5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

Pleural friction	A continuous, low-pitched creaking, or grating sound from	Pleurisy, pneumonia, pulmonary
rub	roughened, inflamed surfaces of the pleura rubbing together.	fibrosis, pulmonary embolism,
	Generally heard during both inspiration and expiration. There	and thoracic surgery.
	is no change with coughing. The patient is usually
	uncomfortable, especially on deep inspiration.
Diminished	Diminished or distant breath sounds.	COPD, drug overdose or major
breath sounds		sedation, neuromuscular
		disease (Guillain-Barré or
		myasthenia gravis), flail chest,
		pleural effusion, and
		pneumothorax.
Whispering	Spoken or whispered syllable more distinct than normal on	Alveolar consolidation and alveolar
pectoriloquy	auscultation.	collapse (atelectasis).

AP, Anteroposterior; COPD, chronic obstructive pulmonary disease.

Self-Assessment Questions

1.Which of the following pathologic conditions increases vocal fremitus?

1.Atelectasis

2.Pleural effusion

3.Pneumothorax

4.Pneumonia

a.3 only

b.4 only

c.2 and 3 only

d.1 and 4 only

2.A dull or soft percussion note would likely be heard in which of the following pathologic conditions? 1. Chronic obstructive pulmonary disease

2. Pneumothorax

3.Pleural thickening

4.Atelectasis

a.1 only

b.2 only

c.2 and 3 only

d.3 and 4 only

3.Bronchial breath sounds are likely to be heard in which of the following pathologic conditions?

1.Alveolar consolidation

2.Chronic obstructive pulmonary disease

3.Atelectasis

4.Fluid accumulation in the tracheobronchial tree

a.3 only

b.4 only

c.1 and 3 only

d.2 and 4 only

4.Wheezing is:

1.Produced by bronchospasm

2.Generally auscultated during inspiration

3.A cardinal finding of bronchial asthma

4.Usually heard as high-pitched sounds

a.1 only

b.1 and 3 only

c.2 and 4 only

d.1, 3, and 4 only

5.In which of the following pathologic conditions is transmission of the whispered voice of a patient through a stethoscope unusually clear?

1.Chronic obstructive pulmonary disease

2.Alveolar consolidation

3.Atelectasis

4.Pneumothorax

a.1 only

b.2 and 3 only

c.1 and 4 only

d.1, 2, and 3 only

6.Which of the following abnormal breathing patterns is commonly associated with diabetic acidosis?

a.Orthopnea

b.Kussmaul's respiration

c.Biot's respiration

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d. Hypoventilation

C H A P T E R 3

The Pathophysiologic Basis for Common Clinical Manifestations

CHAPTER OUTLINE

Normal Ventilatory Pattern

Abnormal Ventilatory Patterns

Dyspnea

The Pathophysiologic Basis of Abnormal Ventilatory Patterns

The Onset/Offset Patterns Associated With Various Cardiopulmonary Disorders

Use of the Accessory Muscles of Inspiration

Scalenes Pectoralis Majors Trapezius

Use of the Accessory Muscles of Expiration

Rectus Abdominis

External Obliques

Internal Oblique Transversus Abdominis Pursed-Lip Breathing

Substernal and Intercostal Retractions

Nasal Flaring

Splinting and Decreased Chest Expansion Caused by Pleuritic and Nonpleuritic Chest Pain

Pleuritic Chest Pain (Pleurisy) Nonpleuritic Chest Pain

Abnormal Chest Shape and Configuration

Abnormal Extremity Findings

Altered Skin Color Cyanosis

Digital Clubbing

Peripheral Edema

Distended Neck Veins and Jugular Venous Distention

Normal and Abnormal Sputum Production

Normal Histology and Mucous Production of the Tracheobronchial Tree Abnormal Sputum Production

Hemoptysis

Cough

Nonproductive Cough Productive Cough

Self-Assessment Questions

CHAPTER OBJECTIVES

After rteading this chapter, you will be able to:

•Discuss the pathophysiologic basis for abnormal ventilatory patterns, including

•Effects of lung compliance

•Airway resistance

•Peripheral chemoreceptors

•Central chemoreceptors

•Pulmonary reflexes

•Pain, anxiety, and fever

•Describe the function of the accessory muscles of inspiration.

•Describe the function of the accessory muscles of expiration.

•Discuss the effects of pursed-lip breathing.

•Describe the pathophysiologic basis for substernal and intercostal retractions.

•Explain nasal flaring.

•Discuss splinting and decreased chest expansion caused by pleuritic and nonpleuritic chest pain.

•List abnormal chest shape and configurations.

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•List abnormal extremity findings.

•Describe normal and abnormal sputum production.

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

KEY TERMS

Abnormal Ventilatory Patterns

Accessory Muscles of Expiration

Accessory Muscles of Inspiration Acute-Onset Conditions

Airway Resistance (Raw)

Aortic and Carotid Sinus Baroreceptor Reflexes Borg Dyspnea Scale

Capability-to-Breathe Cardiac Dyspnea

Cardiopulmonary Exercise Testing Central Chemoreceptors

Central Cyanosis Chronic Conditions Cough

Cyanosis Demand-to-Breathe Digital Clubbing Distended Neck Veins

Dorsal Respiratory Group (DRG) Dyspnea

Eupnea

Exertional Dyspnea External Oblique Muscle Hering-Breuer Reflex Hemoptysis Hypothermia

Hysteresis

Inspiratory-to-Expiratory Ratio (I/E Ratio) intercostal retractions

Internal Oblique Muscle Irritant Reflex

jungular venous distention

Juxtapulmonary-Capillary Receptors (J Receptors) Reflex Lung Compliance (CL)

Modified (British) Medical Research Council (mMRC) Questionnaire Mucociliary Escalator

Mucous Blanket Nasal Flaring

Nonpleuritic Chest Pain

Nonproductive Cough Orthopnea

Paroxysmal Nocturnal Dyspnea Pectoralis Major Muscle Peripheral Chemoreceptors Peripheral Edema

Pitting Edema Pleural Friction Rub Pleuritic Chest Pain Poiseuille's Law Positional Dyspnea

Productive Cough Pulmonary Shunting Pursed-Lip Breathing Rectus Abdominis Muscles Renal Dyspnea

Scalene Muscles Splinting

Sternocleidomastoid Muscles Substernal

Substernal Retraction Tidal Volume (VT) Transairway Pressure

Transversus Abdominis Muscles Trapezius Muscles

Tripod Position Venous Admixture

Ventilation-Perfusion Ratio (V/Q)

Ventral Respiratory Group (VRG)

Work of Breathing (WOB)

As shown in Box 3.1, there are a variety of clinical manifestations commonly observed in examination of the patient with respiratory disease. For example, the patient often demonstrates an abnormal ventilatory pattern, the use of accessory muscles of inspiration, the use of accessory muscles of expiration, purse-lip breathing, substernal or intercostal retractions, nasal flaring, splinting of the chest, abnormal chest shape, clubbing of the toes and/or fingers, a nonproductive or productive cough, and the appearance of cyanosis. Some of these commonly observed clinical manifestations can be objective—such as observed nasal flaring or the use of accessory muscles of inspiration, whereas other clinical observations can be more subjective—for example, the examiner's documentation of the patient's appearance of cyanosis or of his sputum. To further help in the understanding of these commonly observed clinical manifestations, a more in-depth discussion of their pathophysiologic bases is presented in this chapter.

Box 3.1

Common Clinical Manifestations Observed During Inspection

•Anxiety

•Abnormal ventilatory pattern findings

•Use of accessory muscles of inspiration

•Use of accessory muscles of expiration

•Pursed-lip breathing

•Substernal or intercostal retractions

•Nasal flaring

•Splinting or decreased chest expansion caused by chest pain

•Abnormal chest shape and configuration

•Abnormal extremity findings:

•Altered skin color

•Digital clubbing

•Pedal edema

•Distended neck veins

•Cough (note characteristics)

•Expectoration of sputum

•Hemoptysis (note volume)

Normal Ventilatory Pattern

An individual's normal breathing pattern is composed of a tidal volume (VT), a ventilatory rate, and an inspiratory-to- expiratory ratio (I/E ratio). In normal adults, the VT is about 500 mL (7 to 9 mL/kg), the ventilatory rate is about 15 (with

a range of 12 to 18) breaths per minute, and the I/E ratio is about 1 : 2. In patients with respiratory disorders, however, an abnormal ventilatory pattern is often present.

Abnormal Ventilatory Patterns

As presented in Chapter 2, The Physical Examination, there are several abnormal breathing patterns frequently seen in the patient with respiratory problems (see Table 2.4). Thus the respiratory therapist must be strongly proficient in the ability to identify and differentiate such ventilatory patterns as bradypnea, tachypnea, apnea, hypoventilation, hyperventilation, Cheyne-Stokes respirations, Kussmaul's respirations, and Biot's respirations. In addition, the respiratory therapist must have a strong understanding of the meaning and use of the word dyspnea.

Dyspnea

Dyspnea is a general term often used—although incorrectly—to describe the patient's difficulty in breathing. In fact, the term dyspnea is likely the most common symptom the respiratory therapist is asked to evaluate and treat.

Dyspnea is defined as the “breathlessness,” or “shortness of breath,” or the “labored or difficult breathing” felt and

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described only by the patient. Although the onset of dyspnea should not be ignored—and it is always a good reason to seek immediate medical attention—dyspnea should not be assumed by the respiratory therapist's impression of the patient's breathing pattern alone.

The symptoms of dyspnea (“subjective information”) are sensations that can be experienced only by the patient who is having breathing difficulties, not by the observation of the hospital care staff. For example, the patient might say: “I just can't seem to get air into my lung!” Or, “Every time I lie down, I get very short of breath.” These are clearly sensations.

Signs of dyspnea (“objective information”) include audibly labored breathing, hyperventilation, and/or tachypnea, retractions of intercostal spaces, use of accessory muscles, a distressed facial expression, flaring of the nostrils, paradoxical movements of the chest and abdomen, and gasping. These signs of dyspnea are strong indicators of inadequate ventilation and/or an insufficient amount of oxygen in the blood. All of these clinical indicators of inadequate breathing reflecting the patient's reduced capability to breathe should be documented in the patient's chart.

Common types of dyspnea include (1) positional dyspnea, which occurs only when the patient is in the reclining position and is also known as orthopnea, (2) cardiac dyspnea, which is labored breathing caused by heart disease (e.g., congestive heart failure), (3) exertional dyspnea, which is provoked by physical exercise or exertion, (4) paroxysmal nocturnal dyspnea, which is a form of respiratory distress related to posture (especially reclining while sleeping) and is usually associated with congestive heart failure with pulmonary edema, and (5) renal dyspnea, which is difficulty in breathing as a result of kidney disease.

Demand-to-Breathe Versus Capability-to-Breathe

To further our understanding of the sensation of dyspnea, Fig. 3.1 illustrates it as an imbalance of the teeter-totter relationship between the individual's demand-to-breathe and his actual capability-to-breathe. For example, during normal periods of eupnea, the individual has no sensation of difficulty breathing and demand-to-breathe matches capability-to-breathe (i.e., the cardiopulmonary system is able to adequately move oxygen into the body and carbon dioxide out of it. In short, the cardiopulmonary function and reserve are in balance with metabolic needs (see Fig. 3.1A). Eupnea is defined as the normal breathing rate (between 12 and 20 breaths per minute) and regular rhythm and moderate depth for an adult (see Table 2.1).

FIGURE 3.1 The sensation of dyspnea is demonstrated as a balance between the individual's demand-to-breathe and capability- to-breathe. In the normal individual, the demand-to-breathe is driven by (1) oxygen consumption (V̇O2), (2) work of breathing

required by the task at hand, and (3) the person's physical condition. The capability-to-breathe consists of the individual's integrated function and reserve of the cardiopulmonary system (see Figs. 1.2 and 1.3). At rest and with mild to moderate exercise, the reserve of this system is not rate-limiting for exercise. (A) At rest, there is no increased need-to-breathe and therefore there is no sensation of dyspnea (eupnea). The level teeter-totter beam denotes no dyspnea. (B) During exercise in the normal individual, the V̇O2 increases, but is, up to a point, balanced by normal cardiopulmonary function and reserve, which

is adequate to meet the increased metabolic challenge. Although the nonlevel beam denotes dyspnea, this form of dyspnea is normal and can be referred to as effort-appropriate dyspnea. (C) Illustrates an increased demand-to-breathe combined with the reduced capability-to-breathe (caused by a decreased cardiopulmonary reserve and function). This condition causes dyspnea and can significantly limit even modest activities of daily living.

During periods of significant exercise, however, the normal individual's capability-to-breathe may be challenged to meet the increased demand-to-breathe as his oxygen consumption increases. When this occurs, the individual may experience dyspnea, depending on metabolic demands and increased load-related work of breathing associated with the exercise. This demand-to-breathe sensation is normal and can be considered “effort-appropriate dyspnea” (see Fig. 3.1B).

On the other hand, next consider the severely increased demand-to-breathe and dyspnea that occur in the patient performing mild or moderate exercise with an abnormal capability-to breathe because of a reduced cardiopulmonary function and reserve (e.g., chronic bronchitis, emphysema, or congestive heart failure). In this case, the patient's work of

breathing (WOB) and required oxygen consumption (in response to the exercise) are both increased. In fact, many patients with severe cardiopulmonary problems frequently remark that they are short of breath when performing even the most routine day-to-day tasks such as walking, climbing stairs, or dressing (see Fig. 3.1C). For further discussion see text and Chapter 4, Pulmonary Function Testing (section on cardiopulmonary exercise testing).

Chapter 10, The Therapist-Driven Protocol Program, and Chapter 11, Respiratory Insuffiency, Respiratory Failure, and Ventilatory Management Protocol, will stress the importance of prioritizing patient treatments, and the upor downregulating of treatment frequency, dosing, and nature of therapy on the basis of a scheme that in part relies on the severity on the patient's subjective complaints. Not only are severity-based systems used in prioritizing treatments but they are also used in assigning the localization or bedding of patients (e.g., holding areas, intensive care units, step-down units, or rehabilitation units, etc.). Severity-based systems are also an important part of a coding system that determines hospital and physician reimbursement using an alphanumeric coding system (ICD).

The following two methods are commonly used to assess the patient's breathlessness; not surprisingly, they are based on patients' sensation of the severity of their demand-to-breathe—that is, patients’ severity assessment of their dyspnea:

• The Modified (British) Medical Research Council (mMRC) Questionnaire for Assessing the Severity of Breathlessness in those who can speak (Table 3.1).

TABLE 3.1

Modified Medical Research Council (mMRC) Dyspnea Scale

mMRC	Check the Score Box That Best Applies to You (One Box Only)
Score
0	I only get breathless with strenuous exercise.	□
1	I get short of breath when hurrying on level ground or walking up a slight hill.	□
2	On level ground, I walk slower than people of the same age because of breathlessness or have to	□
	stop for breath when walking at my own pace.
3	I stop for breath after walking about 100 m or after a few minutes on level ground.	□
4	I am too breathless to leave the house or I am breathless when dressing.	□

Patients choose a score from the right-hand column that reflects their degree (amount) of shortness of breath (dyspnea).

• The Borg Dyspnea Scale used in patients who cannot communicate because of mouthpieces, endotracheal tubes, tracheotomies, etc. (Table 3.2).

TABLE 3.2

Borg Dyspnea Rating Scale for Use in Patients Unable to Communicate

Scale

Level of Dyspnea

0No shortness of breath (SOB)

0.5	Slight SOB
1

2Mild SOB

3	Moderate SOB
4
5	Strong or hard breathing
6
7	Severe breathing or SOB
8
9
10	SOB so severe I need to stop and rest

Patients indicate their degree of shortness of breath (dyspnea) by pointing (or having the examiner point) to the appropriate number in the rating scale on the left.

The Pathophysiologic Basis of Abnormal Ventilatory Patterns

Although the precise cause of an abnormal ventilatory pattern may not always be known, they are often related to (1) the anatomic alterations of the lungs associated with a specific disorder and (2) the pathophysiologic mechanisms that develop because of the anatomic alterations. Therefore to evaluate and assess the various abnormal ventilatory patterns (rate and volume relationships) seen in the clinical setting, the following pathophysiologic mechanisms that can alter the ventilatory pattern must first be understood:

•Lung compliance

•Airway resistance

•Peripheral chemoreceptors

•Central chemoreceptors

•Pulmonary reflexes

•Hering-Breuer reflex

•Deflation reflex

•Irritant reflex

•Juxtapulmonary-capillary receptors (J receptors) reflex

•Reflexes from the aortic and carotid sinus baroreceptors

•Pain, anxiety, and fever

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Recall the notion put forward in Chapter 1, The Patient Interview, that respiratory disease processes often start slowly but over time even small pathologic changes can produce remarkable signs and symptoms (see Fig. 1.1). The message is clear: In cardiopulmonary disease, “little things (indeed) do mean a lot.” This statement is certainly true for the effects of decreased lung compliance and increased airway resistance on the work of breathing. As discussed in the following section, changes in lung compliance and airway resistance can and do have a profound effect on the patient's ventilatory pattern.

Lung Compliance and Its Effect on the Ventilatory Pattern and Dyspnea

The ease with which the elastic forces of the lungs accept a volume of inspired air is known as lung compliance (Cl). CL is

measured in terms of unit volume change per unit pressure change. Mathematically, it is written as liters per centimeter of water pressure (L/cm H2O). In other words, compliance determines how much air in liters the lungs will accommodate for

each centimeter of water pressure change in distending pressure.

For example, when the normal individual generates a negative intrapleural pressure change of −2 cm H2O during inspiration, the lungs accept a new volume of about 0.2 L gas. Therefore the CL of the lungs and thorax is 0.1 L/cm H2O:

The normal compliance of the lungs is graphically illustrated by the volume-pressure curve seen in (Fig. 3.2). As shown in Fig. 3.3, when CL increases (e.g., emphysema), the lungs accept a greater volume of gas per unit pressure change. When

CL decreases (e.g., pulmonary fibrosis or atelectasis), the lungs accept a smaller volume of gas per unit pressure change.

FIGURE 3.2 Inflation-deflation pressure-volume curve (red dotted line). The direction of inspiration and exhalation is shown by the arrows. The difference between the inflation and deflation pressure-volume curve is a result of the variation in surface tension with changes in lung volume. This effect is called hysteresis. Also note the normal tidal volume (VT) pressure-volume

curves (blue circle hysteresis) that begin and end at the resting functional residual capacity (FRC). TLC, Total lung capacity.

FIGURE 3.3 Effects of increased and decreased compliance on the volume-pressure curve. As the lung compliance decreases, greater pressure change is required to obtain the same volume of 2.5 L (dotted lines).

Although the precise mechanism is not clear, the fact that certain ventilatory patterns occur when lung compliance is altered is well documented. For example, when CL decreases, the patient's breathing rate generally increases while the

tidal volume simultaneously decreases (Fig. 3.4). This type of breathing pattern is commonly seen in restrictive lung disorders such as pneumonia, pulmonary edema, and acute respiratory distress syndrome. In addition, a rapid breathing rate and reduced tidal volume is also commonly seen during the early stages of an acute asthmatic attack when the alveoli are overinflated—CL progressively decreases as the alveolar volume increases. Note that the volume/pressure curve

flattens at high lung volumes (see Fig. 3.2). CL is low at both the high and low ends of the normal pressure-volume curve.

Note the normal resting tidal volume and where it is placed in the pressure volume curve, very near to the normal functional residual capacity, illustrated in blue (see Fig. 3.2). It should be noted that, physiologically, we elect to breathe at the most compliant and efficient portion of our lung volume.

FIGURE 3.4 The effects of increased airway resistance and decreased lung compliance on ventilatory frequency and tidal volume. N, Normal resting tidal volume and ventilatory frequency.

Airway Resistance and Its Effect on the Ventilatory Pattern

Airway resistance (Raw) is defined as the pressure difference between the mouth and the alveoli (transairway pressure)

divided by the flow rate. Therefore the rate at which a certain volume of gas flows through the airways is a function of the pressure gradient and the resistance created by the airways to the flow of gas. Mathematically, Raw is calculated as follows:

For example, if a patient produces a flow rate of 6 L/s during inspiration by generating a transairway pressure difference of 12 cm H2O, Raw would be 2 cm H2O/L/s:

Under normal conditions, the Raw in the tracheobronchial tree is about 1.0 to 2.0 cm H2O/L/s. However, in large airway obstructive pulmonary diseases (e.g., bronchitis, asthma), the Raw may be extremely high. (For a more in-depth discussion

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on this topic, see Chapter 4, Pulmonary Function Testing.) An increased Raw has a profound effect on the patient's

ventilatory patterns. For example, as demonstrated by Poiseuille's Law for pressure and flow, even the slightest reduction in airway diameter can have a remarkable effect on the patient's ability to move air in and out of the lungs (Box 3.2).

Box 3.2

Poiseuille's Law for Flow and Pressure Applied to Bronchial Airways

Poiseuille's law mathematically confirms how small changes in airway diameter can have a profound effect on intrapleural pressure and air flow. For example, consider the mathematics of Poiseuille's law for flow:

where η = the viscosity of a gas (or fluid), ΔP = the change of pressure from one end of the tube to the other, r = the radius of the tube, l = the length of the tube, V = the gas (or fluid) flowing through the tube; and π and 8 = constants, which are excluded from this discussion in the interest of brevity.

The equation shows that flow is directly proportional to P and r4 and inversely proportional to l and η. Thus flow will decrease in response to either a decreased P or tube radius and flow will increase in response to a decreased tube length and fluid viscosity. In addition, the formula shows that flow will increase in response to an increased P and tube radius or decrease in response to an increased tube length and fluid viscosity. Thus assuming that pressure (P) remains

constant, decreasing the radius of a tube by half reduces the gas flow to of its original flow. For example, if the radius of a bronchial tube through which gas flows at a rate of 16 mL/s is reduced from 1 cm to 0.5 cm because of

mucosal swelling, the flow rate through the bronchial tube would decrease to 1 mL/s ( the original flow rate) as graphically illustrated:

To offset this air flow reduction, Poiseuille's law confirms what pressure changes would be needed to maintain the original air flow. When Poiseuille's law is arranged for pressure, it is written as follows:

Using the previous example of reducing the airway from 1 cm to 0.5 cm, if the original driving pressure (i.e., intrapleural pressure) was 1 cm H2O to move gas in and out of the lungs, the patient would need to increase the driving

pressure to 16 cm H2O to maintain the same gas flow as illustrated: