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Acute ventilatory failure (also called acute respiratory acidosis) is a condition in which the lungs are unable to meet the metabolic demands of the body in terms of CO2 removal. As a result, the PaCO2 rises and, without supplemental oxygen, the PaO2 falls. When an increased PaCO2 level

is accompanied by acidemia (decreased pH), acute ventilatory failure, or acute respiratory acidosis, is said to exist. Table 11.3 shows an ABG example of acute ventilatory failure. Clinically, this is a life-threatening medical emergency that requires ventilatory support.

TABLE 11.3

Acute Ventilatory Failure (Acute Respiratory Acidosis)

Arterial Blood Gas Changes	Example
pH: Decreased	7.17
PaCO2: Increased	79 mm Hg
: Increased (but normal)	28 mEq/L
PaO2: Decreased	49 mm Hg*

*Moderate to severe hypoxemia.

Chronic ventilatory failure (also called compensated respiratory acidosis) is defined as a greater-than-normal PaCO2 level with a normal pH

status. The renal system has compensated for the low pH by retaining bicarbonate () and adding it to the patient's blood. Although chronic ventilatory failure is most commonly seen in patients with severe COPD (e.g., chronic bronchitis, emphysema, or cystic fibrosis), it is also seen in several chronic restrictive lung disorders (e.g., obesity, severe tuberculosis, fungal disease, kyphoscoliosis, or interstitial lung disease). Table 11.4 shows an ABG example of chronic ventilatory failure with hypoxemia. Clinically, this is a life-threatening medical emergency that requires ventilatory support.

TABLE 11.4

Chronic Ventilatory Failure (Compensated Respiratory Acidosis)

Baseline Arterial Blood Gas Values*

ABG Changes	Example
pH: Normal	7.37
PaCO2: Increased	77 mm Hg
: Increased (significantly)	43 mEq/L
PaO2: Decreased	61 mm Hg

*NOTE: Chronic ventilatory failure ABG baseline values are much different than the ABG baseline values of the normal individual (e.g., pH: 7.35–7.45; PaCO2: 35–45; : 22–26; PaO2: 80–100).

ABG, Arterial blood gas.

Acute Alveolar Hyperventilation Superimposed on Chronic Ventilatory Failure

Like any other patient (healthy or unhealthy), the patient with chronic ventilatory failure also can acquire a new—that is, additional—acute shunt-producing disease (e.g., pneumonia or pulmonary edema). This is not unusual in the real world of clinical medicine. For example, when such patients have the mechanical reserve to increase their alveolar ventilation significantly in an attempt to maintain their baseline PaO2, their

PaCO2 often decreases from their normally high baseline level. This action causes their pH to increase. As this condition intensifies, the patient's

baseline ABG values can quickly change from chronic ventilatory failure to that of acute alveolar hyperventilation superimposed on chronic ventilatory failure (Table 11.5).

TABLE 11.5

Acute Alveolar Hyperventilation Superimposed on Chronic Ventilatory Failure*

Arterial Blood Gas Changes	Example
pH: Increased	7.51
PaCO2: Increased (but lower than patient's typical elevated baseline level)	52 mm Hg
: Increased (significantly) (but lower than patient's typical elevated baseline level)	40 mEq/L
PaO2: Decreased (but lower than patient's typical low baseline level)	49 mm Hg

*This condition is often seen in patients with acute bronchitis, pneumonia, or pulmonary edema that exacerbates their chronic obstructive pulmonary disease.

Acute Ventilatory Failure (Hypoventilation) Superimposed on Chronic Ventilatory Failure

When the patient with chronic ventilatory failure does not have the additional mechanical reserve to meet the hypoxemic challenge of a new respiratory disorder, the patient begins to breathe less efficiently—that is, the patient hypoventilates.5 This action causes the PaCO2 to increase above the patient's already high PaCO2 baseline level.

As the PaCO2 suddenly increases, the patient's arterial pH level falls, or becomes acidic. As this condition intensifies, the patient's baseline

ABG values change from chronic ventilatory failure to acute ventilatory failure superimposed on chronic ventilatory failure—acute on chronic ventilatory failure (Table 11.6).

TABLE 11.6

Acute Ventilatory Failure Superimposed on Chronic Ventilatory Failure

Arterial Blood Gas Changes	Example
pH: Decreased	7.28
PaCO2: Increased (but higher than patient's typical elevated baseline level)	97 mm Hg
: Increased (significantly) (but higher than patient's typical elevated baseline level)	44 mEq/L
PaO2: Decreased (but lower than patient's typical low baseline level)	39 mm Hg

Table 11.7 provides a summary overview of the ABG findings for (1) chronic ventilatory failure, (2) acute hyperventilation superimposed on chronic ventilatory failure, and (3) acute ventilatory failure superimposed on chronic ventilatory failure.

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TABLE 11.7

Examples of Acute Changes Superimposed on Chronic Ventilatory Failure

Mechanical Ventilation

Before a decision can be made to commit the patient to any form of mechanical ventilation, the respiratory therapist must first answer these questions: Are key clinical indicators of respiratory failure present? Does the patient meet the standard criteria for mechanical ventilation? Does the patient primarily have hypoxemic respiratory failure, hypercapnic respiratory failure, or a combination of both? Which ventilatory support strategy would best serve the patient's short-term or long-term ventilatory needs? Should noninvasive ventilation or invasive ventilation be used? How can the lung be best protected from the harmful effects of mechanical ventilation? Finally, what will be the most effective strategies to “liberate” him from mechanical ventilation?

To satisfactorily answer these questions, it is essential that the respiratory therapist must again use good clinical judgment skills, which are based on the ability to (1) collect all the clinical data relevant to the patient's respiratory status, (2) formulate an objective and measurable respiratory assessment, (3) select and implement a safe and effective ventilatory management plan, and (4) clearly and correctly document the subjective and objective data, assessment, and ventilatory support plan that he has selected in pursuit of these goals.

Standard Criteria for Instituting Mechanical Ventilation

The four standard criteria for mechanical ventilation are (1) apnea, (2) acute ventilatory failure, (3) impending ventilatory failure, and (4) severe refractory hypoxemia. To help determine if the mechanical ventilation should be invasive or noninvasive, the respiratory therapist should also establish if the patient is able to protect his/her own airway during mechanical ventilation with the modality under consideration. Apnea is defined as the complete absence of spontaneous ventilation, which is an absolute indication for invasive mechanical ventilation. Apnea causes the PaO2 to rapidly decrease and the PaCO2 to increase. Death will ensue in minutes unless an airway is established and ventilation is provided.

Acute ventilatory failure is defined as a sudden increase in PaCO2 to greater than 50 mm Hg with an accompanying low pH value (<7.30).

Impending ventilatory failure occurs when the patient demonstrates a significant increase in the work of breathing with borderline acceptable ABG values. Severe refractory hypoxemia (PaO2 <40 mm Hg, SaO2 <75%) reflects a critically low oxygenation status that does not respond well

to oxygen therapy. Severe refractory hypoxemia is often seen in cases of severe pneumonia, interstitial lung diseases, and acute respiratory distress syndrome (ARDS). The PaO2/FIO2 ratio may be used to judge the degree of severity and need for other treatments of this disorder

(Table 11.8). Table 11.9 presents the basic criteria for instituting mechanical ventilation and the primary type of respiratory failure associated with these conditions.

TABLE 11.8

Refractory Hypoxemia

Classifications That May Suggest the Need for Treatment Modalities in Addition to Oxygen

Classification	PaO2/FIO2 Ratio
Normal	350–450 (room air)
Mild (acute) lung injury (acute respiratory distress syndrome)	200–300
Moderate lung injury	100–200
Severe lung injury	<100

TABLE 11.9

Criteria for Instituting Mechanical Ventilation and the Primary Type of Respiratory Failure Associated With These Conditions

Criteria for Instituting Mechanical Ventilation		Primary Type of Respiratory Failure
1.	Apnea	Hypercapnic
2.	Acute ventilatory failure	Respiratory failure
3.	Impending ventilatory failure
4.	Severe refractory hypoxemia	Hypoxemic
		Respiratory failure

Prophylactic Ventilatory Support

In addition to the four standard primary criteria for mechanical ventilation, the decision to place the patient on ventilatory support may be based on prophylactic reasons. For example, prophylactic ventilatory support is sometimes provided to patients in postanesthesia and surgery recovery, particularly in patients with preexisting cardiopulmonary disease, who (especially while still sedated) are at high risk for postoperative complications such as atelectasis, aspiration pneumonia, or ARDS. In addition, prophylactic ventilatory support is often provided to nonsurgical patients who are high risk for pulmonary complications, such as hypercapnic respiratory failure or hypoxemic respiratory failure in COPD, pulmonary, fibrosis, and left articular failure. As discussed in the following section, noninvasive ventilation also belongs in this category of ventilatory support.

Key Clinical Indicators for Ventilatory Support in Hypercapnic and Hypoxemic Respiratory Failure

There are a variety of key clinical indicators (laboratory and bedside) that can be used to help establish the need for ventilatory support. In addition, these clinical indicators can be used to determine the primary type of respiratory failure and the ventilatory strategy that may be used to most safely and effectively ventilate the patient. Table 11.10 lists key clinical indicators for ventilatory support associated with hypercapnic respiratory failure. Table 11.11 provides key clinical indicators associated with ventilatory support for hypoxemic respiratory failure.

TABLE 11.10

Key Clinical Indicators of Hypercapnic Respiratory Failure (Ventilatory Failure)

Clinical Indicator*	Normal Value	Critical Value
Alveolar Ventilation
PaCO2 (acute change)	35–45 mm Hg	>50 mm Hg and rising
pH	7.35–7.45	<7.20
Lung Expansion
Tidal volume (VT)	5–8 mL/kg	<3–5 mL/kg
Respiratory rate (breaths/min)	12–20/min	>30/min, or <10/min
Muscle Strength
Maximum inspiratory pressure (MIP, cm H2O)	−80 to 100 cm H2O	<−20 cm H2O
Vital capacity (VC)	65–75 mL/kg	<10–15 mL/kg
Work of Breathing
Minute ventilation (VE)	5–6 L/min	>10 L/min
VD/VT (%)	25%–40%	>60%

*See a detailed discussion of these clinical indications for hypercapnic respiratory failure in Chapter 4, Pulmonary Function Assessment, and Chapter 5, Arterial Blood Gas Assessment.

TABLE 11.11

Key Clinical Indicators of Hypoxemic Respiratory Failure (Oxygenation Failure)

Clinical Indicator*	Normal Value	Critical Value
Oxygenation Status
PaO2 (mm Hg)	80–100	<60 on FIO2 >0.50
P(A-a)O2 on 100%	25–65	>350
PaO2/PAO2 ratio	0.75–0.95	<0.75
PaO2/FIO2 ratio	350–450	<200
QS/QT (%)	<5	>20

*See a detailed discussion of these oxygen clinical indications in Chapter 6, Oxygenation Assessment.

Ventilatory Support Strategy

The selection of a ventilatory support strategy is based on the type of respiratory failure the patient demonstrates. For example, hypoxemic respiratory failure is treated with various oxygen therapy modalities to manage the patient's oxygenation status. Table 11.12 provides common oxygen treatment modalities for specific causes of hypoxemia.

TABLE 11.12

Common Oxygen Treatment Modalities for Specific Causes of Hypoxemia

Cause of Hypoxemia	Treatment
Alveolar hypoventilation—examples:	Ventilatory support—increased alveolar ventilation
COPD
Drug overdose
Decreased ventilation/perfusion ratio—examples:	Ventilatory support:
COPD	Oxygen
Asthma	CPAP
Pulmonary edema	PEEP
Pulmonary shunting—examples:	Oxygen via:
Pneumonia	CPAP
Atelectasis	PEEP
ARDS
Decreased barometric pressure	Oxygen
High attitude	Move to lower altitude

ARDS, Acute respiratory distress syndrome; COPD, chronic obstructive pulmonary disease; CPAP, continuous positive airway pressure; PEEP, positive end-expiratory pressure.

By contrast, hypercapnic respiratory failure is treated with ventilatory support techniques to manage the patient's PaCO2 levels and acid-base

status. Both oxygen and ventilatory support modalities are used when the patient demonstrates both hypoxemic and hypercapnic respiratory failure (sometimes referred to as Type III respiratory failure). Depending on the clinical situation, either noninvasive ventilation or invasive ventilation can be used as a ventilatory support strategy in all these types of respiratory failure.

Noninvasive Ventilation

Noninvasive ventilation (NIV) is defined as any mode of ventilatory support that does not require an invasive artificial airway (i.e., endotracheal tube or tracheostomy tube). As shown in Box 11.4, NIV has many benefits and is often the first choice for ventilatory support. NIV systems include continuous positive airway pressure (CPAP) ventilation delivered through a nasal or oral mask alone (which is a means to maintain or restore functional residual capacity) or in combination with any mode of pressure-limited or volume-limited ventilation. Both hypoxemic and hypercapnic types of respiratory failure can be managed effectively by NIV.

Box 11.4

Benefits of Noninvasive Ventilation

•Avoids endotracheal intubation

•Reduces problems associated with intubation—for example, airway trauma, increased risk for aspiration, and nosocomial pneumonia

•Maximizes patient comfort

•Decreases mortality

•Increases alveolar ventilation

•Improves alveolar oxygen (PAO2) and carbon dioxide (PACO2) status

•Opens and/or prevents alveolar collapse

•Reduces the work of breathing

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•Decreases oxygen consumption

•Decreases muscle fatigue

The primary indication for NIV is hypercapnic respiratory failure secondary to COPD exacerbation. NIV is also beneficial for a variety of other respiratory disorders when patient are able to protect their airway, including (1) asthma, (2) mild to moderate atelectasis, (3) communityacquired pneumonia, (4) cardiogenic pulmonary edema, (5) ARDS, (6) obesity-hypoventilation syndrome, and (7) neuromuscular diseases such as myasthenia gravis or Guillain-Barré syndrome.

Although NIV is a very safe and effective means of ventilatory support, it may be poorly tolerated, contraindicated, or even harmful in patients with (1) respiratory arrest, (2) cardiac arrest, (3) nonrespiratory organ failure (e.g., severe encephalopathy, severe gastrointestinal bleeding, or hemodynamic instability) (4) upper airway obstruction, (5) excessive or viscous airway secretions, (6) a poor ability to clear secretions, (7) an improperly fitting mask, (8) facial or head trauma or surgery, (9) profound refractory hypoxemia, (10) cardiovascular instability (e.g., hypotension, dysrhythmias, or acute myocardial infarction), (11) an inability to cooperate (e.g., impaired mental status, somnolence), (12) extreme obesity, or (13) the anticipation of a slowly resolving respiratory condition. In these cases, invasive ventilation is required.

Invasive Mechanical Ventilation

Invasive mechanical ventilation is defined as mechanical ventilation via an endotracheal or tracheostomy tube. Both hypoxemic and hypercapnic types of respiratory failure can be managed effectively by invasive mechanical ventilation. Mechanical ventilation protocols are discussed in the following sections.

Mechanical Ventilation Protocols

It is interesting to note that many medical centers have started their therapist-driven protocol (TDP) programs with a Mechanical Ventilation Protocol rather than with one of the relatively simple protocols described in Chapter 10, The Therapist-Driven Protocol Program (e.g., Oxygen Therapy Protocol, Airway Clearance Protocol, Lung Expansion Protocol, or Aerosolized Medical Protocol). The decision to proceed in this manner often appears to be based on humanistic, pathophysiologic, and economic grounds. Indeed, who could defend practices that are unnecessary (if not harmful), uncomfortable, and costly to patients requiring ventilator support?

Unquestionably, the high-technology, high-risk, high-visibility portion of respiratory therapy work is embedded in ventilator management. Much of the success of the TDP movement has occurred because of the dramatic ways in which standardized, data-driven algorithms have improved patient outcomes. Most dramatic reported outcomes include shortened ventilator weaning times, reduction of nosocomial infections, and reduced complications associated with mechanical ventilation (e.g., barotrauma).

Although most Mechanical Ventilation Protocols require the respiratory therapist to select a ventilator mode on the basis of specific patient needs, it is not the intent of this textbook to fully review or discuss the various types, modes, and weaning strategies. Table 11.13, however, does provide an overview of common ventilatory management strategies and good starting points used to treat specific pulmonary disorders.

TABLE 11.13

Common Ventilatory Management Strategies Used to Treat Specific Disorders (Good Starting Points)

		Disease	Ventilator	Tidal Volume			FIO2	General Goals
	Disorder			and Respiratory	Flow Rate	I/E Ratio
		Characteristics	Mode					and/or Concerns
				Rate
	Normal lung	Normal	Volume	4–8 mL/kg of ideal	60–80 L/min	1 : 2	Low to	Care to ensure
	mechanics	compliance	ventilation in	body weight			moderate	plateau pressure of
		and airway	the AC or					≤30 cm H2O.
		resistance	SIMV mode
	But patient has			10–12 breaths/min				Small tidal volumes
	apnea			or slower rates				(<7 mL/kg) should
	(e.g., drug			(6–10				be avoided,
	overdose or			breaths/min)				because atelectasis
	abdominal			when SIMV				can develop.
	surgery)			mode is used
			or pressure
			ventilation—
			either PRVC
			or PC
	Chronic	High lung	Volume	Good starting		1 : 4	Low to	Air trapping and auto-
	obstructive	compliance	ventilation in	point: 4–			moderate	PEEP can occur
	pulmonary	and high	the AC or	8 mL/kg and a				when expiratory
	disease	airway	SIMV mode	rate of 10–12				time is too short.
	(e.g., chronic	resistance		breaths/min				The preferred
	bronchitis or							method of
	emphysema)							managing auto-
								PEEP is to increase
								expiratory time.
			or pressure	Good starting	60–			In severe cases the
			ventilation—	point:(8–10	100 L/min			development of
			either PRVC	mL/kg) and				auto-PEEP may be
			or PC	slightly slower				inevitable. With
				rate (8–10				controlled
				breaths/min)				ventilation, a small
				with increased				amount of PEEP to
				flow rates to				offset auto-PEEP
				allow adequate				may be cautiously
				expiratory time				applied.
			Noninvasive					Inspiratory flow up to
			positive					100 L/min may be
			pressure					helpful in
			ventilation					decreasing
			(NPPV) by					inspiratory time
			nasal or full					and increasing
			face mask is a					expiratory time.
			good
			alternative
			during acute
			exacerbation.
								Tidal volume or rate
								may be decreased
								to reduce
								inspiratory and
								increase expiratory
								time.
								Care to avoid
								overventilation in
								COPD patients

							with chronically
							high PaCO2 levels
Acute asthmatic	High airway	The SIMV mode	Good starting	60 L/min	1 : 2 or 1 : 3	Start at	In severe cases
episode	resistance	is	point: 8–4			100% and	the
	(bronchospasm	recommended	to 8 mL/kg			titrate	development of
	and excessive	to avoid	and rate of			downward	auto-PEEP may
	thick airway	patient	10–12			as pulse	be inevitable.
	secretions)	triggering at	breaths/min			oximetry	With controlled
		an increased	When air			findings	ventilation, a
		rate—leading	trapping is			and	small amount of
		to a decrease	extensive, a			arterial	PEEP to offset
		in expiratory	lower tidal			blood gas	auto-PEEP may
		time and	volume (5–			values	be cautiously
		further air	6 mL/kg)			permit.	applied.
		trapping.	and slower
			rate may be
			required.
Acute respiratory	Diffuse, uneven	Volume	Typically started	60–80 L/min	1 : 1 or 1 : 2.	FIO2 less	The goal is to limit
distress	alveolar injury	ventilation in	at low tidal		Do what is	than 0.6 if	transpulmonary
syndrome		the AC or	volumes and		necessary	possible.	pressure and
		SIMV mode	higher		to meet a		the resultant
		or pressure	respiratory		rapid		barotrauma
		ventilation—	rate. Initial		respiratory		caused by
		either PRVC	tidal volume		rate.		overdistending
		or PC	set at 8 mL/kg				portions of the
			and adjusted				lungs.
			downward to				Maintaining a
			6 mL/kg. May				plateau
			be as low as				pressure of
			4 mL/kg.				30 cm H2O or
			Respiratory				less is
			rates as high as				preferred.
			35 breaths/min				PEEP is usually
			may be				required with a
			required.				low tidal
							volume to
							prevent
							atelectasis.
							The PaCO2 may be
							allowed to increase
							(permissive
							hypercapnia). The
							hypercapnia is not
							a therapeutic goal,
							it is a final tradeoff
							and may be
							accepted as a lung
							protective strategy
							when lower airway
							pressures are
							necessary.
Postoperative	Often normal	SIMV with	Good starting	60 L/min	1 : 2	Low to	PEEP or CPAP of 3–
ventilatory	compliance	pressure	point: 4–			moderate	5 cm H2O may be
support (e.g.,	and airway	support or AC	8 mL/kg and a				applied to offset
coronary artery	resistance	volume	rate of 10–12				the development of
bypass surgery,		ventilation	breaths/min				atelectasis.
heart valve and		are
replacement)		acceptable
		modes or
		pressure
		ventilation—
		either PRVC
		or PC
Neuromuscular	Normal	Volume	Good starting	60 L/min	1 : 2	Low to	PEEP of 3–5 cm H2O
disorders (e.g.,	compliance	ventilation in	point: 4–			moderate	may be applied to
myasthenia	and airway	the AC or	8 mL/kg and a				offset the
gravis or	resistance	SIMV mode	rate of 10–12				development of
Guillain-Barré		or pressure	breaths/min				atelectasis.
syndrome)		ventilation—
		either PRVC
		or PC

AC, Assist-control; breaths/min, breaths per minute; CPAP, continuous positive airway pressure; PC, pressure control; PEEP, positive end-expiratory pressure; PRVC, pressure-regulated volume control; SIMV, synchronized intermittent mandatory ventilation.

Protocol 11.1 provides a good example of a Ventilator Initiation and Management Protocol. Protocol 11.2 illustrates an example of a Ventilator Weaning Protocol.6

Protocol 11.1

Ventilator Initiation and Management PROTOCOL

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Protocol 11.2

Ventilator Weaning PROTOCOL

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Display of Patient on Mechanical Ventilator Supplied With Graphics Package PROTOCOL