Respiratory Physiology Flashcards
What are the functions of the respiratory system
Gas exchanged
Acid base balance
Protect from infection
Communication
What happens in systemic circulation
02 rich blood from L side of heart to tissue
CO2 rich blood from tissue taken to R side
What happens in pulmonary circulation
C02 rich blood from R rich goes to lungs for gas exchange
Returns O2 rich blood to L side
What is the pulmonary circulation compared to systemic
High flow but low pressure as 5l takes same time as it does to go through systemic
How does actual lung tissue get its blood supply
From systemic
Part of bronchial circulation
What is the conducting zone of the respiratory system
Trachea
Primary bronchi
Bronchioles
Resistance decreases as go down as less molecules and more anatomical dead space
What is the respiratory zone / exchange
Alveoli surrounded by pulmonary capillaries
What makes alveoli good for gas exchange
Single layer of epithelium
Elastic fibres that stretch when you breath in creating a recoil
What are type 1 alveoli for
Gas exchange
Simple sqaumous
What are type 2 alveoli for
Producing surfactant - decreased tension, prevent collapse and increase compliance
What are the lungs enveloped in
Visceral (outer surface of lungs) and parietal (inner surface of ribs) pleura
What is the space between lungs and thoracic wall called
Pleural space
Filled with pleural fluid (30ml) which creates a seal holding lungs to thoracic wall to move with breathing
What content state are the lungs in
Wanting to recoil due to inspiration
Elastic recoil pushes chest out when inspire
Creates a negative pressure in the pleural cavity
What are muscles of inspiration
Diaphragm = most important
External intercostal
Accessory
Scalene
SCM
What are muscles of expiration
Passive at rest
Internal intercostal
Abdominal
What is Boyle’s law
Pressure is inversely proportional to volume
As pressure increases volume decreases
What happens in inspiration
Diaphragm contracts pushes abdominal cavity down
External intercostal and scalene pull ribs out
Leads to increase in volume of thoracic cavity
Intrapleural pressure decreases
Alveolar pressure becomes < than atmosphere and air drawn in
What happens in passive expiration
Muscles relax
Elastic recoil of stretched lungs allow them to recoil back to original volume
Decreased volume so increased P and air drawn out
What happens in forced expiration
Contraction of abdominal muscles push thoracic cavity up
Internal intercostal pull ribs in
Alveolar pressure increases pushing air out
Reduces duration of breathing cycle
What happens in forced inspiration
Similar to normal
Requires accessory muscles
SCM, scalene, pec majro and minor, lattismus dorsi, serratura anterior
What is the alveolar pressure
Pressure inside thoracic cavity
Equal to atmosphere
What is intrapleural pressure
Pressur inside pleural cavity
Always -ve due to state of wanting to recoil
What is transpulmonary pressure
Difference between alveolar and intrapleural Always +ve Opposes elastic recoil Dpeendent on volume of lung Larger lung = larger pressure
What happens between breaths at the end of an unforced expiration
No air I flowing
Lungs stretched and attempting to recoil
Chest wall attempting to move out
Creates sub atmospheric intrapleural pressure
Transpulmonary pressure opposes this recoil
What part of brains is involved in subconscious ventilation
Pons
Medulla
What nerves
Phrenic = diaphragm Intercostal = external intercostal
What part of medulla set breathing pattern
DRG - control muscles of inspiration through phrenic and intercostal, receive sensory from vagus
VRG - control muscles of larynx / pharynx
PRG - receive sensory info from DRG, speak with higher brain to initiate and terminate inspiration
How do you change respiratory drive
Emotion via limbic Voluntary Mechano-sensory Swalloing inhibits Drugs Chemical composition detected by chemoreceptors
What is the primary stimulus for changes in ventilation
CO2
Detected by central chemoreceptors in medulla
More sensitive to small changes in PCo2
How do central chemoreceptors work
Detect changes in H+ in CSF which are related to CO2
What happens when there is an increase in CO2
Rate and depth of breathing increases to remove CO2
Where are peripheral receptors located
Carotid and aortic bodies
What do peripheral receptors detect
Change in arterial Po2 NOT CONTENT
Relatively insensitive and require a significant fall in Po2 or rise in H
Can you override peripheral
No Effects are instantaneous Increased RR and TV Blood flow directed to kidney and brain INceased CO
When are peripheral chemoreceptor important
If chronic elevation of PCO2
Central response is blunted
Patients go into hypoxic drive and rely on peripheral receptors to detect O2 falling
Why do you have to be careful in patients who rely on peripheral
Careful when giving O2 to patients with chronic lung disease e.g. COPD
They will have elevated PCO2
Rely only on O2 levels for their breathing
What does hypoventilation cause
Increased CO2
Blood = acidic
COPD / neuro / chest wall
What does hyperventilation cause
Decreased CO2 and alkaline blood
Decreases free Ca = paraesthesia / cramps
Anxiety / HF / PE
What drugs affect ventilation
Opiods / barbiturates = depress
Anasthetic = increase RR but decrease TV
NO = blunts peripheral chemo so if chronic lung = no way to control ventilation
What happens at altitude
Peripheral detect fall in O2 = hyperventilation
Resulting hypocapnia and alkalosis stop any increase in RR due to central chemoreceptors
After a few days kidney works to remove alkalosis so peripheral takes over again
Rise in DPG
Polycythaemia - physiological as erythropoietin produced from kidney but can cause hypervisocotyi
If an anaemic patient has o2 content 1/2 normal what happens to RR + depth
No change
Receptors respond to partial pressure
Amount of O2 in plasma is normal but just decreased RBC to hold O2 so content reduced
Haem saturation will be the same
What is more uncomfortable
1- a high PCo2 and low Po2
2- a low o2 and no CO2
1
PACO2 increased and impairs the gradient so will stay in blood
What is the pressure of O2 and CO2 in artery PA
O2 = 100 CO2 = 40
What is the pressure of O2 and CO2 in alveoli Pa
O2 = 100 CO2 = 40
What is the pressure of O2 and CO2 in venous Pv
O2 = 40 CO2 = 46
What is the difference between partial pressure and o2 content
Content = all 02 in solution Partial = solubility
How does gas exchange work
Gas moves across permeable membrane down pressure gradient until equilibrium reached
What is the rate of diffusion affected by
Directly proportional to gradient Solubility - more soluble = faster SA - larger = faster (alveoli destroyed in emphysema so decreased SA) Distance - smaller = faster Molecular weight - smaller = faster
What diffuses faster CO2 or O2
CO2
Although O2 is smaller but CO2 is much more soluble
Once O2 is in the blood what happens
Binds to haemoglobin = oxyhaemoglobin
Only 3ml O2 dissolves per L plasma so Hg greater increases capacity of O2
Hg = high affinity for O2 so will pull until saturated
Does exercise affect gas exchange
No as only takes 0.25s
What type of molecules does haemoglobin bind
92% = HbA (2 alpha and 2 beta) 8%. = HbF (gamma chains replace beta)
What determines degree of saturation
Partial pressure of O2
When does partial pressure of O2 begin to affect saturation
Almost 100% saturated at normal PaO2 100mHg
90% if PaO2 60
When PaO2 = 40 very difficult to saturate Hg and deliver O2 to cell
If two individuals with partial pressure of 100 and 80 who has most O2
No diff in saturation
Individual with most haemoglobin
What are variables in oxyhemoglobin dissociation curve Acidic PCO2 Hyperventilation Asthma Temp DPG
More acidic = more Co2 and less O2 and curve shifts to right (less saturated)
Increase pCo2 = shifts to R
Voluntary hyperventilation = shifts to the L
Asthma = shifts to R as constricted so decreased ventilation
Temp = shifts to R as want oxygen available for exercise
DPG added = shifts to R as produced when No o2 so want o2 to be available
What type of haem molecules have highest affinity for oxygen
Myoglobin - as muscles need most
Fetal - 2nd most as want to extract from maternal vblood
HbA has least affinity
Can you have a low partial pressure and normal O2 content
No
Partial pressure is what pushes O2 onto haemoglobin
If o2 content low but partial pressure normal then haemoglobin would still be saturated
What happens in anaemia
Partial pressure is normal
O2 content reduced as not enough RBC to carry O2
Ventilatory drive is normal as PaO2 is normal
What happens in CO poisoning
CO binds to haemoglobin
Affinity much greater than O2 and dissociates more slowly
What are the symptoms of CO poisoning
Hypoxia Anaemia Headache Cherry red skin Nausea RR unaffected as PCo2 is normal
How is Co2 transported in the blood
Only 7% dissolves in plasma
93% diffuse into RBC
Converted to H2CO3 with H20 -> HCO3 + H
Products removed to keep reaction going
What enzyme catalyses
Carbonic anhydrase
What are products exchanged for
HCO3 for Cl = chloride shift
H binds to deoxyhaemoglobin to bufer
If CO2 increases not enough Hg = acidosis
How does CO2 go back to alveoli
Pco2 alveoli < venous blood CO2 diffuses out of RBC Disturbes Co2-HCO3 H leaves Hg CL shift reverses Co2 diffuses into alveoli
What needs to be matched adequately
Ventilation
Perfusion
Usually both 5l/ minute
Ideally ratio would be 1
What affects ventilation / perfusion
Disruption of blood flow - influenced by Pa (hydrostatic) and PA (alveolar)
Resistance
What happens as you move from the apex to base of the lung
Ventilation and perfusion rise
Perfusion increases at a greater rate
Pleural pressure greater at base = more compliant and greater ventilation
Hydrostatic pressure is decreased at apex = decreased blood flow and perfusion
What happens at the base of the lung
Blood flow high as Pa is higher Pa > PA Low resistance Blood flow > ventilation V/Q = 0.8
What happens at the apex of the lung
Blood flow low as Pa < PA Alveoli compressed and more compliant Higher resistance Ventilation > blood flow V/Q = 3.3
What happens when perfusion > ventilation
V/Q <1
Po2 falls in the alveoli and Pco2 will rise
Less O2 in alveoli than is being pulled out
Decrease in partial pressure of O2
Increase in partial pressure CO2
Lose gradient so can’t get ri dog CO2 in blood
Shunt form as blood goes from R-L without getting O2
What could cause V/Q <1
Low O2 in air Poor alveolar ventilation as decreased compliance Increased resistance Drug overdose COPD / asthma / pneumonia / IRDS
What happens to deal with this
Hyperventilation
Blood vessels in lung constrict
Mild bronchial relaxation
Causes hypoxia as reduced ventilation, CO2 can still get out as rest of lung takes over so no hypercapnia = type 1
What happens when ventilation > perfusion
V/Q >1
Increase in alveolar O2
What causes V/Q >1
Blood clot / PE
What happens to deal with this
Pulmonary vasodilatation to well perfused areas so V/Q in this is <1
Bronchial constriction if decrease in PCo2
What is type 1 respiratory failure
PaO2 <8kPa
PaCO2 normal or low
Problem is with diffusion or exchange so cannot oxygenate haemoglobin
Unaffected part of lung will keep CO2 out
What is type 2 respiratory failure
PaCO2 >6.5kPA
Respiratory mechanism fails
Not usually primary
What is hypoxia
Insufficient O2 supply
What is hyperaemia
O2 arterial supply low
What causes hypoxaemia in type 1
V/Q mismatch = most common and responds well to increase FIO2
Shunt = no ventilation so respond poorly to FIo2
Alveolar hypoventilation due to reduced res drive - will respond to increase in FIo2
Diffusion impairment if loss of alveoli
