During mechanical ventilation, adjusting the set tidal volume (V_T) or rate (f) can be used to correct respiratory alkalosis or acidosis. These changes are based on the following equation*:

Known PaCO2×KnownV˙E=Desired PaCO2×DesiredV˙E

With this equation, it is assumed that physiological dead space^† and CO₂ production (resulting from metabolism) do not change significantly during a short period. The equation can therefore be modified to read:

Known PaCO2×Known alveolar ventilation per minute (V˙A)=Desired PaCO2×Desired V˙A

If it is appropriate to keep rate (f) constant and change V_T, then the equation becomes:

DesiredVT=KnownPaCO2×KnownVTDesiredPaCO2

If it is appropriate to keep V_T constant and change f, then the equation is written:

Desiredf=KnownPaCO2×KnownfDesiredPaCO2

Respiratory Acidosis: Volume and Pressure Ventilation Changes

When PaCO₂ is elevated (>45 mm Hg) and pH is decreased (<7.35), respiratory acidosis is present and is inadequate. Acute respiratory acidosis is associated with the following:

• Parenchymal lung problems (e.g., pulmonary edema, pneumonia)

• Airway disease (e.g., severe asthma attack)

• Pleural abnormalities (e.g., effusions)

• Chest wall abnormalities

• Neuromuscular disorders (e.g., spinal cord injury, myasthenia gravis)

• Central nervous system (CNS) problems (e.g., drug overdose).1

See Chapter 4 for additional information.

In patients receiving mechanical ventilation, respiratory acidosis generally can be corrected by altering the set V_T or f. Regardless of whether the patient is receiving volume-controlled or pressure-controlled ventilation, increasing will decrease the PaCO₂.

Recommended guidelines are to target the V_T of 5 to 8 mL/kg ideal body weight (IBW) while assuring that the plateau pressure (P_plateau) is maintained less than 30 cm H₂O. As discussed in Chapter 6, tidal volume and breathing frequency adjustments should be based on the patient’s pulmonary pathology. It is important to understand that the 5 to 8 mL/kg range is an average. If the V_T is at the upper limit of this range and/or P_plateau is greater than 30 cm H₂O, then f should be increased.

With PC-CMV, the set pressure is generally increased to obtain the targeted V_T. PC-CMV is time-cycled. If inspiratory time (T_I) is short, increasing it may also increase volume delivery, without requiring an increase in pressure (P) (Fig. 12-2).

 Clinical Scenario

Adjusting PC-CMV in a Patient with Respiratory Acidosis

A 75-kg (165-lb) patient is placed on PC-CMV with a rate of 10 breaths/min, a set pressure of 25 cm H₂O, and a measured V_T of 425 mL. The flow-time curve for this patient is shown in Curve A below. T_I is 0.7 seconds. The ABGs are as follows: pH = 7.30; PaCO₂ = 50 mm Hg; = 23 mEq/L.

To improve ventilation, two things can be adjusted. The T_I can be increased so that the set pressure reaches the alveolar level. This would be apparent when the flow curve shows a time of zero flow during inspiration (Curve B). This strategy may be tried first. If this does not improve volume delivery sufficiently, the set pressure can be increased.

 Clinical Scenario

Respiratory Acidosis: Increasing Tidal Volume

A 50-year-old man with respiratory acidosis is receiving mechanical ventilatory support. He is 6 ft 2 in. tall and weighs 190 lb (81 kg, IBW) (anatomic dead space [V_Danat] = 190 mL). Exhaled V_T measured at the endotracheal tube (ET) is 400 mL. His respiratory rate is 16 breaths/min. The patient is receiving VC-CMV. ABGs show a PaCO₂ of 55 mm Hg and a pH of 7.33. The patient has no pulmonary disease. His desired PaCO₂ is 40 mm Hg. What ventilator change must be made to decrease the PaCO₂?

Because the V_T setting is less than 8 mL/kg and the patient has no pulmonary disease, it is appropriate to hold rate constant and change V_T:

DesiredVT=KnownPaCO2×KnownVTDesiredPaCO2

Desired VT=55×40040=550mL

The new V_T is set at 550 mL (about 7 mL/kg IBW) to achieve a desired PaCO₂ of 40 mm Hg. The alveolar ventilation has been increased appropriately to correct the respiratory acidos is.

 Clinical Scenario

Respiratory Acidosis: Increasing Rate

A 48-year-old woman who is 5 ft 2 in. tall is receiving VC-CMV with no spontaneous breaths. She has a PaCO₂ of 58 mm Hg; pH is 7.28; V_T at the ET is 425 mL. IBW is 115 lb (52 kg); V_Danat is 115 mL. Respiratory rate is 15 breaths/min. How can the ventilator settings be adjusted to achieve a desired Pa₂ of 40 mm Hg?

In this case, the patient’s V_T is set at about 8 mL/kg, so it is appropriate to change f and not increase V_T.

Desiredf=Knownf×KnownPaCO2DesiredPaCO2

Increasing the breathing frequency to 23 breaths/min should decrease the PaCO₂ to 40 mm Hg. It is important to recognize, however, that setting high respiratory rates is associated with air trapping because of a reduced expiratory time.

 Clinical Scenario

Changes During Pressure Ventilation

During PC-CMV, the same types of adjustments for V_T and rate are made based on ABGs, except that the set pressure is increased or decreased to achieve a desired V_T. Exhaled volume is monitored until the desired V_T is obtained. Note that it is important to make sure that T_I is long enough to gain the most benefit from the set pressure (see Case Study 12-1).

 Case Study 12-1

Hyperventilation

A 190-lb (86-kg), 68-year-old man (IBW = 80 kg) is admitted to the hospital. He is placed on mechanical ventilation for acute respiratory failure compounded by a metabolic acidosis. It is found that he has a renal disorder. The physician orders peritoneal dialysis. In the interim, the physician wants the respiratory therapist to target a pH of 7.35 with assisted ventilation. Initial assessment of the patient resulted in the following ABG: pH = 7.22; PaCO₂ = 38 mm Hg; HCO₃⁻ = 15 mEq/L; PaO₂ = 98 mm Hg on F_IO₂ = 0.25.

The ventilator settings are: VC-CMV; f = 24 breaths/min; V_T = 600 mL; F_IO₂ = 0.25.

ABG results on this new setting are pH = 7.37; PaCO₂ mm Hg = 23; = 13.5 mEq/L; PaO₂ = 115 mm Hg.

A flow-time graphic shows the following:

What is the problem, and what would you suggest to correct this problem and still help the patient?

See Appendix A for the answers.

A 75-kg (IBW) patient with respiratory acidosis is receiving PC-CMV (PaCO₂ = 59 mm Hg; pH = 7.31; desired P_ACO₂ = 40 mm Hg). At a set pressure of 10 cm H₂O, the exhaled V_T is 400 mL (5.3 mL/kg) and the rate is 16 breaths/min. The patient is not spontaneously breathing. T_I is set so that the flow returns to zero before the end of inspiration and a P_plateau period can be measured. What ventilator adjustment must be made to decrease his PaCO₂? The V_T setting is less than 8 mL/kg, so it is appropriate to hold f constant and change V_T.

DesiredVT=59×40040=590mlorabout600mL

A set pressure (P) of 10 cm H₂O results in a V_T of 400 mL (0.4 L); what is an estimated pressure that will achieve a V_T of 600 mL (0.6 L)? Assume that compliance does not change. Remember static compliance (C_S) = V_T/(P_plateau − PEEP, C_S = 400/10, and C_S = 40 mL/cm H₂O

DesiredP=DesiredVTCS

DesiredP=600mL(40mL/cmH2O)andP=15cm H2O

Desired pressure is 15cm H2O.

Increasing pressure during PC-CMV will normally increase V_T. Conversely, decreasing pressure decreases V_T for patients with respiratory alkalosis during PC-CMV.

Respiratory Alkalosis: VC-CMV and PC-CMV Changes

When PaCO₂ is decreased (<35 mm Hg) and pH increases (>7.45), then respiratory alkalosis is present and alveolar ventilation is excessive. Common causes of respiratory alkalosis include the following2:

• Hypoxia with compensatory hyperventilation

• Parenchymal lung disease

• Medications (salicylate, xanthines, analeptics)

• Mechanical ventilation

• Central nervous system disorders (meningitis, encephalitis, head trauma)

• Anxiety

• Metabolic problems (sepsis, hepatic disease)

In mechanically ventilated patients, hyperventilation is often the cause of respiratory alkalosis. To correct respiratory alkalosis in this situation, the clinician should decrease minute ventilation during volume-controlled ventilation by decreasing f and, if necessary, by decreasing V_T. If pressure-controlled ventilation is used, the clinician should decrease f first and then decrease set pressure, if necessary.

 Clinical Scanario

Respiratory Alkalosis: Decreasing the Rate

A 35-year-old man with respiratory alkalosis (PaCO₂ = 20 mm Hg; pH = 7.60) is on CMV with no spontaneous breaths and a delivered V_T of 550 mL, a rate of 18 breaths/min, and V_Danat at 150 mL. His desired PaCO₂ is 40 mm Hg. IBW is 70 kg. V_T setting is approximately 8 mL/kg. It is appropriate to decrease f and leave V_T constant:

Desiredf=18×2040=9breaths/min

A new rate of 9 breaths/min should achieve the desired P_ACO₂ of 40 mm Hg. (NOTE: This case did not state whether this was volume-controlled or pressure-controlled ventilation. It does not matter in this situation, however, because the targeted change was the rate.)

 Clinical Scenario

Respiratory Alkalosis: Decreasing the Volume in Pressure-Controlled Ventilation

A 50-year-old woman on PC-CMV originally had a set pressure of 20 cm H₂O, which resulted in a V_T of 450 mL (C_S = 28 mL/cm H₂O). The set rate was 12 breaths/min with no spontaneous efforts. T_I is long enough to provide a slight pause (zero flow) at end inspiration. ABGs on this setting showed a pH = 7.41 and a PaCO₂ of 44 mm Hg. The patient’s IBW is 60 kg.

After 2 days of ventilation on these settings, the pH = 7.51 and the PaCO₂ = 29 mm Hg. The pressure is still at 20 cm H₂O and V_T is 625 mL (10.4 mL/kg IBW). C_S is now 32 mL/cm H₂O. This is a substantial improvement. The V_T is high, based on IBW. What would be an appropriate target volume for this patient?

Desired VT=453or about 450mL

How do you set a pressure to get this V_T?

Remember CS=VT/ΔP,soP=VT/CS

and

P=450mL/(32mL/cm H2O)=14cm H2O

A decrease in pressure to 14 cm H₂O should achieve the new targeted V_T of 450 mL, which is 7.5 mL/kg IBW for this patient.

 Clinical Scenario

Respiratory Alkalosis During Spontaneous Efforts

A 25-year-old man on VC-CMV has a set rate of 14 breaths/min and a V_T of 560 mL. The patient’s IBW is 80 kg (176 lb). The patient is triggering the ventilator an additional 4 breaths/min. Total rate is 18 breaths/min; PaCO₂ is 30 mm Hg; pH is 7.50. What can the respiratory therapist do to improve ventilation? The V_T is 7 mL/kg IBW, which is appropriate for this patient. Suppose the therapist reduces the set f on the ventilator to 10 breaths/min. What impact would this have on ventilation? As long as the patient continues to trigger additional breaths, reducing the set f will have no effect.

Decreasing V_T (or, more specifically, pressure during PC-CMV) may be effective in reducing minute ventilation unless the patient increases his spontaneous rate, thus maintaining high alveolar ventilation. In addition, lowering the V_T to less than 7 mL/kg may result in atelectasis from low V_T ventilation.

In this situation, several alternatives are available: (1) reduce the tidal volume but ensure that an adequate level of PEEP is being administered to reduce the potential for atelectasis; (2) institute another mode, such as synchronized intermittent mandatory ventilation (SIMV) or pressure-supported ventilation (PSV), to allow the patient to breathe without receiving a mandatory breath with every inspiration; or (3) sedate the patient to control breathing better. Sedation may be needed for patients demonstrating extreme agitation, increased work of breathing (WOB), or patient-ventilator asynchrony. It is important to recognize that sedation may not always be the best choice. Whenever possible, the cause of hyperventilation should be investigated and treated. Common causes of hyperventilation include hypoxemia, pain, anxiety, fever, agitation, and asynchrony.

Head injury that results in a high and hyperventilation is sometimes difficult to control, regardless of the mode selected. Some patients with brain injury have a tendency to breathe with a high V_T and f, which is due to a CNS lesion and cannot be corrected.3

The normal ratio of dead space to tidal volume (V_D/V_T) is 0.2 to 0.4. In critically ill patients, this value may be greater than 0.7. Calculation of V_D/V_T ratio uses the Enghoff modification of the Bohr equation: V_D/V_T = (PaCO₂ − )/PaCO₂, where is the partial pressure of CO₂ in the mixed expired gases collected from the patient.* A blood gas sample is collected and the average tidal volume measured while the is being measured. Note that although this method of measuring V_D/V_T ratio can provide useful information on mechanically ventilated patients, it typically requires additional equipment and is not routinely performed.

It is more common in ventilated patients to monitor the end-tidal CO₂ (normal P_ETCO₂ = 35 to 43 mm Hg) and the gradient between arterial and end-tidal CO₂ to determine whether dead space is changing (normal PaCO₂-to-P_ETCO₂ gradient = 1-5 mm Hg). A decrease in end-tidal CO₂ and an increase in the PaCO₂-to-P_ETCO₂ gradient suggest increased dead space. Some clinicians use the mean value of the P_ETCO₂ instead of measuring mixed expired gas to calculate the V_D : V_T ratio.⁶ Advances in capnography using single-breath volumetric CO₂ monitoring offers still another alternative for estimating V_D/V_T. (See Chapter 10 for more details on P_ETCO₂ and volumetric CO₂ monitoring.)

Historically, iatrogenic hyperventilation has been used in patients with acute head injury and increased intracranial pressure (ICP). Hyperventilation reduces CO₂ in the blood, which in turn is associated with constriction of cerebral blood vessels and a decrease in blood flow to the brain. Although this approach was believed by many clinicians to help lower increased ICP, therapeutic guidelines for head injuries with increased ICP do not recommend prophylactic hyperventilation (PaCO₂ <25 mm Hg) during the first 24 hours. Hyperventilation during the first few days following severe traumatic brain injury may actually increase cerebral ischemia and cause cerebral hypoxemia (see Chapter 7 section on closed head injury).

Hyperventilation may be needed for brief periods when acute neurologic deterioration is present and ICP is elevated. Mild hyperventilation (PaCO₂ 30-35 mm Hg) may be used for longer periods in situations in which increased ICP is refractory to standard treatment, including sedation and analgesia, neuromuscular blockade, cerebrospinal fluid drainage, and hyperosmolar therapy.⁷ However, the practice of iatrogenic hyperventilation remains controversial.⁸ Consider the following example.

 Clinical Scenario

Iatrogenic Hyperventilation

A 42-year-old woman who is 5 ft 4 in. tall (IBW = 125 lb, or 57 kg) is on controlled ventilation for 12 hours following a severe cerebral concussion. Her PaCO₂ is 48 mm Hg, her pH is 7.32, and her V_T is 400 mL. Respiratory rate is 12 breaths/min. What are your recommendations? Current V_T is 7 mL/kg. Is it appropriate to change f? In this case, it would be appropriate to increase the f and maintain the PaCO₂ at normal levels for the first 24 hours.

If we change the rate, the following recommendation would apply:

Desiredf=12×4840=14breaths/min

Occasionally, it becomes impossible to maintain normal PaCO₂ levels in a patient without risking lung damage from high pressures and volumes. Patients with acute respiratory distress syndrome (ARDS) or status asthmaticus and sometimes patients with chronic obstructive pulmonary disease (COPD) who require ventilatory support are at risk for ventilator-induced injury. Inappropriate use of mechanical ventilation can result in severe lung injury, activation of inflammatory mediators, and can even potentially lead to multisystem organ failure.9 (See Chapter 17 for additional information on ventilator-induced lung injury.)

A technique referred to as permissive hypercapnia (PHY) has gained popularity as an alternative form of patient management.¹⁰ PHY is a deliberate limitation of ventilatory support to avoid lung overdistention and injury of the lung. During PHY, arterial partial pressures of carbon dioxide (PaCO₂) values are allowed to rise above normal (e.g., ≥50-150 mm Hg), and pH values are allowed to fall below normal (e.g., ≥7.10-7.30). Patients who do not have renal failure or cardiovascular problems usually tolerate a pH of 7.20 to 7.25. Younger patients may tolerate even lower pH values. Many clinicians who use PHY allow for a gradual rise in PaCO₂ because an abrupt increase in PaCO₂ is usually not well tolerated.^11–12

Alterations in PaCO₂ and pH can affect multiple organ systems. Researchers often focus on the effects of severe acidosis because of serious consequences associated with it. Although most investigators agree that a pH of 7.25 or greater is acceptable, no one is certain whether a lower pH is acceptable. Survival without complications has been demonstrated in isolated cases in which the pH dropped as low as 6.6 and the PaCO₂ rose as high as 375 mm Hg when oxygenation was well maintained.^11,13 Similar findings have been shown in studies of patients with ARDS and acute asthma.^14–17

During hypoventilation, increases in PaCO₂ are accompanied by a decrease in PaO₂, so O₂ administration must be provided and oxygenation status monitored carefully. Increases in PaCO₂ and decreases in pH that occur in acute respiratory acidosis also cause a right shift in the oxyhemoglobin dissociation curve. Although this shift in the curve facilitates unloading of O₂ at the tissue level, it also reduces O₂ loading at the lungs and can further compromise gas exchange.

Increases in carbon dioxide have an additional physiological effect. A higher-than-normal PaCO₂ stimulates the drive to breathe. Therefore, it is appropriate to provide sedation to patients with acute lung injury (ALI) in whom permissive hypercapnia is being used. The sedation may improve patient comfort (Key Point 12-1).

Contraindications of Permissive Hypercapnia

Carbon dioxide is a powerful vasodilator of cerebral vessels. Thus, increasing CO₂ levels can result in cerebral edema and increased ICP, which can aggravate cerebral disorders, such as cerebral trauma or hemorrhage, and cerebral-occupying lesions.19,21 For this reason, the use of PHY is contraindicated in the presence of disorders such as head trauma and intracranial disease. Indeed, it is absolutely contraindicated for those patients who demonstrate intracranial lesions.²²

Permissive hypercapnia is relatively contraindicated in patients with preexisting cardiovascular instability. Circulatory effects of PHY can include decreased myocardial contractility, arrhythmias, vasodilation, and increased sympathetic activity. A common finding in patients receiving PHY is increased cardiac output, a normal systemic blood pressure (BP), and pulmonary hypertension.^20,23 If the patient’s sympathetic response is impaired or blocked, or if cardiac function is impaired, then an increase in cardiac output might not occur, allowing the vasodilatation to result in hypotension.¹⁹

The exact response of the cardiovascular system to permissive hypercapnia is difficult to predict; therefore PHY should be used with caution. This is particularly true when working with patients with any of the following cardiovascular conditions: cardiac ischemia, left ventricular compromise, pulmonary hypertension, and right heart failure.²²

Finally, it is worth mentioning that elevated CO₂ or decreased pH may affect regional blood flow; skeletal and smooth muscle function; nervous system activity; and endocrine, digestive, hepatic, and renal system functions. Although these effects have not caused significant concern in the clinical setting, further research in these areas is warranted to improve our understanding of this ventilatory strategy.

 Clinical Scenario

Permissive Hypercapnia

A 30-year-old man with ARDS has been on ventilatory support for a week. Current settings are V_T = 500 mL; f = 12 breaths/min; peak inspiratory pressure (PIP) = 37 cm H₂O; and P_plateau = 29 cm H₂O. The patient is 5 ft 8 in. tall and has an IBW of 70 kg. ABGs show pH = 7.24 and PaCO₂ = 64 mm Hg. What change is appropriate to return his PaCO₂ to normal? If we tried to increase his V_T, pressures would increase. If we increase f, the desired f would be

Desired f=12×6440=19breaths/min

This equation assumes that we want to maintain a normal PaCO₂ of 40 mm Hg. One might suspect that the increased rate would also lead to air trapping, an increase in mean airway pressure, and an increased risk of lung injury. However, in patients with ARDS, lung units are more likely to empty quickly (short time constants). We might increase rate slightly and allow PaCO₂ to remain high (i.e., PHY). To protect the patient from increasing airway pressures, it might be appropriate to use pressure ventilation.

The use of PHY is restricted to situations in which the target airway pressure is at its maximum and the highest possible rates are being used. Although no adverse short-term effects of PHY have been noted for most patients, it is not known whether any long-term effects occur. The risks of hypercapnia are considered by some to be preferable to the high P_plateau required to achieve normal CO₂ levels. This represents a significant shift in thinking in regard to ventilator management and ARDS.²⁴

Suctioning a patient’s artificial airways involves insertion of a suction catheter into the patient’s trachea and the application of negative pressure as the catheter is gradually withdrawn.25 Suctioning a patient with an artificial airway can involve shallow suctioning, in which the catheter is inserted to a depth that approximates the length of the artificial airways, or deep suctioning, where the catheter inserted until a resistance is met. In the latter case, once the resistance is encountered, the catheter is withdrawn approximately 1 cm before applying negative pressure.²⁵

Two methods of suctioning are typically described based on the type of catheter used: the open suctioning technique and the closed suctioning technique. The open-circuit technique requires disconnecting the patient from the ventilator; the closed-circuit technique can be performed without removing the patient from the ventilator. With the closed-circuit technique, a sterile, inline suction catheter is incorporated into the ventilator circuit, thus allowing passage of the catheter into the ET and trachea without disconnecting the patient from the ventilator (Key Point 12-2).

Suction catheters are generally made of transparent flexible plastic that is rigid enough to allow it to be easily inserted into the artificial airway but flexible enough to negotiate turns and not cause trauma to the airway. Catheters are smooth tipped with two or more side holes near the distal end (Fig. 12-3). (It is thought that these smooth-tipped catheters with side holes may help reduce trauma to the mucosa.)²⁶

The proximal end of the catheter connects to a collecting canister via large-bore plastic tube. A thumb port located at the proximal end of the suction catheter allows the operator to control the suction pressure. When it is covered, suction pressure is applied to the catheter and into the airway. The suction pressure applied should be the lowest possible pressure that is required to effectively clear secretions.25 Box 12-2 provides a list of suggested suction pressure levels. These recommended suction levels are based on current practice. It is important to note that to date no experimental studies are available to support these values.

The catheter length should be long enough to reach a main-stem bronchus. This requires a catheter length of about 22 in. (56 cm).26 Note that in infants and in patients with recent tracheal reconstructive surgery or pneumonectomy, the suction catheter should not be inserted more than 1 cm below the distal tip of the ET.²⁷

Remember that the left main-stem bronchus is narrower and branches at a more acute angle than the right bronchus. Consequently, suction catheters often enter the right rather than the left bronchus. A special-tipped suction catheter is available with a bend at the distal end to help facilitate left bronchial suctioning, particularly if the patient is supine or lying on the left side or if the head is turned to the left. Left bronchus suctioning is easier when the patient has a tracheostomy tube in place rather than an ET.²⁷

The diameter of the suction catheter selected is governed by the internal diameter of the artificial airway. It is generally accepted that the diameter of the suction catheter should not exceed 50% of the internal diameter of the artificial airway for children and adults and 30% of the internal diameters for infants.²⁵ Suction catheter sizes are based on French units. French units refer to the circumference of the tube. (NOTE: Circumference equals diameter multiplied times 3.1416 [π].) Because ETs are sized in centimeters and suction catheters are sized in French units, a conversion is required to estimate the correct size (Box 12-3).

Suctioning should be preceded by hyperoxygenation with 100% O₂ for 30 seconds, followed by hyperoxygenation with 100% O₂ for 1 minute after suctioning is complete, especially in patients who are hypoxemic before or during suctioning.²⁸ This can be done manually with a resuscitation bag, although this approach does not guarantee V_T or pressure, and it has been shown to be ineffective in delivering an F_IO₂ of 1.0.²⁵ Hyperoxygenation is therefore best accomplished using a temporary oxygen-enrichment program that is available on many microprocessor ventilators.

The duration of suctioning should be brief and must not exceed 15 seconds.²⁵ Shallow suctioning is recommended over deep suctioning, particularly because deep suctioning has not been shown to be superior and may be associated with significantly greater chance of trauma to the tracheal mucosa. Suction should be applied intermittently rather than continually, and the catheter should be rotated as it is withdrawn.²⁹

Closed-Suction Catheters (In-line Suction Catheters)

The closed-suction procedure is considered equally effective as the standard open-suction procedure.38,39 The closed-suction procedure uses in-line catheters that are encased in clear plastic sheaths. The plastic sheaths are attached to special assemblies that connect to a patient’s ventilator circuit, near the Y-connector (Fig. 12-4).⁴⁰ Notice that inline catheters may add weight and increase the tension on the ET.

The advantage of using the closed-suction technique is that disconnecting the patient from the ventilator can be avoided. This is especially important in patients receiving high F_IO₂s and PEEP because disconnection increases the likelihood of hypoxia and alveolar collapse. Another advantage of this technique is that it reduces the risk for contaminating the airway and lungs when patients are disconnected from the ventilator. For example, using a manual resuscitation bag may introduce contamination into the patient’s lower airways when a single-use disposable suction catheter, which is accidentally contaminated by the handler, is used to suction a patient. Additionally, aerosolized particles from the ventilator circuit can be released into the air during disconnection of the ventilator circuit, thus presenting a potential risk of contamination to the caregiver. Using inline suction avoids these problems and has been shown to reduce the incidence of ventilator-associated pneumonia (VAP).41 Specific indications for closed-suction catheters are listed in Box 12-4.⁴²

Box 12-4

Indications for Using Closed-Suction Catheter Systems

Unstable patients who are ventilated (e.g., in acute lung injury or acute respiratory distress syndrome) and have high ventilator requirements:

• High PEEP ≥10 cm H₂O

• High ≥20 cm H₂O

• Long inspiratory time ≥1.5 s

• High F_IO₂ ≥0.6

• Patients who become hemodynamically unstable during suctioning with an open system and ventilator disconnection

• Patients who desaturate significantly (a drop in SpO₂) during suctioning with an open system and ventilator disconnection

• Patients with contagious infections, such as active tuberculosis, where open suctioning and ventilator disconnect may contaminate health care workers

• Ventilated patients who require frequent suctioning, for example, more than 6 times a day

• Patients receiving inhaled gas mixtures (such as nitric oxide or heliox therapy) that cannot be interrupted by ventilator disconnection.

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Related posts:

1. Ventilator-Associated Pneumonia
2. Basic Concepts of Noninvasive Positive-Pressure Ventilation
3. Initial Patient Assessment
4. Improving Oxygenation and Management of Acute Respiratory Distress Syndrome

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