Control of Ventilation Flashcards
What does ventilatory control require?
- Requires stimulation of the skeletal muscles of inspiration.
- It occurs via the phrenic nerve to the diaphragm (C3,4,5 keeps the diaphragm alive) and intercostal nerves to external intercostal muscles.
- It is entirely dependent on signalling from the brain (sever spinal cord above origin of phrenic nerve (C3-C5) and breathing ceases
Explain the basis of rhythm in respiration
Where does ventilatory control usually reside within? What do they do?
- Resides within Ill-defined centres located in the pons and medulla (known as Respiratory centres)
- Set an automatic rhythm of breathing through co-ordinating the firing of smooth and repetitive bursts of action potentials in DRG- travel to inspiratory muscles initiating inspiration.
Respiratory centres:
- PRG- Pontine respiratory group
- DRG- Dorsal respiratory group- activating muscles of inspiration
- VRG- Ventral respiratory group- activating muscles of expiration. However, it is also involved in output to pharynx, larynx and tongue which keeps the airway patent.
- NTS- Nucleus tractus soliatarius
What can breathing be subject to?
- Normally breathing is subconscious but can be subject to voluntary modulation.
- Respiratory centres adjust this rhythm in response to stimuli
List t_h_e f_a_c_t_o_r_s i_n_v_o_l_v_e_d i_n c_h_a_n_g_i_n_g ‘r_e_s_p_i_r_a_t_o_r_y d_r_i_v_e’,_ r_a_t_e a_n_d d_e_p_t_h o_f _breathing.
- Emotion (via limbic system in the brain)
o i.e. when you laugh, cry, are scared your respiratory pattern changes. - Voluntary over-ride (via higher centres in the brain)
- Mechano-sensory input from the thorax
o Stretch receptors when they reach threshold e.g. stretch reflex
o safety mechanism to stop destruction of alveoli - Chemical composition of the blood (PCO2, PO2 and pH)
o detected by chemoreceptors
o Chemoreceptor input is the most significant factor in ventilatory control
o We do not tolerate partial pressure changes of CO2 very well but can tolerate partial pressure changes of O2.
Identify the function and sites of chemoreceptors and identify the stimuli which activate them.
- They serve to regulate the arterial PCO2
- Include Central and Peripheral Chemoreceptors
outline cerebral chemoreceptors
o Found on the medulla
o Do not respond to direct changes in plasma [H+] because of the blood brain barrier which is highly selective and will not allow any ions to cross it. Gases however can, and will change the PCO2 in the CSF.
o Respond directly to H+ in CSF around brain (wholly derived from CO2-> indirectly monitors the PCO2.)
o The rise in H+ Cause reflex stimulation of ventilation (driven by raised PCO2 = Hypercapnea)
o Ventilation is reflexly inhibited by a decrease in arterial PCO2 (which reduces plasma H+ in the CSF. (hyperventilation)
o Primary ventilatory drive
Peripheral Chemoreceptors are:
o Found on carotid and aortic bodies
o Respond primarily to plasma [H+] and PO2 (and to a lesser extent to PCO2)
o Cause reflex stimulation of ventilation following significant fall in arterial PO2 or a rise in [H+]
o Respond to arterial PO2 not oxygen content
o Increased [H+] usually accompanies a rise in arterial PCO2
o Secondary ventilatory drive
Chronic Lung disease
- Most people rely on CO2 levels for stimulation of ventilation
- But, in chronic lung PCO2 is chronically elevated.
- Individuals become desensitised to PCo2 and instead rely on changes in PO2 to stimulate ventilation.
- Hypoxic drive- driven by a fall in O2 which are detected by our peripheral chemoreceptors.
Knowing now the role of peripheral chemoreceptors, Explain how the peripheral chemoreceptors become important during hypoxia and acid-base imbalance.
- If plasma pH decreases then [H+] increases and then ventilation will be stimulated , blows off CO2 thus lowering H
(acidosis) - if plasma pH increases then [H+] decreases ventilation will be inhibited by retaining CO2 thus increasing H
e. g. vomiting (alkalosis),
The respiration rate in an anaemic patient with a blood oxygen content half the normal value will ?
will stay the same because the partial pressure of CO2 hasn’t changed. There is no problem with ventilation or diffusion. The amount of O2 dissolved in solution is normal. The problem is we don’t have enough RBC to carry oxygen.
Other aspects of control of breathing
- Descending neural pathways from cerebral cortex to the respiratory motor neurons allow for a large degree of voluntary control over breathing.
- Cannot over ride involuntary stimuli such as arterial PCO2 or [H+]
- Breath holding
- Hyper-ventilation- ventilation is reflexly inhibited by an increase in arterial PO2 or a decrease in arterial PCO2/H+
Excess CO2 in our bodies
Example:
- Chamber one-Normal PO2, high PCO2: Chamber two- Low PO2, no PCO2
o Our bodies are programmed to get rid of CO2 and if we are unable to we experience extreme distress.
o Breathing in CO2 increase PACO2 and thus impairs the partial pressure gradient that would usually remove CO2 from the pulmonary artery.
o So CO2 remains in the blood and therefore the partial pressure gradient at the periphery that pulls CO2 out of cells is also lost, causing CO2 to build up in cells.
Respiration in consuming food
- Inhibiting during swallowing to avoid aspiration of food or fluid into the airways. When you finish swallowing you give out an expiration to push out any particles that are dislodged outwards from the region of the glottis.
