Lungs- Structure And Function Flashcards
COMPONENTS OF RESPIRATORY SYSTEM
LUNGS CONDUCTING AIRWAYS CNS CHEST WALL MUSCLES OF INSPIRATION
GROSS STRUCTURE OF LUNGS
Left and right
Right lung larger as left lung makes room for heart
Right lung = upper, middle and lower lobes
Left lung= upper and lower lobes and lingula area. Lingula is projection of upper lobe of left lung.
Right lung broader and left lung longer
More gross structure of lungs
Left lung = lobes separated by oblique fissure
Right lung = upper and middle by horizontal fissure and middle and lower by oblique fissure
Each lung has bronchopulmonary segments- 10 right and 8 left
Pleura - visceral outer and parietal inner. Fluid 10-20ml to lubricate and smooth breathing.
Layers slide over each other as lungs expand and recoil during breathing.
Pleura has a negative pressure naturally and layers of pleura want to stick together as if they don’t, lungs collapse down
Grooves
Visceral and parietal layers stick together
Groove for large vessels in both lungs. Left lung has cardiac notch in lower lobe
ANATOMICAL MARKINGS FOR LUNGS
2.5cm above middle 1/3 clavicle
Anteriorly down to 6th costal cartilage , 7cm lateral to mid line
Laterally down to rib 8
Posterior from T2-T10
Lungs shorter at front and longer at back
Functions of lungs
GSRFPM
Gaseous exchange
Surfactant production - type 2 pneumocytes produce this and keeps alveoli open. Produce in development about week 32.
Reservoir for blood - rich blood supply
Filter - prevent getting infections as lungs trap particles and bacteria
Part of immune system - Large particles trapped in nose, nasopharynx and larynx and we cough them up.
Further in is mucociliary escalator to trap particles and carry debris to pharynx.
If particles get further, macrophages will fight off pathogens before they take hold
Maintains PH blood- maintains ph of blood for enzymes to work well. Lungs control breathing rate and thus, how much co2 exits or is retained inside you.
More Co2= more acidic
Upper respiratory tract, functions and symptoms
Made of : Nose , mouth, pharynx (throat) and larynx (voicebox)
Functions : moisten and warm air, filter particles, swallow and communication through talking
Infection: virus or bacteria, symptoms are cough, sneeze, sore throat and stuffy nose
LOWER RESPIRATORY TRACT COMPONENTS
TRACHEA PRIMARY BRONCHUS SECONDARY BRONCHUS TERTIARY BRONCHUS BRONCHIOLES TERMINAL BRONCHIOLES RESPIRATORY BRONCHIOLES ALVEOLAR DUCTS ALVEOLAR SACS
TRACHEA
Below C6 11cm Long and 2.5cm diameter 15-20 C cartilage rings Gap posterior for oesophagus so you do not swallow and hit cartilage Carina (T5) , bifurcation of trachea
Pathologies : choking, tracheal cancer and floppy trachea (no cartilage)
Primary bronchi
From carina into left and right
C shaped cartilage rings , so airways open
Right one is steeper and wider
So particles likely to enter right lung if it is inhaled
Primary bronchi enter the lungs via the hilum
Pathologies : choking / obstruction and cancer
Secondary bronchi
From primary bronchus
Serves lobes of lungs - right is three and left is two
Cartilaginous plates to keep airways open (not rings)
Pathology : lobar pneumonia
Tertiary bronchi
To bronchopulmonary segments
10 in right and 8/9 in left
Some cartilage plates and less as you go along
Introduction of smooth muscle
So a pathology can constrict airways, reducing air flow and increase resistance to airflow
Pathology : bronchitis (infection and inflammation)
Bronchioles
Come from tertiary bronchi
More smooth muscle than cartilage
Pathology : COPD and fibrosing alveolitis
Terminal bronchioles
From bronchioles
0.3mm - 0.5mm diameter
Smooth muscle and controlled by ANS - sympathetic is bronchodilation and parasympathetic is bronchoconstriction
Pathologies : asthma and fibrosis
Respiratory bronchioles
Each terminal bronchioles branches into many of these
Small, thin and delicate with no cilia
Pathogen will be removed but not able to expel (defence mechanisms rather than physical cough)
Deliver air to gas exchange surfaces of lungs
Alveolar ducts
Joins respiratory bronchioles to alveolar sacs
Affected by cystic fibrosis and pneumonia
Alveolar sacs
Gas exchange site
300 million alveoli - 150 million per lung
Surfactant to keep them open - from type 2 pneumocytes , babies produce this at 32 weeks pregnancy.
If no surfactant, they collapse and gas exchange can’t occur
Pathology : cystic fibrosis or pneumonia
What is bronchial tree divided into?
Conducting and respiratory zones
CONDUCTING ZONE
Trachea to the terminal bronchioles No gas exchange Gas transportation via convection Anatomical dead space - no gas exchange Alveolar dead space would be air in alveoli not used in gas exchange Up to generation 16
Respiratory zone
From respiratory bronchioles to alveoli
Gas exchange in respiratory zone from alveolus to capillary
Gas transport via diffusion
300 million alveoli , large SA for gas exchange
17-23 generations
ALVEOLI CELLS
Type 1 pneumocytes= gas exchange- allows gases to move over alveolar and capillary membranes
Type 2 pneumocytes - produce surfactant to keep alveoli open
Also can produce and divide themselves into type 1 pneumocytes if type 1 cells are damaged
Large capillary network for large SA
Collateral ventilation - interconnections between respiratory bronchioles and the alveoli
PATHWAYS:
Interbronchiolar channels of Martin - between respiratory bronchioles
Bronchiole-alveolar channels of lambert - between respiratory bronchioles to alveoli
Interalveolar pores of Kohn = interconnections between 2 or more alveoli
Allows gas exchange from alveoli from different tracts. If something is blocked off close to the alveolus, we don’t lose the alveoli for gas exchange due to interconnections.
DIAPHRAGM
Major muscle in respiration
Large dome shaped muscle
Contraction = moves down and flattens , ribs move up and out, air moves in down pressure gradient (positive pressure outside and negative alveolar pressure).
Relaxation= moves up and domes out, ribs move down and in , air moves out down pressure gradient (positive alveolar pressure and more negative external pressure)
Movements of diaphragm will alter pressure changes in lungs
Clinically, separated into hemi diaphragms
PULMONARY AND BRONCHIAL CIRCULATORY SYSTEMS
Pulmonary system = involved in. Gas exchange. Takes in 02 and removes CO2. Low pressure system.
Blood flows slow through capillaries for gas exchange
Bronchial circulatory system = higher pressure than pulmonary system and supplies blood to airways themselves- not involved in gas exchange. A lot of blood evened out pressures though (so bronchial system never at too high a pressure).
COMPLIANCE OF LUNGS
Ability of lungs to expand. Lungs are elastic.
Measured as change in volume / change in pressure
Boyle’s law = as pressure increase, volume decreases
As pressure decreases, volume increases
Problems with compliance may be:
Atelectasis- airways collapse down due to lung disease making lungs stiff
Fibrosis - lung tissue damaged and scarred and tissue thickened and stiff
Pneumothorax - collapsed lung / part of lung
Obesity - weight of chest impedes on lung expandability.
Pulmonary vascular engorgement
Pleural effusion- fluid built up between layers of pleura
Resistance
Ease of air flowing through bronchial tree
Consists of = airway resistance and tissue resistance
80% airways resistance in medium size bronchi
20% airway resistance in small size less than 2mm airways
Factors determine resistance
How much lung volume there
Any obstruction in airways like tumour or sputum
State of contraction of smooth muscles
Tissue resistance - ability to move chest wall in breathing. Fracture rib impedes chest wall movement.
Type of airflow
What are the three types of airflow ??
1- Laminar airflow , small airways. Organised air flow where it flows in straight lines.
2- Turbulent airflow, at high velocities in large irregular airways. Disorganised airflow and can form swirling patterns eg, trachea and primary bronchi
3- Transitional airflow - combines laminar and turbulent. At medium sized airways at branch points
ELASTIC RESISTANCE
Elastic resistance - measure of work exerted by resp muscles in inspiration to expand lungs
Elastic recoil= ability of lungs to return to normal shape after expansion in inhalation
Patients can lose elastic recoil of lungs so some air remains in lungs and they are hyper inflated.
WOB - work of breathing
Physical work carried out by muscles in respiration, to overcome elastic resistance in lungs and non elastic resistance in airways.
WOB INCREASES WITH EXERCISE OR PATHOLOGY
Increased WOB is caused by: Poor compliance of lungs Increased resistance - intrinsic airflow and extrinsic tissue Decrease resp. Capacity More elastic resistance
Pressures of alveoli
High pressure needed to open collapsed alveoli
Pathology deflates alveoli, to closing volume and they collapse
Prevent deflation : safety mechanisms like collateral ventilation and some is related to SA
CRITICAL OPENING PRESSURE- maintaining inspiratory effort will inflate most lung tissue
Alveoli tend to remain open and empty at low pressures
STAY Open due to surfactant and collateral channels
SURFACTANT
Liquid with head and tails
Heads hydrophilic
Tails hydrophobic
Heads at alveolar wallls where water is and tails inside where gas exchange occurs
