Obtaining a thorough and accurate patient history is truly an art. One important goal of history taking is to establish a good patient-therapist rapport. The patient must be allowed to explain the history in his or her own words and at a comfortable pace.1 If the therapist appears hurried, distracted, preoccupied, irritated, or uncaring; is often interrupted; or fails to be an attentive listener, the patient-therapist relationship will likely suffer. The interviewer must be careful not to allow personal feelings about the patient’s grooming, appearance, demeanor, or behavior during the interview to unduly question the validity of the chief complaints.2 By the time the patient is referred for physical therapy, he or she may have seen one or more physicians, have been subjected to a number of noninvasive or invasive studies, or have been prescribed oral or inhaled medications with variable or unsatisfactory alleviation of symptoms. The patient is likely to manifest a degree of anxiety and frustration. Therefore, the therapist’s approach, history-taking method, and interviewing style are important for gaining the patient’s confidence and cooperation. The patient history interview can be divided into the data-gathering and interpretative sections.3 The data-gathering segment begins with asking why the patient has sought medical attention and has been referred for physical therapy services. In other words, what is the patient’s chief complaint—the symptom that caused the patient to seek help? The patient should be asked about his or her tobacco-smoking history.3 The number of pack-years of cigarette smoking may be calculated (average number of packs per day multiplied by the number of years smoked) as a relative risk for lung cancer and COPD. Regular smoking of marijuana is more damaging to lung health in the short term as well as potentially long term.4 The family history is useful in evaluating the possibility of hereditary pulmonary diseases, such as alpha1-antitrypsin deficiency, cystic fibrosis, allergic asthma, hereditary hemorrhagic telangiectasia, and others.5,6 A family history of diabetes, hypertension, coronary artery disease (CAD), or rheumatic fever raises the possibility that these conditions might exist in the patient as well.7 Taking an occupational history is particularly important for pulmonary patients who arrive for physical therapy with little or no accompanying medical information. The internal surface of the lung measures 50 to 100 m3 and is in constant contact with the environment.5 Jobs that involve exposure to silica or silicates (e.g., miners, sandblasters, foundry workers, stone cutters, brick layers, and quarry workers) or other inorganic substances place workers at risk for combinations of obstructive and restrictive lung disease (e.g., silicosis). Construction workers, shipyard workers, pipefitters, and other industrial workers exposed to asbestos are at increased risk for developing a restrictive lung disease such as asbestosis.8 Benign pleural plaques may be found on the diaphragmatic pleurae and bilaterally between the 6th and 10th ribs on the anterolateral or posterolateral chest wall. Progressive pleural thickening rarely occurs. These individuals have an increased incidence of malignant neoplastic diseases such as bronchogenic carcinoma and malignant mesothelioma. Some firefighters, iron workers, and other rescuers working at the World Trade Center disaster site following September 11, 2001, have developed respiratory symptoms and disorders.9,10 Coal workers are exposed to coal mine dust. About 10% have simple pneumoconiosis, whereas a smaller proportion develop the complicated form of the condition—progressive massive pulmonary fibrosis.11 A history of paroxysmal coughing, chest tightness, or dyspnea that is worse during the work week but remits on weekends (or other regular days off work) strongly suggests occupational asthma.11 This condition is difficult to diagnose because symptoms commonly occur several hours after exposure to the provoking agent. Causal agents include grain dusts, wood dusts, formalin, enzyme detergents, ethanolamines (in spray paints and soldering flux), nickel, and hard metals (e.g., tungsten carbide). Workers exposed to cotton flax and hemp dusts may develop byssinosis, an obstructive lung disease. In the early stages, this condition is reversible, but long-term exposure over a number of years causes chronic irreversible obstructive lung disease. A history of fever, cough, shortness of breath, and recurrent pneumonias in farmers in the northern United States suggests farmer’s lung.11 This is the most common hypersensitive pneumonitis; it is caused by inhaling fungal agents such as thermophilic actinomycetes. Long-term exposure can lead to pulmonary fibrosis. Numerous occupations expose workers to factors that cause hypersensitive pneumonitis. Questionnaires can be used in a number of ways. Printed symptom or medical questionnaires can be beneficial or detrimental to the patient-therapist relationship, depending on how they are used. Questionnaires can expedite the data-gathering portion of the initial visit by allowing the patient to note in advance all symptoms, medical conditions, surgeries, occupations, medications, and other factors that may influence physical therapy intervention. They can reduce the amount of nontreatment time therapists may otherwise spend inquiring about irrelevant symptoms and conditions. Printed questionnaires also allow patients sufficient time to recall relevant information and respond more accurately than they often do in an interview setting.5 Used in this way, a printed questionnaire can be a valuable tool for expediting a comprehensive evaluation of cardiopulmonary patients. However, if questionnaires are used improperly, they can depersonalize the history-taking portion of the initial visit.1 If the physical therapist allows the printed form to become a substitute for interaction with the patient, patient satisfaction will be low and the patient-therapist relationship will suffer. In addition, questionnaires are being increasingly used as standardized outcome measures to assess activity and participation capacity, as well as quality of life and life satisfaction (see Chapter 17). Many questionnaires have been validated and are reliable when used in the clinical setting. Dyspnea, commonly referred to as breathlessness or shortness of breath, can be defined as the sensation of difficulty in breathing.12 It is one of the most common reasons for patients to seek medical attention. Dyspnea is difficult to quantitate because it is subjective and at times is normal (i.e., at high altitudes and during or following vigorous exercise). Also, patients of different backgrounds use different descriptors for their breathlessness.13 Dyspnea is a symptom of cardiac and pulmonary diseases, among other conditions. When a patient complains of shortness of breath or breathlessness, it should be noted that this complaint is often unrelated to the patient’s arterial oxygen level (PaO2). Many times, it appears that altered mechanical factors during breathing contribute to the sensation of breathlessness.14 Numerous receptors that have a role in sensing dyspnea have been identified; they include vagal receptors (e.g., irritant, stretch, and J-receptors), chemoreceptors, proprioceptive receptors (e.g., tendon organs, muscle spindles, joint and skin receptors), and upper airway receptors.3 Analyzing the oxygen transport system (Figure 8-1) can help the physical therapist to determine the likely cause of each patient’s dyspnea and the most appropriate physical therapy intervention. The delivery of oxygen from ambient air to the mitochondrion within the cell depends on the intact interaction of the respiratory, cardiovascular, and muscular systems. Also, carbon dioxide (CO2) is eliminated in the opposite direction. Dyspnea can be caused by dysfunction in any of the systems. Dyspnea commonly occurs when the body’s requirement for breathing (ventilation) exceeds the body’s capacity to provide it.3 In other words, the symptom varies directly with the body’s demand for ventilation and, inversely, with the body’s ventilatory capacity. There are three basic causes of dyspnea: 12 An increased awareness of normal breathing is usually related to anxiety.5 The patient commonly complains of “not getting a deep enough breath,” a feeling of “smothering,” or “not getting air down in the right places.”15 These sensations have been designated as psychogenic dyspnea. The patient’s breathing pattern is irregular, with frequent sighs. When severe, it is associated with tingling of the hands and feet, circumoral numbness, and lightheadedness. Coaching the patient to hyperventilate and to reproduce the symptoms may help the patient better understand the cause of these symptoms and how to control them.5 The hyperventilation syndrome is properly diagnosed only after organic causes have been excluded and pulmonary function tests indicate normal respiratory mechanics and PaO2. The time course of the appearance and progression of dyspnea should be identified.6,16 Acute dyspnea is common in pulmonary embolism, pneumothorax, acute asthma, pulmonary congestion related to congestive heart failure (CHF), pneumonia, and upper airway obstruction. Most of these conditions require immediate physician evaluation of the acute problem before physical therapy intervention. Subacute or chronic progression of dyspnea generally presents, over time, as increasingly severe dyspnea with exertion. It occurs with emphysema, restrictive lung disorders such as pulmonary fibrosis, chest wall deformities, respiratory muscle dysfunction, occupational lung diseases, chronic CHF, and large pleural effusions. Dyspnea may also be related to body position.16 Therefore, when evaluating dyspnea, the physical therapist should ask whether the patient: A patient who has acute dyspnea requires a rapid and thorough history and physical assessment. The physical therapist should ask several important questions to address the possible causes of acute dyspnea:14 1. Are you short of breath at rest? If the answer is yes, it suggests a severe physiological dysfunction. The patient likely needs prompt evaluation by a physician if this is of recent onset and the patient has not had a medical workup. 2. Do you have chest pain? If so, what part of your chest? Unilateral localized chest pain raises the possibility of spontaneous pneumothorax, pulmonary embolism, or chest trauma. 3. What were you doing immediately before or at the time of the onset of shortness of breath? Approximately 75% of spontaneous pneumothoraces occur during sedentary activity, 20% happen during some strenuous activity, and 5% are related to coughing or sneezing. A history of immobilization of a lower extremity, recent surgery, bed rest, travel requiring prolonged sitting, obesity, CHF, and venous disease of the lower extremities are all risk factors for pulmonary embolism. If the patient’s symptoms are related to chest trauma, the fact that a fall, a blow, or an accident occurred can usually be quickly established. 4. Do you have any major medical or surgical conditions? Cystic fibrosis, chronic obstructive pulmonary disease (COPD), interstitial lung disease, and malignancies are important causes of secondary spontaneous pneumothorax. Acute dyspnea in cardiac patients is difficult to assess because the signs and symptoms are so similar to those caused by pulmonary disease. It is most often due to arrhythmias and acute coronary ischemia with associated left ventricular dysfunction, but it can be caused by any cardiac disorder.16 Dyspnea on exertion is a common complaint of patients with cardiopulmonary dysfunction. Dyspnea during exercise or exertion usually precedes dyspnea at rest.17 It most often is a result of chronic pulmonary disease or CHF. Some causes of dyspnea during exertion or exercise are listed in Table 8-1. Table 8-1 Disorders Limiting Exercise Tolerance, Pathophysiology, and Discriminating Measures
History
The Interview
Whether the individual is an inpatient or an outpatient. Many inpatients have detailed medical records available for the therapist to review. This reduces the amount of information the physical therapist needs to obtain from the patient during an interview. If the information in the chart is scant, or if the individual is an outpatient with only a treatment referral and few or no medical records available, the physical therapist should obtain a more detailed history.
Whether the treatment order is narrow or broad in scope
Smoking History
Family History
Occupational History
Questionnaires
Dyspnea
Has difficulty breathing when reclining horizontally
Finds it necessary to be propped up on several pillows to sleep at night (orthopnea)
Has more difficulty breathing when reclining on one side (trepopnea)
Acute Dyspnea
Dyspnea on Exertion
Disorders
Pathophysiology
Measures That Deviate From Normal
PULMONARY
Obstructive lung disease
↓ Ventilatory capacity due to airflow limitation, increased ventilatory requirement due to V/Q mismatching, hypoxic stimulation to breathing
↓ VO2 max, ↑ VD/VT, ↑ P(a–ET)CO2, ↑ P(A–a)O2, ↓ breathing reserve (MVV−VE2 max), ↓ HR at maximal WR (↑ HR reserve), abnormal (trapezoidal) expiratory flow pattern
Restrictive lung disease
↓ Lung volumes, especially IC and TLC; V/Q mismatching, hypoxemia
↓ VO2 max, ↑ VT/IC, RR >50 at maximal WR, ↓ breathing reserve, ↑ VD/VT, ↑ P(a–ET)CO2, progressively ↓ PaO2 and ↑ P(A–a)O2 with ↑ WRs
Chest wall defects
Respiratory pump dysfunction due to muscle weakness or ↓ chest wall compliance
↓ VO2 max, ↑ VT/IC, ↑ RR at low WRs, nl ΔVO2/ΔWR, ↓ breathing reserve, ↓ HR at maximal WR, nl PaO2
Diseases of pulmonary circulation
↓ Pulmonary perfusion leading to V/Q mismatching
↑ VE at submaximal WRs, ↑ VD/VT, ↑ P(a–ET)CO2, progressively ↓ PaO2 and ↑ P(A–a)O2 with ↑ WRs, ↓ VO2 max, ↓ AT, more shallow ΔVO2/ΔWR as WR is ↑ toward maximum, ↓ O2 pulse (VO2 max/HR)
CARDIAC
Coronary insufficiency
Relative imbalance between myocardial oxygen supply and demand, causing myocardial ischemia
May have chest pain and ischemic ECG changes, ↓ VO2 max, ↓ AT, ↓ O2 pulse, more shallow ΔVO2/ΔWR as WR is ↑ toward maximum, ↑ HR/ VO2, ↑ breathing reserve, metabolic acidosis at low WRs → ↑ WRs→VE, abnormal BP responses
Valvular
Cardiac output limitation due to ↓ effective SV
↓ VO2 max, ↓ AT, ↓ O2 pulse, more shallow ΔVO2 max/ΔWR as WR is ↑ toward maximum, ↑ HR/ VO2, ↑ breathing reserve, metabolic acidosis at low WRs → ↑ VE, abnormal BP responses
Myocardial
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
Get Clinical Tree app for offline access
