ECG in Pulmonary Medicine

Role of ECG in the diagnosis of Pulmonary Diseases


Introduction
Electrocardiography is a useful adjunct to other pulmonary tests because it provides information about the right side of the heart and therefore pulmonary disorders such as chronic pulmonary hypertension and pulmonary embolism. Since the electrical activity of the heart is influenced to an extent by the surrounding lungs, proper evaluation of ECG can throw light to many lung diseases. When the lung hyperinflates the heart become tubular-vertical heart- and the ECG shows corresponding changes. Similarly most of the chronic lung diseases leads on to right ventricular hypertrophy and hence ECG findings reflects that of clockwise rotation of the heart.
For better understanding of the ECG changes in pulmonary diseases, the physician should be aware of the P wave axis, QRS axis, rotation of the heart in vertical and horizontal axis and various arrhythmias.
Basics in ECG

1) Electrical axis of the Heart








• Both I and aVF +ve = normal axis
• Both I and aVF -ve = axis in the Northwest Territory
• Lead I -ve and aVF +ve = right axis deviation
• Lead I +ve and aVF -ve
o lead II +ve = normal axis
o lead II -ve = left axis deviation

Causes of a Northwest axis
• Emphysema
• Hyperkalaemia
• Lead transposition
• Artificial cardiac pacing
• Ventricular tachycardia
Causes of right axis deviation
• Normal finding in children and tall thin adults
• Right ventricular hypertrophy
• Chronic lung disease even without pulmonary hypertension
• Anterolateral myocardial infarction
• Left posterior hemiblock
• Pulmonary embolus
• Wolff-Parkinson-White syndrome - left sided accessory pathway
• Atrial septal defect
• Ventricular septal defect
Horizontal heart
Description of the heart's electrical position; recognized in the electrocardiogram when the QRS in lead aVL resembles that in V6 and QRS in aVF resembles that in V1; also, loosely, when the electrical axis lies between −30° and +30°.
Vertical heart
Loosely descriptive of the heart's electrical axis when it is directed at approximately +90, recognized in the electrocardiogram when the QRS complex in lead aVL resembles V1 while that in aVF resembles V6.
Clockwise and Counterclockwise rotation
Clockwise and counterclockwise rotation refers to a change in the electrical activity in a horizontal plane through the heart. If the electrical activity of the heart has turned more to the right side of the patient this is called counterclockwise rotation. If the electrical activity of the heart has turned more to the left side of the patient this is called clockwise rotation.
Clockwise and counterclockwise rotation can be assessed only in the chest-leads (V1 - V6). Normally the R wave amplitude increases from V1 to V5. Around V3 or V4 the R waves become larger than the S waves and this is called the 'transitional zone'. If the transition occurs at or before V2, this is called counterclockwise rotation. If the transition occurs after V4, this is called clockwise rotation.
Causes of clockwise rotation:
• Intraventricular conduction abnormalities secondary to myocardial degeneration
• Right ventricular heart disease
• Shift of the septum to the left
• Dilated cardiomyopathy
• Shift of the whole heart
• Pulmonary emphysema
• Vertical heart (usually thin and tall persons)
Causes of counterclockwise rotation:
• Electrical shift to the right
• Left ventricular hypertrophy
• WPW Syndrome
• Posterior myocardial infarction
• Left septal fascicular block
• Shift of the septum to the right
• Hypertrophic cardiomyopathy
P-Wave Abnormalities
Right atrial enlargement:
• P-wave axis ≥ +750 (low specificity)
• P-wave > 0.15 mV in V1 or V2 (best criterion)
P Pulmonale
• Peaked P-waves ≥ 0.25 mV in II, III, or aVF
• P-wave axis ≥ +750
• Degree of rightward P-wave axis correlates better with lung disease severity than P-wave amplitude
• P-wave amplitude correlates better with RA strain (may be transient)
Right Ventricular Hypertrophy
• RAD ≥ +110 0
• R/S ratio in V1 or V3R > 1
• qR in V1 or V3R (usually seen in severe RVH)
• rSR’ in V1 with R’ > 0.7 mV
• R/S ratio in V5 or V6 ≤ 1
• R-wave in V1 > 0.7 mV
• S-wave in V2 < 0.2 mV • Onset of intrinsicoid deflection in V1 > 35 ms
Need at least two criteria for definite diagnosis.
• Type A – severe RVH as seen in severe PAH, end- stage COPD, severe VPS
• Type B – mild to moderate RVH (must differentiate from true posterior MI)
• Type C – moderate RVH as seen in Mitral Stenosis, or moderate COPD and occasionally in ASD
• IRBBB – moderate RVH or RVOT hypertrophy as seen in ASD, moderate COPD
All types of RVH are usually associated with some degree of RAD
• Intermittent hypoxia and pulmonary vasoconstriction
• Right atrial “strain”
• Right atrial enlargement
• “Clockwise” rotation of the heart
• RVH (usually mild or mod. unless end-stage)
• Lung hyperinflation
• Depressed diaphragms
• Rightward QRS axis
• P Pulmonale (peaked & >0.25 mV) in II, III, aVF
• Shift of transition leftward
• Low voltage in limb leads
• Type B or C RVH (late)
• Transient atrial arrhythmias
Arrhythmias
Changes in the myocardium due to hypoxia and chamber hypertrophy leads on to many rhythm disturbances. Most of them are tachyarrhythmias especially atrial tachycardia. They include atrial flutter, fibrillation, multifocal atrial tachycardia and rarely ventricular arrhythmias.






ECG Criteria for COPD

COPD due to its hyperinflation retards the transmission of electrical activity to the chest wall. Moreover persistent hypoxia, resultant pulmonary hypertension and cor pulmonale influences the myocardial activity.Hence many ECG changes are observed in COPD.Most of them are non specific and cannot contribute to diagnosis. But proper evaluation ECG is needed in all patients to detect early complications and appropriate interventions.
The most frequently observed findings are
• P pulmonale (peaked P ≥ 0.25 mV in II, III, aVF)
• P wave axis ≥ +800
• QRS amplitude ≤ 0.5 mV in all limb leads
• QRS axis > +900
• QRS amplitude ≤ 0.5 mV in V5 , V6
• S1S2S3 pattern with R/S < 1 in I, II, III • L1 sign of emphysema (Deep S wave in Lead 1) • Atrial arrhythmias (especially MAT) COPD likely to be present if one P and one QRS criterion present Other ECG findings in COPD • P-wave axis > +700 = 89% sensitive and 96% specific
• Degree of QRS RAD correlated with severity, but QRS axis > +900 in only 8%
• P axis > + 600 in 60% of cases
• S1S2S3 pattern in only 25 % of case
• Leftward QRS transition with R/S < 1 in V5 V6 (type C RVH) = severe (end-stage) COPD
• In severe cases of Cor pulmonale, there will be changes of left ventricular involvement such as ST-T changes in left precordial leads, LBBB and ventricular tachyarrhythmias.

ECG in Pulmonary Hypertension

The electrocardiogram (ECG) may demonstrate signs of right ventricular hypertrophy or strain, including right axis deviation, an R wave/S wave ratio greater than one in lead V1, incomplete or complete right bundle branch block, or increased P wave amplitude in lead II (P pulmonale) due to right atrial enlargement. Most ECG signs are specific but not sensitive for the detection of right ventricular disease. ECG changes cannot determine disease severity or prognosis



ECG in Cor Pulmonale

Electrocardiographic (ECG) abnormalities in cor pulmonale reflect the presence of right ventricular hypertrophy (RVH), RV strain, or underlying pulmonary disease. Such ECG changes may include the following:
• Right axis deviation
• R/S amplitude ratio in V1 greater than 1 (an increase in anteriorly directed forces may be a sign of posterior infarction)
• R/S amplitude ratio in V6 less than 1
• P-pulmonale pattern (an increase in P wave amplitude in leads 2, 3, and aVF)
• S1 Q3 T3 pattern and incomplete (or complete) right bundle branch block, especially if pulmonary embolism is the underlying etiology
• Low-voltage QRS because of underlying COPD with hyperinflation

Severe RVH may reflect as Q waves in the precordial leads that may be mistakenly interpreted as an anterior myocardial infarction. Additionally, many rhythm disturbances may be present in chronic cor pulmonale; these range from isolated premature atrial depolarizations to various supraventricular tachycardias, including paroxysmal atrial tachycardia, multifocal atrial tachycardia, atrial fibrillation, atrial flutter, and junctional tachycardia. These dysrhythmias may be triggered by processes secondary to the underlying disease, (eg, anxiety, hypoxemia, acid-base imbalance, electrolyte disturbances, excessive use of bronchodilators, heightened sympathetic activity). Life-threatening ventricular tachyarrhythmias are less common.

ECG in Pulmonary Thromboembolism

ECG findings are mostly nonspecific in pulmonary embolism. Most frequent abnormality is tachycardia followed by ST-T changes. The frequently referred S1Q3T3 sign is seen only in 11-50% of cases.
• Sinus tachycardia: 8-73%
• Sympathetic stimulation
• Acute pulmonary hypertension
• RA & RV strain/dilatation
• Spatial changes (clockwise rotation)
• ↑ RV wall stress leading to RV ischemia
• RV dysfunction
• Sinus tachycardia
• P pulmonale
• RBBB (complete or incomplete)
• Acute rightward axis shift
• S1Q3T3 pattern (? IMI)
• ↓ T V1-V3 (frequently persistent) (? ASMI)
• Atrial arrhythmias (Atrial Fibrillation or Atrial Flutter)
• P Pulmonale: 6-33%
• Rightward axis shift: 3-66%
• Inverted T-waves in ≥ 2 Rt chest leads: 50%
• S1Q3T3 pattern: 11-50%
• S1 – 60%, Q3 – 53%, ↓T3 – 20%
• Clockwise rotation: 10-56%
• RBBB (complete or incomplete): 6-67%
• AF or AFlutter: 0-35%
• No ECG changes: 20-24%





ECG in Dextrocardia
• Global negativity in lead I (a negative P-wave, QRS complex and T-wave)
• Positively deflected QRS complex in aVR
• Negative P-wave in lead II
• Reverse R-wave progression in precordial leads
• Right axis deviation.


The finding of a positively deflected QRS complex in aVR and a negative in lead I should cause concern for the treating paramedic. The most common cause for this finding is reversed electrode placement. If this situation presents and the clinician has assured correct limb lead placement, dextrocardia should be on the list of differentials. Once again, consider ventricular arrhythmias first.
R-wave progression is defined as the transition of a predominantly negative QRS complex in V1 to a predominantly positive QRS complex in V6 on the 12-lead ECG.
The change that is a normal variant with dextrocardia is a reversal of this normal pattern, which would present as a predominant R-wave in V1 and a predominant S-wave in V6.

ECG in Hypoxia
• Shortening of R-R interval
• Increase of P wave
• Prolongation of P-Q
• Deviation of the R vector
• T wave flattening in the left precordial leads

ECG in Pericardial Effusion
• The QRS axis alternates between beats( Electrical alternance)
• ST-segment elevation
• PR-segment depression
• Low voltage complex

ECG in Pneumothorax

• Depend on the size of the pneumothorax
• Caused by displacement of the heart
• Most often RAD, independent of the pneumothorax site
• Low voltage frequently present
• QS complexes in precordial leads also common
• T-wave inversions simulate ischemia
• Occasionally ST elevations mimic injury

ECG in ASD

• Secundum: RAD and IRBBB type RVH (RV volume overload) in ≈ 60%
• Primum: LAFB (almost 100%) ± IRBBB (depending on shunt magnitude)
• Sinus Venosus: Ectopic atrial rhythm
(Inverted P waves II, III, AVF in ≈30%)

ECG in VSD

• LVH or BVH depending on site of the VSD
and magnitude of the L-R shunt
• RVH (usually severe type A) with pulmonary vascular disease (Eisenmenger syndrome)

Conclusion
ECG is an important diagnostic tool in many pulmonary diseases. It can supplement other investigations and in the hands of an expert physician ECG it is a cheap and easily available tool to pinpoint many respiratory diseases.

DM IN PULMONARY MEDICINE

Curriculum for DM Pulmonary Medicine

Introduction

GENERAL GOALS OF THE RESIDENCY TEACHING CUM TRAINING PROGRAM IN DM Pulmonary Medicine

The main goal of the training program is to produce pulmonary physicians with the necessary knowledge, skill and attitude to diagnose and manage in an effective manner, a wide range of clinical problems in Pulmonary Medicine as seen in the community or in secondary/tertiary care setting. Special emphasis is placed on the relatively common and treatable disorders. Possession of clinical skills required for making a diagnosis is given utmost importance.

As a result of training in Pulmonary Medicine, the physician should become competent in life saving interventions, the use of the various diagnostic tests, and interprets their results intelligently & promptly. In addition, trained pulmonary physician should possess knowledge and skills of all the relevant medical fields and  appropriately  deliver  the  required  health  care  in  these  sectors.  It  is considered desirable for the post graduate residents from this specialty to be familiar with the fundamentals of research methodology also.

In order to be considered a competent Pulmonologist, a resident in Pulmonary Medicine must possess humanistic qualities, attitudes and behaviour necessary for the development of appropriate patient-doctor relationship.

SPECIFIC AIMS AND OBJECTIVES OF THE RESIDENT TRAINING PROGRAM IN PULMONARY MEDICINE

As a result of the training under this program, at the end of 3 years of postgraduate training, a resident must acquire the following knowledge, skills and competencies:

1. A thorough knowledge of pathological abnormalities, clinical manifestations, and principles of management of a large variety of medical conditions affecting respiratory system.

2. Skill and competence to choose and interpret correctly the results of the various routine investigations necessary for proper management of the patient. While ordering these investigations, a resident must be able to understand the sensitivity, specificity and the predictive value of the proposed investigation, as well as its cost-effectiveness in the management of the patient.

3. Skill and competence in interventions like endotracheal intubation, needle lung biopsy, bronchoscopy, needle thorococentesis, Intercostal drain placement, pericardiocentesis, thoracoscopy, and various endobronchial procedures.

4. Skills and competence to perform commonly used diagnostic procedures, namely, pleural aspiration, pleural biopsy, lung biopsy, allergy testing, fine needle aspiration, polysomnography, ultrasonography and cardiopulmonary exercise testing.

5.  Skill  and  competence  to  choose  and  interpret  correctly  the  results  of specialized investigations including radiologic, ultra-sonographic, biochemical, hemodynamic, electro-cardio graphic, electrophysiological, pulmonary functional, haematological, immunological, nuclear isotope scanning, arterial blood gas analysis results. polysomnographic and bronchoscopic results.

6. Skill and competence to provide consultation to other medical and surgical specialties and  sub-specialties, whenever needed.

7. Skill and competence to function effectively in varied clinical settings, namely emergency/critical care, ambulatory care, out-patient clinic, in-patient wards.

8. Skill and competence to take sound decisions regarding hospitalization, or timely referral to other consultants of various medical sub specialties recognizing his limitations in knowledge and skills in these areas.

9.  Proficiency  in  selecting  correct  drug  combinations  for  different  clinical problems with thorough knowledge of their pharmacological effects, side-effects, interactions with the other drugs, alteration of their metabolism in different clinical situations, including that in the elderly.

10.Skill   and   competence   to   advise   on   the   preventive,   restorative   and rehabilitative aspects including those in the elderly, so as to be able to counsel the patient correctly after recovery from an acute or chronic illness.

14. Skill and competence to understand research methodology in  Pulmonary Medicine and  to  undertake a  critical appraisal of  the  literature published in various medical journals and be able to apply the same in the setting in which the resident is working.

15. Skill and competence to work cohesively in Resuscitation team along with paramedical personnel and maintain discipline and healthy interaction with the colleagues.

16. Skill and competence to communicate clearly and consciously, and teach other junior residents, medical students, nurses and other paramedical staff, the theory as well as the practical clinical skills required for the practice of Pulmonary Medicine.

Recommendations for D. M Pulmonary Medicine

(3 Year Post Doctoral Course)

There are 52 weeks in a year. Approximately 2 weeks are gazetted / restricted holidays. Therefore, for academic requirements 50 weeks per year are available. Hence, for a three year course 150 weeks are available. Out of these, 10 weeks in three years are not available for hospital work & academics due to
conferences / CMEs / exchange programmes / thesis and case study writing.

Since this speciality demands a 24 hour service to the people, post graduates are required to work 8 hours a day and they are given a day off in a week.

Hours available per day

Six days in a week           8 hours                                   8 hours Total number of hours per week        8X6                     48 hours. Total credit hours available for academics
(No of weeks X No of hours available /week = 150 X 48 = 7200 hrs)

The break up is proposed to be as follows :

A   Bedside teaching / Practicals.

No of weeks( 140) X No of working day / week (6) X No of hours available /day (6)
5040 hrs

B   Thesis / case study writing / conferences / CMEs programmes

(No of weeks ( 10) X No of hours available /week (48) )
480 hrs.

C   Theory

No of weeks( 140) X No of working day / week (6) X No of hours available /day (2)
1680 hrs
Grand total                                                                                             7200 hrs

A.   Practical

1) Skill stations                      140 X 6 hours = 840 hrs.

Duration 6 hrs / week

No of weeks   140.

Skill Stations: Includes all the bedside medical skills pertaining to Pulmonary
Medicine

2) Bed side Medical clerky         140 X 30 = 4200 Hrs

Duration    5 Hrs / day.

30 hrs / week.

Bed side Medical clerky includes case history taking, formulating a working diagnosis, ordering appropriate investigations, and accompanying the patient to the specialized investigation areas, interpretation of all the results and finally starting the treatment protocol for them.

It also lays emphasis on in field resuscitation and transportation of critically ill patients and continuing the care in the ER, ICU and various other places also.

B.  Thesis writing :

NOTE: The 480 hours available should be fruitfully utilized by the student for attending conferences / CME programmes and for dessertation and case study.  Apart  from  this  they  can  utilize  these  hours  for  creating  basic awareness of Pulmonary Medicine among the other specialties and common masses.

C.  Theory

Total Hours Available                             1680 hours.

Besides interactive lectures theory includes Induction, documentation, Orientation, Journal Club, Internal Examination and Final Examination.

Curriculum

Total duration of training program                       3 Years

YEAR I

Introduction and preliminary posting in the

Pulmonary Medicine                                                   3 months

Respiratory Intensive Care Unit                                   3 month

General Medicine / Medical Intensive Care Unit          3months

Cardiology                                                                  2 months

Anaesthesiology                                                          1 month

YEAR II

Pulmonary Medicine                                        3 months

Intensive Respiratory Care Unit                      3 month

Paediatrics / PICU                                         3 months

Emergency Dept                                            2 months

Community Medicine                                     1 month

YEAR III

Pulmonary Medicine                                        6 months

Pulmonary Critical care                                    6month

Final Examination in D M Pulmonary Medicine
At the end of three years of training programme, a post graduate of DM
Pulmonary Medicine should at least possess following skills

CLINICAL SKILLS

1         History taking & Physical examination: Analysis of data for clinical diagnosis
2         Knowledge about common clinical problems, Symptom complex, Diagnostic reasoning
3         Various investigations, interpretation
4         Interventional procedures
5         Critical care, Life saving procedures, Palliation and end of life decisions

COMMUNICATION SKILLS

I          Professional Relationships

A         Patients and relatives B         Colleagues/team work C         Other staff

II         Consultation Skills

II         Record keeping

III       Bereavement Care

A         Breaking bad news

B         Referral for counselling

MANAGERIAL SKILLS

I          Policies/procedures (NHS, Hospital, Departmental) II         Staff management (planning, recruitment, appraisal) III       Equipment (choosing to ordering, medical physics)

IV       Resource management/clinical budgeting

V         Contracting/ setting standards, quality monitoring

VI       Information technology/Health informatics VII      Clinical governance/audit, risk management VIII     Compliments/complaints
IX       Medico-legal statements

X         Committee Work

XI       Liasing with other agencies (e.g. police, coroner) XII      Public Relations/media
XIII     Major Incident planning/exercises

TEACHING SKILLS

I          Lecture preparation

II         Small Group techniques III       Presentation techniques IV       Teaching critique
V         Departmental teaching programme

VI       Professional Development (self-directed learning) VII      Teaching certificate expected

RESEARCH SKILLS

I          Literature survey

II         Scientific study design

III       Data evaluation/Statistics

IV       Preparing publications

PROFESSIONAL ATTRIBUTES

I          Leadership II         Reliability III       Teamwork
IV       Self-motivation (prioritisation, project completion)
SCHEME OF EXAMINATON

Distribution of marks

(Duration – 3 hours each paper)

Paper 1          Applied basic sciences in relation to General Medicine & Pulmonary
Medicine

Paper 2          Non infectious Respiratory Diseases including those affecting
Respiratory centre, Chest wall and Mediastinum

Paper 3          Respiratory Infections including tuberculosis

Paper 4          Respiratory Critical Care and recent advances in Pulmonary
Medicine

Paper I                                                                                                            -- 100marks

a)  2 long essays b)   8 Short notes Model Questions
1) What is acquired immunodeficiency? Discuss the different pulmonary problems in an
immunosuppressed patient.                                                                           20
2) Discuss the central control of Respiration. What you know about hypoventilation syndromes?                                                                                                  20
3) Write short notes on                                                                                 60

a) Thoracic outlet syndrome
b) Role of diaphragm in Respiration c) Dynamic compliance
d) Delayed type hypersensitivity e) Line probe assay
f)  Role of ultrasound in Pulmonary Medicine g) Pressure support ventilation
h) Sepsis syndrome

Paper II                                                                                                          -- 100marks

c)  2 long essays d)   8 Short notes Model Questions
1)   Discuss in detail the relationship between sleep disordered breathing and Hypertension and review relevant studies.                                                                                                   20
2)   Discuss the etiopathogenesis of Lung Cancer.                                                 20
3)   Write short notes on                                                                                       60

 a)   Chylothorax
b)   Asthma mimics
c)    Tiotropium
d)   Congenital cystic adenomatoid malformations e)   Honey comb lung
f)    LVRS
g)    Tracheal stenosis
h)   Primary pulmonary hypertension

Paper III                                                                                                         -- 100marks

e)  2 long essays f)    8 Short notes Model Questions
1) What is pneumonia severity index? Discuss the management of community acquired
pneumonia                                                                                                      20
2) Discuss the relative merits and demerits of revised national tuberculosis control programme.                                                                                                     20
3) Write short notes on                                                                                    60

 a) Mycobacterium growth index tube
b) Acinetobacter
c) XDR TB
d) Exudative effusion
e) Hospital infection control policy
F)  Viral Pandemics g) Haemopysis
h) Hydatid Cyst

Paper IV                                                                                                      -- 100marks

g)  2 long essays h)   8 Short notes Model Questions
1) How will you manage a case of ARDS with multiorgan failure                        20
2) What is health care associated pneumonia ?
How will you manage VAP?                                                                              20
3) Write short notes on                                                                                      60
a) Pulmonary AV fistula b) DLCo
c) Indacaterol
d) Bronchial artery enbolization e) LVEF
f) Toxic gas inhation
g) Diagnosis of Pulmonary thromboebolism h) Lupus pneumonia

Minimum for a pass

Theory aggregate (50% in each paper)                                                      200/400

Clinical/Viva /Dissertations (100+50+50)    (50%)                                    100/200

Grand total                                                                                                300/600

Dissertation                                  Accepted/Not Accepted

(Precondition to appear for the final University Examination)
Clinical         One main case (25x3)                                                -- 75 marks
Two short case(25x2)                                                                    -- 50 marks

Viva-voce/Skill assessment :( 5X10=50marks)

1.  ECG

2.  Radiology (x-rays/ CT)
3.  Sonography(FAST/USG)
4.  Instruments
5.  Ventilatory settings
6.  BLS
7.  Airway and breathing skills( intubation, diagnosed ventilation, needle thorococentesis, intercostals drainage)
8.  Skills related to circulation( central venous cannulation central venous pressure management)
9.  Arrhythmia recognition and management (defibrillation, and
Cardioversion)
10. ABG,Polysomnography PFT Conferences and awards

Moments

PG CME South Zone-2011 at Chennai

COPD-Etiopathogenesis and newer management protocols

Chronic obstructive pulmonary disease (COPD) is a disease characterized by accelerated decline in lung function. Ninety percent of COPD is caused by cigarette smoking; however, only 15% to 20% of chronic tobacco smokers develop COPD, thus implicating additional risk factors in COPD susceptibility. COPD tends to occur more frequently in smokers with family members who have airways obstructive disorders such as asthma and COPD. Thus, there is evidence that accelerated decline in lung function that leads to COPD may be caused by host or genetic factors in a susceptible population of individuals who smoke.

COPD is a complex disorder characterized not only by inflammation but also by tissue remodeling. Remodeling is the net result of tissue destruction and repair. The MMPs and cathepsins are important in tissue destruction and are naturally inhibited by the tissue inhibitor of metalloproteases (TIMP).

It has become clear that the inflammatory process increases in intensity as COPD progresses and does not “burn out” as with many other chronic inflammatory diseases. There is a complex remodeling process in the peripheral lung, resulting in parenchymal destruction (emphysema) and fibrosis of airways (chronic obstructive bronchitis). It is presumed that the inflammatory process leads to these structural changes

COPD pathogenesis can be separated into 4 broad categories: (1) inflammation, (2) age-related changes, (3) genetic associations, and (4) possible therapeutic targets. There is substantial overlap among the categories; however, most of the abstracts fit into the inflammation category.

There is increased inflammation in the bronchial epithelium in smokers with COPD. Smokers without obstruction also had increased numbers of CD4+ cells compared with nonsmokers. CD4+ lymphocytes were increased in the airways of smokers with COPD. Several studies focused on the role of matrix metalloproteases (MMP) in COPD. It is found that the number of airways, type II cells, and macrophages that stained positive for MMP-1 was proportional to severity of emphysema in smokers. Cytokines involved in the inflammatory process of COPD are transforming growth factor-beta (TGF-beta), interferon (IFN)-gamma, stromal cell-derived factor (SDF)-1, urotensin-II, and toll like receptor (TLR)-4.

Aging was also associated with spontaneous changes in the lungs consistent with emphysema. These changes were associated with up regulation of several chemokines (Cxc16, Cxc113, and Cxc19), cell surface receptors (Cd3g, Cd3d and Cd79b), and proteases (MMP12 and MMP9). There were several genetic associations hinting at possible candidate genes that may serve to incite, regulate, or amplify the effects of cigarette smoking-induced airway inflammation.

Candidate genes evaluated for association with the presence or severity of COPD included beta-2 adrenergic receptor, thrombospondin, ADAM33, and TGF-beta. A significant association was found between the Gln27 polymorphism and the presence of COPD in the German population. Risk Factors for COPD

¡        Cigarette Smoking

¡        Exposure to particles

¡        Outdoor air pollution

¡        Genes

¡        Lung Growth and Development

¡        Oxidative stress

¡        Gender

¡        Age

¡        Respiratory infections

¡        Socioeconomic status

¡        Nutrition

¡        Co-morbidities

Systemic Features of COPD

¡        Cachexia: loss of fat free mass

¡         Skeletal muscle wasting: apoptosis, disuse atrophy

¡         Osteoporosis

¡         Depression

¡         Normochromic normocytic anemia

¡         Increased risk of cardiovascular disease

Diagnosis of COPD

Key Indicators for Considering a Diagnosis of COPD

Chronic cough:

¡        Present intermittently or every day, often present throughout the day, seldom only nocturnal.

Chronic sputum production

     Any pattern of chronic sputum production may indicate COPD.

Dyspnea

¡        Progressive (worsens over time).

¡        Persistent (present every day).

¡        Worse on exercise.

¡        Worse during respiratory infections.

History of exposure to risk factors   

¡        Tobacco smoke.

¡        Occupational dusts and chemicals.

¡        Smoke from cooking.

Physical signs

¡         Not specific to the disease and depend on the degree of air flow limitation and hyperinflation

¡         Tachypnoea, purse lip breathing, weight loss, barrel   shaped chest, polyphonic wheezes and crackles

¡          Features of pulmonary hypertension and right heart failure

     Management

Goals of effective management

¡        Relieve symptoms

¡        Prevent disease progression

¡        Improve exercise tolerance

¡        Improve health status

¡        Prevent and treat complications

¡        Prevent and treat exacerbations

¡        Reduce mortality

Current therapy for chronic obstructive pulmonary disease (COPD) has improved the management of this difficult disease, but there is still a pressing need for new therapeutic approaches, particularly in reducing the progression and mortality of this disease. COPD has now become a much greater drain on health resources than asthma, and exceeds the healthcare spending on asthma by some three-fold in industrialized countries. Since the prevalence of COPD is predicted to increase throughout the world by the next 20 yrs, these costs will escalate further. There is no doubt that the management of COPD has improved considerably with the introduction of more effective treatments and the use of non-pharmacological interventions, such as pulmonary rehabilitation and noninvasive ventilation (NIV).

Smoking cessation

Cigarette smoking is the major cause of COPD in the world and smoking cessation is the only therapeutic intervention so far shown to reduce disease progression. Nicotine addiction/dependence is the major problem and treatment should be directed at dealing with this addictive state. At present, several forms of nicotine replacement therapy and some antidepressant drugs are used, but the efficacy of these therapies is low. The most effective therapy available is the atypical antidepressant bupropion and a short course is an effective adjunct for smoking cessation in patients with COPD. However, the relatively poor long-term quit rate (16% at 6 months) indicates that more effective approaches are needed. The partial nicotine agonists that target the α₄β₂ nicotinic acetylcholine receptor, such as varenicline, appear to be promising. Another approach which may have long term benefits is the development of a vaccine against nicotine. The vaccine is designed to stimulate the production of antibodies that bind nicotine so that it cannot enter the brain.

Long-acting bronchodilators

COPD guidelines now recommend the use of long-acting bronchodilators as the mainstay of COPD management. The introduction of the long-acting β₂-agonists formoterol and salmeterol and the anticholinergic tiotropium bromide have been important advances in the management of COPD.

The overall approach to managing stable COPD should be characterized by a stepwise increase in the treatment, depending on the severity of the disease. None of the existing medications for COPD has been shown to modify the long-term decline in lung function that is the hallmark of this disease. Therefore, pharmacotherapy for COPD is used to decrease symptoms and/or complications. The choice between beta-2 agonist, anticholinergic, theophylline, or combination therapy depends on availability and individual response in terms of symptom relief and side effects.

Regular treatment with long-acting inhaled bronchodilators is more effective and convenient than treatment with short-acting bronchodilators, but more expensive. Combining bronchodilators may improve efficacy and decrease the risk of side effects compared to increasing the dose of a single bronchodilator. Current evidence supports the use of at least one of the two classes of long-acting inhaled bronchodilators as initial maintenance therapy for symptomatic COPD. In patients who do not respond satisfactorily to tiotropium or LABA as the initially prescribed single maintenance agent, GOLD guidelines recommend the addition of the alternate class of long-acting inhaled bronchodilator as the next step. The choice of agents will depend ultimately on how well the patient responds to a trial of the drug in terms of both efficacy and side effects, and patient preference and cost.

Indacaterol, (Ultra LABA) significantly improved lung function compared to placebo at 12 weeks in three phase III studies. When given once daily, it showed clinically relevant 24-hour bronchodilation and the onset of action was within five minutes. In a 52-week study, it increased lung function compared to twice-daily Formeterol from day one through one year of treatment.

Treatment with tiotropium provides clinical efficacy in patients with GOLD stage II disease with all levels of FEV1. Aclidinium, the new long acting anticholinergic, provided clinically significant bronchodilation and improvements in dyspnoea and may be a valuable new treatment for COPD.

 Regular treatment with inhaled glucocorticosteroids is appropriate for symptomatic COPD patients with an FEV1 < 50% predicted (Stage III and Stage IV) and repeated exacerbations e.g. 3 in the last three years. Inhaled glucocorticosteroid combined with a long-acting B2-agonist is more effective than the individual components. Chronic treatment with systemic glucocorticoids should be avoided because of an unfavorable benefit-to-risk ratio.

Long Term Oxygen

The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival.

 Avoidance of risk factors

¡            smoking cessation

¡            reduction of indoor pollution

¡            reduction of occupational exposure

Vaccines

¡                    Influenza vaccines

¡                    Pneumococcal polysaccharide vaccine

Newer Drugs

PDE4 Inhibitors: Inhibit neutrophil chemotaxis, adhesion, degranulation and release of proteases. They also reduce exacerbations; improve lung function and health status. The promising drugs in this group are Cilomilast and Roflumilast.

N Acetyl Cysteine

N-acetyl cysteine (NAC) provides cysteine for enhanced production of the antioxidant glutathione and has antioxidant effects in vitro and in vivo. A systematic review of studies with oral NAC in COPD suggested a small reduction in exacerbations.

Other Targeted Drugs

¡        Neutrophil elastase inhibitors

¡        Cysteine protease inhibitors

¡        MMP inhibitors

¡        EGFR inhibitors

¡        Endothelin antagonists

¡        PDE- inhibitors

¡        TNFa inhibitors

¡        IL-8 antagonists

¡        Mucoregulators

Exacerbations of respiratory symptoms requiring medical intervention are important clinical events in COPD. The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified. Inhaled bronchodilators (beta2-agonists and/or anticholinergics), theophylline, and systemic, preferably oral, glucocorticoids are effective for the treatment of COPD exacerbations. Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased volume and change of color of sputum, and/or fever) may benefit from antibiotic treatment. Noninvasive intermittent positive pressure ventilation (NIPPV) in exacerbations improves blood gases and pH, reduces in-hospital mortality, decreases the need for invasive mechanical ventilation and intubation, and decreases the length of hospital stay.

Pulmonary Rehabilitation

        The principal goals are to

¡        Reduce symptoms

¡        Improve quality of life

¡        Increase physical and emotional participation in everyday activities

¡        Improves exercise capacity

¡        Reduces the perceived intensity of breathlessness

¡        Improves health-related quality of life

¡        Reduces the number of hospitalizations and days in  the hospital

¡        Reduces anxiety and depression associated  with COPD

Surgical Options

¡        Bullectomy: When a large unilateral bullae which gradually compresses healthy lung, bullectomy is the best option.This can be done by thoracotomy or through thoracoscopy.

¡        LVRS: When bullous lesions are heterogenous and mainly occupying upper lobes lung volume reduction surgery can be undertaken. This removes mostly diseased part of lung allowing remaining part of lung to inflate adequately. This reduces air trapping and dynamic compression. Three methods are available 1) LVRS by thoracotomy 2) LVRS through VATS and 3) LVRS by endobronchial valves.

¡        Lung Transplantation: Lung transplantation should be offered to patients with diffuse disease who have any of the following

¡        FEV1 <20% predicted

¡        Hypercapnia

¡        Associated pulmonary hypertension

¡        Predicted survival of less than the expected post-transplant survival.

Potential lung transplant recipients must be ambulatory and have a preoperative weight of 70-130% of predicted. Candidates should also be motivated, have adequate social support to deal with the rigorous pre- and post-transplant activities, and have undergone a comprehensive preoperative pulmonary rehabilitation program.

Conclusion

COPD is a disease with progressive deterioration in lung function. There is no effective treatment to revert the pathology, but proper drug selection combined with programmed rehabilitation can improve the quality of life in these patients. For this we need advanced care planning (ACP) and proper implementation of treatment strategy.