SEMINAR ON

DYSPNEA: MECHANISMS, ASSESSMENT & MANAGEMENT

SUBMITTED BY: - PRIYA KUBERAN MODERATED BY: - Dr. VAISHALI RAO

CONTENTS

Respiration: Features and Regulation Dyspnea: Causes and Types Mechanisms of Dyspnea Physiological Mechanisms Pathophysiological Mechanisms Dyspnea Assessment Management of Dyspnea Medical Management Physiotherapy Management

INTRODUCTION

Respiration, the act of breathing, is unique in that, of all the vital functions, it alone is regulated not only by autonomic centers located in the brainstem but also by voluntary signals initiated in the cortex. The goals of respiration are to provide oxygen to the tissues and to remove carbon dioxide. To achieve these goals, respiration can be divided into four major functions: (1) Pulmonary ventilation, which means the inow and outow of air between the atmosphere and the lung alveoli (2) Diffusion of oxygen and carbon dioxide between the alveoli and the blood (3) Transport of oxygen and carbon dioxide in the blood and body uids to and from the bodys tissue cells (4) Regulation of ventilation and other facets of respiration

During normal quiet breathing, all respiratory muscle contraction occurs during inspiration and expiration is almost entirely a passive process caused by elastic recoil of the lungs and the chest cage. Thus, under resting conditions, the respiratory muscles normally perform work to cause inspiration but not to cause expiration.

Mechanics of pulmonary ventilation can be explained by a few important factors. The lungs mainly expand and contract with the help of the diaphragm and the accessory muscles of inspiration and expiration. The pleural, alveolar and transpulmonary pressures help in facilitating the movement of air in and out of the lungs. The compliance of the lung is determined by the elastic forces of the lung tissue itself and the elastic forces caused by the surface tension of the fluid that lines the inside walls of the alveoli and other lung air spaces. The surfactant secreted by the type II alveolar epithelial cells, helps in reducing the alveolar surface tension and thereby reduces the effort required by the respiratory muscles to expand the lungs. The pulmonary volumes and capacities all have established normal values and help in determining any deviation in normal process of respiration.

The regulation of breathing is mainly by : 1. Respiratory centres in the medulla oblongata and pons of the brainstem 2. The Hering Breuer Inflation Reflex 3. Chemical control of respiration 4. Peripheral chemoreceptor system for control of respiratory activity Role of oxygen in respiratory control

The other factors like voluntary control of respiration, effect of irritant receptors in the airways, function of lung J receptors, effect of brain oedema and anaesthesia are some of the other factors that might affect respiration and its regulation. Derangements in the regulation of respiration, ventilatory pump or exchange of gases may lead to uncomfortable breathing sensations, generally referred to as dyspnea by clinicians.

DYSPNEA
Dyspnea is the term generally applied to sensations experienced by individuals who complain of unpleasant or uncomfortable respiratory sensations. Dyspnea has been defined in many ways. Difficult, labored, uncomfortable breathing Awareness of respiratory distress Sensation of feeling breathless or feeling air hunger An uncomfortable sensation of breathing All the above definitions are an amalgamation of the symptoms that the patients feel and the physical signs that the physician observes. There is a deeper interplay between physiological and behavioural factors in producing respiratory discomfort as well as spectrum of phrases used by patients to describe their sensations. Therefore, the American Thoracic Society defined dyspnoea as a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity. Dyspnea, also referred to as shortness of breath or breathlessness is one of the commonest reasons a patient seeks medical attention. The sensations associated with dyspnea range from a slight awareness of breathing to severe respiratory distress and may be mixed with anxiety in severe cases.

SUBJECTIVENESS OF DYSPNEA Dyspnea is often difficult to evaluate as I is highly subjective in nature. The sensation of dyspnea is mainly made up of two components: 1. Sensory input to the cerebral cortex Multiple sources of sensory information from mechanoreceptors in the upper airway, thorax, and muscles integrated in the central nervous system are sent to the sensorimotor cortex in the brain. Thus, the sensation of dyspnea depends on the intensity of the input from the thoracic structures and from the chemoreceptors. It varies directly with ventilatory demand such as exercise and inversely with ventilatory capacity. 2. Perception of the sensation Perception relies on the interpretation of the information arriving at the

sensorimotor cortex and interpretation is highly dependent on the psychological makeup of the person. Dyspnea is a symptom-what the patient feels. A patient may have labored and rapid breathing and deny feeling short of breath. Conversely, a patient may appear to be breathing comfortably and slowly and might still complain of breathlessness.

CAUSES OF DYSPNEA Dyspnea is most often related to pulmonary or cardiac diseases but it is also seen with haematologic, metabolic, chemical, neurologic, psychogenic and mechanical disorders. The clinical types of dyspnea will be as follows: a) Physiologic dyspnea Often associated with exercise, acute hypoxia as in high altitude, breathing high concentration of CO2 in a closed space. Awareness of increased ventilation. Confusion and unconsciousness may occur if the space is devoid or short of O2 b) Restrictive pulmonary dyspnea Often associated with pulmonary fibrosis, chest deformities, pleural effusion, pneumothorax Comfortable at rest Intensely dyspneic when exertion nears patients limited breathing capacity c) Obstructive pulmonary dyspnea Associated with asthma, obstructive emphysema, COPD Increased ventilatory effort Dyspnea is present at rest; breathing is labored and retarded especially during expiration d) Cardiac dyspnea Associated with congestive cardiac failure, pericardial effusion Presence of signs like orthopnea, paroxysmal nocturnal dyspnea, cardiac asthma, periodic respiration

e) Circulatory Associated with chronic anemia, exsanguinating haemorrhage, CO poisoning Dyspnea is present only on exertion unless anemia is severe. Air hunger is a grave sign

f) Chemical Associated with Uremia, kidney failure, hepatic coma,

thyrotoxicosis Dyspnea with severe panting caused by acidosis, heart failure, pulmonary oedema and anemia g) Neurologic Associated with head injury, cerebral lesions like CVA, brain tumour Characterised by hyperventilation, Biots respiration Noisy and stertorous breathing

h) Psychogenic Often seen as pain-related dyspnea, hysterical over breathing, seen in anxiety Continuous hyperventilation or deep sighing respiration at maximal depth. i) Mechanical Associated with chest wall deformities, diaphragmatic paralysis, massive ascites, tumour, pregnancy and obesity

In most dyspneic patients, there is obvious clinical evidence of either cardiac or pulmonary conditions. Like patients with cardiac dyspnea, patients with chronic obstructive lung disease may also waken at night with dyspnea, but, as pointed out above, this is usually associated with sputum production; the dyspnea is relieved after these patients rid themselves of secretions. The difficulty in the distinction between cardiac and pulmonary dyspnea may be compounded by the coexistence of diseases involving both organ systems.

Dyspnea may be acute or chronic, progressive, recurrent, paroxysmal or periodic. Acute dyspnea, in children, is most frequently associated with

asthma, epiglottitis, croup and bronchiolitis. In adults the causes can be asthma, chest trauma, pleural effusion, pneumonia, pulmonary oedema, pulmonary embolism, spontaneous pneumothorax, ARDS, upper airway obstruction in the form of aspirated foreign body or laryngospasm. Chronic dyspnea is almost always progressive in nature. It begins with dyspnea on exertion and over time progresses to dyspnea a rest. The common causes that lead to chronic dyspnea are asthma, congestive cardiac failure, left ventricular failure, cystic fibrosis, pleural effusion, interstitial lung disease, COPD, severe anemia, psychogenic dyspnea and chest wall deformities.

DESCRIPTION AND TERMS ASSOCIATED WITH DYSPNEA

Patients may often complain of dyspnea occurring at certain times of the day, or aggravating on assuming a certain position or during a specific phase of the respiratory cycle. There are a few terms that we need to be aware of when we talk about dyspnea as the patients complaints will often feature them. Inspiratory dyspnea is usually associated with upper airway obstruction and expiratory dyspnea occurs with obstruction of smaller bronchi and bronchioles. Bradypnea denotes less than normal rate of breathing whereas tachypnea indicates rapid rate of breathing. Hypopnea indicates decreased depth of breathing and hyperpnea indicates increased depth of breathing with or without an increased rate. Orthopnea is the inability to breathe when lying down. It is most commonly seen in patients with left ventricular failure and occurs when reclining causes accumulation of fluid in the lungs. Trepopnea is dyspnea caused by lying on one side but does not occur when the patient switches sides. It is often associated with unilateral chest disorders like unilateral pleural effusion or unilateral airway obstruction, bronchiectasis. Platypnea is dyspnea caused by upright position and relieved by recumbent position. Orthodeoxia is arterial oxygen saturation produced by assuming an upright position and relieved by returning to recumbent position. Both platypnea and orthodeoxia are seen together in patients with congenital heart diseases (right-to-left intracardiac shunts) and in patients with venous-

to-arterial shunts in severe lung or liver diseases (cirrhosis). Paroxysmal nocturnal dyspnea (PND) has a strong predictive value for congestive heart failure. The patient usually falls asleep in the recumbent position and awakens, 1-2 hours later, with acute shortness of breath. The patient sits upright on the side of the bed or gets relief after breathing some fresh air. PND occurs due to the transfer of fluid from the extravascular tissues into the blood stream during sleep. It normally takes about 30 minutes for the patient to get some amount of relief and hence the patient must sit up or stand up and ambulate. Functional dyspnea is defined as shortness of breath at rest but not during exertion. It is most commonly seen in young women and usually reassurance is all that is necessary. No unusual findings in the physical examination and pulmonary function tests.

MECHANISMS OF DYSPNEA
The sensation of dyspnea seems to originate with the activation of sensory systems involved with respiration. Sensory information is, in turn, relayed to higher brain centers where central processing of respiratory-related signals

and contextual, cognitive, and behavioral influences shape the ultimate expression of the evoked sensation. The homeostatic systems involved in the regulation of respiration provide a framework for understanding the mechanisms of dyspnea.

Respiratory Control System

Respiratory motor activity emanates from clusters of neurons in the medulla. Efferent respiratory discharges activate the ventilatory muscles that expand the chest wall, inflate the lungs, and produce ventilation. The resulting breathing regulates the oxygen and carbon dioxide tensions and hydrogen ion concentration in the blood and body tissues. Chemoreceptors in the blood and brain as well as mechanoreceptors in the airways, lungs, and chest wall are involved in the automatic regulation of the level and pattern of breathing. Changes in PCO2 and PO2 are sensed by central chemoreceptors in the medulla and peripheral chemoreceptors in the carotid and aortic bodies. Signals from these chemoreceptors are transmitted back to brainstem respiratory centers that adjust breathing to maintain blood-gas and acid-base homeostasis. Afferent impulses from vagal receptors in the airways and lungs also exert important influences on the level and pattern of breathing. Pulmonary stretch receptors are stimulated as the lung expands; irritant receptors around the epithelial cells of the bronchial walls are activated by tactile stimulation in the bronchial mucosa, high rates of air flow, and increases in bronchial smooth muscle tone; and C fibers, found in the interstitium of the lung in proximity to the alveoli and pulmonary capillaries, respond to increases in pulmonary interstitial and capillary pressure.

Feedback

of

afferent

information

from

lung

and

chest

wall

mechanoreceptors provides respiratory motor and pre-motor neurons with important information regarding the mechanical status of the ventilatory pump as well as changes in length and force of contraction of the respiratory muscles. These signals allow adjustments to be made in the level and pattern of brainstem respiratory motor activity to compensate for changes in respiratory muscle function or ventilatory system impedance. Chemoreceptor

as well as lung and chest wall mechanoreceptor afferents may also project to higher brain centers to provide a direct appraisal of the chemical milieu of the body and of the mechanical status of the ventilatory apparatus. Additionally, and very importantly, corollary signals or efferent copies of brainstem respiratory center motor output appear to be transmitted to higher brain centers and result in a conscious awareness of the outgoing motor command. These may all play an important role in shaping the sensation of dyspnea.

PHYSIOLOGICAL MECHANISMS

Respiratory motor command corollary discharge There is a conscious awareness of the outgoing respiratory motor command to the ventilatory muscles. This sense of respiratory motor output is attributed to a corollary discharge from brainstem respiratory neurons to the sensory cortex during automatic reflex breathing or from cortical motor centers to the sensory cortex during voluntary respiratory efforts. Evidence for corollary discharges is functional rather than structural and they are important in shaping the sense of respiratory effort, which intensifies with increases in central respiratory motor command and is proportional to the ration of the pressures generated by the respiratory muscles to the maximum pressuregenerating capacity of those muscles.

Chest wall receptors Projection to the brain of afferent signals from mechanoreceptors in the joints, tendons and muscles of the chest all play a role in shaping respiratory sensations. Afferents from intercostal muscles have shown to project to the cerebral cortex and contribute to proprioception and kinesthesia.

Pulmonary vagal receptors Afferent information from pulmonary vagal receptors project to the brain, and vagal inputs are important in shaping the pattern of breathing. There

is some evidence that vagal influences, independent of any effect on the level and pattern of breathing, may also contribute to the sensation of dyspnea. Vagal receptors may contribute to the unpleasant sensations that result when thoracic expansion is limited and to the dyspnea that accompanies breathholding. Vagal blockade ameliorates dyspnea during exercise and alleviates unpleasant sensations during breathholding. Dyspnea associated with bronchoconstriction is in part mediated by vagal afferents.

Chemoreceptors The dyspnea associated with hypercapnia and hypoxia is largely the result of the chemically induced increases in respiratory motor activity. Sensation of dyspnea may also be directly affected by inputs from chemoreceptors. Relief of exercise-induced hypoxemia by the administration of oxygen results in a reduction of dyspnea out of proportion to the reduction in ventilation.

PATHOPHYSIOLOGY OF DYSPNEA Dyspnea results from a disassociation or a mismatch between central respiratory motor activity and incoming afferent information from receptors in the airways, lungs and chest wall structures. The afferent feedback from the peripheral sensory receptors may allow the brain to assess the effectiveness of the motor commands issued to the ventilatory muscles. When changes in respiratory pressure, airflow or movement of the lungs and chest wall are not appropriate for the outgoing motor command, the intensity of dyspnea is heightened. Therefore, a dissociation between the motor command and the mechanical response of the respiratory system may produce a sensation of respiratory discomfort. Campbell and Howell put forth this theory in the 1960s by using the principle of length-tension inappropriateness. This theory has been generalized to include information arising in the ventilatory muscles and from receptors throughout the respiratory system and has been termed as neuro-mechanical and efferent-reafferent dissociation. Patients with mechanical load on the respiratory system, either resistive or elastic, or respiratory muscle abnormalities will have dissociation between the efferent and afferent information during breathing. This theory explains dyspnea associated with breathholding, the unpleasant sensation of air

hunger experienced by patients receiving mechanical ventilation with small tidal volumes and low inspiratory flow rates, and the discomfort of subjects who voluntarily constrain the rate and depth of their breathing.

Heightened ventilatory demand In normal individuals and in patients with lung diseases, the intensity of dyspnea increases progressively with the level of ventilation during exercise. This is attributed to the increase in respiratory motor output and a corresponding increase in the sense of effort. Many conditions give rise to ventilation that is excessive for the level of physical activity, and consequently cause symptoms of dyspnea. Increase in ventilation is required to compensate for the enlarged dead space that results from lung parenchymal and pulmonary vascular disease. Hypoxemia at altitude and in patients with respiratory disease stimulates arterial chemoreceptors and increases respiratory motor activity. This heightened motor command contributes to dyspnea. Early lactic acid production by skeletal muscles during exercise imposes an additional respiratory stimulus, increases the ventilation at a given level of exercise, and heightens exercise. This, along with the additional burden of advanced age, malnutrition and hypoxemia impair respiratory and peripheral muscle function and lead to limitations in exercise capacity secondary to leg discomfort and dyspnea. The cycle of dyspnea, reduced activity,

deconditioning and more dyspnea is well recognized as a key contributor to the functional decline associated with normal aging and cardiorespiratory illness.

Respiratory muscle abnormalities

Weakness or mechanical inefficiency of the respiratory muscles results in a mismatch between central respiratory motor output and achieved ventilation. This mismatch may explain the dyspnea experienced by patients with neuromuscular diseases affecting the respiratory musculature and patients with respiratory muscle fatigue. For instance, COPD is often characterized by overinflation of the lung and

overexpansion of the thorax. This results in an enlarged FRC and foreshortening of the muscles of inspiration. Based on length-tension properties of muscle, foreshortening of the inspiratory muscles may substantially reduce their force generating capacity. This impairment in the mechanical advantage of the inspiratory muscles contributes importantly to symptoms of dyspnea. Thus, inspiratory muscle shortening with hyperinflation reduces muscle mechanical efficiency.

Abnormal ventilation impedance

Respiratory diseases such as asthma and COPD which narrow airways and increase airway resistance, and diseases of the lung parenchyma, including interstitial pneumonitis and pulmonary fibrosis, which increase lung elastance, commonly cause dyspnea. When ventilatory impedance increases, the level of central respiratory motor output required to achieve a given ventilation rises. When the respiratory effort expended in breathing is out of proportion to the resulting level of ventilation, dyspnea results.

Abnormal breathing patterns

Dyspnea is common in diseases involving the lung parenchyma. It is possible that the rapid shallow breathing often noted in diseases of the lung parenchyma is a reflex response to the stimulation of pulmonary vagal receptors, but there is little direct evidence that pulmonary vagal receptors contribute directly to dyspnea. Pulmonary vagal receptors have been posited to play a role in the dyspnea of severe exercise, pulmonary congestion and pulmonary edema, and recurrent pulmonary embolism.

Blood-gas abnormalities

Blood-gas abnormalities, while among the most serious consequences of

cardiorespiratory disease, poorly correlate with dyspnea in individual patients. Hypoxemia causes respiratory motor activity to increase through

chemoreceptor stimulation. Hypoxia may also have a direct dyspnogenic effect. The dyspnea produced by hypercapnia is largely the consequence of increase in respiratory motor output but there also appears to be a direct effect of PCO2 on the intensity of dyspnea. In patient with chronic hypercapnia, metabolic compensation minimizes any changes in hydrogen ion concentration and consequently limits ventilatory responses and changes in respiratory sensation. The responses to changes in hydrogen ion

concentration may explain the dyspnea of diabetic ketoacidosis and renal insufficiency. The sense of increased work of breathing is a common feature in conditions characterized by dyspnea.

Psychological effects and higher brain center influence

People with dyspnea since a very long time often display anxiety and/or depressive symptoms. At the same time, anxiety, anger and depression can increase symptoms of breathlessness out of proportion to the impairment in cardiorespiratory function. The quality and intensity of dyspnea at a given level of respiratory activity are also thought to be shaped by patient experience, expectation, behaviour and emotional state. Patients who tend to be adaptive and independent tolerate ventilatory loads with relatively few symptoms of dyspnea. Others who are more dependent, anxious, and focused inordinately on their health may experience severe dyspnea with relatively small increases in ventilatory impedance.

DYSPNEA ASSESSMENT
The assessment of dyspnea is a critical part of patient evaluation and

management when cardiopulmonary disease is present. The gold standard for diagnosis and assessment of dyspnoea is the patients self-report. There is no other reliable, objective measure of the disorder. As dyspnea is highly subjective in nature, the patients description of their breathlessness gives the clinician clues about the underlying cause. For instance, patients with asthma tend to use the phrase, I feel a tightness in my chest. Patients with interstitial disease tend to state my breathing is too rapid whereas patients with congestive heart failure often describe their dyspnea as I feel like I am suffocating. Patients with COPD will often complain of not being able to take enough air in. Thus descriptions often can lead to a tentative diagnosis.

History A detailed history regarding the onset of dyspnea has to be taken, as it would help us distinguish between acute or chronic dyspnea. The duration and frequency of dyspneic attacks needs to be asked. The factors that aggravate or relieve dyspnea has to be asked and analysed. The other things to be asked to the dyspneic patient are: Diurnal variation in the episodes of dyspnea Positional variation affecting dyspnea Associated factors Severity of breathlessness

Apart from the description of the symptoms, occupational and personal history also gives a clinician, insights on the possible causes of dyspnea.

Standard spirometry and lung volume and capacity measurements help in distinguishing patients with restrictive pulmonary disease or obstructive pulmonary disease. There is a not so well substantiated claim that dyspnea in a restrictive lung condition is more severe than dyspnea in an obstructive lung condition. Measurement of lung volumes by plethysmography or by gas dilution techniques assesses increase in the dead space which leads to greater ventilatory requirements. Reassessment of lung function following administration of an inhaled

bronchodilator can lead to diagnosis of reversible airway obstruction.

Measurement of gas diffusion can be useful because a decreased diffusing capacity is associated with arterial desaturation, which is commonly found in patients with interstitial lung disease or emphysema, resulting in hypoxia or hypercapnia, thereby leading to distressing urge to breathe. Arterial oxygen saturation can be easily measured by using pulse oximetry. Determination of hypercapnia requires arterial blood sampling. Mixed venous measurement is also infrequently done.

The clinician might also incorporate co-morbid conditions as well as psychological status in the evaluation of significance of symptoms.

The frequent discrepancy between severity of disease and intensity of breathing discomfort has generated attempts to standardize the conditions under which the subjective symptoms are evaluated. Thus, in 1952, Fletcher first published a five-point rating scale which was employed by the Pneumoconiosis Research Unit to rate the impact of dyspnea on activities. A revised version of the scale was published later on, to rate the impact of dyspnea while either walking distances or climbing stairs. This questionnaire is now widely known as Medical Research Council (MRC) Scale.

The Oxygen Cost Diagram is a scale designed to rate activities on a continuum according to the number of calories expended in the performance of the activity. It is a 100 mm vertical visual analogue scale with 13 activities listed at various points along the line corressponding to increasing oxygen requirements for their completion, ranging from sleeping to brisk walking uphill. The potential limitation of the above scales is that they focus on a single dimension provoking dyspnea i.e. magnitude of task. In order to correct this deficiency, Mahler developed the Baseline Dyspnea Index to meausre breathlessness at a single point in time. It is administered during a brief interview and includes measurement of functional impairment and magnitude of effort. It is used to rate a patients dyspnea on each dimension on a scale ranging from o (no impairment) to 4 (extraordinary or severe). The Transition Dyspnea Index was devised to measure changes from an initial baseline state.

The University of California at San Diego Shortness of Breath

Questionnaire (UCSDQ) is a 24-item questionnaire measuring dyspnea during the past week. In the modified version, patients are asked about the frequency of dyspnea when performing 21 different activities on a six-point rating scale.

Despite the advances implicit in these measures, there are recognized limits associated with the assessment process. Most importantly, because the intensity of dyspnea associated with ambulatory activity depends on the rate of work performance (power output), patients may reduce the rate of work performance and thereby minimize the intensity or distress of symptoms. The metabolic cost of ambulatory work increases with the patients weight. Hence, modest ambulatory activity may be associated with dyspnea in obese subjects. Common degenerative diseases associated with aging decrease the efficiency of ambulation. Neural conditions associated with spasticity increase the metabolic cost of activity and thereby increase the ventilatory demands. Arthritis of the hip may also alter the efficiency of walking. The established measures correct some of these limitations but do not deal directly with the suspicion that patients may evaluate their work performance optimistically. To assess symptoms more directly, dyspnea has been evaluated during performance of supervised tasks (e.g., cycle ergometry, 6-min walk, methacholine challenge). In these instances, ratings of dyspnea are obtained from patients at the time of the intervention so breathlessness can be related directly to one or more cardiac or respiratory responses.

Exercise testing is also an important explanatory diagnostic investigation that helps in calculating maximal exercise ventilation to maximal voluntary ventilation ratio, which is used to determine the ventilatory reserve during exercise. The measurement of breathlessness during exercise can be examined in relation to workload, power production, maximal oxygen uptake or interactions among a range of respiratory related variables. The ventilatory capacity measured prior to exercise and ventilation

measured during exercise are related to the intensity of dyspnea using the Borg Scale, Modified Borg Scale or Visual Analogue Scale.

Dyspnea and Quality of Life

Quality of life measures are designed to measure how patients function physically, emotionally, socially and occupationally in their day to day lives as a result of their cardiopulmonary disease. Questionnaires of this type usually appraise dyspnea within the context of a disease that interferes with the patients life.

The Chronic Respiratory Disease Questionnaire (CRQ), developed by Guyatt and colleagues is a 20-item questionnaire evaluating four dimensions of illness: dyspnea, fatigue, emotional function, and mastery. The CRQ is administered by an interviewer and requires 1525 min to complete initially; less time is required for subsequent administrations. To evaluate dyspnea, each patient is asked to select the five most bothersome activities that elicited breathlessness during the last 2 wk. After the patient determines the five most important activities affecting daily life, the severity of breathlessness is determined on a seven-point

scale.

The Saint George Respiratory Questionnaire (SGRQ) is a selfadministered 76-item questionnaire measuring three areas: symptoms, activity, and impact of disease on daily life. Administration time is 20 min. Dyspnea is not evaluated specifically but rather included in the symptom category along with information about cough, sputum, and wheezing.

The Pulmonary Functional Status and Dyspnea Questionnaire (PFSDQ) is a self-administered questionnaire that takes 10 to 15 min to complete, and measures both dyspnea and functional status

independently. The patient assesses his/her ability to perform various activities as well as the amount of associated dyspnea. Dyspnea is also evaluated with three general appraisal questions that create global dyspnea scores that are separate from the score for dyspnea with activity.

The Pulmonary Functional Status Scale (PFSS) is a selfadministered questionnaire measuring the mental, physical, and social functioning of the patient with COPD (119). The PFSS requires 20 min to complete; dyspnea ratings are obtained in relation to several activities and reflected in a dyspnea subscale.

MANAGEMENT OF DYSPNEA

MEDICAL MANAGEMENT

The therapeutic goal of symptomatic management of dyspnea is to relieve the patients sense of the effort of breathing.

Opiods are the first line of therapy for symptomatic control of dyspnea. Opioids decrease exercise-induced dyspnoea and increase exercise tolerance in patients with dyspnea. A typical opioid regimen to control chronic dyspnoea includes both a sustained-release opioid for baseline control and an immediate-release opioid for breakthrough dyspnoea. Opioid receptors have also been identified throughout the tracheobronchial tree, with the highest concentrations in alveolar walls.24 Nebulised opioids, at doses thought to have negligible systemic absorption, have been reported to relieve dyspnoea.

Untreated opioid side-effects, such as constipation, lethargy, and nausea, can affect quality of life. If needed, stimulants (for example, methylphenidate) and antidopaminergic antiemetics (such as prochlorperazine) can be prescribed to control adverse effects for the short term.

Anxiolytics Anxiolytics (such as benzodiazepines) are commonly prescribed for anxiety related to dyspnoea. Treatment of anxiety does have a role in a subset of patients for whom it is a prominent component of the distress. For these patients, benzodiazepines can be safely prescribed at appropriate doses, prescribed in conjunction with opioids without fear of respiratory depression when guidelines are followed. The tranquilliser chlorpromazine and buspirone, a non-benzodiazepine anxiolytic, have been reported to decrease dyspnoea.

Oxygen can reverse hypoxaemia. If this feature is the cause of dyspnoea, oxygen may be the only therapy required. Although there is probably a placebo effect of oxygen and the medical symbolism inherent in its administration, there may be other explanations for its effectiveness. Cool air blowing on the face reduces dyspnoea. Several studies support the hypothesis that stimulation of the trigeminal nerve has central inhibitory effects on dyspnoea. Thus, part of oxygens effect may be due to this sensory

stimulation rather than correction of hypoxaemia or a pure placebo effect. Thus, cool, moving air is a possible option for all dyspnoeic patients.

Apart from symptomatic treatment, the underlying cause of dyspnea needs to be managed appropriately. For instance, bronchodilators incase of airways narrowing or antibiotics in case of respiratory infection or ani-inflammatory agents for inflammation of the respiratory tracts. Steroids have also found to be useful in relieving dyspnea. Inhaled 2 adrenergic agonists, inhaled anti-cholinergics and sustained release

theophylline have all shown to have reduced dyspnea in various trials conducted PHYSIOTHERAPY MANAGEMENT

Various relaxation positions are first taught to the patient to help him relieve dyspnea in case of an acute exacerbation.

Breathing retraining including diaphragmatic breathing and pursed lip breathing has been advocated to relieve dyspnea in patients with obstructive

lung diseases.

Exercise training

Targeted high-intensity exercise training has been shown to improve aerobic capacity and reduce the rate of rise in lactate levels with an attendant reduction in patients with moderate COPD. Controlled studies have shown that exertional dyspnea decreases and exercise tolerance improves in response to exercise training, even in patients with advanced disease.

Supplemental oxygen during exercise

Supplemental oxygen in patients with chronic lung disease can also result in reductions in blood lactate and VE in patients with chronic lung disease. Oxygen may improve ventilatory muscle function so that less efferent stimuli

to breathe is required for any level of VE.

Vibration

The mechanism by which chest wall vibration improves dyspnea is unclear, but the effect is proposed to be from direct influence of afferents from the intercostal muscle spindles on higher brain centers, reflex suppression of brainstem respiratory output, or a decrease in the sense of effort. Studies have demonstrated that application of vibration to intercostal muscles reduced dyspnea in normal control subjects made breathless with an inspiratory resistive load, hypercapneic COPD patients who were dyspneic at rest, and patients with COPD who were made acutely hypercapneic.

Continuous positive airway pressure Low levels of continuous positive airway pressure (CPAP) have been shown to relieve dyspnea during acute bronchoconstriction in asthma, in patients weaning from mechanical ventilation, and during exercise in patients with advanced COPD.

Improving Inspiratory Muscle Strength and Endurance

Dyspnea has been related to weakness and fatigue of respiratory muscles. As previously mentioned, COPD is characterized by hyperinflation, a condition in which the respiratory muscles must function at a mechanical disadvantage. Thus, their ability to generate pressure can fall. If the pressure generated by the inspiratory muscles per breath approaches the maximum pressure that can be achieved, dyspnea worsens. Reduction of ventilatory demand and impedance will ultimately enhance respiratory muscle function, but specific strategies to maintain or improve respiratory muscle function can add to overall dyspnea abatement.

Inspiratory Muscle Training

Because of the association between respiratory muscle dysfunction and dyspnea, an improvement in respiratory muscle function with inspiratory muscle training (IMT) could lead to a reduction in dyspnea. IMT with resistance breathing leads to decrease in levels of dyspnea.

Education

Practitioners of pulmonary rehabilitation generally believe that education about disease and its treatment provide patients with tools for understanding and controlling their symptoms, especially dyspnea. The benefit of education for the treatment of dyspnea has been established for patients with asthma.

Desensitization Desensitization, or exposure to greater than usual sensations of dyspnea in a safe environment, has been theorized to increase a patients self-efficacy for coping with a symptom and potentially heighten the perceptual threshold. The precise mechanism behind these changes in dyspnea, independent of changes in E, is unknown. It is possible that exercise in a monitored and supportive environment may enable patients to overcome apprehension, anxiety, and/or fear associated with exertional dyspnea. Exercise training has been proposed as the most powerful means of desensitization to dyspnea.

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