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Eosinophils 2% to 4%

Basophils 0.5% to 1%

Nongranular Leukocytes

Lymphocytes 20% to 25%

Monocytes 3% to 8%

TABLE 9.3

Common Causes of White Blood Cell Increase

Cell Type

Causes of Increase

Neutrophil

Bacterial infection, inflammation

Eosinophil

Allergic reaction, parasitic infection

Basophil

Myeloproliferative disorders

Monocyte

Chronic infections, malignancies

Lymphocyte

Viral infections

Granular Leukocytes.

The granular leukocytes (also called granulocytes) are so classified because of the granules present in their cytoplasm. The granulocytes are further divided into the following three types according to the staining properties of the granules: neutrophils, eosinophils, and basophils. Because these cells have distinctive multilobar nuclei, they are often referred to as polymorphonuclear leukocytes.

Neutrophils.

The neutrophils make up about 60% to 70% of the total number of WBCs. They have granules that are neutral and therefore do not stain with an acid or a basic dye. The neutrophils are the first WBCs to arrive at the site of infection or inflammation, usually appearing within 90 minutes of the injury. They represent the primary cellular defense against bacterial organisms through the process of phagocytosis (ingestion of foreign material). The neutrophils are one of several types of cells called phagocytes that ingest and destroy bacterial organisms and particulate matter. The neutrophils also release an enzyme called lysozyme, which destroys certain bacteria. An increased neutrophil count is associated with

(1) bacterial infection, (2) physical and emotional stress, (3) tumors, (4) inflammatory or traumatic disorders, (5) some leukemias, (6) myocardial infarction, and (7) burns.

Early (immature) forms of neutrophils are nonsegmented and are called “band” forms. They almost always signify infection if elevated above 10% of the differential. More mature forms of neutrophils have segmented nuclei. They may increase even in the absence of infection (e.g., with stress [exercise] or the use of corticosteroid medication).

Eosinophils.

The cytoplasmic granules of eosinophils stain red with the acid dye eosin. These leukocytes make up 2% to 4% of the total number of WBCs. Although the precise function of the eosinophils is unknown, they are thought to play an important role in the breakdown of protein material. It is known, however, that the eosinophils are activated by allergies (such as an allergic asthmatic episode) and parasitic infections. Their role in the pathogenesis of asthma (see Chapter 14, Asthma) appears to be increasingly important, e.g., eosinophilic asthma. Eosinophils are thought to detoxify the agents or chemical mediators associated with allergic reactions. An increased eosinophil count also may be associated with lung cancer, chronic skin infections (e.g., psoriasis, scabies), polycythemia, and tumors.

Basophils.

The basophils make up only about 0.5% to 1.0% of the total WBC count. The granules of the basophils stain blue with a basic dye. The precise function of the basophils is not clearly understood. Increased basophils are primarily associated with certain myeloproliferative disorders. It is thought that the basophils are involved in allergic and stress responses. They are also considered to be phagocytic and contain heparin, histamines, and serotonin.

Nongranular Leukocytes.

There are two groups of nongranular leukocytes: the monocytes and lymphocytes. The term mononuclear leukocytes is also used to describe these cells because they do not contain granules but have spheric nuclei.

Monocytes.

The monocytes are the second order of cells to arrive at the inflammation site, usually appearing about 5 hours or more after the injury. After 48 hours, however, the monocytes are usually the predominant cell type in the inflamed area. The monocytes are the largest of the WBCs and make up about 3% to 8% of the total leukocyte count. The monocytes are shortlived, phagocytic WBCs, with a half-life of about 1 day. They circulate in the bloodstream, from which they move into tissues—at which point they may mature into long-living macrophages (also called histiocytes).

Macrophages are large wandering cells that engulf larger and greater quantities of foreign material than the neutrophils. When the foreign material cannot be digested by the macrophages, the macrophages may proliferate to form a capsule that surrounds and encloses the foreign material (e.g., fungal spores). Although the monocytes and macrophages do not respond as quickly to an inflammatory process as the neutrophils, they are considered one of the first lines of cellular inflammatory defense. Therefore an elevated number of monocytes suggests infection and inflammation. The monocytes play an important role in chronic inflammation and are also involved in the immune response and malignancies.

Lymphocytes.

Increased lymphocytes are typically seen in viral infections (e.g., infectious mononucleosis). The lymphocytes are also involved in the production of antibodies, which are special proteins that inactivate antigens. For a better understanding of the importance of the lymphocytes and the clinical significance of their destruction or depletion (e.g., in acquired immunodeficiency syndrome [AIDS]), a brief review of the role and function of the lymphocytes in the immune system is in order.

The lymphocytes can be divided into two categories: B cells and T cells. These cells can be identified with an electron microscope according to certain distinguishing surface marks, called rosettes. T cells have a smooth surface; B cells have projections. B cells make up 10% to 30% of the total lymphocytes; T cells account for 70% to 90% of the total lymphocytes.

The B cells, which are formed in the bone marrow, further divide into either plasma cells or memory cells. The plasma

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cells secrete antibodies in response to foreign antigens. The memory cells retain the ability to recognize specific antigens long after the initial exposure and therefore contribute to long-term immunity against future exposures to invading pathogens.

The T cells, which are formed in the thymus, are further divided into four functional categories: (1) cytotoxic T cells (also called killer lymphocytes or natural killer cells), which attack and kill foreign or infected cells; (2) helper T cells, which recognize foreign antigens and help activate cytotoxic T cells and plasma cells (B cells); (3) inducer T cells, which stimulate the production of the different T-cell subsets; and (4) suppressor T cells, which work to suppress the responses of the other cells and help provide feedback information to the system.

The T cells also may be classified according to their surface antigens (i.e., the T cells may display either T4 or T8 surface antigen). The T4 surface antigen subset, which makes up 60% to 70% of the circulating T cells, consists mainly of the helper and inducer cells. The T8 surface antigen subset consists mainly of the cytotoxic and suppressor cells.

Sequence of the Lymphocytic Response to Infection.

Initially, the macrophages attack and engulf the foreign antigens. This activity in turn stimulates the production of T cells and, ultimately, the antibody-producing B cells (plasma cells). The T4 cells play a pivotal role in the overall modulation of this immune response by (1) secreting a substance called lymphokine, which is a potent stimulus to T-cell growth and differentiation; (2) recognizing foreign antigens; (3) causing clonal proliferation of T cells; (4) mediating cytotoxic and suppressor functions; and (5) enabling B cells to secrete specific antibodies.

Because T cells (especially the T4 lymphocytes) have such a central role in this complex immune response, it should not be difficult to imagine the devastating effect that would ultimately follow from the systematic depletion of T lymphocytes. For example, virtually all the infectious complications of HIV/AIDS may be explained with reference to the effect that HIV has on the T cells. A decreased number of T cells increases the patient's susceptibility to a wide range of opportunistic infections and neoplasms. In the healthy subject, the T4/T8 ratio is about 2.0. In the patient with HIV/AIDS, the T4/T8 ratio is usually 0.5 or less.

Platelet Count.

Platelets (also called thrombocytes) are the smallest of the formed elements in the blood. They are round or oval, flattened, and disk-shaped in appearance. Platelets are produced in the bone marrow and possibly in the lungs. Platelet activity is essential for blood clotting. The normal platelet count is 150,000 to 350,000/mm3.

A deficiency of platelets leads to prolonged bleeding time and impaired clot retention. A low platelet count (thrombocytopenia) is associated with (1) massive blood transfusion, (2) pneumonia, (3) cancer chemotherapy, (4) infection, (5) allergic conditions, and (6) toxic effects of certain drugs (e.g., heparin, isoniazid, penicillins, prednisone, streptomycin). A high platelet count (thrombocythemia) is associated with (1) cancer, (2) trauma, (3) asphyxiation, (4) rheumatoid arthritis, (5) iron deficiency, (6) acute infections, (7) heart disease, (8) tuberculosis, and (9) polycythemia vera.

A platelet count of less than 20,000/mm3 is associated with spontaneous bleeding, prolonged bleeding time, and poor clot retraction. The precise platelet count necessary for hemostasis is not firmly established. Generally, platelet counts greater than 50,000/mm3 are not associated with spontaneous bleeding. Therefore various diagnostic or therapeutic procedures, such as bronchoscopy or the insertion of an arterial catheter, are usually considered safe when the platelet count is greater than 50,000/mm3.

Blood Chemistry

A basic knowledge of blood chemistry, normal values, and common health problems that alter these values is an important cornerstone of patient assessment. Table 9.4 lists the blood chemistry tests monitored in respiratory care.

TABLE 9.4

Blood Chemistry Tests Monitored in Respiratory and Cardiac Care

Chemical

Normal Value

Common Abnormal Findings

Glucose

70–110 mg/dL

Hyperglycemia (excess glucose

 

 

level)

 

 

Diabetes mellitus

 

 

Acute infection

 

 

Myocardial infarction

 

 

Thiazide and loop diuretics

 

 

Hypoglycemia (low glucose level)

 

 

Pancreatic tumors or liver disease

 

 

Pituitary or adrenocortical

 

 

hyperfunction

Lactic dehydrogenase (LDH)

80–120 Wacker

Increases are associated with the

 

units

following:

 

 

Myocardial infarction

 

 

Chronic hepatitis

 

 

Pneumonia

 

 

Pulmonary infarction

Serum glutamic oxaloacetic transaminase (SGOT)

8–33 U/mL

Increases are associated with the

 

 

following:

 

 

Myocardial infarction

 

 

Congestive heart failure

 

 

Pulmonary infarction

Aspartate aminotransferase (AST)

7–40 units/L (0.12–

Increases are associated with the

 

0.67 µKat/L)

following:

 

 

Acute aminotransferase

 

 

hepatitis

 

 

Liver disease

 

 

Myocardial infarction

 

 

Pulmonary infection

Alanine aminotransferase (ALT) (previously called serum

5–36 units/L (0.08–

Increases are associated with the

glutamic pyruvic transaminase [SGPT])

0.6 µKat/L)

following:

 

 

Liver damage

 

 

Inflammation

 

 

Shock

Bilirubin

Adult: 0.1–

Increases are associated with the

 

1.2 mg/dL

following;

 

Newborn: 1–

Massive hemolysis

 

12 mg/dL

Hepatitis

Blood urea nitrogen (BUN)

8–18 mg/dL

Increases are associated with acute

 

 

or chronic renal failure

Serum creatinine

0.6–1.2 mg/dL

Increases are associated with renal

 

 

failure

Electrolytes

For the cells of the body to function properly, a normal concentration of electrolytes must be maintained, especially for normal cardiac function. Therefore the monitoring of electrolytes is extremely important in the patient whose body fluids are being endogenously or exogenously manipulated (e.g., intravenous therapy, renal disease, diarrhea). Table 9.5 lists electrolytes monitored in respiratory care. Normal values for blood sodium, potassium, chloride, and bicarbonate should be memorized by the respiratory care practitioner.

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TABLE 9.5

Electrolytes Commonly Monitored in Respiratory Care

Electrolyte

Normal

Common Abnormal Findings

Clinical Manifestations

Value

 

 

 

Sodium

136–

Hypernatremia (excess Na+)

Desiccated mucous membranes

(Na+)

142 mEq/L

Dehydration

Flushed skin

 

 

Hyponatremia (low Na+)

Great thirst

 

 

Sweating

Dry tongue

 

 

Burns

Abdominal cramps

 

 

Loss of gastrointestinal secretions

Muscle twitching

 

 

Use of some diuretics

Poor perfusion

 

 

Excessive water intake

Vasomotor collapse

 

 

 

Confusion

 

 

 

Seizures

Potassium

3.8–

Hyperkalemia (excess K+)

Irritability

(K+)

5.0 mEq/L

Renal failure

Nausea

 

 

Muscle tissue damage

Diarrhea

 

 

Hypokalemia (low K+)

Weakness

 

 

Diuretic therapy

Ventricular fibrillation

 

 

Endocrine disorder

Metabolic alkalosis

 

 

Diarrhea

Muscular weakness

 

 

Reduced intake or loss of K+

Malaise

 

 

Chronic stress

Cardiac arrhythmias

 

 

 

Hypotension

Chloride (Cl

95–

Hyperchloremia (excess Cl)

Deep, rapid breathing

)

103 mEq/L

Renal tubular acidosis

Weakness

 

 

Hypochloremia (low Cl)

Disorientation

 

 

Alkalosis—associated frequently with

Metabolic alkalosis

 

 

hypokalemia; that is, hypokalemic,

Muscle hypertonicity

 

 

hypochloremic metabolic alkalosis

Tetany

 

 

 

Depressed ventilation (respiratory

 

 

 

compensation)

Calcium

4.5–

Hypercalcemia (excess Ca++)

Lethargy, weakness

(Ca++)

5.4 mEq/L

Malignant tumors

Hyporeflexia

 

 

Bone fractures

Constipation, anorexia, renal stones

 

 

Diuretic therapy

Mental deterioration

 

 

Excessive use of antacids or milk

Paresthesia, cramping of muscles, stridor,

 

 

consumption

seizures, mental disturbance,

 

 

Vitamin D intoxication

Chvostek's sign, Trousseau's sign

 

 

Hyperparathyroidism

 

 

 

Hypocalcemia (low Ca++)

 

 

 

Respiratory alkalosis

 

 

 

Pregnancy

 

 

 

Vitamin D deficiency

 

 

 

Diuretic therapy

 

 

 

Hypoparathyroidism

 

Self-Assessment Questions

1.In the healthy woman, what is the hematocrit (Hct)?

a.31%

b.38%

c.42%

d.45%

2.Which of the following represent the primary defense against bacterial organisms through phagocytosis?

a.Eosinophils

b.Neutrophils

c.Monocytes

d.Basophils

3.What is the normal hemoglobin value for men?

a.10 to 12 g%

b.12 to 14 g%

c.14 to 16 g%

d.16 to 18 g%

4.What percent of the normal white blood cell count are neutrophils?

a.20% to 25%

b.40% to 50%

c.60% to 70%

d.75% to 85%

5.In the healthy man, what is the red blood cell count?

a.5,000,000/mm3

b.6,000,000/mm3

c.7,000,000/mm3

d.8,000,000/mm3

6.What is the normal white blood cell count?

a.1000 to 5000/mm3

b.5000 to 10,000/mm3

c.10,000 to 15,000/mm3

d.15,000 to 20,000/mm3

7.Which of the following are activated by allergies (such as an allergic asthmatic episode)?

a.Eosinophils

b.Neutrophils

c.Monocytes

d.Basophils

8.Various clinical procedures such as bronchoscopy or the insertion of an arterial catheter are generally safe when the platelet count is no lower than which of the following?

a.100,000/mm3

b.75,000/mm3

c.50,000/mm3

d.20,000/mm3

9.Which of the following are associated with hyperglycemia?

1.Diabetes mellitus

2.Myocardial infarction

3.Thiazide and loop diuretics

4.Acute infection

a.2 and 4 only

b.2, 3, and 4 only

c.1, 2, and 3 only

d.1, 2, 3, and 4

10.Which of the following are clinical manifestations associated with hyponatremia?

1.Seizures

2.Confusion

3.Muscle twitching

4.Abdominal cramps

a.2 and 4 only

b.2, 3, and 4 only

c.1, 2, and 3 only

d.1, 2, 3, and 4

1TomoTherapy is a type of therapy in which radiation is aimed at a tumor from many different directions. The patient lies on a table and is moved through a donut-shaped device. The radiation source in the machine rotates around the patient in a spiral pattern. Before radiation, a 3D image of the tumor is taken. This helps the physician find the highest dose of radiation that can be used to kill tumor cells while causing less damage to nearby tissue. Tomotherapy is a type of intensity-modulated radiation therapy (IMRT), also called helical tomotherapy.

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S E C T I O N I I I

The Therapist-Driven Protocol Program— The Essentials

OUTLINE

Chapter 10 The Therapist-Driven Protocol Program

Chapter 11 Respiratory Insufficiency, Respiratory Failure, and Ventilatory Management Protocols

Chapter 12 Recording Skills and Intraprofessional Communication

C H A P T E R 1 0

The Therapist-Driven Protocol

Program

CHAPTER OUTLINE

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

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

Severity Assessment

The Essential Cornerstones of a Successful Therapist-Driven Protocol Program

Summary of a Good Therapist-Driven Protocol Program

Common Anatomic Alterations of the Lungs

Clinical Scenarios Activated by Common Anatomic Alterations of the Lungs

Self-Assessment Questions

CHAPTER OBJECTIVES

After reading this chapter, you will be able to:

Describe the therapist-driven protocol (TDP) program and the role of the respiratory care practitioner now and in the future.

Discuss the knowledge base required for a successful TDP program.

Explain the assessment process skills required for a successful TDP program.

Describe the essential cornerstones (Protocols) for a successful TDP program.

List the anatomic alterations of the lungs commonly seen in clinical practice.

Describe the clinical scenarios—chain of events—activated by the common anatomic alterations of the lungs.

Identify the most common anatomic alterations associated with the respiratory disorders presented in this textbook.

Understand in depth the differences between obstructive and restrictive pathophysiology.

Identify the bases for resistance to development of protocol programs, and outline steps to overcome them.

Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.

KEY TERMS

Aerosolized Medication Therapy Protocol

Airway Clearance Therapy Protocol

Anatomic Alterations of the Lung

Assess, Treat, and Teach Protocols

Atelectasis

Bronchospasm

Clinical Manifestation

Clinical Scenarios

Diagnostic Coding

Discharge Planning

Disease-Specific Protocols

Distal Airway and Alveolar Weakening

Evidence-Based Clinical Practice Guidelines

Excessive Bronchial Secretions

Increased Alveolar-Capillary Membrane Thickness

Length of Stay (LOS)

Lung Expansion Therapy Protocol

Oxygen Therapy Protocol

Pathophysiologic Mechanisms

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Patient-Driven Protocols Patient Education Patient Focused Protocols

Patient Protection and Affordable Care Act Protocol Competency Testing Readmission Prevention Teams

Severity Assessment

TDP Safe and Ready Respiratory Therapist

Therapist-Driven Protocol (TDPs)

There is an emerging consensus that the United States health care system is broken and new and innovative solutions to the problem must be sought. The US Department of Health and Human Services (DHHS), Patient Protection and Affordable Care Act, often called the Affordable Care Act (ACA), was made law in 2010 and came into effect in 2014.

One of the earliest effects of the ACA was to institute a system whereby hospitals would be penalized for what were designated as conditions subject to wasteful excess and excessive use of resources—particularly in the general area of length of stay (LOS). Of the seven “index conditions” monitored, five involve significant use of respiratory care services: acute pneumonia, chronic obstructive pulmonary disease exacerbations, postoperative infections, ventilator-associated pneumonia, congestive heart failure/pulmonary edema, and myocardial infarction. Put simply, it was implied that LOS was a good easy surrogate measure for quality of care; if a patient's hospital stay was significantly longer than a “benchmark” (chosen by the DHHS), how could the quality of care and use of precious resources be anything but substandard?

Over the past several years, the following troubling concerns have been noted:

Many hospitals have not been proactive in securing their institutions from possible penalties for exceeding the LOS benchmark—for example, a 5.4-day LOS instead of 5.0 days—and the financial penalties were significant; some hospitals have already found this out with penalties in the neighborhood of hundreds of thousands of dollars!

Many hospital leaders do not know how close their institutions were to the penalty threshold, nor did they appear to be aware of the generally poor results of attempts to remediate the problem published in the current literature—remedies such as, patient education, transition clinics, focused discharge planning, and readmission prevention teams. All have pros and cons, but none has been extremely successful.

What has worked has been precision in discharge diagnostic coding (ICD-10) and cost-effective use of therapeutic modalities. Among the latter are respiratory care services. This latter area is where the therapist-driven protocol (TDP) approach is attractive and where acceptance of its overall effectiveness will be more widely recognized sooner or later.

Clearly, TDPs (also called: patient-driven protocols, or patient focused protocols) have proved to be an important and integral part of respiratory care health services, resulting in superior cost-effective clinical outcomes. According to the American Association for Respiratory Care (AARC), Guidelines for Respiratory Care Departments Protocol Program Directors,1 the purposes of respiratory TDPs are to:

Deliver individualized diagnostic and therapeutic respiratory care to patients

Assist the physician with evaluating patients’ respiratory care needs and optimize the allocation of respiratory care services

Determine the indications for respiratory therapy and the appropriate modalities for providing high-quality, cost-effective care that improves patient outcomes and decreases length of stay

Empower respiratory therapists to allocate care using signand symptom-based algorithms for respiratory treatment

To support the AARC's purpose statement on TDPs, the American College of Chest Physicians (ACCP) initially defined respiratory therapy protocols as follows, with subsequent approval by the National Association of Medical Directors of Respiratory Care (NAMDRC):

TDPs are patient care plans which are initiated and implemented by credentialed respiratory care workers. These plans are designed and developed with input from physicians, and are approved for use by the medical staff and the governing body of the hospitals in which they are used. They share in common extreme reliance on assessment and evaluation skills.

Protocols are by their nature dynamic and flexible, allowing upor down-regulation of intensity of respiratory services. Protocols allow the respiratory therapist authority to evaluate the patient, initiate care, and to adjust, discontinue, or restart respiratory care procedures on a shift- by-shift or hour-to-hour basis once the protocol is ordered by the physician. They must contain clear strategies for various therapeutic interventions, while avoiding any misconception that they infringe on the practice of medicine. All programs must comply with Federal and State regulations and standards including those published by their State Licensing Boards.

TDPs provide the respiratory therapist with a wide-ranging flexibility to both assess and treat the patient—but only within preapproved and clearly defined boundaries outlined by the physician, the medical staff, and the hospital. In addition, respiratory TDPs give the therapist specific authority to (1) gather clinical information related to the patient's respiratory status, (2) make an assessment of the clinical data collected, and (3) start, increase, decrease, or discontinue certain respiratory therapies on a moment-to-moment, hour-to-hour, shift-by-shift, or day-to-day basis. The innate beauty of respiratory TDPs is that (1) the physician should always be in the “information loop” regarding patient care and (2) therapy can be quickly modified in response to the specific and immediate needs of the patient. Numerous clinical research studies have verified these facts: respiratory TDPs (1) significantly improve selected respiratory therapy outcomes and (2) provided appreciably lower therapy costs.

Unfortunately, the implementation of TDPs throughout the United States continues to be slow. In 2008 the AARC Protocol Implementation Committee conducted a survey to evaluate the barriers to implementation. Over 450 respiratory managers responded to the survey. Despite the overwhelming evidence that protocols clearly improve outcomes and reduce cost, the survey showed that less than 50% of respiratory care nationwide was provided by protocols. About 75% of the respondents had at least one protocol in operation. The majority of the respondent hospitals did not have a comprehensive (All-Service,

All-Modality) program in place. According to the study, the department medical directors, managers, nurses, and administrators were not perceived as barriers.

Of significant interest was the fact that the biggest barrier to the implementation of protocols was perceived to be the medical staff itself. The primary reason for the medical staff's resistance was their perception that “staff therapists did not have the skills (i.e., assessment skills) to function under protocols.” The AARC Protocol Implementation Committee stated that “[this] perception must change….”2 To address this concern, many respiratory care departments have established mandatory protocol competency testing on a periodic basis to ensure their employees are “TDP safe and ready respiratory therapists”—that is, up-to-date on the medical staff and specific hospital-approved TDPs used in their place of work. It goes beyond what the respiratory therapy student learns at school, and beyond what is being tested on the National Board for Respiratory Care (NBRC) examinations. It gets right at the issue of the individual therapist's assessment and treatment (i.e., protocol) skills in this hospital at this point in time.

As of the date of this writing there has been some, but far from complete, improvement in this diagnosis/delivery paradox. Overlap of many of the functions potentially seen as within the scope of practice of the respiratory therapist is now being assumed by the physical therapist and certified nurse practitioner. The Advanced Practice Respiratory Therapist (APRT) is a long way from being fully implemented. Only a handful of therapist training programs in this county are training at the level of competency required in the knowledge and skills base described in the following material. Furthermore, the NBRC has not yet developed, let alone implemented, a certifying examination at the APRT level. In fact, licensure at the level of TDP competency is currently available in only a handful of states.

TDPs must be recognized as different from disease-specific protocols (sometimes called disease management protocols), which involve the diagnosis and treatment of individual diseases rather than the use of modalities or medications—for example, an Initial Asthma Management Protocol such as might be used in an emergency department (see Chapter 14, Asthma). Respiratory therapists may be asked to be familiar with certain disease-specific protocols, depending on their work site, but at this juncture should be required to be competent in the use of all the general modalityspecific TDPs (i.e., Oxygen Therapy Protocol, Airway Clearance Therapy Protocol, Lung Expansion Therapy Protocol, Aerosolized Medication Therapy Protocol, and Mechanical Ventilation Protocol).

The essential components of a good TDP program do not come easy. This is because a strong TDP program promises that the respiratory therapist who is identified as “TDP safe and ready” will 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 plan within the limits set by the protocol (Fig. 10.1).

FIGURE 10.1 The promise of a good therapist-driven protocol program.

The converse, however, is also true: When the respiratory therapist is not TDP safe and ready, the systematic 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 (Fig. 10.2). 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 a good deal of 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 10.2 No assessment program in place.

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

As shown in Fig. 10.3 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 specific anatomic lung alterations and pathophysiologic events.

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FIGURE 10.3 Foundations for a strong therapist-driven protocol program. Overview of the essential knowledge base for outcome assessment of respiratory disease.

Hence, it is essential that the respiratory therapist knows and understands that certain anatomic alterations of the lung will lead to specific and often predictable clinical manifestations. Each respiratory disease presented in this textbook describes these four essential knowledge components necessary for TDPs to successfully work in the modern health care setting. 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 previously, the respiratory therapist must 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 the use and evaluation of this process quickly, clearly, and precisely. In the clinical setting, the practice and mastery of the assessment process are absolutely central and essential to the success of a good TDP program (Fig. 10.4). Simply stated, immediately after the respiratory therapist identifies the clinical manifestations (clinical indicators) present, an assessment of the data must be performed and a treatment plan must be formulated. For the most part, the initial 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 10.4 Overview of TDP program. The way knowledge, outcome assessment, and a therapist-driven protocol program interface between each other.

For example, an appropriate assessment for the clinical cause and indicator of wheezing might be bronchospasm—the anatomic alteration of the lungs. If the therapist assesses the cause of the wheezing correctly as bronchospasm, the correct treatment selection would be a bronchodilator treatment from the Aerosolized Medication Therapy Protocol, Protocol 10.4, page 144. If, however, the cause of the wheezing is correctly assessed to be excessive airway secretions, the appropriate treatment plan would entail a specific treatment modality found in the Airway Clearance Therapy Protocol, such as deep breathing and coughing or chest physical therapy, Protocol 10.2, page 140.

Protocol 10.4

Aerosolized Medication Therapy Protocol