Structure and Technique for Interviewing

The ideal interview is one in which the patient feels secure and free to talk about important personal matters. Each interview should begin with the RT introducing himself or herself to the patient and stating the purpose of the visit. The introduction is done in the social space, approximately 4 to 12 feet from the patient. It begins the process of establishing a rapport with the patient and helps the patient feel more comfortable about answering personal questions. Pulling the curtain between the beds of a semiprivate room also may be helpful in making the patient feel more at ease with the interview (Box 15-1).

Next, the RT moves into the personal space (2 to 4 feet from the patient) to begin the interview. In this space, the patient does not have to speak loudly in response to questions. The RT should assume a physical position at the same level with the patient (e.g., by sitting in a chair) before beginning the formal interview. Standing over the patient should be avoided because this position makes the patient feel inferior. Appropriate eye contact with the patient is essential for a quality interview. Eye contact gives the patient more confidence in the interviewer. Eye contact also allows the interviewer to see confusion, anger, frustration, and other emotions that may be expressed by the patient in response to questions.

Using neutral questions and avoiding leading questions during the interview is important. Asking the patient, “Is your breathing better now?” leads the patient toward a desired response and may elicit false information. Asking the patient, “How is your breathing now?” is a better way to get accurate information about the patient’s breathing (Box 15-2).

Common characteristics of symptoms can be identified by asking questions such as the following during the interview:

Identifying these characteristics of any new symptom can be helpful in recognizing the cause and potential therapy; this is primarily the role of the attending physician but sometimes falls to other clinicians in certain settings. Once the symptom or symptoms are established and therapy is started, other questions are used to evaluate the changes in the symptoms over the course of the hospital stay. For example, the clinician may ask, “Has the symptom changed in any way since admission?” or, “Does the therapy seem to make a difference?”

The best interview techniques are of no value if the interviewer is not knowledgeable about the pathophysiology and characteristics of common cardiopulmonary symptoms. The interview is a series of focused questions that pursue specific information related to a tentative diagnosis. The ability to ask the key questions at the right time comes from experience and familiarity with the signs and symptoms of lung disease.

Breathlessness

Breathlessness is the specific sensation of an unpleasant urge to breathe. It is believed to be the conscious perception of intense neural discharge to the respiratory muscles. Breathlessness can be triggered by acute hypercapnia and acidosis and by hypoxemia. A normal experience of breathlessness is the unpleasant throbbing sensation that accompanies prolonged breath holding or feeling “winded” during strenuous physical exercise. However, it is not known how closely normal encounters with breathlessness resemble the sensation that arises during disease because dyspnea in patients with cardiopulmonary disease also is affected by other stimuli that contribute to both the quality and the intensity of the sensation. These include stimuli arising from hypoxemia, irritant receptors in the lungs and airways, and receptors in the blood vessels and heart.

Ultimately, dyspnea and breathlessness are magnified by the emotional distress that accompanies them. This distress is influenced by situation, knowledge, and control. In other words, a healthy person can quickly identify the source of breathlessness and arrest the symptom simply by stopping exercise or the breath hold. In contrast, a patient with cardiopulmonary disease may be unable to control the symptom, let alone be able to identify the source. These factors have a profound emotional impact that must be appreciated by the RT.

Positional Dyspnea

Dyspnea may be present only when the patient assumes the reclining position, in which case it is referred to as orthopnea. Orthopnea is common in patients with congestive heart failure (CHF); it apparently is caused by the sudden increase in venous return that occurs with reclining. The failing left ventricle is unable to accommodate the increased venous return, resulting in pulmonary vascular congestion and dyspnea. Orthopnea is also a symptom of bilateral diaphragmatic paralysis.

Dyspnea in the upright position is known as platypnea. This unusual symptom may accompany arteriovenous malformations in the lung, such as occur in chronic liver disease (hepatopulmonary syndrome), and some hereditary conditions. Platypnea may be accompanied by orthodeoxia, which is oxygen desaturation on assuming an upright position.

Language of Dyspnea

Dyspnea is a subjective experience, and patients possess a nuanced language to describe their sensations. RTs should ask specific questions about the quality and characteristics of the patient’s dyspnea. In this way, the RT might gain insight into the mechanism provoking dyspnea. As the patient describes the sensations, the RT should try to categorize each according to a particular aspect of breathing such as inspiration, expiration, respiratory drive, or lung volume. A remark such as, “I feel that my breath stops,” reflects a problem with inspiration, whereas the remark, “my breath does not go all the way out,” suggests a problem with expiration. Statements such as, “I can’t catch my breath,” suggest that respiratory drive is elevated (i.e., breathlessness).

Different types of lung diseases often evoke unique sensations that may provide clues about the underlying pathophysiology. Patients with asthma frequently complain of chest tightness. In contrast, patients with interstitial lung disease tend to focus on the sensations of increased work of breathing, shallow breathing, and gasping. Patients with CHF are seemingly unique in frequently feeling suffocated. Although the language used to describe dyspnea provides helpful clues, the RT should keep in mind that many lung diseases evoke common sensations.

Patients with cardiopulmonary disease frequently experience several unpleasant breathing sensations simultaneously. A particular sensation may be more prominent than others and may change over time. As mentioned previously, patients with asthma typically complain first about the sensation of chest tightness. However, as bronchoconstriction worsens and the lungs become more hyperinflated, patients often begin to focus more on the sensation of excessive work of breathing, air hunger, and the inability to take a deep breath.

Assessing Dyspnea in the Interview

The assessment of dyspnea is largely determined by the situation. When conducting an interview, the RT should pay particular attention to whether the patient can speak in full sentences. It may be very difficult for patients with severe dyspnea from any cause to speak more than a few words at a time. In this situation, the initial interview should be curtailed, and treatment should be initiated as soon as possible. Questions should be brief and limited to the quality and intensity of dyspnea and the circumstances of symptom onset. Also, the assessment of dyspnea should occur simultaneously with a gross examination of the patient’s breathing pattern (see later section of this chapter). Assessment of dyspnea that arises acutely in patients without a prior history of cardiopulmonary disease typically does not require the same detail as assessment in patients with long-standing cardiopulmonary or neurologic disease.

In patients with chronic cardiopulmonary disease, a detailed and systematic history should cover four major areas, as follows:

Beyond the information gleaned, a detailed conversation about a patient’s struggle with dyspnea allows the patient to share his or her experience and decreases the patient’s sense of isolation.

The intensity of dyspnea can be documented using a numeric intensity or visual analog scale (Figure 15-1). Such scales provide a way to evaluate the patient’s response to treatment over time. These scales are important because objective lung function measurements (e.g., pulmonary function tests, PaO₂) seldom correlate with the degree of dyspnea in many patients.

Psychogenic Dyspnea: Panic Disorders and Hyperventilation

There are perplexing situations in which patients with normal cardiopulmonary function complain of intense dyspnea or suffocation. This condition is known as psychogenic hyperventilation syndrome and is associated with panic disorders. Hyperventilation may coincide with other symptoms such as chest pain, anxiety, palpitations and paresthesia (the sensation of tingling and numbness in the extremities that often accompanies respiratory alkalosis). This syndrome may be either sporadic or chronic and often is self-perpetuating.

Anxiety often is accompanied by breathlessness and hyperventilation. The resulting respiratory alkalosis amplifies the sensation of breathlessness and provokes more anxiety, increasing the intensity of hyperventilation. The classic homespun remedy of having the patient slowly rebreathe into a paper bag holds merit because this can arrest the respiratory alkalosis and help break the cycle. However, rebreathing techniques may require formal behavioral therapy and may not be appropriate in the hospital setting. This condition usually is treated clinically by administering judicious amounts of anxiolytic agents.

The RT always must approach any situation involving hyperventilation or dyspnea as if it had a pathophysiologic basis. The first priority is to measure the vital signs, including arterial oxygen saturation, and perhaps a 12-lead electrocardiogram and arterial blood gases. A psychogenic source should be considered only after a pathogenic source for hyperventilation or dyspnea has been ruled out. Intense pain or fear may provoke anxiety and hyperventilation. The RT must work in concert with nursing and physician colleagues to determine the root cause of any hyperventilation syndrome.

Cough

A cough is the most common, yet nonspecific symptom seen in patients with pulmonary disease. Coughing is a forceful expiratory maneuver that expels mucus and foreign material from the airways. It usually occurs when the cough receptors are stimulated by inflammation, mucus, foreign materials, or noxious gases. The cough receptors are located primarily in the larynx, trachea, and larger bronchi.

The effectiveness of a cough depends on the ability of the individual to take a deep breath, lung elastic recoil, expiratory muscle strength, and level of airway resistance. The ability to take a deep breath or exhale forcefully is often impaired in patients with neuromuscular disease. An effective cough also is impaired secondary to pain; this is typically seen in the early postoperative period in patients following upper abdominal surgery or thoracic surgery or after trauma. Often expiratory flow is limited by factors such as bronchospasm (e.g., asthma) and reduced lung elastic recoil (as in emphysema). Patients with an inadequate ability to cough because of impairment of these factors often have problems with retained secretions and are more prone to the development of pneumonia.

Important characteristics of the patient’s cough to identify include whether it is dry or loose, productive or nonproductive, and acute or chronic and whether it occurs more frequently at particular times (i.e., day or night). Knowledge of such details may help in determining the cause of the cough. A dry, nonproductive cough is typical for restrictive lung diseases such as CHF or pulmonary fibrosis. A loose, productive cough is more often associated with inflammatory obstructive diseases such as bronchitis and asthma. The most common cause of an acute, self-limited cough is a viral infection of the upper airway. Common causes of chronic coughing include asthma, postnasal drip, chronic bronchitis, and gastroesophageal reflux,¹ although combinations of these often exist.² Cough is also associated with the use of certain medications for hypertension (e.g., angiotensin-converting enzyme inhibitors).³

Sputum Production

Healthy airways produce mucus daily. Normally, the quantity of this mucus is minimal, and it is not enough to stimulate the cough receptors. Mucus is gradually moved to the hypopharynx by the mucociliary escalator, where it is either swallowed or expectorated. Disease of the airways may cause the mucous glands, which line the airways, to produce an abnormally increased amount of mucus, which usually stimulates the cough receptors and causes the patient to generate a loose, productive cough. This cough is seen in acute bronchitis or asthma attacks brought on by airway infection.

RTs need to be aware of the terminology associated with sputum. Technically, mucus from the tracheobronchial tree that has not been contaminated by oral secretions is called phlegm. Mucus that comes from the lung but passes through the mouth as it is expectorated is sputum. Because this is how most mucus samples from the lung are obtained, the term sputum is used in this chapter. Sputum that contains pus cells is said to be purulent, suggesting a bacterial infection. Purulent sputum appears thick, colored, and sticky. Sputum that is foul-smelling is said to be fetid. Sputum that is clear and thick is mucoid and is commonly seen in patients with airways disease (i.e., asthma). Changes in the color, viscosity, or quantity of sputum produced are often signs of infection and must be documented and reported to the physician.

Hemoptysis

Coughing up blood or blood-streaked sputum from the lungs is referred to as hemoptysis. Blood-streaked sputum is common in patients with pulmonary disease. Frank hemoptysis is the presence primarily of blood in the expectorant. Hemoptysis is characterized as massive when more than 300 ml of blood is expectorated over 24 hours, and this represents a medical emergency. Hemoptysis must be distinguished from hematemesis, which is vomiting blood from the gastrointestinal tract. Blood from the lung is often seen in patients with a history of pulmonary disease and may be mixed with sputum. Blood from the stomach may be mixed with food particles and occurs most often in patients with a history of gastrointestinal disease.

Nonmassive hemoptysis is caused most often by infection of the airways but also is seen in lung cancer, tuberculosis, blunt or penetrating chest trauma, and pulmonary embolism. Hemoptysis associated with infection usually is seen as blood-streaked, purulent sputum. Hemoptysis commonly is found in patients with bacterial pneumonia. Hemoptysis from bronchogenic carcinoma often is chronic and may be associated with a monophonic wheeze and cough. Common causes of massive hemoptysis include bronchiectasis, lung abscess, and acute or old tuberculosis.

Chest Pain

Most chest pain can be categorized as either pleuritic or nonpleuritic. Pleuritic chest pain usually is located laterally or posteriorly. It worsens when the patient takes a deep breath, and it is described as a sharp, stabbing type of pain. It is associated with diseases of the chest that cause the pleural lining of the lung to become inflamed, such as pneumonia or pulmonary embolism.

Nonpleuritic chest pain is located typically in the center of the anterior chest and may radiate to the shoulder or back. It is not affected by breathing, and it is described as a dull ache or pressure type of pain. A common cause of nonpleuritic chest pain is angina, which classically is a pressure sensation with exertion or stress and results from coronary artery occlusion. Other common causes of nonpleuritic chest pain include gastroesophageal reflux, esophageal spasm, chest wall pain (e.g., costochondritis), and gallbladder disease.

Fever

Fever (an elevated body temperature secondary to disease) is a common complaint of patients with an infection of the airways or lungs. Fever may occur with a viral infection of the upper airway or bacterial pneumonia or tuberculosis. All patients with a fever need further assessment to determine the cause. When infection causes fever, the magnitude of temperature elevation may indicate the type and virulence of the infection. Low-grade fever typically accompanies common upper respiratory tract infections, whereas a high fever occurs with viral influenza infection.

Fever that occurs with a cough suggests a respiratory infection. An infection is even more likely to be the cause of the fever if the patient is producing purulent sputum. In this situation, a persistent fever of at least 38.9° C (102° F) for 2 days accompanied by chills is suggestive of pneumonia. However, the absence of coughing or sputum production does not rule out lung infection. Noninfectious causes of fever include head trauma (secondary to damage of the hypothalamus), cancer, immunologic disorders (e.g., sarcoidosis), an adverse reaction to certain medications (e.g., sulfa drugs), and thromboembolic disorders such as pulmonary embolism.

It was believed for many years that there was a link between fever and atelectasis in postoperative surgical patients. However, more recent evidence has shown no link between the formation of atelectasis and the development of fever (>101.3° F [>38.5° C]) during the first 72 hours after surgery.⁴

Patients with a significant fever have an increased metabolic rate and an increased oxygen (O₂) consumption and carbon dioxide (CO₂) production. The increased need for O₂ intake and CO₂ removal may cause tachypnea. The increased ventilatory demand caused by fever is particularly dangerous for patients with severe chronic cardiopulmonary disease because it may cause acute respiratory failure.

Pedal Edema

Swelling of the lower extremities is known as pedal edema. It most often occurs with heart failure, which causes an increase in the hydrostatic pressure of the blood vessels in the lower extremities. This increase in hydrostatic pressure causes fluid to leak into the interstitial spaces and leads to pedal edema, the degree of which depends on the level of heart failure. There are two subtypes of pedal edema. When pressure is applied with a finger on a swollen extremity, an indentation mark left on the skin is called pitting edema. Weeping edema is when a small fluid leak occurs at the point where pressure is applied.

Patients with chronic hypoxemic lung disease are especially prone to right-sided heart failure (cor pulmonale) because of the heavy demands placed on the right ventricle when hypoxemia causes severe pulmonary vasoconstriction. Eventually, the right side of the heart begins to fail and results in a backup of pressure into the venous blood vessels, especially in the dependent regions such as the lower extremities. This situation promotes high intravascular venous hydrostatic pressures and pedal edema. The patient often complains of “swollen ankles” in such cases.

Body Temperature

The average body temperature for adults is approximately 37° C (98.6° F), with daily variations of approximately 0.5° C (1° F). Body temperature normally varies over a 24-hour day and usually is lowest in the early morning and highest in the late afternoon. Metabolic functions occur optimally when the body temperature is normal.

Body temperature is kept normal by balancing heat production with heat loss. If the body were unable to discharge the heat generated by metabolism, the temperature would increase approximately 2° F (−16.7° C) per hour. The hypothalamus plays an important role in regulating heat loss and can initiate peripheral vasodilation and sweating (diaphoresis) to dissipate body heat. The respiratory system also helps remove excess heat through ventilation by warming the inspired air, which is subsequently exhaled.

An elevated body temperature (hyperthermia or hyperpyrexia) can result from disease or from normal activities such as exercise. Temperature elevation caused by disease is called fever, and the patient is said to be febrile. Fever increases the body’s metabolic rate, increasing both O₂ consumption and CO₂ production. This increase in metabolism must be matched by an increase in both circulation and ventilation to maintain homeostasis; this is why febrile patients often have increased heart and breathing rates. However, not all patients can easily accommodate the need for increased circulation and ventilation, and respiratory failure can result.

A body temperature below normal is called hypothermia. The most common cause of hypothermia is prolonged exposure to cold, to which the hypothalamus responds by initiating shivering (to generate heat) and vasoconstriction (to conserve heat). Other, less common causes of hypothermia include head injury or stroke, causing dysfunction of the hypothalamus; decreased thyroid activity; and overwhelming infection, such as sepsis.

Because hypothermia reduces O₂ consumption and CO₂ production, patients with hypothermia may exhibit slow, shallow breathing and reduced pulse rate. Mechanical ventilators in the control mode may need appropriate adjustments in the depth and rate of delivered tidal volumes as the body temperature of the patient varies above and below normal.

Body temperature is measured most often at one of the following four sites: mouth, axilla, ear (tympanic membrane), or rectum. The oral site is the most acceptable for an alert, adult patient, but it cannot be used with infants, comatose patients, or orally intubated patients. If a patient ingests hot or cold liquid or has been smoking, oral temperature measurement should be delayed for 10 to 15 minutes for accuracy. The axillary site is acceptable for infants or small children who do not tolerate rectal thermometers, but this site may underestimate core temperature by 33.8° F to 35.6° F (1° C to 2° C). The body temperature can also be assessed accurately with the use of a hand-held device to measure the temperature of the eardrum (tympanic membrane). Rectal temperatures are closest to actual core body temperature.

Pulse Rate

The peripheral pulse is evaluated for rate, rhythm, and strength (Box 15-6). The normal adult pulse rate is 60 to 100 beats/min, with a regular rhythm. A condition in which the pulse rate exceeds 100 beats/min is called tachycardia. Common causes of tachycardia are exercise, fear, anxiety, low blood pressure, anemia, fever, reduced arterial blood O₂ levels, and certain medications. A condition in which the pulse rate is less than 60 beats/min is called bradycardia. Bradycardia is less common than tachycardia but can occur with hypothermia, as a side effect of medications, with certain cardiac arrhythmias, and with traumatic brain injury.

The amount of O₂ delivered to the tissues depends on the ability of the heart to pump oxygenated blood. The amount of blood circulated per minute (cardiac output) is a function of heart rate and stroke volume. Pulmonary disease almost always causes a decrease in arterial O₂ content and an increase in O₂ consumption. In this situation, the heart tries to maintain adequate O₂ delivery to the tissues by increasing cardiac output. Cardiac output is increased primarily by increasing the heart rate.

The radial artery is the most common site used to palpate the pulse. The second and third fingertip pads (but not the thumb) are used to palpate the radial pulse. Ideally, the pulse rate is counted for 1 minute, especially if the pulse is irregular. Essential pulse characteristics that should be noted and documented are described in Box 15-6.

Spontaneous ventilation can influence pulse strength, or amplitude. Normally, a slight decrease in pulse pressure is present with each inspiratory effort. This decrease is caused by negative intrathoracic pressure from respiratory muscle contraction during inspiration. The decrease in blood pressure is the result of decreased left ventricular filling from two mechanisms. First, negative intrathoracic pressure pools blood in the pulmonary circulation, which impedes left heart filling. Second, it simultaneously increases venous return (which increases right ventricular volume and pressure) and limits expansion of the left heart during diastole. This mechanism briefly reduces left ventricular stroke volume and decreases systolic blood pressure during inspiration. The slight decrease in pulse pressure (normally <10 mm Hg) with inspiration may not be noticeable with palpation. A significant decrease in pulse strength (>10 mm Hg) during spontaneous inhalation is called pulsus paradoxus, or paradoxical pulse. Pulsus paradoxus can be quantified with a blood pressure cuff (see later section) and is common in patients with acute obstructive pulmonary disease, especially patients experiencing an asthma attack. During respiratory distress, vigorous inspiratory efforts decrease stroke volume by impeding the strength of left ventricular contraction.⁵ Pulsus paradoxus also may signal a mechanical restriction of the pumping action of the heart, as can occur with constrictive pericarditis or cardiac tamponade.

Pulsus alternans is an alternating succession of strong and weak pulses. Pulsus alternans suggests left-sided heart failure and usually is not related to respiratory disease. The pulse also may be assessed by palpating the carotid, brachial, femoral, temporal, popliteal, posterior tibial, and dorsalis pedis pulses. The more centrally located pulses (e.g., the carotid and femoral) should be used when the blood pressure is abnormally low. If the carotid site is used, great care must be taken to avoid the carotid sinus area. Pressure on the carotid sinus area may cause strong parasympathetic stimulation resulting in bradycardia.

Respiratory Rate

The normal resting adult rate of breathing is 12 to 18 breaths/min. Tachypnea is defined as a respiratory rate greater than 20 breaths/min. Rapid respiratory rates are associated with exertion, fever, arterial hypoxemia, metabolic acidosis, anxiety, pulmonary edema, lung fibrosis, and pain. A respiratory rate less than 10 breaths/min is called bradypnea. Although uncommon, bradypnea may occur with traumatic brain injury or hypothermia, as a side effect of certain medications such as narcotics, with severe myocardial infarction, and in cases of drug overdose. In addition to respiratory rate, the pattern of breathing (see later section) is assessed.

The respiratory rate is counted by watching the abdomen or chest wall move in and out. With practice, even subtle breathing movements of a healthy individual at rest can be identified easily. In some cases, the RT may need to place a hand on the patient’s abdomen to confirm the breathing rate. Ideally, the patient should be unaware that the respiratory rate is being counted. One successful method for accomplishing this is for the RT to count the respiratory rate immediately after evaluating the patient’s pulse, while keeping the fingers on the patient’s wrist, giving the impression that the pulse rate is being counted.

Blood Pressure

The arterial blood pressure is the force exerted against the wall of the arteries as the blood moves through them. Arterial systolic pressure is the peak force exerted in the major arteries during contraction of the left ventricle. Arterial blood pressure typically increases with age. Generally, the normal range for systolic blood pressure in an adult is 90 to 140 mm Hg. Diastolic pressure is the force in the major arteries remaining after relaxation of the ventricles; it is normally 60 to 90 mm Hg. Pulse pressure is the difference between the systolic and diastolic pressures. A normal pulse pressure is 30 to 40 mm Hg. When the pulse pressure is less than 30 mm Hg, the peripheral pulse is difficult to detect.

Blood pressure is determined by the interaction of the force of left ventricular contraction, the systemic vascular resistance, and the blood volume (see Chapter 9). The blood pressure is recorded by listing systolic pressure over diastolic pressure (e.g., 120/80 mm Hg).

Hypertension is defined as arterial blood pressure persistently greater than 140/90 mm Hg. Hypertension is a common medical problem in adults, and in approximately 90% of cases the cause is unknown (primary hypertension). There are two subcategories of hypertension.⁶ Stage I hypertension occurs when the systolic blood pressure is 140 to 159 mm Hg or the diastolic blood pressure is 90 to 99 mm Hg. Stage II hypertension occurs when the systolic blood pressure is 160 mm Hg or greater or the diastolic blood pressure is 100 mm Hg or greater. In addition, there is a third category known as prehypertension, which is a systolic blood pressure between 120 mm Hg and 139 mm Hg or a diastolic blood pressure between 80 mm Hg and 89 mm Hg. This last category is not a disease state and does not require treatment but rather is used to assess the risk of eventually developing hypertension.

Mechanically, hypertension results from increased systemic vascular resistance or an increased force of ventricular contraction. Sustained hypertension can cause central nervous system abnormalities, such as headaches, blurred vision, and confusion. Other potential consequences of hypertension include uremia (renal insufficiency), CHF, and cerebral hemorrhage, leading to stroke. Acute, severe elevation of blood pressure can cause acute neurologic, cardiac, and renal failure and is called acute hypertensive crisis.

Hypotension is defined as a systolic arterial blood pressure less than 90 mm Hg or a mean arterial pressure less than 65 mm Hg.⁷ Hypotension also can be defined as a decrease of more than 40 mm Hg from baseline. This expanded definition acknowledges that patients with baseline hypertension may have inadequate tissue perfusion at a blood pressure that may be considered normal for most patients.

Shock is defined precisely as the inadequate delivery of O₂ and nutrients to the vital organs relative to their metabolic demand.⁷ Hypotension is not synonymous with shock. In shock, vital body organs are in imminent danger of receiving inadequate blood flow (underperfusion) and impaired O₂ delivery to the tissues (i.e., tissue hypoxia). For this reason, shock is usually treated aggressively with fluids, blood products, or vasoactive drugs, or a combination of these, depending on the cause and severity of shock.

There are two broad categories of hypotension and shock based on whether they are caused by a hypodynamic or hyperdynamic cardiovascular state.⁸ Hypodynamic states includes left ventricular failure (cardiogenic) and reduced blood volume (hypovolemia or hypovolemic) caused by either hemorrhage or severe fluid loss. Hyperdynamic states occur with profound systemic vasodilation (peripheral vascular failure) associated with overwhelming infection (septic shock), systemic allergic reaction (anaphylaxis), or severe liver failure.

When healthy individuals sit or stand up, there is little change in blood pressure. However, similar postural changes may produce an abrupt decrease in the blood pressure in hypovolemic patients. This condition is called postural hypotension and can be confirmed by measuring the blood pressure in both the supine and the sitting positions or on standing up. Postural hypotension is commonly caused by hypovolemia. A rapid decrease in arterial blood pressure caused by postural hypotension can reduce cerebral blood flow and lead to syncope (fainting). Postural hypotension generally is treated by administration of fluid.

A common technique for measuring arterial blood pressure requires a blood pressure cuff (sphygmomanometer) and a stethoscope (Figure 15-2). When the cuff is applied to the upper arm and pressurized to exceed systolic blood pressure, the brachial artery blood flow stops. As the cuff pressure is slowly released to a point just below the systolic pressure, blood flows intermittently past the obstruction. Partial obstruction of the blood flow creates turbulence and vibrations called Korotkoff sounds. Korotkoff sounds are heard with a stethoscope over the brachial artery distal to the cuff.

To measure the blood pressure, a deflated cuff is wrapped snugly around the patient’s upper arm, with the lower edge of the cuff 1 inch above the antecubital fossa. While palpating the brachial pulse, the clinician inflates the cuff to approximately 30 mm Hg above the point at which the pulse can no longer be felt. The clinician places the diaphragm of the stethoscope over the artery and deflates the cuff at a rate of 2 to 3 mm Hg/sec while observing the manometer.

The systolic pressure is recorded at the point at which the first Korotkoff sounds are heard. The point at which the sounds become muffled is the diastolic pressure. This muffling is the final change in the Korotkoff sounds just before they disappear. At this point, cuff pressure equals diastolic pressure, and turbulence ceases. When muffling begins and the sounds disappear at a wide interval, all three pressures are recorded (e.g., 120/80/60 mm Hg). The clinician must perform the procedure rapidly because the pressurized cuff impairs circulation to the forearm and hand.

The systolic blood pressure usually decreases slightly with normal inhalation. However, a decrease in systolic pressure of more than 6 to 8 mm Hg during a resting inhalation is abnormal and is called paradoxical pulse, or pulsus paradoxus (see Chapter 9). Although simple palpation may be adequate to signal the presence of paradoxical pulse, it can be quantified only by auscultatory measurement. To obtain this measurement, the clinician inflates the cuff until the radial or brachial pulse can no longer be palpated. The clinician slowly deflates the cuff until sounds are heard on exhalation only (point 1). Next, the clinician reduces the cuff pressure until sounds are heard throughout respiration (point 2). The difference between points 1 and 2 indicates the degree of paradoxical pulse.

Most hospitals and clinics have adopted use of the digital blood pressure measuring devices. These devices do not require the health care provider to listen for the Korotkoff sounds and eliminate variances in recorded blood pressures based on human perception. They are considered to be very accurate and simply require the clinician to apply the blood pressure cuff correctly and press the start button. Subsequently, the device takes over and inflates and deflates the cuff automatically. The blood pressure and pulse rate are displayed on a digital screen.

Neck

Inspection and palpation of the neck help determine the position of the trachea and the jugular venous pressure (JVP). Normally, when the patient faces forward, the trachea is located in the middle of the neck. The midline of the neck can be identified by palpating the suprasternal notch. The midline of the trachea should be directly below the center of the suprasternal notch.

The trachea can shift away from the midline in certain thoracic disorders. Generally, the trachea shifts toward an area of collapsed lung. Conversely, the trachea shifts away from areas with increased air or fluid (e.g., tension pneumothorax or large pleural effusion). Abnormalities in the lung bases generally do not shift the trachea.

JVP is estimated by determining how high the jugular vein extends above the level of the sternal angle. JVP reflects the volume and pressure of venous blood in the right side of the heart. Typically, the internal vein is assessed because it is more reliable. Individuals with obese necks may not have visible neck veins, even when the veins are distended.

When lying in a supine position, a healthy individual has neck veins that are full. When the head of the bed is elevated gradually to a 45-degree angle, the level of the blood column descends to a point no more than a few centimeters above the clavicle. With elevated venous pressure, the neck veins may be distended as high as the angle of the jaw, even when the patient is sitting upright.

JVP may vary with breathing. Under normal circumstances, the blood column descends toward the thorax during inhalation and ascends with exhalation. For this reason, JVP should always be estimated at the end of exhalation. Under abnormal conditions (e.g., cardiac tamponade), the JVP may increase during inhalation. This is called Kussmaul sign and is rare.

Jugular venous distention (JVD) is present when the jugular vein is enlarged and it can be seen more than 3 to 4 cm above the sternal angle. The most common cause of JVD is right heart failure (cor pulmonale). Right heart failure frequently occurs in patients with advanced COPD because of chronic hypoxemia. Hypoxemia causes chronic pulmonary vasoconstriction and hypertension, which leads to right heart failure from the excessive workload. Other conditions associated with JVD include left heart failure, cardiac tamponade, tension pneumothoraces, and mediastinal tumors.

The neck is a common place for the physician to palpate for enlarged lymph nodes, which is known as lymphadenopathy. Lymphadenopathy occurs with various medical disorders, including infection, malignancy, and sarcoidosis. Tender lymph nodes in the neck suggest a nearby infection. The lymph nodes are not tender when malignancy is the cause.

Thoracic Configuration

The anteroposterior (AP) diameter of the average adult thorax is less than the transverse diameter. Normally, the AP diameter increases gradually with age but may prematurely increase in patients with COPD. This abnormal increase in AP diameter is called barrel chest and is associated with emphysema. When the AP diameter increases, the normal 45-degree angle of articulation between the ribs and spine is increased, becoming more horizontal (Figure 15-3). Other abnormalities of the thoracic configuration are listed in Table 15-1.

Breathing Pattern and Effort

At rest, a healthy adult has a consistent rate and rhythm of breathing. Breathing effort is minimal on inhalation and passive on exhalation. Abnormal breathing patterns can be broken down into two broad categories. First are breathing patterns directly associated with thoracic or pulmonary diseases that increase work of breathing. Second are patterns primarily associated with neurologic disease (see Chapter 14). Table 15-2 describes common abnormal patterns of breathing.

Cardiopulmonary or thoracic diseases that increase work of breathing typically cause recruitment of the accessory muscles of ventilation. Common causes of an increase in the work of breathing include narrowed airways (e.g., COPD, asthma), “stiff lungs” (e.g., severe pneumonia, pulmonary edema), or a stiff chest wall (e.g., ascites, anasarca, pleural effusions). Increased work of breathing also can result in retractions. Retractions are an intermittent sinking inward of the skin overlying the chest wall during inspiration. They occur when the ventilatory muscles contract forcefully enough to cause a large decrease in the intrathoracic pressure. Retractions may be seen between the ribs, above the clavicles, or below the rib cage. These are called intercostal, supraclavicular, or subcostal retractions. Retractions are difficult to see in obese patients.

Another form of retraction is tracheal tugging, which is caused by extreme negative pressure that pulls the trachea downward during inspiration. This phenomenon is noted by observing the downward movement of the thyroid cartilage toward the chest during inspiration. Typically, this movement occurs in concert with recruitment of the accessory muscles of inspiration, primarily the sternocleidomastoid muscles of the neck.

Generally, two archetypal abnormal breathing patterns exist that provide clues about the underlying pulmonary problem. These patterns fall into two categories: (1) patterns characterized by rapid, shallow breathing and (2) patterns marked by a relatively brief inspiratory phase coupled with an abnormally prolonged exhalation. Rapid, shallow breathing typically occurs in patients with increased lung stiffness, such as patients with pulmonary edema or severe pneumonia. Obstruction of the intrathoracic airways slows lung emptying and results in a prolonged expiratory phase as patients attempt to minimize gas trapping inside the lungs. This prolonged expiratory phase alters the normal ratio of inspiratory to expiratory time from 1 : 2 to 1 : 4 or greater; this always occurs with activation of the expiratory muscles. Obstruction of the extrathoracic upper airway (as with epiglottitis or croup) usually results in a prolonged inspiratory time because airways outside the thorax tend to narrow more on inhalation. Patients with diabetic ketoacidosis often breathe with a deep and rapid pattern that is called Kussmaul breathing.

The diaphragm may be nonfunctional in patients with spinal injuries or neuromuscular disease and may be severely limited in patients with COPD. When the diaphragm is nonfunctional or limited, the accessory muscles of ventilation become active to maintain adequate gas exchange. Heavy use of accessory muscles is reliable evidence of significant cardiopulmonary disease.

In patients with emphysema, the lungs lose their elastic recoil and become hyperinflated. Over time, the hyperinflation forces the diaphragm into a low, flat position. Contraction of a flat diaphragm tends to draw in the lateral costal margins instead of expanding them (Hoover sign) and does little to help move air into the thorax. Ventilation eventually must be achieved by other means and involves heavy use of the accessory muscles. The accessory muscles must assist ventilation by raising the anterior chest in an effort to increase thoracic volume. The severity of lung disease in this situation is often reflected by the magnitude of accessory muscle activity.

Diaphragmatic fatigue is found in many types of chronic and acute pulmonary diseases. When it occurs acutely, diaphragmatic fatigue often manifests with distinctive breathing patterns.⁹ The first sign of acute diaphragmatic fatigue is tachypnea. Sometimes tachypnea is followed by a breathing pattern in which the diaphragm and rib cage muscles alternately power breathing in an attempt to give each muscle group some rest (respiratory alternans). This pattern is noted by the upward motion of the diaphragm during inspiration on a series of breaths, followed by diaphragmatic contractions and inward movement of the abdominal wall on the following series of breaths. When the diaphragm is relaxed, contraction of the rib cage muscles sucks the diaphragm upward and the abdomen inward during inspiration. The opposite phenomenon occurs on breaths when the diaphragm is active. When the rib cage muscles are relaxed, the chest wall may appear to sink in as the abdomen protrudes during diaphragmatic contraction; this often gives the impression that the chest has a rocking motion. Finally, abdominal paradox occurs with complete diaphragmatic fatigue, as the diaphragm is drawn upward into the thoracic cavity with each inspiratory effort of the rib cage muscles. An abdominal paradox also occurs when the diaphragm is paralyzed.

These patterns are not always associated with impending muscle fatigue. Rather, they may be adaptations to high workloads when the respiratory muscle strength is normal.¹⁰ Also, patients with respiratory distress often have tachypnea, along with recruitment of the expiratory muscles. This situation can make it difficult to discern accurately the presence and type of abnormal breathing pattern. The RT must be careful about offering definitive therapeutic suggestions (e.g., absolute need for mechanical ventilation) when he or she perceives the presence of these abnormal breathing patterns.

Palpation

Palpation is the art of touching the chest wall to evaluate underlying structure and function. It is used in selected patients to confirm or rule out suspected problems suggested by the history and initial examination findings. Palpation is performed to evaluate vocal fremitus, estimate thoracic expansion, and assess the skin and subcutaneous tissues of the chest.

Thoracic Expansion

The normal chest wall expands symmetrically during deep inhalation. This expansion can be evaluated on the anterior and posterior chest. To evaluate expansion anteriorly, the RT places his or her hands over the anterolateral chest, with the thumbs extended along the costal margin toward the xiphoid process. To evaluate posteriorly, the RT positions the hands over the posterolateral chest with the thumbs meeting at the T8 vertebra (Figure 15-4). The patient is instructed to exhale slowly and completely. When the patient has exhaled maximally, the RT gently secures his or her fingertips against the sides of the patient’s chest and extends the thumbs toward the midline until the tip of each thumb meets at the midline. The RT next instructs the patient to take a full, deep breath and notes the distance the tip of each of the thumbs moves from midline. Normally, each thumb moves an equal distance of approximately 3 to 5 cm.

Diseases that affect the expansion of both lungs cause a bilateral reduction in chest expansion. Reduced expansion commonly is seen in neuromuscular disorders and COPD. Unilateral reduction in chest expansion occurs with respiratory diseases that reduce the expansion of one lung or a major part of one lung. This condition can occur with lobar consolidation, atelectasis, pleural effusion, or pneumothorax.

Percussion of the Chest

Percussion is the art of tapping on a surface to evaluate the underlying structure. Percussion of the chest wall produces a sound and a palpable vibration useful in evaluating underlying lung tissue. The vibration created by percussion penetrates the lung to a depth of 5 to 7 cm below the chest wall. This assessment technique is not performed routinely on all patients but is reserved for patients with suspected conditions for which percussion could be helpful (e.g., pneumothorax).

The technique most often used in percussing the chest wall is called mediate, or indirect, percussion. A right-handed RT places the middle finger of the left hand firmly against the patient’s chest wall, parallel to the ribs, with the palm and other fingers held off the chest. The RT uses the tip of the middle finger of the right hand or the lateral aspect of the right thumb to strike the finger against the chest near the base of the terminal phalanx with a quick, sharp blow. Movement of the hand striking the chest is generated at the wrist, not at the elbow or shoulder.

The percussion note is clearest if the RT remembers to keep the finger on the patient’s chest firmly against the chest wall and to strike this finger and then immediately withdraw. The two fingers should be in contact for only an instant. As one gains experience in percussion, the feel of the vibration becomes as important as the sound in evaluating lung structures.

Auscultation of the Lungs

Auscultation is the process of listening for bodily sounds. Auscultation over the thorax is performed to identify normal and abnormal lung sounds and to evaluate the effects of therapy. Because auscultation can be performed quickly and is noninvasive, it is a particularly useful tool in many clinical situations. Auscultation is performed with a stethoscope to enhance sound transmission from the patient’s lungs to the examiner’s ears. The clinician always must ensure that the room is as quiet as possible whenever performing auscultation.

Stethoscope

A stethoscope has the following four basic parts: (1) a bell, (2) a diaphragm, (3) tubing, and (4) earpieces (Figure 15-5). The bell detects a broad spectrum of sounds and is very useful for listening to low-pitched sounds (e.g., heart sounds). Proper technique for listening to heart sounds is to place the bell lightly against the chest; this avoids stretching the skin, which makes auscultating heart sounds more difficult by inadvertently filtering out low-frequency sounds. Using the bell to auscultate the lungs is also helpful when emaciation causes rib protrusion that restricts placement of the diaphragm flat against the chest.

The diaphragm is preferred for auscultation of the lungs because most lung sounds are high frequency. The ideal tubing should be thick enough to exclude external noises and approximately 25 to 35 cm (11 to 16 inches) in length. Longer tubing may impair sound transmission.

The clinician should examine his or her stethoscope regularly for cracks in the diaphragm, wax or dirt in the earpieces, and other defects that may interfere with the transmission of sound. The stethoscope should always be cleaned with hospital-approved disinfectant after every patient contact to minimize contamination with microorganisms.11,12 Patients who are placed in contact isolation and patients who are in protective isolation because of immunosuppression should have a dedicated stethoscope in the room to prevent cross infection.

Technique

When possible, the patient should be sitting upright in a relaxed position. The patient should be instructed to breathe a little more deeply than normal through an open mouth. Exhalation should be passive. The bell or diaphragm is placed directly against the chest wall when possible because clothing may produce distortion. The tubing must not be allowed to rub against any objects because this may produce extraneous sounds, which could be mistaken for adventitious lung sounds (discussed later).

Auscultation of the lungs should be systematic and include all lobes on the anterior, lateral, and posterior chest. Auscultation should begin at the lung bases with comparison of breath sounds side to side, working upward toward the lung apexes (Figure 15-6). It is important to begin at the bases because certain abnormal sounds that occur only in the lower lobes may be altered by several deep breaths. At least one full ventilatory cycle should be evaluated at each stethoscope position. If abnormal sounds are present, the clinician should listen to several breaths to clarify the characteristics.

The clinician should listen for and distinguish among the key features of breath sounds. The clinician should identify the pitch (vibration frequency), the intensity (loudness), and the duration of the inspiratory and expiration components of the sound. The acoustic characteristics of breath sounds can be illustrated in breath sound diagrams (Figure 15-7). The features of normal breath sounds are described in Table 15-3. One must be familiar with normal breath sounds before one can expect to identify the subtle changes that may signify respiratory disease.

TABLE 15-3

Characteristics of Normal Breath Sounds

Breath Sound	Pitch	Intensity	Location	Diagram
Vesicular	Low	Soft	Peripheral lung areas
Bronchovesicular	Moderate	Moderate	Around upper part of sternum, between the scapulae
Tracheal	High	Loud	Over the trachea

Mechanisms and Significance of Lung Sounds

The exact mechanisms that produce normal and abnormal lung sounds are not fully known. However, there is sufficient agreement among investigators to allow a general description.

Normal Breath Sounds

Lung sounds heard over the chest of a healthy individual are generated primarily by turbulent airflow in the larger airways. Turbulent airflow creates audible vibrations in the airways, producing sounds that are transmitted through the lungs and chest wall. As this sound travels to the lung periphery and the chest wall, it is altered by the filtering properties of normal lung tissue. Normal lung tissue acts as a low-pass filter, which means it preferentially passes low-frequency sounds. If you place the diaphragm portion of your stethoscope over the chest wall of a friend and listen while he or she speaks, this filtering (attenuation) effect will be evident. The voice sounds are muffled and difficult to understand because of attenuation. This filtering effect explains the characteristic differences between tracheal breath sounds, heard directly over the trachea, and vesicular sounds, heard over the lung periphery. Normal vesicular lung sounds essentially are attenuated tracheal breath sounds.

Bronchial Breath Sounds

Bronchial breath sounds are considered abnormal when they are heard over peripheral lung regions. Normal vesicular sounds are replaced with bronchial sounds when lung tissue density increases, and the attenuation is reduced. When normal air-filled lung tissue becomes atelectatic or consolidated (e.g., pneumonia), the resulting breath sounds are similar to the sounds normally heard over large upper airways.

Diminished Breath Sounds

Diminished breath sounds occur when the sound intensity at the site of generation (larger airways) is reduced, or when the sound transmission through the lung or chest wall is decreased. Sound intensity is reduced with shallow or slow breathing patterns that cause less turbulence in the larger airways, resulting in diminished breath sounds over the entire chest. Sound transmission through the chest wall also is diminished by airways plugged with mucus, hyperinflated lung tissue (e.g., COPD, asthma), air or fluid in the pleural space (e.g., pneumothorax, hemothorax, pleural effusion), and obesity.

Wheezes and Stridor

Wheezes and stridor represent vibrations of airway wall that are caused when air flows at high velocity through a narrowed airway. Airway diameter can be reduced by bronchospasm, mucosal edema, inflammation, tumors, foreign bodies, and pulmonary edema. This narrowing initially causes an increase in the velocity of airflow, which causes the lateral wall pressure to decrease. This decrease in pressure causes the lateral walls of the narrowed airway to pull closer together, and airflow stops. When airflow stops, the lateral wall pressure increases, and the airway opens back to the previous position. This cycle repeats many times per second and causes the airway walls to vibrate and make a musical type of adventitious lung sound similar to a reed instrument.

 Rule of Thumb

Generally, expiratory wheezes indicate obstruction of intrathoracic airways such as occurs with lung diseases (e.g., bronchitis, asthma). Wheezes in such cases are polyphonic. A monophonic wheeze suggests one airway is narrowed and the cause is not likely to be asthma.

It is useful to monitor the pitch and duration of wheezing. Improved expiratory flow is associated with a decrease in the pitch and length of the wheezing. If high-pitched wheezing is present during the entire expiratory time before treatment but becomes lower pitched and occurs only late in exhalation after therapy, the pitch and duration of the wheeze have diminished. This change suggests that the degree of airway obstruction has decreased.

Wheezing may be monophonic (single note) or polyphonic (multiple notes). A monophonic wheeze indicates that a single airway is partially obstructed. Monophonic wheezing may be heard during inhalation and exhalation or during exhalation only. Polyphonic wheezing suggests that many airways are obstructed, such as with asthma, and is heard only during exhalation. Bronchitis and CHF with pulmonary edema can also cause polyphonic wheezing.

Stridor is a serious adventitious lung sound that indicates that the upper airway is compromised. It may occur in patients of any age but most often is heard from the neck of children. In children, laryngomalacia is the most common cause of chronic stridor, whereas croup is the most common cause of acute stridor. Generally, inspiratory stridor is consistent with narrowing above the glottis, whereas expiratory stridor indicates narrowing of the lower trachea.

Crackles

Crackles occur when airflow moves secretions or fluid in the airways. In this situation, coarse crackles are usually heard during inspiration and expiration. These crackles often clear when the patient coughs or when the upper airway is suctioned. Crackles also may be heard in patients without excess secretions. These crackles occur when collapsed airways pop open during inspiration. Airway collapse or closure can occur in peripheral bronchioles or in larger, more proximal bronchi.

Larger, more proximal bronchi may close during expiration when there is an abnormal increase in bronchial compliance or when the retractile pressures around the bronchi are low. In this situation, crackles usually occur early in the inspiratory phase and are referred to as early inspiratory crackles (Figure 15-8). Early inspiratory crackles are usually scant but may be loud or faint. They often are transmitted to the mouth and are not silenced by a cough or a change in position. They frequently occur in patients with COPD (chronic bronchitis, emphysema, or asthma) and usually indicate severe airway obstruction.

Peripheral airways may close during exhalation when the surrounding intrathoracic pressure increases and when surfactant levels are diminished. Fine, late inspiratory crackles are produced by the sudden opening of peripheral airways, usually late in the inspiratory phase. They are more common in the dependent lung regions, where the peripheral airways are most prone to collapse during exhalation. They may clear with changes in posture or if the patient performs several deep inspirations. Late inspiratory crackles are most common in patients with respiratory disorders that reduce gas volume of the lung, such as atelectasis, pneumonia, pulmonary edema, and pulmonary fibrosis (Table 15-4).

TABLE 15-4

Application of Adventitious Lung Sounds

Lung Sound	Possible Mechanism	Characteristics	Causes
Wheezes	Rapid airflow through obstructed airways	High-pitched, usually expiratory	Asthma, CHF
Stridor	Rapid airflow through obstructed upper airway	High-pitched, monophonic	Croup, epiglottitis, postextubation laryngeal edema
Coarse crackles	Excess airway secretions moving through airways	Coarse, inspiratory and expiratory	Severe pneumonia, bronchitis
Fine crackles	Sudden opening of peripheral airways	Fine, late inspiratory	Atelectasis, fibrosis, pulmonary edema

 Rule of Thumb

Fine, late inspiratory crackles suggest restrictive lung diseases such as pulmonary fibrosis.

Pleural Friction Rub

A pleural friction rub is a creaking or grating sound that occurs when the pleural surfaces become inflamed, and the roughened edges rub together during breathing, as in pleurisy. It may be heard only during inhalation but often is identified during both phases of breathing. The rub usually is localized to a certain site on the chest wall. It sounds similar to coarse crackles but is not affected by coughing. The intensity of pleural rubs may increase with deep breathing.

Voice Sounds

If chest inspection, palpation, percussion, or auscultation suggests a lung abnormality, evaluation of vocal resonance may be useful in further assessment. Vocal resonance is produced by the same mechanism as vocal fremitus. Vibrations created by the vocal cords during speech travel down the airways and through the peripheral lung units to the chest wall. The patient is instructed to repeat the words “one,” “two,” “three,” or “ninety-nine” while the clinician listens over the chest wall with a stethoscope, comparing one side with the other side. Normal, air-filled lung tissue filters the voice sounds, producing a significant reduction in intensity and clarity. Pathologic abnormalities in lung tissue alter the transmission of voice sounds, causing either increased or decreased vocal resonance. Increased vocal resonance occurs with lung consolidation, whereas decreased vocal resonance occurs with hyperinflated lung or with pneumothorax.

Inspection and Palpation

Inspection and palpation of the precordium help identify normal or abnormal pulsations. Pulsations on the precordium are created by ventricular contraction. Detection of pulsations depends on the force of ventricular contraction, the thickness of the chest wall, and the quality of the tissue through which the vibrations travel.

Normally, left ventricular contraction is the most forceful and generates a visible, palpable pulsation during systole. This pulsation is called the point of maximal impulse (PMI). In healthy individuals who are not obese (or overly muscular), the PMI can be felt and visualized near the left midclavicular line in the fifth intercostal space. The PMI shifts laterally with left ventricular hypertrophy.

Right ventricular hypertrophy (a common finding in COPD) often produces a systolic thrust called a heave that is felt (and possibly visualized) near the lower left sternal border. To identify the PMI, the clinician places the palmar aspect of the right hand over the lower left sternal border. Right ventricular hypertrophy may be the result of chronic hypoxemia, pulmonary valve disease, or primary pulmonary hypertension.

In patients with chronic pulmonary hyperinflation (emphysema), the PMI may be difficult to locate. Because of the increase in AP diameter and the changes in lung tissue, systolic vibrations are not well transmitted to the chest wall.

The PMI may shift either left or right, following deviations in the position of the lower mediastinum, which may be caused by pneumothorax or lobar collapse. Typically, the PMI shifts toward lobar collapse but away from a tension pneumothorax. The PMI in patients with emphysema and low flat diaphragms may be shifted centrally to the epigastric area.

The second left intercostal space near the sternal border is referred to as the pulmonic area and is palpated to identify accentuated pulmonary valve closure. Strong vibrations may be felt in this area with the presence of pulmonary hypertension or valvular abnormalities (Figure 15-9). Rapid blood flow through a narrowed valve or backflow through an incompetent valve may produce palpable vibrations known as thrills. Thrills are usually accompanied by a murmur (see discussion later).

Auscultation of Heart Sounds

Normal heart sounds are created by closure of the heart valves (see Chapter 9). The first heart sound (S₁) is produced by closure of the mitral and tricuspid (atrioventricular [AV]) valves during contraction of the ventricles. When systole ends, the ventricles relax, and the pulmonic and aortic (semilunar) valves close, creating the second heart sound (S₂). Because pressures in the left side of the heart are higher, mitral valve closure is louder and contributes more to S₁. For the same reason, closure of the aortic valve usually is more significant in producing S₂. If either the AV valves or the semilunar valves do not close together, a split heart sound is heard. A slight splitting of S₂ is normal; it occurs because of increased venous return during spontaneous breathing.

A third heart sound (S₃) can be heard during diastole and is produced by rapid ventricular filling immediately after systole. S₃ is a low-intensity, low-pitched sound best heard over the apex of the heart. In young, healthy children, S₃ is considered normal and is called physiologic S₃. Otherwise, S₃ is abnormal. In older patients with heart disease, S₃ may signify CHF.

A fourth heart sound (S₄) is produced by mechanisms similar to the mechanisms that produce S₃. S₄ may occur in healthy individuals or may be considered a sign of heart disease. S₄ differs from S₃ only in its timing during the cardiac cycle. S₄ occurs later, just before S₁, whereas S₃ occurs just after S₂. A patient with heart disease who has S₃ and S₄ is said to have a gallop rhythm.

Abnormal Heart Sounds

Reduced intensity of heart sounds may result from cardiac or extracardiac abnormalities. Extracardiac factors include alteration in the tissue between the heart and the surface of the chest. Pulmonary hyperinflation, pleural effusion, pneumothorax, and obesity make identification of both S₁ and S₂ difficult. The intensity of S₁ and S₂ also decreases when the force of ventricular contraction is poor, as in heart failure, or when valvular abnormalities exist.

Pulmonary hypertension may cause two abnormalities in heart sounds. First, it increases the intensity of S₂ from a more forceful closure of the pulmonic valve (this is also referred to as a loud P₂). Second, S₂ splitting may be absent. An increased P₂ is identified best over the pulmonic area of the chest (see Figure 15-9).

Cardiac murmurs occur whenever the heart valves are incompetent or stenotic. Murmurs are classified as either systolic or diastolic. Systolic murmurs are produced by an incompetent AV valve or a stenotic semilunar valve. An incompetent AV valve typically produces a high-pitched “whooshing” noise simultaneously with S₁. This noise is caused by a backflow of blood through the AV valve into the atrium. In contrast, a stenotic semilunar valve produces a crescendo-decrescendo sound created by an obstruction of blood flow out of the ventricle during systole.

Diastolic murmurs are created by either an incompetent semilunar valve or a stenotic AV valve. An incompetent semilunar valve allows a backflow of blood into the ventricle simultaneously with, or immediately after, S₂. A stenotic AV valve obstructs blood flow from the atrium into the ventricles during diastole and creates a turbulent murmur.

A murmur also may be created by rapid blood flow across normal valves, such as occurs with heavy exertion. Murmurs are created by the following: (1) a backflow of blood through an incompetent valve, (2) a forward flow of blood through a stenotic valve, and (3) a rapid flow of blood through a normal valve.

Heart sounds can be auscultated by using the bell or diaphragm pieces of the stethoscope. The heart sounds may be easier to identify when the patient leans forward or lies on the left side. This positioning moves the heart closer to the chest wall. When peripheral pulses are difficult to identify, auscultation over the precordium may provide important additional information. Normally, the rate heard over the precordium (the apical rate) should be the same as the palpated peripheral pulse. In patients with atrial fibrillation, the apical rate often is higher than the peripheral pulse (pulse deficit). During atrial fibrillation, the irregular rhythm causes frequent weak ventricular contractions that cannot be detected at peripheral locations.

Clubbing

Clubbing of the digits is a significant manifestation of cardiopulmonary disease. Clubbing is a painless enlargement of the terminal phalanges of the fingers and toes that develops over time. As the process advances, the angle of the fingernail to the nail base increases, and the base of the nail feels “spongy.” The profile view of the digits allows easier recognition of clubbing (Figure 15-10), but sponginess of the nail bed is the most important sign. Causes of clubbing include infiltrative or interstitial lung disease, bronchiectasis, various cancers (particularly lung cancer),¹⁴ congenital heart problems that cause cyanosis, chronic liver disease, and inflammatory bowel disease. COPD alone, even when hypoxemia is present, does not lead to clubbing. Clubbing of the digits in a patient with COPD indicates that something other than obstructive lung disease is occurring.

Cyanosis

Examination of the digits for cyanosis is part of the initial assessment and is done whenever hypoxemia is suspected. Cyanosis can be detected easily because of the transparency of the fingernails and skin.

Cyanosis becomes visible when the amount of unsaturated hemoglobin in the capillary blood exceeds 5 to 6 g/dl; this may be caused by a reduction in arterial or venous O₂ content, or both. Cyanosis of the digits is referred to as peripheral cyanosis or acrocyanosis and may involve extensive portions of limbs. This condition is mainly the result of poor perfusion, especially in the extremities. When capillary blood flow is poor, the tissues extract more O₂, reducing the venous O₂ content and increasing the amount of reduced hemoglobin. The extremities are usually cool to the touch when peripheral cyanosis is a sign of poor perfusion.

Pedal Edema

Pedal edema most often results from heart failure, which causes an increase in the hydrostatic pressure of the venous system and leaking of fluid from the vessels into the surrounding tissues. The ankles are affected most often because they are in a gravity-dependent position throughout most of the day. The edematous tissues “pit,” or indent, when pressed firmly with a finger; this is referred to as pitting edema. The height at which pitting edema occurs can indicate the severity of heart failure. Pitting edema that extends to above the knee signifies a more significant problem than edema limited to around the ankles. Any patient who is suspected to have right-sided or left-sided heart failure is examined for pedal edema.

Capillary Refill

Capillary refill is assessed by pressing briefly and firmly on the patient’s fingernail until the nail bed is blanched. When pressure is released, the speed at which the blood flow and color return is noted. When cardiac output is reduced and the digital perfusion is poor, capillary refill is slow, taking several seconds to complete. In healthy individuals with good cardiac output and digital perfusion, capillary refill time is 2 seconds or less. Capillary refill time should be assessed in the context of whether or not the skin is mottled (i.e., blotched skin shade) and skin temperature.

Peripheral Skin Temperature

When systemic perfusion is poor (as in heart failure or shock), compensatory vasoconstriction in the extremities helps shunt blood to the vital organs. This reduction in peripheral perfusion causes the extremities to become cool to the touch. The extent to which the coolness to touch extends back toward the torso is an indication of the degree of circulatory failure. In contrast, patients with high cardiac output and peripheral vascular failure (as occurs in septic shock) may have warm, dry skin.