| FEV1 | FVC | FEV1/FVC | PEFR | |
|---|---|---|---|---|
| Obstructive Pattern |  | | | |
| Restrictive Pattern | | |   | |
The majority of the time, most of us are not aware of our breathing. At times, however, various physiologic and pathologic conditions may lead to an unpleasant awareness either of breathing itself or of the need to breathe. The principle causes of dyspnea include common and uncommon conditions that are primarily of pulmonary or cardiac origin. In addition, metabolic disturbances and psychogenic factors may cause hyperventilation and shortness of breath. The cause usually becomes apparent through careful history taking, physical findings, or abnormalities on screening tests.
History taking in patients with dyspnea should focus on :
1)Descriptive characteristics of respiratory sensation
2)Onset, frequency, intensity, and duration of the symptoms
3)Most important, activities or conditions that may precipitate breathlessness
Dyspnea may be affected by body position. Trepopnea is dyspnea that occurs in one lateral position but not the other. It may signify unilateral lung disease, such as pleural effusion or obstruction of the proximal tracheobronchial tree. When the patient lies with the affected lung down, gravitational forces increase perfusion of a lung that cannot ventilate well.
Orthopnea is dyspnea in the recumbent position and is usually relieved by sitting upright. It may due to left ventricular failure, obstructive airways disease, or respiratory muscle weakness. Conversely, platypnea is dyspnea in the upright position that is relieved by recumbency.Platypnea may be caused by intracardiac, vascular, or parenchymal lung shunts.
Associated respiratory symptoms should always be noted, including wheezing, cough, sputum production, and pleuritic chest pain.Documentation of exposure in the workplace or at home to tobacco, inhalants, or animals is important. The medication history may reveal drugs that cause pulmonary dysfunction.
Examination of the lungs and heart may confirm such suspected problems as asthma, pneumonia, pneumothorax, or congestive heart failure, but physical findings do not have sufficient sensitivity or specificity to be relied on by themselves. In the absence of a life--threatening situation such as tension pneumothorax( for which treatment must be proceed without confirmation ), others tests are generally needed to definitely explain the cause of dyspnea. Sometimes, as in patients with known asthma or congestive heart failure, treatment can proceed, as long as there is no suggestion of coexisting problems.
On the basis of information obtained from the patient’s history and physical examination, one or more disorders can be suspected.Five cardinals screenings tests are available for the initial evaluation of dyspnea: chest radiograph, electrocardiogram(ECG), pulmonary function testing, determination of arterial blood gas levels, and pulse oximetry.
This is essential in the diagnostic workup. It may suggest several diagnoses: pneumothorax (spontaneous or traumatic), pneumonia, malignant disease, pleural disease
( malignant lesion or effusion ),or pulmonary edema. It may also give clues to other diagnoses (cardiomegaly, deformities of the chest wall, chest trauma and abnormalities of the pulmonary vasculature or in the position of the diaphragm ).
The 12-lead ECG , especially when compared with previous ECGs, may provide important data about myocardial ischemia, arrhythmias, pericarditis, chamber size, or the presence of pulmonary disease.
If pulmonary disease is suspected, pulmonary function testing is often the starting point for investigating exertional dyspnea. Measurement of the peak expiratory flow rate, a simple and inexpensive bedside test, may give evidence of airway obstruction, but is effort-dependent and is not specific for obstructive airways disease. Tests of forced vital capacity and forced expiratory volume in 1 second are also effort-dependent but are more useful in separating obstructive from restrictive pulmonary disease (table 1). Left ventricular failure, as well as pulmonary disease, can cause obstructive changes in pulmonary function tests.
| FEV1 | FVC | FEV1/FVC | PEFR | |
|---|---|---|---|---|
| Obstructive Pattern | | | | |
| Restrictive Pattern | | | | |
Others tests of pulmonary function may be helpful (table 2).Carbon monoxide diffusing capacity of the lungs helps to differentiate an alveolar process from vascular abnormalities.Bronchoprovocation testing, flow volume loops, closing volumes, and respiratory mouth pressures are other noninvasive tests that can be used to evaluate the condition of patients who have suspected respiratory or neuromuscular disease.
| Test | Diagnosis |
|---|---|
| Echocardiography | Structural Abnormalities of Heart |
| Spirometry | Pulmonary Disease(Obstructive X Restrictive) |
| Ventilation-Perfusion Lung Scanning | Pulmonary Embolism |
| Flow-Volume Curves | Upper Airway ObstructiveDiseases |
| Carbon Monoxide Diffusing capacity | Pulmonary Disease(Alveolar X Vascular) |
| Bronchoprovocation Testing | Reactive Airway Disease |
| Cardiopulmonary Exercise Testing | Pulmonary Disease(Obstructive X Restrictive) Cardiac Disease(Ischemia,valvular Abnormalities, Cardiomyopathy) Deconditioning |
| Negative Inspiratory Force | Neuromuscular Disease |
Determination of arterial blood gas levels and pulse oximetry are important in the evaluation of the dyspneic patient.Normal tissue oxygenation requires perfusion with blood that is adequate in oxygen content.The vast majority of oxygen is carried by hemoglobin; only a small amount is dissolved in plasma. Oximetry measures the fraction of oxygen carried in hemoglobin.The PaO2 is a measure only of the dissolved oxygen in arterial blood.Although this fraction is usually only a small part of the oxygen content of blood, it provides the best information about the delivery of oxygen from the atmosphere to the pulmonary capillaries.
Adequate tissue oxygenation is determined not only by oxygen content but also by cardiac output and factors such as pH, body temperature, and the adequacy of red-cell 2,3-disphosphoglycerate concentration , any of which may shift the oxyhemoglobin curve to the right or left. Shifts to the right increase oxygen delivery, while shifts to the left decrease oxygen delivery.
Like oxygen, carbon dioxide is carried in the plasma and erythrocytes. In contrast to the blood transport of oxygen, most of the carbon dioxide produced is carried dissolved in plasma. Minor changes in ventilation therefore affect the PaCO2 level more significantly than the PaO2 level. The presence of extrapulmonary shunts or changes in the alveolar content of oxygen, the diffusion barrier for oxygen between alveoli and capillaries, or the matching between ventilatory and vascular units are more likely to cause changes in PaO2.
In patients with hypoxemia, it is often useful to calculate the alveolar-arterial (A-a) oxygen tension difference (A-aDO2). In the perfect lung, there would be no difference between ventilation and perfusion and the gradient would be zero. The A-a gradient is calculated from the following equation:
A - aDO2= PIO2 - (PaCO2 x 1.2 ) -PaO2
In this equation, PIO2 is the partial pressure of inspired oxygen at local altitude.At sea level, with the patient breathing room air, this is given as average barometric pressure (760 mmHg ) minus the partial pressure for humidification of inspired air (47 mmHg ) times the fraction of oxygen in the inspired air (FIO2 ), or (760-47 ) x .21 = 150.The levels of PaO2 and PCO2 again are obtained from arterial blood gas values. At sea level, in young healthy subjects, a gradient of 10 to 15 is regarded as normal. A simple formula, therefore, for calculating an A-a gradient is: 150 - (PaO2 - PaCO2) while breathing room air, or (700) (FIO2) - (PaO2 + PaCO2 ) at higher inspired oxygen concentrations. The A-a gradient increases with age , with a normal gradient being calculated as less than 4 +(age/4 ).
In general, arterial blood gas levels should be determined in any severely ill patient when an alteration in acid-base status or compromised respiratory function is suspected. However, when the pathologic process is known and an objective measurement is only needed to follow the clinical course and response to treatment, pulse oximetry is a very useful adjunct. At relatively normal cardiac output, the transcutaneous oxygen tension (PtcO2 ) reliably monitors the trend of oxygenation. It correlates roughly with the PaO2 level, especially as the level falls bellow moderately hypoxemic levels.
When PaO2 levels rise above 70 mmHg, however, oxygen saturation does not change proportionately and therefore may be misleading.Transcutaneous oxygen saturation does not take into account the work of breathing. It may also be misleading when hemoglobin is modified or abnormal .Therefore, PtcO2 is better as trending parameter when the underlying of hypoxia is known. At moderate degrees of hypoperfusion, even when not associated with systemic hypotension, the PtcO2 is less reliable.
When cardiac disease is suspected, the Echocardiogram is the best single noninvasive test to define the cause of dyspnea. Information about chamber size, valves, and pericardial disease, as well as ventricular function, may be discerned.
Cardiopulmonary exercise testing should be done when dyspnea cannot be explained after the tests showed above.The objective of such testing is to stress the oxygen transport system in order to identify the particular system affected( lungs, heart, or muscle ).
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