Page 215 - Cardiac Nursing

q
xd
xd
03.
q
q
/29
/09
/09
6
6
/29
c.
In
c.
ara
a
a
7-2
7-2
03.
17
17
In
1
91
A
A
e 1
e 1
91
t
t
ara
p
p
p
6 P
6 P
M
1
0:1
0:1
g
g
g
M
Pa
Pa
K34
0-c
08_
LWB K34 0-c 08_ p p pp177-203.qxd 6/29/09 10:16 PM Page 191 Aptara Inc.
LWBK340-c08_
LWB
C HAPTER 8 / Sleep 191
development of DM, conversely, diabetes itself may contribute to multifactoral and includes nocturnal coughing and dyspnea,
sleep disorders. 252 In patients with diabetes, sleep loss may con- effects of medications (i.e., theophylline), and aging. 257,261
tribute to elevations in HgA1c, and symptoms resulting from di- The cardiovascular consequences in patients with COPD are
abetes, such as nocturia and neuropathic pain, may in turn con- associated with the pulmonary hemodynamic alterations that of-
tribute to sleep disturbance and exacerbate sleep deprivation. 252 ten occur with disease progression. During REM sleep in particu-
lar, patients with COPD often have alveolar hypoxia resulting in
Sleep and Chronic Obstructive pulmonary vasoconstriction, pulmonary artery pressure elevation,
Pulmonary Disease (COPD) and over time pulmonary hypertension (cor pulmonale) may de-
velop and result in right ventricular overload and right-sided HF.
Cardiac patients may have COPD as a comorbidity, and approx- In addition, there is an increase in PVCs in patients with COPD,
imately 10% to 15% of COPD patients experience sleep apnea. although the frequency and clinical relevance of PVCs have not
The term “Overlap Syndrome” describes the relationship between been established in COPD, including whether a low nocturnal
COPD and sleep apnea. Patients with overlap syndrome are char- Sa O2 is the major underlying mechanism. During periods of noc-
acterized by having lower Pa O2 during wakefulness, higher Pa CO2 , turnal desaturation, the maximal myocardial O 2 demands are
elevated pulmonary artery pressure, and more significant episodes considerably higher and often exceed those required for maximal
of nocturnal hypoxemia than sleep apnea patients without exercise testing. It is speculated that in patients with more ad-
COPD. COPD and sleep apnea are each recognized to contribute vanced COPD, this differences in O 2 demand may be one of the
detrimental influence on the respiratory physiology of patients, reasons for higher rates of nocturnal death. 254,256
overall health status and poor quality of life. 253–261 The cornerstone of treatment for COPD remains smoking ces-
Patients with COPD who are hypoxic during wakefulness sation, bronchodilation, and pulmonary rehabilitation. Decreased
become more hypoxic during sleep. 259 A strong association ex- levels of hypoxia in COPD patients are usually achieved by con-
ists between nocturnal O 2 saturation and level of daytime hy- ventional home O 2 therapy (16 to 18 hours/day). Hypnotics are
poxia; with higher daytime hypoxia related to more severe noc- contraindicated in hypercapnic patients and should be used with
turnal desaturation and hypoxia. Desaturation is defined as a caution in hypoxic individuals. Alcohol worsens hypoxia and
drop in Sa O2 of 4 from its baseline level, during quiet breathing should be avoided in the evening in particular, since heavy con-
and just before an episode of hypoxia. Nocturnal desaturation sumption is linked to hypercapnic respiratory failure. Finally, im-
is more severe during REM sleep and may exceed 15 minutes. proving sleep quality will likely improve overall health status and
However, nocturnal desaturation may also occur during non- enhance quality of life in this population. 258,262 This is especially
REM sleep, especially light sleep (stages I and II) but is not as important in those with overlap syndrome whose 5-year survival
severe and of shorter duration. 259–261 Studies have established is lower than that of patients with sleep apnea alone. 253,260
that the most optimal index of sleep-related desaturation is the
mean nocturnal Sa O2 or the mean percentage of recording time Sleep and Depression
under a certain percentage level. In patients with mild daytime
hypoxia Pa O2 60 mm Hg, or with no hypoxia, significant Sleep is an essential component of the pathophysiology and treat-
nocturnal desaturation is defined as a mean Sa O2 90 mm Hg. ment of depression. 263 The majority of people with depressive dis-
The best predictor of nocturnal desaturation in patients with orders experience SPD, and most diagnostic criteria for depression
mild to moderate daytime hypoxia is level of diurnal Pa O2 , but include sleep disturbances. While the likelihood of developing a
daytime Pa CO2 is also an independent predictor of Sa O2 during mood disorder is not simply a consequence of having a sleep pat-
sleep. 257 tern disturbance, longitudinal studies document that insomnia is
Two mechanisms are primarily responsible for worsening hy- a risk factor for onset of depressive disorder 264 and may increase
poxia during sleep in COPD patients: alveolar hypoventilation the risk for relapse in patients with recurrent illness. 265 More than
and ventilation–perfusion mismatching. Alveolar hypoventilation 90% of depressed patients complain about impairments of sleep
differs according to non-REM and REM sleep stages. In non- quality. Typically, patients suffer from difficulties in falling asleep,
REM sleep, alveolar hypoventilation is associated with a lower frequent nocturnal awakenings, and early morning awakening.
basal metabolic rate, reduced ventilatory drive, and an increase in Whereas sleep onset problems and frequent awakenings accom-
upper airway resistance. In REM sleep, ventilatory drive is pany almost any kind of insomnia in the general population, life-
markedly lower, and the hypoxic and hypercapneic responses are time prevalence of depression is approximately 5% to 10%. How-
diminished compared to non-REM sleep or wakefulness. A sec- ever, among patients with cardiovascular disease, these rates of
ond important factor related to REM sleep hypoventilation is a re- depression are two to three times higher. Major depression affects
duction in muscle strength of the respiratory muscles, which likely approximately 15% to 20% of patients with CVD, and minor de-
explains the significant relation between mean nocturnal Sa O2 and pression is present in another 20%. Similar prevalence rates are re-
inspiratory muscle strength; the lower the muscle strength the ported for sleep disturbances in CVD. 213,266 Physiologically, the
lower the nocturnal Sa O2 . Worsening ventilation perfusion mis- brain stem and thalamic nuclei that regulate sleep and the limbic
matching during REM sleep in patients with COPD is largely due mechanisms that modulate mood are implicated in pathogenesis
to reduction in functional residual capacity resulting in closing of of both SPD and depression. 267,268
small airways in dependent areas of the lung. 259,261 Most individuals who are depressed exhibit one or more alter-
Many patients with COPD complain of poor sleep quality ations in sleep neurophysiology. Multiple disturbances in PSG
which often worsens as disease severity increases. In addition, they recordings have been reported in depressed patients during sleep,
experience reduced sleep efficiency with delayed time for sleep on- and these changes are more pronounced as depression increases.
set, a reduction in total sleep time and periods of wakefulness of- The most common sleep disturbances in depression include de-
ten prolonged. Poor sleep quality in patients with COPD is likely creased sleep efficiency, nocturnal and early-morning awakening,