Page 214 - Cardiac Nursing

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190 PA R T I I / Physiologic and Pathologic Responses
audible high-frequency closing clicks and low-frequency sounds The cumulative effects of excess sympathetic activity, in addition
conducted by body tissues that the patient becomes accustomed to other vasoactive factors in response to hypoxia (such as en-
to over time. Although very few interventions have been tested for dothelin), may result in daytime hypertension. Even without day-
their effects on promoting sleep after cardiac surgery, attention to time hypertension, patients with SRBD do not often exhibit the
reducing noxious environmental stimuli is an obvious approach. normal nocturnal dip in blood pressure during sleep due to apnea-
Examples are found in studies reporting positive effects of struc- induced sympathetic activation. Higher nocturnal blood pressure,
tured quiet time, guidelines to reduce noise, and providing pa- independent of daytime hypertension, places the individual at
tients with earplugs while in intensive care units, use of white greater risk for cardiovascular morbidity and mortality. 243,244
noise and music therapy. 217,223 Because sleep disruptions after Patients with SRBD and hypertension experience frequent
cardiac surgery are multifactorial and include environmental, arousals, reduced length and depth of non-REM sleep, and short-
treatment-related, and intrinsic factors, a comprehensive ap- ened REM latency, all of which lead to EDS, fatigue, and im-
proach to management of these problems is essential. paired concentration. 245 Sleep duration has also been recently
shown to influence the risk of hypertension in patients 60 years
Sleep and HF of age who sleep 5 hours per night 246 and is supported by find-
ings from the Sleep Heart Health Study, which suggests a median
SPD are one of the most burdensome and frequently occurring sleep duration of 7 to 8 hours per night increases the prevalence
symptoms in patients with HF. 224,225 Insomnia is the most com- of hypertension. 153 Because hypertension is often associated with
mon SPD, and evidence suggests that up to 70% of patients with other comorbid conditions such HF, obesity, and diabetes, better
HF experience at least one sleep complaint, far exceeding the 10% self-management of these conditions will likely alter the progres-
to 15% reported in the general population. 226 Factors that con- sion of SPD or SRBD, and this is an area for future investiga-
tribute to sleep SPD in persons with HF include increased age, tion. 1,236,247
body mass index, comorbidities, fluid overload, medications, and
psychological distress, particularly depression. 224,227,228 Sleep and Stroke
Sleep-related breathing disorders (SRBD) have been more
widely studied in HF patients than SPDs. Estimates are that Almost every fifth stroke occurs during sleep, yet the data on the
SRBD occur in approximately 50% of HF patients compared to relationship between stroke and sleep are conflicting. 248 Some ev-
5% in the general population. Both OSA and Cheyne–Stokes res- idence suggests that OSA is an independent risk factor for stroke
piration (CSR) with CSA or a mix of both are common in pa- and transient ischemic attack (TIA). Other studies have shown
tients with HF. The hallmarks of CSR–CSA are higher NYHA sleep itself is not a risk factor for stroke because most stroke and
class, atrial fibrillation, frequent nocturnal ventricular arrhyth- TIAs begin between 6:00 AM and noon, while the individual is
mias, lower Pa CO2 and a left ventricular ejection fraction of 20% awake. 249 Some suggest that stroke or TIA is more a cause, rather
or less. 229 Patients with CSR–CSA have interrupted sleep, fre- than consequence of OSA because PSG studies have shown ob-
quent awakenings, and nocturnal O 2 desaturation that results in structive versus central apneas in stroke and equivalent frequency
poor sleep efficiency. Heightened risk for cardiac arrhythmias, and severity of apneas when comparing patients with stroke and
poor clinical outcomes, and increased mortality are also associated TIA. Untreated OSA patients have more strokes, stroke morbid-
with CSR–CSA. 230,231 ity and mortality than those who are treated. Regardless of its role
EDS, poor sleep quality, fatigue, reduced physical function, as a risk factor or consequence, assessment and treatment of OSA
higher depressive symptoms, and a considerably lower quality of in patients with stroke and TIA is advocated. Its contribution to
life are reported among HF patients who experience SPD or hypertension and prothrombosis over time is highly relevant to
SRBD. 229,232,233 PLMs are also associated with SRBD, and con- initial and recurrent stroke. Treating OSA patients with CPAP can
tribute to more frequent nocturnal arousals, poor sleep quality prevent or improve hypertension, reduce abnormal elevations of
and daytime sleepiness. 229 inflammatory cytokines and adhesion molecules, reduce excessive
sympathetic tone, avoid increased vascular oxidative stress, reverse
Sleep and Hypertension coagulation abnormalities, and reduce leptin levels. Grigg-
Damberger 249 recommends a polysomnogram should become
SRBD, particularly OSA, is an independent risk factor for hyper- part of a neurologist’s armamentarium for stroke and TIA.
tension more than any other cardiovascular disease. 234–236 Epi-
demiological studies show that approximately 40% of hyperten- Sleep and Diabetes Mellitus (DM)
sive patients have SRBD, and this number rises to over 80%
among drug-resistant hypertension. 237,238 Recent studies have Given the high prevalence of DM in patients with cardiac condi-
also established a dose–response relationship between severity of tions, it is prudent to note that sleep disordered breathing and
SRBD and hypertension, independent of age, body mass index, sleep loss have been associated with glucose intolerance and in-
gender, alcohol consumption, and smoking. 239–241 For example, sulin resistance. More specifically, a habitual sleep duration of
the Wisconsin Sleep Cohort Study 242 demonstrated that an 6 hours or less or 9 hours or more is associated with increased preva-
apnea–hypopnea index (i.e., the average number of apnea and hy- lence of DM and impaired glucose tolerance. 209 When confound-
popnea events pre hour of sleep) was progressively related to the ing risk factors are rigorously controlled in studies, sleep-related
odds of developing hypertension over the next 4 years compared hypoxemia was also associated with glucose intolerance independ-
to age-matched controls. ent of age, gender, body mass index, and waist circumference and
Elevated nocturnal blood pressure and reduced blood pressure may lead to type 2 DM. 250,251
“dipping” during sleep also suggests a higher probability of un- While recent epidemiological, biological, and behavioral evi-
derlying sleep apnea, even among normotensive individuals. 243 dence suggests that sleep disorders may contribute to the