Portland sleep centre equipment upgrade

Both the Portland and Hamilton Sleep Disorders Centres reopen this coming week, after being closed during the Christmas and January period.

During this period Portland's diagnostic equipment has been upgraded to the E-series making it identical to the Hamilton equipment. This allows for greater clarity in signals, aiding in sleep staging and reporting. With staff at both locations now using the same equipment the ability to train staff will be enhanced and as will trouble shooting when necessary.

The Somte PSG's, that where previously used in Portland will now have the capacity to be used in ambulatory settings. During the last 12 months one unit was utilized for this purpose. It was based at Mount Gambier and sent to Horsham on a needs bases.

Referral forms for both in-laboratory and home sleep studies can be downloaded here.

The referrals forms also provide some guidance as to which patients are appropriate for a home based sleep study and which patients require an in-laboratory based study. It is important to note that in -laboratory studies are still the gold standard for the diagnosis of obstructive sleep apnoea and is an essential adjunct to the diagnosis of many other sleep disorders.

Jessica

Can you change your VO2 max?

For the last two weeks I have been in South Australia on holidays. While over there the state was a buzz because Lance Armstrong was in Adeliade for the tour down under. Everywhere we looked elite and recreational cyclists seemed to have taken over the streets and this was highlighted when the public where invited to join Lance on a community ride around Glenelg (he sent the invitation out through twitter). A staggering 7000 people joined him!

This got me thinking about information I had previously heard about Lance being super human producing extermly low lacate levels (hence not fatiguing as quickly) and having a high VO2 max.

It is reported that his VO2 max is 85 milliliters of oxygen per kilogram of body weight per minute. An average untrained person has a VO2 max of 45 and with training can get it to 60. Exercise physiologists have estimated that an untrained Lance Armstrong would have a VO2 max of 60, hence an average person trained level is his untrained.

So how do you change your Vo2 max? Training volume and training intensity are the key factors. Research has shown the biggest increases can be found in sedendary individuals as they have the most room to improve. Such cases have demonstrated an increase as high as 20%.

Factors other than genetics that influnce VO2 max are age (decrease 30% by the age of 60), gender (female valuse are normally 20% lower than males) and altitude. Altitude is interesting. As there is less oxygen at higher altitudes an athlete will generally have a 5% decrease in VO2 max with a 5000 feet gain in altitude. This is why many athletes undertake altitude training prior to competition.

Vo2 max alone will not predict the winner of an endurance event but most elite althletes will have a VO2 max over 60.

We offer cardiopulmonary testing to community members who are interested in having these results to help inform their training program. Who knows what your potential might be?

Jessica

VO2 max as an indicator for insulin resistance

The measure of VO2 max through cardiopulmonary exercise testing has many uses for both medical and exercise professionals. A quick search of recent studies involving VO2 max (maximal oxygen uptake) revealed many and varied studies. They ranged from the effect of habitual smoking on measured and predicted VO2 max, the relationship between velocity reached at VO2 max and time trial performance in elite Australian rules footballers, determinants of VO2 max decline with age and does respiratory muscle training increase physical performance?

The study that caught my eye was low cardiorespiratory fitness in people at risk for type 2 diabetes: early marker for insulin resistance. Researchers took a group with significant risk factors for type 2 diabetes but were yet to show signs of insulin resistance syndrome (IRS) and compared their cardiorespiratory fitness to a control group from the same area who were deemed to have less association with risk factors for type 2 diabetes. Both groups were matched for sedentary nature, age, gender and BMI. The study showed individuals at risk for IRS and T2DM had a VO2max (22 +/- 6 ml/kg/min) 15% lower than the control group VO2max (26 +/- 9 ml/kg/min) (p <>

An interesting study since the study matched groups for sedentary nature, age, gender and BMI. Gender excluded these are all shown to be some of the highest risk factors for T2DM along with family history, diet, hypertension, gestational diabetes, race and as previously blogged obstructive sleep apnoea.

Jessica

MIP and MEP

Recently a patient was referred to the lab for the above test who presented with a cluster of disabling signs and symptoms who had previously contracted poliomyelitis. Post Polio Syndrome although rarely life threatening can result in under ventilation if the patient has untreated respiratory muscle weakness and aspiration pneumonia from a weakness in the muscles controlling swallowing.
Maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) are measurements that may aid in evaluating respiratory muscle weakness. Measurement of MIPS/MEPS are the most widely used test to assess muscle pressure as it has no adverse effects and is non invasive.
Healthy adults can generate a MIP of greater than -60cmH2O and MEP of greater than 80cmH2O (both pressures tend to be higher in males and decline with age). Pressures lower than these may indicate neuromuscular disease affecting the muscles of respiration. However, other disorders may reduce the pressures by placing the respiratory muscles at a mechanical disadvantage. For example, the pressures may be reduced if there is chest wall deformity. MIP may be reduced by hyperinflation/gas trapping which flattens the diaphragm and places the intercostal muscles at a disadvantage. MEP may also be reduced in severe lung diseases. A MEP of less than 40cmH2O leads to an ineffective cough.
Several studies have demonstrated that MIP and MEP may be very useful in the diagnosis and follow-up of pulmonary and cardiac disease. A reduction in MIP has been shown to be associated with a progressive clinical worsening in patients affected by myasthenia gravis or Guillain-Barré syndrome. In addition it has been suggested that an imbalance between the pressure generated by the inspiratory muscles and the MIP may lead to the development of hypercapnia in patients with COPD. Indeed both MIP and MEP have been shown to be useful in detecting the presence of iatrogenic myopathy, such as steroid-induced myopathy or in predicting post-operative pulmonary complications following coronary artery by-pass surgery.
MIP and MEP are useful in the assessment of respiratory failure. They are sometimes used to predict whether a patient can be weaned from a ventilator. They are occasionally helpful in the diagnosis of unexplained breathlessness in association with a low vital capacity.
However, their usefulness is limited by the wide range of normal values and the fact that the tests are very effort-dependent. MIP and MEP are hard to perform and require a highly motivated subject.

Vanessa

Non-invasive ventilation in acute respiratory failure

I was asked an excellent question on the ward-round recently by one of our clever interns. Confronted by a patient with severe chronic lung disease who has become critically unwell, and having decided that intubation and mechanical ventilation via endo-tracheal tube would not be pursued, I was asked whether we would use non-invasive ventilation (NIV). Non-invasive ventilation involves the application of mechanical breathing support without the use of an endotracheal tube or tracheostomy, usually via an occlusive mask applied over the nose and mouth.

For the benefit of my interns, then, I thought it would be worth reviewing the recent literature on the use of non-invasive ventilation in the acute hospital setting. Unfortunately, there isn’t a hell of a lot of new information by the way of guidelines. However, there is some….

Firstly, in patients with COPD the following guidelines are based on recommendations from the global initiative in obstructive lung disease (GOLD):

• Selection criteria for NIV:
  o Moderate to severe dyspnoea with use of accessory muscles and paradoxical abdominal motion
  o Moderate to severe acidosis (pH <= 7.35) and/or hypercapnoea (PaCO2>45mmHg)
  o Respiratory frequency > 25bpm
  

Now it’s seldom quite so cut-and dried, but for those who like lists then you can learn that one.

There are contraindications to NIV which should be remembered:

Exclusion Criteria:

• respiratory arrest
• cardiovascular instability
• change in mental status / uncooperative patient
• high aspiration risk
• viscous or copious secretions
• recent facial or gastroesophageal surgery
• craniofacial surgery
• fixed nasopharyngeal abnormalities
• burns
• extreme obesity
  

A recent German review of over 2900 publications, weighted according to level of evidence, has come up with the following recommendations for use of NIV in acute respiratory failure – following the motherhood statement that ‘NIV should be preferred to invasive ventilation wherever possible to avoid the risk of ventilator-tube associated complications such as ventilator associated pneumonia’, (a level A recommendation);

• in hypercapnoeic acute respiratory failure (ARF) NIV reduces rate of hospital acquired pneumonia, length of hospital stay and mortality – both in hospital and in ICU (Level A)
• patients with cardiopulmonary oedema should be treated with CPAP or NIV (CPAP is fine. Level A recommendation. Very important – don’t just give them lasix. CPAP treats the heart failure by increasing intrathoracic pressure and reducing venous return – reducing preload on the failing ventricle and allowing it to contract more effectively.... all to do with the Starling curve. Complicated, but CPAP doesn’t just support their breathing, it treats the heart failure. Everyone with APO should get CPAP – says the respiratory physician - but remember that CPAP can drop blood pressure, so be wary in patients with hypotentsion)
• in immunocompromised patients with ARF, for reasons unclear, NIV reduces mortality (Level A)
• to prevent post-extubation failure and to facilitate weaning of intubated patients with hypercapnoeic respiratory failure (Level A)
• in patients who decline invasive intervention, NIV may be an acceptable alternative (Level B)
• to lessen dyspnoea in palliative care (level C)
  

In patients with simply acute hypoxic respiratory failure, the failure rate of NIV is 30 to 50 % and NIV is not generally recommended (except in those immunocompromised patients).

Hope that helps.

Andrew

How much sleep is enough?

What qualifies as a goods night sleep? This is different for everyone but researchers have found that the average number of hours an adult should sleep per night is around 8. That being said some people need as little as six hours while others feel they need nine. The best indicator of if you are getting enough sleep is how you function the next day. If after six hours sleep you wake feeling unrefreshed and experience high levels of daytime tiredness then there is a fair chance that you could do with an extra hour or so per night.

In our society it has become somewhat of a badge of honour to apparently be able to get by on little sleep. Many influentual figures in society have stated they get by on very little sleep. Margaret Thatcher reportedly survived on 4 hours per night and our current PM Kevin Rudd is said to have as little as 3 hours per night. Perhaps we need to take these reported levels of sleep with a grain of salt as they may be used to promote the idea they are hard working and motivated or perhaps it is simply that work interferes with getting an adequate amount of sleep. Not getting enough sleep is a reality for many people not just politicians.

When people have ample opportunity to sleep but have difficulty initiating sleep or maintaining sleep it is described as insomnia. Approximately one third of the population will experience insomnia at some stage during their life. Mostly it is caused by an acute phase in their life such as stress, jet lag, or medical condition and resolves quickly. For others the problem can be ongoing and is thus described as chronic insomnia.

This sleep deprivation can cause impaired judgement, accidents, and mood swings. It is important to establish if there is a reason why enough sleep is not being achieved. It may be due to lifestyle, work, illness, sleeping environment or sleep hygiene.

Sleep hygiene refers to the habits that are established around sleep. Sometimes these habits are reinforced over years and have a disruptive effect on sleep. Recently the partner of a poor sleeper told me they have the TV on all night and her husband wakes several times a night not being able to get back to sleep so has the laptop close to the bed and can spend hour on the Internet. This is not uncommon and is an example of bad habits that have built up over the years having a negative impact not only on the individual but also the bed partner.

Take a look at the sleep hygiene download from our website to see if there is anything you can do to improve your sleep.

Jessica

Can Spiriva® save lives?

Tiotropium (Spiriva®) is almost universally prescribed for treatment of chronic obstructive pulmonary disease. It has been demonstrated to improve lung function (better spirometry, less air trapping) and health-related quality of life, and to reduce the frequency of exacerbations and hospitalizations in studies that compared use of tiotropium to placebo.

But can it save lives?

To date, several interventions in particular clinical settings in patients with COPD have been demonstrated to improve survival. These include; smoking cessation; use of supplemental oxygen in patients with persistent and profound hypoxaemia (low blood levels of oxygen); use of non-invasive ventilation in patients with ventilatory failure (high levels of carbon-dioxide in the blood; and even lung volume reduction in a very select group of patients. An analysis of data collected in the previously-published UPLIFT trial was released in the Blue Journal in mid-November, and suggests that tiotropium used regularly may be added to this list.

This was an interesting study. Two groups of patients (totaling 5993 patients) with COPD were randomized to receive either tiotropium or placebo. They were allowed to take any other inhalers except anticholinergics, and were even allowed to smoke (30% of them were smokers). Many patients discontinued the drug (44.6% in the placebo arm and 36.2% in the treatment arm) but continued in the study over its four year duration, and then a 30 day follow up period, during which tiotropium was stopped and ipratroprium (Atrovent ®) administered. .

During the 1440 days of the treatment period, 411 patients died while receiving placebo and 381 while receiving tiotropium (Hazards ratio (95% CI) 0.84 (0.73-0.97) p-0.016). If those in the two groups who discontinued treatment were included there was still a significant difference ( 491 vs 430, HR 0.87 (0.76-0.99), p-0.034). However, the follow-up period was a particularly bad one for those in the tiotropium group. During that period, 16 patients from the tiotropium group died, as opposed to only four from the placebo group. Six of those ‘tiotropium group’ deaths were patients who had remained on the medication right up until the end of the study – raising the question of whether withdrawal of the medication may have been harmful. By the end of the follow-up period, the survival difference was not statistically significant.

In a sub-group analysis it seemed as if smoking status at baseline might be a significant differentiator. Not too much was made of this in the discussion, but certainly for those patients still smoking there was no difference in risk of death between the two groups (medication vs placebo).

I think that the study design was a bit messy, including smokers and non-smokers and with a real hotch-potch of other inhalers in play. In this regard, however, it can certainly claim to be like real life. This recently-published new analysis of old data from the UPLIFT study gives us even more reason to prescribe tiotropium, and encourage our patients to remain on it.

Andrew