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Topics Covered

Internal and External Respiration

  • Internal Respiration is the intracellular ATP generating processes that use O2 and create CO2
  • External Respiration is the process of exchanging O2 and CO2 between internal and external environment
  • This happens in 4 stages:
    • Ventilation
      • Occurs due to respiratory muscles expanding lungs
      • 2 overall forces involved that cause promote patency of alveoli or collapse:
        • Patency:
          • Transmural pressure gradient
            • The pressure of the pleural cavity surrounding the lung is smaller than the lung itself. This is beneficial as it allows for the unimpeded expansion of the lung.
          • Pulmonary Surfactant -reduces surface tension in alveoli
            • The LAW OF LAPLACE – Smaller alveoli have a higher tendency to collapse under surface tension. So surfactant is most useful for the smallest alveoli
          • Alveolar interdependence
            • If the surface tension of an alveolus causes it to start collapsing – surrounding alveoli that are attached are stretched. Like an elastic band, these stretched alveoli snap back – in turn expanding the original collapsing alveolus.
        • Collapse
          • Elastic recoil of lungs and chest wall
            • This elastic recoil wants to snap back like a rubber band when not being actively stretched by inspiratory muscles – intercostal muscles
          • Alveolar surface tension

Inspiration and Expiration Mechanics

Pulmonary ventilation is the process of air from surroundings entering the lungs.

  • Inspiration– an active process that depends on the contraction of the diaphragm and the intercostal muscles.
  • The contraction of these muscles expand the lung to a greater volume.
  • This causes a decrease in pressure between the lungs and the environment
    • THIS DESCRIBES BOYLES LAW – It essentially states that the pressure of a gas decreases if the volume of the container it is in increases (with constant temperature and mass of gas)
  • Like a vacuum – air from the environment rushes into the lungs to equalise this pressure.
    • Since gas pressure is essentially like a concentration gradient- gases move from high to low concentration gradient until equally spread.
  • Expiration– A passive process driven by opposing forces mentioned above.
    • Upon relaxation of the above inspiratory muscles – the lung volume decreases- due to the elastic property of lung tissue – causing an increased pressure within the lungs HIGHER than atmospheric pressure of the environment
    • This drives the air out of the lungs until the pressures equalise

Gas exchange

There are 2 important components to the efficiency of gas exchange. VENTILATION and PERFUSION

  • Ventilation (V)
  • 2 types:
    • Pulmonary– which is the total air breathed in
    • Alveolar– which is the total air available for gas exchange- this is LOWER than pulmonary ventilation
      • It is lower due to the presence of anatomical alveolar dead space. –
      • ANATOMICAL DEADSPACE IS A CONSTANT value
      • This means that prioritising breathing in DEEPLY is more advantageous for overall oxygenation of blood
  • Perfusion (Q)

Perfusion is the rate at which blood passes through the vasculature surrounding alveoli.

The efficiency of gas exchange is measured using a ratio between Ventilation and Perfusion:

V/Q RATIO – the rates of these values should MATCH for optimum gas exchange.

If an unbalance is present local controls act to constrict smooth muscle present in bronchioles and arterioles.

An example of mismatch is covered on Common Drugs page, which focuses on poor oxygen prescribing in COPD

There are 4 factors that allow for efficient transfer of gases between alveoli and blood:

  • Partial Pressure gradients of CO2 and O2
    • Involves Dalton’s Law of partial pressures
  • Diffusion Coefficient
    • The solubility of gas in the alveolar membrane
    • This is 20 times greater in CO2 than in O2
  • Surface area of alveoli – High surface area so fast transfer
  • Thickness of alveoli – thin walls so fast transfer
    • BOTH follow Fick’s law of diffusion

Lung Volumes

There are a number of lung volumes that are important to understand.

This is easier to understand with the following waveform:

Control of Respiration

The Respiratory Centre is made up of multiple areas in the medulla and the pons: -It is made up of the Pre-Botzinger Complex, Dorsal resp group, Pneumotaxic centre and ventral resp group.

  • The rhythm of respiration (in normal, unconscious respiration) (the pace of inspiration ->expiration->inspiration)
    • Initial impulse generated by the Pre-Botzinger Complex (in the medulla)
      • This excites the dorsal respiratory group
        • This causes contraction of respiratory muscles ->INSPIRATION
      • Excitation of the dorsal resp group in turn excites the pneumotaxic centre (in the pons)
        • This stops the dorsal resp group from firing – when firing stops – respiratory muscles stop contracting -> passively relax
          • Passive relaxation of muscles cause passive relaxation of lungs ->passive expiration
      • If the ventral respiratory group is activated – results in contraction of accessory respiratory muscles -> active, forceful expiration (read more on anatomy page for muscles involved)
  • The Respiratory Centre is modulated through other signals throughout the body namely:
    • Stretch receptors
      • Located in bronchi and bronchioles
      • The afferent limb of the Hering-Breuer reflex
      • Prevents HYPERINLATION OF THE LUNG
      • Signals inhibit respiration – stops firing of the dorsal resp group
    • Joint receptors
      • Impulses generated from moving limbs, namely during exercise – increases ventilation and respiratory rate during exercise.
    • Baroreceptors
      • Increased respiratory rate in response to a drop in blood pressure (sensed by baroreceptors)
  • Chemoreceptors -two types- central and peripheral
    • detect the concentration of CHEMICALS in blood and cerebrospinal fluid (CSF) and influence respiratory centre to correct values via negative feedback control.
    • Play an important role in acid-base balance – more covered on ABG Interpretation page
      • Central – Near surface of medulla
        • Sense H+ in CSF. – An increase H+ leads to increased resp rate to “blow off” CO2
          • This is created through the diffusion and dilution of CO2 from blood to the CSF (fluid that surrounds the brain)
          • This is serves an important function as it only takes a very small increase in CO2 to cause an increase in H+ ion concentration within the CSF (due to the lack of proteins present that result in less of a buffer for increase).
          • A small increase of CO2 therefore can lead to cerebral dysfunction due to the increased acidity.
          • Sensitive sensing within central chemoreceptors is the reason you can only hold your breath for a limited time.
  • Peripheral– In CAROTID and AORTIC body
    • Sense O2, CO2 and H+ (NOTE H+ is linked to CO2 as this gas dissolves in blood to create an increased acidity – so an increased H+) in BLOOD
    • Respiratory rate is INCREASED with a:
      • DECREASED O2
      • INCREASED CO2
      • INCREASED H+
    • Respiratory rate is DECREASED with a:
      • INCREASED O2
      • DECREASED CO2
      • DECREASED H+

Gas Transport in Blood

Oxygen Transport

  • A very small volume (2%) is dissolved in blood itself.
  • The majority (98%) of Oxygen is transported by HAEMOGLOBIN (Hb) in blood.
    • There are FOUR binding sites on Hb for oxygen to bind.
    • These sites have COOPERATIVE AFFINITY
      • This means that as the sites fill up- subsequent unbound sites have a GREATER AFFINITY for the binding of oxygen.
      • This creates the classic sigmoid-shaped O2-Hb dissociation curve
    • This Curve can be SHIFTED :
    • A right shift results in a REDUCED AFFINITY for oxygen
      • INVOLVES THE BOHR EFFECT – this ultimately results in greater oxygen conc in tissues due to O2 unbinding from Hb
      • Anything that signals that cells have undergone CELLULAR RESPIRATION – and so are DEPLETED OF OXYGEN
      • Results in a RIGHTWARDS SHIFT causing replenishing of O2 to tissues via unbinding with Hb – the following are factors that cause this:
        • Increased CO2
        • Increased H+ -from lactate production with respiration
        • Increased temperature (respiration is an energy releasing process)
        • Increased 2,3 DPG – produced in respiration
    • The opposite changes in the same factors (IE No respiration signs so high oxygen saturation in tissues) result in a LEFTWARDS SHIFT and so a high affinity of Hb for Oxygen.

Carbon Dioxide Transport

  • Carbon dioxide is transported in 3 forms:
    • In solution (10%)
    • As bicarbonate (60%)
      • Formation of Bicarbonate from CO2 involves WATER and the catalyst CARBONIC ANHYDARSE (HA)
        • This reaction occurs WITHIN RED BLOOD CELLS (RBCs)- where HA is resident.
        • Formed Bicarbonate LEAVES the RBC via an exchanger- it exchanges bicarbonate for chlorine
          • This exchange is termed CHLORIDE SHIFT
    • As carboamino compounds (30%)
      • The most important compound being carboamino-haemoglobin
        • Essentially CO2 bound to haemoglobin
        • This is facilitated through the HALDANE EFFECT
          • This is the increase in affinity of Hb for CO2 due to unbinding of OXYGEN
            • This means that the Bohr Effect COMPLIMENTS the HALDANE EFFECT
              • OVERALL BOTH the HALDANE and BOHR EFFECT Facilitate:
                • Oxygen exchange INTO tissue
                • Carbon dioxide exchange AWAY FROM tissue (as waste)