Flashcards in Lecture 19: Lung anatomy and mechanics Deck (121):
What is the physiological role of the lungs?
Make oxygen available for metabolism ("internal respiration")
Remove CO2 (metabolic byproduct)
Lobes of right and left lung
Right: upper, middle and lower lobes
Left: upper, lower and lingula (middle lobe)
What surrounds the lungs and their lobes?
What demarcates the thoracic cavity?
Bone: 12 ribs, sternum, vertebrae
Muscle: chest wall muscles and diaphragm
What do the visceral and parietal pleura form?
Pleural sac between lungs and chest wall and diaphragm
Role of the pleural sac
Couples the lungs to the chest wall and the diaphragm
Lubricates: allows sliding movement of the lungs relative to the chest wall and diaphragm
What occurs in pneumothorax?
Loss of lung-throrax coupling (no transmural pressure gradient)
Types of pneumothorax
Primary spontaneous pneumothorax
Risk factors: males, smoking, family history
Secondary spontaneous pneumothorax
With lung disease (COPD, lung infection)
Interstitial lung disease and cancer
Blunt or penetrating injury to the chest wall
Penetration of bony points at rib fracture damages lung
Central venous catheter into chest vein
Positive pressure ventilation (barotrauma)
Trajectory of air through the upper airway
Air enters/exits via the nose & mouth, passing through the pharynx (shared between the digestive and respiratory systems)
Air enters/exits airways via the larynx (contains vocal cords)
Role of epiglottis
Air and food have common passageway
Epiglottis prevents food or drink from entering the airways
Role of upper airways
Airway branching in the human lung, differences?
Anatomy of bronchi
Cartilage in wall
Airway smooth muscle (controls size of airway)
Ciliated pseudo stratified epithelium
Mucous glands (protective)
Anatomy of bronchioles
Terminal bronchioles: no cartilage, reducing smooth muscle, cilia and mucous glands
Respiratory bronchioles: no smooth muscle or cilia, first alveolar bunds
Anatomy of alveolar sacs
Type I and II epithelium
Surfactant (surface tension)
PSNS control of airways - nerve and function
Vagal efferents via muscarinic receptors
Mediate bronchoconstriction, pulmonary vasodilation, mucous gland secretion, mucous gland secretion
SNS control of airways
Bronchial smooth muscle relaxation, pulmonary vasoconstriction, inhibits mucous gland secretion
Non-adrenergic non cholinergic (NANC)
Mixed mediators (ATP, NO, substance P, VIP)
Components of the neural and humeral control of airways
Non-adrenergic non cholinergic (NANC)
Vagal sensory fibers
Stretch, irritant receptors, C fibers, reflex responses (cough, bronchoconstriction, mucous release, heart-lung matching)
Where is the greatest resistance in the respiratory system?
2nd - 5th generation airways (conducting airways)
Resistance is inversely proportional to cross sectional area
Relationship between resistance and cross sectional area
Lower resistance in locations with higher cross sectional area
What effect does bronchoconstriction have on resistance to airflow?
What can induce bronchoconstriction?
PSNS induced airway smooth muscle contraction
Allergic - histamine
Physical - mucous, edema, collapse
Physiologic - neural, local decrease in CO2
What effect does bronchodilation have on resistance to airflow?
What can induce bronchodilation?
Sympathetic nerves - airway smooth muscle relaxation
Physiologic - neural stimulation, hormonal, local increase in CO2
How does gas exchange occur between the alveolar and the capillaries?
Thin interface between the alveolar and the capillaries
Large surface area
Where does blood come from for gas exchange?
Via pulmonary artery (carries deoxygenated blood) and vein (carries oxygenated blood)
What vessels are the airways supported by?
Part of systemic circuit
How can we get air to move in and out of lungs?
Need to create pressure gradients
Lung cannot expand itself, it can only move passively in response to external pressures
What are the two ways to get air into the lung?
Create positive pressure at the airway opening to push air into the lung (in frogs and when a person is manually ventilated with a bag)
Or, create negative pressure within the lung (free breathing in humans)
Anatomy of breathing: respiratory system at equilibrium (end expiration)
Lungs are elastic and want to be smaller
Thorax is elastic and wants to be bigger
Anatomy of breathing: inspiration
Respiratory muscle contraction increases thoracic volume to stretch the lungs
Creates negative pressure (compared to atmosphere) so air moves in
Anatomy of breathing: exhalation
Respiratory muscles relax
Thoracic volume decreases due to pulling forces of the elastic lung
Creates positive pressure so air moves out of lung
What are the two forces that pull the lungs away from the thoracic cage? Opposed by?
The lung's natural tendency to recoil
The surface tension of the alveolar fluid (molecules of fluid lining the alveoli are attracted to each other. This produces surface tension that acts to draw the alveoli together)
Opposed by the natural elasticity of the thorax
Visceral and parietal pleura stay attached by the parietal fluid, so neither the lungs nor the thorax wins
Usual pleural pressure
Due to opposing forces of lungs and thorax
Otherwise, lungs would collapse
What pressures are important in breathing?
Atmospheric pressure (Patm)
Intra-alveolar pressure (Palv)
Intra-pleural pressure (Ppl)
Transmural pressure: difference across a boundary
Important transmural pressures in breathing
Lung wall = Palv - Ppl
Thoracic wall = Patm - Ppl
How does air move during breathing?
Down pressure gradient
Pressure gradients during end expiration
Patm = 0
Palv = 0
Ppl = -5
transmural pressure of lung wall = 0 -(-5) = 5
No air flow
Pressure gradients during inspiration
Thorax and lungs increase in size
Patm = 0
Palv = -1
Ppl = -8
Transmural pressure of lung wall = -1 - (-8) = 7
Air flows into lungs
Lung recoil at functional residual capacity
lung recoil at FRC = chest wall recoil
Lung recoil: % vital capacity vs lung pressure
Recoil force increases as vital capacity and pressure increase
Recoil pressure at different lung volumes
At very negative pressure, the recoil pressure of the lungs is low. The recoil pressure of the thoracic cage is high (wants to expand(
At FRC, the recoil pressure of the lungs is equal to that of the thoracic cage
At tidal volume, the lung recoil pressure is equal to the thoracic recoil pressure
Inspiration: external intercostals, diaphragm
Accessory muscles of inspiration: scaliness, sternocleidomastoid
Muscles of active expiration: abdominal, internal intercostals
Anatomy of inspiration
Diaphragm contracts: moves inferiorly and increases the vertical dimension of the thoracic volume
External intercostals: raise ribs to increase anterior-posterior and lateral thoracic volume
Scalenes and sternocleidomastoid: elevate upper ribs and sternum during exertion
Anatomy of quiet expiration
Muscles relax, lungs and chest wall return to equilibrium
Anatomy of forced expiration
Internal intercostals reduce anterior-posterior and lateral thorax volume
Abdominals force diaphragm up
Ppl becomes positive and larger than Palv = dynamic airway compression
What is compliance?
A measure of the dispensability of a structure
Degree that volume changes in response to change in pressure
delta V / delta P
What part of the pressure volume curve represents compliance?
Compliance vs elastance
Compliance is opposite of elastane
What is lung elastic recoil determined by?
Elastic fibers in lung interstitial (collagen & elastin)
Surface tension of alveolar lining fluid (surfactant)
What determines how much air enters during inspiration?
Pressure-volume relationship in emphysema
Increased lung compliance due to tissue destruction
Steeper slope on Volume vs pressure graph
Person breathes at high lung volume (hyperinflation)
Pressure-volume relationship in fibrosis
Increased lung stiffness (low compliance) due to lung fibrosis
Breathe at very low lung volume
Rapid, shallow breathing
What would happen if the airways and alveoli were lined with water?
Water has highly polarized molecules and high surface tension
High surface tension = decreased compliance
Alveoli could collapse
What reduces surface tension in the alveoli?
Surfactant from alveolar type II cells
Ensures elastic recoil and alveolar stability
Composition of surfactant secreted by alveolar type II cells
Surfactant complex: phospholipids and proteins
Surfactant proteins: SP-A, B, C, D
Main phospholipid: dipalmitoyl-phosphatidylcholine
LaPlace law and elastic recoil
P = (2 x surface tension) / radius
Smaller radius = greater pressure
Lung compliance vs volume
Surface forces in alveoli affect lung compliance
Pressure volume loop in saline-filled lungs
No surface tension
Inflation and deflation curves are similar
Pressure volume loop in lungs with surfactant
Need higher pressure to distend due to greater surface tension
Inflation and deflation curves ar different
What is hysteresis? In lungs?
A property of a system such that an output value is not a strict function of the corresponding input
In an air-filled lung, there is a pronounced difference between the inflation and deflation curves
Surfactant is recruited to alveolus during inflation
Surface tension is lower for exhalation
Change in surfactant during breathing
Inflation of lungs recruits surfactant
Changes in density with increase and decrease in lung size
How is spirometry performed?
Using a spirometer
Measures the volume of air moved during inspiration and expiration maneuvers in time (mL air/min = flow)
What is tidal volume?
TV or Vt
Air inhaled and exhaled with each resting breath
~500 ml in adult
What diseases are associated with a surfactant deficiency?
RDS and ARDS
Respiratory distress syndrome
What is residual volume?
Gas remaining in the lungs at the end of maximal exhalation
What is inspiratory reserve volume?
Volume (above TV) that can be inhaled by maximum effort
What is Expiratory reserve volume?
Volume (below TV) that can be exhaled by maximum effort
What is Functional residual capacity?
Gas in lungs at the end of a resting tidal breath
What is (forced) vital capacity?
VC or FVC
total amount of gas that can be exhaled after a maximal inhalation
What is total lung capacity?
TLC = VC + RV
What is inspiratory capacity?
IC = IRV + Vt
What is used to assess presence of lung disease?
Forced vital capacity maneuver
Forced inhalation from FRC to TLC (~1 sec), followed by forceful exhalation from TLC to RV (~5 sec)
Two types of lung diseases
Obstructive: asthma, emphysema (lungs lose elastic quality), chronic bronchitis (irritation causes increased mucous)
Restrictive: idiopathic pulmonary fibrosis, ILD
What can be determined with FVC maneuver
FVC: forced vital capacity (maximum amount of air forcibly expired after maximal expiration)
FEV1: volume of gas exhaled during first second
What is a heathy FEV1/FVC? Obstructive? Restrictive?
Healthy = 80%
Obstructive = <70%
Restrictive = > 80%
What occurs in obstructive lung disease - resistance, lung volumes, air movement
Airway resistance is increased
FEV1 is decreased, FVC is the same
Less easy to blow air out, air gets stuck inside lungs
What occurs in restrictive lung disease - compliance, air taken in, lung volumes
Lung compliance is reduced
Lung cannot take in as much air
FVC maneuver in airway obstruction
FEV1/FVC < 70%
Airway resistance increased
Scooping in flow-volume curve
Can't move as much air
What occurs in severe obstructive disease - lung volumes
Hyperinflation of lungs
Need FEV1 and FVC to rule out restrictive disorders (airway function)
What forces does lung inflation need to overcome?
1) elastic recoil (including surface forces in alveolae)
2) inertia of respiratory system (negligible)
3) Resistance to airflow
Flow = delta P/resistance
Where is the highest resistance in the respiratory system?
2nd and 5th generation airways
Small cross sectional area and turbulent flow
What happens to airflow as you approach terminal bronchioles
Laminar airflow due to increased cross sectional area
Calibre of these airways can determine airflow resistance
What are characteristics of asthma
obstructive airway disease
Paroxysmal or persistant symptoms (dyspnea, chest tightness, wheeze and cough)
Variable airflow limitation
Airway hyper responsiveness to allergic and non-allergic stimuli
Pathophysiology of asthma
Chronic airway eosinophil and neutrophil inflammation
Associated with reversible airflow limitation caused by airway constriction, edema, mucous secretion
What can happen if asthma is not treated properly?
Can be progressive
Develop airway remodelling, which is linked with fixed airway obstruction (permanent mucous plug, thick smooth muscle)
What are common stimuli used in broncho-provocation challenge test
Chemical (histamine, methacholine, B-agonists)
Physical (exercise, cold air)
Bronchoprovocation test - normal vs mild asthma vs moderate asthma
Normal: eventually, a dose of constrictor will cause muscle to constrict and a plateau is reached
Mild asthma: less constrictor required to drop FEV1. Plateau is higher
Moderate asthma: More sensitive to constrictor. Cannot et to plateau because airways would close completely
What is PC20?
Provocative concentration that drops FEV1 by 20%
PC20 and asthma
asthmatics have a PC20 below 8 mg/mL methacholine
How to test for airway hyper responsiveness?
Broncho-provocation challenge test
How to measure airway function?
Response to bronchodilators
How to use response to bronchodilators in measurement of airway function
1) perform spirometry without bronchodilator
2) inhaled nebulizer or bronchodilator (ex: salbutamol )
3) wait 15+ minutes
4) repeat spirometry
If FEV1 increases greater than 12%, this is a positive result and reversibility is significant
This can be used to guide treatment
What is COPD?
Chronic Obstructive Pulmonary Disease
Inflammatory lung disease (neutrophilic) that affects airways (bronchitis) and lung parenchyma (emphysema)
What changes occur in the airways and lungs of people with COPD?
Airway wall remodelling, pruning of terminal respiratory bronchioles and lung parenchyma destruction (portion of lung involved in gas exchange)
Increased lung compliance = irreversible airway obstruction !!
Incidence of COPD
4th leading cause of death world wide in next decade
Principal cause of COPD
Cigarette smoking (90% of cases)
Chronic dust (silica and cotton) or chemical fume exposure are risk factors
Airway- lung interdependence
Elastic recoil of the lung (alveolar tissue) gives radial traction (parenchyma makes scaffold around alveoli) to tether open airways at larger lung volumes
Airways can collapse during forced expiration
What happens to radial contraction in emphysema?
Radial traction is lost
Patients breathe at higher lung volume to overcome the obstruction due to loss of radial traction on the airways
Lung volume and dynamic airflow resistance (AWR)
Increased lung volume: decreased AWR and increased conductance
Decreased lung volume: increased AWR and decreased conductance
What does radial traction do to airway calibre?
Inspiration: increases calibre
Expiration: decreases calibre
What keeps airways open in quiet breathing?
What happens to pleural pressure during forced expiration?
What is EPP?
Equal pressure point
Pressure inside airway = pleural pressure (peribronchial)
EPP and emphysema
EPP is more easily reached in emphysema
Air becomes trapped
FVC maneuver in restrictive lung disease
ex: idiopathic pulmonary fibrosis (IPF)
FVC is decreased (reduced lung volume due to high stiffness/low compliance)
FEV1 not changed
What is restrictive lung disease?
Diffuse parenchymal lung disease
Infiltration of inflammatory cells with scarring of lung parenchyma and widespread lung fibrosis
Decrease in lung compliance
Broad spectrum of physiology depending on etiology
Idiopathic pulmonary fibrosis - type of disease, prevalence
Restrictive lung disease
Uncommon, unknown etiology
Presents in 5th-7th decade
Idiopathic pulmonary fibrosis - onset and symptpms
Insidious (gradual) onset: progressive dyspnea; persistent dry hacking cough
Chronic alveolar inflammation causes diffuse, progressive lung fibrosis
Altered ventilation, increased work of breathing
Obliterative vascular injury that impairs pulmonary perfusion and gas exchange
What does flow-volume loop reveal
Interplay of lung function determinants
Expiration curve in flow-volume loop
Rapid rise to peak flow in early forced expiration, then descends slowly for remainder of expiration (descending portion is effort independent due to lung elastic recoil and airway resistance)
What can the shape of the flow-volume loop indicate?
Can indicate intrathoracic vs extra thoracic airway obstruction
Inspiratory limb truncation indicates extra thoracic obstruction
Flow volume loop: normal
Maximal inspiratory airflow (MIF) at 50% of FVC is greater than maximal expiratory airflow (MEF) at 50% due to dynamic compression of airways
Flow volume loop: obstructive
Expiratory prolongation with scooping: MEF < MIF
Peak expiratory flow is low, indicates degree of airway obstruction
Flow volume loop: restrictive
Interstitial lung disease
Loop narrowed because of diminished lung volumes (TLC)
Airflow is greater than normal at comparable lung volumes because the increased stiffness of lungs holds airways open