Respiratory Flashcards
where does the trachea bifurcate into lobar bronchi?
T4 (bi-four-cates)
where does the common carotid artery bifurcate into internal and external carotid arteries?
C4
which fissures are on the right side of the lung?
oblique and horizontal
which fissures are on the left side of the lung?
just oblique
how many lobes do each lung have?
right - 3
left - 2
describe the respiratory tree
trachea, left and right main bronchi, lobar bronchi, segmental bronchi, terminal bronchioles, respiratory bronchioles, alveoli
innervation of diaphragm
phrenic C3,4,5
what is pleura?
specialised mesothelium lining body cavities
two continuous layers - visceral and parietal
function of pleural fluid
prevents friction when pleura move against each other during inspiration and expiration
upper airways include? function?
nasopharynx to terminal bronchioles
conductive passage for air
lower airways include? function?
respiratory bronchioles to alveolar sacs
respiratory
exchange of oxygen and carbon dioxide in the lungs
what is respiratory epithelium? (very likely question)
pseudo stratified, ciliated, columnar epithelium with interspersed goblet cells
describe inspiration
phrenic and motor intercostal efferent nerves firing increase
diaphragm and external intercostal contract
thoracic volume increases
thoracic pressure decreases
chest wall (pump handle) and ribs (bucket handle) move up and out, pulling parietal pleura too
alveoli expand
Pressure in alveoli decreases to below atmospheric pressure
air moves into alveoli down pressure gradient
describe expiration
decreased impulses to diaphragm and external intercostals
volume of thorax decreases
pressure in thorax increases
alveoli compress and lung pressure increases
pressure in the alveoli increases to above atmospheric pressure
air passively moves out of alveoli down a pressure gradient
which accessory muscles aid active inspiration?
sternocleidomastoid (sternum, clavicle, mastoid process)
serratus anterior
latissimus dorsi
pec major
which accessory muscles aid active expiration?
internal intercostals
abdominal muscles
in which direction does the chest wall have a tendency to move?
in what direction does the lung have a tendency to move?
what structure ensures they both move in the same direction?
out
in
intrapleural space - parietal and visceral pleura move together
what is transpulmonary pressure?
difference between alveolar pressure and intrapleural pressure
value of transpulmonary pressure
4mmHg
air in pleural space is called?
pneumothorax
what happens to the transpulmonary pressure and lungs in a pneumothorax?
becomes 0
collapse
two main respiratory brain centres?
medullary
pontine
what are the two divisions of the pontine centre?
apneustic and pneumotaxic
function of the apneustic group
pontine centre
acts on dorsal respiratory group to adjust inspiration and increase inspiratory intensity
function of the pneumotaxic group
pontine
allows expiration
overrides apneustic if needed
increased innervation leads to shallower ventilation with increased frequency
function of the DRG
inspiration
stimulate diaphragm and external intercostals
function of the VRG
centre for forced inspiration and expiration
stimulates accessory muscles of ventilation
inhibits apneuistic
other structurs involved in respiration
nucleus tractus solidaris and ambiguous
vagus and glossopharyngeal
limbic system
opiods - depress respiratory drive
amphetamines stimulate
name three pulmonary receptors
slow adapting stretch receptors, rapid adapting stretch receptor, J receptors
where are SASRs located
smooth muscle of the airway
what do SASRs respond to
distension
effect of SASRs
what is is called?
end inspiration and starts expiration (logical, if airway is distended)
Hering Bruer reflex - protective
where are RASRs located
between airway epithelium
what do RASRs respond to?
irritants
effect of RASRs
bronchoconstriction
where are J receptors found?
located in the alveolar walls in close proximity to the capillaries
J = juxtacapillary
what do J receptors respond to?
an increase in lung pressure because of fluid
e.g embolism
effect of J receptors
increase respiratory rate
rapid shallow breathing
bronchoconstriction
which lung receptors are myelinated?
just SASRs and RASRs, not J receptors
two types of lung chemoreceptors
peripheral and central
where are peripheral chemoreceptors located?
aortic arch and carotid sinus
what do peripheral chemoreceptors detect?
change in partial pressure of oxygen
when are peripheral chemoreceptors activated?
partial pressure of oxygen falls below 60% (a significant drop!)
are peripheral or central chemoreceptors faster?
peripheral
what gas is the driver of respiration?
carbon dioxide
where are central chemoreceptors found?
medulla
what do central chemoreceptors detect, and how?
changes of pH by small changes in carbon dioxide partial pressure
H+ cannot cross the blood brain barrier and carbon dioxide can - therefore, central chemoreceptors are not affected by changes in plasma pH
carbon dioxide reacts with water to form carbonic acid, which dissociates to hydrogen carbonate ions and H+
action of central chemoreceptors
increase respiratory rate to compensate
what is V/Q mismatch?
alveolar ventilation and alveolar blood flow are not matched
what is the V/Q ratio?
ventilation to perfusion ratio
in which part of the lung is there more perfusion?
why
bottom
gravity
is V/Q higher of lower at the bottom of the lungs?
lower
in which part of the lung is there more ventilation?
apex
what is physiologic (alveolar) dead space?
ventilated but not perfused alveoli
not the same as anatomical dead space
high V/Q
cause of physiological (alveolar) dead space
pulmonary embolism
what is physiologic shunt?
perfused but not ventilated alveoli
low V/Q
cause of physiologic shunt
pulmonary oedema - collapsed alveoli due to fluid build up
response to dead space
local bronchoconstriction
air diverted to better perfused areas
response to shunt
hypoxic pulmonary vasoconstriction
blood diverted to better ventilated areas
factors shifting curve to left
H+ falls
temperature falls
altitude falls
fall in 2-3 BGP (2,3-diphosphoglycerate/ 2,3 bisphosphoglycerate)
HbF
will a greater affinity for oxygen shift the curve left or right?
left
effect of low pH on the oxygen dissociation curve
curve shifts left
(to remember - carbon dioxide makes blood acidic and you need more oxygen)
effect of low oxygen levels of the oxygen dissociation curve
shifts left
effect of carbon monoxide on the oxygen dissociation curve
shifts left
does HbF have a higher or lower affinity for oxygen?
higher
curve shifts left
units of partial pressure of oxygen
mmHg
x axis
which gas is the driver of respiration?
carbon dioxide
list the mechanisms of carbon dioxide transport in the blood, least to most common
dissolved in plasma
bound to Hb - carbaminohaemoglobin
as HCO3- (buffer equation)
normal pH range
7.35 - 7.45
effect of hypoventilation on blood pH
what does this cause?
increase in carbon dioxide
H+ increases
pH decreases
respiratory acidosis
effect of hyperventilation on blood pH
what does this cause?
decrease in carbon dioxide
H+ decreases
pH increases
respiratory alkalosis
Dalton’s Law
pressure exerted by a mixture of gases in a fixed volume is equal to the sum of the partial pressures that would be exerted by each gas alone in the same volume
Pt = ppA + ppB …
Boyle’s Law
pressure is inversely proportional to volume
P1V1 = P2V2
Henry’s Law
the volume of gas dissolved in a liquid depends on partial pressure and solubility of it
concentration gradient = solubility coefficient x pp
Ohm’s Law
pressure = flow x resistance
V = IR
for trachea, bronchi and bronchioles whereas alveoli have their own equation
alveolar gas equation
PAO2 = PiO2 - PaCO2/R
PA = pressure alveolar oxygen
PiO2 = pressure of inspired oxygen
R is the respiratory coefficient - usually equal to 0.8
Laplace’s Law
alveolar pressure depends on surface tension and radius
P = 2T/r
effect of surfactant on surface tension
decreases surface tension
from which cells is surfactant released?
type II pneumocytes - type of alveolar cells
what is lung compliance?
how easily the lungs expand
which factors determine lung compliance?
surface tension
elasticity of lung tissue
which cells regulate alveolar surface tension?
type II pneumocytes
how is compliance increased?
decrease surface tension by producing surfactant
increase elasticity
what is hypoxia?
low oxygen at tissue level
what is hypoxaemia?
low oxygen in the blood
causes of hypoxaemia
hypoventilation
diffusion impairment - thickening of membrane
shunt - septal defect, perfusing unventilated alveoli
V/Q mismatch
what is hypercapnia?
high carbon dioxide in the blood
constitutes respiratory drive
what causes hypercapnia?
hypoventilation
what is type 1 respiratory failure?
low PaO2
normal PaCO2
what causes type 1 respiratory failure?
pulmonary embolism
what is type 2 respiratory failure?
low PaO2
high PaCO2
cause of type 2 respiratory failure
hypoventilation
why must we be careful when administering oxygen to those with type II respiratory failure?
giving them lots of oxygen leads to hyperventilation
hyperventilation decreases partial pressure of carbon dioxide in the blood
as carbon dioxide constitutes respiratory drive, the patient can no longer breathe
pressure of bronchial circulation (systemic)
120/80
pressure of pulmonary circulation
25/8
effect of hypoxia on bronchial circulation
vasodilation
effect of hypoxia on pulmonary circulation
local vasoconstriction
effect of oxygen on the bronchial circulation
vasoconstriction
effect of oxygen on the pulmonary circulation
vasodilation
function of the bronchial circulation
deliver oxygen to lung tissue
function of the pulmonary circulation
pick up oxygenated blood from lungs
what is pulse pressure?
difference between systolic and diastolic pressures
Poiseuille’s law
a small change in radius leads to a big change in vascular resistance
resistance = 8xlxviscosity / pi x r^4
what is forced vital capacity?
amount of air that can be forcibly exhaled from your lungs after taking the deepest breath possible
what is the peak of the flow/ volume curve?
PEF - peak expiratory flow
what is FEV1?
forced expiratory volume in 1 second
usually 0.75 FVC (FEF75 - forced expiratory flow75)
for a flow/ volume curve, is the part above or below the x axis exhalation?
above
what is FVC?
forced vital capacity
what is respiratory obstruction?
FEV1/ FVC less than 0.7
blocked airways
what causes respiratory obstruction
COPD or asthma
what is respiratory restriction?
FVC less than 0.8 or 80%
decreased expansion ability
what causes respiratory restriction?
pulmonary fibrosis
what is reduced in respiratory obstruction?
FEV1
what is the difference between a volume and a capacity?
a capacity is a combination of more than one volume
what is inspiratory reserve volume?
extra volume that can be inspired above tidal volume, from normal quiet inspiration to maximum inspiration
what is expiratory reserve volume?
extra volume that can be expired below tidal volume, from normal quiet expiration to maximum expiration
what is tidal volume?
volume that enters and leaves with each breath, from normal quiet inspiration to normal quiet expiration
what is residual volume?
air in lungs after max expiration
what is inspiratory capacity?
volume breathed in from quiet expiration to maximum inspiration
what is (forced) vital capacity?
volume that can be exhaled after maximum inspiration (ie. maximum inspiration to maximum expiration)
what is functional residual capacity?
volume remaining after quiet expiration
what is total lung capacity?
volume of air in lungs after maximum inspiration
average tidal volume
0.5L
average inspiratory reserve volume
2.5L
average expiratory reserve volume
1.5L
average residual volume
1.5L
average vital capacity/ forced vital capacity
4.5L
average inspiratory capacity
3L
average functional residual capacity
3L
average total lung capacity
6L
how do you calculate vital capacity?
inspiratory reserve volume + tidal volume + expiratory reserve volume
everything except for residual volume
how do you calculate inspiratory capacity?
tidal volume + inspiratory reserve volume
how do you calculate functional residual capacity?
expiratory reserve volume + residual volume
how do you calculate total lung capacity?
sum of all volumes
IRV + TV + ERV + RV
what is anatomical dead space?
volume of air in the upper and lower respiratory tract that never reaches alveoli
effect of ageing on the lungs
decreased compliance
- stiffer costal cartilages
- decrease in lung elasticity
an increase in V/Q mismatch
a decrease in immunity responses
delayed hypercapnia/ hypoxia response
FEV1 + FVC decrease
- therefore FEV/ FVC ratio decreases
- may falsely show obstruction
types of immunity
innate and adaptive
innate immunity
an example
primitive
non specific
immediate
e.g neutrophils and macrophages
which cells are the main mediators of an inflammatory response?
neutrophils
are neutrophils granulocytes or agranulocytes?
granulocytes
contain primary and secondary granules
adaptive immunity
specific
uses APCs
T and B cells
types of T cells
CD8 - killer cells
CD4 - helper cells induce other cell activation
function of B cells
secrete antibodies
humoural immunity
how many classes of antibodies?
5
name the classes of antibodies?
GAMED
G - most abundant
A - in breast milk, mucosa
M - first in infections
E - allergens
D - unknown, B cell activation?
non immune barriers to lung infection
respiratory epithelium - barrier, anti pathogen proteins, mucus
mucus - lubrication and protection via mucocilliary escalator
coughing - close epiglottis, increase thoracic pressure, air forced out
immune barriers to lung infection
alveolar macrophages
what is hypersensitivity?
allergic hyper-response
type 1 hypersensitivity
IgE
acute anaphylaxis - asthma, hay fever
basophils secrete histamine and prostaglandins
bronchoconstriction and vasodilation and inflammatory response
type 2 hypersensitivity
IgM and IgG mediated
cytotoxic response
autoimmune diseases
tissue damage and altered receptors
type 3 hypersensitivity
IgG
immune complex formation and deposition
type 4 hypersensitivity
T cell mediated
delayed response
what nerve mediates the parasympathetic airway response?
vagus
parasympathetic response on the airways
ACh acts on M3 (muscarinic type 3) receptors on smooth muscle in the airways
vagus
which nerves mediate the sympathetic airway response?
sympathetic chain
sympathetic response in the airways
noradrenaline (NAd) released from adrenal glands after sympathetic stimulation
acts on adrenal medulla to release adrenaline
adrenaline acts on beta 2 receptors on airway smooth muscle (to remember that it is beta 2 and not beta 1, you have 2 lungs and 1 heart)
how do we treat respiratory problems?
bronchodilation
what are the two ways to treat respiratory difficulties?
beta 2 agonists - salbutamol
muscarinic 3 antagonists
what is an agonist?
a drug or substance that binds to a receptor inside a cell or on its surface and causes the same action as the substance that normally binds to the receptor
what is an antagonist?
a substance that stops the action or effect of another substance
equation for pressure of inspired gas
Pi (gas) = P(atm) x Fi(gas)
pressure of inspired gas = atmospheric pressure x fraction of inspired gas
equation for alveolar oxygen
PAO2 = PiO2 - PaCO2/ R
R = 0.8
equation for arterial oxygen
PaO2 = PAO2 - (A - aDO2)
(A - aDO2) means alveolar/ arterial concentration gradient - typically 1
arterial oxygen is usually 1kPa less than alveolar oxygen - natural V/Q mismatch
equation for arterial carbon dioxide
PaCO2 = kVCO2/ VA
typical range of PaCO2 at sea level
4.5 - 6 kPa
typical range of PaO2 at sea level
10.5 - 13.5 kPa
atmospheric pressure
100kPa
what happens to PiO2 with altitude?
falls
what happens to FiO2 with altitude?
stays the same
what happens to atmospheric pressure with altitude?
falls
why does the pressure of inspired oxygen decrease with altitude?
because atmospheric pressure falls and fraction of inspired oxygen stays the same
respiratory response to altitude
hypoxia leads to hyperventilation
PaCO2 falls
heart rate increases
blood pH increases
temporary alkalosis may occur, countered by metabolic hydrogen carbonate excretion
pathologies associated with altitude
acute mountain sickness - only treated by descent
high altitude pulmonary oedema (unacclimated people)
- treated by oxygen treatment and descent
what is 1ATM equivalent to?
100kPa
Boyle’s Law
P1V1 = P2V2
Dalton’s Law
PT = PPA + PPB …
Henry’s Law
the amount of dissolved gas in a liquid is directly proportional to its partial pressure
C = kP
pathologies associated with descent
decompression sickness
- ascend too fast for gas excretion
- inert gas bubbles form in tissues
inert gas narcosis
CNS oxygen toxicity
arterial gas embolism - 15 mins after surfacing
pulmonary barotrauma
what week do the lungs start to develop?
4th
which parts of the embryo form the lung?
endoderm and splanchnic mesoderm
embryology of the lungs
- embryonic
- respiratory diverticulum in the 4th week
- right and left bronchi formed - pseudo glandular
- 5-16 weeks
- right and left bronchi form terminal bronchioles - canalicular
- 16-26 weeks
- terminal bronchioles form respiratory bronchioles
- respiratory bronchioles form a few alveolar ducts - saccular
- 26 weeks - 8 months
- alveolar air ducts grow sacs - alveolar
- 8 months - birth
- alveoli mature
which are the last bronchioles?
respiratory
NOT terminal
name the three embryological shunts
foramen ovale
ductus venous
ductus arteriosus
where is the foramen ovale?
septal hole between the right and left atrium
what is the ductus venosus?
shunt that allows oxygenated blood in the umbilical vein to bypass the liver
what is the ductus arteriosus?
shunts blood from pulmonary artery to aorta
function of umbilical arteries
return deoxygenated blood from foetus to mother
function of the umbilical vein
supplies oxygenated blood from the mother to foetus
how many umbilical arteries do we have?
2
how many umbilical veins do we have?
1
which two organs are bypassed in the foetus?
liver and lungs - because they are not needed
embryology of the first breath
fluid is squeezed out of the lungs
surfactant produced
air inhaled
vasodilaton of pulmonary arteries
what does the umbilical vein become?
ligamentum teres
what does the ductus venosus become?
ligamentum venosus
what does the ductus arteriosus become?
ligamentum arteriosus
what does the foramen ovale become?
fossa ovale
function of alveolar surfactant
decrease surface tension in alveoli
keep alveoli open
when does alveolar surfactant begin to be produced
34 weeks gestation
but dramatic increase 2 weeks pre birth
premature babies often have not made enough surfactant
pre botzinger complex
pacemaker cells located in superior ventral respiratory group
breathing rhythm generators
normal minute ventilation
7.5L/ min but can reach 30L/ min
which cranial nerve monitors carotid peripheral receptor?
glossopharyngeal
which cranial nerve monitors aortic baroreceptor?
vagus
which chemoreceptors are dominant?
central
lung development
from respiratory diverticulum
outbranch from foregut
weeks 4-5
pseudoglandular phase
- development of conducting airways
cannalicular phase
- 16-25
- capillaries, vasculature, alveoli
surfactant produced from week 34 but large increase in production after birth
what is atresia?
failure of oesophagus and trachea to separate
lungs at birth
placenta closes
umbilicaal veins and arteris shut
increase in systemic pressure
amniotic fluid expelled or absorbed
entry of oxygen into lungs causes pulmonary circulation pressure to decrease and flow increases
reduced pressure prevents cardiac shunting, foramen ovale and ductus ateriosus close
oxygen vasodilates pulmonary arteries
first breath
initiates adaptation
oxygen causes pulmonary vasodilation
tissue resistance reduces
vasoconstriction of ductus arteriosus and umbilical arteries
effect of oxygen on pulmonary and systemic systems
pulmonary vasodilator
systemic vasoconstrictor
non immune host defences in the lungs
mucus - mucociliary clearance - mucociliary escalator
coughing and sneezing
antiproteinases
anti-fungal peptides
antimicrobial peptides
opsonins
types of defences in the lung
intrinsic - always present
innate - induced by infection e.g macrophages
adaptive - tailored to a pathogen e.g T cells
consequences of too much mucus
mucus plugs block airways
obstructive lung disease
is lung tissue plastic?
yes
functional plasticity
multipotent basal cell population can differentiate into respiratory epithelial cells if damage occurs
Gell and Coombs Hypersensitivity
4 types
type 1 hypersensitivity
allergies
IgE causes release of histamine from mast cells
vasodilation
gap junctions open
immediate
anaphylaxis
hayfever
type 2 hypersensitivity
autoimmune
IgG binds to self antigens
attack’s body’s own cells
cytotoxic
hours to days
transfusion reactions
type 3 hypersensitivity
immune complex diseases
large scale IgG precipitating, unable to bee cleared by macrophages
type 4 hypersensitivity
delayed type hypersensitivity reaction
T helper cells form granulomas around pathogens with macrophages in a cell mediated response not involving antibodies
tuberculosis
contact dermatitis
innate immunity
dendritic cells
Kupffer cells - liver
alveolar macrophages
initiate acute inflammation via cytokines and antigen presentation
most common leucocyte
neutrophil 70%
primary neutrophil granules
myeloperoxidase
elastase
cathepsins
defensins
secondary neutrophil granules
receptors
lysozyme
collagenase
action of neutrophils
kill bacteria through enzyme release and generation of ROS by NADPH oxidase complex
adaptive immunity
acquired
B and T lymphocytes
humoural and cell mediated respectively
upon binding of receptor, somatic hypermutation occurs to select for receptors with higher affinity (affinity maturation)
T reg cells remove cells that are capable of binding self antigens - immune tolerance
pores allowing movement of macrophages
pores of Kohn
physiological deadspace
175ml
150 anatomical (conducting airway tissues) 25 alveolar (no perfusion)
origin of pulmonary pleurae
mesoderm
layers of gas exchange
apes in capes protect red riding hood
alveolar epithelium
interstitial fluid
capillary endothelium
plasma layer
RBC membrane
RBC cytoplasm
Hb binding site
7 layers
