Week 5: Respiratory Flashcards
Cells Composing the alveolar surface
- Type 1 Alveolar cells
- Type 2 Alveolar Cells
- Fibroblasts
- Capillaries
- Pericytes
- Macrophages
- Immune Cells (T, B, Dendritic)
Type 1 Pneuomcytes (alveolar cells)
- Compose 95% of gas exchange surface
- Facilitate Gas exchange by compromising the exchange membrane
Type 2 Pneumocytes
- about 5% of alveolar surface
- reduce surface tension by secteing surfactant
- Prevent movement of fluid into the alveolus
- can generate type 1 cells
Alveolar Macrophages
- Reside in the mucus layer of the alveolar capillary unit
- can suppress T cell activation
Fibroblasts
- generate and synthesis ‘fibres’ after damage to seal the alveolus off
- type 2 cells attract them when damage occurs
Pulmonary arteries
- Have thinner walls compared to systemic counterparts
- Travel with airways (whereas veins travel between lungs nodes
Hypoxia pulmonary vasoconstriction
Pulmonary pre-capillary arterials contrast in response to alveolar hypoxia, dividing blood to better ventilated areas of the lung
Muscles for respiration and function
- Diaphragm: Contracts/relaxes to expand/reduce thoracic cavity
- External Intercostal: Contracts to elevate ribs (inspiration)
- Internal Intercostal: Contracts to pull ribs down (expiration)
Cough reflex Pathway
- Irritant makes contact with respiratory epithelium
- Innervation of vagal sensory fibres in the pharynx, trachea, & bronchi
Or Modulaion via input from higher brain centres
- Sensory fibres end in nucleus of solitary tract
- Central patter generator motor neurons
- Ventral Resp group motor neurons
- Innervation of respiratory muscles
- Forcefully expiration agasint a closes glottis (ie coughing)
Boyle’s Law
The pressure of a gas is inversely proportional to its volume
This mean that by expanding the lungs, a negative pressure gradient is created pulling air in
Ie: increase lung volume leads to negative alveolar pressure (compare to the atmosphere) and relaxing the diagram resulting in elastic recoil of the lungs results in positive alveolar pressure
Lung compliance
- the stretchiness of the lungs
- formula is Comolaince = (change in volume)/(change in pressure)
Pleural Pressure
Plueral Pressure in negative, creating a vacuum
Sternocleidomastoid muscles
Accessory muscle involved in elevating the sternum and aiding in deep inhalation
Forced Breathing
- aka hypernea
- active, interns inhalation and exhalation involving additional respiratory muscles to meet increased oxygen demands during strenuous activity or when additional ventilation is needed
Quiet Breathing
- aka eupnoea
- Normal, rhythmic inhalation and exhalation during rest or light activities primarily driven by the diaphragm and external intercostal muscles.
Inspiratory Reserve Volume
The maximum additional air that can be inhaled after a normal inhalation.
Tidal Volume
The amount of air inhaled or exhaled during a normal breath.
Expiratory Reserve Volume
The maximum additional air that can be exhaled after a normal exhalation.
Residual Volume
The air remaining in the lungs after a maximal exhalation.
Inspiratory Capacity
The total volume of air that can be inhaled after a normal exhalation, equal to Tidal volume + inspiratory reserve volume
Functional Residual Capacity
The volume of air remaining in the lungs after a normal exhalation, equal to RV + ERV.
Vital Capacity
The maximum amount of air that can be exhaled after a maximal inhalation, equal to IRV + TV + ERV.
Total lung capacity
The total volume of air the lungs can hold, equal to VC + RV.
Pleural and alveolar pressure during expiration and inspiration
Plueral is always negative
Alveolar is negative during inspiration, positive during expiration
Trasmural pressure
- In the context of the lungs, transmural pressure is critical in maintaining airway patency and the integrity of alveolar structures.
Transpulmonary pressure is the difference between the alveolar pressure and the intrapleural pressure in the pleural cavity
Transpulmonary pressure
The pressure difference between alveolar and pleural pressures, maintaining lung expansion.
Lung Compliance
a measure of the lungs’ ability to stretch and expand in response to applied pressure, typically during inhalation.
• It is defined as the change in lung volume per unit change in transpulmonary pressure.
• High lung compliance indicates that the lungs can easily expand with little pressure, whereas low compliance
suggests stiffness or resistance, requiring more effort to inflate the lungs.
• Conditions such as pulmonary fibrosis reduce lung compliance, while emphysema increases it due to the loss
of elastic recoil.
Factors Resisting Airflow
Vagus nerve innervation
causes bronchoconstriction (neural) and adrenaline stimulates beta-2 adrenergic receptors, which then causes bronchodilation (humoral).
Pulmonary surfactant
- secreted by type II alveolar cells in the lungs
- its primary role is to reduce surface tension, thereby decreasing the work of breathing and preventing alveolar collapse (atelectasis).
• The synthesis and release of surfactant are regulated by various factors, including mechanical stretching of the alveoli during breathing and hormonal signals such as cortisol binding.
• Surfactant is stored in lamellar bodies within these cells and is released into the alveolar surface as a fluid film, where it rapidly spreads to reduce surface tension and enhance alveolar stability.
Most common site of nose bleeds
Kiesselbach’s plexus
Factors that influence Pulmonary Vascular resistance
Increase PVR
* Endothelin-1
* Histamine
* Catecholamines (eg adrenaline, noradrenaline)
Decrease PVR
* Nitric oxide via acetylcholine signalling
* Adenosine
Differences between systemic and pulmonary circulation
In Pulmonary Circulation
Arteries travel with airways, veins travel in septa (whereas they travel together in systemic)
Arteries have ticker walls, and are less elastic
Regional (across the lung) differences in blood flow
When standing upright, more blood goes to the lower parts of the lung
Partial Pressure
The amount of the pressure that comes from tat particular gas
It is equal to the total pressure time the fractional concentration of the gas
The Bohr effect
Increased H+ and CO2 promotes offloading of O2 in peripheral tissues (where pCO2 is high), and promotes O2 loading in the lungs (where pCO2 is low)
Oxygen-Hemoglobin Dissociation curve
The Haldane Effect
Greater binding of oxygen with haemoglobin increases the release (offloading) of carbon dioxide, thus, carbon dioxide release is promoted when venous blood is aterilised
Fick’s Law of Diffusion
Rate of gas transfer is proportional to the product of diffusing capacity across a membrane and pressure gradient
** Volume (gas)= Distance (membrane) x (Pressure 1 - Pressure 2)
Diffusing capacity
** The net rate of gas transfer for a partial pressure gradient of 1mmHg **
** Calculated as the net rate of gas transfer / partial pressure gradient **
factors effecting include
* Diffusion Coefficent f the gas
* Membrane surface area (eg height, lung volume, ventilation)
* The physical properties of the membrane (pulmonary congestion, Interstitial oedema, membrane thickening)
* changes in gas up take by RBC (Hb conc, capillary transit time)
V/Q Mathcing
** V= Ventilation Q= amount of blood flow to alveoli **
Because of regional differences within the lung for perfusion and ventilation, there can be a mismatch
Lower VQ=high blood flow, low ventilation
Higher VQ = low blood flow, high ventilation
Factors that influence V/Q Ration
Ventilation
* Gravity (Pleural Pressure Gradient)
* Anatomical expansion (eg larger base of lungs)
* Lung Complaince
* Breathing Pattern
Perfusion
* Gravity (hydrostatic gradient)
* Hypoix pulmonary vasoconstriction
* Pulomary vascular structure
* Lung Volume
Dorsal Respiratory Group
Inspiratory neurons responsible for timing of the respiratory cycle (inspiration)
Within medulla
Ventral Respiratory group
Within the medulla, and is composed of neurons that influence both inspiration and expiration (more so expiration tho)
Pontine Respiratory group
Includes the pneumotaxic centre, responsible for limiting the depth of breathing, and apneustic centre, to delay the inspiratory off-switch
Lung receptors
- Slowly Adapting Stretch Receptors (SASR)
- Rapidly Adapting Stretch Receptors (RASR)
- Vagal C-Fibre nociceptors
Slowly Adapting Stretch Receptors (SASR)
Predominantly in the airways and act as a lung volume sensor
Rapidly Adapting Stretch Receptors (RASR)
Located in the superficial part of the mucosa layer, stimulated by changes in tidal volume, breathing frequency, and lung compliance
vagal C-fibre Nociceptors
Free nerve endings found in both the bronchi and pulmonary capillaries, stimulated by oxidative stress, inflammation or inhaled irritants
Chemical Control of Respiration: central
CO2 passes Blood Brain Barrier
Increase in PCO2 within CSF
H20 + CO2 —> H2CO3 —> H+ + HCO3-
Leads to pH decrease
Detected by central chemoreceptors in the brain and spinal cord, and sends signal to medullary Resp neurons
NB peripheral H+ ions cannot penetrate BBB
Chemical Control of Respiration: central
CO2 passes Blood Brain Barrier
Increase in PCO2 within CSF
H20 + CO2 —> H2CO3 —> H+ + HCO3-
Leads to pH decrease
NB peripheral H+ ions cannot penetrate BBB
Chemical Control or peripheral chemoreceptors
Peripheral chemoreceptors detect PO2 (primarily), PCO2, and H+
Send signal to medullary Resp neurones via the vagus nerve (for aortic arch) and the glossophryngeal nerve (for the sensors in the carotid body)
Leads to change in pulmonary ventilation and metabolism VCO2 or VO2
J receptors
Located near pulmonary capillaries, respond to capillary pressure changes; stimulation leads to tachypnoea
Chest Wall Reflexes
Activated by receptors in the chest muscles, joints, and skin; prevent overinflation or sudden deflation of the lungs, including the hering-Bruner reflex and deflation reflex
Lung Reflexes
Activated by irritant and stretch receptors in lung tissues; detect harmful particles and chemicals; activate coughing and bronchoconstriction; assist in maintaining overall tidal volume
Hearing Breuer reflex
- Inflated lung
- Activation of stretch receptors
- Impulse generated
- Inhibition of inspiratory centre
- Expiration reduces lung inflation
Respiratory Regularon of aid base balace
• Carbon dioxide in the blood can be transported in three predominate forms: o Dissolved gas
o Bound to haemoglobin
o In carbonic acid
• Acid-base balance refers to the homeostatic regulation of pH in extracellular fluid.
• An increase in PCO2 leads to decreased pH, stimulating central chemoreceptors to increase ventilation (VE).
• Respiratory acidosis is caused by hypoventilation, which leads to increased PCO2 and decreased pH.
• Respiratory alkalosis is caused by hyperventilation, which leads to decreased PCO2 and increased pH.
Exercise Hyperpnea
- Aerobic exercise
* 2.a metabolic acidosis
* 3.a Detection by central and peripheral chemoreceptors
AND
* 2.b Mechanical Stress on muscles
* 3.b Dectection by muscle proprioceptors - Initiation of respiratory control centre
- Hyperventilation
- Expulsion of CO2 restoring homeostasis
Spirometry
measures how much and how fast air can be inhaled and exhaled to and from the lungs
Procedure
* Patient is Seated (adults)/Standing (children)
* instructed to fill their lungs completely and then “blast” out air until empty
* They are asked to inhale as fast as possible when empty
* repeat 3-8 times
* then given a bronchodilator, wait 20 mins, then repeat experiment
Pulmonary function Testing (PST) Values
NB:lower normal limit is calculated by subtracting 1.65 standard deviations from the mean, upper is plus
Forced Expiratory volume
* max amount of air that can be expelled in one second
Forced Vital Capacity
* Max amount of air that can be expired in one breath
Peak expiatory flow
* Fastest speed at which air can be expired
Mid forces expiratory flow
* averaged flow rate between 25-75% of FVC
** Forced expiratory time
* Time taken for FVC to be completely expired
Obstructive Ventilatory defects effect on PFT
Cause airflow limitations, thus difficult to empty, results in reduced elastic recoil
Lower FEV, low or normal FVC, FET is normal/high
Restrictive ventilatory defects on PFTs
Low o normal FEV, Low FVC, normal or elevated FEV/FVC, normal or reduced FET
* Flow-volume loop graph follows thin teardrop pattern
Obstructive ventilatory defects
Asthma, Chronic Bronchitis, Emphysema, Foreign bodies (nuts, tumors)
Restrictive ventilatory defects
Congestion, pleural effusion, kyphoscoliosis, Firbosis
Bronchodilator significant in the obstructive pattern PFTs
200ug of salbutamol is given
If FEV1 or FVC increases 10% suggests a reversible or obstructive defect eg asthma
Lung dilation
Used to measure subdivisions of lung volume with H dilation and N washout
STEPS
* patient breathes in a know quantity of a helium oxygen mixture (known H conc)
* inhaled helium mixes with gases present in the lungs, reaching equilibrium
* Patient exhales into a spirometer, measures conc of Helium after each breathe
* using C1V1=C2V2 they can calculate lung volume and other pulmonary parameters
Causes of reduced DLCO and Elevated DLCO
Reduced
* Less Hb available for CO binding
* Anaemia, PE, emphysema
Elevated
* More Hb available for CO binding
* Polycythaemua, erythrocytosis
How does CAD cause Dyspnoea
- CAD
- Stenosis/occlusion
- Myocardial ischemia
- Reduces oxygen to myocardium
- Heart Muscle Damage
- reduced Cardiac output
- Inadequate circulation of oxygenated blood
- increased workload of breathing
How does Cardiomyopathy Cause Dyspnoea
- Cardiomyopathy
- Heart Muscle enlargement/stiffening
- reduced Cardiac output
- Inadequate circulation of oxygenated blood
- increased workload of breathing
How does Pericarditis cause Dyspnoea
- Inflamation of the pericardium
- Fluid build up (pericardial effusion)
- Fluid-reduced contractility
- reduced Cardiac output
- Inadequate circulation of oxygenated blood
- increased workload of breathing
How does valvular disease cause Dyspnoea
- Stenosis/regurgitation
- Increased pulmonary pressure puts strain on heart
- Right Ventricle becomes weakened due to strain
- reduced Cardiac output
- Inadequate circulation of oxygenated blood
- increased workload of breathing
How does Anemia cause Dyspnoea
- Reduced RBC count
- reduced Hb
- receded oxygen carrying capacity
- Insuffinednt oxygen delivery to the tissues and cells
- reduced oxygen availability at the lungs
How does COPD lead to Dyspnoea
- Inflammation leads to narrowed airways
- Obstructed flow of air in/out of the lungs
- reduced oxygen uptake
- reduced oxygen available at the lungs
How does asthma lead to Dyspnoea
- Bronchoconstriction
- Reduced airway diameter
- reduced oxygen intake
- increase workload of breathing
How does pneumonia cause Dyspnoea
*inflammation and fluid build up in the lungs
* Redcued gas exchange capacity
* Inadequate circulation of oxygenated blood
* increased workload of breathing
