obstructive disease

oxygen transport pathway steps

inspired O2 and ambient air quality --> airways --> lungs and chest wall --> diffusion --> perfusion --> myocardial function --> peripheral circulation --> tissue extraction and use of O2 --> return of partially desaturated blood and CO2 to lungs

inspiratory muscles

- diaphragm

- external intercostals

accessory muscles

- SCM

- scalenes

- serratus anterior

- pec major and minor

- upper traps

- ES

- lats

expiratory muscles

- abdominals: recuts, transverse, external oblique, internal oblique

- internal intercostals

mechanics of breathing: inhalation

- active contraction of diaphragm and external intercostal muscles

- thoracic and lung expansion

- negative intrapleural pressure and falling alveolar pressure

- air flows into and inflates lungs

mechanics of breathing: exhalation

- passive relaxation of inspiratory muscles to resting position

- elastic recoil of lungs causes alveolar pressure to rise

- air flows out of lungs

gas exchange (respiration)

- respiratory gas exchange takes place in the alveoli, which have a very large surface area available

- capillary network covers the surface of alveoli

- gas exchange takes place by diffusion across the extremely thin alveolar-capillary membrane

diffusion

- the movement of gases into and out of the blood, the alveolar-capillary membrane

- O2 from alveolar air into blood

- CO2 from blood into alveolar air

- from high to low concentration

diffusion is affected by

- concentration and solubility of gases

- membrane thickness

- surface area

- pathology: fibrosis, fluid, edema, etc

tissue extraction and use of oxygen

- O2 diffuses rapidly out of circulation through cell membrane

- regulated by tissue metabolism and overall demand

- delivery is 3-4x > demand at rest

- VO2 can increase 20x with increased metabolic demands of exercise

- dependent on blood flow: increased blood flow in availability to working tissues

- CO can increase > 5x during strenuous exercise

- rate of O2 extraction is regulated by O2 demand

return of partially desaturated blood and CO2 to lungs

- partially desaturated blood and CO2 removed from cells by venous circulation to R side of the heart and lungs

- CO2 diffuses across alveolar membrane and eliminated through the respiratory system

impaired breathing mechanics

- ineffective (unbalanced) breathing pattern

- impaired lung expansion

- impaired thoracic/chest wall mobility

- ventilatory muscle weakness/fatigue

clinical patterns/diagnosis (cardiovascular - perfusion)

- myocardial pump dysfunction: valve disease, arrhythmias, cardiomyopathy, heart failure

- myocardial vascular dysfunction: CAD, MI, angina, ACS

- peripheral vascular dysfunction: PAD, venous insufficiency, DVT

clinical patterns/diagnosis categories (pulmonary - ventilation)

- obstructive lung dysfunction: COPD, asthma, CF

- restrictive lung dysfunction: pulmonary fibrosis, interstitial lung disease, pneumothorax, pleural effusion, neuromuscular, thoracic cage deformity, obesity, pregnancy, post-op

COPD

- catch all term that is used to both emphysema and chronic bronchitis

- patients with COPD will likely have a mix of both diseases, with one predominating

- clinical presentation varies depending on the primary disease classification

general characteristics of obstructive disease: progressive airway obstruction that involves -->

- inflammation of bronchial walls (increases during exacerbations)

- chronic inflammation leads to narrowing of small airways, destruction of bronchioles

- destruction of lung parenchyma, resulting in loss of lung tissue elasticity

- permanent destruction of alveoli walls

obstructive disease general characteristics

- results in poor gas exchange, air trapping, and hyper inflated lungs

- typically increased use of accessory muscles, altered breathing mechanics

- prone to recurrent respiratory infections

pink puffer

blue bloater

pink puffer

- typically male, middle 50s

- increasing SOB for the last 3-4 years

- thin build with evidence of recent weight loss

- chest is over expanded (barrel chest) increased AP diameter

- cough may be productive (small amounts of white sputum) or absent but GENERALLY non- productive

- increased work of breathing to maintain normal oxygenation

emphysema - signs and symptoms

- progressive dyspnea, especially on exertion

- cough, with variable degrees of productiveness

- decreased breath sounds with prolonged expiratory phase

- possible end-expiratory wheeze on forced expiration

- increased symptoms with acute respiratory infections

- posture: typically leans forward, leans on UE (tripod)

- increased use of accessory muscles

- increased AP diameter from hyperinflation: barrel chest

- hyper resonance to percussion

- flattened diaphragm

emphysema

- characterized by enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of alveolar walls

- diagnosis based on long-term structural and functional changes to lung tissue

destruction of alveoli

- there is MASSIVE loss of surface area for gas exchange as the disease progresses

- increased V/Q mismatching

- decreased perfusion = dead space

emphysema etiology

- most common: cigarette smoking, environmental exposure

- alveoli destruction limited to central part of respiratory bronchiole

- typically most marked in apex of upper lobes, spreads down as disease progresses

- rarer: alpha 1 antitrypsin deficiency, destruction of whole alveoli, more common in lower lobes

emphysema- pathophysiology

- repeated airway inflammation causes progressive lung tissue destruction

- disruption of elastic fiber network --> loss of parenchyma and elastic recoil --> premature closure of airways resulting in air trapping --> increased residual volume

- increased pulmonary vascular resistance (due to loss of lung parenchyma, vascular beds): accelerates pulmonary HTN

barrel chest

air trapping --> increased residual volume and hyper inflated lungs --> increased AP diameter, horizontal ribs = barrel chest

chest x ray

- hyperinflation: dark large lung fields

- horizontal ribs

- flattened low set diaphragms

- vertical, narrow heart/mediastinum

- increased AP diameter

bullae on chest x ray

abnormal air spaces visible on chest x ray when disease is moderately advanced

emphysema: pink puffer

- alveolar (diffusion) problem

- increase in CO2 retention (pink)

- minimal cyanosis

- pursed lip breathing

- dyspneal / increase in respiratory rate

- hyper resonance on chest percussion

- orthopneic

- barrel chest

- exertional dyspnea

- prolonged expiratory time

- speaks in short jerky sentences

- anxious

- use of accessory muscles to breathe

- thin appearance

"blue bloater"

- typically male in his 50s

- H/o chronic and productive cough: cough has progressed from only present in winter months to year round

- SOB, DOE worsening with progressively limited exercise tolerance

- acute exacerbations with purulent sputum becoming more common

- stocky build, with puffy complexion and some cyanosis

- auscultation: adventitious sounds: crackles, rales, rhonchi

- JVD and peripheral edema may be present --> R heart failure (cor pulmonale)

chronic bronchitis signs and symptoms

- cough begins slowly, insidious onset

- cough worsens until chronic, productive

- often more pronounced in the winter months, but may become constant

- progressive DOE: exercise tolerance decreases slowly but steadily, until the individual has essentially no reserve

- normal breath sounds with prolonged expiratory phase

- possible (expiratory) wheezes or crackles

chronic bronchitis

- characterized by idiopathic chronic cough with excessive mucus production

- results from long-term irritation of the tracheobronchial tree

- diagnosis based on subjective report of productive cough on most days for 3 months during 2 consecutive years, when other conditions have been ruled out (diagnosis of exclusion)

chronic bronchitis etiology

- repeated exposure to any inhaled irritant results in chronic inflammation

- cigarette smoking chiefly responsible

- air pollution or industrial smoke

- fires, smoke inhalation

- inhalants are also being used as recreational drugs

chronic bronchitis pathophysiology

- chronic irritation of airways provokes an inflammatory response: mucosal edema, hypersecretion of mucus, destruction of cilia

- irritation of airways can cause bronchoconstriction

- excessive sputum production, increased secretion retention --> decreased ventilation

chest x ray of chronic bronchitis

- may show cardiac enlargement, congested lung fields, scars from old infections along inflamed bronchi

- changes are nonspecific, vary by patient, may show cardiomegaly

chronic bronchitis: blue bloater

- airway flow problem

- color dusky to cyanotic

- recurrent cough and increased sputum production

- hypoxia

- hypercapnia (increase in CO2)

- respiratory acidosis

- increase in hgb

- increase in respiratory rate

- exertional dyspnea

- increase in incidence in smokers

- digital clubbing

- cardiac enlargement

- use of accessory muscles to breathe

- leads to R sided HF: bilateral pedal edema, increase in JVD

pulmonary function in COPD

- spirometry pre/post bronchodilator: to confirm airflow obstruction

- decreased vital capacity, FEV1, and diffusion capacity

- TLC, FRC, and RV are all typically increased in emphysema (from air trapping)

- decreased flow rates with increased expiratory time due to decreased elastic recoil of the lung --> it takes LONGER to get air out due to airway obstruction

- FEV1/FVC (forced expiratory ratio) < 0.7 = obstructive disease

- FEV1 < 65% predicted = diagnostic for chronic airway obstruction

gold classification

- based on FEV1

- in patients with FEV1/FVC < 0.70

Gold 1

Mild FEV1 >/= 80% predicted

Gold 2

Moderate

50%

Gold 3

Severe - 30% ≤ FEV1 < 50% predicted

Gold 4

very severe

FEV1

other obstructive diseases

- bronchiectasis: permanently damaged, widened, thickened bronchi

- mucus build up results in frequent infections and blockages

- cystic fibrosis

- asthma

asthma

- chronic inflammatory condition characterized by hyper responsiveness of the airways to various stimuli, leading to widespread narrowing of the airways

- may have immediate or latent hypersensitivity reaction

- REVERSIBLE airway obstruction

asthma signs and symptoms

- frequently begins in childhood, but may occur at any age

- often a family history

- recurrent and sudden coughing attacks, chest tightness, difficulty breathing

- often accompanied by audible wheezing

- tachypnea

- thick, tenacious sputum

- auscultation: distant breath sounds, prolonged exhalation

- adventitious sounds: high-pitched expiratory, and possibly inspiratory wheezes

status asthmaticus

- severe asthma attack that does not respond to bronchodilators: bronchospasm, airway inflammation, mucus plugging, difficulty breathing, CO2 retention, hypoxemia

- typically presents a few days after onset of a viral respiratory illness, following exposure to a potent allergen or irritant, or after exercise in a cold environment

- associated with symptoms of potential respiratory failure : immediate medical attention is required

status asthmaticus signs and symptoms

- persistent SOB

- breathlessness even while laying down: need to breathe more easily

- chest tightness

- cyanosis

- agitation, confusion, inability to concentrate

- hunched shoulders, strained abs and accessory muscles

asthma pathophysiology

- hypertrophy of airway smooth muscle that contracts during an attack, causing bronchoconstriction

- hypertrophy of mucus glands, edema of the bronchial wall

- V/Q mismatch --> impaired gas exchange, increased work of breathing

- hyperventilation to maintain normal oxygenation

asthma: etiology

- extrinsic: exposure to exogenous allergens sich as pollens, animal danders, feathers, mold spores, dust, food, typically affects children

- intrinsic: precipitated by non-immune mechanisms such as chemical/inhaled irritants, weather, respiratory infections, drugs, emotions/psychological stress

- occupational: result of toxic exposure to various substances in the workplace

- exercise induced

exercise-induced asthma/bronchospasm

- exercise --> loss of heat and/or moisture from airway --> contraction of bronchial smooth muscle without inflammation of mucosa, edema, or mucus formation

characteristics of exercise-induced asthma/bronchospasm

- acute, reversible, usually self-terminating

- triggered by exercise or hyperpnea

- exacerbated by breathing dry and/or cold air

- occurs in 80-90% of known asthmatics

- rarely occurs as the sole trigger of asthma

sympathomimetic (beta 2 agonist)

- example: albuterol (Proventil, Ventolin) short acting, rescue inhaler

- route of administration: aerosol inhalation

side effects of sympathomimetic (beta 2 agonist)

- tremor, shakiness

- palpitations

- tachycardia

- cough

- dry mouth, throat irritation

- dizziness

- nausea, upset stomach

- HTN

- HA

parasympatholytics (anticholinergics)

- ipratropium (atrovent): short acting

- tiotropium (Spiriva): long acting

- route of administration: aerosol or dry powder inhalation

parasympatholytics (anticholinergics) side effects

- dizziness

- nervousness

- drowsiness

- depression

- delirium

- hallucinations

- decreased GI activity

- dry mouth, throat irritation

- HA

combination drugs: long acting beta 2 agonist + inhaled corticosteroid

- symbicort

- advair

- breo

short acting beta2 agonist + short acting anticholinergic

Combivent

physical therapy management

- medical diagnosis, underlying pathology not reversible

- provide non-invasive interventions that can reverse or mitigate insults to O2 transport and reduce, delay, or eliminate need for medical interventions

- optimize cardiovascular and pulmonary function: gas exchange, ventilation, airway clearance, O2 deliverance and utilization

- prevent complications and deconditioning

- modify risk factors

- promote overall physical function

voice sounds

- used to confirm abnormal breath and adventitious sound findings

- vibrations produced by voice, heart through stethoscope as it travels down tracheobronchial tree

- low pitched, muffled over normal lung tissue

- increased or decreased, depending on pulmonary pathology

- increased = consolidation (more fluid filled lung - alveoli)

- decreased = pleural effusion, pneumothorax (fluid/air filled in pleural space, chest wall)

- bronchophony

- egophony

- whispered pectoriloquy

bronchophony

- increased vocal transmission heard in the presence of increased lung density (consolidation due to pneumonia)

- ask pt to say 99: words sound louder and clearer with consolidation indicates retained secretions

- abnormal = + bronchophony

egophony

- voice heard through lungs is increased in intensity and takes on a nasal or bleating quality

- co-exists with bronchophony

- ask pt to say "E--" sound will be heard as "A---" with lung consolidation, retained secretions

- abnormal = (+) egophony test

whispered pectoriloquy

- helpful in identifying smaller or patchy areas of consolidation

- can be present when bronchophony and ego phony are absent

- ask pt to whisper 1,2,3: whispered voice sounds become more distinct and clear in the presence of lung consolidation, retained secretions

- abnormal = + whispered pectoriloquy

tactile fremitus

- formally assess with positive adventitious or voice sounds

- decreased in emphysema: typically less secretions, increased air trapping

- often normal in chronic bronchitis: despite typically increased secretions, air trapping transmits vibrations less

percussion

- formally assess if + adventitious or voice sounds

- hyper resonant in emphysema: air trapping

- often normal resonance in chronic bronchitis

MSK screen: general strength

- 70-80% of age-matched, healthy

- proximal UE strength affected more than distal UE

- respiratory muscle weakness with mod-severe COPD

- inspiratory muscle force more affected than expiratory

acute vs outpatient exercise/activity tolerance evaluation

- bed mobility, transfer, gait

- seated/standing therex

- 6 MWT or variation

- self-paced walk test

- 5xSTS, 30 sec chair rise

- 2 min step test

- chair step test

- monitor O2 sat closely!: may desaturate quickly, observe and document time and interventions to facilitate recovery of SpO2

key impairments: impaired breathing mechanics

- ineffective breathing pattern

- increased accessory muscle use

- not enough diaphragm (flattened)

- impaired breathing control: increased RR

key impairments: impaired ventilatory pump function

- decreased respiratory muscle strength/endurance

- decreased lateral costal expansion (barrel chest)

- air trapping (loss of alveoli elasticity, blocked airways)

key impairments: impaired exercise/activity tolerance

- SOB, DOE

- increased work of breathing

interventions

- breathing strategies: positioning to reduce dyspnea, pursed-lip breathing, paced/breathing control, paired with movement

- promote recruitment of diaphragm vs upper chest/accessories

- thoracic mobility/chest expansion

- respiratory muscle training: inspiratory/expiratory strength, endurance

- airway clearance: mobilization, positioning, postural drainage, cough techniques

interventions cont.

- assess need for adaptive equipment, supplemental O2 therapy

- begin pulmonary rehab within 1 month of acute exacerbation

- education: risk factors, smoking cessation, energy conservation, activity pacing

- aerobic conditioning, endurance and strength training - can reduce frequency/severity of subsequent acute exacerbations

exercise prescription and functional training

- aerobic activity: high intensity is ideal, low intensity intervals OK

- resistance training: upper body strength can reduce RPE and breathlessness

- help to evaluate need for supplemental oxygen

- stop activity with drop in SpO2 > 3-5% from resting, or below 88%

- SpO2 > 85% may be permissible for patients with chronic lung disease

aerobic training

- frequency: > 3x/week, at least 2 sessions supervised

- intensity: prefer high intensity (> 60% HRR), accumulate > 30 min

- low intensity or interval training (repeated bouts of high intensity interspersed with recovery periods) ok

- borg 3-5/10 (mod to strong/hard) or RPE 12-14/20 (somewhat hard)

- type: aerobic = walking, treadmill, cycling

- time: 20-30 min per session

resistance training

- frequency: 2-3x/week, with 1-2 days rest between session

- intensity: 50-60% 1 RM, 1-2 sets, 6-10 reps

- progression: 70-85% 1 RM, 1-2 sets, 8-12 reps

- LE: 5-10% 1 RM

- UE: 5-7% 1 RM

- type: major muscle groups

- multi joint, compound exercises (squats, lunges) for more experienced

- UE training: unsupported UE activities (ADLs) lead to greater dyspnea levels and dyssynchronus breathing

inspiratory muscle training: indications

inspiratory muscle weakness/endurance: diaphragm, intercostals

inspiratory muscle training: goals

- increase ventilatory capacity

- increase strength and endurance

- decrease dyspnea

case study

70 y.o. male brought to the ED yesterday by his

daughter because he was having severe SOB.

HPI: Currently c/o SOB at rest, made worse with

activities such as cleaning and cooking. He is unable to

walk more than 5 min without 3/4 dyspnea and

needing to stop and take a sitting break. SOB when

lying supine. He also reports having a "smoker's

cough", dry with occasional creamy colored phlegm.

Lower legs have been swollen for the past

case study notes

- findings consistent with COPD: barrel chest, SOB at rest, smokers cough, increased accessory muscle usage, smoking for 50 years

- postural deviations: increased thoracic kyphosis, barrel chest

- limitations in ROM/MMT: upper body weakness proximal, limited shoulder flexion

- ask how much mucus coughing up a day

- MSK issues: shoulder impingement, back pain, neck pain

- impairments: decreased aerobic capacity, decreased endurance, decreased inspiratory muscle strength, SOB, cough