Symptom Finder - Dyspnea, Tachypnea and Orthopnea
DYSPNEA, TACHYPNEA, AND ORTHOPNEA
Dyspnea is the subjective feeling of rapid or difficult breathing. The patient will often say: “I can’t get my breath!” Tachypnea is the objective finding of a rapid respiratory rate, and may or may not be associated with the feeling of not being able to breathe properly. One is a symptom and the other is a sign, but the mechanisms for producing them are the same:
inadequate oxygen for body needs or inability to excrete CO2. A few other mechanisms that produce hyperventilation and tachypnea will be discussed later on in this chapter. The best basic science for developing a list of the causes of dyspnea and tachypnea is pathophysiology. Difficulty breathing or rapid breathing will develop when there is decreased intake of oxygen, impaired absorption of oxygen, inadequate perfusion of the lungs with blood, inability of the body to transport enough oxygen to the tissues, increased demand of the tissues for oxygen, and inability of the body to excrete CO2 and other waste products of body metabolism.
Disorders of oxygen intake: In this category are the conditions that may block the respiratory passages such as laryngitis, foreign bodies, an aortic aneurysm or mediastinal tumor pressing on the trachea or bronchi, bronchial asthma, acute infectious bronchitis, and pulmonary emphysema.
Also considered in this category are conditions that interfere with the “respiratory pump” (thoracic cage, thoracic and diaphragmatic muscles, and respiratory centers in the brain) such as kyphoscoliosis, Pickwickian syndrome, myasthenia gravis, Muscular dystrophy and other neuromuscular diseases, peritonitis, encephalitis, and brain tumors.
Disorders of oxygen absorption: Lobar pneumonia, sarcoidosis, silicosis, berylliosis, and various causes of pulmonary fibrosis, and pulmonary edema are considered here. Oxygen diffusion across the alveolocapillary membrane is affected in all of these. Alveolar proteinosis, shock lung, and the adult respiratory distress syndrome must also be considered here.
Disorders of perfusion of the pulmonary capillaries: Pulmonary emboli, hemangiomas of the lungs, and congenital heart increases such as tetralogy of Fallot belong in this category. In all of these conditions unoxygenated blood bypasses the alveoli. Also included in this category are diseases with a ventilation–perfusion defect. In other words, some alveoli are being ventilated but not perfused with blood, while at the same time some alveoli are being perfused but not ventilated. Pulmonary emphysema and the various conditions associated with pulmonary fibrosis (e.g., pneumoconiosis) cause dyspnea on this basis, as well as other physiologic reasons mentioned above.
Disorders of oxygen transport: The tissues will not get oxygen if there is not enough blood to transport it, as in anemia and hemorrhagic shock; if there is not enough blood pressure to perfuse the tissues, as in vasomotor and cardiogenic shock; or if the heart pump fails, as in CHF from many causes. In methemoglobinemia and sulfhemoglobinemia, there may be enough blood, but it is unable to carry the oxygen.
Increased tissue oxygen demand: During exercise and nervous stress, and in febrile states, leukemia and other malignancies, and hyperthyroidism there is an increase in tissue metabolism; consequently, tachypnea may develop to increase the supply.
Inadequate excretion of CO2 and other wastes of tissue metabolism: Inability to excrete CO2 may occur without anoxia in pulmonary emphysema and other chronic obstructive lung diseases and initiate dyspnea, especially on exertion. Other wastes of tissue metabolism may cause an acidosis and stimulate the respiratory centers in this fashion.
Lactic acidosis, diabetic acidosis, and uremia may cause dyspnea on this basis.
From the above discussion, it should be evident that the clinician can develop an excellent list of the causes of dyspnea and tachypnea with an understanding of the pathophysiology involved. A few conditions cannot be recalled with this method: hyperventilation syndrome, ingestion of acids (e.g., methyl alcohol poisoning) and drugs that stimulate the respiratory centers (such as amphetamines), and atmospheric reduction in oxygen tension.
Approach to the Diagnosis
The history and physical examination will almost invariably disclose the cause of dyspnea. If acute respiratory distress syndrome (ARDS) is suspected, look for sepsis from an abdominal source and drug abuse. To confirm pulmonary disease one will order pulmonary function studies, a chest roentgenogram, and arterial blood gases. If routine pulmonary function studies are normal, more sophisticated studies such as the nitrogen washout test and perfusion and ventilatory scans may be necessary. However, a high resolution CT scan (HRCT) is very sensitive in diagnosing interstitial pulmonary disease. To diagnose cardiac conditions, ordering an ECG and echocardiography are most useful.
Any patient with dyspnea and normal physical findings deserves a circulation time to rule out early CHF. A hemogram will diagnose anemias but it will not diagnose methemoglobinemia. A determination of the erythrocytes’ methemoglobin, arterial oxygen saturation, and diaphorase I test must be done.
Other Useful Tests
1. CBC (anemia, polycythemia)
2. Sedimentation rate (pneumonia, subacute bacterial endocarditis
[SBE])
3. Serial cardiac enzymes (acute myocardial infarction)
4. Sputum smear and culture (pneumonia)
5. Lung scan (pulmonary embolism)
6. Sputum for eosinophils (asthma)
7. Toxicology screen (drug abuse)
8. Echocardiogram (CHF, valvular heart disease)
9. Pulmonary angiogram (pulmonary embolism)
10. Trial of diuretics (CHF)
11. Forced vital capacity (FVC) with methacholine challenge (asthma)
12. B-type natriuretic peptide (BNP) assay (CHF)
13. Cardiac catheterization (CHF)
14. Spiral CT scan (pulmonary embolism)
15. Spirometry before and after bronchodilators (asthma)
16. Serum protein electrophoresis (α-1 antitrypsin deficiency)
301
17. Sweat test (Cystic fibrosis)
18. Cardiac CT scan (Coronary Artery Disease)
Dyspnea is the subjective feeling of rapid or difficult breathing. The patient will often say: “I can’t get my breath!” Tachypnea is the objective finding of a rapid respiratory rate, and may or may not be associated with the feeling of not being able to breathe properly. One is a symptom and the other is a sign, but the mechanisms for producing them are the same:
inadequate oxygen for body needs or inability to excrete CO2. A few other mechanisms that produce hyperventilation and tachypnea will be discussed later on in this chapter. The best basic science for developing a list of the causes of dyspnea and tachypnea is pathophysiology. Difficulty breathing or rapid breathing will develop when there is decreased intake of oxygen, impaired absorption of oxygen, inadequate perfusion of the lungs with blood, inability of the body to transport enough oxygen to the tissues, increased demand of the tissues for oxygen, and inability of the body to excrete CO2 and other waste products of body metabolism.
Disorders of oxygen intake: In this category are the conditions that may block the respiratory passages such as laryngitis, foreign bodies, an aortic aneurysm or mediastinal tumor pressing on the trachea or bronchi, bronchial asthma, acute infectious bronchitis, and pulmonary emphysema.
Also considered in this category are conditions that interfere with the “respiratory pump” (thoracic cage, thoracic and diaphragmatic muscles, and respiratory centers in the brain) such as kyphoscoliosis, Pickwickian syndrome, myasthenia gravis, Muscular dystrophy and other neuromuscular diseases, peritonitis, encephalitis, and brain tumors.
Disorders of oxygen absorption: Lobar pneumonia, sarcoidosis, silicosis, berylliosis, and various causes of pulmonary fibrosis, and pulmonary edema are considered here. Oxygen diffusion across the alveolocapillary membrane is affected in all of these. Alveolar proteinosis, shock lung, and the adult respiratory distress syndrome must also be considered here.
Disorders of perfusion of the pulmonary capillaries: Pulmonary emboli, hemangiomas of the lungs, and congenital heart increases such as tetralogy of Fallot belong in this category. In all of these conditions unoxygenated blood bypasses the alveoli. Also included in this category are diseases with a ventilation–perfusion defect. In other words, some alveoli are being ventilated but not perfused with blood, while at the same time some alveoli are being perfused but not ventilated. Pulmonary emphysema and the various conditions associated with pulmonary fibrosis (e.g., pneumoconiosis) cause dyspnea on this basis, as well as other physiologic reasons mentioned above.
Disorders of oxygen transport: The tissues will not get oxygen if there is not enough blood to transport it, as in anemia and hemorrhagic shock; if there is not enough blood pressure to perfuse the tissues, as in vasomotor and cardiogenic shock; or if the heart pump fails, as in CHF from many causes. In methemoglobinemia and sulfhemoglobinemia, there may be enough blood, but it is unable to carry the oxygen.
Increased tissue oxygen demand: During exercise and nervous stress, and in febrile states, leukemia and other malignancies, and hyperthyroidism there is an increase in tissue metabolism; consequently, tachypnea may develop to increase the supply.
Inadequate excretion of CO2 and other wastes of tissue metabolism: Inability to excrete CO2 may occur without anoxia in pulmonary emphysema and other chronic obstructive lung diseases and initiate dyspnea, especially on exertion. Other wastes of tissue metabolism may cause an acidosis and stimulate the respiratory centers in this fashion.
Lactic acidosis, diabetic acidosis, and uremia may cause dyspnea on this basis.
From the above discussion, it should be evident that the clinician can develop an excellent list of the causes of dyspnea and tachypnea with an understanding of the pathophysiology involved. A few conditions cannot be recalled with this method: hyperventilation syndrome, ingestion of acids (e.g., methyl alcohol poisoning) and drugs that stimulate the respiratory centers (such as amphetamines), and atmospheric reduction in oxygen tension.
Approach to the Diagnosis
The history and physical examination will almost invariably disclose the cause of dyspnea. If acute respiratory distress syndrome (ARDS) is suspected, look for sepsis from an abdominal source and drug abuse. To confirm pulmonary disease one will order pulmonary function studies, a chest roentgenogram, and arterial blood gases. If routine pulmonary function studies are normal, more sophisticated studies such as the nitrogen washout test and perfusion and ventilatory scans may be necessary. However, a high resolution CT scan (HRCT) is very sensitive in diagnosing interstitial pulmonary disease. To diagnose cardiac conditions, ordering an ECG and echocardiography are most useful.
Any patient with dyspnea and normal physical findings deserves a circulation time to rule out early CHF. A hemogram will diagnose anemias but it will not diagnose methemoglobinemia. A determination of the erythrocytes’ methemoglobin, arterial oxygen saturation, and diaphorase I test must be done.
Other Useful Tests
1. CBC (anemia, polycythemia)
2. Sedimentation rate (pneumonia, subacute bacterial endocarditis
[SBE])
3. Serial cardiac enzymes (acute myocardial infarction)
4. Sputum smear and culture (pneumonia)
5. Lung scan (pulmonary embolism)
6. Sputum for eosinophils (asthma)
7. Toxicology screen (drug abuse)
8. Echocardiogram (CHF, valvular heart disease)
9. Pulmonary angiogram (pulmonary embolism)
10. Trial of diuretics (CHF)
11. Forced vital capacity (FVC) with methacholine challenge (asthma)
12. B-type natriuretic peptide (BNP) assay (CHF)
13. Cardiac catheterization (CHF)
14. Spiral CT scan (pulmonary embolism)
15. Spirometry before and after bronchodilators (asthma)
16. Serum protein electrophoresis (α-1 antitrypsin deficiency)
301
17. Sweat test (Cystic fibrosis)
18. Cardiac CT scan (Coronary Artery Disease)
