PHYS: Breathing Flashcards
metabolic functions of the lungs
- regulate CO2 levels
- regulate pH (CO2 + H2O -> H2CO3 + H+)
boyle’s law
- P1V1 = P2V2
- if volume increases, pressure decreases (inversely proportional)
- pressure moves from high to low
empyema
- accumulation of pus in pleural cavity
inspiration process
- diaphragm contracts and flattens = increased abdominal pressure
- intercostals contract to move ribs move up and out, causing lungs to expand due to negative pleural pressure
- increased thoracic volume = decreased intrapulmonary (thoracic) pressure
- therefore air rushes in until intrapulmonary pressure is equal to P(atm)
expiration process
- diaphragm relaxes and becomes dome shaped = decreased abdominal pressure
- intercostals relax to move ribs move down and in, causing lungs to recoil due to negative pleural pressure
- decreased thoracic volume = increased thoracic pressure
- therefore air rushes out until intrapulmonary pressure is equal to P(atm)
describe the pressure in the pleural cavity and how does this relate to a pneumothorax
- pleural cavity has negative pressure (756 mmHg which is 4 below P atm)
- this helps hold lungs against inside of thoracic wall
- pneumothorax: air in pleural space (caused by penetrating injury or ruptured lung) reverses the negative pressure
- causes atelectasis since lung isn’t held against the thoracic wall
describe the transpulmonary, intrapleural and intrapulmonary pressure
- P (atm) = 760 mmHg @ sea level - all pressures are relative to this
- intrapulmonary (lung): 760 mmHg (+0)
- intrapleural (pleural cavity): 756 mmHg (-4)
- transpulmonary (between lung and pleural cavity): 760 - 756 = 4 mmHg
2 factors affecting pulmonary ventilation and how to measure
- radius of airways: affects the RATE of airflow (obstructive = decreased radius = decreased FEV1 and therefore FEV1/FVC ratio)
- compliance (ease of expansion): affects the VOLUME of airflow (restrictive = decreased compliance = decreased FEV1 AND FVC = same ratio)
two factors influencing lung compliance
- 1/3 elasticity of issue: collagen and elastin stretch on inspiration and recoil on expiration
- 2/3 surface tension of alveolar air-fluid interface: affects ability for gas exchange to occur (not usually a problem)
Poiseulle’s law
- flow = (P2-P1)/resistance
how to calculate airway resistance
when is airway resistance the highest?
- peaks between the 5-8th generation (medium-sized bronchioles)
- rapidly decreases afterwards b/c cross-sectional area of airway exponentially increases
3 factors which regulate the airway radius
- vagus n. (parasymp) > bronchoconstriction
- inhaled stimuli e.g. cigarettes, dust, cold air > reflex bronchoconstriction
- circulating catecholamines (NA) or sympathetic nerves secrete NA > bronchodilation
lung fibrosis impact on compliance and how will this show on spirometry?
- more collagen and fibroblasts = thickened and less elastic = decreased compliance
- leads to decreased FVC and FEV1 but normal FEV1/FVC ratio
pulmonary surfactant
- where is it produced
- when is it produced
- structure
- function
- produced and secreted by type II alveolar cells
- not produced until 5-7th week of gestation
- mixture of phospholipids, proteins and Ca2+
- weakens H bonds to decrease surface tension in alveoli = remain more open for gaseous exchange = increased compliance
tidal volume vs vital capacity
- TV: air breathed in and out at rest (usually 500mL)
- VC: maximum amount of air that can be inhaled and exhaled (not full volume of lungs because there is always residual volume) - DOESN’T CHANGE DURING EXERCISE
what is total lung capacity and why can’t it be measured during spirometry
- FULL volume of lungs, regardless of residual volume
- spirometry measures airflow in and out so doesn’t take into account RV
2 main purposes of spirometry and how do we measure these?
1) measuring VOLUMES
- breathe in and out normally (TV)
- inhale and then exhale as much as you can (VC)
2) measuring RATE of airflow
- take maximum inspiration and expiration as fast as they can (FVC and FEV1)
- forced vital capacity vs FEV1
- what is a healthy ratio and what happens if it’s less than this?
- FVC = forced vital capacity = maximum air which can be forcefully expired
- FEV1 = air expired in first one second
- FEV1/FVC should be > 75% (i.e. able to expire 75% of functional capacity in at least one second)
- if < 75%, can indicate obstructive lung disease
obstructive vs restrictive lung conditions
- obstructive (hard to exhale all air in lungs due to increased airway resistance e.g. asthma/COPD): reduced FEV1, normal FVC, lower ratio
- restrictive (hard to fully expand lungs due to decreased compliance e.g. fibrosis): reduced FEV1 and FVC but normal ratio
reasons for airway obstruction e.g. asthma
- thickened muscular layer
- increased secretion of mucus
- inflammatory response and oedema in epithelium
Fick’s law equation and 4 factors which affect diffusion (+ extra factor)
diffusion depends on:
- area of membrane available for diffusion (A) - lungs and alveoli expand during inspiration
- thickness of membrane (T)
- solubility (diffusion constant) of gas in water (D)
- pressure gradient across membrane (P1-P2)
- matching of ventilation and perfusion
partial pressure of oxygen and why is this important?
- since normal atmospheric (barometric) pressure is 760 mmHg, and the air is 20% O2
- 0.2 x 760 = 150 mmHg give or take
O2 and CO2 pressure gradients
- pressure gradient = alveolar pressure - pressure in deox blood returning to lungs
- O2 = 100-40 = 60 mmHg
- CO2 = 46-40 = 6 mmHg
pressure gradients:
- high altitude
- underwater/hyperbaric chamber
- high altitudes = decreased barometric pressure = decreased pressure gradient and hence diffusion of O2
- underwater/hyperbaric chamber = increased barometric pressure = increased pressure gradient and hence diffusion of O2
solubility of CO2/O2
- CO2 is much more soluble in water than O2
Dalton’s law
- in a mixture of non-reacting gases, total pressure exerted = sum of partial pressures of each gas
- pressure exerted depends upon temperature and conc. of the gas (higher temperatures increase pressure)
Henry’s law
- conc. of gas in solution depends on atmospheric pressure
- i.e. if the gas particles are in equilibrium between the air and the solution, their partial pressure should be the same
conditions which affect the thickness and SA of the diffusion membrane
- thickness: fibrosis and oedema (make it thicker)
- SA: emphysema - damaged alveoli walls rupture = one larger air space instead of many little ones = decreased SA
how to measure gas diffusion clinically
- pulse oximeter (measures what % of Hb has O2 bound to it)
- ABG: should get PO2 = 100 mmHg and PCO2 = 40 mmHg. lower PO2 can indicate diffusion issues
- diffusion/transfer in the lung of CO (DLCO/TLCO)
why do we use CO to measure diffusion in DLCO?
- diffuses easily across alveolar surface
- highly soluble in blood and has a high affinity for Hb
- not normally present in plasma so we can measure how much is transferred from the inhaled air to plasma
how does the DLCO test work and what is the normal level?
- Pt inhales from bag containing CO and He and holds for 10s
- exhale into separate bag
- difference in CO concentration before and after indicates how much has diffused into the bloodstream (C1V1 = C2V2)
- 25 mLCO/min/mmHg
ventilation (V) vs perfusion (Q) and what are the ideal and normal ratios?
- V = flow of air in/out of alveoli
- Q = blood flow to alveolar capillaries
- ideally they are the same i.e. V/Q = 1 but they are often different due to gravity
- realistically V/Q = 0.8
what happens if V/Q is abnormal?
- if <0.8 this indicates shunting = reduced ventilation e.g. pneumonia/asthma
- if >0.8 this indicates dead space = reduced perfusion e.g. pulmonary embolism
how are the alveoli throughout the lung different?
- alveoli at the top are more stretched because there is more negative pleural pressure
- therefore the base is better ventilated b/c alveoli are squashed and more compliant
- also gravity means perfusion/blood flow is better at the bottom
mechanisms to fix V/Q mismatch
- to match a change in ventilation: diff PO2 levels causes capillaries to dilate or constrict to alter perfusion to match this
- to match a change in perfusion: diff blood flow causes bronchioles to dilate or constrict bronchioles to alter ventilation to match this
how can we clinically measure V/Q
- Pt breathes in radioactive tracer
- allows us to see the circulation of air and blood to determine V/Q
layers oxygen has to go through to bind to Hb on a RBC
- surfactant
- type 1 pneumocyte
- basement membrane
- endothelium
- plasma
- RBC
which type of epithelium lines most of the conducting portion of the respiratory tract and what are the main cell types?
- pseudo stratified ciliated columnar epithelium
- ciliated columnar cells
- goblet cells (secrete mucus)
- basal cells (stem cells)
- Kultschitzky cells (amine precursor uptake and decarboxylation/APUD)
structure of bronchioles
- no cartilage, submucosal glands or goblet cells
- increasing proportion of smooth muscle
- simple columnar epithelium becomes simple cuboidal
- Clara cells - secrete proteins, lysozyme, Ig
2 ways in which O2 is transported
- dissolved in plasma and RBC cytoplasm
- reversibly bound to Hb
structure of Hb
- contains 4 heme groups
- each has an Fe molecule to bind oxygen
oxygen dissociation curve interpretation
- increased PO2 = increased oxygen bound to Hb
- sigmoid shape
- at 100mmHg PO2, all Hb is saturated with O2
- shifts to right mean less O2 is bound to Hb = more easily offloaded to tissues
hypoxia
- when PO2 < 60mmHg
what causes an increased affinity of Hb to O2
- (left shift in graph)
- decreased temp
- less 2,3-DPG
- alkalosis
- decreased PCO2
- increased [CO]
- more oxygen bound to the Hb
what causes a decreased affinity of Hb to O2
- (right shift in graph - think enhanced release of O2 for use by tissues e.g. during exercise)
- increased temp
- increased 2,3-DPG
- acidosis
- increased PCO2
- decreased [CO]
- less oxygen bound to the Hb
3 ways that CO2 can be transported
- dissolved in plasma (CO2)
- chemically bound to Hb in a RBC as carbaminohaemoglobin (HbCO2)
- as bicarbonate ions in plasma (HCO3-) - majority
what is the chloride shift
- when HCO3- moves out of RBCs into plasma but Cl- must move in the opposite direction to maintain electroneutrality
two ways to control breathing
- neural control
- chemical control by chemoreceptors
main inputs for modulation of breathing rate
- peripheral chemoreceptors
- lung and chest wall mechanoreceptors and irritant receptors
- muscles and joints
- these act via the DRG to modulate breathing rate
neural control of breathing
- pneumotaxic centre (pons) inhibits inspiration
- apneustic (pons) stimulates inspiration
- rhythm is initiated by pre-botzinger complex in ventral respiratory group (VRG) - medulla oblongata of brainstem
- then they send signals to the dorsal respiratory group (DRG) which sends it down to the inspiratory motor neurons which cause the diaphragm and intercostals to move
- forced expiration is driven by VRG
two types of chemoreceptors for chemical control of breathing
- central: in medulla (monitor CO2 via H+ in CSF so increased respiration to remove it) - MOST IMPORTANT
- peripheral: in carotid and aortic bodies (monitors for increased CO2 and H+ in arteries, or decreased O2 - in priority order)
which nerves are associated with the carotid and aortic bodies?
- carotid: glossopharyngeal
- aortic: vagus
mechanism behind shallow water drowning
- hyperventilation leads to hypocapnia and still high O2 levels
- the blackout from hypoxia kicks in before the urgent need to breathe due to hypercapnia
- then you urgently breathe whilst unconscious in water and drown
