Chronic Obstructive Pulmonary Disease and Sleep

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Chronic Obstructive Pulmonary Disease and Sleep

• AWAKE Meeting
• February 4, 2009
• Anstella Robinson, MD FCCP FAASM

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Introduction

• Respiratory changes during sleep exacerbate gas
  exchange abnormalities present in those with
  COPD. Subsequent hypoxemia may predispose to
  secondary pulmonary hypertension, heart
  arrhythmias and premature death. More than 40
  of COPD patients complain of sleep disturbances
  including reduced sleep time and increased
  arousals.

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Introduction contd

• COPD patients complain of more daytime sleepiness
  than those without respiratory disease although
  the effects of this on daytime function and
  quality of life have not been studied.

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Respiratory changes during sleep

• During sleep the metabolic rate diminishes.
  Respiratory responses to chemical mechanical and
  cortical inputs are reduced. Increased partial
  pressure of carbon dioxide is a physiological
  response to sleep as is a reduced partial
  pressure of arterial blood oxygen. Reduced tidal
  volume and minute ventilation are also natural
  consequences of sleeping.

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How respiratory function during sleep differs in
COPD

• Normal sleep related respiratory changes can be
  deleterious for those with COPD as they may lead
  to reduced gas exchange and ultimately
  hypoventilation, hypoxemia and hypercapnia
  particularly in REM sleep where muscle atonia is
  the rule. Hypercapnia may lead to a further
  reduction of diaphragmatic contractility and
  ventilatory responsiveness.

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How Respiratory function during sleep differs in
COPD Contd

• Hypoxia may provoke an arousal response although
  this effect varies widely. Patients may continue
  to sleep with significantly impaired oxygen
  levels. Women have an increased responsiveness
  to hypoxemic effects. Impaired respiratory
  muscle activity in COPD patients also effects
  breathing during sleep. Increases in airway
  resistance may cause exaggerated
  broncoconstriction that may be clinically
  significant.

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How Respiratory function during sleep differs in
COPD Contd

• Reduced intercostal muscle activity also affects
  breathing during sleep in those with impaired
  diaphragmatic contraction secondary to
  hyperinflation who may be more dependent on
  accessory muscle function in order to maintain
  ventilation. Hypoxemia and hypercapnia during
  sleep are probably related to hypoventilation in
  patients with reduced respiratory function

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How Respiratory function during sleep differs in
COPD Contd

• Arterial oxygen desaturation during sleep is due
  in mainly to ventilation perfusion mismatch.
  Lung volume changes that occur in sleep include a
  reduction in functional residual capacity. This
  change may lead to ventilation perfusion mismatch
  and significant hypoxemia in patients with COPD.

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How Respiratory function during sleep differs in
COPD Contd

• Reduced FRC is due to
• Respiratory muscle hypotonia
• Diaphragmatic displacement when the patient is
  lying recumbent
• Decreased lung adherence during sleep

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Which COPD Patients Desaturate during sleep and
why?

• The degree of arterial oxygen desaturation
  correlates poorly with measures of pulmonary
  function such as FEV1. arterial oxygen saturation
  while awake is considered to be the best
  predictor of sleep desaturation in patients with
  COPD. Patients with chronic bronchitis (so
  called blue bloaters) have the best correlation
  between awake arterial oxygen saturation and
  minimum arterial oxygen saturation during sleep.

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Which COPD Patients Desaturate during sleep and
why?

• Patients who are hypoxemic while awake are
  typically treated with supplemental oxygen.
  However those whose arterial oxygen saturations
  are borderline while awake and who do not meet
  criteria for supplemental oxygen may develop
  clinically significant hypoxemia while asleep.

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Which COPD Patients Desaturate during sleep and
why?

• Fletcher and colleagues evaluated gas exchange
  and cardiopulmonary hemodynamics in a group of
  COPD patients with borderline oxygen
  desaturations PaO2 gt60mmHg who had significant
  nocturnal oxyhemoglobin desaturation (NOD) and
  compared them to patients with similar pulmonary
  hemodynamics but no NOD

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Which COPD Patients Desaturate during sleep and
why?

• These investigators found
• PaO2 was approximately 12mmHg lower in those with
  NOD compared to those without NOD.
• Arterial/alveolar oxygen tension ratios were more
  abnormal in those with NOD compared to those
  without NOD

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Which COPD Patients Desaturate during sleep and
why?

• Greater arterial oxygen desaturation occurs
  during sleep than in maximal exercise with a
  different mechanism. Awake PaO2 at rest has been
  found to be a better predictor of sleep arterial
  oxygen desaturation than exercise arterial
  desaturation. However awake PaCO2 has not been
  shown as an independent predictor of NOD.

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Coexistent COPD and OSAS (overlap Syndrome)

• Epidemiologic studies show that contrary to what
  one might expect, the prevalence of OSAS in COPD
  patients is similar to that in an age matched
  population without COPD.
• Coexistent COPD and OSAS is associated with more
  severe hypoxemia during sleep.

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Coexistent COPD and OSAS (overlap Syndrome)

• Mean SaO2 is lower in patients with COPD and OSAS
  and the time spent in desaturation is longer than
  those with OSAS alone. Most patients with OSAS
  tend to resaturatre to normal SaO2 levels between
  apneas while those with coexistent COPD may be
  more hypoxemic at the start of the apnea.

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Coexistent COPD and OSAS (overlap Syndrome)

• Thus those with coexistent COPD and OSAS are
  particularly prone to complications of hypoxemia
  such as cor pulmonale. Although early research
  on sleep in COPD had a selection bias towards
  those individuals who sought attention for a
  sleep disorder the Sleep Heart Health Study
  sought to correct this bias by

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Coexistent COPD and OSAS (overlap Syndrome)

• Examining the relationship between COPD and OSAS
  in a large community population of 1132
  participants with predominantly mild COPD who did
  not seek treatment for a sleep disorder. The
  investigation concluded that comorbid COPD and
  OSAS occurred by chance and that a common
  pathophysiological link was unlikely although an
  FEV1/FVC ratio lt65 was associated with an
  increased risk of arterial oxygen desaturation
  during sleep. Greater in patients with COPD and
  OSAS than in those with either disorder alone.

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Cardiac arrhythmias

• In chronic bronchitis patients with basal SaO2
  lt80 studies show multiple atrial and ventricular
  premature contractions as well as other
  abnormalities. Thus sustained hypoxemia
  contributes to myocardial dysfunction and heart
  failure in this subset of patients with COPD.

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Mortality

• Are patients with COPD more likely to die in
  their sleep?
• Some studies suggest that prolonged arterial
  oxygen desaturation during sleep increases the
  risk of death, especially during exacerbations of
  COPD.

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Mortality

• In a study by Fletcher et al 169 patients with
  COPD and daytime PaO2 gt60 mmHG were compared to
  patients with and without NOD. The NOD was
  further characterized as episodic ( desaturation
  occurring mainly in REM sleep) or nonepisodic
  SaO2 lt90 during gt30 of time in bed. At median
  follow up of 3.4 years
• Mortality rated were significantly higher among
  patients with NOD.

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Conclusions

• COPD management must be individualized to each
  patient especially with respect to sleep quality
  and the degree to which COPD sufferers are
  affected by changes in respiratory physiology. It
  is important to perform a sleep history in COPD
  patients as a normal sleep pattern for them might
  actually suggest recurrent nocturnal awakenings
  due to hypercapnia or significant excessive
  daytime sleepiness.

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Conclusions Contd

• Many patients believe that excessive daytime
  sleepiness is a normal part of aging when it may,
  in fact, be part of a treatable condition. Sleep
  studies monitor a number of respiratory and
  neurologic variables and can yield valuable
  information in patients with COPD. Despite new
  research it is unclear how to treat hypoxemia and
  hypercapnia in patients with normal or borderline
  daytime oxygen.
• Coexistent OSAS should be considered in COPD
  patients with snoring or excessive daytime
  sleepiness.

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References

• Fletcher EC, Luckett RA, Miller T et al Pulmonary
  vascular hemodynamics in chronic lung disease
  patients with and without sleep related oxygen
  desaturation during sleep. Chest 1989
  95757-764.
• Sanders MH Newman AB, Hagerty CL et al. For the
  sleep heart health study sleep and sleep
  disordered breathing in adults with predominantly
  mild obstructive airway disease. Am J Respir Crit
  Care Med 2003 1677-14.
• Fleetham JA, Wandersee K. Tosleep perchance to
  breathe How sleep affects patients with COPD.
  Trends and Reviews in COPD 2008 2 4-11.