When the respiratory system fails, your patient may need to be supported by mechanical ventilation (see Indications for mechanical ventilation). Think of it as cruise control for the lungs. As a nurse, what do you need to do? With a plethora of terms and acronyms, it can be very confusing to understand the ventilator settings and how to assess your patient. In this article, we'll give you an overview of ventilatory modes and settings and show you how to ensure optimal care of your patient and avoid complications. First, we'll start with a review of the conditions that often require mechanical ventilation.

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In need of support

Respiratory failure is classified as hypoxemic or hypercapnic and as acute or chronic. The three most common reasons for mechanical ventilation in critically ill patients are pneumothorax, atelectasis, and pulmonary edema. These conditions all fall under the category of hypoxemic respiratory failure. For the purposes of this article, we'll be discussing mechanical ventilation in acute respiratory failure. Your patient may need a mechanical ventilator for the following reasons:

* hypoxemic respiratory failure. Resulting in decreased oxygen in the blood (PaO₂), this type of respiratory failure is the most common and can be associated with almost all acute lung disease. Besides the aforementioned conditions, pneumonia, pulmonary fibrosis, early acute respiratory distress syndrome (ARDS), and smoke inhalation are a few examples of disease processes that can lead to this type of respiratory failure.

* acute severe hypercapnic respiratory failure. Resulting in decreased PaO₂ and normal or increased partial pressure of arterial carbon dioxide (PaCO₂), this type of respiratory failure can be seen in acute chronic obstructive pulmonary disease (COPD) exacerbation, head trauma, and spinal cord injury, to name a few. Hypoventilation due to excessive body fat or central nervous system depressant drugs may also be the culprit.

* bradypnea or apnea with respiratory arrest

* acute lung injury

* tachypnea (respiratory rate of greater than 30 breaths/minute)

* clinical deterioration for another condition unrelated to the lungs

* respiratory muscle fatigue

* coma

* hypotension

* neuromuscular disease.

An endotracheal (ET) tube is necessary for a patient to be placed on mechanical ventilation. The ET tube has two main purposes: It provides a patent airway and its small balloon cuff seals off the trachea to protect the patient from aspiration. The cuff seals off the trachea so the air will go in through the tube and come back out through the tube for measurement by the ventilator, preventing air from entering the stomach. Otherwise, the air would simply escape around the tube and you'd have no idea how much ventilation was actually delivered. The idea is to have minimal to no air leak with the ET tube.

The ET tube's cuff is inflated after tube placement in the trachea has been confirmed. Cuff pressure should be the lowest possible pressure to allow delivery of adequate tidal volume and prevent pulmonary aspiration. Usually, the pressure is maintained at less than 25 mm Hg to prevent injury and at more than 15 mm Hg to prevent aspiration. Cuff pressure should be monitored at least every 8 hours by attaching a pressure gauge monitoring device or using a minimal occlusion volume technique. Follow your facility's policy and procedures for assessing cuff pressure.

After the tube is in place, mechanical ventilation is initiated. Mechanical ventilation will assist your patient in gas exchange, which should be achieved with minimal damage to the lungs. The mechanical ventilator rate is defined as breaths delivered to the patient per minute. The initial rate is set to provide the needed ventilation to achieve a normal PaCO₂ value. Tidal volume is defined as the volume of gas exchanged during each ventilated breath, or the volume of air exhaled per minute. Normal tidal volume in a patient who's breathing spontaneously is 5 to 8 mL/kg. In mechanically ventilated patients, the tidal volume is set to prevent lung injury; the value depends on the patient's lung condition and ideal body weight (IBW). A patient with normal lungs would be ventilated at 10 to 12 mL/kg; COPD, 8 to 10 mL/kg; restrictive lung disease, 4 to 8 mL/kg; and ARDS, 4 to 8 mL/kg.

The ventilator rate and the tidal volume are used to determine the minute ventilation. Minute ventilation is calculated by multiplying the ventilator rate by the tidal volume. Positive end expiratory pressure (PEEP) is the pressure remaining in the lungs at end expiration; it's used to maintain the patency of the alveoli in disease states that cause them to collapse (such as in atelectasis). In a normal, nonventilated patient, 3 to 5 cm H₂O of PEEP is considered physiologically normal. FiO2 is the fraction of inspired oxygen. The FiO₂ value is always expressed as a decimal, not a percentage. An FiO₂ of 1.0 can also be expressed as 100% oxygen; an FiO₂ of 0.5 as 50% oxygen, but it's incorrect to say the patient is on an FiO₂ of 50%. Room air has an FiO₂ value of 0.21, or 21%, but the patient can receive up to 1.0, or 100%, FiO₂. Evaluation of FiO₂ is based on oxygen saturation (SaO₂) and PaO₂ values.

The initial ventilator rate will be adjusted based on the patient's response, his arterial blood gas (ABG) values, and the Pao₂/Fio₂ (P/F) ratio (see Initial ventilator settings). The P/F ratio is a function of gas exchange and is obtained by dividing the PaO₂ by the FiO₂. It's a good indicator of oxygenation and how much oxygen is moving into the circulation. A normal P/F ratio is greater than 300; a value of less than 200 indicates refractory hypoxemia. In addition, the P/F ratio can be used to determine if very badly damaged lungs are improving.

ABG results also help pinpoint when adjustments need to be made. PaO₂ and SaO₂ provide information about oxygenation. The Pao₂ value reflects the oxygen that's dissolved in the blood. Normal PaO₂ is 80 to 100 mm Hg. The SaO₂ value reflects the percentage of saturated hemoglobin. Normal SaO₂ is 95% or greater. The pH and PaCO₂ values are used to determine the ventilatory status. Normal pH is 7.35 to 7.45 and normal PaCO₂ is 35 to 45 mm Hg.

Ventilator modes 101

There are two types of ventilator mode: volume and pressure. The mode of ventilation is chosen based on the needs of the patient. We'll review several possible modes, such as pressure support ventilation (PSV), assist control (AC), synchronized intermittent mandatory ventilation (SIMV), pressure control (PC), pressure regulated volume control (PRVC), and adaptive pressure ventilation (APV).

PSV mode delivers a set pressure that's held during the entire inspiration (each spontaneous breath) while decreasing the patient's work of breathing. In this mode, the tidal volume is determined by the patient's effort, elasticity or compliance of the lungs, and the pressure support setting. The patient must be spontaneously breathing to be placed on a support mode. If he isn't effectively supported by PSV mode, as evidenced by a PaO₂ value of less than 60 mm Hg, the respiratory therapist will change the ventilator to a controlled mode, which allows the patient to receive a set tidal volume.

In AC mode, the patient will receive a set volume with each patient-triggered breath (assisted), as well as the set mechanical rate (controlled). This means that the set mechanical tidal volume is delivered to both the assisted and controlled breaths.

SIMV mode is considered a partial support mode, delivering a set number of breaths and tidal volume while allowing the patient to take spontaneous breaths with a patient-determined tidal volume and rate.

In PC mode, a pressure-limited breath is delivered at a set rate. The tidal volume is determined by the set pressure limit.

Lastly, the ventilator can be set to a dual control mode, such as the PRVC or APV mode. With a dual control mode, the volume is controlled and the pressure regulated. The ventilator will deliver the set tidal volume while adjusting the pressure from breath to breath as the patient experiences changes in airway resistance and compliance (work of breathing). In other words, the set tidal volume is delivered as a pressure-limited (controlled) breath until the desired tidal volume is achieved. The breath is much like a breath in PSV mode, but the ventilator can guarantee the tidal volume. The ventilator monitors each breath and compares the tidal volume delivered with the set tidal volume. If the delivered volume is too low, the pressure is increased on the next breath. If it's too high, the pressure is decreased on the next breath.

Figure. We just need a little help right now.

Putting it all together

Now, let's put everything together using a hypothetical patient scenario. Your patient Alexander Brown, 70, was placed on mechanical ventilation because of persistent apnea following a partial colectomy. He has no history of lung disease. His ventilator settings are:

* SIMV at 10 breaths/minute

* tidal volume of 700 mL

* FiO₂ of 1.0, meaning that he's receiving

* PEEP at 5 cm H₂O.

First, you'll need to evaluate Mr. Brown's pH and PaCO₂. His pH value is within the normal range, and he isn't compensating for a metabolic or respiratory disorder. Hypoventilation causes the patient's pH to drop below 7.35 and his PaCO₂ to rise above 45 mm Hg. This means that the level of ventilation is insufficient to maintain a normal PaCO₂. In hyperventilation, the patient's pH is greater than 7.45 and PaCO₂ is less than 35 mm Hg. This means that the level of ventilation is excessive. But because his pH and PaCO₂ values are both normal, Mr. Brown's level of ventilation is satisfactory.

If Mr. Brown's PaCO₂ value wasn't normal, you'd try to get it back into the normal range by working with the respiratory therapist to change the minute ventilation. PaCO₂ is the respiratory component affecting pH (the kidneys and the HCO₃^- value are the metabolic component). In a patient with hypoventilation, you'd adjust the minute ventilation by increasing the tidal volume or ventilatory rate. These interventions reduce the PaCO₂ back to normal and bring the pH back within the acceptable range.

However, before adjusting the tidal volume, you need to be sure that it's appropriate for the patient based on his IBW, which is used to approximate lung size. Normal lungs typically require a tidal volume between 10 and 12 mL/kg of IBW. Mr. Brown's IBW is 154.4 pounds (70 kg) and his lungs are normal, so a tidal volume between 700 and 840 mL is appropriate. (An even quicker way to set tidal volume for a patient with normal lungs is to add a zero to the patient's IBW in kilograms.)

Next, you'll assess Mr. Brown's oxygenation status by calculating the P/F ratio, which is PaO₂ divided by FiO₂. For example, if the patient's PaO₂ is 225 mm Hg and the FiO₂ is 1.0, the P/F ratio is 225. A number greater than 300 is considered normal. Values between 200 and 300 indicate acute lung injury, and values less than 200 indicate refractory hypoxemia, or hypoxemia that's not responsive to oxygen therapy. Mr. BrownPaO₂ value is 225 mm Hg, which is too low considering that he's receiving 100% oxygen. His PaO₂ should be 500 mm Hg, or five times the percentage of oxygen he's receiving. (Because room air is 21% oxygen, multiplying the percentage of oxygen by 5 is a quick way to estimate PaO₂.) For example, a patient breathing 40% oxygen should have a PaO₂ of about 200 mm Hg. As you increase the delivered FiO₂ you should see a corresponding increase in PaO₂; if not, the patient has refractory hypoxemia.

Mr. Brown's P/F ratio of 225 has already alerted you that he has acute lung injury. The P/F ratio tells you if there's a good relationship between how much oxygen the patient is breathing (FiO₂) and how much is moving through the alveoli into the circulation (PaO₂). If a significant amount of atelectasis causes a low PaO₂, your patient won't respond as he should no matter how much oxygen you administer. The healthcare provider will want to rule out pneumothorax first because increasing ventilator volume delivery will worsen the pneumothorax. If the problem is atelectasis or pulmonary edema, the treatment is to add PEEP.

After delivery of the tidal volume during inspiration, the mechanically ventilated patient is allowed to exhale to a baseline pressure of zero cm H₂O. Low levels of PEEP (3 to 5 cm H₂O) are added to restore the normal volume loss that occurs with intubation, and these levels are well-tolerated by almost all intubated patients. A PEEP level over 5 cm H₂O is considered therapeutic and is used to treat refractory hypoxemia. PEEP restores or maintains lung volume at end expiration by either recruiting collapsed alveoli or preventing further loss of lung volume and atelectasis. Remember that in patients with refractory hypoxemia caused by significant atelectasis, increasing the FiO₂ won't raise the PaO₂ appreciably. In these patients, PEEP is indicated to recruit collapsed alveoli and prevent further loss of lung volume.

Hazards of the road

After the patient is intubated and ventilated, nursing and respiratory therapy must work together to prevent complications related to mechanical ventilation. Emergent intubation places the patient at risk for aspiration, worsening hypoxemia, and increased morbidity and mortality. In addition, mechanical ventilation can lead to several hazards, including:

* barotrauma-injury or damage to the lung tissue. Barotrauma can lead to entry of air into the pleural space (pneumothorax) or the tracking of air along the vascular bundle to the mediastinum (pneumomediastinum). Large tidal volumes and elevated peak inspiratory pressure (PIP) and plateau pressure are risk factors. A PIP of less than 40 cm H₂O and a plateau pressure of 25 to 30 cm H₂O are recommended.

* volutrauma-damage to the lungs caused by too large a volume, leading to a syndrome of symptoms similar to ARDS. When a mechanical ventilation breath is forced into the patient with interstitial lung injury, the positive pressure from the ventilator follows the path of least resistance, which is most often directed to the normal alveoli, leading to overdistension (see Lungs under pressure). The overdistension sets off an inflammatory cascade that calls the inflammatory mediators, or cytokines, to an area of perceived injury, leading to additional damage to previously unaffected alveoli. The increased local inflammation leads to worsening lung injury and ARDS.

* decreased cardiac output and BP-increased pressure in the lungs leads to increased pressure surrounding the heart and major vessels. This increased pressure in the thoracic cavity leads to decreasing blood return to the heart, decreased cardiac output, and eventually decreased BP.

* hospital-acquired infections-possible aspiration of gastric juices or secretions can colonize in the lungs and lead to pneumonia. This is referred to as ventilator-associated pneumonia (VAP)-a new infection of the lungs developing within 48 hours after intubation. VAP is a life-threatening complication, carrying a 33% to 50% mortality rate. The highest risk of VAP is immediately after intubation. VAP should be suspected with new or changing pulmonary infiltrate on the chest X-ray in conjunction with fever, leukocytosis, and a change in the color and amount of secretions. Because the increased pH of gastric juices puts the patient at risk for infection, the recommended prevention strategy is to place him on stress ulcer prophylaxis; these medications decrease gastric pH.

* oxygen toxicity-a combination of increased high levels of oxygen and prolonged use. Oxygen free radicals cause an inflammatory-like response in the lungs that looks and acts much like ARDS. A good rule of thumb is to use the lowest Fio₂ setting that accomplishes the needed oxygenation, preferably less than 6.0, or 60%. Using PEEP allows you to use a lower FiO₂ to reach the target PaO₂.

In addition to monitoring for complications, you must routinely assess the ventilator to make sure it's functioning properly and the settings are appropriate for the patient. Problems can occur in the ventilated patient related to the ventilator, the tubing, the ET tube, or changes in compliance (elasticity) or airway resistance within the lungs. But don't fear, the ventilator gives you a warning alarm or caution lights to help you navigate or troubleshoot your way to success. Never silence an alarm that you can't fix and always provide ventilation while troubleshooting alarms.

There are several types of ventilator alarms to watch out for:

* high PIP-increased airway pressure or decreased lung compliance, most often caused by secretions, coughing, or patient intolerance of the ventilator; always assess breath sounds for increased consolidation, wheezing, bronchospasm, or the possibility of a pneumothorax and check to see if your patient is biting on the tube, if the tubing is kinked, or if the tubing contains increased condensation

* low minute ventilation-if your patient is on control mode, check for a disconnection or leak in the circuit; if he's being weaned off the ventilator, assess for decreased respiratory effort

* apnea-always check for patient effort and check for circuit disconnections that mimic apnea.

A team of mechanics

Critical communication must occur between nursing and respiratory therapy related to patient condition changes and any ordered ventilator changes. Most patients receiving mechanical ventilation will require some form of sedation to offset the anxiety and stress associated with it. Sedation can be administered via a continuous infusion or intermittent doses. Sedation "holidays," during which the patient's level of sedation is lightened for a period of time, need to occur daily to assess his neurologic status and allow him to be reoriented. In addition, the readiness for weaning can be assessed so that mechanical ventilation can be discontinued as soon as possible. The nurse and respiratory therapist must collaborate on when the sedation holiday will occur so both may conduct their neurologic and respiratory assessments.

Another important area where nurses and respiratory therapists can work collaboratively is in the use of protocols for the care of mechanically ventilated patients. Studies have shown that protocols driven by nursing and respiratory therapy safely decrease the number of ventilator days. These protocols allow nurses to titrate sedation medications and allow respiratory therapists to begin spontaneous breathing trials to assess the patient's readiness for weaning. Most of these types of protocols also bundle other treatment strategies that work together to improve the patient's outcome.

Here are a just few measures that should be undertaken for all patients receiving mechanical ventilation unless contraindicated:

* elevating the head of the bed to greater than 30 degrees

* providing mouth care every 4 hours, teeth brushing every 12 hours, and deep oropharyngeal suctioning every 12 hours

* initiating stress ulcer prophylaxis using either histamine₂-receptor blocking agents or proton-pump inhibitors

* initiating deep vein thrombosis prophylaxis.

A road map to success

Learning to care for a patient undergoing mechanical ventilation as a treatment strategy can be smooth driving if you know the right questions to ask. If you answer the questions step by step while working collaboratively with the respiratory therapist, you'll find it's easy to map the destination of oxygen to all the cells in the body!!

Indications for mechanical ventilation

* PaO₂ less than 50 mm Hg with FiO₂ greater than 0.60

* PaO₂ greater than 50 mm Hg with pH less than 7.25

* Vital capacity less than two times the tidal volume

* Negative inspiratory force less than 25 cm H₂O

* Respiratory rate greater than 35 breaths/minute

Initial ventilator settings

The following guide is an example of the steps involved in operating a mechanical ventilator. The nurse, in collaboration with the respiratory therapist, always reviews the manufacturer's instructions, which vary according to the equipment, before beginning mechanical ventilation.

1. Set the machine to deliver the tidal volume required.

2. Adjust the machine to deliver the lowest concentration of oxygen to maintain normal PaO₂ (80 to 100 mm Hg). This setting may be high initially but will gradually be reduced based on ABG results.

3. Record PIP.

4. Set the mode (AC or SIMV) and rate according to the healthcare provider's order. Set PEEP and pressure support if ordered.

5. Adjust sensitivity so that the patient can trigger the ventilator with a minimal effort (usually 2 mm Hg negative inspiratory force).

6. Record minute volume and obtain ABG values to measure PaCO₂, pH, and PaO₂ after 20 minutes of continuous mechanical ventilation.

7. Adjust the setting (FiO₂ and rate) according to the results of ABG analysis to provide normal values or those set by the healthcare provider.

8. If the patient suddenly becomes confused or agitated or begins bucking the ventilator for some unexplained reason, assess for hypoxia and manually ventilate on 100% oxygen with a bag-valve mask.

Lungs under pressure

The best indicator of alveolar overdistension (or too much pressure from mechanically delivered breaths) is peak alveolar pressure, which can be assessed by measuring the plateau pressure, or the pressure applied to the small airways and alveoli during inspiration.

Here's how to measure plateau pressure:

Following delivery of the tidal volume, you'll see a number on the ventilator called PIP, or the amount of pressure it takes to deliver that volume. This number doesn't mean a whole lot and shouldn't be used for trending or evaluation. For example, a PIP of 45 cm H₂O doesn't give you any clinical information because any change in airway resistance or compliance will change the PIP.

If you set the ventilator to achieve a breath hold following delivery of the tidal volume, then you should see the pressure drop from the peak to a holding pressure. This holding pressure is the plateau pressure and should be 30 cm H₂O or less. If the value is higher, overdistension is likely.

Every time you perform a patient and ventilator assessment (sometimes called a ventilator check), assess the plateau pressure. If this value is trending upward or exceeds 30 cm H₂O, talk to the respiratory therapist about alternative, lung-protective strategies, a relatively new but important part of mechanical ventilation. Alternative strategies may include permissive hypercapnia, airway pressure release ventilation, or changing the mode to pressure control ventilation.

If the patient's PIP is increasing but the plateau pressure stays the same, then the reason for the pressure increase is in the ventilator tubing or his tracheobronchial tree. Suppose the patient's PIP is 35 cm H₂O and the plateau pressure is 25 cm H₂O. An hour later, the peak pressure is 65 cm H₂O, but the plateau pressure is still 25 cm H₂O. He isn't in danger of lung damage because the reason for the high PIP is an increase in airway resistance. He may be biting on the ET tube or he may need an inline bronchodilator treatment or suctioning. This is why PIP doesn't mean much by itself and plateau pressure is the more important ventilator pressure to monitor.

Transairway pressure is the difference between the PIP and the plateau pressure; it's typically less than 10 cm H₂O. Investigate any pressure above this level. For example, a sudden increase means an ET tube may be occluded; a more gradual increase may mean the patient is developing bronchoconstriction and may need an inline bronchodilator.

Mr. Brown's status

Cheat Sheet

The following is a summary of our hypothetic patient Mr. Brown's status using the values from the ventilator and his ABG values.

* Mode: volume control SIMV

* pH: 7.38

* Tidal volume: 700 mL

* PaCO₂: 42 mm Hg

* Ventilation rate: 10 breaths/minute

* PaO₂: 225 mm Hg

* FiO₂: 1.0

* HCO₃-: 24 mEq/L

* PEEP: 5 cm H₂O

* P/F ratio: 225

* Total minute ventilation: 9 L (this value includes Mr. Brown's spontaneous breathing in SIMV mode)

* Spontaneous tidal volume: 250 mL

* Spontaneous respiratory rate: 8 breaths/minute

* PIP: 32 cm H₂O

* Breath sounds: bibasilar fine, late-inspiratory crackles

* Plateau pressure: 24 cm H₂O

* Peripheral oxygenation: 100%

Learn more about it

Burns SM. Pressure modes of mechanical ventilation: the good, the bad, and the ugly. AACN Adv Crit Care. 2008;19(4):399-411.

Kallus C. Building a solid understanding of mechanical ventilation. Nursing2009. 2009;39(6):22-28.

Koh SO. Mode of mechanical ventilation: volume controlled mode. Crit Care Clin. 2007;23(2):161-167.

Oakes D, Shortall S. Ventilator Management: A Reference Guide. 3rd ed. Orono, ME: Health Educator Publications; 2009.

Santanilla JI, Daniel B, Yeow ME. Mechanical ventilation. Emerg Med Clin North Am. 2008;26(3):849-862.

Smeltzer SC, Bare BG, Hinkle JL, Cheever KH. Brunner & Suddharth's Textbook of Medical-Surgical Nursing. 11th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:739-746.