Respiratory Physiology
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Inspiration is an active process, but normal expiration is a passive process. Forced expiration recruits the abdominal muscles to help force out air.

Muscles of breathing

  • Diaphragm – this is the main muscle of inspiration. It flattens out. During normal quiet breathing it is only really the diaphragm that does any work (other muscles are often not involved). It is controlled by the phrenic nerve which has nerve roots in C3-5 [Remember: C3,C4,C5 keep the diaphragm alive])
  • External intercostals – they raise the ribcage, and also pull the sternum outwards slightly, which increases the volume of the thorax in a different dimension to the diaphragm (horizontal and vertical vectors)
  • Sternocleidomastoid – this will lift the sternum up slightly
  • Anterior serrate – this lifts up many of the ribs. It attaches to the inside of the scapula, and its other ends attach to the lateral surfaces of the ribs.
  • Scalene – these lift the first two ribs. They attach to the front of the first two ribs, and their other attaches to the transverse processes of the C2-C7 vertebrae.
  • Pectoralis minor – this lifts ribs III-IV
The rectus abdominis and the internal intercostals can aid with expiration when needed.


Compliance is a term used to describe how easily the lungs will expand and contract – how ‘compliant’ they are. The lower the compliance, the greater the pressure needed to fill the lungs. The compliance is determined by the elastin and collagen fibres found in the lung parenchyma. These fibres will help the lung to expel air as a passive process. However, they only account for 1/3 of the contractility of the normal lung. The other 2/3 is caused by the fluid-air surface tension inside the alveoli and other lung spaces as a result of the fluid that lines these spaces.
  • However – it is important to remember that this surface tension is only present when there is an air fluid interface in the lungs. I guess the excess mucus produced in COPD will have an adverse effect on this surface tension effect.  
Surfactants are present in this fluid lining, and these reduce the fluid tension effect, and stop the effect becoming too strong and causing collapse of the lung tissue.

Gas concentrations

The air at the alveoli contains more CO2 than room air because obviously there is a residual volume, thus total gaseous exchange does not occur with each breath – there is some air left in the alveoli that ‘waters down’ air coming in from outside the body.

Normal air

  • 78% nitrogen
  • 21% oxygen
  • 0.5% water
  • 0.04% carbon dioxide

Alveolar Air

  • 75% nitrogen
  • 13.6% oxygen
  • 6.2% water
  • 5.3% carbon dioxide

Expired air

  • 75% Nitrogen
  • 15.7% oxygen
  • 3.6% carbon dioxide
  • 6.2% water
Note that…
Both the composition of air, and the distance it has to diffuse across the alveoli will affect how much gas makes it into the blood stream. Increasing the distance the gas has to diffuse – e.g. due to inflammation or production of excess mucus will decrease the amount of gas getting into the bloodstream.

Nervous control

You cannot continue to breathe if the nervous supply to the muscles is cut off (unlike the heart) because breathing is controlled by skeletal muscle. The breathing centre in the medulla co-ordinates all the muscles required for breathing. However, this can be regulated by conscious activity in the cerebrum.
  • Ondine’s curse – this is a condition where there is damage to the autonomic nervous system such that a person may ‘forget’ to breathe, usually during sleep. It occurs in 1 in 200,000 live births, but can also occur as a result of trauma to the brainstem, or poliomyelitis. These patients will require mechanical ventilation for the rest of their lives (but usually only during sleep). It is also known as primary alveolar hypoventilation.
  • The DRG (Dorsal respiratory group) is a group of neurons in the medulla. They are ‘I’ (inspiratory) neurons. They are active in every breath, whether quiet or forced.
  • The VRG (ventral respiratory group) are also found in the medulla. This contains both I and E (expiratory) neurons, and it is active in forced breathing.
There are also the apneustic (in the pons) and pneumotaxic (in the cerebrum) centres – these regulate the rate and depth of respiration, by causing the activation or inhibition of the DRG and VRG.
The apneustic centre will stimulate the DRG for approxmatley 2 seconds, before stopping stimulation and allowing expiration.
This centre basically controls rate of respiration
The pneumotaxic centre controls the depth of respiration. E.g. an increase in ouput by the pneumotaxic centre will cause a short duration of inspiration, thus reducing the depth of inspiration.

Baroreceptor reflexes

  • When blood pressure falls, respiratory rate increases
  • When blood pressure rises, respiratory rate decreases

The Hering-Breur Reflexes

These are active when there are large tidal volumes, and prevent the lungs from becoming over-inflated or collapsing. They are controlled by stretch receptors that feedback info to VRG and DRG.

Conscious breathing

Bypasses the DRG and VRG altogether, and using pyramidal fibres, will connect directly with the same LMN’s used by the DRG and VRG. This type of breathing is controlled by the motor cortex in the frontal lobe.

Accessory muscles of respiration

By putting your hands on your hips you raise the scapula, and thus raise the pectoralis minor and serratus anterior, thus increasing the distance they can raise the rib-cage.

Gaseous exchange

A normal breath exchanges about 350ml of air in the lungs – compare this to the total lung volume of about 1300ml. This relatively small change prevents sudden changes in gas concentrations in the blood.

Ellicit drugs and the respiratory system

  • Cannabis – increases the risk of COPD. A very heavy cannabis smoker could possibly get COPD in their 30’s or 40’s even without an α-1 antitrpysin deficiency. Some evidence suggests that one spliff is equivalent to smoking 20 cigarettes
  • Cocaine – can cause MI in young people, as well as emphysema
  • Heroin – can cause severe respiratory depression – for which you would give naloxone in the acute situation. This drug can be used to treat respiratory depression in any opioid overdose.

Definitions & Terminology

  • Kussmaul breathing – this is deep, rapid breathing that is induced by acidosis
  • Orthopnoea – this is dyspnoea (shortness of breath) that occurs whilst lying down
  • Eupnoea – normal breathing
  • Respiratory distress syndrome sometimes exists in new born infants – and it is caused by a lack of surfactant – it makes it very difficult for the baby to breathe because the high fluid tension makes it difficult for the lungs to expand.
  • Bronchodilation – is stimulated by adrenaline and the sympathetic nervous system
  • Bronchoconstriction – is stimulated by histamine and the parasympathetic nervous system. Cold air and chemical irritants can also have a similar effect
  • Respiratory rate – the normal respiratory rate in an adult is 12-18 breaths per minute – this is roughly one for every 4 heartbeats. Children will breathe more rapidly at approximately 18-20 breaths per minute.
  • Anatomical dead space – about 150ml of every 500ml of inhaled air (so 30%) will fill the bronchi and not the alveoli – and this air is obviously not available for gaseous exchange. This space that the air fills is known as the anatomical dead space.
  • Physiological dead space – this is the sum of the anatomical dead space, and any extra dead space caused by alveolar damage. In healthy individuals the anatomical dead space = physiological dead space

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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