Test 2 - Shortness of Breath 2

A heterogeneous set of conditions characterized by hypoxia and interstitial (pulmonary vessels, bronchi, connective tissue) abnormalities on chest radiographs. Examples include sarcoidosis, idiopathic pulmonary fibrosis, rheumatoid lung, and pneumoconioses.

Interstitial lung disease

APPROACH TO THE PATIENT: Dyspnea LABORATORY STUDIES

Laboratory studies should include electrocardiography to seek evidence of ventricular hypertrophy and prior myocardial infarction. Echocardiography is indicated when systolic dysfunction, pulmonary hypertension, or valvular heart disease is suspected. Bronchoprovocation testing is useful in patients with intermittent symptoms suggestive of asthma but normal physical examination and lung function; up to one-third of patients with the clinical diagnosis of asthma do not have reactive airways disease when formally tested. Measurement of brain natriuretic peptide levels in serum is increasingly used to assess for CHF in patients presenting with acute dyspnea but may be elevated in the presence of right ventricular strain as well.

APPROACH TO THE PATIENT: Dyspnea DISTINGUISHING CARDIOVASCULAR FROM RESPIRATORY SYSTEM DYSPNEA

If a patient has evidence of both pulmonary and cardiac disease, a cardiopulmonary exercise test should be carried out to determine which system is responsible for the exercise limitation. If, at peak exercise, the patient achieves predicted maximal ventilation, demonstrates an increase in dead space or hypoxemia, or develops bronchospasm, the respiratory system is probably the cause of the problem. Alternatively, if the heart rate is >85% of the predicted maximum, if the anaerobic threshold occurs early, if the blood pressure becomes excessively high or decreases during exercise, if the O2 pulse (O2 consumption/heart rate, an indicator of stroke volume) falls, or if there are ischemic changes on the electrocardiogram, an abnormality of the cardiovascular system is likely the explanation for the breathing discomfort.

Identifying Alarm Symptoms

1) Acute onset and rapid progression of dyspnea are concerning for impending respiratory failure. 2) Always carefully monitor for changes in symptoms because the patient's respiratory status can deteriorate quickly.

Getting Started with the History

1) Begin by assessing the patient's airway, breathing, and circulation. If the patient is unable to complete a full sentence without pausing for a deep breath, move quickly to stabilize the patient. Return to the interview after the patient is more comfortable. 2) Start with an open-ended question that lets the patient describe the dyspnea before asking more focused questions.

Interview Framework

1) First, classify the duration of symptoms as acute or chronic. 2) Listen to the patient's description of dyspnea, particularly exacerbating and alleviating factors and associated signs and symptoms. 3) Ask about risk factors for conditions causing dyspnea from the past medical, social, and family histories.

Dyspnea Caveats

1) The history and physical examination identify the etiology of dyspnea in nearly 70% of cases. The remainder will require more specific testing, such as chest radiographs or pulmonary function tests.3 2) The causes of dyspnea are often multifactorial. For example, heavy smoking is a risk factor for both COPD and coronary artery disease. Patients with chronic lung or heart disease may also suffer from deconditioning. Adequate treatment of the patient requires identification of all causes of dyspnea because the therapies may differ. 3) Platypnea is encountered with right-to-left shunts in the atria or pulmonary vasculature (eg, hepatopulmonary syndrome) and in emphysema. 4) Be particularly cautious about assuming anxiety is the cause of acute or chronic dyspnea because patients with dyspnea caused by organic disease are often anxious.

Dyspnea that occurs in the lateral decubitus position on one side, but not the other.

Trepopnea

Dyspnea can be classified based on the primary physiologic derangement:

- Pulmonary - Cardiac - Hematologic (eg, anemia) - Chest wall or neuromuscular disease - Metabolic (eg, acidosis) - Functional (eg, panic disorders) - Deconditioning

APPROACH TO THE PATIENT: Dyspnea CHEST IMAGING

After the history elicitation and the physical examination, a chest radiograph should be obtained. The lung volumes should be assessed: hyperinflation indicates obstructive lung disease, whereas low lung volumes suggest interstitial edema or fibrosis, diaphragmatic dysfunction, or impaired chest wall motion. The pulmonary parenchyma should be examined for evidence of interstitial disease and emphysema. Prominent pulmonary vasculature in the upper zones indicates pulmonary venous hypertension, while enlarged central pulmonary arteries suggest pulmonary arterial hypertension. An enlarged cardiac silhouette suggests dilated cardiomyopathy or valvular disease. Bilateral pleural effusions are typical of CHF and some forms of collagen-vascular disease. Unilateral effusions raise the specter of carcinoma and pulmonary embolism but may also occur in heart failure. CT of the chest is generally reserved for further evaluation of the lung parenchyma (interstitial lung disease) and possible pulmonary embolism.

CARDIOGENIC PULMONARY EDEMA

Cardiac abnormalities that lead to an increase in pulmonary venous pressure shift the balance of forces between the capillary and the interstitium. Hydrostatic pressure is increased and fluid exits the capillary at an increased rate, resulting in interstitial and, in more severe cases, alveolar edema. The development of pleural effusions may further compromise respiratory system function and contribute to breathing discomfort. Early signs of pulmonary edema include exertional dyspnea and orthopnea. Chest radiographs show peribronchial thickening, prominent vascular markings in the upper lung zones, and Kerley B lines. As the pulmonary edema worsens, alveoli fill with fluid; the chest radiograph shows patchy alveolar filling, typically in a perihilar distribution, which then progresses to diffuse alveolar infiltrates. Increasing airway edema is associated with rhonchi and wheezes.

Conditions that damage heart muscle and may cause heart failure. Etiologies are diverse. Common causes include ischemic heart disease, valvular disease, hypertension, infections, toxins, and genetic disorders.

Cardiomyopathies

Cardiovascular System Dyspnea DISEASES OF THE PERICARDIUM

Constrictive pericarditis and cardiac tamponade are both associated with increased intracardiac and pulmonary vascular pressures, which are the likely cause of dyspnea in these conditions. To the extent that cardiac output is limited (at rest or with exercise) metaboreceptors may be stimulated if cardiac output is compromised to the degree that lactic acidosis develops; chemoreceptors will also be activated.

DYSPNEA DIFFERENTIAL DIAGNOSIS

Dyspnea most often results from deviations from normal function in the cardiovascular and respiratory systems. These deviations produce breathlessness as a consequence of increased drive to breathe; increased effort or work of breathing; and/or stimulation of receptors in the heart, lungs, or vascular system. Most diseases of the respiratory system are associated with alterations in the mechanical properties of the lungs and/or chest wall, and some stimulate pulmonary receptors. In contrast, disorders of the cardiovascular system more commonly lead to dyspnea by causing gas-exchange abnormalities or stimulating pulmonary and/or vascular receptors

A 67-year-old man comes to your clinic for his annual appointment concerned about increasing shortness of breath. A year ago he was able to walk up the stairs to his apartment without difficulty, but now he has a hard time walking one block. He has a 70 pack-year smoking history, and several previous attempts to stop smoking have been unsuccessful. Additional History This patient has had slowly progressive dyspnea with exercise but no symptoms at rest. The chronicity of the patient's symptoms and his ability to engage in conversation reassure you that he does not require urgent intervention. He expresses frustration that he is unable to get a full breath when simply walking around his home. The dyspnea often worsens when he has a "cold," but he denies an acute increase in symptoms. There are no other triggers. When you ask about related symptoms, he describes a persistent cough productive of thick green sputum. The cough has been an irritating presence for the past several months. He denies fevers, chest pain, chest tightness, or orthopnea. Question: What Is the Most Likely Diagnosis? A) Asthma B) Chronic obstructive pulmonary disease C) Congestive heart failure D) Pneumonia

Correct answer: B The most common causes of dyspnea are primary cardiac and pulmonary causes, anemia, deconditioning, and functional dyspnea. The patient describes a productive cough for greater than 3 months and an impressive smoking history; both have high likelihood ratios for chronic obstructive pulmonary disease (COPD). The patient's presentation is highly suggestive of the chronic bronchitis variant of COPD. However, congestive heart failure and COPD frequently occur together; thus a diagnosis of one does not exclude the other. Further evaluation for cardiac causes should be pursued because the patient has several coronary artery disease risk factors (smoking, male sex, and age over 60) and CHF may be contributing to the patient's dyspnea. The classic symptoms of asthma are dyspnea, wheezing, and cough, which overlap with those of COPD, making diagnostic distinction difficult. In this case, the patient's older age of onset makes asthma less likely. Pneumonia is unlikely based on the chronicity of symptoms and lack of systemic symptoms or signs of infection.

Cardiovascular System Dyspnea DISEASES OF THE LEFT HEART

Diseases of the myocardium resulting from coronary artery disease and nonischemic cardiomyopathies cause a greater left-ventricular end-diastolic volume and an elevation of the left-ventricular end-diastolic as well as pulmonary capillary pressures. These elevated pressures lead to interstitial edema and stimulation of pulmonary receptors, thereby causing dyspnea; hypoxemia due to V. /Q mismatch may also contribute to breathlessness. Diastolic dysfunction, characterized by a very stiff left ventricle, may lead to severe dyspnea with relatively mild degrees of physical activity, particularly if it is associated with mitral regurgitation.

Abnormally increased awareness of breathing or sensation of difficulty breathing.

Dyspnea

Serious Diagnoses

Many causes of dyspnea are serious. Patients with acute or severe dyspnea require rapid diagnostic evaluation as they can develop complete respiratory failure. In these cases urgent intubation and mechanical ventilation should be pursued. Fortunately, in the majority of cases, patients are stable enough to provide a comprehensive history. Patients with chronic dyspnea who are able to talk comfortably may have serious underlying disease, but the clinician has more time to evaluate the patient.

Dyspnea when lying flat. Typically described in terms of the number of pillows the patient uses to breathe comfortably to sleep.

Orthopnea

Dyspnea that wakes the patient from sleep. The patient may report waking up gasping for air, and classically finds relief by sitting by an open window.

Paroxysmal nocturnal dyspnea (PND)

Dyspnea that improves when the patient lies down.

Platypnea

Cardiovascular System Dyspnea DISEASES OF THE PULMONARY VASCULATURE

Pulmonary thromboembolic disease and primary diseases of the pulmonary circulation (primary pulmonary hypertension, pulmonary vasculitis) cause dyspnea via increased pulmonary-artery pressure and stimulation of pulmonary receptors. Hyperventilation is common, and hypoxemia may be present. However, in most cases, use of supplemental oxygen has only a minimal impact on the severity of dyspnea and hyperventilation.

the sensation of uncomfortable breathing

Shortness of breath, or dyspnea. This feeling of discomfort may reflect an increased awareness of breathing or the perception that breathing is difficult or inadequate. Dyspnea usually indicates pulmonary or cardiac disease, but can also be the presenting symptom of metabolic derangements, hematologic disorders, toxic ingestions, psychiatric conditions, or simple deconditioning. Dyspnea is the second most common reason for emergency department visits in the United States.

APPROACH TO THE PATIENT: Dyspnea TREATMENT

The first goal is to correct the underlying problem responsible for the symptom. If this is not possible, an effort is made to lessen the intensity of the symptom and its effect on the patient's quality of life. Supplemental O2 should be administered if the resting O2 saturation is ≤89% or if the patient's saturation drops to these levels with activity. For patients with COPD, pulmonary rehabilitation programs have demonstrated positive effects on dyspnea, exercise capacity, and rates of hospitalization. Studies of anxiolytics and antidepressants have not documented consistent benefit. Experimental interventions—e.g., cold air on the face, chest wall vibration, and inhaled furosemide—aimed at modulating the afferent information from receptors throughout the respiratory system are being studied. Morphine has been shown to reduce dyspnea out of proportion to the change in ventilation in laboratory models.

DISTINGUISHING CARDIOGENIC FROM NONCARDIOGENIC PULMONARY EDEMA

The history is essential for assessing the likelihood of underlying cardiac disease as well as for identification of one of the conditions associated with noncardiogenic pulmonary edema. The physical examination in cardiogenic pulmonary edema is notable for evidence of increased intracardiac pressures (S3 gallop, elevated jugular venous pulse, peripheral edema) and rales and/or wheezes on auscultation of the chest. In contrast, the physical examination in noncardiogenic pulmonary edema is dominated by the findings of the precipitating condition; pulmonary findings may be relatively normal in the early stages. The chest radiograph in cardiogenic pulmonary edema typically shows an enlarged cardiac silhouette, vascular redistribution, interstitial thickening, and perihilar alveolar infiltrates; pleural effusions are common. In noncardiogenic pulmonary edema, heart size is normal, alveolar infiltrates are distributed more uniformly throughout the lungs, and pleural effusions are uncommon. Finally, the hypoxemia of cardiogenic pulmonary edema is due largely to V. /Q to mismatch and responds to the administration of supplemental oxygen. In contrast, hypoxemia in noncardiogenic pulmonary edema is due primarily to intrapulmonary shunting and typically persists despite high concentrations of inhaled oxygen.

APPROACH TO THE PATIENT: Dyspnea HISTORY

The patient should be asked to describe in his/her own words what the discomfort feels like as well as the effect of position, infections, and environmental stimuli on the dyspnea (see Fig. 47e-2). Orthopnea is a common indicator of congestive heart failure (CHF), mechanical impairment of the diaphragm associated with obesity, or asthma triggered by esophageal reflux. Nocturnal dyspnea suggests CHF or asthma. Acute, intermittent episodes of dyspnea are more likely to reflect episodes of myocardial ischemia, bronchospasm, or pulmonary embolism, while chronic persistent dyspnea is typical of COPD, interstitial lung disease, and chronic thromboembolic disease. Information on risk factors for occupational lung disease and for coronary artery disease should be elicited. Left atrial myxoma or hepatopulmonary syndrome should be considered when the patient complains of platypnea—i.e., dyspnea in the upright position with relief in the supine position.

APPROACH TO THE PATIENT: Dyspnea PHYSICAL EXAMINATION

The physical examination should begin during the interview of the patient. Inability of the patient to speak in full sentences before stopping to get a deep breath suggests a condition that leads to stimulation of the controller or impairment of the ventilatory pump with reduced vital capacity. Evidence of increased work of breathing (supraclavicular retractions; use of accessory muscles of ventilation; and the tripod position, characterized by sitting with the hands braced on the knees) is indicative of increased airway resistance or stiffness of the lungs and the chest wall. When measuring the vital signs, the physician should accurately assess the respiratory rate and measure the pulsus paradoxus (Chap. 288); if the systolic pressure decreases by >10 mmHg, the presence of COPD, acute asthma, or pericardial disease should be considered. During the general examination, signs of anemia (pale conjunctivae), cyanosis, and cirrhosis (spider angiomata, gynecomastia) should be sought. Examination of the chest should focus on symmetry of movement; percussion (dullness is indicative of pleural effusion; hyperresonance is a sign of emphysema); and auscultation (wheezes, rhonchi, prolonged expiratory phase, and diminished breath sounds are clues to disorders of the airways; rales suggest interstitial edema or fibrosis). The cardiac examination should focus on signs of elevated right heart pressures (jugular venous distention, edema, accentuated pulmonic component to the second heart sound); left ventricular dysfunction (S3 and S4 gallops); and valvular disease (murmurs). When examining the abdomen with the patient in the supine position, the physician should note whether there is paradoxical movement of the abdomen: inward motion during inspiration is a sign of diaphragmatic weakness, and rounding of the abdomen during exhalation is suggestive of pulmonary edema. Clubbing of the digits may be an indication of interstitial pulmonary fibrosis, and joint swelling or deformation as well as changes consistent with Raynaud's disease may be indicative of a collagen-vascular process that can be associated with pulmonary disease. Patients with exertional dyspnea should be asked to walk under observation in order to reproduce the symptoms. The patient should be examined during and at the end of exercise for new findings that were not present at rest and for changes in oxygen saturation.

Dyspnea Prognosis

The prognosis of dyspnea depends on the etiology and severity of the underlying disease. Acute dyspnea is often reversible. Myocardial infarctions, pulmonary emboli, aspiration pneumonia, pneumothoraces, and asthma can generally be successfully treated once diagnosed. In contrast, chronic dyspnea may reflect disease that has progressed to an irreversible stage. Dyspnea associated with chronic pulmonary or cardiac disease may improve if the patient stops smoking and participates in cardiopulmonary exercise training/rehabilitation.

Dyspnea Etiology

The purpose of breathing is to meet the metabolic demands of the body. Thus, any condition that increases the work of breathing (eg, airway obstruction, changes in lung compliance, or respiratory muscle weakness) or increases respiratory drive (eg, hypoxia or acidosis) may result in dyspnea.2 In addition, dyspnea may result from or be exacerbated by primary psychological conditions (eg, anxiety disorders). The differential diagnosis of dyspnea depends on the duration of the symptom and the clinical setting. Conditions associated with acute dyspnea (developing over hours to a few days) are outlined under alarm conditions. Conditions associated with insidious development of dyspnea are outlined below. In an analysis of patients referred to a pulmonary clinic for evaluation of chronic, unexplained dyspnea, 67% suffered from asthma, chronic obstructive pulmonary disease (COPD), interstitial lung disease, or myocardial dysfunction.