copd by magdi sasi 2016

CHRONIC OBSTRUCTIVE AIRWAY DISEASE DR.MAGDI AWAD SASI 2015

COPD

Essential for diagnosis:

H/O cigarette smoking

Chronic cough and sputum production in bronchitis

Exertional dyspnea in smoker in emphysema

Rhonchi with prolonged expiration in local chest examination and decreased

breath sounds in emphysema

PFT---- obstructive pattern

DEFINITIONS:

GENERAL –it is a chronic slowly progressive disorder characterized by airflow obstruction ((

FEV1 < 80% and FEV1/ VC ratio < 70% of predicted values )) which doesn’t change over

several months . Mostly are fixed ( emphysema & bronchitis ) but some reversible

(asthmatic bronchitis).

INDIVIDUAL DEFINITIONS:

1. CHRONIC BRONCHITIS:

Excess mucous production manifested by recurrent productive cough on most days

for > 3 months/years , for > 2 successive years in the absence of other conditions

associated with cough and sputum such as Bronchiectasis ,bronchial asthma ,cystic

fibrosis and mitral stenosis with lung congestion.

It is divided into :

A. Simple chronic bfronchitis ----- when sputum is mucoid

B. Mucopurulent

C. Chronic obstructive bronchitis -----with or without bronchiolitis.

2. Emphysema:

Dilation of air spaces distal to respiratory bronchioles with destruction of bronchial

walls without fibrosis --- clinically it present with hyperinflation.

It is divided into:

1. Centrolobar emphysema ---- in association with chronic bronchitis (( mild ))

2.Panlobular (( panacinar )) emphysema --- in association with bronchiolitis , there

is sever emphysema with minimal features of chronic bronchitis.

PREDISPOSING FACTORS:

1. Cigarettes smoking ---- smoking index 20—30 cigarettes/ day x 20-30 years

Cigarettes smoking

Pulmonary alveolar macrophage Oxidants


Release neutrophil chemtactic factor inactive α 1 antitrypsin

Attract PMNL to alveolus EMPHYSEMA

Neutrophil release

2.Cold dam climate: humidity reduces rate of smoke disposal , and dissolves

some of irritant gases ( esp. sulfur dioxide and tronxide ) and potentiates their

action on bronchial mucosa.

3.Chronic upper respiratory tract infections--- chronic tonsillitis ,sinusitis.

4.Chronic pulmonary congestion:

Mitral stenosis causes winter bronchitis and left ventricular failure.

5. Chronic expiratory effect -----musicians and glass blowers.

6.Genetic predisposition----- α 1 antitrypsin deficiency ( normally it is a potent

enzyme inhibitor against the proteolytic enzyme neutrophil elastase )

transmitted as an autosomal recessive trait and present as sever panlobular

emphysema and liver cirrhosis , very early in life (( 30—40 years of age)).

TOBACCO SMOKE IS BY FAR THE MOST IMPORTANT RISK FACTOR FOR COPD WORL WIDE.

Exposure HOST FACTORS

Smoking Socio-economic Occupation Environmental pollution Diet Recurrent bronchopulmonary infections Perinatal events and childhood illness

Genetic factors Sex Airway hyperreactivity IgE and asthma

PATHOGENESIS:

1. Simple chronic bronchitis: due to bronchial irritation .

It is reversible if the patient stop smoking.

2. Mucopurulent stage: persistence of irritation leads to:

A. Bronchospasm

B. Hypertrophy and hyperplasia of mucus glands ,with excess mucus production.

C. Paralysis of cilia with stasis of mucus blanket.

The traditional view of asthma as a "reversible" disease and COPD as being "irreversible" is no

longer tenable. COPD is now defined as airflow limitation that is "partially reversible"and this

reversibility is generally greater with anticholinergic therapy. Furthermore, asthma probably

becomes less reversible with chronicity and poor control that lead to airway remodeling.


This leads to secondary infection ,commonly with hemophilus influenza and penumococci .

Microascesses forms in wall of bronchi and mucopurulent discharge occurs ,with distortion

of air way ending in irreversible bronchial obstruction.

Chronic obstructive bronchitis : chronic irreversible obstruction , mainly affects small

airways due to :

a. Impaction of mucus in lumen

b. Hypertrophy of bronchial mucosa with infiltration by inflammatory cells

c. Hypertrophy of smooth muscles

d. Peri-bronchial fibrosis

e. The condition may be complicated by emphysema

PATHOPHYSIOLOGY:

The clinical picture of COPD ,depend on whether the dominant effect is wide spread airway

obstruction or emphysema.

Two pure forms (( not common )):

A. PINK PUFFER –TYPE A FIGHTER ----EMPHYSEMA:

1. Loss of alveolar walls ,leads to reduction of the area of alveolocapillary

membrane over which diffusion of O2 &CO2 take place-diffusion defect

2. Diffusion power of CO2 is 20 times more than O2 –hence O2 diffusion is

reduced and CO2 is practically not reduced. Hypoxia with normal/ CO2

3. Normally ,respiratory center is sensitive to increase in CO2 while carotid and

aortic chemoreceptors are sensitive to hypoxia.

4. In emphysema ,hypoxia stimulates chemoreceptors leading to rapid deep

respiration and consequent dyspnea , to improve hypoxia and to wash CO2

5. The patient is termed pink puffer--- not cyanosed (Dyspnea improves hypoxia).

B. BLUE BLOATERS ---TYPE B –NON FIGHTER ---CHRONIC BRONCHITIS:

Puffing increases:

Time of expiration –allowing air to remain longer time in alveoli

Intra-alveolar pressure ,hence increasing back O2 diffusion

1. Diffusion is normal ( alveolar capillary membrane free).

2. Wide spread air way obstruction , impedes ability of air to move in &out

alveoli . This is termed alveolar hypoventilation .

3. Affinity of HB to O2 is very high compared to its affinity to CO2. So initially no

hypoxia occurs since HB will absorb any O2 available , on the other hand

increases CO2 content of alveoli leads to proportionate rise in PCO2 in the

blood , this hypercapnia leads to hyperventilate to wash out CO2.

4. With further progress of bronchial narrowing ,collapse of some areas occurs

with underventilation despite good perfusion.

Hence hypoxia starts with further rise in PCO2 and more hypercapnia.

5. Normal people respond to hypercapnia by hyperventilation ((stimulate RC ))

But in bronchitis ,chronic CO2 retention doesn’t cause hyperventilation.


The respiratory center being set at higher level of PCO2 the only remaining

stimulus for respiration is HYPOXIA (( peripheral chemoreceptor )).

6. The patient is termed blue bloater:

BLUE—due to central cyanosis

BLOATER—hypoxia leads to pulmonary HTN ,cor pulmonale and edema.

Those patients are obese—CO2 retention depress CNSs with lack of activity.

CHARACTERISTIC FEATURES: 80% of patients have had significant exposure to tobacco smoke. In chronic bronchitis , symptoms improve in 90% if they stop smoking. Obstruction is progressive and may be accompanied by airway hyper-reactivity. Progressive disorder of airway obstruction with no or mild reversibility

FEV1 < 80% FEV1 /FVC < 0.7

COMPLICATIONS:

A. CVS:

i. Hypoxia---leads to:

1. Vasosocstriction of pulmonary arteries

2. Vasodilatation of peripheral arteries---- to increase pulmonary blood flow

3. Increased blood viscosity due to polycythemia

4. Depression of myocardial contractility

ii. Cor pulmonale due to secondary pulmonary HTN ---RVH---RVF

iii. Left –side heart failure occurs due to:

A. Two ventricles act as one unit so failure of one will affect the other

B. Reversed Bernheim effect –push RT IVS to the left & decrease LV

C. Associated LV disease---coronary artery disease.

B. Renal regulation in COPD:

Increased PCO2 is compensated by renal reabsorption of Na HCO3 from tubules.

This leads to peripheral edema.

This is seen in blue bloater in absence of corpulmonale.

CLINICAL PICTURE:

The patient is usually a male ,above 50 years ,heavy smoker

Symptoms—in advanced cases due to hypoxia ,hypercapnia and corpulmonale.

General weakness ,easy fatigue ,anorexia ,weight loss

Due to hypercapnia ---brain edema (( increase ICP )) may lead to:

Drowsiness

Headache

Impaired sensorium

Astrexis—flapping tremors

Coma—CO2 narcosis

Ankle edema-----due to corpulmonale and renal regulation.

Chest symptoms:

1. TRIAD OF COUGH ,DYSPNAE ,WHEEZE.


COUGH---special history of chronic cough ,with mucoid or mucopurulent

expectoration of 3 months for 2 consecutive years .

Frequent exacerbations leading to eventual disability.

DYSPNEA—gradual onset ,progressive course first on exertion ,progressive

to symptoms at rest but no orthopnea in sever disease.

CHEST PAIN—may occurs due to:

i. Pleurisy due to pneumonia

ii. Pneumothorax due to rupture emphysematous bullae

iii. Strain of intercostals muscles due to chronic cough

WHEEZING

HAEMOPTYSIS—may be the only recent symptom of lung cancer.

ON EXAMINATION:

CLINICAL ABNORMALITIES IN ADVANCED AIRFLOW OBSTRUCTION: Loss of weight ---often stimulates unnecessary investigation. Pursed lip breathing –physiological response to decrease air trapping. Central cyanosis. Flapping tremor and bounding pulse 2ry to hypercapnea. Peripheral edema –2ry to cor pulmonale. Raised JVP , Right parasternal heave ,loud P2 , Tricuspid regurgitation.

ON CHEST EXAMINATION: Reduction in the length of the trachea above the sterna notch. Tracheal descent during inspiration –tracheal tug. Contraction of sternomastoid and scalene muscles on inspiration. Excavation of suprasternal & supraclavicular fossae during inspiration. Indrawing of costal margins and intercostals spaces. Increased antero-posterior diameter of the chest relative to lateral diameter Rhonchi especially on forced expiration.

A. Vital signs:

Large pulse volume due to V/D (( vasodilatation )).

Small pulse volume due to corpulmonale.

A.F. with multifocal extrasystole –in sever hypoxia.

RR—tachypnea with working accessory respiratory muscles.

Contracted sternocleomastoid muscles with neck shortening with

tracheal tug

HEAD EXAMINATION: Puffiness of eye lids due to chronic cough Fundus---increased ICP leads to papillodema ,engorged fundal veins with small pupils Central cyanosis may be present Flushed face due to polycythemia

B. NECK EXAMINATION:

Neck veins are usually congested due to increased intrathoracic pressure and as a sign for

the development of cor pulmonale.


C. UPPER LIMB EXAMINATION:

Clubbing is not a common features of COPD

If present ,it indicate Ca or bronchiectasis.

D. LOWER LIMB EXAMINATION:

Edema ----corpulmonale or salt and water retention

E. ABDOMEN:

The lower border of the liver may be felt due to :

Depression of the liver by flat diaphragm—non tender

Cor pulmonale---tender liver

F. Ascites may be present.

CHEST EXAMINATION:

a. Manifestation of airways obstruction:

Due to chronic bronchitis—

Vesicular breath sounds with prolonged expiration

Generalized wheezes

Prolonged forced expiratory time (( N= 3-4 sec )).

b. Manifestation of hyperinflation :

Due to emphysema –

INSPECTION---barrel chest Horizontal ribs Wide intercostals spaces and wide subcostal angle > 90 Manubro-sternal angle is prominent Respiration is mainly abdominal –chest moves up and down as one unit Bilateral limitation of chest expiration Suction of supraclavicular ,suprasternal and lower intercostals spaces during

inspiration with fullness during expiration Absent or weak cardiac pulsation

PALPATION Trachea is central TVF is decreased bilaterally Tenderness due to rib fracture 2ry to malignancy

AUSCULTATION

Vesicular breath sounds

With prolonged expiration

Decreased breath sounds all over

Distant heart sounds

Marked crepitation may be due to bronchiectasis ,LVF ,pneumonia

Lower diaphragm---

Epigastric pulsation due to RV enlargement with palpable lower border of liver


COMPLICATION: 1. Bronchopneumonia 2. Bronchial obstruction -----collapse 3. Respiratory failure:

Type I ----pure emphysema Type II----mixed or pure chronic bronchitis

4. Corpulmonal with RHF , LHF may also occurs later 5. Pneumothorax ---- due to rupture emphysematous bulla 6. Peptic ulcer in 20% in cases due to:

a) Devitalization of mucosa by hypoxia b) Hypercapnia ----vagal center ----hyperchlohydria c) Drugs : Steroids , Aminophylline and smoking

Gastro-esophageal reflux disease , GE sphincter dilatation 7. Prolonged cough may lead to:

A) Intra ocular pressure ----puffy lower lid ,retinal haemorrhage B) Intracranial pressure ---- cerebral and subarachnoid haemorrhage –bleeding C) Increased intrathoracic pressure may leads to:

Rupture bulla ----pneumothorax Muscle strain ----chest pain Rib fracture Hemoptysis Syncope ---prevention of blood inlet and exit Increased intraabdominal pressure ---hernia ,prolapsed –rectal ,incontinence Insomnia Dissemination of infection

8. Secondary polycythemia may lead to embolization any where due to stasis.

INVESTIGATION:

1. CBC ----Increased in polycythemia with low ESR

2. CHEST X RAY:

Signs of hyperinflation -- > 6 anterior ribs

Hypertranlucency of lung with transverse ribs and wide intercostals spaces

Low flat diaphragm

Heart shadow is elongated ( tubular heart )

There may be emphysematous bullae

Exaggerated brocho-vascular markings

Decreased peripheral vascular markings


3. PULMONARY FUNCTION TEST:

Pulmonary function testing is used in the diagnosis of chronic obstructive

pulmonary disease (COPD) and the staging of COPD severity. The current

diagnostic criterion for airflow obstruction is a ratio of forced expiratory

volume in 1 second (FEV1)to forced vital capacity (FVC) < 70%. However this

absolute definition can lead to false-negative determinations in younger

patients and false-positive determinations in the elderly.

Spirometry should be complemented by measurement of lung volumes using

body plethysmography in those with evidence of airflow obstruction.

Small airways disease can be detected by various techniques that measure

airway and total respiratory system resistance. There is renewed interest in

the forced oscillation technique and impulse oscillometry because of their

noninvasiveness and potential ability to distinguish small from larger airway

disease. Finally, pulmonary function testing has an important role in

preoperative risk assessment; for example, in patients being considered for

lung volume reduction surgery or resection of a lung nodule.

It is indicated in :

A. Early detection ---before ECG ,ABG and CXR changes

B. Assess severity

C. Must be done before any major operation :


If FVC , FEV 1 ,MVV below 50% of predicted values -----operation must be

delayed or counseled due to increased risk of respiratory failure.

D. Reversibility ----- in asthmatic bronchitis

Progressive decline in forced expiratory volume in 1 second (FEV1) in

patients with chronic obstructive pulmonary disease.

Obstructive -----FEV1< 80% ,FEV1/FVC <70% , TLC , RV

FVC is reduced in sever disease.

DL CO is decreased in emphysema.

The normal rate of decline of FEV1 is typically 25 to 30 mL/year but this

decline is accelerated in smokers and might be as high as 100 mL/year in

severe COPD patients. The rate of decline of FEV1 is also influenced by

exacerbations, with more frequent exacerbations accelerating the decline.

Staging of chronic

obstructive pulmonary

disease based on the

forced expiratory volume

in 1 second (FEV1). The

left panel depicts the

American Thoracic

Society staging from

1995.

Current opinion is moving away from severity staging based on FEV1 to staging based on

clinical markers such as persistent symptoms and frequent exacerbations.


Dynamic changes in

operational lung volumes

during exercise contrasting

normal subjects with chronic

obstructive pulmonary

disease (COPD) patients. In

normal subjects, end-

expiratory lung volume

decreases; whereas with

COPD patients, it increases.

For example, when normal

subjects exercise tidal volume

increases by virtue of both

increased end-inspiratory lung

volume (EILV) and reduction

in end-expiratory lung volume

(EELV) or functional residual

capacity (FRC) .

By contrast, COPD patients

exhibit increases in EELV with

exercise thus reducing

inspiratory capacity and

causing EILV to encroach toward total lung capacity (TLC).

POSTGRADUATE DISCUSSION:

Hyperinflation can be thought of as having "static" and "dynamic" components. Although

the degree of hyperinflation is probably constantly changing, concomitant with

fluctuations in EELV, it is instructive to consider separate contributory factors for the static

and dynamic components. Static hyperinflation is a permanent elevation of EELV due to

changes in the elastic properties of the lungs that progress over time and cause increasing

lung volumes. Dynamic hyperinflation recognizes that the degree of lung emptying from

breath to breath is also dependent

on expiratory airflow and the time

available for expiration. The airflow

limitation changes with bronchial

smooth muscle tone and airway

inflammation, so dynamic

hyperinflation also changes. A

component of static hyperinflation

probably exists because of fixed

airflow limitation. However, in these

circumstances EELV is still

determined by the available


expiratory time and can usually be reduced by slowing respiratory rate.

The degree of hyperinflation can be determined by measuring inspiratory capacity (IC).

several studies have measured lung volumes including, TLC, by body plethysmography

and then used IC maneuvers with simple spirometry to determine EELV. This technique

assumes that TLC remains constant, which is thought to be true over short time periods

and also during exercise. The bronchodilator studies have established that IC as a measure

of hyperinflation correlates better with dyspnea and exercise performance that FEV1.

This finding also offers an explanation as to why FEV1 has traditionally been recognized to

correlate poorly with dyspnea and exercise performance such as 6-minute walking

distance.

Summary of the finding: 1. Residual volume increased 2. Vital capacity decreased 3. Maximum voluntary ventilation decreased 4. PEFR -----peak expiratory flow rate decreased 5. Forced expiratory volume in first second ----decreased 6. FEV1 / FVC ---decreased

Reversibility testing to salbutamol and ipratropium is necessary to detect patient with

substantial increase in FEV1 who really have asthma and to establish the post

bronchodilator FEV1 which is the best predictor at long term prognosis.

Significant reversibility is defined as 15 % and at least 200ml increase in FEV1 .Evidence at

a similar objective response to a course at oral prednisolone ((30mg /2 weeks )) should be

performed in all patients with COPD.

One of the common problems encountered with COPD patients is an inability to perform a

complete or adequate exhalation thus resulting in an underestimate of FVC and

overestimate of FEV1:FVC ratio. These inaccuracies result in a tendency to diagnose a

restrictive ventilatory abnormality and a risk of missing airflow obstruction. For this

reason the measurement of the forced expiratory volume in 6 seconds (FEV6) has been

advocated along with the FEV1:FEV6 ratio. Whichever approach is used, two reproducible

measures should be obtained (where the largest values for FEV1 and FVC are within 200

mL) from a maximum of eight tests.

In most patients with evidence of airflow obstruction on spirometry, additional useful

information can be obtained by measuring the subdivisions of lung volume. The primary

measurement is functional residual capacity (FRC) in conjunction with a slow vital capacity

maneuver, which allows other lung volumes to be determined.

Body plethysmography is the preferred method because this measures the entire thoracic

gas volume (TGV). Gas dilution methods tend to underestimate lung volumes because of

insufficient distribution of the marker gas to lung regions with slow time constants for

airflow as well as failure to penetrate non-communicating gas spaces such as bullae. A

clinically meaningful difference (e.g., 200 mL) between FRC measured by body

plethysmography and helium dilution implies air trapping.


The diffusing capacity of the lung for carbon monoxide (DLCO) is useful in detecting the

presence of emphysema in patients with airflow obstruction.

To get the most accurate results from breathing tests:

■ Do not smoke for at least 1 hour before the test.

■ Do not drink alcohol for at least 4 hours before the test.

■ Do not exercise heavily for at least 30 minutes before the test.

■ Do not wear tight clothing that makes it difficult for you to take a deep breath.

■ Do not eat a large meal within 2 hours before the test.

■ Ask your health care provider if there are any medicines that you should not take on the

day of your test.

4. ABG

Very important for two reasons:

1. To indicate O2 concentration by mask ( high in type I emphysema and low

type II (( bronchitis ))

2. If P Co2 > 45 mmHg ----- there is risk from muscle relaxants and anesthetics

5. ECG:

Sinus tachycardia

SVT ,ventricular ectopics

Cor-pulmonale

6. Sputum culture and sensitivity:

Streptococcus pneumonia , Haemophilus influenza

7. Estimation of serum α 1 ---antitrypsin ---decrease in 1ry emphysema

ASSESSMENT OF COPD:

1. Chest x ray

2. ABG

3. Spirometry

4. Bronchodilator response

5. Trial of oral steroids > 15 % increase FEV1 for 2 weeks—30mg prednisolone

WHO TO ADMIT?

1. Acute exacerbation that fail to respond to OPD treatment

2. Cor-pulmonale

3. Pneumothorax

4. Acute respiratory failure

5. Pneumonia

6. CNS symptoms of acute onset

7. Sudden dyspnea


TREARMRNT:

NON PHARMACOLOGICAL

A. Stop smoking

Completely and permanently together with use of nicotine replacement therapy.

In well motivated patients ,Bupropion (( 150 mg once daily increasing to 150mg

/twice daily )) commenced 1—2 weeks prior to stopping smoking .

Bupropion is contraindicated in epileptic patients or CNS tumor

It is used for 7 – 9 weeks.

B. Encourage exercise

C. Treat poor nutrition or obesity

D. Change residence ---away from areas with heavy pollution

E. Pulmonary rehabilitation

F. Pneumococcal and influenza vaccine

PHARMACOLOGICAL

INFECTION , BRONCHOCONSTRICTION ,WHEEZING ,SPUTUM

A. Treatment of infections:

Infection is considered to be present if there is purulent noneosinophilic sputum.

Respiratory infection should be treated promptly because it aggravates dyspnea

and may precipitate type II respiratory failure in patients with severe airflow

obstruction.

The usual causative organisms are streptococcus pneumonia or H.Iinfluenzae.

Influenza immunization should be offered to all patient each year.

Amoxicillin 250mg 8 hour 1 X 3 X7 days

Co –amoxiclav 375 mg 1 X 3 X 7 days—B lactamase bacteria

Doxycycline 100mg 1 X 2 X5 days

Clarithromycin 250 –500 mg 12 hour X 7 Days—if penicillin sensitive

B. Bronchodilators are the most important agents.

Anticholinergic , Sympathomimetics , Methyl xanthine inhibitors

Short acting B agonists –Salbutamol ,Albuterol ,Metoprotrenol

Shorter onset of action, used in acute situations in mild to moderate cases.

Long acting B 2 agonist –Salmeterol , Formoterol , Sustained R. albuterol

It has no clear role unless there is reversibility demonstrated by spirometry

after broncho-dilator test i.e. in asthmatic bronchitis.

They are used twice daily like Salmeterol in later situation.

Ipratropium bromide—2 –4 puffs via MDI / 6hr

Used by nebulizer and inhalers.

It is first line therapy ,long acting , no side effect

Theeophylline is of limited value especially if patient is smoker because

higher dose will be needed and toxicity may be more than benefit , But

there will be indication in patient who develop corpulmonale because

there is evidence that it may help in diaphragmatic contraction beside

being a bronchodilator.


Oral theophylline is 3rd line agent

IPRATROPIUM AND B AGONIST TOGETHER ARE MORE EFFECTIVE.

Short acting bronchodilators can increase exercise tolerance acutely in COPD.

Anticholinergics given daily can improve health ststus over a 3 month period.

Long acting B agonists improve health ststus ,possibly more than regular ipratropium .

B agonists reduce symptoms ,rescue medication use and increase the time between exacerbations.

Combining long acting inhaled B agonists and ipratropium leads to fewer exacerbations than either drug alone.

Combining long acting B agonist and theophylline produces a greater spirometric change than either drug alone.

Tiotropium improves health status and reduces exacerbation and hospitalizations compared with both placedo & regular ipratropium.

C. CORTICOSTEROIDS:

COPD is generally not steroid responsive .10% of stable out patients will have >

20% increase in FEV1 compared with placedo. BTS recommend prednisolone

30mg/d/2 weeks to check FEV1 reversibility (( > 15 % ))

Beclomethazone 250 mg 1 X 4 upto 2 X 4 according to the response

In patients with advanced COPD (( FEV1 <50%)) ,there is evidence that inhaled corticosteroids can reduce the number of exacerbations per year.

D. Expectorants and mucolytic agents are of NO value

E. O2 therapy:

O2 therapy should not with held for risk of worsening academia in hospitalized pt.

For most patients ,a flow rate of 1—3 L achieves a PaO2 > 55%.

It results in long survival ,exercise ,sleep reduced hospitalization ,and better

quality of live in advance disease.

It is of value in preventing cor pulmonale.

Indicated with hypoxia < 40mmHg with exertion or <55mmHg at rest.

Dose --- > 15 hours per day of nasal O2.

Indication ---PaO2 <7.3 kPa ((55mmHg)) . Goal---SaO2>90% during rest ,sleep &exertion

INDICATIONS OF HOME O2 THERAPY(LTOT—long term O2 therapy):

1. Clinically stable non smoker with PaO2<55 mmHg((7.3 kpa))

Sa O2 ≤ 88% taken at rest breathing room air

2. During sleep nocturnal O2:

i. Pao2 ≤ 55mmHg for a patient whose awake PaO2 ≥ 56mmHg

ii. Decrease PaO2 > 10mmHg or decrease Sa O2 > 5% associated with

symptoms and signs attributed to hypoxia.

iii. During exercise :

PaO2 ≤ 55mmHg during exercise OR

There is evidence that O2 supplements improves hypoxia.


iv. PaO2 56—60mmHg or SaO2 89% if thete is:

A. HCT > 56%

B. ECG –P PULMONALE > 3 mm

C. DEPENDENT OEDEMA –RVF

F. Surgical measures:

Bullectomy

Single lung transplantation

Volume reduction surgery

G. Pulmonary rehabilation:

It is a multidisciplinary programme of care that is individually tailored and

designed to optimize physical and social performance and autonomy.

It includes:

1. Exercise training

2. Education

3. Psychological /behavioural intervention

4. Nutritional therapy

SEVERITY OF COPD –GOLD

MILD FEV1 50----80% PREDICTED smokers cough ,exertional dyspnea -+

MODERATE FEV1 30----49% PREDICTED Exertional dyspnea ,-+ wheeze,cough -+sputum

SEVER FEV1 > 30% CORPULMONALE Dyspnea , wheeze and cough prominent OR FEV1 < 30%

Patients with FEV1 30—50% with evidence of right heart failure or PaO2 < 6.7kPa or

central cyanosis is considered to be sever.

MORE ADVANCED COPD:

a) Pulmonary rehabilitation ---opiates ,Benzodiazepines ,Antidepressents

b) Monitor blood level of theophylline

c) Consider LTOT if PaO2 < 7.3 kPa

d) Asses home setup and support needed

e) Lung volume reduction surgery

f) Non invasive positive pressure ventilation

TREATMENT ACCORDING TO STAGES:

MILD Antimuscurinic (( ipratropium )) or B2 agonist

MODEARTE Antibiotic for exacerbations Bronchodilatation

1. Regular ipratropium /Tiotropium 2. Long acting B2 agonist (Salmetrol) +

inhaled steroids (Fluticosone) 3. If FEV1 < 50% and excebations ≥ 2 year

SERETIDE


4. Symbicort is Budesonide + Formoterol 5. Oral theophyllin

SEVER Combination therapy with: 1. Regular short acting B2 agonist +

anticholinergic 2. Consider steroid trial 3. Asses for home nebulizer 4. Refer to specialist

PULMONARY HTN Asses the need for LTOT Treat edema with diuretics

PATTERNS OF COPD DIFFERENTIATING POINTS

CHARACTER PINK PUFFER ((A)) EMPHYSEMA BLUE BLOATER((B))CHRONIC BRONCHITIS

AGE After 50 years Late 30—40 years

DYSPNEA Sever progressive mild

COUGH Rare ,little mucoid sputum Chronic ,frequent ,excess mucopurulent

WHEEZING Little if any episodic

BODY BUILT Thin obese

CENTRAL CYANOSIS absent marked

HEART FAILURE Rare ,in end stage --terminal Common ,early

CHEST Barrel shaped ,distant sounds Normal ,wheezing ,noisy

HEART SOUNDS Distant and weak normal

INVESTIGATION HB ABG Pa O2 PaCO2

Normal Increased alveolar ventilation Normal to decreased 65-75mmhg Normal to 35—70 mmHg

Increased 15—18g/dl Decreased alveolar ventilation Reduced 45—60mmHg High 50—60 mmHg

CHEST X RAY Hyperinflated Flat diaphragm Deceased vascular marking

Increased interstitial marking—dirty lung especially at bases Diaphragm not inflated

PFT Air flow obstruction TLC increased DL CO decreased

Air flow obstruction TLC normal but may be slightly increased DL CO normal

SPECIAL INVESTIGATION V/Q MATCHING HEMODYNAMIC NOCTURNAL VENTILATION EXERCISE VENTILATION

Increased ventilation to highV/Q High dead space COP N PUL P. mildly with exercise Mild to mod. Degree of O2 desaturation without obs.sleep A Increased minute ventilation MV for level of of O2 consumption PaO2 tend to decrease

Increased perfusion to low V/Q COP N PUL. P. markedly ,worsen w execise Sever O2 desaturation with obstructive sleep apnea Decrease M.V.for level of O2 consumption PaO2 may raise PaCO2 rise signficantly

copd by magdi sasi 2016

Documents