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PULMONARY REHABILITATION

Upper Respiratory Tract The structures of the upper respiratory tract are the nasal cavity, pharynx, and larynx. As air is brought into the body, the nasal cavity and pharynx filter and remove particles in the air and begin to humidify and warm it to body temperature. The larynx, which extends from C3 to C6, controls airflow; and when it contracts rapidly, the epiglottis prevents food, liquids, or foreign objects from entering the airway

food, liquids, or foreign objects from entering the airway Lower Respiratory Tract The lower respiratory tract

Lower Respiratory Tract The lower respiratory tract is composed of conducting airways of the tracheobronchial tree and the terminal respiratory units. There are approximately 23 generations (branchings) of the structures within the tracheobronchial tree, which extends from the trachea to the terminal respiratory units of the lungs. The first 16 airway branchings of the lower respiratory tract primarily conduct air, whereas the last 6 are respiratory airways that end (in the mature lung) in approximately 300 million alveoli. The diameter of the airways becomes increasingly smaller with each successive generation of the tracheobronchial tree.

each successive generation of the tracheobronchial tree. The trachea is an oval, flexible tube supported by

The trachea is an oval, flexible tube supported by semicircular rings of cartilage. It extends from C6 in an oblique, downward direction to the sternal angle level of rib 2 and T6, at which point it bifurcates into two mainstream bronchi: the right, which is directed almost vertically, and the left, which is directed more obliquely. The two mainstem bronchi then divide into five lobar bronchi: three on the right and two on the left. Mainstem and lobar bronchi have a great amount of cartilage, which helps maintain airway patency. Each of the lobar bronchi divide into two or more segmental bronchi: 10 on the right and 8 on the left. Segmental bronchi have scattered cartilage, smooth muscle, elastic fibers, and a capillary network. The mainstem, lobar, and segmental bronchi have a mucous membrane essentially the same as the trachea. Segmental bronchi divide into subsegmental bronchi and

bronchioles, which have less and less cartilage and ciliated epithelial cells. These bronchioles divide into the terminal bronchioles, which are distal to the last cartilage of the tracheobronchial tree. Terminal bronchioles contain no ciliated cells. Terminal bronchioles divide into respiratory bronchioles and provide a transitional zone between the bronchioles

and alveoli. These respiratory bronchioles divide into alveolar ducts and alveolar sacs. One duct may supply several sacs. The ducts contain smooth muscle, which narrows the lumen of the duct with contraction. The alveoli are located in the periphery of the alveolar ducts and sacs and are in contact with capillaries (alveolar-arterial membrane). Gas exchange occurs here.

The lungs are elastic structures, containing collagen and elastic fibers that resist expansion. For normal lungs to contain air, they must be distended either by a positive internal pressurei.e., by a pressure in the airways and alveolar spacesor by a negative external pressurei.e., by a pressure outside the lung. Ventilation is the process whereby the lungs replenish the gas in the alveoli. Measurements of ventilatory function in common diagnostic use consist of quantification of the gas volume contained in the lungs under certain circumstances and the rate at which gas can be expelled from the lungs. Because the various lung volumes and capacities are often abnormal in people with pulmonary disorders, they are routinely measured in such patients. The original clinical measuring device, a spirometer, was a simple instrument utilizing a hollow bell inverted over water. Now patients simply blow into a small electronic measuring device. Spirometry is most useful for evaluating losses in respiratory function and for following the course of certain respiratory diseases.

is most useful for evaluating losses in respiratory function and for following the course of certain
is most useful for evaluating losses in respiratory function and for following the course of certain

Although it cannot provide a specific diagnosis, it can distinguish between obstructive pulmonary disease involving increased airway resistance (such as chronic bronchitis) and restrictive disorders involving a reduction in total lung capacity resulting from structural or functional changes in the lungs (due to diseases such as tuberculosis, or to fibrosis due to exposure to certain environmental agents such as asbestos). Increases in TLC, FRC, and RV may occur as a result of hyperinflation of the lungs in obstructive disease, whereas VC, TLC, FRC, and RV are reduced in restrictive diseases, which limit lung expansion.

Two other useful tests are FVC and FEV. FVC, or forced vital capacity, measures the amount of gas expelled when a subject takes a deep breath and then forcefully exhales maximally and as rapidly as possible. FEV, or forced expiratory volume, determines the amount of air expelled during specific time intervals of the FVC test. For example, the volume exhaled during the first second is FEV 1 . Those with healthy lungs can exhale about 80% of the FVC within 1 second. Those with obstructive pulmonary disease exhale considerably less than 80% of the FVC within 1 second, while those with restrictive disease can exhale 80% or more of FVC in 1 second even though their FVC is reduced.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Chronic obstructive pulmonary diseases (COPD) are diseases of the respiratory tract that produce an obstruction to airflow and that ultimately can affect both mechanical function and gas exchanging capacity of the lungs.

COPD is also known as chronic obstructive airway disease (COAD) and chronic obstructive lung disease (COLD)

Certain physical symptoms are characteristic of COPD. This includes:

Chronic cough

Expectoration of mucus

Wheezing

Dyspnea on exertion

EPIDEMIOLOGY

COPD is the fourth leading cause of death and affects >16 million persons in the United States. COPD is also a disease of increasing public health importance around the world. Global Initiative for Chronic Obstructive Lung Disease (GOLD) estimates suggest that COPD will rise from the sixth to the third most common cause of death worldwide by 2020.

ETIOLOGY

Genetic predisposition

Environmental factors ( allergic diseases , e.g. asthma)

Respiratory infections (e.g. bronchopneumonitis)

Chemical inflammation (e.g. cigarette smoke, asbestosis)

Metabolic abnormalities (e.g. alpha 1-antitypsin def)

Cigarette smoking (main cause: chronic bronchitis, emphysema)

Smokers are 3.5-25 times more likely (depending on amounts smoked) to die of COPD than non- smokers

PATHOPHYSIOLOGY

Changes Associated with Obstructive Lung Diseases:

Narrowing & obstruction of airways

Inflammation of the airways

Destruction of alveolar & bronchial walls

Increased production & retention of mucus

Abnormal pulmonary function tests:

- decreased vital capacity & expiratory reserve volume

- increased residual volume

- decreased expiratory flow rates Asthma

EARLY OBSTRUCTIVE LUNG CONDITION

BRONCHOPULMONARY DYSPLASIA

Bronchopulmonary dysplasia is a chronic lung disease of infancy, characterized by respiratory distress and oxygen dependency lasting beyond 1 month of age; that follows the use of oxygen and ventilatory support to treat neonatal respiratory distress.

Etiology

Barotrauma(injury due to pressure)

Intubated infants

High oxygen concentration(oxygen toxicity)

Pulmonary interstitial edema

Infection

Congestive heart failure

Clinical manifestations

Mild BPD

Transient tachypnea

Cyanosis with feeding or crying

Severe BPD

Tachypnea

Cyanosis on room air

Suprasternal, intercostals and subcostal retractions

Nasal flaring

Grunting

Pulmonary HPN

R sided heart failure

Pathophysiology

Partial expiratory flow volume (PEFV) reveals low forced expiratory rates

Generally decreased lung compliance and functional residual capacity @ early stages

Persistent ventilation-perfusion mismatching results in hypoxemia and need for long-term oxygen therapy and possible ventilator support

Ground-glass appearance is seen on xrays indicating hyaline membrane disease

CYSTIC FIBROSIS

Cystic fibrosis is a genetic disorder characterized by dysfunction of the exocrine glands with abnormal secretions in the respiratory tract, sweat glands, mucosal glands of the small intestine, the pancreas, and bile ducts of the liver. Abnormally think, tenacious mucus along with impaired mucociliary clearance results in COPD and frequent respiratory infections.

Etiology

Cystic fibrosis is an autosomal recessive genetic disease caused by mutations in the gene (long arm of chromosome 7) encoding the cystic fibrosis transmembrane conductance regulator (CFTR).

Pathophysiology

An acute inflammatory/allergic process produces hyperreactive airways and chronic inflammation of airways which results in increased V/Q mismatching ad therefore increased work of breathing

Clinical manifestations

children with CF usually small for their age due to pancreatic malfunction leading to food mal- absorption.

exocrine gland dysfunction within pulmonary. increased production of viscous mucus. airway

obstruction.

.Chronic airway obstruction + pooling of secretions: vulnerable to pulmonary

infection.

Manifests as chronic productive cough; dyspnea, tachypnea; cyanosis.

Clinical hallmark: chronic coughing & production of copious amount of thick, purulent mucus

PFT show decrease expiratory flow rates; increase residual volume over time (due to hyperinflation of the lungs)

Average patient survives into the late 20s or early 30s. Pulmonary complications eventually the cause of death.

Cystic fibrosis Triad

Chronic pulmonary disease

Pancreatic deficiency

Abnormal high levels of sweat electrolytes: increased NaCl content

ASTHMA

Asthma is a chronic inflammatory disease of the airways characterized by increased responsiveness of the tracheobronchial tree to a variety of stimuli. Widespread narrowing of the airways occurs when the individual comes in contact with these stimuli. Generally asthma is episodic in nature, with acute episodes being separated by symptom-free time periods.

Asthma that begins in childhood as is triggered by allergens is called extrinsic asthma. Asthma that begins after age 35 is called intrinsic asthma and is more severe in nature.

Etiology

Allergens

Exercise

Infections

Occupational stress

Environmental stress

Pharmacologic stress

Emotional stress

Pathophysiology

Predominant feature seen in PFT: obstruction to airflow, either episodic or continual with varying severity

o

Decreased FEV1 and FEV1:FVC

o

Decreased VC

o

Increased FRC and RV

Hyperreactivity of airways to various stimuli results in bronchial smooth muscle contraction and hypertrophy, inflammation of the mucosa and overproduction of viscous, tenacious mucus.

Severity of airway obstruction may be no uniform in the lungs so that distribution of ventilation is uneven

o

Initially perfusion is diverted away from underventilated

o

If obstruction becomes widespread and severe, ventilation-perfusion mismatching worsens and arterial hypoxemia occurs

Clinical manifestations

intermittent wheezing and dyspnea

cough

respiratory distress

hyperinflated chest, hyperresonant to percussion

auscultation reveals prolonged expiratory phase

status asthmaticus

o

patients with a severe persistent attack of asthma that is refractory to bronchodilators

o

usually in severe respiratory distress and have cyanosis

o

become physically exhausted by the increased work of breathing and from sleep deprivation

BRONCHIECTASIS

Bronchiectasis is a permanent, abnormal dilation and distortion of one or more bronchi that is caused by destruction of the elastic and muscular components of the bronchia walls.

Etiology

Necrotizing infection or a series of multiple infections involving the tracheonbronchial walls and adjacent lung parenchyma

Bacterial pneumonias

o

S. aureus

o

Klebsiella pneumonia

o

P. aeruginosa

Bronchial obstruction

Mucoid impaction

Pathophysiology

Bronchial obstruction produces atelectasis which increases the intrathoracic pressure required to overcome greater elastic resistance and causes dilation of the bronchi.

Prolonged bronchial obstruction increases the risk of secondary infection which results in destruction of the bronchial walls and dilation of the bronchi leading to reparative laying down of the fibrous tissue.

Arterial hypoxemia may develop due to ventilation-perfusion mismatching

Extensive pulmonary anastomoses occur at precapillary level in the granulation tissue surrounding bronchiectatic segments. These can lead to bronchial artery enlargement and left to right shunts (recirculation of oxygenated blood).

Clinical manifestations

Cough

Copious mucopurulent sputum and fetid (having disagreeable odor)

o Separates into three layers in standing characteristic of the disease

Upper layer of white/slightly greenish brown frothy secretions

Middle thin mucoid layer

Bottom layer of thick greenish plugs

Recurrent pulmonary infections

Recurrent hemoptysis

Abnormalities on auscultation

o

Moist rales/crackles over involved lobes

o

Rhonchi during mucus retention

o

Dullness to percussion and decreased breath sounds during mucus plugging

ADULT OBSTRUCTIVE LUNG CONDITIONS

CHRONIC BRONCHITIS

Chronic bronchitis is characterized by excessive mucus production in the bronchial tree with a chronic or recurrent productive cough that lasts at least 3 months and recurs over at least 2 consecutive years. Hypersecretion begins in the large airways and is not associated with airway obstruction (simple bronchitis). Later, hypersecretion progresses to the smaller airways where the airway obstruction begins initially (chronic bronchitis)

Etiology

Cigarette smoking

Air pollution

Second-hand smoke

Occupational exposure to dusts, such as gold, coal, fluorspar and asbestos

Occupational exposure to vegetable dusts, such as cotton, flax or hemp

Pathophysiology

Initially, there is respiratory bronchiolitis with inflammatory and obliterative changes that have been initiated by inhaled irritants.

Small airway disease may not be detectable

Clinical manifestations

Chronic productive cough with morning expectoration and clearing of secretions accumulated during the night

Sputum is usually clear and mucoid but can become purulent during the presence of infection.

Recurrent chest infections

Overweight with a cyanotic cast to their lips and nailbeds; “blue bloater”

Rhonchi and wheezes are frequently heard

Prolonged expiratory phase

EMPHYSEMA

Emphysema, an alveolar or parenchymal disease, is an abnormal and a permanent enlargement of the air spaces distal to the terminal nonrespiratory bronchioles, accompanied by destructive changes of the alveolar walls. Disturbances in lung function result from these anatomic changes, including loss of elastic recoil, excessive collapse of airways on exhalation and chronic airflow obstruction.

4 basic types:

1. Centrilobular emphysema (CLE)

Alveoli arising from the respiratory bronchiole or the proximal portion of the acinus are most affected

Normal alveolar ducts and alveolar sacs

No respiratory disability

2. Panlobular emphysema (PLE)

All alveoli within acinus are affected to the same degree

A nearly uniform destruction f most of the structures within a lobule is seen

associated with alpha antitrypsin deficiency and unilateral hyperlucent lung syndrome

o A.antitrypsin, enzyme produced in the liver inactivates elastase, which if unchecked destroys lung elastic tissue

3. Paraseptal emphysema

Enlarged air spaces are at the periphery of the acinus, just under the pleura or along connective tissue septa

These thin-walled, inflated areas located at the pleural surface may become bullae

4. Irregular emphysema

Located in the vicinity of scars and is related to the effects of scarring and contraction

Etiology

Cigarette smoking

Environmental air pollution

Hereditary deficiency of alpha1-antitrypsin

Pathophysiology

Repeated inflammation of the airways along with the development of partial or complete bronchiolar bronchiolar obstruction results in:

Air trapping and alveolar overdistention which causes fragmentation of the intraalveolar elastic tissue and rupture of the attenuated interalveolar septa, leads to coalescence of several alveoli and bullae formation.

Release of proteases which causes progressive lung destruction

Loss of functional alveoli results in gross V/Q mismatching throughout the lungs which increases the work of breathing and creates potential for ventilatory muscle fatigue.

Also increased V/Q mismatching produces increased hypoxemia and possibly CO2 retention resulting in increased RR and use of accessory muscles and even greater work of breathing.

Loss of large portions of lung parenchyma decreases the number of pulmonary capillaries which leads to increased pulmonary hypertension.

Clinical manifestations

Shortness of breath

Scant sputum production

Barrel-shaped configuration of chest wall with increased subcostal angle

Hypertrophied accessory muscles of respiration

Pursed-lip breathing even at rest

Shoulders frequently rounded

Thin, sometimes cachectic in body build with rosy skin tones; “pink puffer”

DIFFERENTIAL DIAGNOSIS

Diagnosis

Suggestive features

COPD

Mid-life onset Slowly progressing symptoms Long history of smoking

Asthma

Early onset Varying symptoms Symptoms during the night/early morning Presence of allergy, rhinitis and/or eczema A family history Airflow limitation that is largely reversible

Congestive heart

Fine basilar crackles on auscultation Dilated heart on chest radiography Pulmonary oedema Volume restriction not airflow limitation on pulmonary function tests

failure

Bronchiectasis

Large volume of purulent sputum Commonly associated with bacterial infection

 

Coarse crackles/clubbing on auscultation Bronchial dilation and bronchial wall thickening on chest radiography/CT

Tuberculosis

Onset at all ages Lung infiltrate on chest radiography Microbiological confirmation High local prevalence of tuberculosis

Obliterative

Younger onset and in non-smokers History of rheumatoid arthritis/fume exposure? Hypodense areas on expiration on CT

bronchiolitis

Diffuse

Effects mostly male nonsmokers Almost all have chronic sinusitis Diffuse small centrilobular nodular opacities and hyperinflation on chest radiography and HRCT CT: computed tomography; HRCT: high-resolution computed tomography.

panbronchiolitis

GENERAL MEDICAL MANAGEMENT

Pharmacologic therapy

o

vaccination against influenza and pneumococcal pneumonia

o

inhaled quaternary anticholinergic

o

b20adrenergic agonist bronchodilators

o

inhaled corticosteroids

o

oral theophylline can improve respiratory muscle endurance

exposure to environmental and occupational pollution must be prevented

α1-antitrypsin augmentation therapy in those with emphysema

smoking cessation

noninvasive mechanical ventilation

lung volume reduction surgery

combined long-acting β-agonists with inhaled corticosteroids

oxygen therapy

PT GOALS

Decrease amount and viscosity of secretions and prevent respiratory infections.

Remove or prevent accumulation of secretions.

Promote relaxation of accessory muscles of inspiration.

Improve patient’s breathing pattern and ventilation.

Minimize or prevent episodes of dyspnea.

Improve mobility and lower thorax as well as posture.

Increase exercise tolerance.

Improve overall fitness.

PT MANAGEMENT

Breathing exercises and ventilatory training are fundamental interventions for the prevention or comprehensive management of impairments related to acute or chronic pulmonary disorders. It increases the effectiveness of the cough mechanism, improves strength endurance and coordination of the muscles of ventilation , correct inefficient/abnormal breathing patterns and decrease the work of breathing, relieves dyspnea during exertion among others.

o

Diaphragmatic breathing

Patients with primary or secondary pulmonary dysfunction can be taught how to control breathing by optimal use of the diaphragm and decreased use of accessory muscles.

Improve efficiency of ventilation

Decrease work of breathing

Increase the excursion of the diaphragm

Improve gas exchange and oxygenation

o

Segmental breathing

Teach patient how to expand localized areas of lungs while keeping other areas quiet.

Done during postural drainage or following thoracic surgery when it is important to emphasize expansion of problem areas of lungs and chest wall

o

Inspiratory resistance training

Uses pressure- or flow-based devices to provide resistance to airflow

Designed to improve the strength and endurance of muscles of inspiration and decrease the occurrence of inspiratory muscle fatigue

o

Incentive spirometry

Form of ventilatory training that emphasizes sustained maximum inspirations

 

using a small hand-held spirometer that provides visual/auditory feedback about whether a target max inspiration is reached.

o

Pursed-lip breathing

Lightly purse lips together during controlled exhalation

Adopted spontaneously by patients with COPD to deal with episodes of dyspnea

o

Positive expiratory pressure breathing

Resistance to airflow is applied during exhalation

Similar to pursed-lip except that that patient breathes through a specially designed mouthpiece or mask that controls resistance to airflow.

Used to hold airways open during exhalation to mobilize accumulated secretions and improve their clearance.

Respiratory muscle endurance training and helps to reduce fatigue.

Airway clearance strategies are mandatory to reduce the work of breathing, improve gas exchange and limit infection. This is indicated for persons with

o

Abnormal cough mechanics

Muscle weakness

o

Altered mucus rheology

Cystic fibrosis

o

Structural airway defects

Bronchiectasis

o

Altered mucociliary clearance

Primary ciliary dyskinesia

Techniques for clearing secretions include

o Postural drainage

Aka bronchial drainage

Consists of positioning the patient according to bronchopulmonary anatomy so that a particular lung segment is placed with its bronchus perpendicular to gravity.

Goal is to facilitate drainage of secretions into the segmental bronchus from

which they can be removed by coughing

o

Manual/device-induced airway oscillation

o

Chest percussion

 

Rhythmically and alternately striking the chest wall over specific lung segments wit cupped hands to mechanically jar and dislodged retained secretions

PT molds his hands to fit the contour of the area being treated and applies a force that is appropriate t the individual patient

Force is adjusted according to patent tolerance and should not be uncomfortable for it is not the force but the cupping that is effective

It

should be continued for 2-5mins per lung segment then followed by vibration

 

and coughing or suctioning.

o

Vibration

 
 

Consists of chest compression with manual vibration produced by tensing all muscles in the upper extremities in cocontraction.

Performed during exhalation only, it aims at moving the mucous that was dislodged during percussion toward the larger airways.

PT hand placement can be on both sides of the patient’s chest or one hand on top of the other

Patient takes a deep inspiration and then chest compression with vibration are

performed throughout exhalation for 6-8 breaths .

o

Shaking and rib springing

 

Shaking is similar to vibration except that it consists of gentle thrusts in and out rather than vibrations with chest compression

Rib springing is a more vigorous form of shaking in which the ribs are pumped in

a

springing fashion 3-4x during exhalation

Contraindicated in patients with rigid chest walls, osteoporosis or other bone abnormalities.

o

Coughing

 

Primary means of clearing airways of excess secretions and foreign material

Either a reflex or voluntarily, an effective cough consists

deep inspiration

closure of the glottis with contraction of the abdominal muscles

opening of the glottis with expulsion of the trapped air by forceful abdominal contraction

impairment results in retained secretions and bronchial obstruction

Teach patient the importance of an effective cough, how to produce an efficient and controlled voluntary cough and when to cough.

For chest PT to be effective, mucoactive medications must be given

o

Expectorants

o

Mucolytics

o

Bronchodilators

o

Surfactants

o

Mucoregulatory agents

o

Antitussives for uncontrolled coughing

Chest mobilization exercises

o

Maintain and improve mobility of chest wall, trunk and shoulder girdle when it affects ventilation or postural alignment.

o

Combine stretching of hypomobile trunk muscles with deep breathing

Exercise conditioning

o

A candidate must demonstrate a decrease in functional exercise capacity as a result of a pulmonary disease and be able to participate safely in a rigorous cardiorespiratory endurance training program.

o

Cardiorespiratory exercise training is often effective for decreasing exertional dyspnea.

o

In patients with COPD, cardiorespiratory endurance exercise therapy has been shown to improve maximum or symptom-limited aerobic capacity, timed-walk distance and health- related quality of life. Adding resistance training to the rehabilitative program can provide additional benefits such as increased fat-free mass and muscle strength.

o

Several adjunct modalities might reduce the extreme breathlessness ad peripheral muscle fatigue that prevent patients with severe COPD from exercising at higher intensities.

Continuous positive airway pressure and NIPPV during exercise might reduce the perception of dyspnea.

Adding electrical stimulation to strength exercises for peripheral muscles has been shown to further improve muscle strength in patients with COPD.

Oxygen supplementation, even in patients who don’t desaturate during exercise allows for higher exercise intensities and produces a superior training effect.

High intensity physical group training in water can produce significant benefits as well.

Continuous outpatient exercise training, home-based or community-based exercise programs or exercise training in groups of persons with COPD is necessary to sustain the benefits acquired during the initial rehabilitation program.

Restrictive Lung Dysfunction

Etiology

Restrictive Lung Dysfunction (RLD) is an abnormal reduction in pulmonary ventilation.

Lung expansion is diminished.

The volume of air or gas moving in and out of the lungs is decreased.

Pulmonary edema

o

Extravascular water in the lungs, usually caused by back pressure from failing left heart.

o

Main symptom: BREATHLESSNESS

Pulmonary emboli

o Blockage of the pulmonary vasculature, usually by a blood clot

Restrictive Lung Dysfunction is not a disease. In fact, this dysfunction may result from many different diseases arising from the pulmonary system or almost any other system in the body. It can also result from trauma or therapeutic interventions, such as radiation therapy or the use of certain drugs.

Pathogenesis

Three major aspects of pulmonary ventilation must be considered to understand the pathophysiology of RLD. They are compliance of both the lung and the chest wall, lung volumes and capacities, and the work of breathing.

Compliance

Physiologic link that establishes a relationship between the pressure exerted by the chest wall or the lungs and the volume of air that can be contained within the lungs.

With RLD chest wall or lung compliance, or both, is decreased.

Lung Volumes

Restrictive lung dysfunction eventually causes all the lung volumes and capacities to become decreased.

Because the distensibility of the lung is decreased, the inspiratory reserve volume (IRV) is diminished.

Work of Breathing

With RLD the work of breathing is increased.

Clinical Manifestations

6 Classic Signs

1. Tachypnea or an increased respiratory rate. Early in the course of RLD there may be overcompensation, with the respiratory rate increasing to the point that minute ventilation is

increased and alveolar hyperventilation occurs, resulting in greater exhalation of carbon dioxide (CO2).

2. Hypoxemia. A condition in which arterial oxygenation is below normal.

Ventilation-perfusion

hypoxemia. This mismatching may be due to changes in the collagenous framework of the lung, scarring of capillary channels, distortion or narrowing of the small airways, compression from tumors within the lung or bony abnormalities of the chest wall, or a variety of other causes. Even if patients are not hypoxemic at rest, they may quickly become hypoxemic with exercise.

to

mismatching,

an

invariable

finding

in

RLD,

leads

3. Decreased breath sounds with dry inspiratory rales (Velcro cracles)

4. Decrease in lung volumes and capacities

5. Diffusing capacity (DL CO ). This arises as a consequence of a widening of the interstitial spaces due to scar tissue, fibrosis of the capillaries, and ventilation-perfusion abnormalities. In RLD the DL CO has been measured at less than 50% of predicted.

6. Cor Pulmonale. Right-sided heart failure is due to hypoxemia, fibrosis and compression of the pulmonary capillaries, which leads to pulmonary hypertension.

Other signs:

Decrease in chest wall expansion

Possible cyanosis or clubbing

3 Hallmark Symptoms

1.

Dyspnea

2.

Irritating, dry, non-productive cough.

3.

Wasted, emaciated appearance

 

Signs and Symptoms of Restrictive Lung Dysfunction

Signs

Symptoms

Tachypnea Hypoxemia Decreased lung volumes Decresed diffusing capacities Decrease breath sounds Altered chest radiograph (often reticulonodular pattern) Pulmonary hypertension

Dyspnea

Cough

Weight loss

Muscle wasting

Differential Diagnosis

In Restrictive Lung Disease Forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) are reduced so theFEV1/FVC ratio is normal.

In Obstructive Lung Disease FEV1 is reduced while the FVC is normal thus the FEV1/FVC ratio is lower.

Medical Management

1. Supplemental Oxygen to support the arterial partial pressure

2. Antibiotic therapy to fight secondary pulmonary infection

3. Measures to promote adequate ventilation and prevent accumulation of pulmonary secretions

4. Good nutritional support

However, if the changes that are causing the RDL are acute and reversible (pneumothorax) or chronic but reversible (Guillain-Barre syndrome), the treatment consists of specific corrective interventions (e.g., chest tube placement) as well as supportive measures (e.g., temporary mechanical ventilation) to assist the patient to maintain adequate ventilation until the patient is again able to be independent in this activity.

RLD Management Goals

1.

Improve exercise tolerance of the patient

2.

Increase/bring back to normal lung volume of patient

3.

Decrease/bring back to normal patient’s work of breathing

4.

Bring relief of pain, anxiety or tension, fatigue

Physical Therapy Management

1. Treatment program that includes:

Low-level activity initially with gradual progression

Periodic rest periods to increase patient tolerance of more vigorous activities

Coordination of breathing with activity

Techniques to increase pulmonary compliance

o

Breathing exercises

o

Thoracic mobility and posture exercises

o

Soft tissue mobilization

Bronchial hygiene techniques if secretion management is a problem

o

Postural Drainage with percussion and/or vibration (PD&P) (PD&V)

o

High Frequency Compression/Oscillation Therapy

o

Flutter Valve

o

IntraPulmonary Percussive Ventilation

o

Positive Airway Pressure Techniques

o

Positive Expiratory Pressure Therapy (PEP)

Relaxation techniques

2. Aerobic or endurance training

Exercise involving large muscles of the body, which is sustained continuously for at least 20 to 30 minutes at an intensity of 70% to 85% of maximal predicted heart rate (according to age) and performed at least 3 days per week

3.

Breathing pattern control

Teach patients specific breathing strategies including diaphragmatic breathing, pursed-lip breathing to reduce work of breathing by slowing the respiratory rate or eliminating accessory muscle activity, especially during exertion.

4. Positioning

Lung compliance decreases and work of breathing increases progressively from standing, to sitting, to supine. In supine, lung volume is restricted by the load of the viscera, increased thoracic blood volume, and small airway closure.

No physiotherapy should be carried out without consideration of the position in which it is performed.

5. Deep breathing

Accurately position patient, usually side-lying-inclined-towards-prone to facilitate maximum expansion of the base of the uppermost lung

If side-lying is impossible, upright sitting may be done

When patient is ready, he/she is asked to breathe in deeply and slowly through the nose, then sigh out through the mouth

After every few breaths, patient should relax and regain his/her rhythm

Breathing rate and pattern should be observed at this time

6. AROM exercises strengthening exercises, bracing

Required for patients with paralysis

7. Teach patients to increase and strengthen endurance of remaining ventilator muscles by:

Use of an inspiratory muscle trainer

Resistance exercise to the diaphragm

Incentive spirometer

8. Patient must learn to perform:

Active and passive chest wall stretching (rolling, positioning, side leaning, air shift maneuvers)

9. PROM may be done immediately

Sources:

Braddom, R.L. (2011). Physical Medicine & Rehabilitation. 4 th ed. Singapore: Elsevier Pte. Ltd.

Hillegas, A. & Sadowsky, H. (2001). Essentials of Cardiopulmonary Physica Therapy. 2 nd ed. USA: W.B. Saunders Company.

Kisner, C. & Colby, L.A. (2007). Therapeutic Exercise: Foundations and Techniques. 5 th ed. PA: F.A. Davis Company.

Watchie, J. (1995). Cardiopulmonary Physical Therapy.: A Clinical Manual. USA: W.B. Saunders Company.