Basic principles of mechanical ventilation

Alveolar ventilation and the equation of motion

Alveolar ventilation denotes fresh gas delivery to the gas - exchanging regions of the lungs. Mathematically this is expressed as:

where VA = alveolar ventilation per minute, f = breathing frequency, VT = tidal volume, and VD = wasted ventilation or dead space per breath. Alveolar ventilation needs to be adequate for the rates of tissue oxygen consumption (VO ₂ ) and carbon dioxide production (VCO ₂ ). By convention, CO ₂ transport, as expressed by the relationship between VCO ₂ and the steady-state arterial PCO ₂ , is used to quantify VA:

The difference between total ventilation (f × VT) and VA is VD.

The lungs are inflated by mechanical ventilation when a dynamic pressure increment or flow is applied at the airway opening. These applied forces interact with respiratory system compliance (both lung and chest wall components), airway resistance, and, to a lesser extent, respiratory system inertance and lung tissue resistance to effect gas flow. For simplicity, inertance and tissue resistance are relatively small and for clinical purposes can be ignored, so that the interactions of pressure, flow, and volume with respiratory system mechanics can be expressed by the simplified equation of motion:

In the mechanically ventilated patient, this relationship is expressed as:

where ΔPcir is the change in ventilator circuit pressure above baseline (peak pressure minus end-expiratory pressure: Ppeak − PEEP); ΔPmus is inspiratory muscle pressure generated by the patient (if present); $\dot{\text{V}}$ is the flow into the patient’s lungs; R is the resistance of the external circuit, artificial airway, and natural airways combined; V t is the tidal volume; and C rs is the respiratory system compliance. If intrinsic or auto-PEEP (PEEPi) is present, muscle and circuit pressure must overcome this end-expiratory bias before flow and volume can be delivered, and thus PEEPi will add to the pressure requirement.

When flow is paused and pressure is held constant at end inspiration ( $\dot{\text{V}}$ = 0, Pmus = 0), the ventilator circuit pressure levels off at a pressure commonly referred to as the “plateau” pressure (Pplat). By use of this inspiratory hold, the components of Pcir required for flow and for respiratory system distention can be separated to describe R and Crs:

Importantly, airway pressure measurements made under no-flow conditions are alveolar pressures and are determined by the pressure needed to distend the lung and the chest wall at that volume (Pplat at end inspiration, PEEP at end expiration). However, it is only the pressure across the lungs (transpulmonary pressure [TPP]) that affects alveolar stretch, drives regional ventilation, and maintains end-expiratory lung volume. TPP can be directly measured if an estimate of average pleural pressure (approximated by esophageal pressure) is available. Thus TPP = alveolar pressure minus pleural pressure = Paw − Ppl.

In practice, because chest wall compliance (the major determinant of Ppl) is generally high, Ppl changes over the respiratory cycle are usually small, and measurements of airway Pplat and PEEP are reasonable approximations of TPP. In contrast, under conditions of very low chest wall compliance (e.g., obesity, anasarca, abdominal compartment syndrome, tight bandages), Ppl may be quite high, and thus the measured Pplat and PEEP will markedly overestimate the actual TPP. This influence needs to be considered when setting the upper limits of ventilator settings in such patients and may require actual measurements of Ppl (Pes) to be safe.

In situations where spontaneous efforts occur, no-flow conditions at end inspiration are difficult to obtain, and consequently Pplat may be impossible to measure in real time. One solution to approximate Pplat under these conditions would be to deliver a controlled (i.e., passive) breath with an inspiratory pause using a similar VT and PEEP. Alternatively, there are proprietary monitors that can analyze the expiratory flow pattern during a passive exhalation to calculate respiratory system compliance and resistance and then determine a Pplat.

Flow-targeted vs. Pressure-targeted breaths

As noted earlier, there are two basic approaches to delivering positive-pressure breaths: flow targeting and pressure targeting. With flow targeting, the clinician sets inspiratory flow so that circuit pressure is the dependent variable. With pressure targeting, the clinician sets an inspiratory pressure target (with either time or flow as the cycling criterion) so that flow and volume are dependent variables (i.e., varying with lung mechanics and patient effort). With a flow-targeted breath, changes in compliance, resistance, or patient effort will change Pcir (but not flow); in contrast, with a pressure-targeted breath, similar changes in compliance, resistance, or effort will cause a change of tidal volume (but not Pcir).

Each strategy has advantages and disadvantages. ^, For flow-targeted breaths, a minimal tidal volume can be guaranteed. For pressure-targeted breaths, the rapid initial flow and subsequent declining flow of pressure targeting may enhance gas mixing and patient synchrony. As noted earlier, on modern ventilators, a variety of feedback mechanisms can combine features of flow- and pressure-targeted breaths.

Intrinsic (auto) peep

PEEPi is the positive end-expiratory pressure that develops within alveoli because of insufficient expiration time, either because of inadequate time allowed between breaths by the ventilator or patient or because of increased expiratory resistance and collapse (flow limitation). ^, PEEPi depends on three factors: the minute ventilation, the expiratory time fraction, and the respiratory system’s expiratory time constant (the product of resistance and compliance). The potential for developing PEEPi rises with increases in the minute ventilation, decreases in the expiratory time fraction, or increases in the expiratory time constant (i.e., with higher R or C rs values).

The development of PEEPi will have different effects during pressure-targeted compared with flow-targeted ventilation. In flow-targeted ventilation, the constant delivered flow and volume (and thus ΔPcir) means that a rising PEEPi will increase both the Ppeak and the Pplat. In contrast, in pressure-targeted ventilation, the set Pcir limit coupled with a rising PEEPi level will decrease ΔPcir and, with it, the delivered tidal volume (and minute ventilation). Importantly, this accommodation may help limit the buildup of PEEPi.

In the patient without respiratory effort, PEEPi can be recognized in two ways. First, when an inadequate expiratory time produces PEEPi, analysis of the flow graphic will show that expiratory flow has not returned to zero before the next breath is given. Second, PEEPi in alveoli with patent airways can be quantified during an expiratory hold maneuver that permits equilibration of the end-expiratory pressure with Pcir. Note that total end-expiratory pressure is the sum of applied PEEP and PEEPi. Importantly, in patients with airway collapse, the expiratory hold maneuver will not detect the presence of PEEPi in units peripheral to the zone of closure.

In the patient with respiratory efforts, PEEPi can function as an inspiratory threshold load that produces delayed or even missed triggering of the desired breath. In those cases with tidal flow limitation, this load can be counterbalanced with the judicious application of applied PEEP, guided either clinically or with Pes measurements.