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How to Write Ventilator Orders 

How to Write Ventilator Orders
How to Write Ventilator Orders

John W. Kreit

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date: 05 July 2020

Now that you’ve learned all about ventilator terminology, modes and breath types, and the indications for mechanical ventilation, you’re ready to write ventilator orders. As you’ll see, this is really pretty easy, but it’s important that you take an orderly, step-by-step approach.

This chapter is divided into three sections:

  • Initial ventilator orders—How to choose appropriate settings immediately after intubation

  • Adjusting ventilator settings—How to make changes throughout the course of your patient’s illness

  • Weaning from mechanical ventilation—How to write orders for “spontaneous breathing trials”

Initial Ventilator Orders

Step 1: Choose a Mode of Mechanical Ventilation

As discussed in Chapter 5, the CMV mode is ideal for critically ill patients with respiratory failure because it guarantees a clinician-set number of mechanical breaths, allows the patient to control the total respiratory rate, and requires very little patient inspiratory effort and work of breathing.

My recommendation:

  • Always use CMV as the initial mode of mechanical ventilation.

Step 2: Choose the Type of Mechanical Breath

Here you get to choose between five breath types (described in Chapter 5): volume control (VC), pressure control (PC), adaptive pressure control (aPC), pressure support (PS), and adaptive pressure support (aPS). I prefer to initially use VC or aPC breaths in all patients because they provide a clinician-set tidal volume. The combination of VC or aPC breaths with the CMV mode guarantees a minimum, safe minute ventilation.

My recommendation:

  • Use VC or aPC breaths with the CMV mode.

Step 3: Select Settings Based on the Type of Mechanical Breath

Remember that each breath type requires you to set specific parameters. So, your next set of orders depends on whether you’ve picked VC or aPC breaths in Step 2. If you chose VC breaths, you must specify the delivered tidal volume (VT) and, depending on the ventilator, set either the peak inspiratory flow and the flow profile or the inspiratory time (TI). If you selected aPC breaths, you have to set the VT and TI.

My recommendations:

  • VC breaths

    • Tidal volume:

      • ~ 8 ml/kg ideal body weight (IBW)

      • ≤ 6 ml/kg IBW in patients with the acute respiratory distress syndrome

    • Peak inspiratory flow: 60–80 L/min

    • Flow profile: Descending ramp

    • Inspiratory time: 0.6–0.8 second

  • aPC breaths

    • Tidal volume: Same as for VC breaths

    • Inspiratory time: Same as for VC breaths

Step 4: Specify Other Basic Settings

Fractional Inspired Oxygen Concentration (FIO2)

Hypoxemia is bad! Always start with a high FIO2 and decrease it later, if possible. Never start low and work your way up.

My recommendations:

  • Patients with a high oxygen requirement prior to intubation should initially receive an FIO2 of 1.0.

  • In patients with acute or acute-on-chronic hypercapnia and modest oxygen requirements, an initial FIO2 of 0.5 is usually okay.

Mandatory Respiratory Rate (RR)

This is the number of guaranteed breaths each minute, and it must be specified in the CMV and SIMV modes.

My recommendations:

  • As a general rule, the mandatory rate should initially be set between 10 and 14 breaths per minute.

  • Patients with chronic hypercapnia may only need 6–10 breaths per minute.

Positive End-Expiratory Pressure (PEEP)

PEEP is used to help open or “recruit” atelectatic alveoli and improve PaO2 in patients with extensive alveolar filling. In many hospitals, a small amount of PEEP (e.g., 5 cmH2O) is routinely used in all mechanically ventilated patients to prevent atelectasis.

My recommendations:

  • Patients with severe air flow obstruction are likely to have dynamic hyperinflation and intrinsic PEEP. Set PEEP at zero for these patients.

  • In all other patients, start at a PEEP of 5.0 cmH2O.

Trigger Type

Very sensitive techniques have shown that, when compared with pressure-triggering, flow-triggering decreases the time between the onset of patient inspiratory effort and gas entry into the lungs and reduces patient work of breathing. The magnitude of this difference, though, does not appear to be clinically relevant, and these two triggering methods should be considered interchangeable. Refer to Chapter 4 for a review of pressure and flow-triggering.

My recommendation:

  • Select either pressure or flow triggering.

Trigger Sensitivity

The effort required to trigger the ventilator increases as pressure sensitivity becomes more negative and flow sensitivity becomes more positive. Ideally, sensitivity is set to allow easy triggering with low risk of auto-triggering (see Chapter 11).

My recommendations:

  • Set pressure sensitivity at –1 or –2 cmH2O.

  • Set flow sensitivity at 1 or 2 L/min.


Table 8.1 provides an example of initial ventilator orders.

Table 8.1 Initial Ventilator Orders

Ventilator mode:


Breath type:

VC or aPC

Tidal volume:

500 ml

Inspiratory time:*

0.7 seconds

Peak flow:*

60 L/min

Flow profile:*

Descending ramp


1.0 or 0.5

Mandatory rate:

12 breaths/minute


5 cmH2O

Trigger type:



–2 cmH2O

* Set either inspiratory time or peak flow and profile depending on the ventilator.

CMV = continuous mandatory ventilation; VC = volume control; aPC = adaptive pressure control

Adjusting Ventilator Settings

After you write your initial orders, you’ll need to make adjustments during the time your patient is on the ventilator. Most will be in response to one or more of the following conditions: high or low PaO2 and SpO2, respiratory acidosis, or respiratory alkalosis.

High PaO2 and SpO2

If you follow my recommendation and start with a high FIO2, you’ll often need to reduce it after your first arterial blood gas (ABG) measurements. You will also be able to decrease the FIO2 as your patient’s underlying lung disease improves. You should reduce the FIO2 as much as possible, while keeping the PaO2 between about 70 and 80 mmHg. Unfortunately, there’s no reliable way to predict what effect a decrease in the FIO2 will have.

That’s because the relationship between the FIO2 and PaO2 depends on the type and severity of the underlying gas exchange abnormality. As shown in Figure 8.1A, V˙/Q˙ mismatching causes a curvilinear relationship that varies with the severity and extent of disease. Notice that even when V˙/Q˙ imbalance is severe, PaO2 increases dramatically at high FIO2. That’s because, as long as some ventilation is present, even very low V˙/Q˙ alveoli will eventually fill with O2, and the blood leaving them will have a high PO2 and hemoglobin saturation.

Figure 8.1 The calculated mean alveolar PO2 (PA¯O2) increases linearly with FIO2. As the severity of V˙/Q˙ mismatching increases (A), the relationship between the fractional concentration of inspired oxygen (FIO2) and the arterial partial pressure of oxygen (PaO2) becomes increasingly curvilinear. In the presence of a right-to-left shunt (B), there is a linear relationship between FIO2 and PaO2. As shunt fraction (expressed as percent of cardiac output) increases, there is a smaller and smaller rise in PaO2 with FIO2.

Figure 8.1 The calculated mean alveolar PO2 (PA¯O2) increases linearly with FIO2. As the severity of V˙/Q˙ mismatching increases (A), the relationship between the fractional concentration of inspired oxygen (FIO2) and the arterial partial pressure of oxygen (PaO2) becomes increasingly curvilinear. In the presence of a right-to-left shunt (B), there is a linear relationship between FIO2 and PaO2. As shunt fraction (expressed as percent of cardiac output) increases, there is a smaller and smaller rise in PaO2 with FIO2.

When intrapulmonary shunting is present, some alveoli receive no ventilation. Increasing the FIO2 has no effect on the shunted blood and, above a certain level, cannot further increase the saturation of blood passing through ventilated alveoli. This produces a linear relationship between PaO2 and FIO2 (Figure 8.1B) that flattens as the shunt fraction (the percentage of the cardiac output flowing through unventilated alveoli) increases.

Since lung disease often produces both V˙/Q˙ mismatching and shunt, there’s no way to predict the PaO2–FIO2 relationship in a particular patient. So, here’s what you do. First, make sure that the hemoglobin saturation measured by pulse oximetry (SpO2) is accurate by comparing it with the saturation measured from an ABG (SaO2). If it is, simply reduce the FIO2 in small increments until the SpO2 is consistently around 93%. I like to shoot for 93% because, even under the best of circumstances, the SpO2 may be off by 2%. Further decreases in the FIO2 should be based on PaO2 and SaO2 measurements.

Low PaO2 and SpO2

If your patient has extensive airspace filling, it’s likely that, at some time during the course of their illness, the PaO2 and SpO2 will be low even when they’re receiving high FIO2. At that point, the first step is to gradually increase the level of PEEP. By increasing mean alveolar pressure, PEEP opens or “recruits” atelectatic alveoli and reduces intra-pulmonary shunting. In general, PaO2 increases with increments in PEEP; but be careful. As discussed in Chapter 3, PEEP reduces venous return and increases RV afterload, which can significantly decrease LV preload, cardiac output, and tissue O2 delivery. I suggest that you increase PEEP in increments of 3–5 cmH2O while monitoring stroke volume or cardiac output, or at least watching closely for signs of impaired tissue perfusion. PEEP levels over 20 cmH2O are rarely used. PEEP and other ways of increasing PaO2, including prone positioning, neuromuscular blockade, and inhaled vasodilators, are discussed in detail in Chapter 12.

Respiratory Acidosis

In Chapter 2, you learned that hypercapnia and respiratory acidosis occur when alveolar ventilation is insufficient to excrete the CO2 produced by the body, and that this can result from low minute ventilation (V˙E), high dead space ventilation (V˙D), or high CO2 production (V˙PCO2).


When caring for critically ill patients, there’s typically little you can do to significantly reduce V˙PCO2 or V˙D, so, regardless of the underlying cause, your response to respiratory acidosis must be to increase V˙E. You could do this using a trial-and-error approach and gradually increase V˙E while following serial ABGs, but there’s a better way. If we make the reasonable assumption that V˙PCO2 and V˙D remain constant over a short period of time, then PaCO2 is inversely related to V˙E, and Equation 8.1 becomes:


We can then set up a proportion between the current PaCO2 (PaCO2-1) and V˙E(V˙E­1), and the V˙E needed (V˙E­2) to give the PaCO2 that we want (PaCO2-2).

PaCO2­-1×V˙E­-1 = PaCO2­-2 ×V˙E­-2



If tidal volume isn’t changed1, we can substitute respiratory rate (RR) for V˙E and rewrite this equation as:

PaCO2­-1/RR­-2 = PaCO2­-2/RR­-1

Solving for RR-2 gives us


So, let’s say that a patient is being ventilated at a rate of 10 breaths per minute and has a PaCO2 of 65 mmHg. The rate needed to reduce the PaCO2 to 40 mmHg is (65/40) x 10, or about 16 breaths per minute. When doing these calculations, it’s important to recognize that it takes a while to see the full effect of a change in ventilation. That’s because the body contains an enormous store of CO2 (about 120 L) that exists in a variety of different forms. So wait for at least 20 minutes before checking to see if the change in respiratory rate was effective.

Respiratory Alkalosis

Hypocapnia and respiratory alkalosis occur when minute ventilation exceeds that needed to maintain a normal PaCO2. This may be due to patient agitation or discomfort, and in these cases, the problem often resolves with appropriate sedation or analgesia. Much more often though, respiratory alkalosis occurs simply because the mandatory rate has been set too high. You can easily distinguish between these two possibilities by comparing the set and total respiratory rates displayed on the user interface of the ventilator. If they’re the same, the patient’s respiratory alkalosis is iatrogenic, and you need to reduce the set rate. You can use the method we just discussed to calculate the rate needed to return the PaCO2 and pH to normal, or you can simply decrease the set rate until the patient begins to trigger spontaneous breaths.

Weaning from Mechanical Ventilation

Once the underlying cause of respiratory failure has resolved or significantly improved, you need to determine whether or not your patient is ready for extubation. This is most often done by evaluating a number of parameters, including tidal volume, respiratory rate, and vital capacity during so-called spontaneous breathing trials. These trials can be truly spontaneous; that is, the patient is disconnected from the ventilator, or they can be performed using low-level pressure support breaths. I prefer the latter approach because it maintains functioning ventilator alarms, compensates for the extra work needed to breathe through the endotracheal tube, and eliminates the need to disconnect and reconnect the patient.

Table 8.2 shows the orders needed to perform an on-ventilator spontaneous breathing trial. Chapter 15 provides an in-depth discussion about how to discontinue mechanical ventilation.

Table 8.2 Orders for a Spontaneous Breathing Trial

Ventilator mode

Spontaneous ventilation

Breath type:


Pressure support level:

5 cmH2O


0 or 5 cmH2O


Same as on CMV

Trigger type:



–2 cmH2O

PS = pressure support


1 Recall from Chapter 2 that any change in VT changes the V˙E needed to maintain a given PaCO2 because it alters the ratio of dead space to tidal volume (VD/VT). That’s why we always change RR rather than VT.