11- Respiratory Structures and the mechanics of breathing Flashcards
what do the chest call and lungs both have in common
elastic structures
Alveolar Pressure (P or PA )
Pressure within alveoli (equal to atmospheric when there is no airflow).
Pleural Pressure (Ppl)
Pressure within pleural space(is sub- atmospheric when there is no airflow
Transpulmonary or Recoil Pressure (PTP or PRe)
Difference between pleural and alveolar pressures (reflects elastic recoil pressure of the lung)
values at end expiration
Ppl is -5, PRe is 5, PA is O cmH2O
values during inspiration
Ppl is -8, PRe is 7, PA is -1 cm H2O
what happens during inspiration
diaphragm contracts
pleural space is expanded which decreases pleural pressure
Sequence of events during a normal breath
During Inspiration:
1. The brain initiates diaphragm and/or intercostal muscles contraction.
- Pleural space increases as chest wall expands.
- When the pleural space increases, the PPL becomes more negative countering recoil pressure thereby expanding alveoli.
- Alveolar pressure falls below atmosphere pressure
- Air flows into alveoli to equalize alveolar and atmospheric pressure.
sequence of events during normal expiration
- The brain ceases inspiratory command.
- Inspiratory muscles relax.
- Thoracic volume decreases causing PPL to become less negative and decreasing the alveolar pressure gradient.
- Alveolar elastic recoil increases alveolar pressure above atmospheric
providing airflow until alveolar and atmospheric pressure equalize.
Changes in PA and PPL during a breath
PA changes less than PPL during a breath because a
portion of PPL is used to overcome lung recoil
Reflects lung compliance
∆V/∆PTP
Airway resistance
R=PA /airflow
what happens to lung recoil pressure (PRe) as lung volume increases?
lung recoil pressure (PRe) increases
- lungs always want to be at a 0 pressure so the further away it is from 0 the more likely it is to collapse
- lung pressure and volume have a direct (non-linear) relationship
lung recoil, tissue elasticity, and surface tension
- large pressure change required to initially inflate with air
- lung recoil due to elastic tissue and surface tension
density of surfactant molecules determines surface tension
- higher density of surfactant in small alveoli prevent these alveoli from empting into large alveoli
- phospholipids in surfactant minimize surface tension in the lung
Atelectasis
Collapse of Alveoli
- caused by obstruction of airway and subsequent absorption of gases
- absence of surfactant facilitates this b/c of high collapsing pressure (spend a lot of energy trying to reopen the lungs everytime)
Sighs
large tidal volumes that alleviate atelectasis (large negative pleural pressure to pop open the alveoli that have collapsed)
emphysema
destruction of lung elastic tissue (less surfactant)
lung compliance and 2 diseases
Lung compliance is…
- increased in pts with emphysema
- decreased in pts with pulmonary fibrosis
Vital capacity vs pressure graphs
emphysema (closest to y-axis) -> normal -> fibrosis
Elastic Characteristics of the Chest Wall
Equilibrium position 60% of vital capacity (VC)
Chest wall compressed to residual volume (RV)
- attempts to expand
- exerting a force of 40cm H20
Chest wall forced to total lung capacity (TLC)
- attempts to collapse
- exerting a force of about 15mmHg
Elastic Characteristics of the Chest Wall and lung
-the lung recoil pulls the chest in and the chest recoil pulls the lungs out
abnormalities of chest wall (pretty low yield info here)
Most abnormalities decrease chest wall compliance to decrease TLC and capability for chest wall expansion.
- Ankylosing spondylitis- stiff chest wall (inflammatory induced fibrosis) 2. Kyphosis (anteroposterior angulation)
- Scoliosis (excessive lateral curvature)
- Obesity (soft tissue restriction)
- Aging (fibrosis)(Infants have a very compliant chest wall) Patients with an abnormal chest wall are dyspneic
airway resistance
Determined primarily by diameter of airways.
The total area of multiple small airways is greater than that of the large airways.
Thus, resistance is greater in the trachea than in the combined terminal bronchi.
airway resistance v. volume
airway resistance decreases as lung volume increases
what acts like springs to expand the airways
elastic recoil of the alveolar septa attached to airways
what happens to flow and lung volume during expiration
flow decreases as lung volume decreases
what occurs at low lung volumes
flow is effort independent
increments in PA are offset by airway constriction
emphysema and pulmonary fibrosis effect on expiratory flow
Emphysema and pulmonary fibrosis decrease maximal effort expiratory flow
one reason breathing is regulated
to avoid high and low lung volumes
four major diseases of increased airway resistance
- Emphysema – due to decreased tethering of airways by lung elastic tissue, airway diameter is below normal.
- Bronchitis – reduced airway diameter due to increased mucous and airway inflammation.
- Asthma – hyperactive airway smooth muscle causes excessive muscle contraction that narrows airways.
- Obstructive Sleep Apnea – Closure or compression of pharyngeal airway due to excessive adipose tissue and/or reduced airway dilator muscle activity.
“time constant” of airway
reflects rate of alveolar filling when a pressure change is applied
what happens if one lung is partially constricted?
one will start moving air into the constricted one so its not getting as much fresh air. also the not constricted one will move a lot faster at those conditions where you breath more
correct sequence of changes during an inspiration
- increased diaphragm activity
- expansion of pleural space
- decreased pleural pressure
- decreased alveolar pressure
- inspired flow
correct sequence of changes during an expiration
- increased diaphragm activity
- decreased pleural pressure
- decreased alveolar pressure
- expiration
