Ventilation - the neural control of breathing Flashcards
location of the primary respiratory centre
‘Centres’ located in medulla oblongata and pons
• Collect sensory information about O2 and CO2 levels in blood
• Determines signal sent to respiratory muscles which leads to alveolar ventilation
• Four major sites responsible for the adjustment:
– Respiratory control centre (source of central pattern generator)
– Central chemoreceptors
– Peripheralchemoreceptors
– Pulmonary mechanoreceptors
where are the dorsal and ventral respiratory groups located and where does it receive sensory supply input from
nucleus tractus solitarius and organs of thorax and abdomen
what is the character of these neurones
• Neurons in this group emit repetitive bursts of inspiratory neuronal action potentials
• Cause of repetitive bursts not known
• Involves respiratory ramp for 2 seconds
followed by cessation for 3 seconds
• Ramp can be altered by
- Controlling rate of increased of ramp (heavy breathing, ramp increases rapidly so lungs fill rapidly)
– Controlling limiting point at which ramp suddenly stops (control rate of respiration)
Pneumotaxic & Apneustic Centres
Centres modulate, but are not essential for, normal respiratory output
Pneumotaxic centre
located dorsally in nucleus parabrachialis medialis of upper pons
- 1o effect is to control switch-off point of inspiratory ramp (so controls filling phase of lung cycle)
- Strong pneumotaxic signal - inspiration may last for less than 0.5 second while a weak pneumotaxic signal - inspiration may last for 5 or more seconds
• Ultimate goal of ventilation
to maintain proper levels of PO2, PCO2 & pH (H+)
Hypercapnia
(↑PCO2) and acidosis (↓pH) detected by central respiratory centre
Hypoxia
(↓PO2) detected by peripheral chemoreceptors in carotid and aortic bodies, also detects Hypercapnia (PCO2) and acidosis (pH)
Mechanism of Action of Central Chemoreceptors
- Chemosensitive area located bilaterally beneath ventral surface of the medulla
- Neurons very sensitive to H+ ions (may be only important direct stimulus)
- H+ ions do not cross blood brain barrier very well, however, CO2 crosses easily
• increases in blood PCO2 causes
PCO2 to increase in interstitial fluid of medulla and CSF
• CO2 combines with H2O to form H+ ions by action of carbonic anhydrase
The Carotid Body
• Bodies have multiple highly characteristic glandular-like cells (Glomus cells) that
synapse directly or indirectly with nerve endings
• Both sympathetic & parasympathetic NS innervate carotid body
• Senses decreased arterial PO2
– Low PO2, but normal PCO2 and pH
– increase in firing rate of carotid sinus nerve
– At normal values of PCO2 and pH a decrease of PO2 causes progressive increase in firing rate
• Can sense increases in arterial PCO2
– Results show graded icnreases in PCO2 at a fixed blood pH (7.45) and fixed PO2 (80mmHg), produced graded increases in firing rate of carotid sinus
• Can sense decreases in arterial pH (e.g. metabolic acidosis)
– Blood pH (7.25) and fixed PO2 (80mmHg), firing rate of carotid sinus nerve is greater over all PCO2 values
Respiratory system receives input from 2 other sources:
– Stretch and chemical/irritant receptors
– Higher CNS centres that control non-respiratory activity
• Slowly adapting pulmonary stretch receptors
– Hering-Breuer reflex (1868)
– Helps to prevent over-inflation of the lungs
– Stretch receptors located in muscular portions of walls of bronchi and bronchioles
– Send signals thro’ vagal nerves to DRG neurons when lungs overstretched
– Feedback response initiated that ‘switches off ‘ inspiratory ramp
– In humans reflex not activated until tidal volume es to about 3 times normal (i.e. 1.5L / breath)
Modulation of Respiratory Output
• Rapidly adapting pulmonary stretch (Irritant) receptors
– Epithelium of trachea, bronchi and bronchioles contains sensory nerve endings,
pulmonary irritant receptors
– Responsible for coughing and sneezing
Modulation of Respiratory Output
• C-fibre receptors (J Receptors)
– Receptors in alveoli and conducting airways close to capillaries
– Respond to chemical and mechanical stimuli
– Stimulated during conditions like pulmonary oedema, congestion, pneumonia, Also from endogenous chemicals such as histamine
– Induces apnea
Cough Reflex
- Nerve endings of vagus and/or visceral afferent fibres are activated by irritation of trachea or bronchi
- Action potentials travel to medulla and spinal cord respectively
three phases of the cough reflex
– Preparatory inspiration
– Compressive phase
• Glottis closed by vagal efferent activity
• Forced expiration against a closed glottis
• Pressure increases
– Expulsive phase
• Glottis suddenly opens and trapped air is expelled at high speed by contraction of internal intercostals and abdominal muscles
• Result is to dislodge mucous covering airways and carry irritant away to mouth
Higher Brain Centre Activity
Some cortical neurons send axons to respiratory centres in medulla
Some cortical premotor neurons send axons to motor neurons controlling respiratory muscles