Respiratory Reflexes

This lecture had a fair bit of new content. It's not as difficult conceptually as that last cardiovascular lecture, but it is still way too much for a Monday afternoon IMO :P (Okay, it wasn't that bad, but I feel like there were a few little bits and pieces that just slid past me.)

Describe the inputs to the central rhythm generator.

As mentioned in my previous post, respiratory rhythm arises largely from the medulla. The centres in the medulla involved in control of respiration can be influenced by a variety of factors, such as feedback from peripheral receptors, emotion and temperature. (Temperature doesn't really have a massive effect on ventilation in humans, but in some animals, such as dogs, it can cause panting.) Voluntary control of ventilation is separate to the rhythm control in the medulla.

List the three types of lung receptors

The three types of lung/lower airway receptors include slowly adapting receptors (SARs), rapidly adapting receptors (RARs) and C-fibres. I'll describe them in more detail soon.

Describe the Hering-Breuer reflex.

As mentioned here, the Hering-Breuer reflex prevents overinflation of the lungs. It does this by suppressing inhalation when the lungs are already inflated. The vagus nerve is vital to this reflex- if you cut it, the reflex disappears. The Hering-Breuer reflex is not particularly strong in conscious humans, but it is important in animals (and may also be important in anaesthetised humans).

Explain the role of SAR and their stimulation and effects.

SAR, or Slowly Adapting Receptors, help detect the volume of the lungs. They are activated when the lungs are stretched, and as they do not adapt to the stretch (or at least they adapt very slowly, hence their name), they keep firing while the lungs are inflated. These may contribute to the Hering-Breuer reflex, which I just described.

SARs are myelinated fibres which have a conduction velocity of 15-30m/s (which is pretty standard for myelinated fibres). As mentioned above, they are stimulated by stretch. They do not respond to deflation, unlike RARs as I'll discuss shortly. The effects of SAR activation include reduced tidal volume, shorter respiratory time and bronchodilation.

Describe the reflex effects of RAR and the stimuli that activate them

RAR, or Rapidly Adapting Receptors, help detect changes in volumes of the lungs. Located within or near the epithelium, they are activated when stretching occurs, but their response is rapidly "switched off." They respond in response to both inflation and deflation, and the frequency of their impulses depends on the rate of change of volume of the lung (which is also related to inspiratory flow rate).

RARs, like SARs, are myelinated fibres with a conduction velocity of 15-30m/s. As well as being stimulated by stretch, they are also stimulated by irritants such as acid, smoke and dust. They produce reflexes such as coughing, tachypnea (abnormally rapid breathing), hyperventilation and bronchoconstriction.

Describe the activation and reflexes produced by C-fibres.

C-fibres, unlike RARs and SARs, are unmyelinated and thus their conduction velocity is much slower (1m/s). They come in two flavours: bronchial and pulmonary. They are present in the airway epithelium, as well as in other places around the lung.

Stimulants of C-fibres include capsaicin (as I'll explain shortly), acid and/or hypertonic saline (for bronchial C-fibres) and oedema and/or large amounts of inflation (for pulmonary C-fibres). It should be noted, however, that they are generally not very responsive to inflation. Activation of C-fibres produces bronchoconstriction, bradycardia, and sometimes cough. Initially, C-fibre activation can produce apnoea, but later on hyperpnea can be produced instead. (See here if you don't remember what these terms mean.)

One thing that is kind of unique about C-fibres is that they contain both afferent and efferent fibres, allowing the signal to branch out more easily (I think... there were quite a few tidbits in this lecture that I didn't quite get). C-fibres also contain neurotransmitters, including peptide neurotransmitters such as tachykinins. These can cause vascular leak (contraction of endothelial cells, increasing the amount of space between them), mucous production and bronchoconstriction. (I think. As I said, there were quite a few bits in this lecture that slid over me. I blame the time in the afternoon.)

Recall the receptors activated by capsaicin.

C-fibres can be activated by capsaicin, the component of chilli that makes it hot. Capsaicin activates vallinoid receptors (VR1), which are TRP (transient receptor potential) channels. Activation of VR1s produces the sensation of heat. Over long periods of time, capsaicin can actually kill off C-fibres, making you more tolerant to hot foods.

Explain the detection of cough.

This was hardly covered in the lecture, but the summary slide says that RARs and maybe C-fibres can detect cough. Receptors in the upper airways might help as well.

Describe the effects and activation of upper airway cool receptors.

Receptors in our upper airways can respond to changes in temperature, such as what happens when we exhale air from outside. Stimulation of these receptors makes us feel like we are breathing, so receptor stimulation suppresses further ventilation. On the other hand, when these receptors are blocked, we can feel like we can't breathe even though our blood gas concentrations might be normal.

Aside from cool receptors, there are quite a few other receptors in the upper airway (nose and larynx). These can cause laryngospasm (closing off of the larynx). These receptors can respond to flow, temperature, pressure, upper airway muscle contraction, snoring and obstruction.

Describe the effects of menthol.

Menthol stimulates cool receptors, making it feel like you are getting more airflow than you actually are.

Explain the muscle proprioception reflexes including the spindle and tendon organ

Muscles have a couple of different proprioception reflexes. We didn't go into too much detail on them in the lecture though. Apparently this was covered to some extent in PHYL2002, which I didn't do, so...

Muscle spindles can measure muscle length, and sudden change in spindle length (as might happen when you tap someone on the knee) can cause a reflex contraction. The Golgi apparatus can also play a role in measuring force on the tendon. Such receptors are present in a lot of skeletal muscles, but the diaphragm has few of them. Hence, a lot of the proprioception reflexes involved in breathing actually come from the abdominal muscles and intercostal muscles.

Define dyspnea.

Dyspnea is the feeling that you can't breathe, even though blood gases might be normal. There are several different mechanisms that might trigger this, such as mucus covering the cool receptors (as happens during a cold).