Obstructive sleep apnea (OSA) is a common disorder associated with an
increased risk of cardiovascular disease and stroke. As it is strongly
associated with known cardiovascular risk factors, including obesity,
insulin resistance, and dyslipidemia, OSA is an independent risk factor
for hypertension and has also been implicated in the pathogenesis of
congestive cardiac failure, pulmonary hypertension...
Obstructive sleep apnea (OSA) is a common disorder associated with an
increased risk of cardiovascular disease and stroke. As it is strongly
associated with known cardiovascular risk factors, including obesity,
insulin resistance, and dyslipidemia, OSA is an independent risk factor
for hypertension and has also been implicated in the pathogenesis of
congestive cardiac failure, pulmonary hypertension, arrhythmias, and
atherosclerosis [1].
Obstructive sleep apnea is part of a spectrum of sleep-related
breathing disorders that includes snoring, upper airway resistance
syndrome (increased respiratory effort without apnea or hypopnea), and
central sleep apnea (CSA) (apnea without respiratory effort). The OSA
syndrome is the combination of obstructive apneas with daytime tiredness
or recurrent awakenings or gasping episodes [1].
Clinical suspicion of OSA is usually raised by complaints of snoring
and daytime tiredness, despite an adequate duration of sleep. Mainly, OSA
patients are managed clinically by sleep physicians with a background in
respiratory medicine or neurology. Atypical presentations are not
uncommon, however, and result in OSA patients presenting to a variety of
medical specialists.
Obstructive sleep apnea is now recognized to be an independent risk
factor for daytime hypertension. An association between OSA and
hypertension was suggested by a series of population and cohort studies,
observational studies in patients attending hypertension clinics and sleep
clinics [2,3]. Increased variability of blood pressure and loss of the
nocturnal blood pressure dip were also reported [4]. A recent
prospective, randomized, placebo-controlled comparison between therapeutic
and subtherapeutic CPAP reported a reduction in blood pressure,
particularly in those with more severe OSA [5].
Patients with OSA have many features in common with the “metabolic
syndrome,” including systemic hypertension, central obesity [6], and
insulin resistance [7]. The AHI correlates with BMI, waist-to-hip ratio,
hypertension, and diabetes, whereas trends toward lower high-density
lipoprotein and elevated triglycerides are reported for OSA subjects
<_65 years="years" old="old" _8.="_8." p="p"/> The role of sleep-disordered breathing in arrhythmias in heart
failure is still being defined. In a study of 81 males with stable heart
failure, incidences of atrial fibrillation and ventricular tachycardia
were significantly higher in sleep apnea subjects (AHI The risk of experiencing angina or an acute coronary syndrome is
increased in the hours after waking from sleep. In OSA, cyclical
variations in heart rate and blood pressure are dramatic [12], more so
than many hemodynamic stresses in daily life, and occur during sleep, a
time when in normal subjects blood pressure and heart rate are the lowest
and least variable. In OSA, increased peripheral sympathetic nerve
activity during sleep persists during wakefulness at approximately twice
the normal levels [13] and may affect acute coronary events in the early
hours of the day.
Patients with heart failure can have a combination of CSA and OSA,
which can vary during sleep or over time. In one study, within-night
changes were documented with progression from predominantly OSA early in
the night to CSA, presumably due to the fall in the arterial pCO2 level to
below the apneic threshold [14].
Positive airway pressure has been known to help acute cardiogenic
pulmonary edema for decades. The beneficial effects are thought to operate
via an increased intrathoracic pressure and reduced left ventricular
transmural pressure gradient, increased lung volume, assistance to
inspiratory respiratory muscles and stabilisation of the upper airway.
Cardiac work is reduced as a result [15].
In patients with established congestive heart failure is likely to be
a marker of advanced disease, via the mechanisms of impaired cardiac
output and elevated sympathetic activity, hyperventilation, reduced lung
volume and circulatory delay. Importantly, such patients who have not
responded to maximal medical therapy might be responsive to positive
airway pressure.
Sincerely
Dr. Murat Enoz
References
1- The report of an American Academy of Sleep Medicine Task Force.
Sleep-related breathing disorders in adults: recommendations for syndrome
definition and measurement techniques in clinical research. Sleep
1999;22:667–89.
2- Gislason T, Almqvist M. Somatic diseases and sleep complaints: an
epidemiological study of 3,201 Swedish men. Acta Med Scand
1987;221:475–81.
3- Worsnop CJ, Naughton MT, Barter CE, Morgan TO, Anderson AI, Pierce
RJ. The prevalence of obstructive sleep apnea in hypertensives. Am J
Respir Crit Care Med 1998;157:111–5.
4- Wilcox I, Grunstein RR, Collins FL, Doyle JM, Kelly DT, Sullivan
CE. Circadian rhythm of blood pressure in patients with obstructive sleep
apnea. Blood Press 1992;1:219–22.
5- Pepperell JCT, Ramdassingh-Dow S, Crosthawaite N, et al.
Ambulatory blood pressure after therapeutic and subtherapeutic nasal
positive airway pressure for obstructive sleep apnoea: a randomised
parallel trial. Lancet 2001;359:204–10.
6- Grunstein R, Wilcox I, Yang TS, Gould Y, Hedner J. Snoring and
sleep apnoea in men: association with central obesity and hypertension.
Int J Obes Relat Metab Disord 1993;17:533–40.
7- Elmasry A, Lindberg E, Berne C, et al. Sleep-disordered breathing
and glucose metabolism in hypertensive men: a population-based study. J
Intern Med 2001;249:153–61.
8- Newman AB, Nieto FJ, Guidry U, et al. Relation of sleep-disordered
breathing to cardiovascular disease risk factors: the Sleep Heart Health
Study. Am J Epidemiol 2001;154:50–9.
9- Javaheri S, Parker TJ, Liming JD, et al. Sleep apnea in 81
ambulatory male patients with stable heart failure: types and their
prevalences, consequences, and presentations. Circulation 1998;97:2154–9.
10- Javaheri S. Effects of continuous positive airway pressure on
sleep apnea and ventricular irritability in patients with heart failure.
Circulation 2000;101:392–7.
11- Garrigue S, Bordier P, Jais P, et al. Benefit of atrial pacing in
sleep apnea syndrome. N Engl J Med 2002;346:404–12.
12- Mayer J, Becker H, Brandenburg U, Penzel T, Peter JH, von Wichert
P. Blood pressure and sleep apnea: results of long-term nasal continuous
positive airway pressure therapy. Cardiology 1991;79:84–92.
13- Carlson JT, Hedner J, Elam M, Ejnell H, Sellgren J, Wallin BG.
Augmented resting sympathetic activity in awake patients with obstructive
sleep apnea. Chest 1993;103:1763–8.
14- Tkacova R, Niroumand M, Lorenzi-Filho G, Bradley TD. Overnight
shift from obstructive to central apneas in patients with heart failure:
role of PCO2 and circulatory delay. Circulation 2001;103:238–43.
Positive-pressure ventilation may be associated with adverse
cardiovascular effects, particularly when using large tidal volumes and /
or high PEEP. The increased intra-thoracic pressure decreases venous
return to the heart with subsequent reduction of cardiac filling, cardiac
output and blood pressure. On the other hand, positive-pressure
ventilation may have beneficial hemodynamic effects. If the pos...
Positive-pressure ventilation may be associated with adverse
cardiovascular effects, particularly when using large tidal volumes and /
or high PEEP. The increased intra-thoracic pressure decreases venous
return to the heart with subsequent reduction of cardiac filling, cardiac
output and blood pressure. On the other hand, positive-pressure
ventilation may have beneficial hemodynamic effects. If the positive
airway pressure is timed to occur during systole and the airway pressure
is released during diastole, cardiac output can sometimes be increased and
the mechanical ventilator can actually function as a partial ventricular
assist device ( as if the ventilator is squeezing the heart when the intra
-thoracic pressure is increased during systole) . Based on clinical
observation, many patients with decompensated heart failure (who were
intubated and ventilated because of acute pulmonary oedema) improved
significantly several hours after mechanical ventilation. Compensatory
tachycardia, ventricular ectopics and gallop rhythm decreased and many
patients showed much better diuretic response. In addition, some patients
with underlying Coronary artery disease - CAD - demonstrated ECG evidence
of improved myocardial ischemia after initiation of positive- pressure
ventilation (nitrates and calcium antagonists were not given to those
patients with borderline B.P for fear of exaggerated ventilator - induced
hypotension). It should be remembered that ventilator-induced hypotension
is a potential complication in volume-depleted patients rather than the
fluid-overloaded patients with heart failure. We can assume that
mechanical ventilator may be particularly useful to patients with
decompensated heart failure as it may augment ventricular contraction,
improve arterial oxygenation and hence myocardial O2 supply and reduce
preload (as a result of increased intra-thoracic pressure and reduced
venous return). Preload reduction not only reduces pulmonary congestive
symptoms but also decreases left ventricular end-diastolic diameter (
L.V.EDD ), L.V wall tension and therefore cardiac work and myocardial O2
demand (the same mode of action of nitrates that may explain the ECG
evidence of improved ischemia in some patients with CAD shortly after
intubation. It is to be remembered that L.V wall tension depends on
L.V.EDD - determined by preload - and intra-ventricular pressure -
determined by after load. Positive - pressure ventilation may also be
beneficial in the clinical setting of acute pulmonary oedema in which up
to 40 – 50 % of the cardiac output may be taken up by the overacting
respiratory muscles of the severely distressed patients. After intubation,
ventilation and sedation (with or without muscle paralysis), mechanical
ventilator provides "rest" to the overacting respiratory muscles and
allows redistribution of the cardiac output from the respiratory muscles
to the heart, brain and kidneys. This may lead to improved coronary blood
flow and myocardial O2 supply which may further enhance myocardial
contractility and reduce myocardial ischemia. In addition, renal blood
flow may also be increased which may explain the enhanced diuretic
response in heart failure patients after intubation and mechanical
ventilation. In conclusion, positive-pressure ventilation may have several
beneficial effects in patients with decompensated heart failure who are
intubated because of acute pulmonary oedema and hypoxemic respiratory
failure. This may include increased cardiac output, improved myocardial
ischemia (due to increased O2 supply and reduced O2 demand) and increased
renal perfusion and diuretic response. Finally, this issue needs more
evaluation using echocardiography (to assess L.V function and regional
wall motion), invasive hemodynamic monitoring (to measure cardiac output,
PCWP and pulmonary artery pressure) as well as biochemical markers of
heart failure such as the recently available B-type natriuretic peptide
that may be of value in assessing the severity of heart failure.
References
1. Pinsky HR. Cardiovascular effects of ventilatory support and withdrawal. Anaesth. Analg 1994; 79: 567 – 576
2. Veisprille A. The pulmonary circulation during mechanical ventilation. Acta Anesthesiol Scand 1990; 34 (Suppl):51-62.
I read with interest this article in Thorax and have been worried by the comments in "Pulse" which followed (9 December 2000).
The lack of information about the general practitioner (GP) consultations, and the non-
availability of records is alarming and dispiriting. Particularly when
nowadays much information is computerised and records can in emergency
situations, given the hard work of Health...
I read with interest this article in Thorax and have been worried by the comments in "Pulse" which followed (9 December 2000).
The lack of information about the general practitioner (GP) consultations, and the non-
availability of records is alarming and dispiriting. Particularly when
nowadays much information is computerised and records can in emergency
situations, given the hard work of Health Authorities pass between
practices in days.
It would be helpful to know what physical signs might have been
missed, indeed the selection process does not define presenting clinical
signs (beyond absence of life). So we have no denominator of cases where
we might need to think harder to avoid these events. As an habitual
"examiner" after ten years in general practice (and ten in hospital
medicine) I have been surprised by the paucity of physical signs in
patients with cough fever and purulent sputum. In these days of
evidenced based guidelines leading us away from the use of antibiotics we
need something hard to guide us to avoid the tragic but extremely rare
cases described.
It is a sad fact that subtle physical signs can be missed - even if
they are indeed present. Ten years in general practice has taught me
that serious illness changes quickly from minor symptoms to dire straits.
The only similar case in my recollection was a young woman sent home from
casualty to return moribund to hospital the same day with lobar pneumonia.
Steven Stern, MB ChB BSc MRCP
Principal in General Practice
I was interested to see the work of Figueroa-Munoz and colleagues
showing an association between obesity and wheeze.[1] I would like to
caution against their conclusion. In their study asthma is defined
according to "asthma attack" and parental reports of wheeze. Several
studies have shown parental reporting of wheeze to be unreliable.[2][3][4]
Please can the authors clarify who defined, "asthma att...
I was interested to see the work of Figueroa-Munoz and colleagues
showing an association between obesity and wheeze.[1] I would like to
caution against their conclusion. In their study asthma is defined
according to "asthma attack" and parental reports of wheeze. Several
studies have shown parental reporting of wheeze to be unreliable.[2][3][4]
Please can the authors clarify who defined, "asthma attack?" I see that
their data independent of reported wheeze supports their conclusion but it
would be a stronger argument if parents were not the only ones relied on
to report asthma symptoms. The assumption that all that wheezes is asthma
may lead to the omission of other diagnoses or the inappropriate
prescription of inhaled corticosteroids.
May I be so bold as to suggest an
alternative title for this important work: "Association of obesity and
respiratory symptoms in children"?
References
(1) Figueroa-Munoz JI, Chinn S, Rona RJ. Association of obesity and asthma in 4-11 year old children in the UK Thorax 2001;56:133-7.
(2) Elphick HE, Sherlock P, Foxall G et al. Survey of respiratory sounds in infants. Arch Dis Child 2001;84:35-9.
(3) Cane RS, McKenzie SA. Parents' interpretations of children's respiratory symptoms on video Arch Dis Child 2001;84:31-4.
(4) Cane RS, Ranganathan SC, McKenzie SA. What do parents' of wheezy
children understand by "wheeze". Arch Dis Child 2000;82:327-32.
The observational data presented by Macfarlane et al on the aetiology of
acute lower respiratory tract illness in the community[1] confirm that the
often stated assertion that these illnesses are usually caused by viral
infection is incorrect. The high prevalence of bacteriological and
atypical pathogens, and in particular the high prevalence of C pneumoniae
in these patients is of interest and points to the n...
The observational data presented by Macfarlane et al on the aetiology of
acute lower respiratory tract illness in the community[1] confirm that the
often stated assertion that these illnesses are usually caused by viral
infection is incorrect. The high prevalence of bacteriological and
atypical pathogens, and in particular the high prevalence of C pneumoniae
in these patients is of interest and points to the need for further
studies to clarify the clinical significance of these isolates. The lack
of correlation between indirect evidence of infection (radiographic and
CRP levels), GP assessment of the need for antibiotics and pathogen
isolation are also of great interests and have important messages for
those working in the community.
The outcome conclusions from this study do however need to be treated with
some caution.
The authors state that outcomes were similar whether or not
antibiotics were used, but as this was an unrandomised observational
study, we cannot say that the groups of patients who were and were not
given antibiotics by the GPs in the study were comparable. The experienced
GP researchers in this study may well have had particular reasons for
giving or withholding antibiotics, and the significance of similar
reconsultation rates in these groups is open to interpretation.
In the accompanying editorial,[2] the authors state that systematic
reviews of randomised controlled trials of antibiotic prescription for
acute bronchitis do not support antibiotic treatment, and evidence based
educational initiatives aimed at GPs are advocated as one of the
strategies to alter clinical behaviour.
Having recently reviewed the
literature on this important clinical topic myself,[3] I cannot agree with
their assessment of the current evidence. The more recent review they
quote[4] has been criticised on methodological grounds, and the most
recent and extensive systematic review of this clinical problem, published
on the Cochrane database,[5] comes to very different conclusions,
commenting that "the review confirmed the impression of clinicians that
antibiotics have some beneficial effects in acute bronchitis". The
benefits are probably small and confined to certain patient subgroups, but
the quantification of benefit and the definition of the characteristics of
responder groups need further studies to delineate.
The world literature
currently consists of eight randomised controlled trials of variable
quality, some 20 years old, that use different antibiotic regimens and
different outcome measures. Several of these studies have concluded that
the antibiotic regimens used did improve outcomes.
The recent enquiry into community acquired pneumonia deaths in young
adults published in this journal,[6] revealed that the primary care
management of these patients at the severe end of lower respiratory tract
infection spectrum was deficient in many cases - three quarters of patients
had seen their GP for the illness without a correct diagnoses and few had
received antibiotics from their GP. There are many areas of uncertainty
remaining in this field, and while observational studies such as this help
to bring some clarity into this confused area of daily clinical practice,
well designed randomised controlled trials are still needed to produce the
evidence based guidance that GPs require. The current evidence is
inadequate to meet the challenge identified by Macfarlane et al,[1] that
of identifying the cohort of patients who will benefit from antibiotics.
Dr Mike Thomas
Clinical Research Fellow
Department of Primary Care Respiratory Medicine
University of Aberdeen, UK
References
(1) Macfarlane J, Holmes W, Gard P, Macfarlane R, Rose D, Weston V.
et al. Prospective study of the incidence, aetiology and outcome of lower
respiratory tract illness in the community. Thorax 2001;56:109-14.
(2) Steele K, Gormley G, Webb CH. Management of adult lower
respiratory tract infection in primary care. Thorax 2001;56:88.
(3) Thomas M. The management of acute respiratory tract infection in
adults in primary care. Primary Care Respiratory Journal 200;9:4-7.
(4) Fahey T, Stocks N, Thomas T. Quantitative systematic review of
randomised controlled trials comparing antibiotic with placebo for acute
cough in adults. BMJ 1998;316:910.
(5) Becker L, Glazier R, McIsaac W, and et al. Antibiotics for acute
bronchitis. Douglas R, Bridges-Webb C, Glasziou P, and et al. (1). 1998.
Oxford, Update software. Acute Respiratory Infections Module of the
Cochrane database of systematic reviews.
(6) Simpson JCG, Macfarlane JT, Watson J, Woodhead M. A national
confidential enquiry into community acquired pneumonia deaths in young
adults in England and Wales. Thorax 2000;55:1040-5.
I read with great interest the article of Nakayama et al about tuberculin
responses and risk of pneumonia in immobile elderly patients. It is known
that TH1 cells are important in delayed type hypersensitivity responses to
tuberculin. The authors' findings are important in assessment of
pathogenesis of pneumonia in elderly patients. But I have some doubts
about the analysis of data. The groups were compared...
I read with great interest the article of Nakayama et al about tuberculin
responses and risk of pneumonia in immobile elderly patients. It is known
that TH1 cells are important in delayed type hypersensitivity responses to
tuberculin. The authors' findings are important in assessment of
pathogenesis of pneumonia in elderly patients. But I have some doubts
about the analysis of data. The groups were compared by using Student's t
test although the groups were less than 30. So Mann Whitney U test must be
used instead of Student t test.
We fully appreciate Dr Furness's comments on the limitations of the
definition of asthma based on parents' reports of symptoms and we have
contributed on the subject.[1] Epidemiological studies of asthma have to
rely on reported symptoms,[2][3] but a better understanding of what
parents call wheeze would be of great importance, especially in a
multicultural society. The validity of reported asthma symptoms...
We fully appreciate Dr Furness's comments on the limitations of the
definition of asthma based on parents' reports of symptoms and we have
contributed on the subject.[1] Epidemiological studies of asthma have to
rely on reported symptoms,[2][3] but a better understanding of what
parents call wheeze would be of great importance, especially in a
multicultural society. The validity of reported asthma symptoms has been
demonstrated in adults[4] and the symptoms analysed in the validation were
not dissimilar from those used in our study.
We have discussed that parents' perceptions of asthma may vary
according to ethnicity and social background.[5][6] False positive and
false negative responses could arise if parents mislabel other respiratory
symptoms as wheeze or if persistent wheeze is unrecognised.[7] Persistent
wheeze is unrecognised as asthma in a large percentage of children from
the ethnic minorities and inner city areas. We performed the analysis
using either parental reports of persistent wheeze or asthma attacks in
order to overcome these differences and the results were consistent. We
adjusted for ethnicity and study area in the analysis of the inner city
sample to account for the variation in perception.
References
(1) Jones CO, Qureshi S, Rona RJ, et al. Exercise-induced bronchoconstriction by ethnicity and presence of asthma in British nine
year olds. Thorax 1996;51:1134-6.
(2) Burney PGJ, Chinn S, Rona RJ. Has the prevalence of asthma
increased in children? Evidence from the National Study of Health and
Growth 1973-86. BMJ 1990;300:1306-10.
(3) The International Study of Asthma and Allergies in Childhood
(ISAAC) Steering Committee. Worldwide variations in the prevalence of
asthma symptoms: The International Study of Asthma and Allergies in
Childhood (ISAAC). Eur Respir J 1998;12:315-35.
(4) Burney PG, Laitinen LA, Perdrizet S, et al. Validity and
repeatability of the IUATLD (1984) bronchial symptom questionnaire: an
international comparison. Eur Respir J 1989;2:940-5.
(5) Duran-Tauleria E, Rona RJ, Chinn S, Burney P. Influence of ethnic
group on asthma treatment in children in 1990-1: national cross sectional
study. BMJ 1996;313:148-52.
(6) Duran-Tauleria E, Rona RJ. Geographical and socioeconomic
variation in the prevalence of asthma symptoms in English and Scottish
children. Thorax 1999;54:476-81.
(7) Cane RS, Ranganathan SC, McKenzie SA. What do parents of wheezy
children understand by wheeze? Arch Dis Child 2000;82:327-32.
Gupta and colleagues [1] present the epidemiology of pneumothorax in
England using national data from the Hospital Episode Statistics for
emergency hospital admissions, which in turn is reliant on information
provided from local National Health Service (NHS) trusts. However, little
is known of the reliability of these locally collected data on the
incidence of pneumothorax.
Gupta and colleagues [1] present the epidemiology of pneumothorax in
England using national data from the Hospital Episode Statistics for
emergency hospital admissions, which in turn is reliant on information
provided from local National Health Service (NHS) trusts. However, little
is known of the reliability of these locally collected data on the
incidence of pneumothorax.
We prospectively evaluated data from The Ipswich Hospital NHS Trust
over a four-year period (2001 – 2004). Data for episodes of pneumothorax
were obtained from hospital records identified through the appropriate
discharge codes. Chest X-ray reports which demonstrated the presence of
pneumothorax, acted as the ‘gold-standard’ of which the reliability of
data was assessed, as every pneumothorax episode would have required
radiological confirmation.
The number of pneumothorax episodes as recorded by the hospital
database was 135 compared to 210 reported on chest radiographs, indicating
that the former correctly identified 64% of pneumothorax episodes compared
to the latter.
Formal data recording of pneumothorax episodes is unreliable in our
locality, and if our experience is mirrored in other local NHS trusts,
this may well influence the national epidemiology of pneumothorax as a
whole in England. A more reliable method of identifying pneumothorax
episodes is now urgently needed.
References
(1) Gupta D, Hansell A, Nichols T, et al. Epidemiology of pneumothorax
in England. Thorax 2000;55:666-71.
Several measures exist to aid the diagnosis of upper airway obstruction (UAO). These include subjective clinical signs such as the presence of stridor and objective measures such as the pattern of the flow-volume curve. However, by far the simplest and easily measured, but yet relatively unknown and underutilised, is the forced expiratory volume in 1 second (FEV1) / peak expiratory flow (PEF) rat...
Several measures exist to aid the diagnosis of upper airway obstruction (UAO). These include subjective clinical signs such as the presence of stridor and objective measures such as the pattern of the flow-volume curve. However, by far the simplest and easily measured, but yet relatively unknown and underutilised, is the forced expiratory volume in 1 second (FEV1) / peak expiratory flow (PEF) ratio. We wish to reignite attention to the use of this uncomplicated measurement through presentation of an interesting clinical case.
A 57-year old lady presented to our respiratory clinic with a complaint of inspiratory stridor. She did not have any other significant respiratory symptoms. There were no overt symptoms of gastroesophageal reflux or oesophageal dysfunction. On direct questioning, she denied any symptoms consistent with collagen vascular disease or vasculitis, except Raynaud’s phenomenon. Her medications included losartan for hypertension and amitriptyline for depression. She is a never-smoker. Clinical examination was unremarkable apart from a soft inspiratory stridor, which was heard best above the suprasternal notch. Her blood biochemistry, haematology, autoimmune, and vasculitic screen were unremarkable. Spirometry showed FEV1 of 2.79L (110% predicted), forced vital capacity (FVC) of 3.57L (120% predicted), FEV1/FVC ratio of 78%, and PEF of 396L/min (105% predicted). Her calculated FEV1/PEF ratio was 7.05ml/L/min. The pattern of the expiratory flow-volume curve was normal with a slight plateau in the inspiratory flow-volume curve (Figure 1). Flexible fibre-optic bronchoscopy demonstrated a subglottic stenosis (Figure 2).
Several pioneering studies have previously determined the usefulness of the FEV1/PEF ratio in diagnosing UAO.1-3 FEV1 is defined as the volume measured during the initial 1 second of a forced expiration from full inspiration and PEF is defined as the maximum flow rate maintained for at least 10 milliseconds during a forced expiration from full inspiration. Therefore, in UAO where the embarrassment is in the pre-carina upper airway, one would intuitively expect the FEV1/PEF ratio to increase, as chronologically, PEF would be affected more than FEV1, with the former reflecting more proximal airway per se. Evidently, the FEV1/PEF ratio has been shown to be significantly higher in patients with UAO compared to patients with asthma, chronic obstructive pulmonary disease, and normal subjects.1;2 A value of above 10ml/L/min was initially thought to represent UAO,1;2 although this was subsequently found to vary between 7ml/L/min and 12ml/L/min depending on the different subgroups of UAO such as extrathoracic, fixed, and variable intrathoracic.3
Therefore, although definitive procedures such as flexible fibre-optic bronchoscopy are needed to confirm the diagnosis of UAO, straightforward practical measurements that are useful in day-to-day clinical practice such as the FEV1/PEF ratio, which is easily obtainable through simple spirometry, may aid in either prompting initial consideration or confirming clinical suspicion of such a diagnosis.
Daniel K C Lee, MB, BCh, MRCP, MD
Prashant S Borade, MB, BS, MD
Nicholas J Innes, MB, BS, FRCP
Department of Respiratory Medicine, Ipswich Hospital, Heath Road, Ipswich IP4 5PD, Suffolk, England, United Kingdom
Rotman HH, Liss HP, Weg JG. Diagnosis of upper airway obstruction by pulmonary function testing. Chest 1975; 68: 796-799.
Mellisant CF, Van Noord JA, Van de Woestijne KP, Demedts M. Comparison of dynamic lung function indices during forced and quiet breathing in upper airway obstruction, asthma, and emphysema. Chest 1990; 98: 77-83.
Figure 1
Expiratory and inspiratory flow-volume curve
Figure 2
Subglottic stenosis found on flexible fibre-optic bronchoscopy
The review of Pulmonary Rehabilitation in the UK (Thorax, 2001: 56:
827-834) by Dr MDL Morgan begins by noting the lag between the quality of
pulmonary rehabilitation services in the USA compared to their virtual
absence in the UK. Dr Morgan goes on to mention that psychology is one of
the disciplines included in the multiple disciplines that comprise an
effective pulmonary rehabilitation program. In fact, most of the le...
The review of Pulmonary Rehabilitation in the UK (Thorax, 2001: 56:
827-834) by Dr MDL Morgan begins by noting the lag between the quality of
pulmonary rehabilitation services in the USA compared to their virtual
absence in the UK. Dr Morgan goes on to mention that psychology is one of
the disciplines included in the multiple disciplines that comprise an
effective pulmonary rehabilitation program. In fact, most of the leading
hospitals in the US that have pulmonary rehabilitation programs are indeed
truly "multidisciplinary" and the psychosocial and emotional functioning
of the clients constitutes an important ingredient of such programs.
However, the "most recent definition of pulmonary rehabilitation" cited by
Dr Morgan waters down the role of psychology and the program that he
recommends for the UK appears to be primarily exercise based and
physiotherapy-led. In fact,the process and components of pulmonary
rehabilitation described by Dr Morgan comprise almost entirely of
exercise. Dr Morgan acknolwedges only that the "coexistence of reduced
self-efficacy and the affective component is likely to have an effect on
performance," and even so, in the next sentence he, astonishingly,
essentially dismisses the need for a psychologist in such programs:
"psychological and behavioural intervention is already embedded in the
structure of rehabilitation programmes through the delivery of education,
small group discussions and relaxation therapy.... The role of
specific, individual or group psychotherapy is also unclear." According
to him, the only area where psychologists may contribute is in the
assessment of motivation!
Dr Morgan recommends the usage of mental health
questionnaires, presumably psychosocial and mental health variables are
only to be measured not targeted for treatment -- as the presumtion sems
to be that with improved lung function, all such parameters will
automatically improve as well. If this were so, then we would hope that
problems in treatment compliance, severe panic attacks with or without
agoraphobia, debilitating anxiety, depression, fear of death and dying
frequently seen in COPD patients will also automatically resolve without
the need for a professional psychologist on a pulmonary rehabilitation
program. When read closely, the program described in this article does
not resemble a multidisciplinary program at all and hence it should simply
be called a Physiotherapy or Exercise-Based program. Sadly, the kind of
program described will fail many of the COPD patients and Pulmonary
Rehabilitation in the UK will continue to be well behind the well-rounded,
well-funded multidisciplinary prgrams in the US.
Dear Editor,
Obstructive sleep apnea (OSA) is a common disorder associated with an increased risk of cardiovascular disease and stroke. As it is strongly associated with known cardiovascular risk factors, including obesity, insulin resistance, and dyslipidemia, OSA is an independent risk factor for hypertension and has also been implicated in the pathogenesis of congestive cardiac failure, pulmonary hypertension...
Dear Editor
Positive-pressure ventilation may be associated with adverse cardiovascular effects, particularly when using large tidal volumes and / or high PEEP. The increased intra-thoracic pressure decreases venous return to the heart with subsequent reduction of cardiac filling, cardiac output and blood pressure. On the other hand, positive-pressure ventilation may have beneficial hemodynamic effects. If the pos...
I read with interest this article in Thorax and have been worried by the comments in "Pulse" which followed (9 December 2000).
The lack of information about the general practitioner (GP) consultations, and the non- availability of records is alarming and dispiriting. Particularly when nowadays much information is computerised and records can in emergency situations, given the hard work of Health...
I was interested to see the work of Figueroa-Munoz and colleagues showing an association between obesity and wheeze.[1] I would like to caution against their conclusion. In their study asthma is defined according to "asthma attack" and parental reports of wheeze. Several studies have shown parental reporting of wheeze to be unreliable.[2][3][4]
Please can the authors clarify who defined, "asthma att...
The observational data presented by Macfarlane et al on the aetiology of acute lower respiratory tract illness in the community[1] confirm that the often stated assertion that these illnesses are usually caused by viral infection is incorrect. The high prevalence of bacteriological and atypical pathogens, and in particular the high prevalence of C pneumoniae in these patients is of interest and points to the n...
I read with great interest the article of Nakayama et al about tuberculin responses and risk of pneumonia in immobile elderly patients. It is known that TH1 cells are important in delayed type hypersensitivity responses to tuberculin. The authors' findings are important in assessment of pathogenesis of pneumonia in elderly patients. But I have some doubts about the analysis of data. The groups were compared...
We fully appreciate Dr Furness's comments on the limitations of the definition of asthma based on parents' reports of symptoms and we have contributed on the subject.[1] Epidemiological studies of asthma have to rely on reported symptoms,[2][3] but a better understanding of what parents call wheeze would be of great importance, especially in a multicultural society. The validity of reported asthma symptoms...
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Gupta and colleagues [1] present the epidemiology of pneumothorax in England using national data from the Hospital Episode Statistics for emergency hospital admissions, which in turn is reliant on information provided from local National Health Service (NHS) trusts. However, little is known of the reliability of these locally collected data on the incidence of pneumothorax.
We prospectively...
Dear Editor,
Several measures exist to aid the diagnosis of upper airway obstruction (UAO). These include subjective clinical signs such as the presence of stridor and objective measures such as the pattern of the flow-volume curve. However, by far the simplest and easily measured, but yet relatively unknown and underutilised, is the forced expiratory volume in 1 second (FEV1) / peak expiratory flow (PEF) rat...
The review of Pulmonary Rehabilitation in the UK (Thorax, 2001: 56: 827-834) by Dr MDL Morgan begins by noting the lag between the quality of pulmonary rehabilitation services in the USA compared to their virtual absence in the UK. Dr Morgan goes on to mention that psychology is one of the disciplines included in the multiple disciplines that comprise an effective pulmonary rehabilitation program. In fact, most of the le...
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