusion

Pulmonary critical care medicine is an extremely complex discipline. It often requires expert consultation and advice from a host of sources to manage these incredibly ill patients. However, with even just a general knowledge of respiratory mechanics and the technology available for respiratory care, any level provider can appropriately care for these patients, and maybe even improve outcomes. 

References

1. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301–1308.
2. Crapo JD. Morphologic changes in pulmonary oxygen toxicity. Annu Rev Physiol. 1986;48:721–731.
3. Ben-Haim SA, Amar R, Shofty R, et al. The effect of positive end-expiratory pressure on the coronary blood flow. Cardiology. 1989;76(3):193–200.

Resources

• Courey A, Hyzy R. (July 2, 2014.) Overview of mechanical ventilation. UpToDate. Retrieved Nov. 15, 2014, from www.uptodate.com/contents/overview-of-mechanical-ventilation.
• Dushianthan A, Grocott MP, Postle A, et al. Acute respiratory distress syndrome and acute lung injury. Postgrad Med J. 2011;87(1031):612–622.
• Hansen-Flaschen J, Siegel M. (June 25, 2014.) Acute respiratory distress syndrome: Clinical features and diagnosis in adults. UpToDate. Retrieved Nov. 15, 2014, from www.uptodate.com/contents/acute-respiratory-distress-syndrome-clinical-features-and-diagnosis-in-adults.
• Hyzy R. (March 21, 2014.) Modes of mechanical ventilation. UpToDate. Retrieved Nov. 15, 2014, from www.uptodate.com/contents/modes-of-mechanical-ventilation.
• Siegel M, Hyzy R. (Dec. 8, 2014.). Mechanical ventilation in adults in acute respiratory distress syndrome. UpToDate. Retrieved Dec. 15, 2014, from www.uptodate.com/contents/mechanical-ventilation-of-adults-in-acute-respiratory-distress-syndrome.
• ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: The Berlin definition. JAMA. 2012;307(23):2526–2533.

 

IPPV is typically applied to an intubated patient; however, while not optimal, it can be successfully achieved via supraglottic or emergency adjunct airways.

 

Sidebar: VLV & PLV Modes

VLV Modes

Assist/Control Ventilation (A/C): A/C is probably the most common ventilator mode that will be seen by the provider. A/C on some ventilator models can also be called continuous mandatory ventilation (CMV). While A/C and CMV are now relatively synonymous with one another, true CMV is an out-of-favor form of A/C where the patient is unable to trigger any breaths. In A/C, the ventilator will deliver a minimum MV based on the RR and VT set by the provider. However, if the patient triggers more breaths than the set RR, these patient-triggered breaths will be delivered at the set volume entered by the provider. This means that the MV is variable based on the patient’s demand, but the VT for each breath will never change.

Synchronized Intermittent Mandatory Ventilation (SIMV): SIMV is quite similar to A/C in the fact that the minimum MV is set by the provider. In SIMV, a set number of breaths (the RR) is delivered at a set VT. However, unlike A/C, if the patient triggers a breath, the breath is delivered but “unassisted” by the ventilator. In other words, for each of the patient-triggered breaths, the VT will vary based on how much air the patient can pull without any support from the ventilator.

Unique to SIMV is synchronization that occurs between the patient-triggered and the ventilator’s assisted breaths. This point can be tricky, so let’s look at it in terms of a real world example. You’ve set a ventilator to the mode SIMV and have set the RR to 12 and the VT to 500 mL, but the patient is over-breathing at a rate of 20. Twelve of the 20 patient-triggered breaths will be delivered at a VT of 500 mL. The remaining eight breaths will be delivered based on the patient’s own effort with a variable VT. This particular mode is often used as a tool to help wean patients from the ventilator whove been ventilated for some period of time.

Pressure Regulated Volume Control (PRVC): This mode is another variation of A/C. With PRVC, the patient receives a set MV, but each breath’s flow and inspiratory time is variable based on the airway pressures. The computer within the ventilator adjusts over how long a breath is delivered and at what force based on the maximum amount of pressure that can be delivered in each breath. These pressure settings are entered by the provider in addition to the other settings typically entered for VLV.

PLV Modes

Pressure Assist/Control (PA/C): PA/C (also known as pressure control) is the most common mode of PLV used today. PA/C can be thought of as the pressure-limited form of A/C. A breath can be triggered by the ventilator or the patient. The inspiratory phase of the breath is then terminated once the PIP and inspiratory time are reached. There’s no guarantee of a set VT or MV. Thus in all actuality, there’s also no guarantee the patient would be ventilated at all. While rare, there’s the possibility of inadequate air movement all together with PLV modes.

Pressure-Limited SIMV: This mode is nearly identical to its volume-controlled counterpart. However, the difference here again is how the breath is terminated based on inspiratory time and PIP, not the volume delivered.

Airway Pressure Release Ventilation (APRV): APRV is a unique form of PLV. APRV utilizes CPAP to recruit and maintain patent alveoli. CPAP can be thought of as a pressure similar to PEEP, but maintained throughout the entirety of the breath. The general way APRV works is that a high level of CPAP (P high) is given over each breath for a specific period of time (T high). Then a lower level of CPAP (P low) is given for a shorter period of time (T low). This allows for maximum alveolar recruitment during the T high phase.

During the T low phase, the alveoli can get a bit of a reprieve from the higher pressure and the lungs are able to more fully deflate, releasing residual CO2 trapped in the lungs during T high. Patients with a spontaneous respiratory drive are able to trigger their own breaths in this mode. This mode of ventilation has been shown to decrease the amount of time patients with ARDS require mechanical ventilation. However, there’s  no decrease in mortality associated with the use of APRV.1 There are also alternate forms of this mode that are known as Intermittent Mandatory Airway Pressure Release Ventilation (IMAPRV) and Biphasic Ventilation (BV). These two forms are synonymous with APRV, and generally just augment the traditional APRV settings to achieve different outcomes.

High-Frequency Oscillatory Ventilation (HFOV): HFOV is a bit of an outlier in the world of PPV. HFOV delivers relatively minute VT at very high RR. Because of the high RR, it’s actually not measured in breaths per minute, but in hertz (Hz). While the VT is dependent on several factors and the particular patient population, the RR can often exceed 150 Hz and can get as high as 300 Hz. This particular mode is used in neonates more frequently, but has limited promise in adults with ARDS refractory to other treatments.2 In this particular form of ventilation, patients are generally heavily sedated and paralyzed, as the patient can’t have a respiratory drive in this form of PPV.

Adaptive Support Ventilation (ASV): This particular mode is very dependent on the computing power of the ventilator. This mode takes into account the readings from the ventilator such as airway pressures, VT, intrinsic I:E, and other measurements to deliver a form of PLV that is unique to each individual patient. ASV can be used in patients with or without their own respiratory drive.

References

1. Putensen C, Zech S, Wrigge H, et al. Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury. Am J Respir Crit Care Med. 2001;164(1):43–49.
2. Ferguson ND, Cook DJ, Guyatt GH, et al. High-frequency oscillation in early acute respiratory distress syndrome. N Engl J Med. 2013;368(9):795–805.