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Archived Training Days

NET Training Day: Royal Free Hospital 07/02/18

In February we were welcomed to the Royal Free Hospital by Dr James Goldring. Many thanks to him for organising the day, and to everyone facilitating such interesting sessions.

Obesity and sleep disordered Breathing,

Dr Swapna Mandal began the day with an update on obesity. She reminded us that physiology is different in people with obesity. When load outweighs the capacity of the respiratory system, compensatory mechanisms kick in. However, in our severely obese patients neural drive is unable to respond and respiratory failure ensues. BMI has a measurable effect on lung volumes, expiratory flow and the work of breathing. No wonder these people feel breathless!

Not only do obese patients have an increased neural respiratory drive, but this is reduced on treatment with CPAP.

The true prevalence of OSA is unknown. Estimates are that 1/270 adults in US have OSA. Series have suggested that 30% of obese patients admitted to hospital have OSA.

Not all obese patients have the same risk profile. Compared to eucapnic obese counterpoints those with hypercapnoea are more likely to need ICU, more likely to die, and have an increased cost of care pre-diagnosis. Untreated OHS has a significant impact on mortality.

  • Nowbar, Sogol, et al. “Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome.” The American journal of medicine 116.1 (2004): 1-7.

Diagnosis involves sleep studies. Multi-channel PSG is the gold standard. Limited poly (resp flow, SpO2, thoraco-abdo movements, ECG) is commonly used. In some places only oximetry is available.

Important parameters are: pCO2 >6, BMI >30, pHTN, no evidence of other cause e.g. neuromuscular disease. >25% sleep time spent with pCO2 >6.65 (use transcutaneous CO2). Oximetry trace can be suggestive – prolonged periods of hypoventilation suggest OHS.

ABGs can be tricky to access in outpatients. Can we rely on serum HCO3? Are there surrogates to streamline who to do ABGs on? Dr Mandel suggests:

  • Men: FVC <3.5L SpO2 <95%
  • Women FVC <2.3L SpO2 <93%

If oximetry only is available, then the % <90% sats is predictive of who may be hypercapnoeic. Cut off is 30%. Consider ABG and/or limited PSG.

Treatment options are CPAP vs NIV. The battle continues on which is most appropriate. Obesity is the most common reason for starting NIV.

How does NIV work?
– Pressure support – more PS = higher Vt
– Back up rate = higher RR
– EPAP – flushes out physiological dead space, increases alveolar recruitment, reduces threshold load.
– Oxygen if required

Studies to date have mainly looked at short term outcomes. The Pickwick study will investigate mid and longterm efficacy, and aim to tease out phenotypes in OHS. It is still recruiting. It is a large european study. AHI >30 vs <30.  Initial findings at 2/12 NIV and CPAP > control but no difference between NIV and CPAP groups. We will need to wait and see the longer term effects and outcomes. As in previous studies, it appears compliance is key.

ST – Spontaneous/Timed mode —> set EPAP/IPAP parameters
AVAPS – Average Volume Assured Pressure Support —> set target Vt
iVAPS – Intelligent Volume Assured Pressure Support

AVAPS/iVAPS is potentially a more efficient way to manage hypercapnoeic respiratory failure as there is quicker improvement in pCO2 and GCS and theoretically a shorter LOS – this is yet to be proved.

Acetazolamide for COPD or OHS? If cannot tolerate CPAP/NIV then there is limited evidence for this treatment. However, the conclusion of the Cochrane review was “Acetazolamide can produce a small increase in arterial PO2 and fall in PCO2. These conclusions are drawn from a few small short studies that were not all of high quality. It is not known whether this physiological improvement is associated with clinical benefit.”

Bariatric surgery should be considered. It forms part of the NICE guidelines. Surgery leads to improvements in metabolic state, PFTs, and polycythaemia.

This pilot RCT of NIV in addition to rehab vs NIV alone showed more weight loss, increased exercise capacity,improved breathlessness, and improved hypertension. Think holistically.

Sleep disordered breathing in COPD

Dr Patrick Murphy talked more about patients with COPD and hypercapnoea, both those with stable disease and post exacerbation, with an update from the HOT-HMV trial.

The basic problem is increased respiratory load vs reduced neural respiratory drive & reduced muscle capacity. This imbalance leads to alveolar hypoventilation. It is important to remember that the normal effects of sleep are a respiratory insult! There are changes in the upper airways, respiratory pattern, respiratory muscle function, and chemical control of breathing. Remember that the phases of sleep are relevant. In REM sleep all muscles are paralysed except the diaphragm.

50% of patients on LTOT may have significant hypoxia overnight. Resting sats are not a helpful marker for nocturnal sats. Those with hypercapnoea are the ones most likely to have significant nocturnal hypoventilation/ low sats.

Stable hypercapnoeic COPD
The EuroVent study showed huge variation across Europe in the provision of domiciliary NIV for COPD. If you are in Italy you are much more likely to get NIV for COPD than in Poland or Denmark. Shapiro published the first big study into NIV in COPD in 1992 in the Lancet. 184 patients received negative pressure ventilation titrated to diaphragm EMG vs sham. NIV in this group was poorly tolerated. This is perhpas not surprising as the mode of ventilation was the Poncho wrap!! Find some great images on the history of ventilators on the American Association for Respiratory Care’s Virtual Museum.

Then came positive pressure ventilation – NIV for COPD.

When at first you don’t succeed, do another study. When you still don’t succeed do another bigger study. When you still don’t succeed do a meta-analysis!

Why were these studies unsuccessful? Does NIV really not work? Looking closer at the details of the trials provides some answers. The German study took a high intensity approach. The aim was to meet either: 20% reduction in pCO2, or <6.5kPa pCO2. This trial achieved a reduction in pCO2 within 14 days and showed improved HRQoL (SGRQ, SF36), lower all cause mortality 21% over 12 months. Benefit occurred within 90 days. NNT = 5 with home NIV to save 1 life over 12 months. That’s a pretty great NNT! As a comparator, for PCI the NNT = 40. It is important to consider the limitations of this study. These patients had preserved exercise capacity – so is this evidence applicable to other hyercapnoeic COPD patients? What about frequent exacerbators? Patient phenotyping is key.

Domiciliary NIV following acute NIV
1/5 admissions in medicine are for COPD. 25% have respiratory failure and 13% receive NIV. There is a 33% readmission at 90 days (data from BTS audit). There is a huge undisputed evidence base for acute NIV for decompensated hypercapnoeic respiratory failure. This is best practice, and the gold standard. There is a reduced mortality with an  NNT=8. There has been a growing use of NIV – 8% admissions now. This is huge numbers of patients. However these patients have poor outcomes after discharge. In the first 3 – 12/12 there is a 30% mortality (depending on cohort).

RESCUE trial (Struik et al 2014)  assessed the impact of home NIV following an acute exacerbation of COPD. IPAP median 19 EPAP 5 RR 15. No 1yr benefit, no longer term benefit (admission free survival). Why did this study have a negative outcome? There was no clinically significant reduction in pCO2 (even if statistically significant). In the standard care arm patients mostly recovered pCO2 -therefore they were not chronically hypercapnoeic. Again, patient phenotyping is key. Persistent respiratory failure = worse prognosis. Transient respiratory failure has much better outcomes whatever treatment is given.

HOT-HMV (JAMA 2017 Murphy, Rehal, Arbane et al.) RCT of NIV after acute hypercapnoeic exacerbation of COPD. At 2 wks if persistent hypercapnoea pCO2 >7 randomise to LTOT or LTOT and home NIV. Aggressive titration. Primary outcome = admission free survival. HOT-HMV took a long time to recruit – most common reason to not include was that at 2/52 pCO2 <7 – patients had recovered. The study population had severe COPD (FEV1 0.6, MRC 5, pCO2 7.5). Median LTOT 1L. Median IPAP 24, median EPAP 4, median backup rate 14.

Outcomes: NIV controlled nocturnal hypoventilation (tcCO2) – so there was effective ventilation. There was an improvement in gas exchange – within 3/12.  Patients in HOT arm switched to HOT-HMV arm if met criteria later (i.e. recurrent exacerbations, later pCO2 rise) – so some attenuation of effect as intention to treat analysis. HOT-HMV increased time to readmission or death by 90 days, reduced likelihood of readmission or death by 50%. Early effect on QoL within first 6/52. Over 12/12 some attenuation. But importantly there was no evidence of worsening QoL. Interestingly most deaths in this severe COPD group were Respiratory (rather than CV in COPD patients overall). There was 1 fewer exacerbation per patient per year for patients on HMV.

In the per-protocol analysis there were enhanced physiological outcomes including pCO2. Adjusted HR 0.41 for admission free survival. There was a statistically significant reduced mortality in HMV arm (trend only in ITT analysis).There were 2 fewer exacerbations per patient per year in per-protocol analysis. There was no evidence of favourable baseline predictors of mortality in compliers – similar at baseline. Health economic analysis: £756 more expensive per patient to deliver HMV. Cost per QALY £15k. Cost-effectiveness analysis: probability intervention more expensive and more effective 46.9%. Probability that is was more effective and less expensive 30%.

So what have we learned?

  • Patient selection is essential – phenotype is everything.
  • The ventilation strategy is vital.
  • When employed in the right way in the right patients domiciliary NIV in COPD delays time to readmission, reduces exacerbations, and possibly reduces cost.

There has been some reluctance to ventilate at high pressures due to concerns about tolerance. Dreher (2010, 2011) showed good tolerance of high intensity ventilation, and that it does not lead to deterioration in sleep quality (which had been cited as a concern). Patients use the ventilator more if ventilate at higher pressures – they feel better, and so are more likely to use ventilator. There has also been a debate over high backup rates vs high pressures. Dr Murphy believes it is probably not as important as improving pCO2 – whatever method works.

Assessment of patients who have had acute NIV at 2-4wk is now part of the German guidelines, and coming to Swiss guidelines. It will not be included in NICE recommendations as the study was published after the guideline consultation came out.

COPD-OSA overlap
This is very common, and getting more common. This is a combination of the 2 most prevalent respiratory conditions, with some shared risk factors. COPD has a  huge burden of nocturnal symptoms with a significant impact on QoL. Evidence suggests thats is not impacted by PR or bronchodilators. We don’t ask about sleep enough. With OSA there is an increased risk of exacerbations. Treatment with CPAP reduces exacerbation frequency in observational studies, but there has been no RCT.

There is also a mortality benefit, but this is dependant on actually using CPAP! Compliance is a very significant issue.

Why do so many COPD patients decline CPAP? The application of extrinsic PEEP can worsen hyperinflation, and lead to poor sleep quality. This is associated with higher breathlessness during wakefulness. More breathlessness on CPAP leads to worse compliance. One contributor may be the use of autoCPAP in many sleep services. The algorithms used by these machines are not validated for COPD patients and can lead to inappropriately high pressures as they try to overcome flow limitation due to COPD airflow limitation (not upper airway). They therefore may be over-titrating. Novel modes using non flow-based algorithms may be better and lead to enhanced compliance and therefore better outcomes for these patients.

Paddy is now the Journal Club editor for Thorax. Email him and contribute to “What’s hot that the other lot got?”

Ventilation in Neuromuscular disease

Professor Anita Simonds, from the Royal Brompton Hospital, talked to us about goal setting in NIV in NMD and encouraged us to be clear about what is trying to be achieved.

– extend survival
– improve QoL
– treat acute exacerbation (reduce freq?)
– relief of dyspnoea
– control symptoms e.g. sleep disordered breathing, headaches
– impact on chest wall (?pulmonary) development in paediatric population
– improve concurrent resp/cardiac symptoms e.g. COPD, heart failure
– allow effective treatment if other symptoms eg opiates for patin without worsening resp failure, CO2 narcosis or over sedation – palliative setting
– buy time to resolve affairs, say goodbye
– provide individual with sense of control/ autonomy over end stage disease – can choose to start it, can choose to discontinue it
– ceiling of care in do-not-intubate patients
– intermediate step before tracheotomy ventilation

There are many issues to consider when deciding on timing of NIV initiation in MND. Recommendations primarily come from consensus statements.

RCT of initiation of NIV at time of development of nocturnal hypoventailtion in NMD (hypercapnia at night, normal gases in the day)

In this study there was a significant reduction in time tcCO2 >6.5 and increased mean SpO2 in the NIV group. Those who develop nocturnal hypoventilation at night soon develop daytime hypercapnia (i.e. in control group symptomatic, often need NIV anyway) – can plan ahead and start at appropriate planned time.

There has been a significant growth in paediatric patients transitioning to adult care (with NM disease and needing NIV). In the Brompton cohort 40% paediatric NIV patients transition to adult care.

NICE guideline 2010 updated 2016. Recommends initiation of NIV if SpO2 <92% if lung disease, <94% if no lung disease. If pCO2 >6 this is a  major warning, that the patient may be close to ventilatory failure – must refer for NIV assessment.
FVC is useful but may fall late. SNIP very useful as more linear decline than FVC.

In an RCT of  NIV in MND there was a survival advantage of 7 months. There was a greater survival advantage for those with mild-mod bulbar disease, rather than severe bulbar involvement. There was improved QoL mainly for those with mild-mod not severe bulbar involvement.

Symptoms are different in lower motor neurone bulbar group vs pseudo bulbar group. Cough assist devices can be very helpful.

Indications for tracheostomy in progressive NM disease:

– bulbar dysfunction, aspiration pneumonia
– failure to wean onto NIV following acute decompensation
– combination 24hr ventilator dependance and reduced bulbar function
– vocal cord dysfunction/ upper airway problems/choking episodes
– patient preference

Advantages of trache: more secure interface, face free from interface, may be easier to manage 24hr ventilation, access to power airways for suctioning, necessary if secretions/aspiration, speaking valves usually allow speech and swallowing
Disadvantages of trache: may circumvent pulmonary defence mechanisms, may generate sputum, risk of sputum plugging, dislodgement, greater expertise required, can impede phonation, can result in trauma, granuloma, stenosis and haemorrhage.
Few trials of NIV vs tracheostomy.

Trache and NIV are not directly comparable. They are often used at different stages of disease. Individual decision making is necessary – advantages and disadvantages may be weighed differently by different patients. Consideration must be given to the practicalities of the care package required, family support, location of care.

Is palliative NIV recommended/justifiable? The benefit from palliative NIV should be assessed by time based symptom control, not by ABG. Patients do not fail NIV, NIV fails patients for a number of reasons. Advanced care planning is key. Decisions evolve over time.

Useful resources:

Cough Augmentation Techniques explained

Stephanie Mansell, Consultant Physiotherapist shared with us her love of phlegm! She loves getting phlegm out of people’s lungs.

Cough physiology
The cough: irritation, inspiration, compression (closed glottis), expulsion!
NMD respiratory assessment: inspiratory phase, glottis closure, expiratory phase.

– Inspiratory phase problem: Spirometry, SNIP
– Glottis closure problem: staccato expiration from max insp capacity e-e-e-e-e
– Expiratory phase problem: Peak cough flow (PCF) – if >270L/min not too concerned, able to clear phlegm. 160-270 likely to need some help, <160L/min ineffective cough.

Maximum insufflation capacity techniques
Breath stacking – need good glottic control. Most people can get 3, some 5. Example video. 
Glossopharyngeal breathing (frog breathing) – used a lot in 1970/80s. Example video: ‘pharyngeal breathing in MDA.
Lung Volume recruitment bag – £23. Includes 1 way valve. Useful for bulbar involvement. Augment breath stacking. Much cheaper than cough assist.

Manually assisted cough – requires patient to co-operate with you for timing. Like an abdominal thrust / Heimlich. Physios can get wrist injuries – watch out! Also useful in ICU patients – no cough at all.
Mechanical insufflation exsufflation (MI:E). Previously called cough assist – old machines only.

The MI:E increases peak cough flow
and reduces need for intubation and minitrachs in NMD patients with acute infection.  It also reduces treatment time (when treatment time exceeds 30min). Physios are resource stretched. There is a campaign from charity for all hospitals to have MI:Es.

Relative contraindication is bulbar involvement- due to variable response to pressure. Requires experience and individualised approach. Not indicated for COPD patients – can increase hyperinflation.

Sleep beyond breathing

Dr Brian Kent from Guys and St Thomas’ Hospital refreshed our memories on a typical hypnogram of an adult. There are 4 stages of sleep – 3 NREM 1 REM. We spend most of first 1/3 night in slow wave sleep. As the night goes on, we spend less time in slow wave sleep, more time in REM sleep. N1 5%, N2 light sleep 45-55%, N3 slow wave sleep 20-25% (decreases with age), REM sleep 20-25%. These proportions change with age. N3 is probably the most important – important physiologically. Deprivation of N2 sleep causes major problems. Deprivation of REM sleep does not appear to be a real problem. On antidepressants people have very little REM sleep but few problems. What is REM sleep for? This is unclear.

Wakeful chemicals – monoamines. NA, serotonin, dopamine. ACh-R —> nocturne keeps you awake.
Sleep chemicals – GABA neurones in the ventrolateral preorbital nucleus. Negative feedback to wakefulness centres. Benzos are GABA-A antagonists – interact with this pathway.

Orexin, and hypocretin 1 are important for stabilising wake and sleep.

ACh is very active during wakefulness and REM sleep. Monoamines are active during wakefulness, less in NREM sleep, absent in REM sleep. Orexin is very active in wakefulness, not in any type of sleep.

Hypersomnias: Central

– Narcolepsy
– Idiopathic hypersomnia
– Kleine-Levin syndrome

Hypersomnias: Secondary

– sleep disrupting pathology
– sleep restriction
– drugs – obvious e.g. valium. But also high dose gabapentin, opiates etc Some antidepressants interrupt sleep.
– depression – mental health has a massive effect on daytime function, but also effect on sleep, and ability to stay awake in the day

In Narcolepsy there is a breakdown between wake and sleep, as well as NREM and REM sleep. The main symptoms are: excessive daytime sleepiness, hypnogogic hallucinations, sleep paralysis, cataplexy. Cataplexy is usually segmental – patients are usual able to protect themselves and get to the ground/safely fall. Less dramatic than examples seen on TV! There are many examples online.
Differentiating cataplexy vs pseudocataplexy is tricky!

Narcolepsy incidence is 1/2000 in UK – variable dependant on ethnicity. Unheard of in Ashkenazi Jews. Very common in Japanese people. It is substantially under-diagnosed. There is a bimodal peak of onset – mid teens and mid 30s. Orexin is key in narcolepsy. Orexin stops people going into REM sleep. Lack of Orexin means patients are unable to stop going into REM sleep. Inappropriate activation of spinal interneurones- lose tone in muscles, cataplexy. Orexin is also very key in stabilising histamine signally in the hypothalamus. Sleepiness.
Genetic factors are relevant. Is is usually sporadic. HLA-DQB1*0602. Only 25% twin concordance. It is thought to be an autoimmune disorder. T cell receptor polymorphisms. Antibodies to Trib2. Worry about secondary narclopsy in those who develop symptoms in later age. Associated with brain damage.

Diagnosis:  Type 1, classic. Sleepiness. Diagnostic MST and cataplexy OR CSF hypocretin <110ng/L

Diagnosis: Type 2. Sleepiness, plus diagnostic MSLT. ? is this really narcolepsy or something else.

NPSG, MSLT, HLA typing (not that helpful), CSF hypocretin (only if diagnosis unclear)
MSLT: 4 nap opportunities, approx 2hrs apart. Sleep latency recorded. 20mins sleep recorded. Normal: sleep latency >10mins. No REM sleep. Narcolepsy: sleep latency <5mins, sleep-onset REM in 2 of 4 naps. Limitations: procedural issues, 5.9% males and 1.1% females have positive MSLT in cohort of 556 subjects. 15% of BIISS (behaviourally induced insufficient sleep syndrome) have positive MSLT. Cannot interpret in isolation. Impact of positive predictive value. 70x more likely to diagnose BIISS than narcolepsy.

Can be caught out by people’s terrible sleep patterns. Actigraphy is useful in this context. All tests are data points, which need to put alongside history and overall assessment.

For daytime sleepiness – stimulants (modafinil 1st line, amphetamines e.g. Ritalin. If they don’t work then give people actual speed = dexamphetamine), sodium oxybate, pitolisat. For cataplexy – antidepressants (clomipramine), sodium oxybate

RCT of modafinil as a treatment for the excessive daytime somnolence of narcolepsy. Common side effects are nausea and headache. Worrying are palpitations, breathlessness, and chest pain.

Sleep-stage sequencing of sleep-onset REM in periods in MSLT predicts treatment response in patients with narcolepsy. Modafinil nearly complete response in 45%. Methylphenidate 35%, dexamphetamine 15%. Quite a high proportion of treatment failure. 55% treatment failure in dexamphetamine.

Sodium oxybate is GHB, a Class II controlled drug. It binds to GABA-B – makes people sleep. Also inhibits REM. Suppresses cataplexy.

This is a systematic review and meta-analysis of 2 trials! The newest drug is a H3 inverse agonist, Pitolisant. It potentiates effects of histamine and has equivalence of response with modafinil. Negotiations are ongoing with the drug company on cost.

Idiopathic insomnia is excessive daytime sleepiness, with no other explanation. It is uncommon, and not easy to treat. If you think it’s idiopathic hypersomnia it probably isn’t, so get the patient a psychiatric assessment.

Diagnosis is based on history, and video PSG (mainly used to exclude other disorders). The parasomnias are a family of disorders in which people are doing or experience things during sleep that they don’t want to happen.

The Nightmare, Henry Fuseli, 1781

NREM parasomnias
Sleep walking
Night terrors
Sleep related eating disorder
Confusional arousals

REM sleep parasomnias
REM sleep behavioural disorder
Sleep paralysis

NREM parasomnias are common in children (up to 20%) and rarer in adults (4%). 85% of adult sleep walkers had childhood somnambulism. There is a significant genetic predisposition. NREM parasomnias occur during Slow wave sleep. They are often triggered by stress, sleep deprivation, Alcohol, or sleeping tablets. They occur with sporadic frequency, and are not very predictable. They are usually in the first half of the night. People are capable of complex behaviours whilst asleep and have little or no recollection of events. During night terrors people can interact with their environment. They may be inconsolable.

Treatment: trigger avoidance, harm avoidance, stress reduction, clonazepam/BZDs, melatonin, antidepressants, CPAP. Evidence for drugs is poor. Clonazepam usually first line.

REM parasomnias include REM sleep behavioural disorder in which there is a loss of brainstem mechanisms mediating tone in REM sleep demonstrated on PSG. Typically people have no recollection but may recall dreams. Often violent, repetitive dreams. Kicking, punching, swearing are common. Injuries may occur (to themselves or their bed partner). People have their eyes closed, and rarely get out of bed. They occur predominantly in the second half of sleep. Men>Female.
RBD is associated with neurodegenerative disorders including parkinsons, DLB, MSA. In one large series, over the course of 15yrs 95% of those with ‘idiopathic RBD’ developed neurodegenerative disease.

Other associations: narcolepsy, drugs, restless legs.

Nocturnal frontal lobe epilepsy is a very important differential for parasomnias. It can occur throughout the night, there may be multiple episodes, and it is often proceeded by stereotyped motor patterns.

Restless legs is common, and causes a lot of distress. International Restless legs Syndrome Study Group suggest that it affects 2-15% population and 25% pregnant women. It is mainly idiopathic. Always check for Fe deficiency, CKD, peripheral neuropathy.
1st line drug treatment is ropinirole 0.25-4mg ON. Alternative is pramipexole. Can cause impulsive disorder as it is a dopamine agonist. Can cause augmentation – symptoms in the day. Alternatives – gabapentin or pregabalin, Clonazepam, Opiates.

Come and do a visit. Come and do a fellowship for post-CCT fellowship.

Sleep reporting workshop

Dr Swapna Mandel gave a masterclass in sleep study reporting.
We reviewed limited cardiorespiratory polygraphies. The AASM manual for the scoring of sleep and associated events costs £100 as a book; and is cheaper online and if you are a member
Channels: nasal flow; thoraco-abdominal movement; Sats; HR; thermistor to measure snoring +/- sound +/- pressure.

An event may be a:
Apnoea: 90% reduction in flow/thermister, lasting 10sec. Does not have to have desaturation following it.
Hypopnea: >30% fall in nasal flow for at least 10sec, in association with desaturation (3-4%)

Is the event central or obstructive?
Obstructive: Ongoing thorax-abdominal movement, snoring
Central: flat line, no movement
Can get mixed events.

TcCO2 = pCO2 >6.65 for more than 10min

More info on current rules for scoring sleep studies available from AASM. 

The afternoon ended with some excellent NIV simulation stations and sleep reporting workshops. Thanks to James and Nirav for making these interactive!


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