Pulmonary Disease in Elderly

Dr S.K.Jindal

                                                          It is only recently that health problems of the elderly have drawn our more active attention in this country. The number of people beyond 65 years of age have significantly increased in the last one or two decades or so. This is partly because of the increase in the total population and partly because of an increase in life span. Many individuals who earlier used to die young, now live longer into old age. This has obviously happened because of the general improvements in socio-economic standards and health care. As a result, one sees more and more elderly people in the hospitals seeking solutions for their health problems.

                                                                        The issues related to health care of elderly have evoked great interest of internists and the specialists. Old age is one special area of medicine which is rather specialized for handling. Yet one needs to manage an old person as a general physician more often than a specialist.

                                                                        All body systems including the respiratory tract age with time. But the different alterations which occur in one particular system (e.g. respiratory) are also reflected in the functioning of the other. This is particularly true in old age.

                                                                        The anatomical and physiological alterations which take place with age not only affect the normal functioning of respiratory system but also the occurrence and course of different diseases. It is important to discuss the different age related changes before we deliberate upon diagnosis and management of diseases.

                Age-related changes in Respiratory System

 I. Structural changes

1. Lung elasticity: The two major tissues of lung parenchyma affected by aging are lung elastin and collagen. Due to changes and loss of elastin, there is loss of elasticity resulting in alveolar dilatation, lung hyperinflation and inadequate deflation. Lungs therefore become voluminous and rounded in shape  an appearance similar to that of emphysema. It is for this reason that the terminology senile emphysema got popular although the lungs are not emphysematous in true histological sense.

                                                                    There is also a progressive increase in respiratory bronchioles and alveolar ducts   ductectasia. But the alveolar septae become shortened and flattened causing a decrease in the surface to volume ratio. Collagen, which is metabolically inert, is present in abundance in lungs. Due to an increase in the number of cross-links between sub-units of collagen, there is increased rigidity.

2. Changes in chest wall: There is sclerosis and calcification of joints of ribs with sternum and spinal column. In addition, osteoporosis of vertebrae may cause kyphosis. The chest wall changes decrease its compliance limiting chest expansion. Changes in compliance of lung parenchyma and chest wall take place in opposite directions. Since the increase in chest wall rigidity is far more than the decrease in lung elastic recoil, the overall change is that of a decrease in compliance of the respiratory system, causing increased work of respiratory muscles.

3. Respiratory muscles: Respiratory muscles atrophy with age causing decrease in respiratory muscle strength and endurance. Both maximal inspiratory (Pimax) and expiratory (Pemax) pressures decrease in both sexes. There is a marked inter-individual variability in respiratory pressures. Physically active individuals have greater muscle endurance because of the training effects.

4. Miscellaneous changes: There are some alterations in respiratory control i.e. a diminished responsiveness to hypoxaemia and/or hypercapnia. This could further be attributed to changes in function of the peripheral chemo-receptors or the respiratory centre or both.

                                                          Alterations in pulmonary circulation are generally mild. There is a minor increase in pulmonary vascular resistance and pulmonary artery wedge pressure during exercise. These changes have little physiological or clinical significance.

II. Functional changes

                                                                    Alterations of lung functions are important and clinically relevant. There is a gradual decline in vital capacity (VC) and forced expiratory volume in first second (FEV1). On the other hand, the residual lung volume, functional residual capacity (FRC) and the total lung capacity are increased. These changes indicate some degree of air trapping in the lung. The air flows are reduced and the percent ratio of FEV1 to VC may also be low. Total airway resistance at FRC does not change but the significant increase which occurs in the peripheral airway resistance is compensated by a decrease in central airway resistance.

                                                                        There is a gradual decline with age of diffusion capacity (DLCO) of the lungs. Both the membrane component (Dm) and pulmonary capillary blood volume (VC) decrease but the decline in Dm is greater. Low DLCO along with increased ventilation   perfusion mismatching cause an age-related fall in arterial oxygen pressure (PaO2). The alveolar oxygen pressure (PAO2) remains unaltered but the alveolar arterial oxygen gradient (PA-aO2) is increased. There are no alterations in either PaCO2 or pH of arterial blood.

                                                                    Besides the functions of other organ systems, exercise, sleep, psychological and sexual activities also alter with age and affect the functioning of respiratory system either directly or indirectly. Exercise capacity is decreased and sleep disturbed. The diminished gastrointestinal motility, limited neurological responses, diminished cardiac output and increased dysfunction, all affect the normal functions of respiratory systems, occurrence of diseases and their management strategies.

III. Impaired Defence Mechanisms

                                                                    Both the local and systemic defence mechanisms are altered in old age. There is impairment of cough and other respiratory reflexes. Mucociliary function of the respiratory tract is depressed and the clearing of aspirated particles is delayed. The immunological defences involving different cells including the lymphocytes and macrophages are altered. There is decreased phagocytosis and microbial killing by the macrophages. Both antigen presentation and cytokine production are impaired. In view of the impairment of both non-immunological and immunological mechanisms, the chances of occurrence of respiratory infections are increased and their resolution delayed.

Respiratory disease in elderly

                                                                    In addition to the above listed factors which predispose to disease occurrence, there are several other variables which influence the clinical spectrum and behaviour of different respiratory diseases. The cumulative effect of exposure to different disease-producing agents which has taken place in the preceding years, becomes manifest. Tobacco smoking, occupational and environmental exposures are important examples of some of these exposures. Similarly, the presence of comorbid conditions such as diabetes mellitus, hypertension and other cardiovascular diseases, presence of gastrointestinal and neurological illnesses affect the occurrence and management of respiratory diseases.

Specific Diseases

I. Infections

1. Pneumonia: Pneumonia is the most frequent respiratory infection of old age. The factors predisposing to respiratory infection have been listed earlier. Pneumococcal pneumonia is perhaps the commonest form of community acquired pneumonia. Nosocomal pneumonia in hospitalized patients occur due to Klebsiella and other Gram negative bacilli or sometimes, staphylococci.

                                                                        Haemophilus influenza, influenza, other viral and mycoplasma pneumonias are also common especially in patients with chronic obstructive pulmonary disease (COPD). Both viral and bacterial pneumonias constitute an important cause of increased morbidity and mortality.

                                                                        Diagnosis of pneumonia is suspected from the clinical picture of fever, increased malaise, fatigue and weakness, cough with or without sputum production and/or hemoptysis. Diagnosis is established on presence of polymorphonuclear leucocytosis and chest roentgenological findings. Sputum should be examined by Gram’s staining and culture. If sputum is not available, or patient shows poor (or no) response to treatment, bronchoscopic examination or other invasive procedures may be required to obtain material for microbiological investigations.

                                                       Treatment is administered with antibiotics and other supportive measures. Choice of antibiotic depends upon the causative organism which is either established or suspected.

2. Tuberculosis: Old age is particularly susceptible to tuberculosis. It is mostly reactivation of a previously quiescent tubercular focus due to a recent insult or impairment of immunological defences which causes active tuberculosis. Primary tuberculosis due to reinfection may also occur. Symptoms are relatively fewer and physical examination nonspecific. Tuberculin test cannot be relied upon in view of its being positive in over 50 percent of healthy population of this country. Moreover, it is frequently negative in old age even in the presence of an active disease.

                                                                      Diagnosis of tuberculosis is generally made on clinical features and roentgenological appearances of upper lobe infiltrates with/without cavitation, or a diffuse miliary pattern. Sputum, if available, offers the best choice for diagnosis. Smear examination if repeated thrice, is likely to be positive in upto 60 percent of patients with active tuberculosis. Many a patients either do not produce sputum or are unable to cough it out. Bronchoscopy is helpful in such cases and examination of bronchial secretions offers an additional positivity of about 20 to 30 percent. Transbronchial lung biopsy is of great help in patients with diffuse miliary disease.

                                                                    Tuberculosis is managed on similar lines as in any other case. The initial intensive phase involves administration of four potent drugs (isoniazid, rifampicin, pyrazinamide and ethambutol) for two months followed by four months of isoniazid and rifampicin. Aminoglycosides such as streptomycin and amikacin are avoided in old age. Similarly, ethambutol dosage should not be high and duration not prolonged for fear of ocular toxicity. It may not always be easy to monitor for visual field defects in old age.

3. Fungal and parasitic infections: These are more likely to occur in immuno-compromised patients such as those with diabetes mellitus or malignancies and those on immunosuppressive drugs, such as corticosteroids, for other indications. Aspergillosis, Cryptococcosis and histoplasmosis are important fungal infections. Diagnosis and management are done on similar lines as in other categories of patients.

II. Chronic Obstructive Pulmonary Disease (COPD)

                                                            COPD characteristically starts in middle or past middle age and progresses slowly. A patient who has developed the disease at about 50 years of age, therefore, is likely to have a well established and advanced disease by the time he reaches 65 years or over. He is severely disabled because of breathlessness and suffers from frequent exacerbations due to recurrent infections and other complications.

                                                            COPD encompassing chronic bronchitis and emphysema, occurs most often in chronic and heavy smokers. Old age by itself does not cause COPD although the structural and functional alterations which take place with age, do contribute to lung function impairment, disease morbidity and mortality. Senile emphysema, a term which connotes age related emphysema is more a misnomer, than a disease. It only implies the presence of hyperinflated lungs due to increased elasticity. There is no true alveolar destruction unless the individual resorts to smoking which is likely to initiate true emphysematous changes and accelerate lung function decline.

                                                                        Dyspnoea is a common symptom in the elderly even in the absence of COPD. This, in part is a general symptom and in part, related to increased cardio-respiratory demands. With aging, there is progressive worsening of cardiac disorders contributing to dyspnoea. It is worse if there is associated obesity, which is not uncommon in old age. Obesity causes increased work of breathing and respiratory muscle weakness.

                                                                        Diagnosis of COPD is relatively simple. Clinical features and chest roentgengraphy, further aided by spirometric measurements are fairly diagnostic. Electrocardiography, echocardiography and sometimes exercise testing are required for cardiopulmonary assessment. Blood gas measurements are required to diagnose the presence and severity of respiratory insufficiency. COPD is managed with general advice of stopping smoking, bronchodilators, expectorants and treatment of infections. For long term rehabilitation programmes, inspiratory muscle training and general exercise reconditioning are very useful. Domiciliary, long term oxygen therapy has been shown to benefit most such patients.

                                                          Acute exacerbations and respiratory failure are managed more actively with antibiotics, increased oxygen administration and other supportive therapy. Endotracheal intubation and a short period of assisted ventilation may be required in a severely hypoxic and hypercapnic patient.

                                                                    It is better to manage these patients conservatively rather than aiming to achieve normal blood gas values. Mechanical ventilation, even if required, should be weaned off as early as possible. When prolonged, there develops respiratory muscle weakness and dependence on assisted ventilation. Unfortunately, we do not have a back up system of domiciliary care to provide home ventilation and other supports. Invariably therefore, a prolonged period of assisted ventilation becomes a source of an unending agony and misery to the patient and the family. It also burdens severely the already strained public health services in most instances.

Bronchial Asthma

                Chronic airways obstruction in old age is more often caused by COPD but can occasionally be attributed to asthma which is either present from younger age or rarely starts de novo at old age. Asthma in the elderly needs to be differentiated from other causes of wheezing of which COPD is the most important. Left heart failure, pulmonary thromboembolism and central airway obstruction due to lung tumours are some other important causes.

                                                                        Eosinophilic syndromes, bronchial carcinoids or foreign body aspiration may also simulate a clinical picture of asthma. Early recognition of asthma is important for efficient management. Asthma in the elderly is relatively poorly tolerated and requires more aggressive management requiring hospitalization earlier than late. An acute episode can prove to be fatal unless managed in time.

                                                            Bronchial hygiene is of particular interest in the elderly especially in the presence of airways obstruction. In view of the impaired defence mechanism, poor reflexes and weak respiratory muscles, an elderly patient is unable to cough and expectorate effectively. Bronchial secretions, being viscid and thick, may block respiratory passages and rapidly cause pneumonia and respiratory failure. Nebulization of bronchodilators and mucolytic agents and maintenance of hydration are important in liquefying the secretions. Parenteral corticosteroids and antibiotics are also required for acute exacerbations.

                                                                    Respiratory physiotherapy is important to maintain bronchial patency. Expulsive coughing and other chest physical therapy (CPT) procedures such as chest percussion and vibration are helpful.

III. Lung Tumours

                                                                    Both primary and metastatic lung tumours are common. Metastases may arise from cancers of breast, gastrointestinal tract, kidneys and urinary bladder, prostate and genital tract. Primary Lung cancer occurs more commonly in the 6th and 7th decades of life. The mean age of lung cancer in India is reported to be lower (54-56 years) than in the West where it is above 65 years, in both males and females. There is evidence to suggest that the mean age of lung cancer is rising. In fact, the age incidence in India is similar to what was reported in the West some 40 years ago.

                                                                        There are some differences in the histological types of cancer amongst smokers and nonsmokers in patients above 40 years of age. Squamous cell is most common amongst smoker and denocarcinoma amongst the nonsmokers.

                                                                    Diagnosis of cancer poses special problems. Invasive investigations are often required for which the patient is generally hesitant. Management plans involving both surgical and nonsurgical treatments are also cumbersome and generally tiring for a old person. Both radio and chemotherapy are poorly tolerated. Above all, the results are not curative in most instances. It is therefore palliative treatment which is often resorted to.

IV. Miscellaneous respiratory problems

1. Primary alveolar hypoventilation

                                                                                            This may result from either a low perfusion state in the region of central respiratory chemo-receptors or the brain micro-infarcts. Both these changes are more likely in the aged. The syndrome is characterized by chronic arterial hypoxaemia and hypercapnia. The patient therefore, presents a picture simulating that of chronic cor pulmonale and respiratory failure.

2. Obesity hypoventilation syndrome

                                                                                            A clinical picture of chronic hypoxaemia and hypercapnia is seen in obese patients - obesity hypoventilation syndrome. The primary cause in this condition is decreased respiratory centre responsiveness due to alterations in hormonal function. Weight reduction and progesterone therapy is the treatment of choice.

3. Altered breathing

                                                                                            Cheyne-Stokes breathing is common in the elderly. It is characterized by regular cycles of gradually increasing and decreasing depth of respiration. It is perhaps because of hypoperfusion of the respiratory centre. Its presence in patients of congestive heart failure supports this mechanism.

4. Sleep apnoea syndromes (SAS)

                                                                                            Although sleep apnoea syndromes are not age-specific, they tend

to occur more commonly in the old because of the factors described earlier i.e. hypoperfusion, micro-infarcts, hormonal and neuromuscular changes. Both central and obstructive sleep apnoea may occur. There are frequent periods of apnoea or hypopnoea during sleep. This causes arterial oxygen desaturation and effects of hypoxaemia.

5. Pulmonary Aspiration

                                                                                Aspiration of gastric contents is common due to reduced levels of consciousness and gastroesophageal motility problems. This is even more likely in semiconscious and unconscious patients following strokes, seizures or other diseases concurrently present in the aged. While acute massive aspiration may prove to be fatal, pneumonia is a common sequelae of aspiration.

Dr S.K.Jindal, Professor & Head,

            Postgraduate Institute of Medical Education and Research,

Chandigarh, India.

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Lungs  in Pregnancy

                                                                                                                                                                                        Prof. S.K.Jindal

Introduction

                                                                     Pregnancy induces a number of alterations in anatomy and Physiology

which have got important pulmonary and cardiovascular consequences. some of the changes that occur during pregnancy are briefly described below. Airways: There occurs hyperemia, edema and hypersecretion in the upper airways during pregnancy. These changes can induce or aggravate nasal obstruction and obstructive sleep apnea syndrome. Respiratory Muscles & Rib Cage: Diaphragm is displaced upward but the excursion remains the same. The tone of the abdominal muscle decreases. Physiological Changes: The expiratory reserve volume decreases by 8-40% and residual volume reducers by 7-22%. The functional residual capacity therefore decreases by 10-25%. There is no change in vital capacity, total lung capacity and lung compliance. The total pulmonary resistance falls by 50% during pregnancy. There is rise in tidal volume by about 20% which causes an increase in minute ventilation.

Cardiovascular changes:

                                                            There is an increase in the heart rate and stroke volume, as a result the cardiac output increases. There is fall in the systemic and pulmonary vascular resistances during second trimester of pregnancy. Due to this fall in systemic vascular resistance, there is an increase in the level of aldosterone which induces an increase in plasma volume compared to red cell mass (This is responsible for physiological anaemia of pregnancy).

Dyspnoea during pregnancy:

                                                            About 40-60% of pregnant females complain of dyspnoea during pregnancy. Physiological hyperventilation of pregnancy is caused by altered chest wall muscle proprioception due to an increase in respiratory stimulation, physiological dyspnoea occurs early in the pregnancy and improves during labour and does not occur at rest. The important common pulmonary causes of dyspnoea during pregnancy are asthma, aspiration, pulmonary thromboembolism, pneumonia, amniotic fluid embolism and air embolism etc.

1. Asthma in pregnancy: If asthma is not controlled during pregnancy, it can increase the incidence of preterm labour and growth retardation. In various studies, it was shown that about  35% of cases of asthma will worsen, 30% will improve and rest will remain unaltered during pregnancy. Therapy of asthma during pregnancy does not differ from that in a non pregnant patient. If the patient is on oral or inhaled steroids, she should be started on parental hydrocortisone before labour.

2. Restructive lung disease during pregnancy: Most of the restrictive lung diseases constitute relative contraindications to pregnancy. However, if FVC is less than 1L, pregnancy should be avoided. The clinical course of sarcoidosis is not altered by pregnancy. However, pregnant patient of sarcoidosis who have stage IV disease, or have advanced age will have poor prognosis. In progressive systemic sclerosis with renal failure, the pregnancy should be avoided. Worsening of systemic lupus erythematosus is uncommon during pregnancy.

3. Deep venous and pulmonary thromboembolism: Pregnancy is a hypercoagulable state (venous stasis, increased clotting factors and decreased fibrinolytic activity. Heparin is the drug of choice for anticoagulation. Warfarin is given between 6-12 wks can produce embryopathy (stippled epiphyses, nasal hypoplasia).

4. Amniotic Fluid Embolism: I t presents as a sudden, unexpected shock during or after labour followed by respiratory distress. About 10-15% patients develop seizures and disseminated intravascular coagulation. The diagnosis is made on clinical grounds and confirmed by taking a sample from pulmonary artery and showing fat globules. Pathophysiologically, there is mechanical obstruction of pulmonary vasculature, increased alveolar capillary leakage and anaphylaxis due to foetal antigens. Management is largely supportive. Mechanical ventilation and diuresis may be required.

5. Pleural Diseases: During pregnancy due to increased blood volume, there is increased incidence of benign pleural effusion. Choriocarcinoma may metastasize to the lung or pleura producing haemorrhagic pleural effusion.

6. Pneumonia complicating pregnancy: The incidence of pneumonia is not increased during pregnancy. However, if pneumonia occurs, it can have progressive course. Mortality is increased due to : reduced lymphocyte proliferation, reduced cell mediated cytotoxicity and reduced lymphokine response.

Tuberculosis and pregnancy:

                                                                        Some studies have shown an increased incidence of relapse of tuberculosis during post partum period. In preantibiotic era, there was increased maternal mortality from untreated tuberculosis. Treatment of tuberculosis is similar to that of non pregnant patient. Streptomycin is contraindicated for fear of ototoxicity. Some studies have shown that use of Rifampicin during pregnancy can produce limb reduction, central nervous system abnormality and decreased prothrombin levels. But Rifampicin continues to be given during pregnancy.

Deptt. of Pulmonary Medicine, PGI Chandigarh

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Respiration & cardio-vascular system

The effect of Respiration on the cardio-vascular system 

                                                                                                                                                   Prof. S. K. Jindal

                                                                      The heart and great vessels are within the chest, and consequently are subject to the changes in intrathoracic pressure associated with respiration. The effects are relatively mild in the normal subject. These effects are easily observed at the beside as sinus arrhythmia, splitting of the second heart sound, and by small variations in the systolic blood pressure. Certain produce marked fluctuations in blood pressure with respiration: detection is essential for appropriate diagnosis and treatment. A review of this interaction physiology and pathophysiology is useful to emphasize the cardiovascular system as a complete circuit, separation the transient effects from the steady-state effects, and to clarify the concepts of venous return and cardiac output.

                                                                     In the steady-state, venous return and cardiac output are identical in volume per minute, although cyclical changes with respiration may affect one more than the other transiently. Considerations of a complete circuit also require that the changes in output of the right ventricle must be accounted for in the return to the left ventricle within a short time (1-2 beats). Similarly, the left ventricular output must be accounted for in the systemic venous return in a steady-state, although the transportation lag is substantially longer for the systemic transient changes in the left ventricular output may be delayed several seconds, and are generally more damped in appearance in the systemic venous return. Certain definitions are descriptions are important to consider before analyzing the effects of respiration on the cardiovascular system. First, it is helpful to bear in mind two types of vascular pressures. In analyzing the flow of blood around the circuit, the intravascular pressure relative to atmospheric pressure is used in determining pressure gradients. In considering the diameter of a cardiovascular chamber, the distending pressure must be considered.

                                                                     This is also called the transmural pressure, and is simply the internal pressure minus the pressure outside the wall. The transmural pressure should not be used in considering flow or pressure drop across part of the vascular bed. The transmural pressure is vital in determining the filling of cardiac chambers.

A. NORMAL RESPIRATION

                                                                     Pleural Pressure The force that lowers the intrathoracic pressure with inspiration is produced by inspiratory muscles, primarily the diaphragm and thoracic skeletal musculature. The inspiratory drop in pleural pressure is transmitted to all intrathoracic structures, including the heart and great vessels.

                                                                        If there were no change of volume in these chambers, the pressure could be transmitted quite faithfully, but flow usually continues into and out of the chamber, so that the intravascular pressure with not precisely reflect the fluctuations in intrathoracic pressure. This transmission of the intrathoracic pressure in utilized clinically by measuring the intrathoracic pressure via an esophageal balloon.

                                                                     Pericardial Pressure The pericardium forms the immediate milieu for the heart, and it transmits the pleural pressure accurately in its fluctuation with respiration, but as the heart fills, during diastole, the pericardial pressure will increase above the intrathoracic pressure. This difference is relatively small in the normal subject, but may be quite important in abnormal states, and when calculation ventricular function curves from filling pressure against stroke volume.

                                                            Venous Return The return of systemic blood to the right atrium is driven by pressure gradient from the systemic veins to the right atrium. The venous pressure outside the thorax is above atmospheric pressure and as he intrathoracic pressure fall with inspiration, the pressure gradient favoring flow into the thorax is enhanced. Since the pulmonary artery (upstream of the pulmonary veins) and the left atrium and left ventricle (downstream of the pulmonary veins) are all subject to the intrathoracic pressure, there should be little, if any, direct effect of inspiration on the pulmonary veins. Most of the change in flow in the pulmonary veins with inspiration results from transmission of the output from the right ventricle. Studies timing this relationship have shown that the major flow pulse from the right ventricle appears in the pulmonary veins in the same cardiac cycle.

                                                                     Consequently, the increased volume of the right ventricle with should appears in the pulmonary veins in the same cycle, and should be reflected increased left ventricular stroke volume after one or two beats. This is should be reflected in increased left ventricle would occur in the first one or two cardiac cycles after the onset of inspiration, since the lowest point in the right ventricular stroke volume cycle is just prior to the onset of inspiration. The enhanced right ventricular stroke volume does account for a commonly observed auscultator finding. With inspiration, the normal healthy young subject will demonstrate splitting of the second heart sound at the pulmonic area. This reflects the relative increase in the right ventricular stroke volume, which requires a greater ejection time, thereby delaying the pulmonic closure beyond that of the aortic valve, sufficiently to produce audible separation of the two closing sounds. (The aortic closure always precedes the pulmonic in the normal subject).

                                                                     Arterial Effects (After load) The intrathoracic blood vessels are exposed to the drop in pressure with inspiration of approximately 7 mmHg. For the left ventricle, the effective pump level drops by that amount, since the bulk of the systemic circulation is outside the chest, at atmospheric pressure. To maintain the same pressure in the peripheral circulation, an increase in pressure generated by contraction of the left ventricle would have to be developed. This slight increase in after load for the left ventricle has relatively little effect on the stroke volume of the left ventricle under normal conditions of respiration and circulation, but does account for the slight respiratory fall in systolic blood pressure that can be easily measured in the normal subject. By contrast, the right ventricle ejects into the pulmonary circulation within is entirely within the thorax and therefore the right ventricle experiences no change in after load.

                                                                        Reflex Effects In healthy subject at rest, inspiration is associated with an acceleration of the heart rate, and a deceleration occurs with expiration. This phenomenon, sinus arrhythmia, occurs under conditions of vagal control over the cardiac pacemaker, via neural radiation from the respiratory centre in the medulla to the cardiovascular centre. This has a major effect on stroke volume of the two ventricles, through changes in the filling interval for the ventricles. With inspiratory acceleration, the filling interval is diminished and the stroke volume for both ventricles becomes smaller. With sinus arrhythmia, the varying diastolic interval becomes the single most important determinant of the stroke volume, and effect of enhanced venous return are less obvious. When the subject is stressed, resulting in an increased sympathetic tone and diminished vagal tone, tachycardia results, and the variation of filling interval disappears. At that time, the effect on stroke volume of enhanced venous return to the right heart with inspiration is much more pronounced.

B. CARDIAC TAMPONADE

                                                                     Pleural Pressure During tamponade normal respiration persists, and the wings of intrapleural pressure do not change significantly, an average of 7 mmHg. Thus, in tamponade, the phenomenon of pulsus paradoxus (a drop in systolic blood pressure with inspiration of greater than 10 mmHg) cannot be attributed to a direct transmission of intrathoracic pressure.

                                                                        Pericardial Pressure The peak-to peak pressure change with respiration in the pericardium is exactly the same as the pleural pressure. However, since pericardium is distended with fluid, its overall pressure is substantially; elevated. This increased pressure reduces the transmural or distending pressure for the heart, and drastically interferes with filling of the two ventricles. The rise in pericardial pressure is not limitless, since all circulation will cease when the pericardial pressure rises above 20 mmHg. Near that point, all of the diastolic pressure throughout the heart will be similar, in both atria and both ventricles.

                                                                        The pericardial effusion does not shield the heart from the changing intrathoracic pressure of respiration, which is superimposed on the high pressures due to the tamponade. The pericardial pressure will also fluctuate with the cardiac cycle, to a much greater extent than the normal, since the pericardium is quite full, and small changes in volume will produce large changes in pericardial pressure.

                                                                     The pericardium is capable of a slow stretching, and if the fluid accumulates very slowly, the pressure will not necessarily rise, and sometimes a rather large effusion can be tolerated without tamponade and pulsus.

                                                                        Venous Return A high rate atrial pressure, as the downstream pressure of the systemic circulation, has a markedly inhibiting effect on systemic venous return. This is the case in tamponade, and shock is usually present with very high venous pressure. The 7 mmHg. Drop with normal inspiration is effective in temporarily increasing   venous return to the right heart. Since the stroke volume is   markedly limited by the limited diastolic filling, the enhanced venous return will make an obvious improvement in the stroke volume of the right ventricle with inspiration. After 1-2 beats, that stroke volume will appear in the left ventricular output, but that increase will be delayed by 2-3 beats from the onset of inspiration, and therefore systolic blood pressure will be at its lowest during inspiration.

                                                       The effect of inspiration on the pulmonary veins, as discussed under the normal circulation, is minimized by the fact that the pulmonary vein and the left heart are subjected to the same intrathoracic pressure. An earlier theory of pulsus paradoxus contended that the pulmonary veins actually pooled blood temporarily with inspiration, through an increased transmural pressure, whereas the left ventricle was shielded from the effects of inspiration by the pericardial effusion.

                                                                        Another theory explaining pulsus paradoxus that remains popular is that  the enhanced venous return to the right ventricle with inspiration successfully competes for the fixed volume available within the pericardium. With a fixed total volume, and increase in right ventricular filling would competitively inhibit left ventricular filling, leading to a decrease in the stroke volume which in turn would lead to low systolic pressure during inspiration that is characteristic of pulsus paradoxus. It has been shown in human subjects with tamponade that, indeed, the ventricular septum is displaced into the left ventricular cavity during inspiration. That this could also be attributed to a diminished left ventricular volume of the delayed effect of the expiratory decrease in right ventricular stroke volume. Arterial Effects (After load) Since the fall in pleural pressure with tamponade is the same as in the normal, increased after load cannot reasonably explain the substantially greater all in systolic blood pressure. The slight increase in after load for the left ventricle could have a negative effect on the left ventricular stroke volume, but both by percentage and by actual volume, the effect would be trivial.

                                                                     Reflex Effects In tamponade, a shock-like state exists, and invariably there is tachycardia and generalized vasoconstriction, which probably involves the veins as well as the arteries. Without this reflex adjustment, the mean circulatory pressure could not be increased, and circulation would cease at as earlier point in the disorder.

C. OBSTRUCTED BREATHING

                                                                     Pleural Pressure With increased airway resistance, the fluctuations in pleural pressure are exaggerated over those of normal breathing. Expiratory obstruction may lead to active expiratory effort, and positive intrathoracic pressure, but since dynamic compression of the airway limits any increase in airflow, patients gain little benefit and rarely develop a positive pleural pressure greater than a few centimetre of water.

                                                                        During as asthmatic attack there is also marked obstruction to inspiratory air flow, and these patients breathe at a high lung volumes in order to maintain airway patency. These factors combine to produce extremely negative pleural pressures, as much as  40 cm H2O with inspiration.

                                                            Venous Return The negative intrathoracic pressure will enhance venous return, but the effect is limited by collapse of the veins. Nevertheless, there will be an inspiratory increases in right ventricular stroke volume, which should appear after a couple of beats in the left ventricular stroke volume. Although the inspiratory-expiratory variation in venous return is exaggerated the mean cardiac output is not necessarily altered.

                                                                     Arterial Effects (After load) The left ventricle, subjected to an intrathoracic pressure of  40 cm H2O during inspiration, has to pump phill  to maintain forward flow in the peripheral circulation. This very substantial after load results in a transient reduction in the left ventricular stroke volume and a marked drop in systolic blood pressure.

                                                                     Obstructed breathing thus causes marked pulsus paradoxus, which can be used clinically as an index of the severity of air flow impairment. The pulsus paradosux of tamponade can easily be distinguished from obstructed breathing by the absence of respiratory distress.

D. POSITIVE PRESSURE BREATHING

                                                                     Pleural Pressure A mechanical ventilating device delivers a tidal volume at a positive airway pressure to inflate the lungs; deflation is by elastic recoil with an open airway at atmospheric pressure. At the end of exhalation, the lung volume (FRC) and pleural pressure are about the same as during spontaneous breathing. However during the inflation phase, the pleural pressure rises (becoming less negative or slightly positive).

                                                                        Pericardial Pressure The pericardial pressure will follow the pleural pressure fluctuations but may be at a slightly higher mean level. Cardiac pulsation will be superimposed and may be of substantial magnitude, relative to the respiratory fluctuations. Venous Return As the pleural pressure rises, the pressure in the venae cavae ad right atrium will rise, and the venous return will fall. Consequently, the right ventricular stroke volume will fall during inflation. However, the pulmonary capillaries will be compressed by the increased alveolar size and pressure, and  pulmonary venous flow will be enhanced. Thus, return to left atrium is increased, and the left ventricular stroke volume will actually be increased initially during the lung expansion. Within a few heart beats the decreased right ventricular output causes left ventricular output to fall, usually coincident with expiration. Accordingly the cycle of rising and falling left ventricular stroke volume is reversed from that of normal respiration.

                                                            Arterial Effects (After load) Although the left ventricle theoretically is at a slight advantage with the positive pleural pressure, relative to the peripheral vasculature at atmospheric pressure, this slight reduction in after load is more than offset by the hindrance of venous return to the right heart. Reflex Changes Positive pressure ventilation usually induces an increase in sympathetic tone so that the heart rate is somewhat increased and there is constriction of the capacitance vessels, the veins, which help maintain a higher venous pressure, allowing partial restoration of venous return. The steady-state cardiac output is usually diminished.

E. POSITIVE END-EXPIRATORY PRESSURE (PEE)

                                                                     In some mechanically ventilated patients, improved alveolar oxygenation can be obtained by maintaining a positive airway pressure at all times, even during passive exhalation. The end-expiratory lung volume (FRC) is increased above the normal volume. The effects are essentially the same as with positive pressure ventilation, but the effects on cardiac output are substantially greater, since the pleural pressure is increased above normal throughout all phases of respiration.

                                                            The continuing impairment of venous return results in a decrease in mean stroke volume of right and left ventricles. The usual clinical index of left ventricular filling, the left atrial or pulmonary wedge  pressure, will be elevated due to the increased intrathoracic pressure even though left atrial transmural pressure, left atrial volume, and left ventricular end diastolic volume are all reduced.

                                                            The addition of 5-10 cm H2O of PEEP is well tolerated by patients with normal to high intravascular volume but can markedly reduce cardiac output if initial volume is low. PEEP of 15-20 cm H2O will reduce cardiac output by 20% or more in most patients unless added volume is given. In some cases continuous positive airway pressure (CPAP) is maintained while the patients breathes spontaneously. The end-expiratory pleural pressure will still be elevated but it will decreased with inspiration rather than increasing further so venous return is less compromised and cardiac output better maintained than with comparable levels of PEP and mechanical ventilation.

F. CARDIOPULMONARY RESUSCITATION (CPR)

                                                          In patients with asystole, or ventricular fibrillation, cardiac output adequate to maintain cerebral and coronary circulation, can be maintained by external compression of the chest. It has generally been assumed that the effective mechanism was compression of the ventricles directly against the spine, forcing blood out into the aorta.

                                                            This assumption rested on the fact that during cardiac surgery, with the chest open, the cardiac output could be maintained by massaging the heat directly. Recently however, observation of patients who fibrillated during cardiac catheterization have suggested an alternate explanation for maintaining forward flow. These conscious patients were asked to cough vigorously at 1 or 2 second intervals, and the cardiac output was maintained by this method for over one minute. Since the heart was fibrillating, and no external pressure was applied to the pericardium, it was concluded that the driving force was the marked increase in intrapleural pressure produced by the cough.

                                                                        As has been shown with positive pressure ventilation, blood is expelled from the pulmonary veins into the heart, and apparently through the heart into the aorta with the sharp cough. The caval pressure is also elevated by this means, but the transport lag across the peripheral vascular bed allows the flow pulse to be effective, since the venous pressure dropped quickly, and its retrograde progress was impeded by the venous valves. It is now considered likely that compression of the pulmonary vasculature, rather than the ventricle, may be important aspect of external compression must be intermittent, allowing refill with elastic recoil before subsequent compression would be effective.

Deptt. of Pulmonary Medicine, PGIMER, Chandigarh, India.

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Osteoarthritis: Current concepts

                                                                                                                                                                            K.M. Marya, MS (Orth)

What Is Osteoarthritis?

                                                Also known as degenerative joint disease or osteoarthrosis, osteoarthritis is a joint disease that affects cartilage, the tissue that covers the ends of bones in a joint. Healthy cartilage allows bones to glide over one another, absorbing the shock of sudden physical movements. When a person has osteoarthritis, cartilage breaks down and wears away, and the bones eventually rub against each other. The resulting damage to the bones and underlying tissue can lead to tenderness, swelling, loss of joint motion, and chronic pain.

                                                            As the stress on the joint continues, it may lose its normal shape. Bone spurs (tiny growths called osteophytes) also may develop. Small pieces of bone and cartilage can break off and float into the joint space, and fluid may accumulate within the joint if the tissue lining the joint becomes inflamed.

                                                            Osteoarthritis commonly occurs in such weight-bearing joints as the knees and hips. It can also affect joints in the hands, fingers, lower back, and neck. What Causes Osteoarthritis? The cause of osteoarthritis is still unknown, but many factors can increase a person's risk for developing the disease. These risk factors include:

* A family history of the disease. Genetics accounts for more than 50 percent of all cases of osteoarthritis.

* Inactivity. If joints are not used in a long time, the cartilage protecting the joints becomes weak and may eventually lose its function.

* Age. As the body ages, cartilage becomes less flexible and loses its ability to regenerate. Also, the repeated wear and tear on these joints over the years  an lead to osteoarthritis.

* Traumatic injury to the joint. Former athletes and ballet dancers in particular are susceptible to developing the disease from repeated injuries to various joints.

*Obesity. Extra weight puts more strain on the joints.

* Lack of vitamin D. Low levels of vitamin D make bones more susceptible to osteoarthritis.

What Are Symptoms of Osteoarthritis?

                                                Osteoarthritis usually develops very slowly. Initially the symptoms are mild, but they may eventually get worse.  Symptoms include:

+ Steady or intermittent  pain in a joint + Stiffness after getting out of bed

+ Joint  swelling or tenderness

+ Crunching feeling or sound in the joint (called crepitus)

+ Enlarged, gnarled finger joints, which can be a sign of osteoarthritis in the hands

+ Limited joint movement. People with osteoarthritis may experience referred pain, or pain in areas of the body on the same nerve pathway as the affected joint. For example, an arthritic hip may cause pain in the groin, buttock, or knee.

Diagnosing Osteoarthritis

                                                                     If you think you have osteoarthritis, see your doctor. After a physical examination and a discussion of your symptoms, your physician might assess your reflexes, muscle strength, and your ability to walk, bend, and perform regular day-to-day activities. Depending on the assessment, your physician might order other tests. X-rays can help detect cartilage loss, bone damage, and bone spurs.

Current Treatments

                                                The goals of osteoarthritis treatment are to improve your joint function and quality of life. Treatments for osteoarthritis include preventive measures to stop or slow disease progression, self-management, medication, and surgery. Some complementary therapies are available, as well. Prevention If you have a mild case of osteoarthritis, you and your doctor can develop a preventive plan to keep the disease from progressing. The following preventive interventions can help:

+ Exercising on a regular basis to keep the joints moving

+ Managing your weight to reduce the stress on the joints

+ Increasing your vitamin D intake

+ Limiting your participation in high-risk sports such as football, tennis, rugby, and basketball.

                                                       Medications  your physician may prescribe one of the following medications to treat osteoarthritis pain and help improve joint function: + Nonsteroidal anti-inflammatory drugs (NSAIDs). These medications include aspirin, ibuprofen, ketoprofen, and naproxen sodium. NSAIDs, which can help relieve inflammation, joint pain, and swelling, are available by prescription or over the counter. NSAIDs block the body's production of prostaglandins, chemicals that are released when the body is in pain. Prostaglandins can contribute to the pain, heat, and swelling that occur after tissue has been damaged. Using NSAIDs for a long time could lead to ulcers, bleeding, and damage to the stomach lining. + Acetaminophen.

                                                Topical pain-relieving creams. Creams such as those that contain capsaicin can numb the skin temporarily. + Corticosteroids. Your physician may inject these powerful anti-inflammatory hormones into the affected joint to relieve pain, but  they are not recommended for long-term use. + Hyaluronic acid. This new medicine, used to treat osteoarthritis of the knee, is a normal component of the joint involved in lubrication and nutrition. Most patients feel relief from arthritic pain after 3 to 5 injections of hyaluronic acid. + Glucosamine and chondroitin sulphate. These components of cartilage are available as supplements that can help ease pain. Initial research showed that taking the supplements for a month relieved symptoms in some patients with arthritis.

Self-Management

                                                          In addition to preventive measures and medications, patients with osteoarthritis can work with their doctor to develop habits and

skills to manage pain and disability :

+ Warm towels or hot packs, warm-water therapy, and cold therapy can help ease joint pain and increase mobility.

+ Supportive shoes with rubber soles will absorb shock and reduce further damage to your joints.

+ Special exercises can restore joint movement and strength. Work with your doctor to create an exercise program for your individual needs and abilities.

+ Weight-management programs help reduce the amount of stress you

put on your joints.

Surgical Treatments

                                                                     In some cases, a joint is so damaged that it might need to be surgically repaired or replaced in one of the following procedures:

+ Joint replacement (arthroplasty). After removing the ends of the damaged bones, a surgeon will replace them with artificial joints made of metal, ceramic, or plastic.

+ Bone repositioning (arthrodesis / fusion). During this procedure, a surgeon immobilizes the joint to reduce pain. Because the surgery limits patient's mobility, it's often performed on the smaller joints of the foot and hand.

+ Joint resurfacing (arthroscopic surgery). Surgeons remove such inflammatory particles as torn or damaged cartilage or bone from the joint. The procedure offers short-term relief.

Complementary Therapies for Osteoarthritis

                                                          Some complementary therapies can help ease the pain associated with  osteoarthritis:

+ Relaxation techniques. Meditation and yoga help relieve pain by relaxing muscle tension. Relaxation techniques also can help people manage stress and anxiety.

+ Tai chi. This ancient Chinese discipline stretches joints in a series of light, controlled movements. Its emphasis on deep breathing and inner stillness can relieve stress and anxiety.

+ Acupuncture. Some people have found pain relief through acupuncture. An acupuncturist inserts fine needles at specific points on the skin, penetrating just  below  the skin's top layer. The needles do not draw blood or cause discomfort.

Research

+ Osteoarthritis detection. Researchers hope to discover new ways to detect the disease in its early stages. Scientists are developing noninvasive urine, blood, and imaging tests that would detect changes in the tissues around joints.

+ Genetic tests. Scientists continue to search for more genes associated with the breakdown of cartilage production. Researchers have identified one genetic defect  that leads to the early onset of osteoarthritis. They hope to identify more of these genetic markers to develop screening tests and genetic therapies to help prevent the disease.

+ Cartilage production. Preliminary evidence links a decreased number of cartilage cells to the development of osteoarthritis. Researchers are examining why cartilage cells die faster than new ones can grow, and several studies are examining the effects of certain proteins and molecules that could stimulate growth in cartilage. A growth factor called human osteogenic protein 1 has been found to be very successful in stimulating cartilage protein production. Scientists hope to determine if vitamin C and certain chemicals called nitric oxide inhibitors can prevent cartilage damage.

                                                Researchers also hope to develop monoclonal antibodies (cells produced by the immune system) that can identify the breakdown of protein molecules in the cartilage of people with osteoarthritis. Additionally, scientists are continuing to learn how certain enzymes called metalloproteinases break down and destroy cartilage. By understanding this mechanism, scientists hope to discover new therapies that can block cartilage destruction by these substances.

+ Joint replacement. To increase the range of motion after joint replacement, researchers are developing bioengineered, cell-based materials to replace the metal and cements currently used.

+ Acupuncture. The National Centre for Complementary and Alternative Medicine (NCCAM) at Harvard University in Boston is conducting several studies to determine if acupuncture relieves pain and helps improve joint function. In one study, researchers are comparing the effects of acupuncture, fake acupuncture (or placebo), and patient education; another study will examine acupuncture in combination with exercise and Physical  Therapy.

+ Glucosamine and chondroitin sulphate. A study sponsored by the NCCAM and the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) will evaluate the effectiveness of these supplements in relieving pain associated with osteoarthritis of the knee.

+ Magnetic resonance imaging (MRI). Research funded by the Arthritis Foundation is exploring the use of MRI to monitor very early changes in certain cartilage proteins called proteoglycans. bigI

+ Medications. New medications may help improve the quality of life of people with osteoarthritis. New compounds called viscosupplements are injected into the joint to help provide pain relief for those with osteoarthritis of the knee. Researchers are studying a drug called doxycycline to determine if it may help prevent or slow down the progression of osteoarthritis. Scientists have found that doxycycline works against enzymes that break down cartilage.

Future Researchers are investigating better ways to prevent and treat  osteoarthritis:

+ Geneticists will continue to explore the role of genetic factors in the development and progression of osteoarthritis.

+ Researchers will determine if estrogen or hormone replacement therapy (HRT) help prevent the disease.

+ Scientists will continue to investigate new methods of stimulating cartilage production.

+ Researchers will study various complementary and alternative therapies to determine their usefulness in easing symptoms of osteoarthritis.

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 Colour Vision and Occupation  

                                                                                                                                                                  Shankaran Ramaswamy

Colour Blindness

                                                                        The term colour blindness is a common but misleading term that implies total loss of colour vision. In most cases the defect is usually only partial and the term “colour defective vision”  would be more appropriate. The commonest defect is in the red/green part of the visual spectrum. Males are more commonly affected; about 8% of all males and 0.5% of females are affected to a varying degrees.

                                                                  There are other defects due to failure in the blue receptors, a total failure of all receptors and a failure of the other retinal receptor, the rod

Mechanism of defect

                                                                        All colours can be made by mixing the three primary colours; red, green and blue in varying amounts and the eye sees colours by detecting the amounts of these primary colours. This processing is done by special nerve endings in the retina of the eye. One type of nerve ending, the cone, has three special pigments which detect one colour, either red, green or blue. If one of these nerve types is impaired there is a colour defect.

                                                                        Males are more affected because the genes that control the development of these colour sensitive nerve endings are carried on the x chromosome, which is the chromosome that determines male characteristics. Females are rarely affected, but may be carriers of the trait and up to one in seven are carriers.

                                                                        Colour defects can also be acquired and a common cause in our community is cataracts. As the cataract becomes more dense it filters out all colours, but the bright reds, yellows, greens and blues are more affected. It has been said that the changing colour choices of many famous painters has been due to the affect cataracts have had on their colour vision. Other diseases affecting the optic nerve and the retina also affect colour vision but these are rare and often only affect one eye.

Type of defects

                                                            The defects are named after the Greek words for the three primary colours: Protos for red, Deutros for green and Tritos for blue. Someone who has a complete red defect is said to have Protanopia and if he only has partial defect he is said to have Protanomaly. The commonest defect involves the green receptors and it accounts for over half of the defects; 4% of all males have a partial defect and 1% have a complete defect. As the loss of colour vision is in the middle of the visual spectrum this defect causes the least awareness. The problem is the inability to distinguish red and green but they are sensitive to red light.

                                                The next most common defect is due to failure in the red receptors, and it affects 1% of males. These people also confuse red and green but are not sensitive to red light. There are other defects due to failure in the blue receptors, a total failure of all receptors and a failure of the other retinal receptor, the rod

Colour Vision and Occupation

                                                            Colours are constantly used to distinguish the difference between objects in everyday life. For many centuries colour has been an important part of many occupations and professions. Today the use of colour and colour coding has become much more widespread, a fact that undoubtedly influences the career choices of those with a colour vision deficiency. The use of colour extends to the work environment, and so it affects jobs and careers which require some degree of colour identification. These careers vary in the extent of reliance on colour vision, and so have been grouped into categories depending on if it is desirable or vital for operatives to have

normal colour vision. This list can never be comprehensive and many jobs fall into several categories, as there are often different activities within a specific trade, profession or occupation.

Careers/Jobs/Occupations/Industries requiring perfect colour vision.

Armed Forces

Air Forces - certain grades

Navy - certain grades

Civil aviation

Colour matcher in dyeing, textiles, paints, inks, coloured paper,  ceramics, cosmetics.

Carpet darner/inspector, spinner, weaver, bobbin winder

Electrical work -

electrician

electronics technician

colour TV mechanic

motor mechanic

telephone installer

fisherman

railways

Police - certain grades

CAREERS ADVICE 

                                                When occupational advice is given, the risk of an error being made and the consequences of the possible errors must be estimated. This is done by first testing the person and then, from the results, determining their suitability to the particular profession.

                                                            In some occupations the use of colour, and the complexity of its use may increase as a person is promoted, therefore the job may have no prospects for someone with a colour deficiency. This has to be considered when a person with a colour deficiency is hired and should also be explained to the person before they accept the job. Another point to consider is if the person may want to transfer, there is a possibility that although the work may be exactly the same at another company, they may have different policies on hiring people with colour deficiencies.

DAY-TO-DAY PROBLEMS

                                                Most defective colour vision does not seriously handicap those suffering from it in day-to-day life, this is because they adapt to their deficiency and most have normal visual acuity. However, some problems arise in tasks that people with normal colour vision take for granted. Judging the ripeness of fruit, selecting coloured clothes, choosing decorating materials, checking if meat is cooked, reading maps and playing sporting games such as snooker are just a few of many examples.

                                                            Probably one of the most   hazardous day-to-day  problems is in driving. Traffic signals are the only connotative colour codes which people use regularly and, although many colour deficient people are able to distinguish traffic lights by the position and different intensities of lights on the column, some do report having problems.

                                                            About a third of colour deficient people feel uncomfortable driving at night due to the overhead street lights. The street lights can often cause colour confusion  and small lights are often mistaken for red stop signals. Red and green ‘cats-eyes’ which mark the lanes of motorways are also often confused. Regardless of the possible complications of driving that colour deficient people have, statistics have shown that colour deficient drivers are involved in fewer accidents, a fact that suggests that they learn to adapt to their difficulties by taking more care. 

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