Flashcards in 207 -Obstructive Sleep Apnoea Deck (25):
define obstructive sleep apnoea
the stopping or slowing of breathing during sleep due to closing of the upper airway. Sleep causes pharyngeal incompetence (muscles relax) causing a collapse of the upper airway. Incr. in PaCO2 causes the px to wake up causing broken sleep and daytime sleepiness.
what are the risk factors for OSA?
*Obesity/lower facial shape *tonsil/nasal problems
*hypothyroidism *alcohol/sedatives *smoking
*being male *ty II DM *snorers *40-60 y/o
how might a px with OSA present?
*Excessive daytime sleepiness - assess with Epworth Sleepiness scale
*partner notices px stop breathing at night
*morning headaches, dry throat, anxiety, poor concentration, irritability
*sweats, reduced libido
how would you investigate suspected OSA?
*overnight oximetry tracing - shows pattern of regular desaturation
*measure nasal flow
*measure throax/abdo movements
how would you manage a px with OSA?
*treat underlying disorder - hypothyroidism, bariatric surgery
*lifestyle changes - smoking, alcohol in eve, weight, posture
*ventilation - Continuous positive airway pressure (CPAP) - continuously blows column of air down airway
what can untreated OSA lead to?
*sleepiness at work/job problems
*relationship problems & sexual dysfunction
*risk of sudden death and cardiac problems
*commonest cause of 2ry hypertension
*poor diabetic control
what ABG changes would you see in a px with type I respiratory failure?
*PCO2 normal or low
*pH normal or alkalytic
*HCO3 normal or low
what ABG changes would you see in a px with type II respiratory failure?
*pH acidotic or normal
*HCO3 high or normal
what FEV1 and FVC changes would you see in a px with restrictive lung disease
both FEV1 and FVC reduced and ration between them normal or incr. as full expiration achieved rapidly
what ABG changes would you see in a px with respiratory acidosis and why?
caused by incr. in CO2 so incr. PaCO2, decr. pH & incr HCO3. Acute - slight incr. in HCO3 as more CO2 for dissociation. compensated - kidneys compensate over time gently incr. HCO3 retention
what ABG changes would you see in a px with respiratory alkalosis and why?
caused by decr. in CO2 so decr. PaCO2, incr. pH & decr HCO3. Acute - slight decr. in HCO3 as more CO2 eliminated. compensated - kidneys compensate over time gently decr. HCO3 retention
what ABG changes would you see in a px with metabolic acidosis and why?
caused by incr. in H+ due to incr. lactic acid production/decr. H+ elimination (renal failure) so normal/decr. PaCO2, decr. pH & decr HCO3. Acute - marked decr. in HCO3 as used to buffer acid. compensated - further decr. HCO3 due to hyperventilation
what ABG changes would you see in a px with metabolic alkalosis and why?
caused by decr. in H+ due to loss of H+(vomit gastric acid)/excess bicarbonate infusion so normal/decr. PaCO2, incr. pH & incr HCO3. Acute - marked incr. in HCO3 as no acid to conjugate. compensated - further incr. HCO3 due to hypoventilation
where does the automatic rhythm of breathing originate and what does it act upon?
the medulla oblongata (lowest segment of brainstem). Impulses are sent down the spinal cord to phrenic nerve & intercostals & via CN12 to the pharynx larynx. Compression of medulla causes respiratory depression
what 3 medullary regions are responsible for impulses driving respiration?
*Parafacial Respiratory Group (PFRG) - originate action potentials just before inspiration
*Dorsal Respiratory Group (DRG) - action potentials during inspiration (stimulate muscles of insp)
*Ventral Respiratory Group (VRG) - mostly action potentials during expiration
From where do the 3 medullary regions receive inputs from?
*chemoreceptors - via CN9/10 - monitor arterial blood gas/acid conc.
*higher CNS (cerebral cortex, hypothalamus) via Pontine Respiratory Group (PRG) in pons which fine tunes respiratory rhythm (sets vol when insp turns to exp)
what ventilatory rhythm pacemaker models are there?
*distributed network model
*multiple oscillator models
*single oscillator models
*couple oscillator model - insp rhythm originates in pre botzinger complex (PBC) and exp in PFRG
what is the group pacemaker hypothesis of signal generation?
*beginning of cycle - all neurones hyperpolarised
*recovery - some neurones recover and depolariseto cause Action potential
*recurrent excitation - AP stimulate other neurones to depolarise
*burst - incr. stimulation leads to all neurones to depolarise
what innervates the muscles of respiration
*phrenic nerve supplies diaphragm for C3/4/5
*intercostals supplied by respective thoracic segments
where in the brain does voluntary control originate?
from cerebral cortex via pyramidal tracts direct to effector muscles - voluntary control bypasses the medulla (Px can still breathe if medulla damaged)
reflexes can also modify resp rhythm via vagus (sneeze/cough in U/LRT, pulmonary stretch receptors, irritant receptors in epithelial cells, j-receptors in alveolar walls)
why is chemoreception important?
maintains PaO2 to maintian O2 supply to tissue
maintains PaCO2 to keep pH of tissues constant
how do chemoreceptors affect ventilation during exercise?
ventilation incr with work as chemoreceptors sense incr. in PaCO2 (due ro CO2 production in metabolism) to keep PaO2 and PaCO2 constant
which chemoreceptors sense CO2 and O2?
CO2 - both central and peripheral (main stimulus for breathing)
o2 - peripheral only (stimulates breathing when PaO2 <60mmHg)
where are central chemoreceptors located and what stimulates them?
*neurones on surface of ventro-lateral medulla (medullary raphe, retrotrapezoid)
*stimulated by [H+} in CSF that bathes medulla (indirectly determined by PaCO2 as CO2 diffuses from cerebral arteries to CSF and some [H+]blood - central more sensitive to resp acidosis than metabolic but slow acting due to diffusion