The essential components of a good TDP program do not come easy. This is because a strong TDP program promises that the respiratory care practitioner, who is identified as “TDP safe and ready,” be qualified to (1) systematically collect the appropriate clinical data, (2) formulate a uniform and accurate assessment, and (3) select a uniform and optimal treatment within the limits set by the protocol (Figure 9-1). The converse, however, is also true: When the respiratory care practitioner is not “TDP safe and ready,” the collection of clinical data is not done at all or is incomplete. As a result, nonuniform or inaccurate assessments are made, resulting in nonuniform or inaccurate treatment selections (Figure 9-2). This inappropriate and ineffective type of respiratory therapy leads to the misallocation of care, the administration of unneeded care, and—most important—the nonprovision of needed patient care. The bottom line is poor-quality patient care and unnecessary costs. To be sure, the development and implementation of a strong TDP program require some fundamental knowledge, training, and practice, but the benefits are worth the price. The essential components of a good TDP program are discussed in the following paragraphs.

FIGURE 9-1 The promise of a good therapist-driven protocol program.

FIGURE 9-2 No assessment program in place.

The “Knowledge Base” Required for a Successful Therapist-Driven Protocol Program

As shown in Figure 9-3, the essential knowledge base for a successful TDP program includes (1) the anatomic alterations of the lungs caused by common respiratory disorders, (2) the major pathophysiologic mechanisms activated throughout the respiratory and cardiac systems as a result of the anatomic alterations, (3) the common clinical manifestations that develop as a result of the activated pathophysiologic mechanisms, and (4) the treatment modalities used to correct them. In other words, the clinical manifestations demonstrated by the patient do not arbitrarily appear but are the result of anatomic lung alterations and pathophysiologic events.

FIGURE 9-3 Foundations for a strong therapist-driven protocol program. Overview of the essential knowledge base for assessment of respiratory disease.

Hence, it is essential that the respiratory practitioner know and understand that certain anatomic alterations of the lung will lead to specific—and often predictable—clinical manifestations. Each respiratory disease chapter presented in this textbook describes these four essential knowledge components necessary for TDP work. In the clinical setting this knowledge base enhances the assessment process essential to a good TDP program.

The “Assessment Process Skills” Required for a Successful Therapist-Driven Protocol Program

Using the knowledge base described above, the respiratory care practitioner must also be competent in performing the actual assessment process. This means that the practitioner can (1) quickly and systematically gather the clinical information demonstrated by the patient, (2) formulate an accurate assessment of the clinical data (i.e., identify the cause and severity of the problem), (3) select an optimal treatment modality, and (4) document this process quickly, clearly, and precisely. In the clinical setting, the practice—and mastery—of the assessment process is absolutely central and essential to the success of a good TDP program (Figure 9-4). In other words, immediately after the respiratory care practitioner identifies the appropriate clinical manifestations (clinical indicators), an assessment of the data must be performed, and a treatment plan must be formulated. For the most part the assessment is primarily directed at the anatomic alterations of the lungs that are causing the clinical indicators (e.g., bronchospasm) and the severity of the clinical indicators.

FIGURE 9-4 The way knowledge, assessment, and a therapist-driven protocol program interface.

For example, an appropriate assessment for the clinical indicator of wheezing might be bronchospasm—the anatomic alteration of the lungs. If the practitioner assesses the cause of the wheezing correctly as bronchospasm, then the correct treatment selection would be a bronchodilator treatment from the Aerosolized Medication Therapy Protocol (see Protocol 9-4, page 122). If, however, the cause of the wheezing is correctly assessed to be excessive airway secretions, then the appropriate treatment plan would entail a specific treatment modality under the Bronchopulmonary Hygiene Therapy Protocol, such as cough and deep breathing or chest physical therapy (see Protocol 9-2, page 120).

Table 9-1 illustrates common clinical manifestations (i.e., clinical indicators), assessments, and treatment selections routinely made by the respiratory care practitioner.

TABLE 9-1

Clinical Manifestations, Assessments, and Treatment Selections Commonly Made by the Respiratory Care Practitioner

Clinical Data (indicators)	Assessments	Treatment Selections
Vital Signs
↑Breathing rate, ↑blood pressure, ↑pulse	Respiratory distress	Treat underlying cause
Abnormal Airway Indicators
Wheezing	Bronchospasm	Bronchodilator treatment
Inspiratory stridor	Laryngeal edema	Cool mist
Rhonchi	Secretions in large airways	Bronchial hygiene treatment
Crackles	Secretions in distal airways	Treat underlying cause—e.g., congestive heart failure (CHF)
		Hyperinflation treatment
Cough Effectiveness Indicators
Strong cough	Good ability to mobilize secretions	None
Weak cough	Poor ability to mobilize secretions	Bronchial hygiene treatment
Abnormal Secretion Indicators
Amount: >30 ml/24 hrs White and translucent sputum Yellow or opaque sputum Green sputum Brown sputum Red sputum Frothy secretions

Excessive bronchial secretions

Normal sputum

Acute airway infection

Old, retained secretions and infections

Old blood

Fresh blood

Pulmonary edema

Bronchial hygiene treatment

None

Treat underlying cause

Bronchial hygiene treatment

Notify physician

Treat underlying cause—e.g., congestive heart failure (CHF)

Hyperinflation treatment

Abnormal Lung Parenchyma Indicators Bronchial breath sounds Atelectasis Hyperinflation treatment, oxygen treatment Dull percussion note Infiltrates or effusion Treat underlying cause Opacity on chest X-ray Fibrosis No specific treatment Restrictive pulmonary function test values Consolidation No specific, effective respiratory care treatment Depressed diaphragm on X-ray Air trapping and hyperinflation Treat underlying cause Abnormal Pleural Space Indicators Hyperresonant percussion note Pneumothorax Evacuate air* and hyperinflation treatment Dull percussion note Pleural effusion Evacuate fluid* and hyperinflation treatment Abnormalities of the Chest Shape and Motion Paradoxical movement of the chest wall Flail chest Mechanical ventilation* Barrel chest Air trapping (hyperinflation) Treat underlying cause—e.g., asthma Posterior and lateral curvature of spine Kyphoscoliosis Bronchial hygiene treatment Arterial Blood Gases—Ventilatory pH↑, Paco₂↓,

↓ Acute alveolar hyperventilation Treat underlying cause pH N, Paco₂↓,

↓↓ Chronic alveolar hyperventilation Generally none pH↓, Paco₂↑,

↑ Acute ventilatory failure Mechanical ventilation* pH N, Paco₂↑,

↑↑ Chronic ventilatory failure Low-flow oxygen, bronchial hygiene Sudden Ventilatory Changes on Chronic Ventilatory Failure (CVF) pH↑, Paco₂↑,

↑↑, Pao₂↓ Acute alveolar hyperventilation on CVF Treat underlying cause pH↓, Paco₂↑↑,

↑ Pao₂↓ Acute ventilatory failure on CVF Mechanical ventilation* Metabolic pH↑, Paco₂ N, or ↑,

↑, Pao₂ N Metabolic alkalosis Give potassium*—Hypokalemia Give chloride*—Hypochloremia pH↓, Paco₂ N or ↓,

↓, Pao₂↓ Metabolic acidosis Give oxygen—Lactic acidosis pH↓, Paco₂ N or ↓,

↓, Pao₂ N Metabolic acidosis Give insulin*—Ketoacidosis pH↓, Paco₂ N or ↓,

↓, Pao₂ N Metabolic acidosis Renal therapy* Indication for Mechanical Ventilation pH↑, Paco₂↓,

↓, Pao₂↓ Impending ventilatory failure Mechanical ventilation pH↓, Paco₂↑,

↑, Pao₂↓ Ventilatory failure pH↓, Paco₂↑,

↑, Pao₂↓ Apnea Oxygenation Status Pao₂ < 80 mm Hg Mild hypoxemia Oxygen treatment and treat underlying cause Pao₂ < 60 mm Hg Moderate hypoxemia Pao₂ < 40 mm Hg Severe hypoxemia Oxygen Transport Status ↓Pao₂, anemia, ↓cardiac output Inadequate oxygen transport Oxygen treatment and treat underlying cause

^*These procedures should be performed only as ordered by the physician.

Severity Assessment

The frequency at which a respiratory therapy modality is to be administered is just as important as the correct selection of a respiratory therapy treatment. Often the frequency of treatment must be up-regulated or down-regulated on a shift-by-shift, hour-to-hour, minute-to-minute, or even (in life-threatening situations) second-to-second basis. Such frequency changes must be made in response to a severity assessment. In a good TDP program, the well-seasoned respiratory care practitioner routinely and systematically documents many severity assessments throughout each working day. For the new practitioner, however, a predesigned Severity Assessment Rating Form may be used to enhance this important part of the assessment process. One excellent, semiquantitative method of accomplishing this is illustrated in Table 9-2. The clinical application of this severity assessment is provided in the following case example.

TABLE 9-2

Respiratory Care Protocol Severity Assessment

Item	0 Points	1 Point	2 Points	3 Points	4 Points
Respiratory history	Negative for smoking or history not available	Smoking history <1 pack a day	Smoking history >1 pack a day	Pulmonary disease	Severe or exacerbation
Surgery history	No surgery	General surgery	Lower abdominal	Thoracic or upper abdominal	Thoracic with lung disease
Level of consciousness	Alert, oriented, cooperative	Disoriented, follows commands	Obtunded, uncooperative	Obtunded	Comatose
Level of activity	Ambulatory	Ambulatory with assistance	Nonambulatory	Paraplegic	Quadriplegic
Respiratory pattern	Normal rate 8-20/min	Respiratory rate 20-25/min	Patient complains of dyspnea	Dyspnea, use of accessory muscles, prolonged expiration	Severe dyspnea, use of accessory muscles, respiratory rate >25, and/or swallow
Breath sounds	Clear	Bilateral crackles	Bilateral crackles and rhonchi	Bilateral wheezing, crackles, and rhonchi	Absent and/or diminished bilaterally and/or severe wheezing, crackles, or rhonchi
Cough	Strong, spontaneous, nonproductive	Excessive bronchial secretions and strong cough	Excessive bronchial secretions but weak cough	Thick bronchial secretions and weak cough	Thick bronchial secretions but no cough
Chest X-ray	Clear	One lobe: infiltrates, atelectasis, consolidation, or pleural effusion	Same lung, two lobes: infiltrates, atelectasis, consolidation, or pleural effusion	One lobe in both lungs: infiltrates, atelectasis, consolidation, or pleural effusion	Both lungs, more than one lobe: infiltrates, atelectasis, consolidation, or pleural effusion
Arterial blood gases and/or oxygen saturation measured by pulse oximeter (Spo₂)	Normal	Normal pH and Paco₂ but Pao₂ 60-80 and/or Spo₂ 91-96%	Normal pH and Paco₂ but Pao₂ 40-60 and/or Spo₂ 85-90%	Acute respiratory alkalosis, Pao₂ < 40 and/or Spo₂ 80-84%	Acute respiratory failure, Pao₂ < 80 and/or Spo₂ < 80%

Severity Index
Total Score	Severity Assessment	Treatment Frequency
1-5	Unremarkable	As needed
6-15	Mild	Two or three times a day
16-25	Moderate	Four times a day or as needed
Greater than 26	Severe	Two to four times a day and as needed;
Greater than 26	Severe	Alert attending physician

Severity Assessment Case Example

A 67-year-old man arrived in the emergency room in respiratory distress. The patient was well known to the therapist-driven protocol (TDP) team; he had been diagnosed with chronic bronchitis several years before this admission (3 points). The patient had no recent surgery history, and he was ambulatory, alert, and cooperative (0 points). He complained of dyspnea and was using his accessory muscles of inspiration (3 points). Auscultation revealed bilateral rhonchi over both lung fields (3 points). His cough was weak and productive of thick gray secretions (3 points). A chest x-ray film revealed pneumonia (consolidation) in the left lower lung lobe (3 points). On room air his arterial blood gas values were pH 7.52, Paco₂ 54, 41, and Pao₂ 52—acute alveolar hyperventilation on chronic ventilatory failure (3 points).

Using the Severity Assessment Form shown in Table 9-2, the following treatment selection and administration frequency would be appropriate:

Total score: 17

Treatment selection: Chest physical therapy

Frequency of administration: Four times a day; and as needed

The Essential Cornerstone Respiratory Protocols for a Successful Therapist-Driven Protocol Program

Although there are many “assess and treat” respiratory care protocols used throughout the health-care industry today, the following respiratory protocol examples provide the “essential foundation” of a successful TDP program:

• Oxygen Therapy Protocol (Protocol 9-1)

• Bronchopulmonary Hygiene Therapy Protocol (Protocol 9-2)

• Aerosolized Medication Therapy Protocol (Protocol 9-4)

• Lung Expansion Therapy Protocol (Protocol 9-3)

• Mechanical Ventilation Protocol (Protocol 9-5 and Protocol 9-6)

• Mechanical Ventilation Weaning Protocol (Protocol 9-7)

The vast majority of the daily work performed by the respiratory practitioner involves assessments and treatments associated with these protocols. Most patients with respiratory problems require care found in one or more of these protocols. These respiratory protocols are the essential cornerstones of a good TDP program. For example, a patient experiencing a severe asthmatic episode would likely demonstrate a variety of objective clinical indicators to justify the assessments that call for the administration of oxygen therapy (e.g., to treat hypoxemia), an aerosolized bronchodilator (e.g., to treat bronchospasm), bronchial hygiene therapy (e.g., to mobilize the thick white secretions associated with asthma), and mechanical ventilation (e.g., to treat acute ventilatory failure).

As shown in the algorithms in Protocols 9-1 through 9-7, a step-by step, branching logic process directs the practitioner to (1) gather clinical data (clinical indicators), (2) make assessment decisions based on the clinical data, and (3) either start, up-regulate, down-regulate, or discontinue a treatment modality. In fact, the primary reason a good TDP program works is because a specific treatment modality cannot be started, stopped, or modified unless there are specific—and measurable—clinical indicators identified to justify the assessment and treatment decision.

The treatment selections outlined in each of the listed protocols are based on current AARC’s Clinical Practice Guidelines (CPGs), which provide the most recent scientific evidence that justifies the administration of a specific treatment modality. Using the evidence-based method mandated by the scientific community, CPGs provide the indications, contraindications, hazards and complications, assessment of need, assessment of outcome, and appropriate monitoring techniques used for specific therapy modalities. In other words, the CPGs are the gold standards used by the respiratory care practitioner to start, adjust, or discontinue a specific treatment modality. In Box 9-1, excerpts from the AARC’s CPG on oxygen therapy for adults in the acute care facility provide a representative example of a CPG—and, more important, the scientific basis for the Oxygen Therapy Protocol (Protocol 9-1).*

Box 9-1 Oxygen Therapy for Adults in the Acute Care Facility

AARC Clinical Practice Guideline (Excerpts)*

Indications

• Documented hypoxemia. Defined as a decreased Pao₂ in the blood below normal range.

• Pao₂ < 60 mm Hg or Sao₂ < 90% in subjects breathing room air

• Acute care situations in which hypoxemia is suspected

• Severe trauma

• Acute myocardial infarction

• Short-term therapy or surgical intervention (e.g., postanesthesia recovery, hip surgery)

Contraindications

• No specific contraindications to oxygen therapy exist when indications are present.

Precautions and/or Possible Complications

• Pao₂ > 60 mm Hg may depress ventilation in some patients with elevated Paco₂.

• Fio₂ > 0.5, may cause absorption atelectasis, oxygen toxicity, and/or ciliary or leukocyte depression.

• Supplemental oxygen should be administered with caution to patients with paraquat poisoning or to those receiving bleomycin.

• During laser bronchoscopy, minimal Fio₂ should be used to avoid intratracheal ignition.

• Fire hazard is increased in the presence of increased oxygen concentration.

• Bacterial contamination associated with nebulizers or humidifiers is a possible hazard.

Assessment of Need

• Need is determined by measurement of inadequate oxygen tension and/or saturation, by invasive or noninvasive methods, and/or the presence of clinical indicators.

Assessment of Outcome

• Outcome is determined by clinical and physiologic assessment to establish adequacy of patient response to therapy.

Monitoring

• Patient

• Clinical assessment including cardiac, pulmonary, and neurologic status

• Assessment of physiologic parameters (Pao₂, Sao₂, Spo₂) in conjunction with the initiation of therapy or:

Within 12 hours of initiation with Fio₂ < 40

Within 8 hours with Fio₂ ≥ 0.40 (including postanesthesia recovery)

Within 72 hours in acute myocardial infarction

Within 2 hours for any patient with principal diagnosis of COPD

• Equipment

• All oxygen delivery systems should be checked at least once per day.

• More frequent checks are needed in systems:

Susceptible to variation in oxygen concentration (e.g., hood, high-flow blending systems)

Applied to patients with artificial airways

Delivering a heated gas mixture

Applied to patients who are clinically unstable or who require Fio₂ > 0.50

• Care should be taken to avoid interruption of oxygen therapy in situations including ambulation or transport for procedure.

^*See http://www.aarc.org/ (Clinical Practice Guidelines) for the most recent and complete list of clinical practice guidelines.

From Respir Care 47(6):717-720, 2002. See this article for the complete guidelines.

Several different treatment selections are listed under each of the protocols. In essence, the various treatment selections serve as a “therapy selection menu.” When the patient demonstrates the clinical indicators associated with any of these protocols, the respiratory therapist is expected to select and administer the most efficient and most cost-effective treatment to the patient. As already discussed, the treatment selection decision and the frequency with which the therapy is to be administered are based on (1) the identification of the appropriate clinical indicators, (2) the severity suggested by the clinical information, (3) the patient’s ability to perform or tolerate the therapy, and (4) the patient’s response to the therapy.

For example, the implementation of the Lung Expansion Therapy Protocol (Protocol 9-3) would likely be indicated after thoracic surgery to prevent, or correct, atelectasis. If the patient were unconscious or unable to follow directions, a continuous positive airway pressure (CPAP) mask would be a more appropriate treatment selection (under the Lung Expansion Therapy Protocol) than, say, incentive spirometry—even though both are designed to treat or prevent atelectasis. In this example, the CPAP mask therapy would be more expensive but more appropriate than the less expensive incentive spirometry.

Remember, the treatment portion of a protocol is based on the therapy that will best work to correct or offset the anatomic alterations and pathophysiologic mechanisms caused by the respiratory disorder in a timely and cost-efficient manner. Finally, even when the patient is transferred to the intensive care unit, intubated, and placed on a mechanical ventilator, the respiratory care practitioner must usually still administer one or more of the first four respiratory therapy treatment protocols listed in this section. For example, the patient would likely need CPAP or positive end-expiratory pressure (PEEP) to offset any alveolar atelectasis caused by bronchial airway mucous plugs via the Lung Expansion Therapy Protocol. Or, the patient would likely require a bronchodilator agent to offset bronchospasm via the Aerosolized Medication Therapy Protocol.

The following sections provide an overview of the respiratory care practitioner’s most sophisticated and refined protocols—the Mechanical Ventilation Protocol and the Mechanical Ventilation Weaning Protocol.

Mechanical Ventilation Protocol

It is interesting to note that many medical centers have started their TDP programs with a Mechanical Ventilation Protocol rather than with one of the simpler protocols described in this chapter (e.g., Oxygen Therapy Protocol, Bronchial Hygiene Protocol, Lung Expansion Protocol, or Aerosolized Medication 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 actually harmful), uncomfortable, and costly to patients requiring ventilator support?

Although there are a number of good ventilatory management strategies used to treat specific respiratory disorders, the need for a standardized approach to ventilator management has required the development of Mechanical Ventilation Protocols. Protocol 9-5 provides an example of a Mechanical Ventilation Protocol. Protocol 9-6 further illustrates a more comprehensive—and operational—protocol for Mechanical Ventilator Management, and Protocol 9-7 illustrates an example of a comprehensive operational Mechanical Ventilation Weaning Protocol.*

The primary objectives of mechanical ventilation are (1) to reverse acute ventilatory failure, (2) to maintain normal respiratory balance, or homeostasis—especially the acid-base balance of the blood and the amounts of CO₂ and O₂ exchange, (3) to improve oxygenation and increase lung volume, (4) to reduce the work of breathing, (5) to permit sedation or paralysis (or both), and decrease systemic and/or myocardial oxygen consumption.

Achievement of these objectives reverses acute ventilatory failure (also called acute respiratory acidosis) and corrects the patient’s acid-base balance and oxygenation status, reverses or prevents atelectasis and stabilizes the chest wall, reverses muscle fatigue, allows sedation and/or neuromuscular blockade, and decreases systemic or myocardial oxygen consumption—a daunting list, indeed! Furthermore, the attainment of these goals and objectives results from an intelligent assessment of the patient’s needs, an understanding of the pertinent pathophysiology, and knowledge of ventilator management techniques most likely to meet the needs of the moment. This is the cornerstone of the “assess and treat” paradigm of the Mechanical Ventilation Protocol.

Unquestionably, the high-technology, high-risk, high-visibility portion of respiratory care 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 are shortened ventilator weaning times, reduction of nosocomial infections, and reduced complication rates of mechanical ventilation (e.g., barotrauma).

Mechanical ventilation may be delivered by endotracheal tube (most common), by tracheostomy, by a face mask, or by a cuirass-type device. Ventilator modes include assist-control (A/C) and synchronized intermittent mandatory ventilation (SIMV) with or without pressure support (PS). Much less commonly used modes include SIMV alone, inverse-ratio ventilation (IRV), and airway pressure release ventilation (APRV). In general, the goal of mechanical ventilation is to totally or partially replace the gas exchange function of the lungs, with as few complications as possible.

Although most Mechanical Ventilation Protocols require the respiratory care practitioner 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 ventilator modes and weaning strategies. Table 9-3, however, does provide an excellent overview of common ventilatory management strategies and good starting points used to treat specific pulmonary disorders.

TABLE 9-3

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

Disorder	Disease Characteristics	Ventilator Mode	Tidal Volume and Respiratory Rate	Flow Rate	I : E Ratio	Fio₂	General Goals and/or Concerns
Normal Lung Mechanics	Normal compliance & airway resistance	Volume ventilation in the AC or SIMV mode.	10-12 ml/kg of ideal body weight	60-80 L/min	1 : 2	Low to moderate	Care to ensure plateau pressure of 30 cm H₂o or less.
But patient has apnea			10-12 bpm or slower rates (6-10 bpm) when SIMV mode is used				Small tidal volumes (<7 ml/kg) should be avoided, since atelectasis can develop
(e.g., drug overdose or abdominal surgery)		Or pressure ventilation—either PRVC or PC
Chronic Obstructive Pulmonary Disease	High lung compliance and high airway resistance	Volume ventilation in the AC or SIMV mode	Good starting point: 10 ml/kg and a rate of 10 to 12 bpm	60 L/min	1 : 2 or 1 : 3	Low to moderate	Air trapping and auto-PEEP can occur when expiratory time is too short. The preferred method of managing auto-PEEP is to increase expiratory time.
(e.g., chronic bronchitis or emphysema)		Or pressure ventilation—either PRVC or PC	A smaller tidal volume (8-10 ml/kg) and slightly slower rate (8-10 bpm) with increased flow rates to allow adequate expiratory time	60-100 L/min			In severe cases, the development of auto-PEEP may be inevitable. With controlled ventilation, a small amount of PEEP to offset auto-PEEP may be cautiously applied.
		Noninvasive positive pressure ventilation (NPPV) by nasal or full face mask is a good alternative during acute exacerbation					Inspiratory flow up to 100 L/min may be helpful in decreasing inspiratory time and increasing expiratory time
							Tidal volume or rate may be decreased to reduce inspiratory and increasing expiratory time
							Care to avoid overventilating COPD patients with chronically high Paco₂ levels
Acute Asthmatic Episode	High airway resistance (bronchospasm and excessive thick airway secretions)	The SIMV mode is recommended to avoid patient triggering at an increased rate—leading to a decrease in expiratory time and further air trapping	Good starting point: 8 to 10 ml/kg and rate of 10-12 bpm When air trapping is extensive, a lower tidal volume (5-6 ml/kg) and slower rate may be required

60 L/min 1 : 2 or 1 : 3 Start at 100% and titrate downward as pulse oximetric findings and arterial blood gas values permit In severe cases, the development of auto-PEEP may be inevitable. With controlled ventilation, a small amount of PEEP to offset auto- PEEP may be cautiously applied. Acute Respiratory Distress Syndrome Diffuse, uneven alveolar injury

Volume ventilation in the AC or SIMV mode

Or pressure ventilation— either PRVC or PC

Typically started at low tidal volumes and higher respiratory rate

Initial tidal volume set at 8 ml/kg and adjusted downward to 6 ml/kg

May be as low as 4 ml/kg

Respiratory rates as high as 35 bpm may be required

60-80 L/min

1 : 1 or 1 : 2

Do what is necessary to meet a rapid respiratory rate

Fio₂ less than 0.6 if possible

The goal is to limit transpulmonary pressure and the resultant barotraumas caused by overdistending portions of the lungs

Maintaining a plateau pressure of 30 cm H₂O or less is preferred

PEEP is usually required with a 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 tradeoff and may be accepted as a lung protective strategy when lower airway pressures are necessary.

Postoperative Ventilatory Support
(e.g., coronary artery bypass surgery, heart valve and replacement) Often normal compliance and airway resisitance

SIMV with pressure support or AC volume ventilation are acceptable modes

Or pressure ventilation—either PRVC or PC

Good starting point: 10 to 12 ml/kg and a rate of 10 to 12 bpm

However, a larger tidal volume (12-15 ml/kg) and slower rate (6-10 bpm) may be used to maintain lung volume

60 L/min 1 : 2 Low to moderate PEEP or CPAP of 3 to 5 cm H₂O may be applied to offset the development of atelectasis Neuromuscular Disorder
(e.g., myasthenia gravis or Guillain-Barre syndrome) Normal compliance and airway resistance

Volume ventilation in the AC or SIMV mode

Or pressure ventilation—either PRVC or PC

Good starting point: 12 to 15 ml/kg and a rate of 10 to 12 bpm 60 L/min 1 : 2 Low to moderate PEEP of 3 to 5 cm H₂O may be applied to offset the development of atelectasis

AC, Assist-control; SIMV, synchronous intermittent mandatory ventilation; PRVC, pressure regulated volume control; PC, pressure control; CPAP, continous positive airway pressure; bpm, breaths per minute.

Ventilatory Management in Catastrophes

The risk of major catastrophes continues to increase as a result of many factors, including the threat of bioterrorism, the growing mobility of the world’s population, and numerous viruses. For example, the events that occurred immediately after September 11, 2001 and the recent reports of the person-to-person transmission of avian influenza identified in Thailand and H1N1 (“swine flu”) in the United States are powerful reminders that the population at large is vulnerable to both known and unknown dangers. In addition, it should be understood that because epidemics and bioterrorist attacks can result in conditions that cause acute ventilatory failure, large numbers of mechanical ventilators (which are limited in supply) will certainly be needed should such an unfortunate event occur.

Figure 9-5, a photograph taken during the great poliomyelitis epidemic in the early 1950s (over 50,000 people were stricken), reminds the reader of a need for such intervention. Note the nurse-to-patient ratio of 1 : 2. At the time, each nurse was ready to step in and manually operate the “iron lungs” of two patients in the event of a power outage. Today, it is very unlikely that our health-care system could adequately provide this type of ventilator care and coverage.

FIGURE 9-5 Iron lungs in gym. Iron lungs were in high demand during the polio epidemic of 1951 to 1953. (Courtesy Rancho Los Amigos National Rehabilitation Center. From http://en.wikipedia.org/wiki/File:Iron_Lung_ward-Rancho_Los_Amigos_Hospital.gif.)

With the realization that many factors may result in a large demand for ventilator management, some thought is now being offered in the literature that suggests how this might be done. The choices and alternatives are grim ones and are illustrated in a representative three-tier criteria system provided in Box 9-2. As shown, Tier 1 is directed only to acute ventilatory failure with shock and multiple organ dysfunction. Tier 2 presents criteria for high potential for death, prolonged ventilation, and high levels of resource use. Tier 3 criteria may entail additional restrictions or a scoring system and are implemented to maintain consistent standards of care.*

Box 9-2 Three Tiers of Criteria

Tier 1: Do not offer and withdraw ventilatory support for patients with any one of the following:

1. Respiratory failure requiring intubation with persistent hypotension (systolic blood pressure <90 mm Hg for adults) unresponsive to adequate fluid resuscitation after 6 to 12 hours of therapy and signs of additional end-organ dysfunction (e.g., oliguria, mental status changes, cardiac ischemia)

2. Failure to respond to mechanical ventilation (no improvement in oxygenation or lung compliance) and antibiotics after 72 hours of treatment for a bacterial pathogen (timeline may be modified based on organism-specific data)

3. Laboratory or clinical evidence of more than four organ systems failing

a. Pulmonary (acute respiratory distress syndrome, ventilatory failure, refractory hypoxemia)

b. Cardiovascular (left ventricular dysfunction, hypotension, new ischemia)

c. Renal (hyperkalemia, diminished urine output despite adequate fluid resuscitation, increasing creatinine level)

d. Hepatic (transaminase greater than two times normal upper limit, increasing bilirubin or ammonia levels)

e. Neurologic (altered mental status not related to volume status, metabolic, or hypoxic source, stroke)

f. Hematologic (clinical or laboratory evidence of disseminated intravascular coagulation)

Tier 2: Do not offer and withdraw ventilatory support from patients with respiratory failure requiring intubation with following conditions (in addition to those in Tier 1):

Patients with pre-existing system compromise or failure including the following:

1. Known congestive heart failure with ejection fraction <25% (or persistent ischemia unresponsive to therapy and pulmonary edema)

2. Acute renal failure requiring hemodialysis (related to illness)

3. Severe chronic lung disease including pulmonary fibrosis, obstructive or restrictive diseases requiring continuous home oxygen use before onset of acute illness.

4. Acquired immunodeficiency syndrome (AIDS), other immunodeficiency syndromes at stage of disease susceptible to opportunistic pathogens (e.g., CD4 <200 for AIDS) with respiratory failure requiring intubation

5. Active malignancy with poor potential for survival (e.g., metastatic malignancy, pancreatic cancer)

6. Cirrhosis with ascites, history of variceal bleeding, fixed coagulopathy, or encephalopathy

7. Acute hepatic failure with hyperammonemia

8. Irreversible neurologic impairment that makes patient dependent on personal care (e.g., severe stroke, congenital syndrome, persistent vegetative state)

Tier 3: Specific protocols to be agreed on by guideline development committee. Possibilities include the following:

1. Restriction of treatment based on disease-specific epidemiology and survival data for patient subgroups (may include age-based criteria)

2. Expansion of preexisting disease classes that will not be offered ventilatory support

3. Applying Sequential Organ Failure Assessment scoring to the triage process, and establishing a cutoff score above which mechanical ventilation will not be offered

Overview Summary of a Good Therapist-Driven Protocol Program

Figure 9-6 provides an overview of the essential components of a good TDP program. As illustrated, the implementation of every respiratory care plan must be directly linked to (1) a physician’s order, (2) the identification and documentation of specific clinical indicators (obtained from both the patient’s chart and physical examination), (3) a bedside respiratory assessment and severity assessment, (4) a treatment selection that is both therapeutic and cost-efficient, and (5) the reevaluation of the patient’s response to the treatment.

FIGURE 9-6 Overview of the essential components of a good therapist-driven protocol program.

This step-by-step process mandates that the respiratory care practitioner (1) have a strong knowledge base of the major respiratory disorders, and (2) be competent in the actual assessment process (see Figure 9-4). Figure 9-7 provides an assessment form with common examples for each category (i.e., clinical indicators, respiratory assessments, and treatment plans). The examples shown in Figure 9-6 can easily be transferred to the subjective-objective-assessment-plan (SOAP) format. The SOAP format used in the assessment of respiratory diseases is discussed in more detail in Chapter 10.

FIGURE 9-7 Respiratory care protocol program assessment form.

Common Anatomic Alterations of the Lungs

Although the respiratory care practitioner may at some time treat one or two cases of every respiratory disorder presented in this book, most of the respiratory care practitioner’s professional career will be spent caring for patients with only a few of them. For example, the diagnosis-related group (DRG) and International Statistical Classification of Diseases and Related Health Problems (ICD-9) identification systems show that more than 80% of the respiratory care practitioner’s work is concerned with intelligent assessment and treatment selection for a relatively short list of respiratory illnesses (Table 9-4).

TABLE 9-4

Common Respiratory Disorders

Respiratory Disorder	DRG Number*	ICD-10 Code^†
Chronic bronchitis	088	491.1, 491.9
Emphysema	088	492.8
Asthma	096	493.0
Acute pneumonia	079, 089, 090	(see below)
Aspiration pneumonia	079	507.0
Atelectasis	101/102	518.89
Adult respiratory distress syndrome	099/102	518.82
Interstitial fibrosis	089	515.0
Pulmonary edema/congestive heart failure	127	402.91
Acute respiratory failure	087	518.81
Respiratory failure with ventilatory support	475	96.7
Respiratory failure/tracheostomy/ventilatory support	483	96.72/31.1

^*Respiratory disorders can be identified by their respective diagnosis-related group (DRG). DRG is an identification system used to categorize and document diseases, primarily for use in health care reimbursement (such as Medicaid and Medicare). Patients are routinely assigned a DRG based on their admitting diagnosis, and each DRG communicates information about patients. Because the use of DRGs is prevalent, respiratory care practitioners should recognize and understand the DRGs that they will commonly encounter.

^†The ICD-10 code numbers are used for reimbursement with other third party payers. The ICD-10 system is more specific than the DRG system. For example, pneumococcal pneumonia is listed as ICD # 418.0, Haemophilus influenzae is ICD # 482.2, etc.

Therefore the most common anatomic alterations of the lungs treated by the respiratory care practitioner can be derived by recognizing the most common DRG respiratory disorders identified in Table 9-4. The major anatomic alterations include (1) atelectasis (e.g., which can occur from mucous plugging, upper abdominal surgery, or pneumothorax), (2) alveolar consolidation (e.g., pneumonia), (3) increased alveolar-capillary membrane thickness (e.g., acute respiratory distress syndrome [ARDS], pneumoconiosis, or pulmonary edema), (4) bronchospasm (e.g., asthma), (5) excessive bronchial secretions (e.g., chronic bronchitis, asthma, pulmonary edema), and (6) distal airway and alveolar weakening (e.g., emphysema). Each of these anatomic alterations of the lung in turn leads to a chain of events that can be summarized in the following clinical scenarios.

Clinical Scenarios Activated by Common Anatomic Alterations of the Lungs

For the purposes of this text, we have chosen to refer to the interrelationship among the major anatomic alterations of the lung, the pathophysiologic mechanisms, and the clinical manifestations that result as “clinical scenarios.” Specific anatomic alterations of the lung (such as the ones listed previously) lead to the activation of specific and predictable pathophysiologic mechanisms and to their effects. The more common pathophysiologic mechanisms are listed in Box 9-3. The pathophysiologic mechanisms in turn activate specific and predictable clinical manifestations (see Figure 9-3). To enhance the reader’s knowledge and understanding of commonly encountered respiratory disorders, clinical scenarios for the anatomic alterations presented in the following paragraphs are provided.*

Key to Abbreviations in Figures 9-8 through 9-13
ABG	=	Arterial blood gas
ARDS	=	Acute respiratory distress syndrome
CPAP	=	Continuous positive airway pressure
CPT	=	Chest physical therapy
Do₂	=	Total oxygen delivery
ERV	=	Expiratory reserve volume
FEF	=	Forced expiratory flow, midexpiratory phase
FEV₁	=	Forced expiratory volume in 1 second
FEV_T	=	Forced expiratory volume timed
FRC	=	Functional residual capacity
FVC	=	Forced vital capacity
IC	=	Inspiratory capacity
MVV	=	Maximum voluntary ventilation
O₂ER	=	Oxygen extraction ratio
PD	=	Postural drainage
PEEP	=	Positive end-expiratory pressure
PEFR	=	Peak expiratory flow rate
PFT	=	Pulmonary function test
	=	Shunt fraction
RV	=	Residual volume
	=	Mixed venous oxygen saturation
TLC	=	Total lung capacity
VC	=	Vital capacity
	=	Ventilation-perfusion ratio

Atelectasis

Figure 9-8 shows the pathophysiologic mechanisms caused by atelectasis (e.g., from a pneumothorax), the clinical manifestations that result, and the treatment protocols used to offset them. The hypoxemia that results from atelectasis is caused by capillary shunting. This type of hypoxemia is often refractory to oxygen therapy. Therefore the implementation of the Lung Expansion Therapy Protocol may be more beneficial in the treatment of hypoxemia than the Oxygen Therapy Protocol in such a patient.

Alveolar Consolidation

Figure 9-9 shows the pathophysiologic mechanisms caused by alveolar consolidation (e.g., pneumonia), the clinical manifestations that result, and the treatment protocols used to offset them. The hypoxemia that develops as a result of consolidation is caused by capillary shunting. This type of hypoxemia is often refractory to oxygen therapy.

Depending on the severity of the alveolar consolidation, the Lung Expansion Therapy Protocol or the Oxygen Therapy Protocol may be beneficial. In general, however, there is no effective, specific respiratory care treatment modality for alveolar consolidation. With pneumonia, the great temptation for the respiratory care practitioner is to do too much, such as instituting lung expansion therapy, bronchodilator therapy, and bronchial hygiene therapy. Such treatment protocols generally are not indicated, especially during the early stages of the disease process. Appropriate antibiotics (prescribed by the physician), bed rest, fluids, and supplementary oxygen are all that is usually needed. When pneumonia is in its resolution stage, however, the patient may experience excessive secretions and atelectasis, accompanied by bronchoconstriction. At this time, other treatment modalities may be indicated.

Increased Alveolar-Capillary Membrane Thickness

Figure 9-10 illustrates the major pathophysiologic mechanisms caused by increased alveolar-capillary membrane thickness (e.g., postoperative ARDS, pulmonary edema, asbestosis, chronic interstitial lung disease), the clinical manifestations that develop, and the treatment protocols used to offset them. The hypoxemia that develops as a result of an increased alveolar-capillary membrane thickness is caused by an alveolar diffusion block. This type of hypoxemia often responds favorably to oxygen therapy.

Bronchospasm

Figure 9-11 shows the major pathophysiologic mechanisms activated by bronchospasm (e.g., asthma), the clinical manifestations that result, and the appropriate treatment protocols used to offset them. The Aerosolized Medication Therapy Protocol (Bronchodilator Therapy) is the primary treatment modality used to offset the anatomic alterations of bronchospasm (the original cause of the pathophysiologic chain of events). The Oxygen Therapy Protocol and Mechanical Ventilation Protocol are secondary treatment modalities used to offset the mild, moderate, or severe clinical manifestations associated with bronchospasm. In other words, when the patient responds favorably to the Aerosolized Medication Therapy Protocol, the need for the Oxygen Therapy Protocol may be minimal and the Mechanical Ventilation Protocol may not be necessary at all.

Excessive Bronchial Secretions

Figure 9-12 illustrates the major pathophysiologic mechanisms caused by excessive bronchial secretions (e.g., chronic bronchitis, asthma), the clinical manifestations that result, and the appropriate treatment protocols used to correct them. The Bronchopulmonary Hygiene Therapy Protocol is the primary treatment modality used to offset the anatomic alterations associated with excessive bronchial secretions. When the patient demonstrates chronic ventilatory failure during the advanced stages of respiratory disorders associated with chronic excessive airway secretions (e.g., chronic bronchitis), caution must be taken not to overoxygenate the patient.

Distal Airway and Alveolar Weakening

Figure 9-13 illustrates the major pathophysiologic mechanisms caused by distal airway and alveolar weakening (e.g., emphysema), the clinical manifestations that result, and the appropriate treatment protocols used to offset them. Pulmonary rehabilitation and oxygen therapy may be all the practitioner can provide to treat the symptoms associated with distal airway and alveolar weakening. When the patient demonstrates chronic ventilatory failure during the advanced stages of the disorder, caution must be taken with the Oxygen Therapy Protocol not to over-oxygenate the patient.

Overview of Common Anatomic Alterations Associated with Respiratory Disorders

When the respiratory therapy practitioner knows and understands the chain of events (clinical scenarios) that develop in response to common anatomic alterations of the lungs, an assessment and an appropriate treatment protocol can be easily determined. Table 9-5 provides an overview of the most common anatomic alterations associated with the respiratory disorders presented in this textbook.

TABLE 9-5

Common Anatomic Alterations of the Lungs Associated With Respiratory Disorders

Respiratory Disorder	Atelectasis	Alveolar Consolidation	Increased Alveolar-Capillary Membrane Thickness	Bronchospasm	Excessive Bronchial Secretions	Distal Airway Weakening
Chronic bronchitis				X*	X
Emphysema				X	X*	X
Bronchiectasis	X	X		X	X
Asthma				X	X
Pneumonia		X	X		X*
Lung abscess		X			X
Tuberculosis		X	X
Fungal diseases		X	X
Pulmonary edema	X		X		X
Pulmonary embolism	X			X
Flail chest	X	X
Pneumothorax	X
Pleural diseases	X
Kyphoscoliosis	X				X*
Pneumoconiosis			X	X
Cancer of the lung	X	X			X
Adult respiratory distress syndrome	X*	X	X
Chronic interstitial lung diseases			X	X*
Guillain-Barré syndrome	X*	X*			X*
Myasthenia gravis	X*	X*			X*
Meconium aspiration syndrome	X	X			X
Transient tachypnea of newborn			X		X
Infant respiratory distress syndrome	X	X			X
Pulmonary air leak syndromes	X
Respiratory syncytial virus	X	X			X
Bronchopulmonary dysplasia	X		X		X
Diaphragmatic hernia	X
Cystic fibrosis	X*			X*	X
Near drowning	X	X	X	X
Smoke inhalation and thermal injuries	X	X	X	X
Postoperative atelectasis	X

^*Common secondary anatomic alterations of the lungs associated with this disorder.

Figure 9-14 provides a three-component overview model of a prototype airway to further enhance the reader’s visualization of anatomic alterations of the lungs commonly associated with the obstructive respiratory disorders (e.g., asthma, bronchitis, or emphysema) and the treatment plans commonly used to offset them.