control of breathing Flashcards
sleep: explain the effect of sleep on breathing and blood gases; explain the apnoeic threshold and how this may lead to central sleep apnoea; explain the influences of sleep on the upper airway and how this may lead to obstructive sleep apnoea; explain how cardiorespiratory disease may be exacerbated by changes in breathing control during sleep
respiratory centre input
reflex/automatic brainstem only (not voluntary behavioural motor cortex or emotional limbic system, which are only when awake);uses bulbospinal pathway from respiratory neurones of medulla
what is the PreBotzinger complex
network of cells (not pacemaker) in medulla brainstem which reciprocally inhibit each other to generate rhythm; close to surface of medulla to detect pH in CSF based on CO2 levels
change in minute ventilation and SaO2
breathing becomes more shallower in sleep but at same rate (hypoventilation); minute ventilation decreases (lower tidal volume); SaO2 decreases very slightly but barely changes as on flat of oxygen-dissociation curve
changes in PaO2 with sleep
PaO2 reduces but saturation stays high (oxygen saturation curve); if lower PaO2 when awake, much lower saturarion when asleep (as curve)
changes in PaCO2 with sleep
PaCO2 increases slightly when asleep as tidal volume decreases; if it doesn’t you won’t breathe as no change in pH detected
hypercapnia: ventilatory sensitivity to CO2
when asleep less sensitive to CO2 hence bigger increase in PaCO2 when asleep to breathe
apnoeic sleep threshold and central sleep apnoea
PaCO2 threshold at which you don’t breathe by reducing tidal volume - must exceed to stimulate breathing; central sleep apnoea is the failure of tidal volume to decrease due to issue in medulla or muscles controlled by medulla (stroke or central congenital hypoventilation syndrome), so no effort made to breathe
obstructive sleep apnoea
upper airway above trachea (no cartilage) becomes obstructed when asleep (obesity, size of jaw), so effort to breathe but ineffective (thorax and abdomen still work when airflow ceases)
causes of occlusion of phalangeal airway in obstructive sleep apnoea
reduced upper airway muscle activity as loses tone and becomes floppy; negative intra-luminal pressure during inhalation can force shut rather than allow air to enter - exacerbated by excess adipose tissue in tongue and neck as applies external positive pressure
obstructive sleep apnoea cycle
effort to breathe against closed airway → arousal → increased ventilation → sleep restarts → decreased accessory muscle function leads to hypercapnia and return of apnoea; can lose emotional intelligence due to being very tired as no deep sleep
how is COPD exacerbated by sleep
further left on SaO2 curve so less SaO2 (accessory muscles paralysed so worse)
effect of heart failure on central sleep apnoea
causes pulmonary congestion, which irritates receptors, causing hyperventilation; this lower PaCO2 below apnoeic threshold, causing cessation of breathing due to central sleep apnoea