27. Respiratory Failure and Sleep Apnoea Flashcards
Define hypoxia (numerically). What could cause it?
What are the 3 main functions of the lungs?
Briefly describe ventilation.
How is ventilation controlled?
PaO2 <8.0 kPa. Altitude, pathological (tumour etc.), damage e.g. smoke damaging alveoli, pneumonia/fibrosis damaging alveolar wall.
Ventilation. Gas exchange. Lung perfusion.
Inspiration: intercostal rib and diaphragm muscles contract, pressure in chest < outside, air sucked into lungs.
Expiration: intercostal rib and diaphragm muscles relax, elastic recoil of lungs forces them to contract, pressure in chest > outside, air pushed out of lungs.
Stimulation of breathing centre in brain (medulla) -> controls rate and depth of breathing -> blood O2 and CO2 levels monitored and fb sent to medulla.
What can go wrong in gas exchange (5 things)?
What are the following causes of hypoxia in the 4 pathology images (from your answers to the question above).
Failure of overall ventilation - hypoventilation (less air reaches alveoli e.g. hyperinflation, kyphoscoliosis). Failure of GE (diffusion). V/Q mismatch (areas of lungs don’t reveive both their blood supply and ventilated air). R -> L cardiac shunt. Low inspired O2.
Kyphoscoliosis - hypoventilation
Lobar pneumonia - V/Q mismatch
Asthma - hypoventilation
Sarcoidosis - diffusion abnormality
What are the following causes of hypoxia in the 4 pathology images (from the 5 things that can go wrong in GE)?
Thoracoplasty for TB - hypoventilation
Lobar collapse - V/Q mismatch
High altitude - low inspired O2
Pulmonary emboli - V/Q mismatch
What are the following causes of hypoxia in the 4 pathology images (from the 5 things that can go wrong in GE)?
Pulmonary fibrosis - diffusion abnormality
COPD - hypoventilation (L), diffusion abnormality (R)
MND and MD - hypoventilation
Air-flight - low inspired O2
What are the following causes of hypoxia in the 3 pathology images (from the 5 things that can go wrong in GE)?
Pneumothorax - V/Q mismatch
Morbid obesity - hypoventilation
Eisenmenger syndrome - R -> L shunt (congenital heart disease)
What are 4 causes of hypoventilation?
What is diffusion abnormality, and what can it be caused by?
What is V/Q mismatch (give reasons for both V and Q mismatch)?
1) Obstruction to airways - COPD, severe asthma
2) Hyper-expanded lungs - COPD
3) Thoracic cage problems - kyphoscoliosis and thoracoplasty, obesity
4) Weakness of respiratory muscles e.g. MND, muscular dystrophy
Ventilation normal but barrier to diffusion of O2 alveoli -> blood. Causes: fibrosis, sarcoidosis, asbestosis, emphysema (COPD) but also hypoventilation.
Area of lung perfused but not ventilating: lung airspaces filled with fluid (pneumonia, pulmonary oedema), lung collapse (pneumothorax, lung collapse)
OR
Area of lung ventilated but not perfusing: pulmonary emboli.
How does the consequences of hypoxia differ in:
a) diffusion abnormality
b) V/Q mismatch
c) hypoventilation
Describe type 1 respiratory failure. What are some causes?
a) Increased ventilation -> more CO2 exhaled -> hypoxic but not hypercapnic.
b) Increased ventilation -> more CO2 exhaled -> hypoxic but not hypercapnic.
c) Increased ventilation -> unable to increase ventilation -> hypoxic AND hypercapnic.
* HYPOVENTILATION ONLY MECHANISM OF HYPERCAPNIA.*
Hypoxia only - failure of oxygenation. PaO2 < 8.0 kPa, SaO2 about 90%. Increase in resp drive -> increase ventilation. PCO2 drops.
Causes: diffusion abnormality (pulm fibrosis, emphysema in COPD), V/Q mismatch: reduced V (pneumonia, pulm oedema, pneumothorax, lung collapse) OR reduced Q (PE), low inspired O2.
Describe type 2 respiratory failure. What are some causes?
How is type I acute respiratory failure treated?
Hypoxic and hypercapnic - failure of ventilation. PaO2 < 8.0 kPa, can’t increase ventilation. pCO2 rises to > 6.7 kPa. CO2 dissovles in blood -> carbonic acid. pH falls (<7.35) = acidosis.
Causes: obstruction to airways (COPD, asthma), hyper-expanded lungs (COPD), thoracic cage problems (kyphoscoliosis, thoracoplasty, obesity), weakness of respiratory muscles (MND, DMD).
Correct hypoxia with high flow O2, 60 - 100% O2 via mask, keep O2 sats >95%. Treat underlying cause (pneumonia/pulm oedema/pulm embolism/non-severe asthma), consider CPAP if continuing hypoxia.
What is CPAP?
How is type II acute and chronic respiratory failure treated?
Continuous +ve airway pressure, pushes pressure into airways mainly during expiration. Can expand collapsed portions of lungs which are under-ventilated. Improves V/Q matching and hypoxia. Keeps airways open in sleep apnoea. Doesn’t overcome hypoventilation. (pic)
Make sure don’t give too much O2: give enough so not hypoxic BUT not too much b/c may suppress resp drive - aim for sats 88-92%.
Acute type II: use controlled O2 therapy: 0.5 - 2L/min via nasal cannulae, 24-28% masks using venturi valves. Regular blood gases to monitor CO2. Consider NIV if pH and CO2 not improving. Acute NIV in acidotic type II COPD.
What is NIV?
What are some consequences of type I chronic respiratory failure?
What is the tx?
Delivers high pressure during inspiration to improve ventilation. Also improves hypoventilation and oxygenation. Prevents/reduces hypercapnia. Useful in all conditions causing hypoventilation and type II resp failure - both acute (in hosp for COPD exacerbations) and chronic (at home for kyphoscoliosis, NMD, obesity hypoventilation syndrome, COPD etc.) Need to make sure they don’t mouth breathe.
Pulm hypertension (hypoxia -> blood redirected to parts of lungs that get more O2 -> BV vasoconstrict), cor pulmonale (R HF), peripheral oedema, 2o polycythaemia - stroke, symptoms from ischaemic heart/peripheral vascular diseases, poor sleep, neuro-psychiatric, fatigue.
LTOT improves survival in COPD pts with hypoxia (PaO2 <7.3 kPa). Reduces complications of hypoxia: cor pulmonale, polycythaemia. Pts given O2 concentrator to deliver O2 for at least 15hrs/d.
Differentiate simply between causes of hypoxia vs hypercapnia.
What tx would you use for acidotic type II in COPD?
What is obstructive sleep apnoea?
What are the 2 types?
Hypoxia has many causes; hypercapnia is only a result of hypoventilation.
Acute NIV. (Chronic NIV in other causes of hypoventilation).
Repetitive episodes of partial or complete upper airway obstruction during sleep. Cessation of breathing for 10s, or normal breathing dropped by 90% or more for 10s during sleep. (<5 apnoeas/night = normal)
1) Obstructive: something closes upper airway completely obstructed, stop breathing but still try and breathe against it; abdo movement and chest movement in opposite directions
2) Central: no movement of chest wall or abdo muscles and cessation of breathing. Due to brain/CNS.
How do you diagnose sleep apnoea (what 3 things do you need to measure)?
What is the AHI?
Where is the problem in this picture of OSA?
What occupation must you check for in OSA?
1) Airflow (nasal cannula)
2) Abdo/chest movement (bands)
3) O2 levels (pulse ox)
Apnoea and Hypopnoea Index: number of apnoeas and hypopnoeas/hr of the study (equivalent to RDI (resp disturbance index). Measures OSA severity. 0-5 within normal. 5-15 mild. 15-30 moderate. 30+ severe. (Apnoea = complete cessation of airflow for at least 10s. Hypopnoea = reduction in airflow to <50% of by 30% for at least 10s with desat of at least 4%).
Soft palate compressed by tongue and fat.
HGVs. DVLA should be informed of dx by pt.
What are some predisposing factors for obstructive sleep apnoea?
What abnormal anatomy can be associated with sleep apnoea?
What systemic conditions can be associated with sleep apnoea?
What scale can be used to measure daytime sleepiness?
Obesity (narrows upper airway), neck circumference increases risk esp if >16.5 inches, male (longer pharyngeal airway), Afro-Caribbean x2 risk of Caucasians/Asians.
Abnormal anatomy: Micrognathia (undersized jaw). Tonsillar hypertrophy. Acromegaly (excess GH after growth plates closed. Initial symptom typically enlargement of hands and feet. May be enlargement of forehead, jaw, and nose). Down’s syndrome.
Hypothyroidism, Cushing’s. T2DM, HT.
Epworth Sleepiness Scale out of 24. >10 = abnormal.
What are some other medical consequences of OSA?
What are some tx for OSA?
What is used for pts with moderate or severe SA?
CDV mortality, systemic HT, insulin resistance and T2DM, coronary artery disease, stroke, CCF, pulmonary HT, cardiac arrhythmias e.g. AF. B/c e.g. if O2 levels decrease and HR increases during apnoea -> HT and arrhythmias -> coronary artery disease, stroke etc.
Wt loss, avoid alcohol and sedatives, non-supine sleep (on side instead), tonsillectomy, mandibular advancement splints (if jaw backset) (L pic), palatal surgery, maxillofacial surgery, tx medical cause e.g. Cushings.
CPAP (R pic) - reduces daytime sleepiness, RTAs, BP, CDV events. Improves cognitive performance, mood, QoL. Helps prevent pulm HT and R HF.
