0901- Control of breathing- CG

Question 1

Outline the central organisation of breathing

Answer 1

Arterial CO2 controls respiration rate, but this relationship can be changed in metabolic acidosis (increased ventilation even if paCO2 low), or sleep, COPD, drugs and anaesthetics (ventilation doesn’t change as much in response to increases in PaCO2)

Question 2

Where and how CO2, O2 and pH are sensed and how these regulate respiration

Answer 2

Chemoreceptors – Central (most important for control- located behind the BBB. H+ and HCO3 doesn’t penetrate BBB, only CO2 does) High CO2 (receptors sense local H+) = increased ventilation Sensitivity reduced by sleep, old age, athletes, divers, morphine, barbiturates Mechanism CSF more acidic than blood = higher [CO2] in CSF Metabolic acidosis (↑H) - indirectly increase blood CO2 , hence decrease CO2 diffusion into CSF (preventing it from activating central chemoreceptor) – Peripheral (less important, takes over if chronic high CO2- high altitude, COPD [develop a tolerance to CO2 due to increased HCO3- in CSF) Normal CO2 = kicks in when O2 is seriously low) low O2= increased ventilation, Mechanism Glomus cells in carotid body- increase respiration if low O2 and H+ (via CN IX) In COPD- only way of controlling respiration due to central tolerance. If O2 given to COPD patient: no more ventilatory drive H+ (ketoacidosis)- stimulates ventilation when pH drops, difficult to separate from PaCO2

Question 3

Name and describe the 3 different tracheobronchial receptors

Answer 3

f

Question 4

describe how the respiratory CPG works (central pattern generator)

Answer 4

Important for controlling breathing reflex- output (ie muscle tone) maintained during sleep (reduced tone = snoring) Both skeletal and blood vessels involved- both CNS and ANS - CNS- cranial, spinal nerves (ie tongue [XII], larynx[X]- all involved in breathing) - ANS- PNS (vagal), SNS (from spinal levels) Overridden by voluntary control (high centres)

Question 5

Describe the anatomical components of the breathing CPG

Answer 5

Location: Diffuse, distributed controller, set of nuclei with no central centre- spinal cord, brainstem (medulla), pons and other cortical/spinal areas (modulation) Medullary respiratory nuclei 2 groups- inspiratory (dorsal resp group, intermediate ventral resp group) and expiratory (rostral and caudal VRG- not activated during quiet breathing) They inhibit each other via inhibitory interneurons, and elements within the groups are linked to AB reflexes (CVS)

Question 6

What are the Effectors during breathing?- numerous, complex

Answer 6

Muscle groups recruited in order: 1. Innervation of upper airway muscles (nares, tongue, larynx/pharynx). 2. Diaphragm and muscles of the rib cage. 3. Opening of glottis ahead of decrease in tracheal pressure (inspiration): – if the two occur at the same time, flow↑ causes upper airway collapse (tongue & pharynx).

Question 7

Identify respiratory control during special circumstances (i.e. exercise, high altitude) and recognise some abnormalities in respiratory control.

Answer 7

Damage to neural elements result in specific ‘patterns’ At TV, inspiration uses muscle contraction; expiration passive (no phrenic activity). Vagal breathing: bradypnoe & large volumes. Patterns under pathological conditions ○ – Cheyne-Stokes: periods of apnoea followed by hyperventilation; seen at high altitude and during sleep, severe heart disease and brain damage. Mechanism ? (delay between peripheral and central chemoreceptors). ○ – Ataxic breathing: brain damage ○ – Apneustic breathing: after head trauma with damage to pons: inspiratory breathholds of many seconds followed by brief exhalations. ○ – Sleep apnoea: see other lectures.