There are several types of sleep apnea that exist, but the most frequently diagnosed is obstructive sleep apnea (OSA), which occurs when muscles relax in the throat causing an airway blockage. The blockage causes people to snore and/or wake up during the night multiple times. A victim to this disorder becomes sleepy during the day, turning it into the source of poor performance at work and even car crashes. While day time sleepiness and fatigue are largely reported as the most common symptoms by patients, OSA can have a bad effect on the cardiovascular system that often goes unnoticed.
“The evidence is very strong for the relationship between sleep apnea and hypertension and cardiovascular disease generally, so people really need to know that,” said Donna Arnett, Ph.D., chair and professor of epidemiology at the School of Public Health at the University of Alabama at Birmingham and the president of the American Heart Association. According to an American Thoracic Society study of people with hypertension, about 30% have obstructive sleep apnea. If they have obstructive sleep apnea, there is a 50% chance they also have hypertension.
Why does blood pressure rise due to sleep apnea? When someone who suffers from sleep apnea stops breathing during the night, their oxygen levels fall drastically. The effects of this is that the brain will tell the blood vessels to increase pressure by narrowing or tightening up so that the body can receive more oxygen flow. In a sleep study, a sleep doctor can measure the severity of the sleep apnea and determine whether the patient has mild sleep apnea, characterized by five to 15 episodes per hour; moderate sleep apnea, defined by 15 to 30 per hour; or severe sleep apnea, meaning more than 30 each hour.
Oral appliance therapy can help control the symptoms of sleep apnea and prevent heart-related problems associated with sleep apnea. “The good news is treatment that keeps the breathing passages open and oxygen flowing can yield fast results,” Dr. Arnett said. “Blood pressure comes down really quite quickly.”
Reference sleepfoundation.org, heart.org, thoracic.org, harvard.edu
Updated August 4th 2017
When the weekend rolls around, many of us can admit to staying up later and sleeping in longer than usual.
Turns out, you might want to think twice before turning into a night owl on the weekends. If you’ve got a regular sleep schedule during the workweek and you mix it up on the weekends, you may be jeopardizing your health.
A recent study by researchers at the University of Arizona found that shifting your sleep habits over the weekend could pose great risks to your health. By analyzing 984 adults, ages 22 to 60, and asking about their sleep patterns, the researchers found a link between shifting sleep patterns and heart disease, depression and other health conditions.
Using the term “social jetlag” to describe the time difference between when your body wants to sleep and when you actually go to sleep, the researchers found that it’s not only the amount of sleep that matters, but also the consistency. “These results indicate that sleep regularity, beyond sleep duration alone, plays a significant role in our health,” said Sierra Forbush, a research assistant at the University of Arizona.
So, how do you know if you’re experiencing social jetlag? For the study, researchers found the midpoint between when participants fell asleep and when they woke up -- both on weekends and weekdays -- and calculated the difference between them. So, if you typically go to sleep at 11 p.m. and wake up at 7 a.m. during the week, and at 1 a.m. and 9 a.m. over the weekend, that’s two hours of social jetlag. So, “catching up on sleep” over the weekend is, in fact, not the best idea.
"With social jetlag, you are more likely to have heart disease, to feel fatigued, to feel tired and to have a worse mood," Forbush said. The study revealed that for every hour of social jetlag weekly, a person’s likelihood of suffering from heart disease increases by a whopping 11 percent. Not only that, but participants who recorded one hour of social jetlag were 22 percent more likely to rate their health as good, but not excellent, and 28 percent were more likely to describe it as poor or fair.
Updated August 3 2017
Getting good quality sleep is critical for the endocrine system to properly operate. Ninety percent of cell and tissue growth and regeneration in the brain and the human body occur during the third stage of sleep, so this means that the number of uninterrupted hours of sleep is of greater importance than the number of hours itself.
Research shows that hormone levels affected “multiple physiological changes, including increased cortisol and … impaired metabolism” when sleep was disrupted as a result of subjects only receiving four hours per night. For example, the pineal gland releases melatonin, which causes drowsiness and sleep and activated during REM sleep and immobilizes the body and initiates rapid eye movement (REM). The pons is a structure at the base of the brain that is active during REM sleep and signals nerves in the spine to immobilize the body and also initiates REM.
Diabetes and thyroid disease are common among the many hormone-related disorders that an individual can develop when their quality of sleep is poor. In children, the endocrine and nervous systems are also interrelated and disorders of the endocrine system can manifest neurological symptoms such as headache, altered mentality, abnormal muscle tone and strength, and developmental delay.
What does uninterrupted sleep mean? It means that we go through the four stages of non-rapid eye movement (NREM), which make up 75 percent of the night and REM for 25 percent of the night, which occurs about every 90 minutes during sleep. However, when sleep is interrupted, the pattern starts all over at NREM and allows less opportunity to reach REM, which restores the brain and body.
A Johns Hopkins University School of Medicine study suggests that continued sleep fragmentation negatively affected mood and “reduced feelings of sympathy and friendliness.”
“The lack of sufficient slow-wave sleep had a statistically significant association with the subjects’ reduction in positive mood,” the researchers say.
Quality sleep is especially critical to the development of children and adolescents. Snoring, mouth breathing and apnea can have serious behavioral and social-emotional consequences for children including hyperactivity, emotional symptoms such as anxiety and depression, peer relationship problems, conduct problems such as following rules and social behavior toward others.
When considering how and if an individual is getting good quality sleep, it is important to also determine the method of breathing. Breathing through the nose is now known to be vital to good health Researchers in the late 1990s, found that Nitric Oxide (NO) gas was discovered in the nasal passage that was produced continuously prevented bacterial growth; mouth-inhaled air does not benefit the lungs and body the same way as air inhaled through the nose. Nitric Oxide (NO) Gas plays a role in the function of most organs and kills some bacteria and viruses, has anti-inflammatory effects and may play an important role in heart disease and aging.
A child with normal breathing and sleep patterns has a “pediatric upper airway appears to dynamically regulate airflow.” As the child matures and transitions into puberty, the “compensatory response to upper airway response pressure loading declines with age.” Additionally, a child’s sleep pattern changes as they approach puberty; where they go to bed on average nearly one hour later and sleep about 30 minutes less. This change in sleep pattern occurs before their physical changes are apparent.
Technology and screens that emit blue light on phones and tablets can affect sleep cycles by disrupting the circadian rhythm, the body’s biological clock. The blue light from our devices has a high concentration of short-wavelengths, which suppresses the production of the calming hormone melatonin that promotes sleep. Behavioral sleep deprivation is associated with shorter slow wave sleep (SWS), increasing levels of pro-inflammatory cytokines and low grade inflammation. Significant hormonal changes affecting hypothalamic-pituitary-adrenal axis activity take place in the setting of sleep deprivation and affect the immune system. Scheduling time to wind down and having a ritual helps to create a healthy sleep schedule.
Dr. Elliott J. Alpher, Lily Mai.
Updated August 2 2017
4. Slip on some socks. Some people have the unlucky lot in life of colder-than-comfortable extremities. But having warm hands and feet seems to predict how quickly you'll fall asleep, according to a 1999 study. Speed up the process by pulling on a pair of clean socks before climbing into bed.
Updated August 1st 2017
Sleeping badly could be driving weight gain, scientists fear, after finding that people who slept just six hours a night had waist measurements an inch greater than those who get nine hours. The results strengthen the evidence that insufficient sleep could contribute to the development of metabolic diseases such as diabetes.
The study by the University of Leeds involved 1,615 adults who reported how long they slept and kept records of food intake. It also measured other indicators of overall metabolic health such as blood pressure, blood cholesterol, blood sugar, and thyroid function as well as weight and waist circumference recorded.
Those who slept for six hours or less a night had waists that were on average 1.1 inches (3cm) larger than those who slept for nine hours.Shorter sleep was also linked to reduced levels of good cholesterol, which helps remove fat from the body and protects against conditions like heart disease.
Dr Greg Potter, a researcher in metabolism at Leeds University, said: “The number of people with obesity worldwide has more than doubled since 1980. Obesity contributes to the development of many diseases, most notably type 2 diabetes. Understanding why people gain weight has crucial implications for public health."
Crucially, the study did not find any relationship between shorter sleep and a less healthy diet - a fact that surprised the researchers.
Other studies have suggested that shortened sleep can lead to poor dietary choices. But the new research suggests that it is the sleep itself, which is driving the effect.
Dr Laura Hardie, the study's senior investigator, added: "Because we found that adults who reported sleeping less than their peers were more likely to be overweight or obese, our findings highlight the importance of getting enough sleep.
“How much sleep we need differs between people, but the current consensus is that seven to nine hours is best for most adults."
The findings add to the growing body of evidence showing just how important a good night's sleep is to health.
Updated 29th July 2017
If you, or a loved one, is a chronic snorer, you should do something about it. Serious snoring can signal sleep apnea, a very dangerous condition. A new study from the National Center for Biotechnology Information suggests there may be a simple solution and it’s as easy as standing up.
The researchers recruited 16 snorers for their research. All of them were healthy, normal weight people. After measuring the fluid volume in the volunteers’ calves, the researchers asked them to sit for four hours—and then tracked their snoring that night.
Why the interest in leg fluid? As the researchers point out in the study: “Prolonged sitting may promote leg fluid retention that redistributes to the neck during sleep and contributes to snoring.” The researchers also wanted to test a potential solution: Half of the volunteers pressed their feet against pedals to keep their calf muscles active while sitting; the other half let their legs hang limply the way we all do at work and on the couch.
A week later, the researchers reversed the groups—the inactive volunteers pressed pedals, the pedal-pressers sat idly—before tracking nightly snoring again.
Sure enough, the volume of lower-leg fluids actually tripled when volunteers sat quietly, and they snored up a storm that night. But when volunteers worked the pedals—keeping the blood pumping and fluids moving in their calves—they had less fluid buildup, and their snoring dropped by more than half when they hit the sack.
“If there is excess fluid in the neck it will make your windpipe or esophagus more narrow,” says sleep doctor Michael Breus, MD. When you lay down after a long day of sitting, excess fluid in the legs can flood up to the neck, compressing your windpipe. “This forces the air to move faster and this can cause a vibration and then a snore. It is an airway thickness issue,” explains Dr. Breus.
Around 12 to 15 percent of American men have sleep apnea, and roughly 45 percent of people snore, according to Dr. Breus. Luckily, as the study suggests, there’s an easy fix. “My suggestion is to make sure that people take advantage of walking and moving whenever possible,” says Dr. Breus. “Getting up every two hours for a five-minute walk, parking your car far away to walk to work and cycle or walk to work.”
He also likes the idea of under-the-desk fitness equipment.
You can get a stair-stepper, peddler or elliptical that can keep your calf muscles busy throughout the day. Just remember that this is one small study, and leg exercise may not be everyone’s snoring solution; if you’re a heavy snorer, get checked out by a sleep specialist. In the meantime, there’s nothing wrong with getting more exercise.
Updated July 19th 2017
For the first time, researchers have demonstrated the causal context of why deep sleep is important to the learning efficiency of the human brain. They have developed a new, non-invasive method for modulating deep sleep in humans in a targeted region of the brain.
Most people know from their own experience that just a single sleepless night can lead to difficulty in mastering mental tasks the next day. Researchers assume that deep sleep is essential for maintaining the learning efficiency of the human brain in the long term.
While we are awake, we constantly receive impressions from our environment, whereby numerous connections between the nerve cells, so-called synapses, are excited and intensified at times. The excitation of the synapses does not normalize again until we fall asleep. Without a recovery phase, many synapses remain maximally excited, which means that changes in the system are no longer possible: Learning efficiency is blocked.
Causal connection between deep sleep and learning efficiency
The connection between deep sleep and learning efficiency has long been known and proven. Now, researchers at the University of Zurich (UZH) and the Swiss Federal Institute of Technology (ETH) in Zurich have been able to demonstrate a causal connection within the human brain for the first time. Reto Huber, professor at the University Children's Hospital Zurich and of Child and Adolescent Psychiatry at UZH, and Nicole Wenderoth, professor in the Department of Health Sciences and Technology at the ETH Zurich, have succeeded in manipulating the deep sleep of test subjects in targeted areas. "We have developed a method that lets us reduce the sleep depth in a certain part of the brain and therefore prove the causal connection between deep sleep and learning efficiency," says Reto Huber.
Subjective sleep quality was not impaired
In the two-part experiment with six women and seven men, the test subjects had to master three different motoric tasks. The concrete assignment was to learn various sequences of finger movements throughout the day. At night, the brain activity of the test subjects during sleep was monitored by EEG.
While the test subjects were able to sleep without disturbance after the learning phase on the first day, their sleep was manipulated in a targeted manner on the second day of the experiment, using acoustic stimulation during the deep sleep phase. To do so, the researchers localized precisely that part of the brain responsible for learning the abovementioned finger movements, i.e., for the control of motor skills (motor cortex). The test subjects were not aware of this manipulation; to them, the sleep quality of both experimental phases was comparable on the following day.
Deep sleep disturbances impair learning efficiency
In a second step, researchers tested how the manipulation of deep sleep affected the motoric learning tasks on the following day. Here, they observed how the learning and performance curves of the test subjects changed over the course of the experiment. As expected, the participants were particularly able to learn the motoric task well in the morning. As the day went on, however, the rate of mistakes rose. After sleep, the learning efficiency considerably improved again. This was not the case after the night with the manipulated sleep phase. Here, clear performance losses and difficulties in learning the finger movements were revealed.
Learning efficiency was similarly as weak as on the evening of the first day of the experiment. Through the manipulation of the motor cortex, the excitability of the corresponding synapses was not reduced during sleep. "In the strongly excited region of the brain, learning efficiency was saturated and could no longer be changed, which inhibited the learning of motor skills," Nicole Wenderoth explains.
In a controlled experiment with the same task assignment, researchers manipulated another region of the brain during sleep. In this case, however, this manipulation had no effect on the learning efficiency of the test subjects.
Use in clinical studies planned
The newly gained knowledge is an important step in researching human sleep. The objective of the scientists is to use this knowledge in clinical studies. "Many diseases manifest in sleep as well, such as epilepsy," Reto Huber explains. "Using the new method, we hope to be able to manipulate those specific brain regions that are directly connected with the disease." This could help improve the condition of affected patients.
Updated July 16 2017
Obstructive sleep apnoea (OSA) in type 2 diabetes patients increases the risk of developing diabetic retinopathy, according to new research from the University of Birmingham.
The study of 230 type 2 diabetes patients at hospitals in the Midlands is published in the American Journal of Respiratory and Critical Care Medicine.
Patients were assessed for diabetic retinopathy using specialist retinal imaging, while OSA was diagnosed using a home-based cardiorespiratory portable device. The prevalence of diabetic retinopathy was higher in those with OSA at 42.9% than those without the condition (24.1%).
Follow-up appointments more than three years later found that patients with OSA were more likely to develop moderate to severe retinopathy. The longitudinal research found that 18.4% of patients with OSA developed this level of severity, compared to 6.1% of patients without the condition.
The study also found that patients who received treatment for OSA with a machine designed to unblock the airways during sleep had a lower chance of developing advanced diabetic retinopathy compared to patients who did not receive the therapy.
Study author, Dr Abd Tahrani, said “clinicians should consider testing type 2 diabetes patients for OSA. It is important that clinicians treating patients with type 2 diabetes are aware that their patients who also have OSA are particularly at increased risk of developing advanced retinopathy and, hence, appropriate preventative measures should be put in place,” he emphasised.
Updated July 13th 2017
Many of us struggle to get a good night's sleep.
A sense of purpose aids sleep, US scientists find in a new study that explored the relationship between having a sense of purpose in life and quality of sleep in older adults.
The study analysed data from 800 older adults with an average age of 80 in the US.
Researchers found that generally, having a greater sense of purpose in life was associated with better quality of sleep, as well as a decreased likelihood of sleep disorders such as sleep apnoea and restless leg syndrome. Although these are interesting findings, it's not possible to rule out the influence of other factors.
The fairly abstract concept of "sense of purpose" may be influenced by various health and lifestyle factors, such as levels of physical activity and mental health problems, and these may all in turn affect quality of sleep. But this study wasn't able to pull out all of the intricacies of this complex relationship. Problems with sleep are more common in the UK than most people realise, but there are proven ways to help combat insomnia.
As for having a sense of purpose, research has shown that volunteering your time for a cause or charity you believe in can help improve your mental wellbeing. The study was carried out by researchers from Northwestern University in the US, and was funded by the National Institute on Aging Grant Numbers and the Illinois Department of Health. It was published in the peer-reviewed journal Sleep Science and Practice. The analysis of data from two cohort studies set out to explore the relationship between having a sense of purpose in life and quality of sleep.
Previous research has suggested that having a sense of purpose in life could protect against several negative health outcomes, one being sleep disturbances. Sleep disturbance is known to be more common among older adults. Studies have also observed the prevalence of sleep disturbance to be higher among African Americans than white people. The researchers wanted to investigate this further. Cohort studies are useful for looking at an association between an exposure and an outcome. But the study design means it isn't possible to fully rule out the influence of other confounding factors and prove that a purpose in life directly leads to better sleep.
What did the research involve?
The data sample for this analysis was taken from two ongoing Chicago-based cohort studies: the Minority Aging Research Study (MARS) and the Rush Memory and Aging Project (MAP).
MARS is a study of risk factors for cognitive decline that recruits older African Americans who haven't had a diagnosis of dementia.
MAP aims to look at the brain changes associated with ageing and cognitive decline. It recruited older adults of mostly white ethnicity (88%) without a diagnosis of dementia who agreed to annual clinical assessments, as well as brain autopsy after they died.
The analysis included 825 older adults with an average age of 79.
Purpose in life was measured at the start of the studies using a modified 10-item assessment derived from the Ryff and Keyes' Scales of Psychological Well-Being, a tool used to assess sense of purpose. As part of the assessment, individuals were asked to respond to statements like "I feel good when I think of what I've done in the past and what I hope to do in the future", and "Some people wander aimlessly through life, but I am not one of them". Participants used a five-point scale for their responses, ranging from 1 strongly disagree to 5 strongly agree. Higher scores were used to indicate higher levels of purpose in life.
Sleep quality and symptoms of potential sleep disorders were assessed using a 32-step questionnaire derived from the Pittsburgh Sleep Quality Index (PSQI), the Berlin Questionnaire, and the Mayo Sleep Questionnaire (MSQ). The questionnaire was given to participants at the end of each annual visit. The PSQI assessed sleep quality, specifically looking at how long it takes to fall asleep, sleep duration, and how much you actually sleep during the night.
The Berlin questionnaire assessed risk of sleep apnoea, and the MSQ assessed the presence of restless leg syndrome and REM behaviour disorder, where dreams are acted out (for example, through sleepwalking or shouting out). Sleep data was collected at baseline and follow-up points at the end of the first, second and third year. The researchers analyzed any links with purpose in life, adjusting for potential confounders like age, sex, race and years of education. Changes in quality of sleep over the course of the two-year study were also taken into account.
What were the basic results?
How did the researchers interpret the results?
The researchers concluded that, "In a biracial sample of over 800 older adults, the present findings provide support for the hypothesis that purpose in life is related to sleep quality, with indications that it could be a potentially useful clinical tool for assessing older adults." They added: "We found that higher levels of purpose in life at baseline predicted better sleep quality at baseline, as well as increased change in sleep quality over a one-year period, a finding that is consistent with previous studies."
Conclusion.
This study explored the relationship between having a sense of purpose in life and sleep quality and sleep disorders.
Researchers found generally, having a greater sense of purpose in life was associated with better quality of sleep and a decreased likelihood of sleep disorders like sleep apnoea and restless leg syndrome.
Updated July 11 2017
RECOMMENDATIONS FROM THE NATIONAL SLEEP FOUNDATION
Sleep protects our physical and mental health and insufficient sleep is the cause of some serious health problems including strokes, high blood pressure, overweight and obesity, diabetes, dementia and occular problems.
The amount of sleep that a person needs to stay healthy, alert and active depends on their age and will vary from one person to another, but there are now some recognized guidelines.
The National Sleep Foundation (NSF) evaluated 300 studies and recently released an age-based sleep recommendation scale.
Newborns (0 to 3 months): 14 to 17 hours of sleep
Infants (4 to 11 months): 12 to 15 hours of sleep
Toddlers (1 to 2 years): 11 to 14 hours of sleep
Preschoolers (3 to 5 years): 10 to 13 hours of sleep
School-agers (6 to 13): 9 to 11 hours of sleep
Teenagers (14 to 17 years): 8 to 10 hours of sleep
Young adults (18 to 25 years): 7 to 9 hours of sleep
Adults (26 to 64 years): 7 to 9 hours of sleep
Older adults (65 years +): 7 to 8 hours of sleep
Gender Differences.
Women often sleep more than men and their sleep is lighter and more easily disrupted. Pregnancy and hormonal changes related to menopause influence sleep health. Traditionally, tending to babies and children was “the woman’s job” but today the modern man shares those nocturnal duties.
Other Factors that Disrupt Sleep
Depression, stress, arthritis, fibromyalgia, muscle pain, epilepsy, heart disease and substance abuse. Restless Leg Syndrome is another sleep disrupter.
Updated July 10th 2017
Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression.
Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years there have been important advances in understanding the pathophysiology of sleep-related breathing disorders, including habitual snoring, increased upper airway resistance syndrome, and sleep apnea. Sleep-related breathing disorders have been recognized as important causes of morbidity and mortality. Among adults, sleep apnea is more common than asthma. In the United States, approximately 12 million people 30 to 60 years of age have obstructive sleep apnea and 38,000 die each year from cardiovascular disease attributed to sleep related breathing disorders. Among the approximately 31 million US citizens aged 65 years and older, nearly 7.5 million have sleep apnea, including 46% with moderate or severe disease. Among nursing home residents, up to half have clinically important sleep apnea.
In two recent studies, approximately 40% to 50% of outpatients with asymptomatic or mildly symptomatic congestive heart failure had obstructive sleep apnea or Cheyne-Stokes respiration with central sleep apnea. Sleep-related breathing disorders may contribute to progression of heart failure and worsen its prognosis.
In this article, we review the cardiovascular consequences of sleep-related breathing disorders, including the acute effects of apnea on the cardiovascular system, and the associations between sleep-related breathing dis- orders and hypertension, cardiac arrhythmias, pulmonary hypertension, and congestive heart failure. Epidemiologic studies have demonstrated that sleep- related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
There are several types of sleep-related breathing disorders. Sleep apnea is defined as repetitive prolonged cessation of airflow associated with sleep arousal and at times with oxygen desaturation. Sleep apnea can be obstructive, in which respiratory effort persists despite occlusion of the oropharyngeal airway; central, in which both respiratory efforts and airflow cease; or a mixed central/obstructive pattern. Hypopnea is defined as a greater than 50% reduction in air flow with either an oxygen desaturation of greater than 3% or an arousal. A respiratory effort-related arousal event occurs when increasing effort leads to an arousal from sleep that does not meet the criteria for apnea or hypopnea. Increasing respiratory effort or out-of-phase breathing is the hallmark of in- creased upper airway resistance syndrome. However, the measurement of respiratory effort during sleep is difficult, because there are no non-invasive ways to measure increased resistance to breathing. Current techniques include respiratory inductance plethysmography and measurement of nasal pressure, change in pulse transit time is being evaluated as a measure of increased respiratory effort. Because there is night-to-night variability in the frequency of respiratory events in patients with milder forms of sleep-related breathing disorders, a “negative” polysomnogram does not rule out sleep-related breathing disorders in a symptomatic patient.
The usual daytime manifestations of sleep-related breathing disorders are excessive sleepiness, fatigue, un- refreshing sleep, and poor concentration. The constellation of obstructive sleep apnea, oxygen desaturation, and excessive sleepiness has been termed the obstructive sleep apnea syndrome.
A recent statement of the American Academy of Sleep Medicine and the American Thoracic Society outlined the diagnostic criteria for sleep-related breathing disorders. Obstructive sleep apnea-hypopnea syndrome requires excessive daytime sleepiness that is not better explained by other factors, as well as five or more obstructed breathing events (apnea, hypopnea, or respiratory effort-related arousals) per hour during sleep. The number of these events per hour of sleep determines the Respiratory Disturbance Index (RDI). The severity is rated as mild when there are 5 to 15 events per hour, moderate at 15 to 30 per hour, and severe at greater than 30 events per hour.
Apneic or hypopneic events are commonly associated with oxygen desaturation and are terminated by arousal. These repetitive events are associated with substantial changes in sympathetic discharge and in intrathoracic pressure that affect cardiovascular function.
Acute and transient effects of sleep-related breathing disorders on the cardiovascular system.
In normal subjects, systemic blood pressure decreases approximately 10% to 15% during sleep, with the greatest reductions occurring in non-rapid eye movement (non- REM) stages 3 and 4. Cardiac output also decreases by approximately 10% during non-REM sleep. The decrease in cardiac output results from reductions in heart rate and stroke volume. Because systemic blood pressure decreases substantially in conjunction with a less pronounced decrease in cardiac output, systemic vascular resistance probably declines slightly during non-REM sleep.
In contrast with the normal physiologic effect of sleep on the cardiovascular system, the hemodynamic response to apnoeic stimuli is more complex. The acute hemodynamic consequences of obstructive sleep apnea include systemic and pulmonary hypertension, increased left ventricular afterload, and decreased cardiac output. These changes are primarily the result of sympathetic stimulation, alterations in intra-thoracic pressure, and hypoxia and hypercapnia.
Neurohumoral Response to Apnea.
Apnoeic events result in brief surges in sympathetic nervous system activity, vasoconstriction, and transient hypertension. Systemic blood pressure is usually lowest during the early to middle portion of most apneic episodes. A gradual increase in pressure is then observed, and a sudden elevation occurs after termination of apnea.
During apneic episodes that are 35 to 40 seconds in duration, cardiac output decreases by approximately one-third. After termination of apnea, cardiac output increases by 10% to 15% above baseline. The combination of increasing systemic pressure and decreasing cardiac output indicates that systemic vascular resistance increases during apnea. Systemic vasoconstriction is believed to be mediated by alpha sympathetic neural activity, because patients with Shy-Drager syndrome, who are sympathetically denervated, have minimal changes in heart rate or systemic pressures in response to apnea. During hypoxia and at the termination of apnea, serum catecholamine levels increase, causing acute elevation in pulmonary and systemic blood pressures. Some of these alterations persist during wakefulness. The sympathetic neural response to apnea is, in large part, related to hypoxemia and hypercapnia, although cardiac sympathetic function and integrity, as assessed with radionuclide imaging, are impaired in sleep apnea. During the apnoeic period, heart rate slows in proportion to the duration of apnea and the degree of oxyhemoglobin desaturation. Increased vagal efferent activity partly mediates these reductions in heart rate, as atropine usually ameliorates apnea-related bradycardia. The resumption of ventilation is associated with a rapid increase in heart rate, presumably in response to a decrease in vagal tone.
Brady and tachy arrhythmias are common during sleep in patients with obstructive sleep apnea syndrome. In addition, several other types of arrhythmias can occur, including sinus pauses of 2 to 13 seconds in duration, ventricular ectopy, and complete heart block. Whereas supraventricular bradyarrhythmias and tachyarrhythmias during sleep is mainly the result of an alteration in sympathetic nervous system tone, ventricular arrhythmias are related to marked hypoxia, because they usually occur when oxyhemoglobin saturation falls below 60%.
Increased venous return causes a leftward shift of the interventricular septum (ventricular interdependence), thereby reducing left ventricular compliance and decreasing left ventricular end-diastolic volume. Further, the decrease in intrathoracic pressure delays blood leaving the intratharacic aorta, hence increasing left ventricular afterload. The combination of decreased left ventricular end- diastolic volume and increased left ventricular afterload results in decreased stroke volume and cardiac output. As a result of these hemodynamic changes and the surges in catecholamine levels, systemic blood pressure increases cyclically during sleep.
Effect of Hypoxia.
Changes in blood oxygen tension are sensed primarily by the carotid chemoreceptors, which, when activated, lead to bradycardia, arteriolar constriction in many vascular beds, and increased secretion of catecholamines. Hypoxia induced systemic vasoconstriction occurs during apnea, especially when the oxyhemoglobin saturation falls below 65%. The resulting hypertension is transient.
Pulmonary vasoconstriction occurs in response to alveolar hypoxia in order to match lung perfusion with ventilation. In patients with obstructive sleep apnea, recurrent episodes of hypoxemia during sleep lead to repeated acute increases in pulmonary artery pressures However, fewer than 20% of these patients develop sustained daytime pulmonary hypertension (mean pulmonary artery pressure greater than 20 mm Hg). Right ventricular hypertrophy can occur in patients with more marked obstructive sleep apnea and oxygen desatu- ration. However, overt pulmonary hypertension with right ventricular failure is seen primarily in patients with obstructive sleep apnea who also have chronic alveolar hypoventilation and hypercapnia.
Chronic cardiovascular effects of sleep-related breathing disorders.
Sleep-related breathing problems are associated with several cardiovascular diseases. Although a review by Wright et al on the health effects of obstructive sleep apnea dismissed these effects, citing the lack of controlled prospective studies, several recent epidemiologic studies and trials have demonstrated a strong association between sleep-related breathing disorders and cardiovascular disease that is independent of shared risk factors, such as obesity, age, and male sex.
Hypertension.
More than half of patients with obstructive sleep apnea have systemic hypertension compared with an expected prevalence of 20% in middle-aged obese men. Approximately 25% of patients with hypertension have obstructive sleep apnea. For example, one study found that 30% of hypertensive men had sleep apnea, with an apnea index greater than 10, compared with only 9% of controls.
A greater prevalence of cardiovascular complications is seen throughout the spectrum of sleep-related breathing disorders, from snoring to obstructive sleep apnea. A study of 3,323 Danish men found an association between self-reported snoring and blood pressure, but the association was lessened when other risk factors were taken into account. Lindberg et al prospectively studied 2,668 men aged 30 to 69 years for the development of hypertension in relation to snoring, excessive daytime sleepiness, and other known cardiovascular risk factors during a 10-year follow-up period. Of the habitual snorers, 12.5% reported that they had developed hypertension, compared with 7.4% of the remaining subjects.
In one study, the blood pressure–lowering effect of CPAP was seen only in patients whose blood pressure did not decrease during sleep, “nondippers,” with obstructive sleep apnea syndrome. Some of the effects of CPAP on blood pressure may have been in part the result of weight loss. In one study, patients with sleep apnea who were successfully treated had a substantial reduction in cardiovascular events compared with equally affected patients who refused treatment.
The mechanisms underlying the development of sustained hypertension in sleep-related breathing disorders are not known. Possibilities include hypoxemia, repeated arousals, sustained increases in catecholamine levels and sympathetic tone, enhanced endothelin secretion, and altered eicosanoid activity. Furthermore, carotid chemoreceptors may maintain in- creased peripheral sympathetic activity and blood pressure after cessation of asphyxia or exposure to hypoxia. Increased ventilatory and pressor responsiveness to isocapnic hypoxia has been demonstrated in awake young subjects with mild hypertension. Brief exposure to hypoxia may result in sustained increases in peripheral sympathetic activity.
Coronary Artery Disease.
A greater risk of coronary artery disease in sleep-related breathing disorders is suggested by several retrospective and cross-sectional studies. The prevalence of sleep-related breathing disorders (measured as RDI of 10 or more) was 37% among men and 30% among women with angiographically verified coronary artery disease. In another study, clinically important sleep apnea was found in 50% of patients with coronary artery disease. Nearly 30% of patients with coronary artery disease and concomitant sleep apnea experienced myocardial ischemia during apnea, primarily during REM sleep. Patients with coronary artery disease should be screened for sleep-related breathing disorders.
Idiopathic Cardiomyopathy and Congestive Heart Failure.
Idiopathic cardiomyopathy and congestive heart failure have been reported in patients with obstructive sleep apnea. Left ventricular hypertrophy was more common in 30 normotensive patients with obstructive sleep apnea than in controls. In one study, all 8 patients with congestive cardiomyopathy of unknown origin had obstructive sleep apnea, and 4-week treatment with nasal CPAP increased the mean left ventricular ejection fraction significantly from 37% to 49%.
Respiratory Disturbance Index.
After adjustment for age, body mass index, weight gain, smoking, alcohol consumption, and physical activity, habitual snoring was an independent predictor for the development of hypertension, with an odds ratio of 2.6 [95% confidence interval (CI), 1.5 to 4.5)]. In a cross-sectional study of 805 Wisconsin state employees aged 30 to 60 years, polysomnography data were analyzed in relation to blood pressure measurements made before bedtime and after rising. Compared with subjects who did not have sleep-related breathing disorders, and after adjustment for body mass index, age, and sex, sleep- related breathing disorders were associated with cardio- vascular disease. The dose–response relation be- tween sleep-related breathing disorders, including snoring, and hypertension was independent of known confounders.
Sleep-related breathing disorders were risk factors for cardiovascular diseases in a 10-year prospective study in 3,100 men, in which the age-adjusted mortality was 2.9 (95% CI, 1.3 to 6.7) times greater in men with snoring and excessive daytime sleepiness compared with men who did not have these symptoms. Further adjustment for body mass index, hypertension, cardiac disease, and diabetes reduced the relative risk of cardiovascular mortality to 2.0 (95% CI, 0.8 to 4.7). These studies suggest that snoring and the increased upper airway resistance syndrome may be associated with an increased risk of cardiovascular disease.
The evidence supporting a possible cause–effect relation between obstructive sleep apnea and hypertension comes primarily from intervention studies, which have often observed both acute and chronic reductions in blood pressure after treatment of the sleep disorder.
Cerebrovascular Disease.
Two studies found that about one-third of strokes apparently occurred during sleep. Among potential risk factors for stroke in one study, only snoring was significantly associated with stroke in sleep. In the other study, sleep-related breathing disorders were associated with a threefold increase in the risk of stroke.
The hemodynamic changes associated with disordered breathing during sleep may stress the cerebral circulation. In several cross-sectional studies, patients with a history of transient ischemic attacks or stroke have had a greater prevalence of sleep-related breathing disorders than control subjects. However, it is not clear whether sleep-related breathing disorders were an independent risk factor for stroke or increased stroke risk because of associated hypertension.
Sleep-related breathing disorders affect cerebral hemodynamics, including a greater than 50% reduction in cerebral blood flow during apnoeic and hypopneic events. The reduction in blood flow is related to the duration of hypopneas and the degree of oxygen de- saturations. In addition, there is also increased platelet activation and aggregation in the obstructive sleep apnea syndrome.
SUMMARY
Sleep-related breathing disorders are a group of conditions that range from simple snoring with sleep disruption, to the increased upper airway resistance syndrome, to sleep apnea. These disorders may be associated with substantial cardiovascular morbidity and mortality, and early recognition and treatment may be effective in reducing these complications.
Francoise Roux, MD, Carolyn D’Ambrosio, MD, Vahid Mohsenin, MD
Updated July 9th 2017
The pressure to work more and sleep less is driving a global epidemic with worrying consequences, says neuroscientist Matt Walker.
“Back in the 1940s people were sleeping on average just a little bit over eight hours a night, and now in the modern age we’re down to around 6.7, 6.8 hours a night,” says Matt Walker, professor of neuroscience and psychology at the University of California, Berkeley.
“So that’s a staggering loss of sleep within the space of just 70 years, we’re now almost at the stage where we’ve lopped off 20% of that.”
For adults, the modern world is full of things which reduce sleep. Caffeine, which keeps us awake, and alcohol, which fragments our sleep and suppresses dreaming.
Although we’ve improved the conditions for sleeping, with everything from better mattresses to smoke-free homes, our controlled environment may also have created problems, Walker says.
“One, which people may find surprising, is central heating and central air conditioning. So, when the sun sets, temperature drops dramatically and when the sun rises it starts to pick back up. Our bodies expect that beautiful thermal lull and what we have done is dislocate ourselves from the natural ebb and flow that tells us when it’s time to sleep and actually helps us get to sleep.”
Alcohol, coffee and even air conditioning can affect how we sleep, Walker says, and then there’s technology. No longer just artificial light, but all sorts of devices with LED screens, emitting a powerful form of blue light.
“Now that blue light unfortunately will put the brakes on the release of a hormone called melatonin at night, and melatonin signals when you should sleep.Technology also causes sleep procrastination. Midnight is the time when we think we should probably send our last email or check Facebook one more time. And to all this, we can add the modern offspring of the early rising movement – the economic and social pressure to work more, sleep less, and be more like some famous world leaders – including Donald Trump, Barack Obama and Margaret Thatcher – who have claimed to exist on five hours of sleep a night or less.
But should we be aspiring to be more like George W. Bush, who reportedly went to bed around 9pm and got as much as nine hours sleep each night? Based on probably about 10,000 research study papers now, the number of people who can survive on six hours of sleep or less and show no impairment, rounded to a whole number and expressed as a per cent, is zero.”
Professor Walker says "with anything less than seven hours’ sleep, we start to see health consequences. Every major disease that is killing us in the developed world, alzheimers, cancer, obesity, diabetes, anxiety, depression, suicide; all of them have direct and very strong causal links to deficient sleep.”
Updated 8th July 2017
