Pulmonary System

pulmonary system

requires ventilation while removing CO2 from the blood through external ventilation

ventilation

ability to move air in and out of the lungs via a pressure gradient

respiratory system goes thorugh

upper airway, lower airway

terminal respiratory unit

Acinus

everything outside the respiratory unit

deadspace

Respiration

gas exchange that supplies O2 to and removes CO2 from the blood

upper airway consist of

nasal cavities, sinuses, pharynx, tonsils, larynx

Lower airway consist of

trachea, bronchi, bronchioles, lobes of the lungs

alveolar duct consist of

respiratory bronchioles & alveolar sacs

respiratory unit is from the

respiratory bronchioles through the alveoli

the conducting airway, aka the dead space consist of

trachea, segmental bronchi, nonrespiratory bronchioles

Major sequelae of pulmonary diseases or injury

hypoxia, hypoxemia, hypercapnia

hypoxemia

deficiency of oxygen in arterial blood

hypoxia

decreased availability of oxygen to body tissue

Prolonged hypoxia leads to ___ _____

cell death

impairments in the pulmonary system have

systemic, widespread effects

hypercapnia

elevation in CO2 leads to acidosis (decreased pH)

Normal PaO2 level

80-100mmHg (95-100% pulse ox)

irregualr (low) PaO2 levels symptoms include

tachycardia, respiratory distress, DOE, LH, nausea, dyscoordination, malaise, confusion, labored breathing, arrhythmia, cardiac arrest, lethargy

hyperventilation

increased volume of air moving in/out of the alveoli; resulting in increased blood CO2, decreased in blood O2

Cough (s/s of respiratory system)

physiological response to clear irritants (antigens) from the airway

Dry & persistent cough reasons

tumor, congestion, hypersensitive airway

productive cough reason

inflammation, infection, irritation

hemoptysis cough reasons

bloody sputum, indicative of tumor, abscess, infarct

rust colored sputum reasons

may indicate pneumonia or hemoptysis

s/s of pulmonary disease

dyspnea, chest pain, cyanosis, clubbing, altered breathing patterns, altered breath sounds

dyspnea

shortness of breath

chest pain

usually substernal or over involved lung fields

chest pain can radiate to the

neck, upper trapezius, costal margins, thorax, scapulae, shoulder, pleural irritation

cyanosis

blueish color of skin or mucous membrane (lips, eyes, fingers, toes)

clubbing

thickening & widening of the terminal phalanges (chronic tissue perfusion/nutrition due to hypoxia)

altered breathing patterns

changes in rate, depth, & regularity of breathing

hypoventilation

decreased volume of air moving in/out of the alveoli (blood: increased CO2, decreased O2)

hyperventilation

increased volume of air moving in/out of the alveoli (blood: decrease CO2, increase O2)

RR

12-20 breaths/min

Stridor

Harsh inspiratory sound, indicates laryngeal obstruction

Wheezing

Continuous high-pitch whistling sound during expiration (bronchospasm, airway constriction)

Crackles/Rales

discontinuous low-pitched sounds during inspiration (indicate secretion fluid in the peripheral airways)

crackles/rales is indicative of

pneumonia, pulmonary edema

Implication for PT clinical practice

1. Patients with pulmonary, cardiovascular, and neuromuscular diseases are at risk for deficient oxygen transport ± may have altered breathing patterns.

2. impacts respiration + ventilation (multiple systems)

3. Exercise stresses the oxygen transport system therefore monitoring of cardiopulmonary status is important

4. VITAL SIGNS

Lung Dysfunction: 2 main classifications

restrictive lung dysfunction (RLD) & obstructive lung dysfunction (OLD)

obstructive lung dysfunction (OLD)

airflow is impeded, less & slower air out of the lungs

obstructive lung dysfunction (OLD) pathologies

Emphysemia, [chronic] bronchitis, asthma, cystic fibrosis

restrictive lung dysfunction (RLD)

Volume (ventilation) of air is reduced (less air in lungs) due to restriction expansion of the lungs or chest wall.

pulmonary function testing (PFT)

decrease in mostly all volumes & capacities, relatively normal flow rate, decreased diffusion capacity (DLCO)

restrictive lung dysfunction (RLD) pathologies

aging, septic, pleural, cardiovascular, neuromuscular, musculoskeletal/connective tissue, occupational/environemental, pulmonary, maturation/developmental

Pathogenesis of restrictive lung dysfunction (RDL)

1. Impaired pulmonary compliance (decreased in chest wall or lung tissue compliance)

2. altered lung volumes & capacities (decreases)

3. increased work of breathing (WOB) (increased ventilation, therefore SOB)

Pathogenesis of restrictive lung dysfunction (RDL): Impaired pulmonary compliance

1. Chest wall: reduced expansion results in decreased lung volume

2. Lung with decreased compliance: stiffer, less elastic, more difficult to expand

decreased compliance results in increased pressure needed to maintain ventilation (work harder to breathe)

Pathogenesis of restrictive lung dysfunction (RDL): altered lung volume & capacities

1. Lung volume: eventually all of the lung volumes decrease

2. Lung capacity: if all lung volumes are reduced, lung capacities will reduce as well (>/= 2 lung volumes added together)

Pathogenesis of restrictive lung dysfunction (RDL): work of breathing

work of breathing increases (greater transpulmonary pressure are needed to achieve the same tidal volume)

1. muscles (diaphragm + accessory) must work harder

2. respiratory rate increases, tidal volume decreases (increase energy expenditure

With an increase in WOB respiratory rate_________ & tidal volume _______.

increases & decreases

Tidal volume

inhale/exhale in normal breaths at rest; not under conscious control

inspiratory reserve volume

additional air that can inhaled past tidal volume

Inspiratory capacity

tidal volume + inspiratory reserve volume

expiratory reserve volume

additional air that can be exhaled past tidal volume

residual volume

volume still in lungs after max expiratory effort (preventing collapse)

functional residual capacity

expiratory reserve volume + residual volume

vital capacity

inspiratory reserve volume + tidal volume_ expiratory reserve volume

total lung capacity

max volume to which the lung scan be expended (VC + residual volume)

RDL signs

1. tachypnea

2. VQ mismatching

3. decreased breath sounds

4. PFT

5. decreased diffusing capacity of lung for carbon monoxide

6. cor pulmonale

Tachypnea

increased RR & decreased TV to overcome decreased compliance & maintain minute ventilation

VQ perfusion/mismatching

Damage to lung tissue/ capillaries airways or bony abnormalities lead hypoxemia

decreased breath sounds + dry inspiratory crackles especially at bases

due to atelectasis: reduced lung volumes

Cor pulmonale

pulmonary HTN leading to RHF

Cor Pulmonale reason for HTN & RHF

Increased pressure in pulmonary circulation, increasing work on the right ventricle.

fibrotic pulmonary capillary —> less CO/CO2

PFT

decreased lung volumes & capacities by spirometry

Decreased diffusing capacity of lung for carbon monoxide (DLCO)

due to widened interstitial spaces due to scarring, VQ abnormality, capillary fibrosis

RLD classic symptoms

dyspnea/SOB, dry-nonproductive cough, muscle wasting

RLD symptom: muscle wasting

emaciated appearance due to cachexia

RLD symptoms: dysnpea/SOB

initially with exercise, then at rest

what are the contributing factors to the 6 classic signs & 3 classic symptoms of RLD?

1. Decreased lung volume & capacities

2. decreased chest wall compliance, decreased lung tissue elasticity

3. increased WOB, increased RR to maintain minute ventilation

RDL treatment

1. Supplement O2

2. Treat infections

3. Airway clearance techniques (ACTs)

4. Promote ventilation

5. Ventilatory muscle training (endurance; provide resistance)

6. Nutrition