Central Sleep Apnea (CSA)
or Cheyne Stokes Respiration (CSR):
In pure CSA,
the brain's respiratory control centers are imbalanced during sleep;
blood levels of carbon dioxide and the neurological feedback mechanism
that monitors them, do not react quickly enough to maintain an even
respiratory rate, with the entire system cycling between Apnea and Hyperpnea,
even during wakefulness; the sleeper stops breathing and then starts
again; there is no effort made to breathe during the pause in breathing:
there are no chest movements and no struggling; after the episode of
Apnea, breathing may be faster 'Hyperpnea' for a period of time, a compensatory
mechanism to blow off retained waste gases and absorb more oxygen.
While sleeping, a normal individual is at rest as far as cardiovascular
workload is concerned; breathing is regular in a healthy person during
sleep and oxygen levels and carbon dioxide levels in the bloodstream
stay fairly constant; the respiratory drive is so strong that even conscious
efforts to hold one's breath do not overcome it; any sudden drop in
oxygen or excess of carbon dioxide, even if tiny, strongly stimulates
the brain's respiratory centers to breathe.
In CSA,
the basic neurological controls for breathing rate malfunction and fail
to give the signal to inhale, causing the individual to miss one or
more cycles of breathing; if the pause in breathing is long enough,
the percentage of oxygen in the circulation will drop to a lower than
normal level 'Hypoxaemia' and the concentration of carbon dioxide will
build to a higher than normal level 'Hypercapnia'; in turn, these conditions
of Hypoxia and Hypercapnia will trigger additional effects on the body.
Brain cells need constant oxygen to live and if the level of blood oxygen
goes low enough for long enough, the consequences of brain damage and
even death will occur; fortunately, CSA
is more often a chronic condition that causes much milder effects than
sudden death; the exact effects of the condition will depend on how
severe the SA
is and on the individual characteristics of the person having the SA.
In any person, Hypoxia and Hypercapnia have certain common effects on
the body; the heart rate will increase, unless there are such severe
co-existing problems with the heart muscle itself or the autonomic nervous
system that makes this compensatory increase impossible; the more translucent
areas of the body will show a bluish or dusky cast from 'Cyanosis',
which is the change in hue that occurs owing to lack of oxygen in the
blood and turns the skin bluish; overdoses of drugs that are respiratory
depressants, such as Heroin, and other opiates, kill by damping the
activity of the brain's respiratory control centers; in CSA,
the effects of sleep alone can remove the brain's mandate for the body
to breathe.
Normal Respiratory Drive:
After exhalation, the blood level of oxygen decreases and that of carbon
dioxide increases; the exchange of gases with a lungful of fresh air
is necessary to replenish oxygen and rid the bloodstream of built up
carbon dioxide; oxygen and carbon dioxide receptors in the blood stream,
called 'Chemoreceptors', send nerve impulses to the brain, which then
signals reflex opening of the larynx, so that the opening between the
vocal cords enlarges, and movements of the rib cage muscles and diaphragm;
these muscles expand the thorax, chest cavity, so that a partial vacuum
is made within the lungs and air rushes in to fill it.
Physiologic effects of Central Sleep Apnea (CSA):
During CSA,
the central respiratory drive is absent and the brain does not respond
to changing blood levels of the respiratory gases; no breath is taken
despite the normal signals to inhale; the immediate effects of CSA
on the body depend on how long the failure to breathe endures; at worst
CSA may
cause sudden death; short of death, drops in blood oxygen may trigger
seizures, even in the absence of epilepsy; in people with epilepsy,
the Hypoxia caused by Apnea may trigger seizures that had previously
been well controlled by medications; in other words, a seizure disorder
may become unstable in the presence of SA.
In adults with coronary artery disease, a severe drop in blood oxygen
level can cause Angina, Arrhythmias, or Heart
Attacks 'Myocardial Infarction'; longstanding recurrent episodes
of Apnea, over months and years, may cause an increase in carbon dioxide
levels that can change the pH of the blood enough to cause a Metabolic
Acidosis; it also causes
a slight struggling that the person is not aware of; if not recognised
by anyone awake it may lead to death, or any other problems; this is
similar to an Asthma attack but not
quite the same, it gives you a feeling as if you are being strangled
by someone.
Mixed Apnea and Complex Sleep Apnea, a mix of (Obstructive Sleep
Apnea (OSA) and Central Sleep Apnea (CSA):
Some people with SA
have a combination of both types; when the OSA
syndrome is severe and longstanding, episodes of CSA
sometimes develop; the exact mechanism of the loss of central respiratory
drive during sleep in OSA
is unknown but is most commonly related to acid base and CO2 feedback
malfunctions stemming from heart failure; there is a constellation of
diseases and symptoms relating to body mass, cardiovascular, respiratory
and occasionally, neurological dysfunction that have a synergistic effect
in SDB;
in some cases, a side effect from the lack of sleep is a mild case of
EDS
where the subject has had minimal sleep and this extreme fatigue over
time takes its toll on the subject; the presence of CSA
without an obstructive component is a common result of chronic opiate
use, or abuse, owing to the characteristic respiratory depression caused
by large doses of narcotics.
What are the Symptoms of Sleep Apnea (SA)?
The risk of OSA
rises with increased body weight, active smoking and age; in addition,
patients with Diabetes
are up to three times more likely to suffer from OSA;
people with low muscle tone and soft tissue around the airway, such
as with those who are clinically obese, and structural features that
give rise to a narrowed airway are at high risk of OSA
and the elderly and men are more likely to have OSA
than young people and women; although unfortunately, it is not uncommon
in women and children.
Common symptoms include loud snoring, restless sleep and sleepiness
during the daytime and sufferers complain about EDS,
fatigue and impaired alertness, a slower reaction time and vision problems;
early reports of OSA
in the medical literature described individuals who were very severely
affected, as often being affected with severe Hypoxemia, Hypercapnia
and Congestive Heart Failure.
Snoring is a common finding in people with this syndrome; snoring is
the turbulent sound of air moving through the back of the mouth, nose
and throat; although not everyone who snores is experiencing difficulty
breathing, snoring in combination with other conditions such as overweight
and obesity has been found to be highly predictive of OSA
risk; the loudness of the snoring is not indicative of the severity
of obstruction, however; if the upper airways are tremendously obstructed,
there may not be enough air movement to make much sound; even the loudest
snoring does not mean that an individual has the SA
syndrome; the sign that is most suggestive of SAs
occurs when the snoring stops.
Due to the disruption in daytime cognitive state, behavioral effects
are also present, which include moodiness and belligerence, as well
as a decrease in attentiveness and drive; these effects become very
hard to deal with, thus the development of depression may transpire
and unfortunately, due to the many factors that could lead to some of
the effects previously listed, some patients are not aware that they
suffer from SA
and are either misdiagnosed, or just ignore the symptoms altogether.
Other indicators include, but are not limited to, Hypersomnolence, Obesity
BMI >30, Large
Neck Circumference (16 in (410 mm) in women, 17 in (430 mm) in men),
Enlarged Tonsils and Large Tongue Volume, Micrognathia, Morning Headaches,
Irritability, Mood Swings, Depression, Learning and/or Memory Difficulties
and Sexual Dysfunction.
The term SDB
is commonly to describe the full range of breathing problems during
sleep in which not enough air reaches the lungs 'Hypopnea' and 'Apnea';
SDB
is associated with an increased risk of Cardiovascular
Disease, Stroke,
High Blood Pressure, Arrhythmias, Diabetes
and sleep deprived driving accidents.
When high blood pressure is caused by OSA,
it is distinctive in that, unlike most cases of High Blood Pressure
'Essential Hypertension', the readings do not drop significantly when
the individual is sleeping.
How is Sleep Apnea (SA) Diagnosed?
The diagnosis of SA
is based on the conjoint evaluation of clinical symptoms, such as excessive
daytime sleepiness and fatigue, and of the results of a formal sleep
study 'Polysomnography or a 'Reduced Channels Home Based test; the latter
aims at establishing an objective diagnosis indicator linked to the
quantity of Apneic events per hour of SA
Hypopnea Index (SAHI) or Respiratory Disturbance Index (RDI), associated
to a formal threshold, above which a patient is considered as suffering
from SA and the
severity of their SA
can then be quantified.
Nevertheless, due to the number and variability in the actual symptoms
and nature of Apneic events, such as Hypopnea vs SA
and CSA
vs OSA,
the variability of patients' physiologies and the intrinsic imperfections
of the experimental setups and methods, this field is opened to debate;
within this context, the definition of an Apneic event depends on several
factors, such as the patient's age, and account for this variability
through a multi criteria decision rule described in several, sometimes
conflicting, guidelines.
One example of a commonly adopted definition of an Apnea, for an adult,
includes a minimum 10 second interval between breaths, with either a
neurological arousal (a 3 second or greater shift in EEG frequency,
measured at C3, C4, O1, or O2) or a blood oxygen desaturation of (3
to 4)% or greater, or both arousal and desaturation.
Oximetry, which may be performed overnight in a patient's home, is an
easier alternative to formal sleep study 'Polysomnography; in one study,
normal overnight oximetry was very sensitive and so if normal, SA
was unlikely; in addition, home oximetry may be equally effective in
guiding prescription for automatically self adjusting continuous positive
airway pressure.
Patients are often examined using 'Standard Test Batteries' in order
to further identify parts of the brain that are affected by SA;
the tests have shown that certain parts of the brain cause different
effects; the 'Executive Functioning' part of the brain affects the way
the patient plans and initiates tasks; the part of the brain that deals
with attention causes difficulty in paying attention, working effectively
and processing information when in a waking state and the part of the
brain that uses memory and learning is also affected.
How is Sleep Apnea (SA) Treated?
Some treatments involve lifestyle changes, such as losing weight, quitting
smoking, avoiding alcohol or muscle relaxants, sleeping pills and other
sedatives, which can relax throat muscles, contributing to the collapse
of the airway at night; therefore, treatment often starts with behavioral
therapy; for mild cases of SA,
physicians often recommend sleeping on one's side, as opposed to on
one's back, which can prevent the tongue and palate from falling backwards
in the throat and blocking the airway; this probably works owing to
changes in the pulmonary oxygen stores.
Many people also benefit from sleeping at a 30 degree elevation of the
upper body or higher, as if in a recliner; doing so helps prevent the
gravitational collapse of the airway; lateral positions, such as sleeping
on a side, as opposed to supine positions, sleeping on the back, are
also recommended as a treatment for SA,
largely because the gravitational component is smaller in the lateral
position.
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