Respiration Flashcards
effect of removal on breathing
cortex and pons: slow gasping breaths
medulla: breathing stops
expiratory neurons
inhibit inspiratory neurones.
inspiratory neurones activate expiratory neurones
lung receptors
c fibre endings, afferent nerve fibres carried in vagus
chemoreceptors
central = fast response to arterial pO2 on surface of medulla , arterial pCO2, arterial {H+} and peripheral pCO2
Slowly Adapting Receptors (SARs)
aka stretch receptors, mechanoreceptors situated close to airway smooth muscle, stimulated by stretching of airway walls during inspiration, help inititate expiration and prevent overinflation. afferent fibres= myelinated
rapidly adapting receptors (RARs)
aka irritant receptors, located airway epitheloim, respond to rapid inflation, smoke, dust , RARs in trachea initiate cough, mucus, bronchocontricition
myelinated
C-fibre endings
unmyelinated nerve endings, stimulated by increased interstitial fluid (oedema) and inflammatory mediators
hypoxia and co2 buildup
common in copd patients, leads to chronic hypercapnia, loss of sensitivity of central chemoreceptors. ig given o2 abolishes drive to breathe as has become controlled by hypoxia
drug respiratory depressants
anaesthetics, opiod analgesics, sedatives
drug respiratoy stumlants
doxapram, b2 agonsits aka bronchodilators
regulation of breathinh
Midbrain neural activity stimulates breathing during
wakefulness (“wakefulness drive to breathe”)
During sleep:
• Respiratory drive decreases (loss of wakefulness drive)
– reduction in metabolic rate
– reduced input from higher centres such as pons and cortex
upper airway muscle activity
phasic: contraction of upper airway muscles, opening of upper airway, facilitates inward flow
tonic: continous background activity, maintains airway
during sleep loss of tonic activity
apnoea= cessation of breathing
obstructive sleep apnoea
important cause of rtcs
rfs: obesity, alcohol, nasal obstruction `
respiratory rhythm originates in medulla
hypoxia and hypercapnia feedback via chemoreceptors
elastic recoil
lung= inward
chest wall= outward
inspiration
alveolar pressure
expiration
Alveolar pressure > atmospheric
what causes SOBOE in COPD
decreased lung elastic recoil
obstruction, inability to increase tidal volume effectively
inspiration is active
expiration is passive ( recoil)
breathing disrupted by
airflow obstruction - copd and asthma
weakness of expiratory muscles (MND. advanced respiratory disease, diaphragm failure)
lung tissue damage (emphysema)
thoracis cage disorders ( ankylosing spondylitis, kyphoscoliosis)
dalton’s LAW
gases in a mixture exert pressures that are independant of each other
henry’s law
the concentration o a fissolved gas is dirctly proportional to its partial pressure
nitrogen in blood
high atmospheric content, low water solublility, under high pressure has an anasthetic effect, nitrogen narcosis, on reduction of pressure N2 emboli cause local ischaemia - bends
2,3 -bisphosphoglcerate
binds to deoxy-Hb and lowers Hb affinity for o2 imroving o2 delivery to tu=issues
foetal Hb has a lower affinity for 2,3 BPG so has a higher oxygen affinity than Hba
Haemoglobin
A tetramer: 2 alpha and 2 beta subunits
Each subunit has a Haem group
• A porphyrin with a central Ferrous atom: binds O2
• Combines loosely with Oxygen
• Combination alters its shape and charge
Oxygen/Hb Dissociation
The affinity of binding O2 increases with each successively bound O2
molecule: Allosteric Effect
• Once bound a number of factors can change the ability of Hb to take
up and liberate oxygens
• Ultimately we want Hb to take up O2 in the lung and liberate O2 at
the tissues (muscles)
in practice
nearly all the oxygen carried in the blood is bound to haemoglobin
Partial pressure of oxygen PO2
kPa
Gas exchange is driven by partial pressure • Partial pressure of oxygen in the alveolus equals the partial pressure in the blood draining the alveolu The partial pressure of oxygen in mixed alveolar gas is higher than that of arterial blood • This is due to shunting
shunting
To move something from one place to another, usually because that thing is not wanted, without considering any unpleasant effects Anatomical shunts • A small amount of arterial blood doesn’t come from the lung (Thebesian veins) • A small amount of blood goes through without seeing gas (bronchial circulation) • Physiological shunts (V) and alveolar dead space (Q) • Not all lung units have the same ratio of ventilation (V) to blood flow (Q) • V/Q mismatch
Summary
Gas exchange allows oxygen into blood and CO2 out
• The passage of oxygen to the blood is by diffusion
• The carriage of oxygen is mainly performed by Hb
• The level of oxygen in the blood is roughly the same as that in the
alveolus in health
What causes a low level of oxygen in the blood?
Hypoventilation
• Hypoventilation allows less air (and oxygen) to enter the alveoli so
less oxygen available to the blood
• Decreased environmental oxygen e.g. altitude
• A problem with the alveolar/capillary membrane
• Miss-match of ventilation and perfusion (next lecture)
What can increase the partial pressure of oxygen?
Hyperventilation
• Administration of oxygen
Increase in available PO2
in healthy state
• At a normal PO2
, blood carries nearly as much oxygen as it
possibly can
• Therefore increasing the PO2 has very little effect on the
oxygen content
• However in disease oxygen therapy is a key intervention
CO2 changes dynamically with hyper and
hypoventilation
whilst o2 stays fairly constant
Normal” V/Q mismatch
• Less airflow and blood flow at the top of the lung but V>Q = high V/Q • Middle of lung V/Q normal • Bottom of lung more ventilation and more blood flow but V
Increased V/Q Ratio
Lots of ventilation to alveoli, not much blood • Alveoli and blood reach an equilibrium which is closer to air • PO2 is therefore higher • (and PCO2 is lower)`
Low V/Q ratio
Less ventilation to alveoli, lots of blood • Alveoli and blood reach an equilibrium which is closer to venous blood • PO2 is therefore lower (and PCO2 is higher)
Physiological Dead Space
Physiological Dead Space
V/Q mismatch
Calculate the expected alveolar PO2 (PAO2 ) using the alveolar gas equation • Compare with the measured arterial PO2 (PaO2 ) • If PAO2 = PaO2 then no mismatch
A-a Gradient
Tells us the difference between alveolar and arterial oxygen level • Can help to diagnose the cause of hypoxaemia • High A-a gradient • Problem with gas diffusion • V/Q mismatch • Right to left shunt
CO2 is mostly dissolved in blood
o2 bound to hb
Won’t breathe: control failure
Brain failure to command e.g. drug overdose
Can’t breathe: broken peripheral mechanism
- Nerves not working e.g. phrenic nerve palsy
- Muscles not working e.g. muscular dystrophy
- Chest can’t move e.g. severe scoliosis
- Gas can’t get in and out e.g. asthma/COPD
Type 2 respiratory failure
Decrease in PO2 • Increase in PCO2 • Common causes in hospital: • Severe COPD (can be acute or chronic) • Acute Severe Asthma • Pulmonary Oedema in acute Left Ventricular failure • Due to hypoventilation as main feature
Give oxygen
• Controlled in COPD patients with chronic respiratory failure
• Treat the underlying cause to reverse hypoventilation e.g.
bronchodilators for acute asthma or opiate antagonists for overdoses
• Support ventilation
• Non-invasive ventilation
• Invasive ventilation
What causes V/Q mismatch?
Most lung diseases effecting the airways and parenchyma • Lung infection such as pneumonia • Bronchial narrowing such as asthma and COPD (although they can also progress to type 2 resp failure) • Interstitial lung disease • Acute lung injury (COVID) Pneumonia causes mismatch
What happens to arterial CO2 in V/Q mismatch?
• Blood leaving areas of low V/Q ratio has
• Low PaO2
• High PaCO2
• High PaCO2 stimulates ventilation
• ‘Extra’ ventilation goes to areas of normal
lung and areas with high V/Q ratio so get
blood with low CO2
• Blood from both areas mixes so overall
CO2
is normal
What happens to arterial O2 In V/Q mismatch
• Blood leaving areas of low V/Q ratio has • Low PaO2 • High PaCO2 • High PaCO2 stimulates ventilation • ‘Extra’ ventilation goes to areas of normal lung and areas with high V/Q ratio • But extra ventilation can’t push O2 content much higher than normal • Blood from both areas mixes but cannot overcome the low oxygen level
How do we treat respiratory failure
Give Oxygen
• Treat the underlying cause
V/Q mismatch due to perfusion
problems
Pulmonary embolism
• Can range form small PTE causing no problem with gas exchange
ranging to massive PE with hypoxia
• Emboli effectively cause areas of dead space where there is
ventilation but no perfusion causing hypoxia
• Massive emboli can cause circulatory failure and death
Treatment of Pulmonary Emboli
Oxygen in acute episode
• Anticoagulation to stop further clot propagation
• Thrombolysis in some cases where circulatory compromise
Asthma and Respiratory Failure
Hypoxaemia suggests significant asthma attack • Bronchospasm and mucous plugging causes ventilation defects and V/Q miss match • Type 2 resp failure develops when severe bronchospasm causes hypoventilation of alveoli or exhaustion • The patient needs oxygen to survive • Invasive ventilation may be required
COPD and Respiratory Failure
• COPD is a mixture of chronic airways inflammation and narrowing and emphysema • Problems with V/Q mismatch and hypoventilation • May present acutely with respiratory failure type 1 or type 2 • May have chronic type 2 respiratory failure in advanced disease • Treat respiratory failure with oxygen but with caution in chronic type 2 respiratory failure
Masks
Variable performance • Cheap and cheerful • Exact inspired O2 concentration not known • Fixed function • Constant, known inspired concentration • Reservoir mask • High inspired concentration of O2 Controlled oxygen therapy: Venturi Mask`
