Initiation of Mechanical Ventilation ?Choosing ventilator settings

Mode: At ENH, we use mainly volume-cycled (assist control) mechanical ventilation. There is increasing evidence that using this modality, especially with a strategy to avoid ventilator-induced lung injury (VILI), outcomes can be improved for several disease processes. No such data exists, to date, to substantiate the efficacy of pressure control ventilation (PCV) and there are theoretical reasons that may limit extrapolation of the assist control data to PCV.

Initial ventilator settings: When choosing ventilator settings for any given patient, we choose the respiratory rate and tidal volume (the parameters that contribute to the pCO2) and the FiO2 and PEEP (the parameters that contribute to the PO2). Generally, in a patient who has not been excessively sedated and/or muscle relaxed we choose a respiratory rate of 12-14/min realizing that patients with intact neuromuscular capacity will "trigger" as many breaths as they need to maintain pH where their brain wants it. The only caveat is that occasionally, the rate must be turned lower to prevent hyperventilation. In general, letting the patient "choose" their own rate by setting a rate that is somewhat lower than their indigenous rate, is preferable in that it prevents iatrogenic hyperventilation. We choose ONLY the initial tidal volume by weight, realizing that it is nonsensical to maintain tidal volume by weight (to do so denies the pathophysiology of illness). As soon as the patient is comfortable on the ventilator, we measure the plateau (static) airway pressure, which is the most accurate reflection of distal airspace over- or underdistension and titrate to a tidal volume that yields a pressure, ideally, in the 20-25 cmH2O range. We do not tolerate plateau pressures above 30-35 cmH2O except in cases of profound obesity and/or PEEP>15 cmH2O in which the high static airway pressure is unlikely to represent a threat to the patient. Notice that peak airway pressure is not used to titrate tidal volumes because it is a function of both static and dynamic pressures in the lung. Ptotal (also called Ppeak) is the sum of the static pressure (=elastance*tidal volume) and the resistive pressure (=flow*resistance). Since much of the resistive airway pressure is dissipated on the robust upper airways (and endotracheal tube), a high peak airway pressure is only problematic if it is caused by a high plateau pressure which is associated with VILI (see reference by Manning and the ACCP consensus statement below).

Regarding oxygenation, begin with 100% FiO2 and PEEP=0 for obstructive lung disease and PEEP=5 for everyone else.

An arterial blood gas must be performed within 15 minutes of initiating mechanical ventilation to assure adequate ventilation/oxygenation. In patients with shock, when getting an ABG can be difficult before resuscitation, a venous blood gas (to estimate pH) and pulse oximetry saturation can be monitored until a true ABG can be obtained.

**Initial ventilator settings should deliver breaths with inspiratory flows that allow sufficient time for exhalation, otherwise the ventilator can be dangerous to the patients. Inspiratory:expiratory ratios should be 1:4 or less for most conditions; obstructive lung diseases generally require more exhalation time than this, while collapsing lung conditions (with low airway resistance) can be treated safely with less exhalation time.

Ratios approaching 1:1 (or even 1:2) should be avoided without the input of a pulmonologist/intensivist. In general a square inspiratory waveform at 60 LPM is a safe starting point for most conditions.

If the pulse oximetry waveform is good (3 stars) and correlates with the ABG, we titrate the FiO2 down in 10% decrements until we get to 50-60% ("non-toxic" concentrations of oxygen) so long as pulse ox is>90%. If the pulse ox drops to <90% before reaching an FiO2 of 60%, we gradually increase the PEEP (2-5 cmH2O at a time) which usually allows us to decrease the FiO2 to non-toxic levels. Never decrease the FiO2 with O2-saturations<90%! If the pH of the initial ABG is <7.30, then increase the respiratory rate. Note, we do not change the tidal volume if the plateau airway pressure is 20-25 cmH2O ? changes in minute volume, to affect pCO2, are achieved through changes in the respiratory rate once "safe" (i.e. not over- or under-distending) tidal volumes are reached.

Note that the ventilator can be very uncomfortable for some patients, coughing and overbreathing can be dangerous (causing VILI). Accordingly, great care should be taken to assure patient-ventilator synchrony which means the patient breaths pretty much with the ventilator and isn't fighting breaths. When such "bucking" causes high airway pressures, think about ways that you might adjust the ventilator to make the patient more comfortable. Changes in tidal volume or inspiratory flow characteristics (shape and magnitude of the flow) can establish patient comfort without resorting to large doses of sedatives. Make sure that as you titrate ventilator settings to achieve comfort that you observe the plateau airway pressure rules and I:E rules sugggested above. Use escalating doses of sedatives when the patient is bucking and having dangerous airway pressures (peak>60 with plateau greater than 35 cmH2O) and there is insufficient time to try these titrations and/or when the titrations fail. See section on Sedatives and Analgesia.

Once the patient has been stabilized on the ventilator attention turns to treating the cause of respiratory failure. Patients require ventilators for one of three reasons: hyopoxemic respiratory failure (due to shunt from flooding, blood, pus, fluid - or atelectasis), hypercapnic respiratory failure (due to failure of the respiratory pump, overloading of the pump or both), or simply because the patient needs an artificial airway.

Special Cases: ARDS and severe airflow obstruction

1. Severe airflow obstruction -- status asthmaticus. The available data suggests that the ventilator can kill patients with severe asthma (through dynamic hyperinflation) and that by simply allowing enough time for exhalation, VILI and depression of the circulation can be eliminated. The most powerful means of extending expiratory time is to reduce the minute volume. In these gas hungry patients very large amounts of sedatives and/or muscle relaxation may be required to reduce the minute volume sufficiently to reduce dynamic hyperinflation and keep the plateau airway pressure in the safe (<30 cmH2O) range. A plateau pressure based strategy, with permissive hypercapnia if necessary, has been shown to reduce mortality compared to historical controls.
2. ARDS ? Choosing a tidal volume of 6 ml/kg then customized to maintain plateau airway pressures less than 30 cmH2O resulted in a 25% reduction in mortality, presumably by attenuating VILI which then causes less systemic inflammatory response and multiple organ failure. Prone ventilation does not reduce mortality but has a role in refractory hypoxemia in which clinicians have difficulty decreasing the FiO2 to £ 60% despite high PEEPs (>15 cmH2O). Alternating recumbent with prone ventilation (every 6-12 hours) can allow use of non-toxic (£ 60%) oxygen in these most difficult cases.

Although primary failure of the neuromuscular circuit may occur (e.g. drug intoxications, ALS, Guillian Barre, myasthenia gravis), hypercapnic respiratory failure most often results from overloading of the respiratory muscles. The ventilator can be used to quantify loads each day, allowing the determination of the degree to which overloading caused respiratory failure in the first place and loads that bind patients to the ventilator each day. The work of breathing can be summarized as the work it takes to drive gas across the conducting airways (analagous to a straw) and the work it takes to expand the lung and chest wall from equilibrium/FRC (analagous to a balloon at the end of the straw). Therefore the two principle mechanical loads of breathing are the resistance of the conducting airways and the stiffness (elastance; 1/compliance) of the lung and chest wall. Minute volume is a third, non-mechanical load, that if elevated requires more breaths to maintain eucapnia, and therefore more resistive and elastic work. Clinicians should measure each of these three loads daily in order to identify and treat reversible causes of respiratory failure, thereby minimizing the duration of ventilator dependence.

Total airway pressure, also called peak airway pressure is the sum of the pressures it takes to drive a volume through the conducting airways (the resistive pressure) and to expand the lung and chest wall from FRC to the given volume (the elastic pressure). So:

P_peak=P_resistive+P_elastic

Since:

P_resistive=flow*resistance

P_elastic=elastance*volume

Then:

P_peak= (flow*resistance)+(elastance*volume)

The ventilator gives a peak airway pressure for every breath, therefore to solve the equation all one needs is to determine one of the two remaining variables. This is done by simply stopping flow in the system just following delivery of a tidal volume. Since flow=0, P_resistive during the cessation of flow is zero and the remaining pressure registered by the machine is the P_elastic, which is also called the "static airway pressure" (because there is no flow) or the "plateau airway pressure" because it looks like a plateau following a peak when one looks at pressure tracings. Now, since two variables have been measured directly, P_resistive can be computed by:

P_resistive=P_tot-P_elast or the "resistive pressure=peak minus plateau"

If one uses a square (constant) inspiratory flow to measure the peak airway pressure and the magnitude of that flow is 60 LPM (1 L/s), then

P_resistive =1*R= P_tot-P_elast and,

mathematically, the peak minus the plateau yields airway resistance in cmH2O/L/s (<15 is normal).

The ventilator displays the spontaneous minute volume on line. Therefore all three loads, resistance, compliance (tidal volume/plateau-PEEP) and minute volume are EASILY quantified.

Quick differentials for excess loads:

1. High resistance: (>15 cmH2O/L/s) - Think about what could be occluding the airways from the top down: kinked or bitten endotracheal tube, excessive secretions, bronchospasm. Rx: Assure that a suction catheter can pass through the tube without excess resistance, suction secretions and treat bronchospasm with bronchodilators.
2. Low compliance/high stiffness: (Compliance<35 ml/cmH2O) ? Think about conditions that can make either the chest wall or lung stiff. For stiff chest wall, think obesity and large ascites. For stiff lung, think about infiltrative pulmonary disease (pneumonia, edema, fibrosis), large pleural effusions (rarely cause big stiffness), and dynamic hyperinflation (auto-PEEP, present usually when patients are "gas-trapping" due to high airway resistance).
3. High minute volume: Occurs either because of increased CO2 production (sepsis, overfeeding) or ineffective elimination through an elevated dead space (pulmonary embolus, severe emphysema, hypovolemia).

Overloading is the most common reason for respiratory muscle failure; so identification and treatment of elevated loads is essential. Reversible causes of reduced respiratory muscle strength that are common in critically ill patients include: sepsis, electrolyte deficiencies, drugs (corticosteroids), malnutrition.

Remember FIX THE PATIENT

If hypoxemia binds them to a ventilator (i.e. their PaO2/FiO2<120 and/or they require PEEP>5 cmH2O) then they have shunt caused by flooding with blood, pus or fluid OR atelectasis. Identify the causes and reverse them.

If the work of breathing binds them to the ventilator (i.e. they breathe rapidly and shallowly when they are taken off the ventilator), then identify the elements of reduced neuromuscular capacity AND elevated loads that can be reversed and aggressively fix them.

There are recently published data to suggest that attention to the identification of the remediable elements of respiratory failure hastens liberation from the ventilator (see article by Smyrnios below).

The overwhelming preponderance of evidence suggests that physicians, nurses and respiratory therapists inadvertently impede liberation from mechanical ventilation when they fail to test readiness each day. By simply testing readiness to breathe each day, outcomes are markedly improved.

So for any patient who does not require pressors to maintain the circulation and who does not have an evolving MI AND whose PaO2/FiO2 is greater than 120, a daily trial of spontaneous breathing (SBT) is indicated. This trial can be pressure support£ 7 cmH2O, CPAP=5 cmH2O, flow-by, or T-piece. The first trial need only last 30 minutes. There are no data to suggest optimal duration of subsequent trials in patients who fail a first trial; most use 30-120 minutes. Success of a trial is guided by how the patient looks and feels subjectively, whether there have been significant increments (>10) of heart rate, respiratory rate or blood pressure during the trial and some also use an arterial blood gas. If a patient passes, then airway competence must be determined (adequate cough without excessive secretions) and if satisfactory a trial of extubation can follow. If the patient fails (i.e. the SBT, evaluation of airway competence, or a trial of extubation), attention turns to define (the pathogenesis) why they've failed.