The Respiratory System Flashcards
Nasal cavity
- breathing through nose is preferred (protective mechanism of lungs)
- nasal cavity lined with hairs to aid in removal of course particles, releases mucous to trap small particles and watery excretions which contain lysosomes to attack and destroy particles
- smaller hairs line inner nasal cavity which assist in moving mucous down to pharynx to be swallowed and destroyed by stomach acid.
- watery excretions humidify incoming air to make it suitable for passing through airways
- nasal conchi is a membrane which protects the nasal cavity.
- slow movements of air create turbulent flow allowing humidifying to occur more quickly
Larynx & pharynx
Larynx- deciphers between food and water
Pharynx- filters air that we breath
Trachea
- 10-12cm diameter 2cm
- tube made up of smooth
Muscle. - cartilaginous rings every cm allows airways to be open at all time
- horseshoe structure to prevent food from being stuck
- internal lining- pseudo stratified (single layer), epithelial (surface of body), columnar, goblet cells (mucous production)
- mucous lines wall of trachea
- cilia move pathogens up and swallow again to reach stomach to be destroyed
Cells of alveoli
- simple squamous epithelium (type 1) - wall of alveoli. These are unusually thin to optimise gas exchange.
- macrophages - remove debris and microbes from inner surface of alveoli to protect from inflammation which would prevent efficient gas exchange
- surfactant secreting cells (type 2 cells) produce surfactant which is a watery substance. This lowers the surface tension on the alveolar surface which is produced by the cohesive nature of water, thus it acts as a detergent by interacting with water molecules Tor deuce cohesiveness to allow efficient inflation and deflation of alveoli.
Ventilation perfusion
Perfusion is adjusted to changes in ventilation.
Eg. Decreased blood flow, reduced PO2 in blood vessels, vasoconstriction of pulmonary vessels, decreased blood flow, blood flow matches airflow
Inspiration
ACTIVE PROCESS
- diaphragm and external intercostal muscles contract
- external intercostal muscles elevate the rib cage; the sternum moves anteriorly
- diaphragm flattens and moves inferiorly
- thoracic cavity volume increase
- intrapulmonary pressure drops to -1mmHG
- air flows into lungs down its pressure gradient until intrapulmonary pressure is 0
Expiration
PASSIVE PROCESS
- Inspiratory muscles relax (diaphragm rises; rib cage defends due to recoil of costal cartilages)
- thoracic cavity volume decreases
- elastic lungs recoil passively; intrapulmonary volume decreases
- intrapulmonary pressure rises to +1 mmHG
- air flows out of lungs down its pressure gradient until intrapulmonary pressure is 0
Thoracic cavity
Lined with serous membrane, allowing lung to attach to it, so they can move simultaneously.
Visceral membrane- attached to lung
Parietal membrane- attached to thoracic wall
Intrapleural fluid found between the lungs and thoracic wall to prevent lungs from collapsing.
Intrapleural pressure is negative within pleural cavity due to surface tension of alveolar fluid, elasticity of the lungs, elasticity of the thoracic wall
Forced inspiration
Greater contraction of diaphragm and external intercostal muscles, aiding muscles also help to lift rib cage upwards
Heavy expiration
Active process
Abdominal muscles squeeze listing the diaphragm and reducing thoracic volume. Internal intercostals push on thoracic wall
Respiratory volumes
Tidal volume- 500ml- amount of air inhaled or exhaled with each breath under resting conditions
Inspiratory reserve volume- 3300ml amount of air that can be forcefully inhaled after tidal volume
Excitatory reserve volume- 1000ml - amount of air that can be forcefully exhales after tidal volume
Respiratory capacity
Total lung capacity - 6000ml- max amount of air contained in the lungs at full capacity
Vital capacity- 4800ml - maximum amount of air that can be inspired or expired
Alveolar and tissue respiration
Tissues- O2 from systemic capillaries into cells, CO2 from cells into systemic capillaries
Alveoli- O2 from alveoli into pulmonary capillaries, CO2 from pulmonary capillaries into alveoli
Influenced by surface area, partial pressure gradient and rate of blood flow
Ficks equation
Mass/time (diffusion) = K (Kroghs diffusion constant) X area (surface area of respiratory membrane) X change in concentration gradient // thickness of respiratory membrane
Anything which increases alveolar thickness will reduce diffusion
CO2 More soluble than O2,
Impacts on capacity to diffuse from alveoli to blood - need moreO2 to account for amount of CO2
Alveolar pressures
Partial pressure of alveoli differ from those in the atmosphere due to
- humidification of inhaled air
- mixing of old and new air- first 150ml of 500 ml is dead space
- gas exchange between alveoli and pulmonary capillaries
Hypoventilation
Decreases alveolar ventilation. This causes PO2 to drastically decrease. Decreased CO2 can cause temporary paralysis- permanent state of contracted muscle, blood vessels in brain contract to allow build up of CO2 leading to diziness and unconsciousness
Factors affecting ventilation
Resistance within the airways
Airflow = change pressure / resistance
Lung compliance- the stretch ability of elastic fibres of lung tissues
Inspirstion
Diaphragm and external intercostal muscles contract
Thoracic cavity volume increases
Lungs stretc- intrapulmonary volume increases, and intrapulmonary pressure decreases
Alveoli expand and air flows into lungs
Intrapleural pressure
The pressure within the pleural cavity The pressure is always negative, which acts like a suction to keep the lungs inflated Neg pressure due to: Surface tension of alveolar fluid Elasticity of lungs Elasticity of thoracic wall
Ventilation eqns
Pulmonary ventilation = tidal volume X frequency of breaths
Alveolar ventilation = (tidal volume - dead space) X frequency
Changes in ventilation
Hypoventilation- high levels of CO2, low levels of O2
Hyperventilation- high levels of O2, low levels of CO2
Gas carriage
Gases are:
Dissolved in plasma
Chemically combined with haemoglobin
Converted into a different molecule
Oxygen transport
- 5% in plasma and erthrocyte cytosol (fluid of RBC)
- 5% combined with haemoglobin (fully saturated 4 out attached to each heme group is called oxyhemoglobin)- this is fully reversible and generally occurs in pulmonary capillaries
In areas of poor O2, HbO2 becomes Hb + O2- no enzymes required
foetus has two alpha and two gamma chains to increase affinity of O2 for development
Oxygen binding to haemoglobin
Only free haemoglobin contributes to partial pressure. Therefore when haemoglobin is present, there is a greater oxygen concentration as it holds four oxygen particles
Oxygen - haemoglobin dissociation curve
Increasing PO2 increased haemoglobin saturated. @ PO2 100, haemoglobin is 99% saturated, higher PO2 would not be beneficial, and a PO2 drop within 20% would have little impact on saturation.
A small drop in PO2 means a large amount delivered to tissue.
Oxygen loading/ unloading
Cardiac output is the amount of time to deliver blood around body- it delivers 250ml of oxygen per min. Oxygen is unloading during the steepest part of the O2/Hb curve. At this point, small decreases in tissue PO2 will lead to large unloading of O2
Factors that affect O2- Hb saturation curve
DPG- chemical used to increase O2 binding. No DPG shifts to left, added DOG shifts to right
Temp- low temp shifts to left, high temp shifts to right
Acidity- low acidity to left, high acidity to right
Carbon dioxide transport
7% dissolved in and
23% combined with glob in part of Hb does not compete with oxygen, but has greater affinity when not fully saturated with O2 (HbCO2 carbaminohaemoglobin)
70% converts to bicarbonate
In red blood cells:
CO2 + H20 > H2CO3 > H+ + HCO3
Thus decreases pH when excess PCO2
Hb Buffers out H+ so pH doesn’t change dramatically. Approx 200ml of CO2 delivered to the blood per min
Control of breathing
Basic rhythm is controlled by respiratory systems in the medulla and pons of the brain. Sets the rhythm by automatically initiating inspiration. It sends impulses along the phrenic nerve to the diaphragm and along intercostal nerves to external intercostal muscles
Central chemoreceptors
Basic rhythm is modified by input from central chemoreceptors which are located in the medulla. They monitor the pH associated with CO2 concentrations in he brain. CO2 is the most important factor controlling rate and depth of breathing.
Peripheral chemoreceptors
Located in aortic arch and carotid arteries. Sensitive to pH, PCO2 and particularly PO2. Chemosensory neurons inform the ventilation control centre in the medulla to increase rate of ventilation.
A severe reduction in PO2 can result in hyperventilation.
Effects on ventilation
Regardless of the source, increases in the activity of the blood cause hyperventilation, even if co2 levels are driven to abnormally low levels.
Lung compliance
A measure of the lungs distensibility (ease at which lung can be stretched or inflated) . When compliance is abnormally high, the lungs are prone to collapse. When compliance is abnormally low, the work of breathing is increased.
Low compliance - more work required to inflate the lungs go bring normal tidal volume eg. Chronic fibrosis
High compliance- low elastic recoil, increased effort to get air out of the lungs. Eg emphysema
Effects of exercise on ventilation on blood gases
Significantly increased pulmonary ventilation, no change in pO2, at intense workout point decreased CO2
This is NOT due to negative feedback. This may be an anticipatory effect
No single mediator or mechanism identified explaining why ventilation remains so closely matched to CO2 production
Hypoxic or hypercarbic mechanisms do not llay a significant role
Mechanisms believed to contribute: neural inputs from motor cortex to medullary respiratory centres, affairs by from muscle and join mechanoreceptors
Anaerobic threshold/ lactate threshold
Point at which lactic acid starts to accumulate in the blood stream- production is faster than ability to remove. Hence, decreased pH, stimulate peripheral chemoreceptors, increased ventilation
Respiratory centres
Higher brain- voluntarily control our breathing
Stretch receptor- prevents over breathing by reducing our capacity
Irritant receptors- inhibit breathing when irritants present, stops breathing to allowing coughing
Non co2 acid ventilation
May be due to exercise. Detected by peripheral chemoreceptors as opposed to central, this is due to BBB not allowing hydrogen ions to enter brain and be detected by central chemoreceptors
