Accelerated junctional rhythm (AJR)

Accelerated junctional rhythm (AJR) occurs when the rate of an AV junctional pacemaker exceeds that of the sinus node. This situation arises when there is increased automaticity in the AV node coupled with decreased automaticity in the sinus node. Causes of AJR are digoxin toxicity, use of beta-agonists, e.g. isoprenaline, adrenaline, Sick sinus syndrome, myocardial ischaemia, myocarditis (acute rheumatic fever, lyme disease, Diphtheria) and metabolic states with increased adrenergic tone. Certain drugs which can cause bradycardia such as beta blockers, calcium channel blockers and antiarrhythmic agents can also induce AJR.

Fig-1: ECG of a 25 year old female having dextrocardia, situs inversus and congenital cyanotic heart disease. 

Junctional rhythms are classified by their rate as 1) Junctional Escape Rhythm: 40-60 bpm 2) Accelerated Junctional Rhythm: 60-100 bpm and 3) Junctional Tachycardia: > 100 bpm.

They may also be classified by aetiology as automatic Junctional Rhythms (e.g. AJR) = Due to enhanced automaticity in AV nodal cells or re-entrant Junctional Rhythms (e.g. AVNRT), due to re-entrant loop involving AV node.

Fig-2: Example of an accelerated junctional rhythm (courtesy ECG library)

ECG Features of AJR

·         Narrow complex rhythm; QRS duration < 120ms (unless pre-existing bundle branch block or rate-related aberrant conduction).

·         Ventricular rate usually 60 – 100 bpm.

·         Retrograde P waves may be present and can appear before, during or after the QRS complex.

·         Retrograde P waves are usually inverted in the inferior leads (II, III, aVF), upright in aVR + V1.

·         AV dissociation may be present with the ventricular rate usually greater than the atrial rate.

·         There may be associated ECG features of digoxin effect or digoxin toxicity.

Periods of junctional rhythm are not necessarily associated with an increase in mortality. If an obvious cause is present, such as complete heart block or sick sinus syndrome, then the morbidity or mortality is directly related to that and not to the junctional rhythm mechanism, which is serving as a "backup rhythm" during the periods of bradycardia. Accelerated junctional rhythms may be a sign of digitalis toxicity.

ECG features may be mistaken for that of dextrocardia as this patient is having dextrocardia and situs inversus. In dextrocardia inverted P wave is seen only in Lead-1 and upright P in aVR. Other features are right axis deviation, positive QRS complexes (with upright P and T waves) in aVR, inversion of all complexes (global negativity) in Lead I and absent R-wave progression in the chest leads.

Complications

Complications of junctional rhythm are usually limited to symptoms such as dizziness, dyspnea, or presyncope. Exacerbation of cardiac comorbidities, such as congestive heart failure and rate-related cardiac ischemia, may occur.

Multiple congenital defects in a young adult with features not limited to a syndrome A rare case report

Multiple congenital defects in a young adult with features not limited to a syndrome

A rare case report

Summary

We report the case of a 25-year-old female, presenting to the hospital with history of fever, cough and breathlessness of 3 days duration.  She was diagnosed to have congenital cyanotic heart disease in early childhood, but no intervention was done till date. She used to get recurrent respiratory infections which were treated as outpatient. On examination she is of short stature with kyphoscoliosis, having triangular face with retrognathia, hypertelorism, prominent epicanthal fold, low set ears, broad nose base and low posterior hair line. Her oxygen saturation with 4 litres oxygen was only 49%. She also had conductive deafness on the left ear. Patient’s genitalia and secondary sexual characters were well developed and her menstrual period last for 6-8 days with menorrhagia and dysmenorrhea. Other important features noted are cubitus valgus, pes cavus and systolic murmur suggestive of VSD. Echocardiography revealed dextrocardia, large VSD, pulmonary stenosis, double outlet right ventricle, right ventricular hypertrophy and transposition of great arteries. Ultrasonography revealed situs inversus and splenomegaly. Her ECG features were in favour of accelerated junctional rhythm. HRCT thorax to rule out bronchiectasis could not be performed as the clinical condition deteriorated rapidly and patient succumbed to her illness. This patient in spite of having multiple congenital defects that are fatal beyond infancy if not corrected lived up to 25 years. Not all her clinical features are limited to a known syndrome. Here we postulate that she had most of the features of Noonan syndrome or Noonan variant along with features of heterotaxy syndrome. A clinical syndrome with all these features is not so far reported in the literature.

Background

Noonan Syndrome (NS) is a relatively common congenital disease that affects both males and females equally. This is an autosomal dominant disorder with an incidence of 1 in 1000 to 2500 live births¹. This is caused by mutations in one of many genes such as PTPN11, SOS1, RAF1, RIT1, KRAS, NRAS, BRAF, and MAP2K1. The clinical features of NS include broad or webbed neck, low posterior hair line, typical chest deformity, short stature, ocular hypertelorism, epicanthal folds, triangula facies, micrognathism, kyphoscoliosis, cubitus valgus, pulmonary stenosis, ventricular or atrial septal defect and right ventricular hypertrophy.

Leopard syndrome is a Noonan Variant with features of hyperpigmented macules over the face and trunk (Lentigenes), electrocardiographic conduction defects, ocular Hypertelorism, pulmonic stenosis, abnormalities of genitalia, retardation of growth and deafness.

Hetrotaxy syndrome has situs ambiguous or situs inversus. Situs ambiguous is a rare congenital defect where most organs are heterogeneously distributed in the chest and abdomen. In situs inversus, organs in the chest and abdomen are reversed. Paired organs may show isomerism. Isomerisms can be isolated, but can also be part of various syndromes, the best known of which—for its respiratory disorders—is immotile cilia syndrome, that includes Kartagener syndrome. This syndrome shows a recessive inheritance and is associated with situs inversus, heart defects, bronchiectasis, sinusitis, and otitis media as well as sterility in males².  Abnormal intestinal rotations are commonly found in patients with heterotaxy syndrome.^3,4 Heterotaxy can also cause polysplenia or asplenia associated with congenital heart defects. The heterotaxy syndrome associated with asplenia has a worse prognosis, because it is commonly associated with significant heart anomalies which include double outlet right ventricle, transposition of great arteries and ventricular septal defect.^5,6 However, the advances made in recent years in heart surgery and the early detection of heart disorders by prenatal ultrasonography have prolonged survival in patients with heterotaxy.^4,7

We report the case of a 25-year old adult female presenting with features of Noonan variant syndrome (Leopard syndrome) having additional features of Heterotaxy syndrome. This type of clinical presentation, which satisfies the diagnosis of both Leopard syndrome and Heterotaxy syndrome, is extremely rare and is not reported so far. More over this patient has congenital cardiac defects, which are not compatible with life if not corrected, and she has lived up to 25 years without surgical correction remains a mystery in clinical medicine.

Case presentation

A 25 year old female, from a low socioeconomic background, presented with complaints of fever, vomiting and increased breathlessness of 3 days duration. There is no history of cough with sputum production, orthopnea, PND, chest pain or palpitations. She gives history of recurrent chest infections since childhood. She also had left ear infections and bluish discoloration of hands and lips. There is no significant antenatal history, but her milestones were delayed and started walking at 7 years of age. She attained menarche at 16 years of age with regular cycle, associated with menorrhagia and dysmenorrhea. One of her maternal aunt had kyphoscoliosis and facial features similar to her. One child in her family died at 9 days of life.

She is short statured with a height of 146 cm and has clubbing and cyanosis. Her SaO2 is 49% on 4 ltrs. of O2. Other general physical features include widely set eyes, triangular face with broad forehead and micrognathia, broad nose base, low set ears, crowded teeth with gum hypertrophy, short and broad neck, low posterior hair line, hyper-pigmented macules over the trunk, kyphoscoliosis, cubitus valgus and pes cavus. Other features include asymmetrical chest, underdeveloped left mammary gland and precordial bulge. She has dextrocardia and situs inversus. Echocardiogram showed features of pulmonary stenosis, double outlet right ventricle, large VSD, right ventricular hypertrophy and transposition of great arteries. Neurological examination revealed conduction deafness on the left side. Ultrasound examination confirmed situs inversus and a large spleen.

Fig-1: Demonstrating the important clinical findings such as cyanosis (A), low posterior hair line (B) and thoracic kyphoscoliosis (C).Multiple hyper-pigmented macules are also seen on the back.

Investigations

Blood examination showed elevated total count with neutrophilic leukocytosis. ESR was 54 mm fall/1st hour. Platelet count was 1,18,000 cells/cmm.

X ray chest showed scoliosis of thoracic spine and dextrocardia. Stomach air bubble is not seen on the left side. ECG showed tachycardia and inverted P wave in all leads except aVR and V1. Echocardiographic features include situs inversus with dextrocardia, Double outlet right ventricle (DORV) with Transposition of grat arteries (TGA), subaortic ventricular septal defect (VSD), Pulmonary stenosis (TOF Physiology), dilated coronary sinus with SVC draining in to CS and normal biventricular function.

Ultrasound examination of abdomen revealed situs inversus with large spleen on the right side. Both kidneys were normal except increased echogenicity. Uterus and adenexia appeared normal.

Her renal function was altered with a blood urea of 88 mg% and serum creatinine of 3.2 mg%. Arterial blood gas analysis showed PaO2 24, PaCO2 30, HCO3 22 and a PH of 7.21

HRCT could not be performed to rule out Kartagener’s syndrome as the patient’s condition deteriorated rapidly.

Fig-2: X ray chest showed scoliosis of thoracic spine and dextrocardia. Stomach air bubble is not seen on the left side.

Fig-3: ECG showing tachycardia and inverted P wave in all leads except aVR and V1.

Discussion

Noonan Syndrome (NS) is a relatively common congenital disease that affects both males and females equally. This is an autosomal dominant disorder with an incidence of 1 in 1000 to 2500 live births¹. This is caused by mutations in one of many genes such as PTPN11, SOS1, RAF1, RIT1, KRAS, NRAS, BRAF, and MAP2K1. Noonan syndrome was first described in 1963 by Noonan and Ehmke⁹. It is also known by synonyms such as male turner syndrome or female pseudo turner syndrome. These patients were previously thought to have a form of Turner syndrome, with which Noonan syndrome shares numerous clinical features. Patients with Noonan syndrome have normal karyotypes to differentiate it from Turner syndrome. Classical Noonan phenotype has features such as short stature, short or webbed  neck, low posterior hair line, ocular hypertelorism, short nose with broad base, low set ears with posterior folding, triangular facies with small chin, padded fingers and toes, lymphedema, mental retardation, pulmonary stenosis, atrial or ventricular septal defects, hypertrophic cardiomyopathy and bleeding tendency. Rarely coarctation of aorta and tetralogy of Fallot (TOF) were also reported¹⁰. This patient has most of these features to satisfy the diagnosis of Noonan Syndrome. Presence of sexual characteristics with regular menstrual cycles rule out the possibility of Turners syndrome. We could not do karyotyping to establish mutations responsible for this syndrome.

There are few clinical features in this patient which cannot be explained by Noonan syndrome. These are multiple hyper-pigmented macules over the trunk (lentigenes), electrocardiographic conduction defect in the form of accelerated junctional tachycardia and conduction deafness. These features are described in Leopard syndrome which is a Noonan variant.  Leopard syndrome is a complex dysmorphogenetic disorder of variable penetrance and expressivity, first described by Zeisler and Becker in 1936¹¹. Gorlin et al introduced the acronym LEOPARD as the name of the syndrome in 1969¹² to highlight the main features of the disorder such as Lentigines (L), electrocardiographic conduction abnormalities (E), ocular hypertelorism (O), pulmonary stenosis (P), abnormalities of genitalia (A), retardation of growth (R) and deafness (D). Not all of the findings are present in any given patient. LEOPARD syndrome, also known as Noonan syndrome with multiple lentigines, is a rare autosomal dominant disorder most often caused by missense mutations in the PTPN11 gene, which encodes the protein tyrosine phosphatase SHP2¹³.

Presence of dextrocardia, situs inversus, double outlet right ventricle and transposition of great arteries were never reported in Noonan syndrome or Leopard syndrome. These features make this patient unique in clinical presentation. It is very rare to see significant structural abnormalities of heart in dextrocardia with situs inversus. The structural abnormalities detected in this patient are all serious conditions with which patient cannot survive beyond infancy if not treated. This patient lived up to 25 years without undergoing any intervention is also unique. These features are explained in heterotaxy syndrome. Heterotaxy have been recognized since 1933 (complete) ¹⁴ and 1826 (incomplete)¹⁵. The habitual and orderly arrangement of the organs in the human body is determined early in the embryonic development and is based on genetic information¹⁶. The loss of such orderly arrangement may characterize situs inversus or a disordered and variable arrangement (heterotaxy syndrome). Heterotaxy syndrome has an approximate incidence of 1:10,000 births and is slightly more prevalent in men, at a ratio of 2:1.

Hetrotaxy syndrome has situs ambiguous or situs inversus.  Situs ambiguous is a rare congenital defect where most organs are heterogeneously distributed in the chest and abdomen. In situs inversus, organs in the chest and abdomen are reversed. Paired organs may show isomerism. Isomerisms can be isolated, but can also be part of various syndromes, the best known of which—for its respiratory disorders—is immotile cilia, that includes Kartagener syndrome. This syndrome shows a recessive inheritance and is associated with situs inversus, heart defects, bronchiectasis, sinusitis, and otitis media as well as sterility in males².  Abnormal intestinal rotations are commonly found in patients with heterotaxy syndrome. Heterotaxy can also cause polysplenia or asplenia associated with congenital heart defects. The heterotaxy syndrome associated with asplenia has a worse prognosis, because it is commonly associated with significant heart anomalies which include double outlet right ventricle, transposition of great arteries and ventricular septal defect.^5,6 At least 12% of primary ciliary dyskinesia (PCD) patients have heterotaxy.¹⁷ Cyanosis or poor peripheral perfusion is the most common findings in patients with heterotaxy. The liver may be on the left, rather than on the right, and it may span the abdomen. Dextrocardia may be identifiable. Other components of the syndrome include situs inversus totalis, dTGA, DORV, VSD, growth retardation and delayed milestones.

Conclusion

We report a rare case in a 25-year old female with a unique combination of clinical features. She has all clinical manifestations of Noonan variant- Leopard syndrome, and in addition has features of heterotaxy syndrome. Available literature did not show any similar case report. The cardiac defects are all serious and not compatible with life beyond infancy if not surgically corrected. This patient lived up to 25 years without any surgical correction. This syndrome may be called Leopard-Heterotaxy syndrome considering the clinical features of both Leopard syndrome and heterotaxy syndrome in one patient.

References

1. Bhambhani V, Muenke M. Noonan syndrome. Am Fam Physician 2014; 89 (1):37-43.

2. Fuster Siebert M, Cabanas Gancedo R, Cuevas Alvarez J, et al. Heterotaxia cardiaca y anomalías filiares. Medicina Clínica 1983; 80: 231–32.

3. Peeters H, Devriendt K. Human laterality disorders. Eur J Med Genet 2006; 49: 349–62.

4. Choi M, Borenstein SH, Hornberger L, et al. Heterotaxia syndrome: the role of screening for intestinal rotation abnormalities. Arch Dis Child 2005; 90: 813–15.

5. Salomon LJ, Baumann C, Delezoide AL, et al. Abnormal abdominal situs: what and how should we look for? Prenatal Diag 2006; 26: 282–85.

6. Syamasundar Rao P, Molthan M, Ariz P. Systemic venous anomalies and partial heterotaxia with normal heart. Am J Dis Child 1973; 125: 749–52.

8. Beck A, Hudgins L. Congenital cardiac malformations in the neonate. Am Acad Pediatr 2003; 4.

9. Porciello R, Divona L, Strano S, Carbone A, Calvieri C, Giustini S. Leopard syndrome. Dermatol Online J. 2008; 14(3):7.

10. Romano AA, Allanson JE, Dahlgren J, et al. Noonan syndrome: clinical features, diagnosis, and management guidelines. Pediatrics. 2010; 126(4):746-59.

11. Li R, Baskfield A, Lin Y, Beers J, Zou J, Liu C, et al. Generation of an induced pluripotent stem cell line (TRNDi003-A) from a Noonan syndrome with multiple lentigines (NSML) patient carrying a p.Q510P mutation in the PTPN11 gene. Stem Cell Res. 2019; 34:101374.

12. Begic F, Tahirovic H, Kardaševic M, Kalev I, Muru K. Leopard syndrome: a report of five cases from one family in two generations. Eur J Pediatr. 2014; 173(6):819-22.

13. Roberts AE, Allanson JE, Tartaglia M, Gelb BD. Noonan syndrome. Lancet 2013; 381(9863):333-42.

14. Kartagener M. [Zur pathogenese der bronchiektasien: bronchiektasien bei situs viscerum inversus] [German]. Beitr Klin Tuberk. 1933. 83:489-501.

15. Martin G. [Observation d'une deviation organique de l'estomac, d'une anomalie dans la situation et dans le configuration du coeur et des vaisseaux qui en partent ou qui s'y rendant] [French]. Bull Soc Anat Paris. 1826. 1:40-8.

16. Shiraishi I, Ichikawa H. Human heterotaxy syn-drome – from molecular genetics to clinical fea-tures, management, and prognosis –. Circ J.2012; 76:2066–75

17. Shapiro AJ, Davis SD, Ferkol T, et al. Laterality defects other than situs inversus totalis in primary ciliary dyskinesia: insights into situs ambiguus and heterotaxy. Chest 2014 Nov. 146 (5):1176-86.

COVID 19- How to tackle community spread?

COVID 19- How to tackle community spread?

Corona virus infection of 2019 (COVID 19) which started first in China is now showing all features of a pandemic with more than 100 countries affected. It appears to be a fast spreading viral infection and needs community participation to contain it. Disease is mild with mortality risk of about 3.4%. However it has created panic all over the world. The main concern is international travel and the ability of the virus to spread through contacts. This can be attributed to the high reproductive number (R0 value) of 2.28 the virus boasts coupled with the fact that the virus chose the most populous country in the world to wreak havoc. This high R0 value stresses the need for strict infection control and management to contain this illness.

As per preliminary reports death rate is not very high, but may differ from one country to other due to climate, geographical, ethnic and genetic factors. Most important factor in containing this epidemic is through community participation. Govt. should issue directions regarding the measures to be undertaken for controlling the spread. These directions are binding to all citizens across the region. Restricting international travel is one important measure, especially travel in and out of most affected countries is to be strictly restricted. Avoidable travel, travel for tourism purpose etc. can be cancelled or postponed to a later date.

Next important measure is surveillance in international airports; where in all international passengers are screened by a team of health care providers. Symptomatic should be isolated in health care facilities and treated and asymptomatic contacts can be quarantined in their homes so that mixing with other public is strictly restricted for at least 14 days. All contacts and suspects should be tested for presence of viral antigen.

Since the initial symptoms of the disease are like any other flu illness, even a minor running nose has created an undue fear amongst the people. Seeking early professional advice puts these patients at a higher risk of acquiring Covid 19 from the hospitals. Hence, self-quarantine is of paramount importance and needs to be stressed. Patients need to initially isolate themselves from their immediate kin, wear a surgical mask and follow strict hygiene measures to restrict transmission. Initially, symptomatic measures such as anti pyretics, adequate hydration and nasal decongestants may be taken. Professional help need only be sought if the symptoms persist.

A monitoring cell under the district health authority is to be formed and that is responsible for treating symptomatic, tracking contacts, allaying fear among public and to give directions to the public. There will be state cell to coordinate district activities and to provide money and materials to the district units. Health centers designated for quarantine of suspects should have chambers with negative pressure to contain the spread of the virus. Health workers should also be equipped with adequate supplies of gloves, N95 masks, respirators, goggles, face shields, gowns and aprons. It cannot be emphasized enough that these workers, being at the forefront of combating this illness, need to be protected at all costs. All details about each individual case so far reported should be traced with special details regarding mode of acquisition, age, travel and contact history, symptoms and signs, investigation reports, severity of disease, co morbidities, course of the disease and outcomes.

Contact tracing of a case suspect is of paramount importance to prevent spread in the community, especially in a highly populous country like India. Both primary and secondary contacts should be tracked and put on strict home quarantine. Meticulous planning and sincere effort done by the Govt. of Kerala in this direction is a model being appreciated by all.

There should be directions to avoid mass gatherings especially, festivals, meetings, marriage celebrations where large number of people are exposed.  It will be better to close all educational institutions for a period till containment is achieved. News bulletins, public awareness programmes through social media are essential to give updated information to the public. At the same time care should be taken not to create panic among citizens. Awareness about cough hygiene, hand hygiene and other general measure with special emphasis on early reporting and reassurance are the need of the hour.

WHO has declared Covid 19 as a pandemic and wanted all the countries to take urgent measures to contain the disease. The report from China is hopeful that number of new cases reported is coming down drastically. Hope that, with the concerted efforts of all we will be able stop the onslaught of 2019-nCoV.

AIR POLLUTION

AIR POLLUTION IN DELHI AND THE HEALTH EMERGENCY

Ravindran Chetambath, Jesin Kumar C

Dept. of Pulmonary Medicine

DM Wayanad Institute of Medical Sciences, Kerala

Delhi, a city which was once known for the various architectural tourist attractions, is now a city smothered in smog which often compromises the visibility of these historic structures. As the festival of lights approached this year, the people of Delhi faced a dilemma that they have of late become familiar with. In a city where the growing levels of pollution have forced their residents to wear surgical masks outdoors; use of firecrackers seemed to only aggravate the problem. Hospitals in the ‘’world’s most polluted capital’’ have seen an increase in patients reporting with respiratory illnesses. Children residing in the city also develop irreversible lung damage at a very young age.

Environmental air pollution, the fifth largest killer in India, has probably been a constant source of health issues since the discovery of fire millions of years ago¹. Its use in cooking and heating purposes is still a major reason for respiratory illnesses. The rise in the number of power plants and motor vehicles in the city has resulted in the emergence of newer and more harmful pollutants like sulfur oxide, nitrogen oxide, ozone and polycyclic aromatic hydrocarbons in the atmosphere. It was estimated that about 3000 metric tons of air pollutants were emitted every day in Delhi, with a major contribution from vehicular pollution (67%), followed by coal-based thermal power plants (12%). There was a rising trend from 1989 to 1997 as monitored by the Central Pollution Control Board (CPCB). The concentrations of carbon monoxide from vehicular emissions in 1996 showed an increase of 92% over the values observed in 1989.

Since the atmosphere in Delhi contains a complex mixture of pollutants, it is often difficult to find out the individual health effects of each pollutant. Our respiratory system is equipped with defence mechanisms to protect us from these harmful pollutants. However, it is becoming increasingly difficult for our body to cope with the pollutants in Delhi due to its harmful properties. Particulate matter pollutants are classified based on their size into PM₁₀ (<10 µm diameter) and PM_2.5 (<2.5 µm diameter) particles. As per the Air Quality Index (AQI) data of 2019², Delhi now has a PM_2.5 level of 185µg/m³. This high level of minute PM_2.5 particles in our capital helps these substances to evade the filtration mechanisms in our nose and airways and penetrate the alveoli to spread to the other vital organs³. The oxidative burden posed by air pollutants like ozone, in Delhi, is often so large that it overwhelms the innate antioxidant system in our body⁴. The ensuing oxidative stress is linked to a wide range of diseases including, asthma, diabetes, cardiovascular disorders, Alzheimers disease, Parkinson’s disease, depression, infertility and cancer.

World Health Organization in September 2011 reported⁵ that Delhi has exceeded the maximum PM10 limit by almost 10-times at198μg/m³. Major concerns for human health from exposure to PM10 include effects on respiratory systems, damage to lung tissue, cancer and premature death. Elderly persons, children and people with chronic lung disease, influenza or asthma are especially sensitive to the effects of particulate matter. These pollutants can cause widespread airway injury like respiratory bronchiolitis and can also result in exacerbations of pre-existing respiratory illnesses like asthma and chronic obstructive pulmonary disease. The rise in the incidence of lung cancer, now becoming increasingly common in young never smokers, can also be attributed to these pollutants⁶. It was found that Delhi had 1.7-times higher prevalence of respiratory symptoms compared with rural controls (P < 0.001); the odds ratio of upper respiratory symptoms in the past 3 months in Delhi was 1.59 (95% CI 1.32-1.91) and for lower respiratory symptoms was 1.67 (95% CI 1.32-1.93)⁷.

The months of October and November are the months when Delhi really chokes. Inhaling the air during these months is equivalent to smoking 45 to 50 cigarettes per day⁸. The bursting of firecrackers during festivals hampers the hazardous atmosphere in Delhi. Unfortunately, the city is not entirely to blame for the predicament it finds itself in during these months. The burning of organic matter like crop residues in the states of Punjab and Haryana during these months have contributed to about 26% of the particulate matter in Delhi’s air⁹.

The trend of worsening air quality in Delhi is bound to continue if drastic measures are not implemented at the earliest. Measures taken by the chief minister like the implementation of the odd-even rule for vehicles and distribution of surgical masks to school children are steps in the right direction but need to be preceded by scientific studies to elucidate the quantity of air and the problem posed by these pollutants. These include large scale epidemiological studies, animal and in vitro research. Experimental studies subjecting animals or humans to varying concentrations of the pollutants in a controlled environment may be needed to elucidate the harmful effects of these pollutants. In vitro research helps to study the effects of these pollutants on a cellular level¹⁰.

The onus is on the people of Delhi to contribute in whatever way possible to curb this menace. Car-pooling and the use of bicycles, CNG filled cars and public transports are some ways in which vehicular emission can be controlled. Reforms by the government like improving the quality of public transport, marking out bicycle lanes on the roads and reducing taxes on CNG filled cars; can also aid in this¹¹. As far as industries in the suburb are concerned, drastic measures like shutting them down or relocating them are needed. It was reported that use of lower-emission motor vehicles resulted in a significant gain in disability-adjusted life-years in Delhi. Another study found significant evidence for reduction in respiratory illnesses following introduction of control measures¹².

The problem Delhi faces is huge and seems unsurmountable at times. However cities like Beiijng faced similar problems decades earlier and have managed to overcome them to a certain extent¹³. Enormous investment of time, resources and political will is needed in order to improve the air quality of Delhi. The thought of children being exposed to such hazardous air should propel us to act promptly. At least for them, let us take an oath to be a part of the solution and not the problem.

REFERENCES:

1.      Air pollution 5th largest killer in India. The Economic Times [Internet]. 2013; Available from: https://economictimes.indiatimes.com/news/environment/pollution/air-pollution-5th-largest-killer-in-india-study/articleshow/18486354.cms

2.      Mishra R. Delhi air quality takes a hit, thick smog covers sky. India today. 2019.

3.      Balakrishnan K, Ganguly B, Ghosh S, Sambandam S, Roy S, Chatterjee A. A spatially disaggregated time-series analysis of the short-term effects of particulate matter exposure on mortality in Chennai, India. Atmos Heal. 2011

4.      Jerret M, Burnett R, Pope C, Ito K, Thurston G, Krewski D. Long-term ozone exposure and mortality. N Engl J Med. 2009;360:1085–95.

5.      WHO Air quality guidelines for particulate matter, ozone, nitrogen dioxide and sulfur dioxide, Global update 2005, Summary of risk assessment. Available from http://whqlibdoc.who.int/hq/2006/WHO_SDE_PHE_OEH_06.02_eng.pdf.

6.      Murray JF, Nadel JA. Textbook of Respiratory Medicine. 6th ed. Philadelphia: Elsevier 2016; p 1332.

7.      Epidemiological Study on Effect of Air Pollution on Human Health (Adults) in Delhi, Environmental Health Series: EHS/1/2008, Central Pollution Control Board, Ministry of Environment & Forests, Govt. of India. 2008. Aug, Available from: http://cpcb.nic.in/upload/NewItems/NewItem_161_Adult.pdf.

8.      Delhi air right now is like smoking 50 cigarettes a day. The Economic Times [Internet]. 2019 Oct; Available from: https://economictimes.indiatimes.com/news/politics-and-nation/delhi-air-right-now-is-like-smoking-50-cigarettes-a-day/killer-air/slideshow/71789493.cms

9.      Sharma M, Dikshit O. Comprehensive study on air pollution and greenhouse gases in Delhi [Internet]. Kanpur; 2016. Available from: http://cerca.iitd.ac.in/files/reports/IITK study 2016.pdf

10.  Cho C, Hsieh W yeh, Tsai C hung, Chen C yi, Chang H fang, Lin C sheng. In vitro and in vivo experimental studies of PM2.5 on disease progression. Int J Environ Res Public Health. 2018

11.  Badami MG. Transport and urban air pollution in India. Environ Manage. 2005

12.  Nidhi, Jayaraman G. Air quality and respiratory health in Delhi. Environ Monit Assess. 2007; 135:313–25. [PubMed] [Google Scholar]

13.  Secretiat C. Beijing’s air quality improvements are a model for other cities. Climate and clean air coalition [Internet]. 2019; Available from: https://www.ccacoalition.org/en/news/beijing’s-air-quality-improvements-are-model-other-cities.

Do we need lumpers or splitters in Pulmonary Practice?

Pulmonary Medicine is the subspecialty of internal medicine (even we can call it as super-specialty) that focuses on the diagnosis and management of disorders of the respiratory system, including the lungs, upper airways, thoracic cavity, mediastinum and chest wall. Although most common respiratory problems are treated by general internists and other specialty physicians, those practicing pulmonary medicine (often referred to as “pulmonologists”) are frequently called upon to help diagnose unknown disorders and assist in managing difficult, unusual, or complicated diseases of the respiratory system.  

There is an unfinished debate on the issue of treating pulmonology as a sub- (or super-) specialty of medicine. Why I call it subspecialty is that it is an integral part of internal medicine, not separated, but deals with science of respiratory system. In that count cardiology, neurology, nephrology etc. are also sub-specialties. Basic knowledge of medicine is essential to practice these subspecialties. In the United States, an applicant for a fellowship in pulmonary (or any other sub-specialty) must be previously certified in internal medicine by the American Board of Internal Medicine (ABIM). This is also the case in India for super-specialties, such as Cardiology, Nephrology, Gastroenterology, Neurology and others.

Pulmonologists have expertise in structural, inflammatory, infectious, and neoplastic disorders of the lung parenchyma, pleura and airways, pulmonary vascular disease and its effect on the cardiovascular system, and detection and prevention of occupational and environmental causes of lung disease. Diseases commonly evaluated and treated by pulmonologists include asthma, chronic obstructive lung disease (COPD), lung cancer, interstitial and occupational lung diseases, complex lung and pleural infections including tuberculosis, pulmonary hypertension, and cystic fibrosis. Some pulmonologists focus on sleep-disordered breathing (such as sleep apnea) and may provide diagnostic and therapeutic services in sleep laboratories. 

Even though, we have our subspecialty named as pulmonology or Pulmonary Medicine, there is a trend among our colleagues to further split the specialty. In 1960s and 70s, Internal medicine or general medicine suffered from this splitter syndrome, wherein most of the specialties started separating from the parent discipline and started independent practice. Now almost all diseases are shared by these splinter groups and M D in general medicine is like a “glorified MBBS’. This has a long-lasting impact in a country like India where family practice or general practice (GP) is not mandatory for specialty consultation. This was welcomed by all doctor groups looking at the lucrative names and the fame attached to it, ignoring the fundamental principles of medical practice. The terms used by our colleagues as intensivist or interventionist point to such a phenomenon in pulmonary medicine and I am afraid that history is being repeated.

I am writing this based on my recent experiences while formulating a scientific programme for the just concluded Napcon 2019 at Kochi. As you all know preparing a scientific programme of that magnitude was a herculean task. I have done my level best to invite topics in each subcategory from colleagues working in different capacities. To my surprise I got very good topics worth of three Napcons. I had to spend a lot of time to carefully select the best out of that and to fit in to the scientific programme. Then the task is to allot topics to appropriate faculty. Two organizations representing pulmonologist of India are responsible for conducting Napcon. Preferences in selection of faculty will always be there and as organizing team we must respect these rules. We had about 350 to 400 faculties in the wish list. Out of these some 30% faculties are known to me and the rest are not in my remote sense. Allotting topics to these faculties is always going to be a problem unless their interests and preferences are known. What we have done next is to send e mails to all prospective faculties to inform us about their preferences and choices of topics. Only 20 % faculties responded and since we are bound to respect the timelines also, topics were randomly allocated to faculties.

Now the real problem surfaces, as mails started flowing saying that the topic allotted to them are not according to their interest or field of practice. Few replies really shocked me. One was like this. “The topic allotted to me for a guest lecture is foreign to me. I am in no way related to this topic and I regret to inform that I cannot take up this assignment”. I looked up at the qualification, designation and affiliation of this faculty. He is a fully qualified professor in a reputed national institute teaching both undergraduates and postgraduates.

This really disturbed me a lot. If a section of Pulmonary Medicine is ‘foreign’ to a professor of a medical institute, how the teaching in that department goes. During discussion in a postgraduate symposium, if this topic is brought in what will be the response of this faculty. Forget about postgraduates, undergraduate teaching is to be a little broader and if one aspect is not touched by a faculty, how are we going to complete the teaching.

This is where lumping and splitting comes. Both have its own merits and demerits, especially in science. As per Wikipedia definition, a "lumper" is an individual who takes a gestalt view of a definition, and assigns examples broadly, assuming that differences are not as important as signature similarities. A "splitter" is an individual who takes precise definitions and creates new categories to classify samples that differ in keyways. There are lumpers, who like to group things into broad categories, and there are splitters, who divide things into smaller categories. Splitting often leads to “distinction without difference”, ornamental or fussy categories, and failure to see underlying similarities.

When we look at the history of training in Pulmonary Medicine, it started with a course of diploma in tuberculosis after the degree of under graduation (MBBS) to tackle the problem of tuberculosis. Later, this diploma course was upgraded to the degree of MD (Tuberculosis and Chest Diseases) to tackle the high incidence of pulmonary tuberculosis. As the time went on, when specialized work started then we tried to ignore the basic things and concentrated on sophisticated work. This is the inherent issue when we start splitting everything in small specific compartments. What has happened to tuberculosis now, will happen to pneumonia, asthma or COPD in future.

We should never be ignoring the basic sciences, because we have sophisticated equipments and other paraphernalia to take care of. A pulmonologist these days need to engage with a bit of several other sub-specialties, especially rheumatology and immunology, cardiology and cardiothoracic surgery, environmental and occupational medicine, aviation and diving medicine, oncology, sleep medicine and many others. Respiratory critical care is a major component of pulmonary medicine. It includes the mandatory components of cardio-pulmonary resuscitation, intubation and mechanical respiratory supports. Lungs constitute an important target of damage of most of the life-threatening diseases with mechanical ventilation as the prime focus of critical care management. It is, therefore, important to include critical care as an integral component of pulmonology subspecialty programmes.

Every institute taking up postgraduate training in Pulmonary Medicine should have all facilities to train the students to equip them to meet the challenges of practice. Trained specialists should undergo continuing medical education periodically to abreast their knowledge or participate in hands on workshop to improve their skills. This will prepare them to become a ‘complete specialist’ confident enough to meet any challenges in clinical medicine. It is an insult that a qualified postgraduate is not trained in bronchoscopy or thoracoscopy during their course. Many institutes have now started fellowship in critical care, intervention, allergology etc. to compartmentalize the specialty. Those who acquire this fellowship would love to call them as specialist in that category and their knowledge and practice get narrowed down. This is the main demerit of splitting.

I consider that Pulmonary medicine, whether a subspecialty or super-specialty, remain as a single discipline. We don’t promote splitting it up as intensivist, interventionist, allergologist etc. Tuberculosis shall continue to bother pulmonologists more than the internists and other specialty physicians. Pulmonogists must engage themselves with TB and RNTCP as one of their prime curricular and practice needs. A pulmonologist should also possess the skill to perform diagnostic tests and therapeutic interventions in addition to the cognitive knowledge of diseases and their management. All fellows in pulmonary medicine should be able to identify and manage all pathological conditions related to this specialty and try to get an integrated approach when multiple specialist services are needed. One should be able to treat tuberculosis, ARDS or tracheal tumors with the same spirit and vigor. Let us be lumpers rather than splitters. That is good for the specialty too.

Further reading

1.     1.  Jindal SK. Pulmonary training facilities in medical colleges in India. Indian J Chest Dis & Allied Sci 1989; 31:295-98.  

2.     2.  HS Hira. Training of pulmonary medicine in India. Lung India 2006; 23 (3):132.

3.    3. American Board of Medical Specialties/Internal Medicine/Pulmonary diseases. Available from URL: www.abms.org (Accessed on March 16, 2013).

4.     4. Jindal SK. Pulmonary and critical care medicine: objectives of training (Part I). Lung India 1997; 15:112-14. 

5.      5. Jindal SK. Pulmonary and critical care medicine: curriculum and evaluation (Part II). Lung India 1997; 15:164-67.

6.      6.. Ravindran C: Critical Thinking in Clinical Practice; Pulmon 2006; 8:3:73-75

(Author is presently working as Professor and Head of Pulmonary Medicine in DM Wayanad Institute of Medical Sciences, Wayanad, Kerala. He has worked in the capacity of Principal of Govt Medical College, Kozhikode and Managing Director of Academy of Medicine Sciences, Pariyaram, Kannur. He has 35 years of teaching experience in Pulmonary Medicine. He was the organizing chairman of just concluded Napcon 2019 at Kochi, Kerala)

AGING LUNG

AGING LUNG- Review Article 

Introduction Demographic transition in India is showing an increased proportion of aged population in the country. The overall life expectancy rate in India is 69.1 years, and it is 67.8 years for males and 70.5 years for females respectively. In the state of Kerala, the average life expectancy is 74.9 years with a break up of 72 years for males and 77.8 years for females. The absolute number of over 60 populations was 78 million in 2001 and is projected to be 137 million in 2021. These demographic changes influence the health, economic activity and social condition of the people. As age advances every organ in the body undergoes structural and functional decline. It is evident when we see the wrinkled skin and flabby muscles of an elderly person. These changes are natural and compatible with comfortable living as physical and intellectual activities are less in such advanced age. Groundwork of whether a person will age well, or age poorly, begins early in life. By the time we are in our second or third decade, biological aging and chronological aging do not proceed in parallel steps1. Some biologic measures are more predictive of whether an individual will have a life of relatively good health, or develop chronic diseases, and die early. Pulmonary disease has significant consequences for the aging population. Changes in the respiratory system are also natural, as our lungs enter their "golden years". However, these changes should be gradual and subtle. The normal ageing process brings about changes to the respiratory system which mean older people are at increased risk of respiratory compromise. Our lungs mature by the time we are about 20-25 years old. After about the age of 35, it is normal for the lung function to decline gradually as age advances. Forced vital capacity (air that is expelled after a forcible exhalation) can decrease by about 200 ml per decade (20 ml/year), even for healthy non smoking person. This decline becomes 35ml/year after the age of 65 years. Forced expiratory volume in one second (FEV1) declines by 1 to 2 percent per year after about the age of 35.The respiratory system has numerous functions in addition to its central role in gaseous exchange; it has a role in regulating blood pH and maintaining mechanical and immune defenses. Lung function seems to play a significant role in healthy aging2,3. 

Case Scenario-1: I recollect the story of an 80 year old retired nurse referred as a case of interstitial lung disease. She started experiencing shortness of breath on walking or climbing stairs for the last 3 years which is gradually progressing, affecting her house hold work. As she is living alone she has to attend to all her personal needs including cooking food. The referring physician detected fine crackles in the left lung base and advised X Ray chest which was reported as normal. Her cardiac work up was also normal. A spirometry attempted recorded poor values due to improper effort. On evaluation her respiratory system appeared normal for her age and the basal crackles detected in the left lung base is part of aging process and not due to any lung disease. This is important as the closing volume increases as age advances and left lower lobe being compressed by the left ventricle has more impact than right lower lobe. But it is difficult to convince a person who is self dependant for years and developed symptoms only recently. An HRCT thorax was advised which also reported normal with age related changes. It is important to have knowledge on lung function decline as age advances and all activities should be modified to ones comfort level. Trying to stretch it beyond a certain level to satisfy our needs make one symptomatic. Another thing which can be tried here is to build exercise tolerance. This has to be started early in life so that the impact of aging process on respiratory system will be slower. 

Structural and functional changes with aging Chest wall is vital for optimal lung function. Changes to the spine, muscles, and ribs with aging impact normal lung function. As people normally age, narrowing of the intervertebral disc spaces causes increased kyphosis of the spine. This curvature decreases the space between the ribs and creates a smaller chest cavity4. After age 40, the kyphosis angle begins to increase more rapidly in women than men, from a mean of 43° in women aged 55–60 years, to a mean of 52° in women 76–80 years of age5. It is reported that with increasing vertebral angle there is a significant decline in the forced expiratory volume in 1 second (FEV1) and vital capacity (VC). The angle of the muscle fibers in relation to the ribs may also affect the efficiency and decrease the movement of the lower ribs during inspiration6 . These changes are structural and based on the origin and insertion of the muscles. Aging is associated with reduced inspiratory and expiratory muscle strength. Overall muscle function in the body decreases by 2% annually as we age7. The most important respiratory muscle, the diaphragm, undergoes structural changes such as flattening, fibrosis and regional weakness leading to functional decline. Respiratory muscle decline can lead to an inability to ventilate in the face of increasing demands, such as that seen in respiratory disease. There is also evidence that at the cellular level, the muscles of elderly individuals have less mitochondrial adenosine triphosphate reserves to sustain a sudden increase in metabolic demand8. If an elderly person becomes ill with pneumonia, and therefore has increased metabolic demands for oxygen in the setting of decreased respiratory muscle strength and decreased cellular energy reserve, he or she may not be able to meet those demands. This leads to an increased risk of respiratory failure in older individuals9. With aging there is a decreased ability to clear mucus from the lungs. Two mechanisms primarily contribute to this decline: 1) reduced cough strength and 2) alterations in the body’s ability to clear particles in the airways. Any decrease in the strength of the respiratory muscles will greatly impact an individual’s ability to generate the force required for an effective cough10. Aging is associated with reduction of both inspiratory and expiratory muscle strength. There is age-related atrophy of muscle fibers, termed sarcopenia, which may also explain the reduced respiratory strength in the elderly. The decrease in muscle fiber strength can be as high as 20% by age 7011. The elasticity of the lung is reduced. Elasticity is the important factor for inflation and deflation of lungs. Once it is reduced the natural capacity to inhale and exhale effectively is affected. Along with that the alveoli are enlarged. This leads to retention of more air in the lungs. This is called senile emphysema. These changes are much more in smokers when compared to non smokers. 

Physiological changes with aging: Number of alveoli, alveolar ducts, and capillary segments are stable once adulthood is reached and total lung volume remains the same12. There will be reduction in functional capacity of the lung. The alveolar-capillary surface area increases13 and elasticity decreases, resulting in an increase in resting functional residual capacity and an increase in end-expiratory lung volume. In healthy older adults, these functional changes may only be felt during extreme exertion14, but age-related changes in capacity must be accounted for when diagnosing lung disease. 

Case Scenario-2: A 75 year old nonsmoker used to complain of exertional breathlessness. He had multiple consultations for this and is using inhaled bronchodilator on a presumptive diagnosis of COPD. Otherwise healthy person, he has no identifiable cardiovascular morbidity. Looking at his occupation which he is doing for the last 50 years, it is evident that he is overstretching his respiratory reserve at this age. He is working as electric welder and has to manage metal rods and sheets which precipitate his breathlessness. This scenario indicates that although there may be global reduction in lung function, it is slow in development and the individual can cope up with these changes by life style modification, so that there is less work load on respiratory system. 

FVC and FEV1, or the ratio of FEV1/FVC, change in a linear manner with age. The reference values inferred from younger populations are inaccurate when applied to older adults and can lead to a misdiagnosis of COPD15. These physiologic changes to the lungs contribute to changes in lung function and susceptibility to disease (Table 1) 12, 13. Lung diseases such as COPD and pulmonary fibrosis increase with age, as does the incidence of pneumonia16. In some cases, such as pulmonary fibrosis, the development of disease is clearly linked to cellular senescence such as mitochondrial dysfunction17. Measures of Lung Function Changes With Age Total lung volume No change Alveoli (number) No change Alveoli (size) Increases Alveoli (elasticity) Decreases Functional residual capacity Increases due to changes in elasticity and enlargement of airways End-expiratory lung volume Increases due to changes in elasticity and enlargement of airways Apparent diffusion coefficient Increases due to airspace enlargement FEV1/FVC Decreases due to changes in elasticity, airspace enlargement, and other physiologic changes Airspace wall surface area per unit volume of lung tissue Decreases due to airspace enlargement Table-1: Showing physiological changes in lung function due to aging 

Immunological changes with aging Lung, over the course of an average life is exposed to particulates, ozone, aerosols, infections, allergens, and pollutants. In addition to this some people are exposed to cigarette smoke, radiation, drugs and medications, mechanical injury, and exposure to industrial pollutants. Consequently, tissue repair is of paramount importance in the lungs as we age. Inappropriate or ineffective repair can lead to fibrosis, dysplasia or remodeling. Tissue repair and remodeling are orchestrated by epithelial cells, immune cells, fibroblasts, and progenitor cells, all of which undergo age-related changes that affect function. It is found out that there is basal activation of the innate immune system in aged individuals in the absence of an immunologic threat18. This phenomenon, referred to as “inflammatory aging”, is marked by elevated levels of tissue and circulating pro-inflammatory cytokines in aged subjects. Related to inflammatory aging is the blunted immune response, known as “immune-senescence”, following a pathogenic threat or tissue injury18. Multiple studies have established reduced levels of mediators such as TNF-α, IL-6, interferon-γ, nitric oxide, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1α after different types of antigenic stimulation in aged animals19. The interplay between inflammatory aging and immune-senescence, leads to disruption in the balance of pro- and anti-inflammatory mediators in favour of a pro-inflammatory environment with advanced age, which subsequently retards an appropriate adaptive immune response. This imbalance of immune mediators, delayed immune activation, and protracted course of inflammation may result in increased morbidity and mortality in aging individuals following infection, environmental exposures, or systemic injury. 

Pathological changes with aging Chronic respiratory diseases, such as asthma, emphysema, chronic bronchitis, bronchiectasis, and interstitial lung diseases have higher mortality among people aged 65 years and older. Many respiratory diseases develop exclusively in the elderly. Similarly many diseases have poor out come in the elderly when compared to their younger counterparts. Pneumonia severity is assessed by CURB65 score. According to this score individual aged 65 or more are at risk of developing severe pneumonia. Resolution of pneumonia is delayed and mortality is very high in elderly individuals. COPD usually starts after the age of 50 years. The prevalence of COPD is two to three times higher in people over age 60. The increased burden of COPD seen in the elderly population may be due to age-associated changes in the structure and function of the lung, increasing the susceptibility to COPD. It is a progressive disease and cause significant morbidity after 65 years of age. Acute infective exacerbations, hospitalizations and ICU admissions are more in the elderly. It is reported that infective exacerbations due to fungal infections is more common in elderly COPD patients20. Idiopathic pulmonary fibrosis is another disease of the elderly. Due to immunological injury and repair, progressive fibrosis develops. This causes irreversible damage to the lungs leading to compromised respiratory function. Lung cancer also is frequently manifested in the elderly individuals. Due to exposure to smoke and irritants there will be dysplastic changes. Due to poor defense in the elderly, irritants are not effectively removed from the respiratory tract. This can lead to metaplastic and neoplastic changes as age advances. Many systemic diseases of the elderly are also linked with poor respiratory function. It is well proved that development of Type-2 diabetes, a disease of the elderly, is linked to functional decline of the lungs. Individuals whose FEV1 and FVC are at the lower end of the normal range develop many diseases of elderly such as cardiovascular disease, type 2 diabetes and cognitive decline, earlier than those with normal lung function. A chest wall change such as increased kyphosis due to spondylosis reduces respiratory compliance. Dementia and Parkinsonism are frequent causes for aspiration related lung diseases in the elderly. It is reported that low lung function is an accelerant to the aging process; and in turn can be considered as a predictor for development of any of the age-related conditions. Consistent with this statement, a study of middle-aged adults found that lower FEV1 and FVC at baseline correlated with lower cognitive function and an increased risk of being hospitalized for dementia. 

Interventions to reduce respiratory morbidity in the elderly • Avoid smoking: Cigarette smoking is found to be the most important risk factor for COPD, Idiopathic pulmonary fibrosis and lung cancer. Smoking also increases the chance of development of respiratory infections such as pneumonia and tuberculosis. • Avoid air pollution: Indoor and outdoor air pollutants can damage the lungs. Secondhand smoke, outdoor air pollution, chemicals in the home and workplace can cause or worsen lung diseases such as asthma and COPD. • Exercise: Regular exercise can improve the exercise tolerance and patients feel better and comfortable at that functional level. • Rehabilitation: Especially vocational rehabilitation is essential as age advances. It is important to understand that the decline in pulmonary function occur as age advances and the same level of work load will not be tolerated at an advanced age.. • Weight reduction: Abdominal fat can impede the diaphragm's ability to fully expand the lungs. A combination of both healthy eating and exercise will help in maintaining the optimal weight. • Immunization: It is better to have prophylactic influenza and pneumococcal vaccine after the age of 65 years. This is especially important in patients suffering from COPD and other chronic lung diseases. 

Conclusion Lung health is intimately associated with good health in older adults. There are many age-associated changes in the respiratory system. An efficient respiratory system is essential for health and longevity, but age brings about changes that reduce its efficiency. As the body ages, respiratory muscles lose strength, lung tissues lose elasticity, the alveolar surface area diminishes and lung capacity is reduced. As age increases, the respiratory system is less able to expel inhaled irritants and pathogens due to a reduced cough reflex and a decline in muco-ciliary clearance. There are many complex changes in immunity with aging that increase susceptibility to infections. It is pertinent to know the changes associated with age in order to make a proper clinical diagnosis and offer treatment. Unnecessary investigation and medication may further worsen the respiratory function. Proper counseling and precautionary measures may help the patient to lead a comfortable life with an aged lung. 

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