Recent studies have shown in both patients and clinical studies that sleep depri
ID: 3479351 • Letter: R
Question
Recent studies have shown in both patients and clinical studies that sleep deprivation causes elevated heart rate and hypertension. a) From the literature, what is the cause of the increased heart rate and hypertension in the sleep deprived? (need more than 3 references; b) What are the cellular mechanisms behind the increase in heart rate? c) What effect would this have on the kidney? d) How would sleep deprivation affect venous return, cardiac output and central venous pressure? (I need cell and tissue mechanisms and graphs; 20pts)e) How would sleep deprivation alter pre-load, afterload and the length-tension curve of the left ventricle?
Explanation / Answer
a) Sleep is essential for a healthy heart. People who don't sleep enough are at higher risk for cardiovascular disease—regardless of age, weight, smoking and exercise habits. One study that examined data from 3,000 adults over the age of 45 found that those who slept fewer than six hours per night were about twice as likely to have a stroke or heart attack as people who slept six to eight hours per night.
It's not completely clear why less sleep is detrimental to heart health, but researchers understand that sleeping too little causes disruptions in underlying health conditions and biological processes like glucose metabolism, blood pressure, and inflammation. One of the reasons we know how vital sleep is to the heart is that patients with sleep apnea (which causes them to wake frequently throughout the night) often have compromised heart health. This is because, without long, deep periods of rest, certain chemicals are activated that keep the body from achieving extended periods in which heart rate and blood pressure are lowered. Over time, this can lead to higher blood pressure during the day and a greater chance of cardiovascular problems. Many studies have shown the relationship between sleep apnea and cardiovascular disease. One found that over an eight-year period, men with severe sleep apnea were 58 percent more likely to develop congestive heart failure than men without the nighttime breathing disorder. But it doesn't take a severe underlying sleep disorder to see effects on the heart.
Recent research has shown that too little sleep earlier in life could take its toll as well. For example, in one study, adolescents who didn't sleep well were at greater risk of developing cardiovascular problems. Those teens had higher cholesterol levels, a higher body mass index, larger waist sizes, higher blood pressure, and an increased risk of hypertension. It's easy to see how these alterations in childhood health could snowball into major concerns later on, and why it's important to protect sleep at every age.
b) Short sleep duration was associated with the development of HT (Hypertension). This may be attributable in part to autonomic dysregulation that changes the predominant neutral interaction of sympathovagal balance during sleep into the increased sympathetic tone. In 24 hr ambulatory blood pressure monitoring (ABPM) studies, BP tended to rise the day after sleep deprivation in both normotensives and hypertensives. Similarly, Tochikubo et al. showed significant increases in BP, low-frequency/high-frequency (LF/HF) ratio, and urinary excretion of norepinephrine, especially in the evening, the day after sleep deprivation in 18 male technical workers aged 23 to 48 years. These data suggest that a lack of sleep may increase sympathetic nervous system activity the next day. Zhong et al. assessed cardiovascular autonomic modulation during 36 hr of total sleep deprivation in 18 normal healthy subjects. LF was significantly increased at 12 and 24 hr, as was LF/HF at 12 hr, whereas HF was decreased at 12 hr of sleep deprivation.
Using polysomnography, Irwin et al. examined whether or not nocturnal vagal tone indexed by HF was related to measures of sleep depth and daytime perceptions of sleep quality, sleepiness, and fatigue in alcohol-dependent patients. Compared with the controls, these patients showed the decrease in delta sleep time along with impairments in sleep quality, daytime energy, and the HF component both before and during sleep.
Irwin and Ziegler investigated whether or not sleep deprivation induces differential cardiovascular and sympathetic responses, and measured heart rate, BP, and circulating sympathetic catecholamines in 36 abstinent alcohol-dependent men and 36 age-, gender-, and ethnicity-matched controls. Although baseline heart rate, BP, and sympathetic catecholamines were similar in both groups, partial night sleep deprivation induced greater increases in heart rate and circulating levels of norepinephrine and epinephrine in the alcohol-dependent men than in controls.
Vascular lesions with atherosclerosis are filled with immune cells that affect inflammatory responses. These responses are suggested to initiate plaque activation that progress hypertensive status. Born et al. have shown that stimulated ex vivo production of interleukin-2 (IL-2) is higher during sleep suggesting that this effect is dependent on sleep. Conversely, partial night sleep deprivation induced decreases in stimulated production of IL-2 and natural killer cell responses.
Irwin et al. measured circulating levels of catecholamines and IL-2 sampled every 30 minutes during two nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600) in 17 healthy male volunteers. On the PSD-L night, levels of norepinephrine and epinephrine significantly increased in association with nocturnal awakening. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or various sleep stages.
Elevated plasma concentrations of C-reactive protein (CRP) are indicative of systemic inflammation. Circulating CRP levels are representative marker of vascular damage progression. In this point, higher CRP level would be associated with incidence of HT. Meier-Ewert et al. measured high-sensitivity C-reactive protein (hs-CRP) collected every 90 minutes for 5 consecutive days in 10 healthy adults who stayed awake for 88 continuous hours. The hs-CRP concentrations and systolic BP increased during that period.
Additionally, excessive waking periods would induce long-standing psycho-social stress. Recently, stress exposure has been found to lead to increased salt intake and inhibition of renal salt excretion. These processes may be related to HT development during volume overload for 24 hr and to arterial remodelling.
In short, sleep deprivation is associated with increased sympathetic tone. Sleep loss might serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.
c) Kidney function is actually regulated by the sleep-wake cycle. It helps coordinate the kidneys’ workload over 24 hours. We also know that nocturnal patterns can affect chronic kidney disease and that people who sleep less usually have faster kidney function decline.
Better understanding how the kidneys work and interact with our hormones at night might also help determine better nutrition guidelines and optimized times for medication delivery. This is because the kidneys’ ability to process medications and nutrients like sodium and potassium changes between day and night.
Although it is commonly accepted that patients with Chronic Kidney Disease (CKD) experience poor sleep quality, not much is known about the physiological mechanisms underlying this phenomenon. According to Hildreth, patients with CKD often exhibit sympathovagal imbalance due to baroreceptor reflex function impairment in which there is hyperactivity of the sympathetic nervous system and decreased vagal tone. In healthy individuals, sleep is accompanied by a decrease in sympathetic activity and an increase in a vagal tone that leads to a nocturnal dipping of blood pressure. However, patients who have sleep disorders resulting in hypoxemia and sleep fragmentation have been shown to have increased sympathetic nervous system stimulation and decreased parasympathetic activity, which results in a reduced fall in nocturnal blood pressure.
Blood pressure regulation by the autonomic nervous system during sleep also affects the renin-angiotensin-aldosterone system. As blood pressure decreases during the normal sleeping period, there is a reflexive increase in plasma renin activity and aldosterone. As an individual goes through cycles of rapid eye movements (REM) and non-REM (NREM) sleep, there are oscillations of cardiac sympathovagal balance and plasma renin levels. Plasma renin activity and aldosterone peaks during NREM sleep more specifically stages 3 and 4 and dips during REM sleep. This oscillatory nature of PRA is absent in patients who experience a night of sleep deprivation. However, decreased sleep duration is not the only factor affecting nocturnal PRA and aldosterone secretion. Sayk et al showed that decreased sleep quality induced by suppressing slow-wave sleep (stages 3 and 4) also reduced nocturnal blood pressure dipping, which would affect the RAA system as well. It is believed that the lack of nocturnal blood pressure dipping is an important risk factor for progression of CKD. Reducing nighttime blood pressure by means of carefully timed antihypertensive therapy in the evenings may reduce the risk of progression of CKD to ESRD (End Stage Renal Disease).
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