Related Information
How to get a good night’s sleep?
Getting a good night’s sleep requires more than just going to bed on time. Try following these four sleep tips to give yourself the best chance of getting consistent, quality sleep each night. And if you feel like you’re doing everything you can to get a good night’s sleep but no longer have the energy to do the things you love, there might be more to the story. Sleep apnea (also spelt sleep apnoea) affects three in 10 men and nearly two in 10 women .1 Talk to your doctor and ask about a sleep apnea test – which can be done in a sleep lab or the comfort of your own home.
- Allocate enough time for sleep. Sleep is just as important as diet and exercise, so it’s important to allocate the right amount of time in your day for sleep and plan the rest of your schedule accordingly. Getting a good night’s sleep means 7–8 hours each night for adults (including older adults), 9–10 hours for teens, at least 10 hours for school-aged children and 11–12 hours for preschool-aged children.
- Create consistent sleep habits. As creatures of habit, we’re usually more successful when following a routine. Sleep is no different. From your pre-sleep ritual to going to bed and waking up at the same time, you’ll find that consistency makes it easier to fall asleep each night.
- Create a comfortable sleep environment. Make sure your bedroom is cool, quiet and comfortable – especially your bed. It may take some experimenting and an investment on your part, but finding an ultra-comfortable bed and pillow is invaluable. We spend one-third of our lives in bed, making it the one area of your life you don’t want to compromise on comfort.
- Turn it off before bed. Whether it’s television, reading, email or texting, give yourself a nice window of time to unplug and relax before bedtime. Your body should associate your bed with sleep and these activities ramp up your brain activity rather than relaxing it. Television and bright light can also suppress melatonin production – making it difficult to fall asleep.
Reference
- 01 Peppard et al. Increased prevalence of sleep-disordered breathing in adults Am J Epidemiol. 2013;177(9):1006–14.
The Importance of Airway Clearance
Airway clearance and lung expansion are critical components for respiratory health.
Respiratory health depends on consistent clearance of airway secretions. Normal airway clearance is accomplished by 2 important mechanisms: the mucociliary clearance system and the ability to cough. Impaired mucociliary clearance is linked to poor lung function in a broad range of diseases and disabilities.1
Because at-risk individuals are prone to recurrent episodes of respiratory inflammation, infection, and, eventually, irreversible lung damage, improvement of mucociliary clearance is a vital treatment goal—one that can be accomplished with an individualized bronchial hygiene plan that includes effective airway clearance therapy.2
Additionally, lung health can be compromised by atelectasis. Atelectasis can occur in any patient who cannot or does not take deep breaths periodically. Patients who have difficulty taking deep breaths without assistance include those with significant obesity, those with neuromuscular disorders, those who are under heavy sedation, and those who have undergone upper abdominal or thoracic surgery.3
Unresolved atelectasis and lack of airway clearance are critical concerns, and are associated with manydiseases and conditions. By offering you clinical evidence and tools regarding airway clearance, Hill-Rom demonstrates a high level of dedication to keeping your respiratory system healthy.
References
- Houtmeyers E, Gosselink R, Gayan-Ramirez G, et al. Regulation of mucociliary clearance in health and disease. Eur Respir J. 1999;13(5):1177-1188. Review.
- Braverman J. Maintaining healthy lungs: the role of airway clearance therapy. Exceptional Parent Magazine. August 2001.
- Wilkins RL, et al. Basic Therapeutics. Egan’s Fundamentals of Respiratory Care, 9th edition. Mosby, Inc. 2009;904-905.
What causes snoring?
What causes snoring is a question that can be answered multiple ways. From an anatomical standpoint, snoring is caused by a partially closed upper airway (the nose and throat). Everyone’s neck muscles relax during sleep, but sometimes they relax so much that the upper airway partly closes and becomes too narrow for enough air to travel through to the lungs.
Why do people snore?
Why do some people snore and others don’t? Those who have enlarged tonsils, an enlarged tongue or excess weight around the neck are more prone to snoring. And structural reasons like the shape of one’s nose or jaw can also cause snoring. The snoring sound itself is a result of the narrowing of a person’s airway, which causes a throat vibration and the snoring sound. No matter the reason, 40% of normal adults snore regularly,1 whether they realize it or not.
Snoring and sleep apnea
Snoring and sleep apnea (also spelt apnea) are linked at an alarming rate – three in 10 men and nearly two in 10 women who are habitual snorers suffer from some degree of obstructive sleep apnea.2 Sleep apnea prevents you from getting the healthy sleep you need to lead a refreshed, energetic life. So regardless of what is specifically causing snoring for you, if you snore — or if you suspect you snore — consider it a sign that something might not be right. Take our short sleep apnea quiz or find a sleep testing facility near you.
01 Ohayon MM et al. Snoring and breathing pauses during sleep: telephone interview survey of a United Kingdom population sample. BMJ. 1997;314:860–3
02 Young T et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993; 328(17):1230–5
Why is sleep important?
To understand why sleep is important, think of your body like a factory that performs a number of vital functions. As you drift off to sleep, your body begins its night-shift work:
- Healing damaged cells
- Boosting your immune system
- Recovering from the day’s activities
- Recharging your heart and cardiovascular system for the next day
We all know the value of sleeping well, and we’ve all experienced the feeling of being refreshed after a good night’s sleep – and the feeling of fatigue after a poor night’s sleep. But even though we know this, in our busy society, many of us are not getting the quality sleep needed to truly receive the health benefits of sleep.
Understanding the sleep cycle
Understanding what happens during sleep also means understanding the sleep cycle, which consists of two recurring phases: REM (rapid eye movement) and NREM (non-REM or non-rapid eye movement). Both phases are important for different functions in our bodies.
NREM sleep typically occupies 75–80% of total sleep each night. Many of the health benefits of sleep take place during NREM sleep – tissue growth and repair occurs, energy is restored and hormones that are essential for growth and development are released.
REM sleep typically occupies 20–25% of total sleep each night. REM sleep, when dreaming occurs, is essential to our minds for processing and consolidating emotions, memories and stress. It is also thought to be vital for learning, stimulating the brain regions used in learning and developing new skills.
If the REM and NREM cycles are interrupted multiple times throughout the night — either due to snoring, difficulties breathing or waking up frequently throughout the night — then we miss out on vital body processes, which can affect our health and well-being the next day and long term.
What happens if you don’t get enough sleep?
If your body doesn’t get a chance to properly recharge – by cycling through REM and NREM – you’re already starting the next day at a disadvantage. You might find yourself:
- Feeling drowsy, irritable or sometimes depressed
- Struggling to take in new information at work, remembering things or making decisions
- Craving more unhealthy foods, which could cause weight gain1
If this happens night after night, it places a tremendous strain on your nervous system, body and overall health. So if you’re not sleeping well or aren’t feeling rested when you wake up in the morning, it’s important to talk to your doctor and ask if a sleep study is right for you.
References
- Morselli L et al. Role of sleep duration in the regulation of glucose metabolism and appetite. Best Pract Res Clin Endocrinol Metab 2010;24(5):687–702.
What happens during normal breathing?
To find out what could be affecting your ability to breathe properly, it’s helpful to first understand what normal breathing looks like.
Breathing is automatic
It might sound simple, but it’s important to realize that breathing is not something we have to consciously remember to do. It’s a reflex that is controlled by nerve cells in the brain and spine.
The upper and lower airways
The respiratory system is made up of 2 parts: the upper and lower airways.
Upper airway
Lower airway
The lower airway is protected by the chest cavity, which also contains the heart and lungs.
The breathing process
What starts the breathing process is actually the effort you make (from your chest) to draw air into your body.
When you breathe, the air entering your nose is cleaned, warmed and moistened. It then travels through your throat to the windpipe, and down to the bronchi in the lungs.
As you inhale and exhale, your chest and ribs expand and contract to allow for the air going in and out.
Abnormal breathing
As you can imagine, the everyday act of breathing can become very difficult if you have a respiratory condition that affects the muscles, nerves, reflexes or organs involved in breathing.
Learn more about respiratory conditions:
- COPD
- Neuromuscular disease
- Cheyne-Stokes respiration
- Respiratory conditions in children
- OHS
- Restrictive lung disease
Medical Terms
cmH2O:
A centimeter of water or cmH2O is a unit for pressure. The normal range of the CPAP device is 4-20 cmH2O.
It is defined as the pressure exerted by a column of water of 1cm in height at 4 C (temperature of maximum density) at the standard acceleration of gravity.
SpO2:
SpO2 (pulse oximetry) is a measurement of arterial oxygen saturation, the amount of oxygen being carried by hemoglobin in the blood, given in as a percentage (%). Normal values range from 90%-100%.
AHI:
Apnea Hyponea Index (AHI) is the total number of complete cessations (apnea) and partial obstructions (hyponea) of breathing occurring per hour of sleep.
By the definition from the American Academy of Sleep Medicine and the American Thoracic Society, “Sleep Apnea” means repetitive episodes of cessation of breath and arousals associated with a reduction in blood oxygen saturation (SpO2 drops >3%).
RDI:
Respiratory Disturbance Index (RDI) is the total number of apneas, hypopneas and respiratory event related arousals (RERA) per hour of sleep.
Mild: AHI: 5-15 / RDI: 5-20
Moderate: AHI: 15-30 / RDI: 20-40
Severe: AHI: >30 / RDI: >40
BMI:
Body Mass Index (BMI) is a key index defines by the World Health Organization (WTO). It is a tool for indicating weight status, correlates with body fat.
Underweight: BMI < 18.5 Normal: BMI 18.8 – 24.9 Overweight: BMI 25 – 29.9 Obese: BMI > 30
The above information is for reference only. Please consult your doctors for the detail information.
CPAP Therapy
Principle of CPAP:
CPAP works by creating a pneumatic splint in the upper airway. A flow generator sends pressurized air through the nose or mouth to the upper airway. The pressurized air prevents the soft tissues of the upper airway from narrowing and collapsing.
During sleep, the PAP machine blows air at a prescribed/ titrated pressure. Pressure is measured by centimeter of water (cmH2O). With most patients being adequately treated with pressure between 6-14 cmH2O.
Type of PAP:
PAP therapy is divided into 4 types: Fixed Pressure, Auto-adjusting Pressure, Auto-adjusting Bi-level Pressure and Adaptive Servo Ventilation.
Fixed Pressure (CPAP):
The titrated pressure is delivered throughout sleep at the constant pre-set pressure (normally 4-20 cmH2O). Once the pressure set, the patient cannot change it unless the physician prescribe a new pressure setting. The patient can ask the device provider to make this change.
Auto-adjusting Pressure (APAP):
The pressure delivered to the patients varies throughout the night. It is a dynamic device and pressure varies depending on the patency of the upper airway. Patients report it is more comfortable as the pressure delivered changes with individual’s needs.
For example, if a patient changes their position during sleep and has several obstructive upper airway events, the pressure increases. When obstructive events stop, the pressure decreases. This type of treatment is optimal for patients whose pressure needs vary greatly throughout the night.
Auto-adjusting Bi-level Pressure (Vauto):
It is for patients requiring both higher pressures and greater pressure relief. Particularly for non-compliance OSA patients that cannot use both CPAP and APAP. It combines pressure relief with the dynamic response of the AutoSet algorithm.
Adaptive Servo Ventilation (ASV):
It continuously adapts pressure support to maintain the patient’s target ventilation, rapidly stabilizing their breathing pattern and arterial blood gases.
The algorithm also contains a unique physiological waveform for a more comfortable breathing experience.
It designed for Congestive Heart Failure (CHF) patients who have Cheyne Stokes Respiration (CSR) or Central Sleep Apnea (CSA) with or without Obstructive Sleep Apnea (OSA).
AutoSet™ technology
Changes in sleep stage, weight, body position, and other factors can alter a patient’s airway pressure treatment requirements from night to night, hour to hour and breath to breath. At times they may need higher pressure to maintain airway patency, and at times their pressure needs may be lower. ResMed’s AutoSet™ automatic positive airway pressure (APAP) devices monitor a patient’s airway on a breath-by-breath basis and deliver only the pressure that patients need—when they need it.
- Our AutoSet devices are designed to provide the minimum pressure required at each point in time to treat apneas/hypopneas and upper airway resistance.
- Patients report better subjective sleep and achieve a significant reduction (37%) in median treatment pressure with consequently lower system leaks than fixed-pressure therapy (CPAP).1
- Patients on treatment pressures of 10 cm H2O or higher, or who have side effects from CPAP treatment, experience more benefit from auto-adjusting therapy such as AutoSet.2,3,4
- ResMed’s AutoSet devices use a patented algorithm that responds to flow limitation (the earliest sign of impending airway collapse), snoring and apnea on a breath-by-breath basis.5-6
Reference
- Teschler H, Wessendorf TE, Farhat AA, Konietzko N, Berthon-Jones M. Two months auto-adjusting versus conventional nCPAP for obstructive sleep apnea syndrome Eur Respir J 2000;15(6):990-5.
- Hukins C. Comparative study of autotitrating and fixed-pressure CPAP in the home: a randomized, single-blind crossover trial. Sleep 2004;27(8):1512-7.
- Resta O, Carratu P, Depalo A, Giliberti T, Ardito M, Marrone O, Insalaco G. Effects of fixed compared to automatic CPAP on sleep in Obstructive Sleep Apnea Syndrome. Monaldi Arch Chest Dis 2004;61(3):153-6.
- Massie CA, McArdle N, Hart RW, Schmidt-Nowara WW, Lankford A, Hudgel DW, Gordon N, Douglas NJ. Comparison between automatic and fixed positive airway pressure therapy in the home. Am J Respir Crit Care Med 2003; 167(1):20-3.
- Ayappa I, Norman RG, Hosselet JJ, Gruenke RA, Walsleben JA, Rapoport DM. Relative occurrence of flow limitation and snoring during continuous positive airway pressure titration. Chest 1998;114(3):685-90.
- Farre R, Montserrat JM, Rigau J, Trepat X, Pinto P, Navajas D. Response of automatic continuous positive airway pressure devices to different sleep breathing patterns: a bench study. Am J Respir Crit Care Med 2002;166(4):469-73.
Three Lines of Defence of AutoSet Algorithm
- Flow Limitation – Phenomena: Narrowing of upper airway, affecting the inspiration flow curve shape.
- Snore – Phenomena: Sound generated by vibration of the upper airway walls, usually caused by flow limitation.
- Apnea – Phenomena: Severely or completely obstructed upper airway.
AutoSet Response:
- Both 3 type of indications will lead to pressure increase.
- If there is no sort of event above for a period of time, this will lead to pressure decay.
What to look for in a sleep therapy equipment provider
If you have recommended that your patient be treated with positive airway pressure therapy, their next important step is to visit a therapy equipment supplier – sometimes called a home medical equipment (HME) provider – to buy their therapy equipment.
Some patients may not know where to start looking and may ask you for guidance. So it’s helpful for you to have a list of preferred equipment suppliers to recommend.
Patient education | Do their staff explain the importance of treatment, and how to use and take care of their equipment? |
Mask choices | Do they offer a wide variety of masks to suit your patient’s unique anatomy and lifestyle needs? |
Proper fitting setup | Do they ensure that patients achieve proper mask fit by fitting them in a reclining position? |
Objective compliance data | Does the sleep therapy equipment include compliance monitoring tools that provide you with detailed data on your patient’s therapy usage and efficacy? |
Patient follow-up | Do they call patients straight after set-up and throughout the first week on therapy to answer questions and address any issues that may arise? Do they regularly remind patients when it’s time to service their equipment or replace any accessories to ensure their system is working optimally? |
On-call patient support | Can their staff be easily reached to assist patients with therapy issues? Do they have convenient hours of operation? |
Again, some patients may not know where to find a dental sleep specialist and may ask you for guidance. It is helpful for you to have a list of preferred clinicians to recommend. If you are interested in finding a clinician who uses ResMed’s Narval CC, please contact us.
Like you, dental sleep specialists play a major role in ensuring your patients achieve long-term adherence and healthy outcomes, so it’s important to refer your patients to providers who offer the following:
- Extensive dental sleep experience: Are they able to provide you with their credentials specific to dental sleep (eg, AADSM certifications, etc.) and most recent CE efforts? Is Dental Sleep and active part of their practice (dental sleep patients/month > 10)?
- Referral partnership protocol: Are they able to provide you with a workflow that will complement your practice (eg, patient case notes/SOAP notes)? Can they share case studies and documentation to support how they will interface with your office/how they interface with other referral sources?
- Oral appliances choices: Do they offer a wide variety of oral appliances to suit your patient’s unique anatomy and lifestyle needs?
- Proper setup: Can they walk you through the patient experience and explain their metrics for patient success? (Will they use screening questionnaires or home sleep testing to define success? What do you prefer based on the patient’s level of OSA severity?)
- Patient follow-up: When does the patient return for titration visits? Generally how many appointments are required in a given three-month span to find the optimal titration setting? Do they have a follow-up protocol after optimal titration is reached and success is agreed to by you and the clinician (eg, every 6 months or annually)?
- Patient support: Can their staff be easily reached to assist patients with therapy issues? Do they have convenient hours of operation? Do they accept medical insurance to cover the oral appliance or do they provide support in submitting claims for payment?
Spirometric Data Quality as Assessed by Repeatabliy in COPD Exacerbations
AJ Harrison¹, G Sowman², H Kaur-Nagra PhD², D Price³, M Brown³, P Ford MD³.
Introduction
Spirometry is one of the few clinical measurements that requires maximum patient eort in order to achieve acceptable and repeatable results. Obtaining valid Spirometry data from chronic obstructive pulmonary disease (COPD) patients who present to the clinic with an exacerbation can be challenging.
Pharmaceutical trials are reliant on accurate data to meet endpoints. We will demonstrate that by using standardised equipment and Over-Reading² we can maintain excellent data quality in this challenging patient population. The patient factor is signicant when low values are expected for COPD patients struggling with an exacerbation. Having well-trained clinical staff who can coach these patients correctly can have a signicant impact on the quality of Spirometry. The accuracy and quality of Spirometry is also particularly important in clinical trials where Spirometry data are used as primary endpoints.
A total of 93 moderate to very severe COPD patients performed 672 Spirometry sessions. Out of those sessions, 96% met the ATS/ERS FVC repeatability criteria¹ and 99% met the FEV repeatability criteria¹. The ATS/ERS 2005 criteria are widely used in clinical trials as a benchmark for the quality of Spirometry.
Methods
In an international multicentre trial, 93 COPD patients (Gold II – IV) aged 43-80 years old and presenting with a COPD exacerbation were randomised into a clinical trial. Spirometry was performed at both the initial visit and subsequent sessions over a 6 month follow-up period. The Spirometry was conducted by well-trained technicians in 8 centres in 3 European countries. In total, 672 Spirometry sessions were performed. An average patient therefore performed 7 Spirometry sessions. At all sites, the Spirometry was performed using the Vitalograph Spirometry System (including Vitalograph Pneumotrac™ (Fleisch) spirometer run on Spirotrac® software customised for the trial) with Over-Reading.
Training
Before the trial commenced all technicians were trained in the correct use of the equipment and trial specific procedures. In addition, all technicians were required to demonstrate their ability to perform acceptable and repeatable Spirometry sessions prior to gaining trial accreditation. Throughout the trial
each centre was monitored for spirometric quality to ensure that site re-training was undertaken if required.
OVER-READING
After primary review by the technician, the sessions were transmitted to a central database at Vitalograph and QA reviewed (“Over-Read”) by one of three expert Over-Readers within 1-2 business days of receipt. All of the Over-Readers reviewed each session according to the trial-specic acceptability criteria (based on the ATS/ERS Guidelines¹).
As per the ATS/ERS standards¹, the protocol allowed up to eight manoeuvres per session which
needed to meet the FVC and FEV acceptability criteria. The repeatability for both FEV and FVC was calculated as the dierence between the two highest acceptable readings of a session.
Results
A total of 672 (100%) spirometric sessions were recorded at 8 sites in 3 European countries by 93 patients (Country A – 41 patients, Country B – 30, Country C – 22) presenting with a COPD exacerbation. The repeatability for both FEV and FVC was calculated as the difference between the two highest acceptable readings (Figure 1).
The mean figures for each country’s repeatability (Figure 1) are within the ATS/ERS recommendation of 150ml. The overall mean repeatability was 69 for FVC and 40 for FEV. Country C had both the lowest FVC and FEV mean repeatability (but also the fewest patients).
The distribution of the repeatability as a percentage for all sessions were graded (Table 1).
TABLE 1: % OF TOTAL SESSIONS WITHIN REPEATABILITY GRADE BY COUNTRY
Repeatability (ml) | Country A (%) | Country B (%) | Country C (%) | Overall (%) |
---|---|---|---|---|
FVC | ||||
<50ml | 45.5 | 70.6 | 53.4 | 48.5 |
<100ml | 78.2.5 | 93.9 | 84.5 | 79.3 |
<150ml | 94.4 | 99.7 | 96.6 | 96.0 |
>150ml | 5.6 | 0.3 | 2 | 4.0 |
FEV1 | ||||
<50ml | 73.8 | 50.9 | 71 | 72.9 |
<100ml | 93.1 | 79.5 | 96.6 | 93.8 |
<150ml | 98.1 | 97.6 | 100.0 | 99.0 |
>150ml | 1.9 | 2.4 | 0.0 | 1.0 |
Overall 4% of FVC manoeuvres were outside the ATS/ERS repeatability limit and just 1% for FEV.
Conclusion
With standardised equipment, well-trained technicians and QA review by independent Over-Readers, patients presenting to clinic with COPD exacerbations can produce reliable and repeatable data in clinical trials.
Bibliography
1. M.R. Miller et al. ATS/ERS Task Force: Standardisation of Spirometry, Eur Respir J 2005; 26: 319-338 2. AJ Harrison, et al. Quality control of respiratory measurements in global trials. ERJ 2006; 28: S50, 984
Acknowledgements
Novartis International AG for use of their data.
Differentiating Asthma from COPD
Whilst asthma and COPD are different diseases they cause similar symptoms, which can present a challenge in identifying which of the two diseases a patient is suffering from. A patient survey by the British Lung Foundation (BLF) showed that nearly 39% of COPD patients had been told they have asthma.
There are, however, some important distinctions between asthma and COPD. COPD causes chronic symptoms and narrowed airways which do not respond to treatment to open them up. In the case of asthma the constriction of the airways through infl ammation tends to come and go and treatment to reduce infl ammation and to open up the airways usually works well.
COPD is more likely than asthma to cause a chronic cough with phlegm and is rare before the age of 35 whilst asthma is common in under-35s. Disturbed sleep caused by breathlessness and wheeze is more likely in cases of asthma, as is a history of allergies, eczema and hayfever. Differentiating between COPD and asthma requires a history of both symptoms and spirometry. The spirometry history should include post bronchodilator measurements, the degree of reversibility and, ideally, home monitoring which gives a history of diurnal variation.
What are the definitions?
Airflow Obstruction: Both asthma and COPD are characterised by airflow obstruction. Airflow obstruction is defined as a reduced FEV1 and a reduced FEV1/FVC ratio, such that FEV1 is less than 80% of that predicted, and FEV1/FVC is less than 0.7.
Asthma: Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread, but variable, airflow obstruction within the lung that is often reversible either spontaneously or with treatment1.
COPD: COPD is a chronic, slowly progressive disorder characterised by airflow obstruction (reduced FEV1 and FEV1/VC ratio) that does not change markedly over several months. The airflow obstruction is not fully reversible2.
Clues to the Difference Between COPD and Asthma
History | COPD | Asthma |
---|---|---|
Age | Over 35 | Any age |
Dyspnoea varies | A little | A lot |
Onset of dyspnoea | Gradually | Sudden bouts |
Dyspnoea at rest | Uncommon | Common |
Smoking history | > 20 pack years | Variable |
Wheezing as a child | Uncommon | Common |
Productive cough | For many years | Associated attacks |
Morning coughing fits | Common | Uncommon |
Nocturnal cough wakes | Uncommon | Common |
Family history | Uncommon | Usually |
Atopy | Unusual | Often |
Steroid responsiveness | Weak | Strong |
Morning coughing fits | Common | Uncommon |
Anticholinergic response | Usually good | Beta-agonists better |
Beta-agonist response | Anticholinergics better | Very good |
Note: COPD is more likely to affect older people. The vast majority of sufferers are aged 70 to 85. COPD patients also tend to have frequent acute respiratory infections which can also accelerate the decline of FEV1.
Confirm or Preclude COPD or Asthma with Spirometry
Spirometry | COPD | Asthma |
---|---|---|
VC | Reduced | Nearly normal |
FEV1 | Reduced | Reduced in attack |
FVC (or FEV6) | Reduced | Nearly normal |
FEV1 Ratio (of VC/FVC/FEV6) | Reduced anytime | Reduced in attack |
FEV1 as % of predicted (or SDS*) | <LLN | Reduced in attack |
Bronchodilator reversibility | A little | Marked if in attack |
Serial spirometry | Progressive deterioration | Constant or erratic |
Home monitoring | Use for alerts | Use for variability |
Peak Flow measurement | Not useful | As above |
Peak Inspiratory Flow measurement | Not useful | Not useful |
* SDS = Standard Deviation Score. In comparing your test subject to a ‘normal population’ using SDS or LLN (Lower Limit of Normality) is preferred to percent of predicted because the latter gives false negatives for younger people and false positives for older people.
Serial Spirometry
The most important objective measurement of all in lung disease management is serial spirometry. Taking a single lung function measurement may or may not yield useful information. But comparing that spirometry test data, particularly the FEV1, with data from the previous few years yields invaluable, yet simple, information.
As a normal growing child it is fairly obvious that the lung function values will rise according to the individual’s growth centiles. After achieving adulthood, and a period of a few years without change in values, every normal person will have a gradual decline lung function. In disease this pattern may radically change.
In older people, the rate of decline of a COPD sufferer can be two or three times the FEV1 decline in normal people. Medical intervention can bring this back to a normal rate of decline, but not back to the level of a normal person. For this reason early detection is crucial. It is very possible to detect this accelerated rate of decline even when the patient is in ‘normal range’. An accelerated rate of decline detected by serial spirometry is definitely abnormal, no matter if the patient still has ‘good’ lung function values3.
A serial spirometry plot like the one pictured here is typical of uncontrolled COPD, such as a sufferer who keeps smoking4.
Serial spirometry is impossible without spirometry quality control. Without consistently accurate measurements, the serial data will be useless, or worse, misleading. Although serial spirometry can help identify device or procedural problems, this is shutting the door after the horse has bolted. The real answer is training and quality control.
Spirometry Quality Control
Spirometer accuracy: An accuracy check is a is a two minute check that you do just before starting your asthma or COPD clinic and is as simple as setting the device to ‘accuracy check’ mode (for ATPS measurement) then pumping the 3-L syringe. If all is well the device will measure 3L ±3%. It is important not to confuse ‘calibration’ with an accuracy check. Calibration is an annual certifi cation of traceability to international measurement standards which may or may not involve adjustment prior to certifi cation.
Test acceptability: When testing, each forced expiratory blow comprising part of the session data must be acceptable. This means that there is a good start of test, no artefacts such as coughing and a good end expiratory plateau and a test duration of over 6-s (3-s in children under 10 years). Premature test termination is the most common error in spirometry.
Number of blows: The spirometry guidelines require that a test session comprise of a minimum of 3 satisfactory blows to ensure that the forced expiratory volumes are ‘the best’. Of course usually more blows are required as there are usually some unsatisfactory blows, especially if a slow VC test does not precede the FVC, or the operator fails to use a disposable noseclip.
Repeatability: The satisfactory blows must be repeatable within 5% on both FEV1 and FVC. In practice this means the best two blows.
Training & Over-reading: None of the above can be achieved without proper training. The use of over-reading for ECG interpretation is widely used, but over-reading spirometry reports is relatively new in primary care. New technology is making automation of over-reading possible.
Home Monitoring
Home monitoring of lung disease is important to alert the patient of exacerbations and for providing invaluable objective data to the practitioner. Additionally, the patient may be given an ‘action plan’ for helping them to manage their condition or to know when to seek medical intervention. According to BTS/SIGN5 “Written personalised action plans as part of selfmanagement education have been shown to improve health outcomes for people with asthma” and “Prior to discharge, in-patients should receive individualised asthma action plans, given by clinicians with appropriate training in asthma management.”
The use of mechanical peak flow meters may not be adequate for lung diseases other than asthma6. Today accurate and inexpensive home monitors are available which record FEV1 and even FEV6 as well as having the facility to set a personalised action plan for the patient. For PEF measurement in asthmatics, inexpensive electronic home monitors can also be used which avoids the need for paper records and misleading ‘false reporting’.
References:
1. Global Strategy for Asthma Management and Prevention. Global Initiative for Asthma (GINA), 2011. Available from www.ginasthma.org
2. Global Initiative for Chronic Obstructive Pulmonary Disease: NHLBI/WHO workshop report. 2001 National Institutes of Health. Bethesda, MD: publication No. 2701 http://www.goldcopd.com
3. P. Vineis, Smoking and Impact on Health, Eur. Respir. Rev 2008: 17: 110, 182-186. World Asthma Day 2009 is on May 5th.
4. Anthonisen NR, Connett JE, Kiley JP, et al. Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA 1994; 272: 1497–1505.
5. British Thoracic Society, Scottish Intercollegiate Guidelines Network. British Guideline on the Management of Asthma. SIGN; 2010. http://www.sign.ac.uk
6 Chronic Obstructive Pulmonary Disease. National clinical guideline on management of chronic obstructive pulmonary disease in adults in primary and secondary care Thorax March 2004, Volume 59, Supplement 1.
How Does Smoking Contribute to COPD?
The air you breathe travels down through the windpipe, eventually making its way into bronchial tubes. Bronchial tubes then stretch out into much smaller tubes known as bronchioles, which have minuscule clusters of air sacs at the end called alveoli.
Within the small air sacs are tiny blood vessels known as capillaries. When you inhale, the oxygen moves through the air sacs and into the blood of the capillaries that are located within the air sacs. Simultaneously, carbon dioxide is moved from the blood vessels into the air sacs in a process known as gas exchange.
The elasticity in the air sacs enables this exchange to occur smoothly as they inflate and deflate with each breath. People who smoke suffer lung damage which allows less air to flow in and out of the air pathways due to:
- stiffening of air sacs
- degradation of wall between air sacs
- thickening and inflammation of air pathway walls
- increasing mucus in the air pathways, causing build-up and air obstruction
Cigarette smoke contains harmful toxins that affect lung functionality. Toxins that are inhaled directly into the lungs over prolonged periods of time can lead to high levels of abnormal lung irritation, causing the onset of COPD. As long-term exposure to cigarette smoke continues, the lungs incur more damage, including lung inflammation, and breakdown of the lung’s filter system.
Can You Reverse Cigarette Damage?
Unfortunately, there is no cure for COPD. Damage to the lungs can’t be reversed. COPD is treated using several different methods including changes in lifestyle, therapy, and prescription drugs. When used in combination, these treatment methods can slow down the progression of the disease and bring relief to the patient by causing symptoms to subside. The best way to stop the disease from worsening is for people who smoke to quit immediately and avoid secondhand smoke. People who continue to smoke put themselves at increased risk of accelerating the disease and its symptoms, as well as premature death.
Sleep apnea and cardiovascular issues
An abundance of research has focused on the connection between sleep apnea and cardiovascular or heart issues. Some of the key findings include:
- Causes hypoxia, increased intrathoracic pressure swings due to the attempts to breathe during an apnea, and activation of the sympathetic nervous system—all of which have many negative consequences for the cardiovascular system.1-4
- Is strongly associated with hypertension, independent of all relevant risk factors.5-8
- Is present in more than 30% of patients with hypertension.9
- Occurs in 80% patients with drug resistant hypertension.10
Treated with CPAP may result in a clinically significant drop in blood pressure. This drop is sufficient to reduce risk of a coronary heart disease event by 37% and stroke risk by 56%.11,12,13
Treatment with CPAP in patients who also have heart failure, improves left ventricular function.15
Is common in patients with cardiovascular disease and occurs in 50% atrial fibrillation patients.16
Patients have increased levels of inflammatory, oxidative and vascular endothelial effect markers, which are associated with atherogenesis. These markers are improved when the sleep apnea is treated with CPAP.17-20
When severe, significantly increases the risk of cardiovascular events. Treatment with CPAP reduces this risk.21,22
References
01 Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA 2003;290:1906-14.
02 Lattimore JD, Celermajer DS, Wilcox I. Obstructive sleep apnea and cardiovascular disease. J Am Coll Cardiol 2003;41:1429-37.
03 Bradley TD, Floras JS. Sleep apnea and heart failure: Part I: obstructive sleep apnea. Circulation 2003;107:1671-8.
04 Peker Y, Hedner J, Norum J, Kraiczi H, Carlson J. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow-up. Am J Respir Crit Care Med 2002;166:159-165.
05 Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342:1378-1384.
06 Lavie P, Herer P, Hoffstein V. Obstructive sleep apnea syndrome as a risk factor for hypertension: population study. BMJ 2000;320:479-82.
07 Nieto FJ, Young TB, Lind BK, Shahar E, Samet JM, Redline S, D’Agostino RB, Newman AB, Lebowitz MD, Pickering TG. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. JAMA 2000;283:1829-1836.
08 Bixler EO, Vgontzas AN, Lin HM, Ten Have T, Leiby BE, Vela-Bueno A, Kales A. Association of hypertension and sleep-disordered breathing. Arch Intern Med 2000;160:2289-95.
09 Sjostrom C, Lindberg E, Elmasry A, Hagg A, Svardsudd K, Janson C. Prevalence of sleep apnoea and snoring in hypertensive men: a population based study. Thorax 2002;57:602-7.
10 Logan AG, Perlikowski SM, Mente A, Tisler A, Tkacova R, Niroumand M, Leung RS, Bradley TD. High prevalence of unrecognized sleep apnoea in drug-resistant hypertension. J Hypertens 2001;19:2271-7.
11 Logan AG, Tkacova R, Perlikowski SM, Leung RS, Tisler A, Floras JS, Bradley TD. Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreflex. Eur Respir J 2003;21:241-7.
12 Becker HF, Jerrentrup A, Ploch T, Grote L, Penzel T, Sullivan CE, Peter JH. Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation 2003;107:68-73.
13 Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, Mullins R, Jenkinson C, Stradling JR, Davies RJ. Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet 2002;359:204-10.
14 Shahar E, Whitney CW, Redline S, Lee ET, Newman AB, Javier Nieto F, O’Connor GT, Boland LL, Schwartz JE, Samet JM. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med 2001;163:19-25.
15 Kaneko Y, Floras JS, Usui K, Plante J, Tkacova R, Kubo T, Ando S, Bradley TD. Cardiovascular effects of continuous positive airway pressure in patients with heart hailure and obstructive sleep apnea. N Engl J Med 2003;348:1233-1241.
16 Lanfranchi PA, Braghiroli A, Bosimini E, Mazzuero G, Colombo R, Donner CF, Giannuzzi P. Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure. Circulation 1999;99:1435-40.
17 Teschler H, Dohring J, Wang YM, Berthon-Jones M. Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure. Am J Respir Crit Care Med 2001;164:614-9.
18 Pepperell JC, Maskell NA, Jones DR, Langford-Wiley BA, Crosthwaite N, Stradling JR, Davies RJ. A randomized controlled trial of adaptive ventilation for Cheyne-Stokes breathing in heart failure. J Respir Crit Care Med 2003;168:1109-14.
19 Topfer V, El-Sebai M, Wessendorf TE, Moraidis I, Teschler H.[ Adaptive servoventilation: effect on Cheyne-Stokes-Respiration and on quality of life ]Pneumologie 2004;58:28-32.
20 Schadlich S, Konigs I, Kalbitz F, Blankenburg T, Busse HJ, Schutte W.[ Cardiac efficiency in patients with Cheyne-Stokes respiration as a result of heart insufficiency during long-term nasal respiratory treatment with adaptive servo ventilation (AutoSet CS) ]Z Kardiol 2004;93:454-62.
21 Philippe C; Stoica-Herman M; Drouot X; Raffestin B; Escourrou P; Hittinger L; Michel P-L; Rouault S; d’Ortho M-P. Compliance with and effectiveness of adaptive servoventilation versus continuous positive airway pressure in the treatment of Cheyne-Stokes respiration in heart failure over a six month period. Heart 2006;92(3):337-42.
22 Gami AS, Pressman G, Caples SM, Kanagala R, Gard JJ, Davison DE, Malouf J, Ammash N, Friedman P, Somers VK. Association of atrial fibrillation and obstructive sleep apnea. Circulation 2004;110(4):364-7.
23 Ip MS, Tse HF, Lam B, Tsang KW, Lam WK. Endothelial function in obstructive sleep apnea and response to treatment. Am J Respir Crit Care Med 2004;169:348-53.
24 Ip MSM, Lam B, Chan LY, Zheng L, Tsang KWT, Fung PCW, Lam WK. Circulating nitric oxide is suppressed in obstructive sleep apnea and is reversed by nasal continuous positive airway pressure. Am J Respir Crit Care Med 2000;162:2166–2171.
25 Shamsuzzaman AS, Winnicki M, Lanfranchi P, Wolk R, Kara T, Accurso V, Somers VK. Elevated C-reactive protein in patients with obstructive sleep apnea. Circulation 2002;105:2462-4.
26 Dyugovskaya L, Lavie P, Lavie L. Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients. Am J Respir Crit Care Med 2002;165:934-9.
27 Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005;365(9464):1046-53.
28 Doherty LS, Kiely JL, Swan V, McNicholas WT. Long-term effects of nasal continuous positive airway pressure therapy on cardiovascular outcomes in sleep apnea syndrome. Chest 2005;127