The respiratory system Flashcards
Respiratory quotient
Ratio of CO2: O2 - depends on food consumed
Trachea and bronchi
Rigid tubes - rings of cartilage avoid collapse
Bronchioles
No cartilage, smooth muscle walls, sensitive to some hormones/chemicals
Alveoli
Thin walled inflatable sacs
Pulmonary capillaries around each alveolus for good blood supply
Large SA and thinner - efficient gas exchange 0.5 microm
Type I alveolar cells
1 cell layer thick - flattened
Type II alveolar cells
Secrete surfactant (phospholipid)
Alveolar macrophages
Guard lumen to prevent infection
Pores of Kohn
Airflow between neighbouring alveoli - collateral ventilation
Lined with ciliated epithelia and bathed in mucous - much-ciliatory escalator
Pleural sac
Double-walled, closed sac separating from thoracic wall
Pleural cavity = interior
Intracellular sac secreted by pleura surfaces - lubrication, protection
Diaphragm
Skeletal muscle separating thoracic and abdominal cavity
Function of respiratory system
Exchange of gases in air/blood, homeostatic regulation of pH, defence against inhaled pathogens, vocalisation, thermoregulation, water loss
Pressures in the respiratory system
Atmospheric (barometric) pressure Intra-alveolar pressure (intrapulmonary) Intrapleural pressure (intrathoracic) Alveolar pressure atmospheric = air out of lungs
Boyle’s Law
Any constant temperature, the pressure exerted by a gas varies inversely with the volume of gas
Lung mechanics
No muscles, relies on difference in pressure (transpulmonary pressure = Palv - Pip) and compliance (stretch)
Respiration muscles attached to chest wall and contract and real to change chest dimensions, causing TP change
Inspiration
Diaphragm domed -> phrenic nerve -> contracts and flattens
Intercostal muscles -> intercostal nerve
Expansion of thoracic cavity decrease in intrapleural pressure - increasing ling volume and lowers intra-alaveolar pressure than atmospheric so air enters
Expiration
Relaxation of inspiratory muscles - diaphragm and chest wall muscles decrease chest cavity size
Intrapleural pressure increases, compresses lungs, intra-alveolar pressure increases - above atmospheric -> air out
Contraction of expiration muscles -> abdominal wall and internal intercostal
Elastic recoil of alveoli
Highly elastic connective tissue, alveolar surface tension
Lung compliance
Effort to stretch lungs Change in volume to given force/pressure = change in V/Change in P Ease with with volume can be changed Reciprocal of elastane High compliance = easy chest expansion
Law of LaPlace
Surface tension P=2T/R
P in large alveolus > smaller - small may collapse
Sufacant lowers surface tension o liquid lining alveoli so pressure to hold alveoli open = reduced
Airway resistance, R
R proportional to Ln/r^4
Upper airways diameter constant
Mucus accumulation can increase resistance
Bronchioles - collapsible tubes increase R
Bronchoconstriction (asthma) and dilation can occur
Tidal volume, TV
Volume of air/breath
Inspiratory reserve, IRV
Extra volume that can be maximum inspired
Inspiratory capacity, IC
= IRV + TV
Expiratory reserve, ERV
Extra volume that can be expired by max contraction beyond normal
Residual volume, RV
Minimal volume remaining in lungs after max expiration
Functional residual capacity, FRC
Volume of air in runs after normal expiration
= ERV + RV
Vital capacity, VC
Max volume of air in single breath maximum inspired
IRV + TV + ERV
Total lung capacity, TLC
Mac volume lungs can hold
VC + RV
Forced expiratory volume in 1 second, FEV
Volume of air during first second of expiration in VC determination
Anatomical dead space
Conducting airways, no gas exchange occurs ~150ml
Physiological dead space
Anatomical dead space + alveolar dead space
Alveolar dead space = non-functioning alveoli e.g. absence of blood flow
Minute ventilation
Volume breathed in per min
Pulmonary ventialton
Tidal volume x respiratory rate
Alveolar ventialtion
TV-dead space x respiratory rate
Pulmonary circulation
Conc O2 + CO2 in arterial blood is contents, O2 in same rate as consumers, CO2 out same rate as produced
Gas exhange
Simple diffusion of O2/CO2 down partial pressure gradients
pp exerted by each gas in mixture = total pressure x fractional composition of gas in mixture
Diffusion gradients in lungs and tissue affected by conc grad, SA and permeability
Dalton’s law
P total = P1 + P2….
Air — becomes moist —> alveoli –> water vapour reduced N2/O2 levels
Establishment of gradients
P(air) = PN2, PO2, PH2O, PCO2
Air through conducting zone - humidified to saturation
Solubility of gases
Any pp cones of dissolved gases differ - some more soluble
Henry’s law
C = kP (pp in atmosphere)
Air flows down conc gards
Air -> alveoli PO2 down
PCO2 down
Due to continuous gas exchnage alveoli/capillaries, air mixes with alveoli air, alveoli air saturated water vapour
Exchange of O2 and CO2
In alveoli = rapid
In tissue = diffusion grads. PCO2 depends on metabolic activity and blood flow to tissue. Large grads = more exchange
Venous blood active tissue, down PO2 and up PCO2
Venous blood right atrium mixed PCO2 and PO2 average
Determinants of alveolar PO2 and PCO2
PO2 and PCO2 in inspired air, minute ventilation, rate respiration tissue consumes O2/produces CO2 - alveolar ventilation exceeds demands of tissue: PO2 up and PCO2 down
Matching ventilation to perfusion
Ratio alveolar ventilation to pulmonary blood flow (Va/Q - 0.8 av)
Upright = gravity increases pulmonary arterial hydrostatic pressure at base than apex - alveolar ventilation varies in same direction as blood flow
Ventilated alveoli close to perfused capillaries ideal for gas changes.
Top blood flow not as good - middle = best
Airway obstruction - V/Q = 0 no ventilation
Vascular obstruction - V/Q = infinity = no perfusion
Perfusion
Delivery of blood to tissue
Haemoglobin
Hb + O2 HbO2 - each carries 4 O2 molecules PO2 100mgHg (normal) = Hb 98% sat
O2/Hb dissociation curve
ppO2 high (lungs) sat high
ppO2 low (tissue) sat low - dissociation
Plateau where ppO2 high - lungs
Steep - systemic Hb unloads O2 to tissues
Sigmoidal curve
1O2 bound increase affinity for Hb for next O2
O2 binding = conformational changes
Lower affinity shifts curve right - higher pO2 to achieve saturation
Higher affinity shift to left - lower PO2 to achieve sat
Temp increase - to right
pH acidity up, affinity down, to left
Myoglobin
O2 binding protein in skeletal muscle - higher affinity for O2 than Hb
Low pO2 50% saturated
Liberates O2 when pO2 to 10mmHg
Foetal Hb
PaO2 20mmHg low sat - 60% sat
Co2 combined with water
Bicarbonate ion -> carbonic acid
Hypoventilate
PCO2 and H+ ions up, lower pH, inc HCO3- respiratory acidosis - kidneys conserve HCO3-
PO2 down stimulates increase in breaths and depth
Hyperventilate
PCO3 and H+ ions down, higher pH, decrease in HCO3- - respiratory alkalosis - renal compensation excretes HCO3
APO2 up - reduced lack of CO2 - decrease breaths and depth
‘Black box’ control of breathing
Respiratory neurons in medulla inspiration and expiration
Neurons in pons modulate ventilation
Rhythmic pattern breathing
Ventilation modulated chemical factors and higher brain centres
What controls breathing rhythm
Medulla oblongata
Dorsal respiration group - in region in nucleus tracts solitairus (NTS)
Vagus nerve and higher brain centres alter DRG/VRG
Chemoreceptors
Monitor PO2, PCO2, in carotid and aortic bodies
Type I peripheral chemoreceptors
Contact blood - afferent nerves - NT
Type II peripheral chemoreceptors
Glial cell like - repair and nutrient supply
Central chemoreceptors
Ventral surface medulla - H+ ions stimuli pH change cerebrospinal fluid
H+ don’t cross, CO2 does
Chemoreceptor reflex
Central and peripheral respond PCO2 changes
