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VOLGOGRAD STATE MEDICAL UNIVERSITY PATHOLOGICAL PHYSIOLOGY GENERAL MEDICINE FACULTY THEME: HYPOXIA TITLE: HYPOXIA: PREVENTION, TREATMENT AND PECULIARITY OF MONITORING NAME: ISYAFIQ QAMAAL BIN AHMADI GROUP: 36

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Page 1: Hypoxia

VOLGOGRAD STATE MEDICAL UNIVERSITY

PATHOLOGICAL PHYSIOLOGY

GENERAL MEDICINE FACULTY

THEME: HYPOXIA

TITLE: HYPOXIA: PREVENTION, TREATMENT AND PECULIARITY OF MONITORING

NAME: ISYAFIQ QAMAAL BIN AHMADI

GROUP: 36

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CONTENT(1)Treatment for hypoxic hypoxia

- Cardiopulmonary resuscitation (CPR)- Artificial respiration- Mechanical ventilation- Intubation- Oxygen concentrator

(2)Hypoxia with low partial pressure of atmospheric oxygen such as found at high altitude- Acclimatization- Altitude training

(3)Treatment for hypoxia with decrease in oxygen saturation of the blood caused by sleep apnea or hypopnea- Treatment for sleep apnea

(4)Treatment for hypoxia when the blood fails to deliver oxygen to target tissues- Treatment for carbon monoxide poisoning- Treatment for methemoglobinemia

(1)TREATMENT FOR HYPOXIC HYPOXIA

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Cardiopulmonary resuscitation (CPR)

Cardiopulmonary resuscitation (CPR) is an emergency procedure for people in cardiac arrest or, in some circumstances, respiratory arrest. CPR is performed both in hospitals and in pre-hospital settings.

CPR involves physical interventions to create artificial circulation through rhythmic pressing on the patient's chest to manually pump blood through the heart, called chest compressions, and usually also involves the rescuer exhaling into the patient (or using a device to simulate this) to ventilate the lungs and pass oxygen in to the blood, called artificial respiration. Some protocols now downplay the importance of the artificial respirations, and focus on the chest compressions only.

Artificial respiration

Artificial respiration is the act of simulating respiration, which provides for the overall exchange of gases in the body by pulmonary ventilation, external respiration and internal respiration. This means providing air for a person who is not breathing or is not making sufficient respiratory effort on their own (although it must be used on a patient with a beating heart or as part of cardiopulmonary resuscitation to achieve the internal respiration).

Pulmonary ventilation (and hence external respiration) is achieved through manual insufflation of the lungs either by the rescuer blowing into the patient's lungs, or by using a mechanical device to do so. This method of insufflation has been proved more effective than methods which involve mechanical manipulation of the patient’s chest or arms, such as the Silvester method. It is also known as Expired Air Resuscitation (EAR), Expired Air Ventilation (EAV), mouth-to-mouth resuscitation, rescue breathing or colloquially the kiss of life.

Artificial respiration is a part of most protocols for performing cardiopulmonary resuscitation (CPR)[4][5] making it an essential skill for first aid. In some situations, artificial respiration is also performed separately, for instance in near-drowning and opiate overdoses. The performance of artificial respiration in its own is now limited in most protocols to health professionals, whereas lay first aiders are advised to undertake full CPR in any case where the patient is not breathing sufficiently.

Mechanical ventilation involves the use of a mechanical ventilator to move air in and out of the lungs when an individual is unable to breathe on his or her own, for example during surgery with general anesthesia or when an individual is in a coma.

Insufflations (Mouth-to-mouth insufflations)

Insufflation, also known as ‘rescue breaths’ or ‘ventilations’, is the act of mechanically forcing air into a patient's respiratory system. This can be achieved via a number of methods, which will depend on the situation and equipment

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available. All methods require good airway management to perform, which ensures that the method is effective. These methods include:

1. Mouth to mouth - This involves the rescuer making a seal between their mouth and the patient's mouth and 'blowing', to pass air into the patient's body

2. Mouth to nose - In some instances, the rescuer may need or wish to form a seal with the patient's nose. Typical reasons for this include maxillofacial injuries, performing the procedure in water or the remains of vomit in the mouth

3. Mouth to mouth and nose - Used on infants (usually up to around 1 year old), as this forms the most effective seal

4. Mouth to mask – Most organisations recommend the use of some sort of barrier between rescuer and patient to reduce cross infection risk. One popular type is the 'pocket mask'. This may be able to provide higher tidal volumes than a Bag Valve Mask.[6]

5. Bag valve mask (BVM) - This is a simple device manually operated by the rescuer, which involves squeezing a bag to expel air into the patient.

6. Mechanical resuscitator - An electric unit designed to breathe for the patient

Adjuncts to insufflations

Most training organisations recommend that in any of the methods involving mouth to patient, that a protective barrier is used, to minimise the possibility of cross infection (in either direction).[7]

Barriers available include pocket masks and keyring-sized face shields. These barriers are an example of Personal Protective Equipment to guard the face against splashing, spraying or splattering of blood or other potentially infectious materials.

These barriers should provide a one-way filter valve which lets the air from the rescuer deliver to the patient while any substances from the patient (e.g. vomit, blood) cannot reach the rescuer. Many adjuncts are single use, though if they are multi use, after use of the adjunct, the mask must be cleaned and autoclaved and the filter replaced.

The CPR mask is the preferred method of ventilating a patient when only one rescuer is available. Many feature 18mm inlets to support supplemental oxygen, which increases the oxygen being delivered from the approximate 17% available in the expired air of the rescuer to around 40-50%.

Tracheal intubation is often used for short term mechanical ventilation. A tube is inserted through the nose (nasotracheal intubation) or mouth (orotracheal intubation) and advanced into the trachea. In most cases tubes with inflatable cuffs are used for protection against leakage and aspiration. Intubation with a cuffed tube is thought to provide the best protection against aspiration. Tracheal tubes inevitably cause pain and coughing. Therefore, unless a patient is unconscious or anesthetized for other reasons, sedative drugs are usually given to provide

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tolerance of the tube. Other disadvantages of tracheal intubation include damage to the mucosal lining of the nasopharynx or oropharynx and subglottic stenosis.

In an emergency a Cricothyrotomy can be used by health care professionals, where an airway is inserted through a surgical opening in the cricothyroid membrane. This is similar to a tracheostomy but a cricothyrotomy is reserved for emergency access. This is usually only used when there is a complete blockage of the pharynx or there is massive maxillofacial injury, preventing other adjunts being used.[8][edit] Efficiency of mouth to patient insufflation

Normal atmospheric air contains approximately 21% oxygen when created in. After gaseous exchange has taken place in the lungs, with waste products (notably carbon dioxide) moved from the bloodstream to the lungs, the air being exhaled by humans normally contains around 17% oxygen. This means that the human body utilises only around 19% of the oxygen inhaled, leaving over 80% of the oxygen available in the exhalatory breath.

This means that there is more than enough residual oxygen to be used in the lungs of the patient, which then crosses the cell membrane to form oxyhemoglobin.

Oxygen

The efficiency of artificial respiration can be greatly increased by the simultaneous use of oxygen therapy. The amount of oxygen available to the patient in mouth to mouth is around 16%. If this is done through a pocket mask with an oxygen flow, this increases to 40% oxygen. If a Bag Valve Mask or mechanical respirator is used with an oxygen supply, this rises to 99% oxygen. The greater the oxygen concentration, the more efficient the gaseous exchange will be in the lungs.

Mechanical Ventilation

In medicine, mechanical ventilation is a method to mechanically assist or replace spontaneous breathing.

This may involve a machine called a ventilator or the breathing may be assisted by a physician or other suitable person compressing a bag or set of bellows. Traditionally divided into negative-pressure ventilation, where air is essentially sucked into the lungs, or positive pressure ventilation, where air (or another gas mix) is pushed into the trachea.

It can be used as a short term measure, for example during an operation or critical illness (often in the setting of an intensive care unit). It may be used at home or in a nursing or rehabilitation institution if patients have chronic illnesses that require long-term ventilatory assistance.

Owing to the anatomy of the human pharynx, larynx, and esophagus and the circumstances for which ventilation is required then additional measures are often required to "secure" the airway during positive pressure ventilation to allow unimpeded passage of air into the trachea and avoid air passing into the esophagus and stomach. Commonly this is by insertion of a tube into the trachea which

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provides a clear route for the air. This can be either an endotracheal tube, inserted through the natural openings of mouth or nose or a tracheostomy inserted through an artificial opening in the neck. In other circumstances simple airway maneuvres, an oropharyngeal airway or laryngeal mask airway may be employed. If the patient is able to protect their own airway such as in non-invasive ventilation or negative-pressure ventilation then no airway adjunct may be needed.

Mechanical ventilation is often a life-saving intervention, but carries many potential complications including pneumothorax, airway injury, alveolar damage, and ventilator-associated pneumonia.

In many healthcare systems prolonged ventilation as part of intensive care is a limited resource (in that there are only so many patients that can receive care at any given moment). It is used to support a single failing organ system (the lungs) and cannot reverse any underlying disease process (such as terminal cancer). For this reason there can be (occasionally difficult) decisions to be made about whether it is suitable to commence someone on mechanical ventilation. Equally many ethical issues surround the decision to discontinue mechanical ventilation.

Intubation

In medicine, intubation refers to the placement of a tube into an external or internal orifice of the body. Although the term can refer to endoscopic procedures, it is most often used to denote tracheal intubation. Tracheal intubation is the placement of a flexible plastic tube into the trachea to protect the patient's airway and provide a means of mechanical ventilation. The most common tracheal intubation is orotracheal intubation where, with the assistance of a laryngoscope, an endotracheal tube is passed through the mouth, larynx, and vocal cords, into the trachea. A bulb is then inflated near the distal tip of the tube to help secure it in place and protect the airway from blood, vomit, and secretions. Another possibility is nasotracheal intubation where a tube is passed through the nose, larynx, vocal cords, and trachea. Extubation is the removal of the tube.

Oxygen concentrator

An oxygen concentrator is a device used to provide oxygen therapy to a patient at substantially higher concentrations than available in ambient air. They are used as a safer, less expensive, and more convenient alternative to tanks of compressed oxygen. Common models retail at around US$800. Leasing arrangements may be available through various medical-supply companies and/or insurance agencies. Oxygen concentrators are also used to provide an economical source of oxygen in industrial processesHow they work

The simplest oxygen concentrator is capable of continuous delivery of oxygen and has internal functions based around two cylinders, filled with a zeolite material, which selectively adsorbs the nitrogen in the air. In each cycle, air flows through one cylinder at a pressure of around 20 lbf/in² (138 kPa, or 1.36 atmospheres) where the nitrogen molecules are captured by the zeolite, while the other cylinder is

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vented off to ambient atmospheric pressure allowing the captured nitrogen to dissipate.

Typical units have cycles of around 20 seconds, and allow for a continuous supply of oxygen at a flow rate of up to approximately five liters per minute (LPM) at concentrations anywhere from 50 to 95 %. This process is called pressure swing adsorption (PSA). Since 1999, concentrators providing up to 10 LPM have been available for high flow patients, in sizes not much larger or heavier than 5 LPM concentrators.

Portable oxygen concentrators

Since 2000, a number of manufacturers have introduced portable oxygen concentrators. Typically, these produce less than one liter per minute (LPM) of oxygen and use some version of pulse flow or demand flow to deliver oxygen only when the patient is inhaling. However, there is a portable oxygen concentrator with up to 3 LPM of continuous-flow oxygen. This device also has pulse flow available to either provide higher flows or reduce power consumption. These portable concentrators typically plug into a wall outlet like the larger, heavier stationary concentrators.

Portable oxygen concentrators usually can also be plugged into a vehicle DC adapter, and most have the ability to run from battery power as well, either for ambulatory use or for use away from power or for airplane travel. The FAA has approved portable oxygen concentrators for use on commercial airlines, although it is necessary to check in advance whether a particular brand or model is permitted on a particular airline.

Historically, demand or pulse flow concentrators have not been used for nocturnal use—sleeping. If the nasal cannula moves such that the concentrator is not able to detect when the patient is inhaling, it is unable to deliver the pulse while the patient is inhaling.

Safety

In both clinical and emergency-care situations, oxygen concentrators have the advantage of not being as dangerous as oxygen cylinders, which can, if ruptured or leaking, greatly increase the combustion rate of a fire. As such, oxygen concentrators are particularly advantageous in military or disaster situations, where oxygen tanks may be dangerous or infeasible.

Oxygen concentrators are considered sufficiently non-volatile to be leased to individual patients as a prescription item for use in their homes. Typically they are used as an adjunct to CPAP treatment of severe Sleep apnea. There also are other medical uses for oxygen concentrators, including emphysema and other respiratory diseases.

Used, refurbished, and temperamental units are worthless to the medical community since an individual's health frequently relies on the constant extended operation of the unit. However, such units are valuable to metal and glasswork

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hobbyists. Oxygen is one of the more expensive bottled gases. Medical oxygen concentrators or dedicated industrial (non-medical) oxygen concentrators can be made to operate a small oxy-acetylene torch quite easily, if only at lower pressures.

(2)HYPOXIA WITH Low partial pressure of atmospheric oxygen such as found at high altitude

Acclimatization

Acclimatization or acclimation is the process of an organism adjusting to change in its environment, allowing it to survive changes in temperature, water and food availability, other stresses and often relates to seasonal weather changes. Acclimatization occurs in a short time, (days to weeks) and within one organism's lifetime (compare adaptation). This may be a discrete occurrence or may instead represent part of a periodic cycle, such as a mammal shedding heavy winter fur in favor of a lighter summer coat. Acclimation is an important characteristic among many organisms because it allows them to evolve over time while changes are also simultaneously occurring in their environment. Organisms adjust their morphological, behavioral, physical, and/or biochemical traits in response to these environmental changes that they are faced with.

Altitude training

Altitude training traditionally referred to as altitude camp, is the practice by some endurance athletes of training for several weeks at high altitude, preferably over 2,500 m (8,000 ft) above sea level, though more commonly at a lower altitude due to the lack of availability of a suitable location. At this altitude the air still contains approximately 20.9% oxygen, but the barometric pressure and thus the partial pressure of oxygen is reduced.[1][2] More common nowadays is the use of an altitude simulation tent, altitude simulation room, or mask-based hypoxicator system where the barometric pressure is kept the same, but the oxygen content is reduced which also reduces the partial pressure of oxygen. Such devices have enabled different altitude training techniques including Live High, Train Low, or the practice of merely performing occasional exercise sessions at altitude.

Depending very much on the protocols used, the body may adapt to the relative lack of oxygen hypoxia in one or more of a number ways such as increasing the mass of red blood cells and hemoglobin, and non-hematolological responses.[3][4][5] Proponents claim that when such athletes travel to competitions at lower altitudes they will still have a higher concentration of red blood cells for 10-14 days, and this gives them a competitive advantage. Some athletes live permanently at high altitude, only returning to sea level to compete, but their training may suffer due to less available oxygen for workouts.

Background History

The study of altitude training was heavily delved into following the 1968 Olympics, which took place in Mexico City, Mexico: elevation 7,349 feet (2,240 m). It was during these Olympic Games that endurance events saw significant below-record

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finishes and anaerobic, sprint events broke all types of records[6] It was speculated prior to these events how the altitude might affect performances of these elite, world class athletes and most of the conclusions drawn were equivalent to those hypothesized: that endurance events would suffer and that short events would not see significant negative changes. This was attributed not only to less resistance during movement-due to the less denser air[7]-but also the anaerobic nature of the sprint events. Ultimately, these games inspired investigations into altitude training from which unique training principles were developed with the hope of avoiding underperformance.

Principles and mechanisms

Athletes or individuals who wish to gain a competitive edge for endurance events tend to take advantage of exercising at altitude due to the physiological changes that occur from the environmental differences compared to that at sea level. High altitude is typically defined as any elevation above 5,000 feet (1,500 m). It is further broken down that elevations above 11,500 feet (3,510 m) are very high altitude and elevations at or above 18,000 feet (5,500 m) are extreme altitude. The differences between sea level and high altitude are characterized by the density of air and atmospheric pressure. At sea level, air is extremely dense due to higher atmospheric pressure, which results in more molecules of gas per liter of volume air. At levels of high altitude, the atmospheric pressure is less dense, resulting in less molecules of gas per liter of volume air. This leads to a decrease in partial pressures of gases in the body, which elicits a variety of physiological changes in the body that occur at altitude.[8]

One suggestion for optimizing adaptations and maintaining performance is the live high, train low principle. This training idea emphasizes living at higher altitudes in order to experience the physiological adaptations that occur, such as increased Erythropoietin(EPO) levels, increased Red Blood Cell levels, and higher VO2 max, while maintaining the same exercise intensity at sea level. Due to the environmental differences at altitude, it may be necessary to decrease the intensity of workouts. Studies examining the live high, train low theory have produced varied results, which may be dependent on a variety of factors such as individual variability, time spent at altitude, and the type of training program.[9][10] For example, it has been shown that athletes performing primarily anaerobic activity do not necessarily benefit from altitude training as they do not rely on oxygen to fuel their performances.

Synthetic EPO also exists. Injections of synthetic EPO and blood doping are illegal in athletic competition because they cause an increase in red blood cells beyond the individual athlete's natural limits. This increase, unlike the increase caused by altitude training, can be dangerous to an athlete's health as the blood may become too thick and cause heart failure (see polycythemia). The natural secretion of EPO by the human kidneys can be increased by altitude training, but the body has limits on the amount of natural EPO that it will secrete, thus avoiding the harmful side effects of the illegal doping procedures.

Scientific studies[citation needed] have shown that altitude training can produce increases in speed, strength, endurance, and recovery. Opponents of altitude

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training argue that an athlete's red blood cell concentration returns to normal levels within days of returning to sea level and that it is impossible to train at the same intensity that one could at sea level, reducing the training effect and wasting training time due to altitude sickness. Altitude simulation systems have enabled protocols that do not suffer from such compromises, and can be utilized closer to competition if necessary. Some devices would be considered portable.

A 2005 study showed that although the boosted VO2 max had returned to normal 15 days after the conclusion of an 18-day Live High Train Low protocol, the submaximal performance at ventilatory threshold was enhanced upon initial return to sea-level, and was even greater 15 days later.

Numerous other responses to altitude training have also been identified, including angiogenesis, glucose transport, glycolysis, and pH regulation, each of which may partially explain improved endurance performance independent of a larger number of red blood cells.[4] Furthermore, exercising at altitude has been shown to cause muscular adjustments of selected gene transcripts, and improvement of mitochondrial properties in skeletal muscle.

In Finland, a scientist named Heikki Rusko has designed a "high-altitude house." The air inside the house, which is situated at sea level, is at normal pressure but modified to a low concentration of oxygen, about 15.3% (below the 20.9% at sea level), the same concentration as that at the altitudes often used for altitude training. Athletes live and sleep inside the house but perform their training outside (at normal oxygen concentrations at 20.9%). Rusko's results show improvements of EPO and red-cell levels. His technology has been commercialized and is being used by thousands of competitive athletes in cycling, triathlon, olympic endurance sports, professional football, basketball, hockey, soccer, and many other sports that can take advantage of the improvements in strength, speed, endurance, and recovery.

Physiological Adaptations

While performing endurance activities it has been observed that maximal and submaximal aerobic power and capacity decreases with increasing elevation. Submaximal endurance activities at altitude reveal an increase in heart rate and respiratory ventilation in order to compensate for the lesser availability of oxygen. At altitude there is a decrease in oxygen hemoglobin saturation. In order to compensate for this, Erythropoietin (EPO), a hormone secreted by the kidneys, stimulates red blood cell production from bone marrow in order to increase hemoglobin saturation and oxygen delivery. While EPO is naturally occurring in the body, it is also made synthetically to help treat patients suffering from kidney failure and during chemotherapy. Over the past thirty years EPO has become popularly abused by competitive athletes through blood doping and injections in order to gain advantages in endurance events. Abuse of EPO, however, increases RBC counts beyond normal levels (polycythemia) and increases the viscosity of blood possibly leading to hypertension and increasing the likelihood of a blood clot, heart attack or stroke. Though at altitude it is known EPO stimulates production of RBC’s, it is uncertain how long this adaptation takes as various studies have found different conclusions based on the amount of time spent at altitude. One study

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concluded that individuals who lived at sea level and came to live at altitude had lower VO2max’s compared with individuals who had lived at high altitude their entire lives. This implies a more significant adaptation to altitude in individuals who have been at high elevations for most of their lives, allowing for more complete adaptations. It has also been found that VO2max decreases with increasing altitude. One study concluded that this decrease in VO2 at altitude is likely due to the decrease in arterial oxygen saturation, possibly causing a decrease in cardiac output.[17] This decrease in cardiac output occurs as a means to compensate for the decreased availability of oxygen to the working muscles. In addition to cardiovascular and respiratory adaptations, significant changes in the musculature have also been observed with altitude adjustments. In a study comparing rats active at altitude versus rats active at sea level, with two sedentary control groups, it was observed that muscle fiber types changed according to homeostatic challenges which led to an increased metabolic efficiency during the beta oxidative cycle and citric acid cycle, showing an increased utilization of ATP for aerobic performance.

(3)TREATMENT FOR HYPOXIA WITH DECREASE IN OXYGEN SATURATION OF THE BLOOD CAUSED BY SLEEP APNEA OR HYPOPNEA

Treatment for sleep apnea

The most common treatment for sleep apnea is the use of a continuous positive airway pressure (CPAP) device,[25] which 'splints' the patient's airway open during sleep by means of a flow of pressurized air into the throat. However, the CPAP machine only assists inhaling, whereas a BiPAP machine assists with both inhaling and exhaling and is used in more severe cases.[citation needed]

In addition to CPAP, a dentist specializing in sleep disorders can prescribe Oral Appliance Therapy (OAT). The oral appliance is a custom-made mouthpiece that shifts the lower jaw forward, which opens up the airway. OAT is usually successful in patients with mild to moderate obstructive sleep apnea. Precise control of the position of the mandible is crucial to the success of an oral appliance.

OAT is a relatively new treatment option for sleep apnea in the United States, but it is much more common in Canada and Europe.In Singapore, there is a new treatment.

CPAP and OAT are generally effective only for obstructive and mixed sleep apnea.

In mild cases of obstructive sleep apnea, use of a specially shaped pillow or shirt may reduce sleep apnea episodes, usually by causing users to sleep on the side instead of on the back or in a reclining position instead of flat.

For patients who do not tolerate or fail nonsurgical measures, surgical treatment to anatomically alter the airway is available. Several levels of obstruction may be addressed, including the nasal passage, throat (pharynx), base of tongue, and facial skeleton. Surgical treatment for obstructive sleep apnea needs to be individualized

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in order to address all anatomical areas of obstruction. Often, correction of the nasal passages needs to be performed in addition to correction of the oropharynx passage. Septoplasty and turbinate surgery may improve the nasal airway. Tonsillectomy and uvulopalatopharyngoplasty (UPPP or UP3) is available to address pharyngeal obstruction. Base-of-tongue advancement by means of advancing the genial tubercle of the mandible may help with the lower pharynx. A myriad of other techniques are available, including hyoid bone myotomy and suspension and various radiofrequency technologies. For patients who fail these operations, the facial skeletal may be advanced by means of a technique called maxillomandibular advancement, or two-jaw surgery (upper and lower jaws). Technically, this is accomplished by a surgery similar to orthognathic surgeries addressing an abnormal bite. The surgery involves a Lefort type one osteotomy and bilateral sagittal split mandibular osteotomies.

Other surgery options may attempt to shrink or stiffen excess tissue in the mouth or throat, procedures done at either a doctor's office or a hospital. Small shots or other treatments, sometimes in a series, are used for shrinkage, while the insertion of a small piece of stiff plastic is used in the case of surgery whose goal is to stiffen tissues.

Possibly owing to changes in pulmonary oxygen stores, sleeping on one's side (as opposed to on one's back) has been found to be helpful for central sleep apnea with Cheyne-Stokes respiration (CSA-CSR).

Medications like Acetazolamide lower blood pH and encourage respiration. Low doses of oxygen are also used as a treatment for hypoxia but are discouraged due to side effects.

Alternative treatments

A 2005 study in the British Medical Journal found that learning and practicing the didgeridoo helped reduce snoring and sleep apnea as well as daytime sleepiness. This appears to work by strengthening muscles in the upper airway, thus reducing their tendency to collapse during sleep.

A program that uses specialized "singing" exercises to tone the throat, in particular the soft palate, tongue and nasaopharynx, is 'Singing for Snorers' by Alise Ojay.[32] Dr. Elizabeth Scott, a medical doctor living in Scotland, had experimented with singing exercises and found considerable success, as reviewed in her book The Natural Way to Stop Snoring (London: Orion 1995) but had been unable to carry out a clinical trial. Alise Ojay, a choir director singer and composer, began researching the possibility of using singing exercises to help a friend with snoring and came across Dr. Scott's work. In 1999, as an Honorary Research Fellow with the support of the Department of Complementary Medicine at the University of Exeter, Alise conducted the first trial of singing exercises to reduce snoring.[33] The results were described by Ojay as promising and after two years of investigations, she designed the 'Singing for Snorers' program in 2002.

The independent nonprofit UK consumer advocacy group Which? reviewed Singing for Snorers. Their physician Dr. Williams "feels the company is ethical in 'offering

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aims not claims' until research is complete" and the review stated: "Combining the programme with diet and exercise, the snorer in our test couple found real improvements in the volume and frequency of his snoring after six weeks. His partner is sleeping better, too." In the case of snorers who also have sleep apnea, there is anecdotal evidence from some of the users of Ojay's program, as she reports on her page, as reported by an American, Charley Hupp, who flew to the UK to personally thank her, on his web page and as reported by one user in the UK on the discussion forum of the British Snoring and Sleep Apnoea Association. This person reported that sleep tests before and after the program showed a significant effect: "My apnoeas had gone down from 35 to 0.8 per hour."

Benefits and risks for treatment by surgery

CPAP is functional in sleep apnea and cost-efficient for the health care system, but it is a symptomatic therapy and does not cure the disease. In contrast, although not well known, surgery is more expensive and can treat directly the causes of sleep apnea: The Stanford Center for Excellence in Sleep Disorders Medicine achieved a 95% cure rate of sleep apnea patients by surgery. Maxillomandibular advancement (MMA) is considered the most effective surgery for sleep apnea patients, because it increases the posterior airway space (PAS).The main benefit of the operation is that the oxygen saturation in the arterial blood increases. In a study published in 2008, 93.3.% of surgery patients achieved an adequate quality of life based on the Functional Outcomes of Sleep Questionnaire (FOSQ). Surgery led to a significant increase in general productivity, social outcome, activity level, vigilance, intimacy and sex, and the total score postoperatively was P = .0002. Overall risks of MMA surgery are low: The Stanford University Sleep Disorders Center found 4 failures[which?] in a series of 177 patients, or about one out of 44 patients.

Surgery and anesthesia in patients with sleep apnea

Several inpatient and outpatient procedures use sedation. Many drugs and agents used during surgery to relieve pain and to depress consciousness remain in the body at low amounts for hours or even days afterwards. In an individual with either central, obstructive or mixed sleep apnea, these low doses may be enough to cause life-threatening irregularities in breathing or collapses in a patient’s airways.[43] Use of analgesics and sedatives in these patients postoperatively should therefore be minimized or avoided.

Surgery on the mouth and throat, as well as dental surgery and procedures, can result in postoperative swelling of the lining of the mouth and other areas that affect the airway. Even when the surgical procedure is designed to improve the airway, such as tonsillectomy and adenoidectomy or tongue reduction, swelling may negate some of the effects in the immediate postoperative period. Once the swelling resolves and the palate becomes tightened by postoperative scarring, however, the full benefit of the surgery may be noticed. Individuals with sleep apnea generally require more intensive monitoring after surgery for these reasons.

Sleep apnea patients undergoing any medical treatment must make sure his or her doctor and/or anesthetist are informed about their condition. Alternate and emergency procedures may be necessary to maintain the airway of sleep apnea

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patients. If an individual suspects he or she may have sleep apnea, communication with their doctor about possible preprocedure screening may be in order.

(4)TREATMENT FOR HYPOXIA WHEN THE BLOOD FAILS TO DELIVER OXYGEN TO TARGET TISSUES

Treatment for carbon monoxide poisoning

Initial treatment for carbon monoxide poisoning is to immediately remove the person from the exposure without endangering further people. Those who are unconscious may require CPR on site.Administering oxygen via non-rebreather mask shortens the half life of carbon monoxide to 80 minutes from 320 minutes on normal air. Oxygen hastens the dissociation of carbon monoxide from carboxyhemoglobin, thus turning it back into hemoglobin. Due to the possible severe effects in the fetus, pregnant people are treated with oxygen for longer periods of time than non-pregnant patients.

Hyperbaric oxygen

Hyperbaric oxygen is also used in the treatment of carbon monoxide poisoning, as it may hasten dissociation of CO from carboxyhemoglobin and cytochrome oxidase to a greater extent than normal oxygen. Hyperbaric oxygen at three times atmospheric pressure reduces the half life of carbon monoxide to 23 minutes, compared to 80 minutes for regular oxygen. It may also enhance oxygen transport to the tissues by plasma, partially bypassing the normal transfer through hemoglobin. However it is controversial whether hyperbaric oxygen actually offers any extra benefits over normal high flow oxygen, in terms of increased survival or improved long term outcomes. There have been randomized controlled trials in which the two treatment options have been compared; of the six performed, four found hyperbaric oxygen improved outcome and two found no benefit for hyperbaric oxygen. Some of these trials have been criticized for apparent flaws in their implementation. A review of all the literature on carbon monoxide poisoning treatment concluded that the role of hyperbaric oxygen is unclear and the available evidence neither confirms nor denies a medically meaningful benefit. The authors suggested a large, well designed, externally audited, multicentre trial to compare normal oxygen with hyperbaric oxygen.Other

Further treatment for other complications such as seizure, hypotension, cardiac abnormalities, pulmonary edema, and acidosis may be required. Increased muscle activity and seizures should be treated with dantrolene or diazepam; diazepam should only be given with appropriate respiratory support. Hypotension requires treatment with intravenous fluids; vasopressors may be required to treat myocardial depression. Cardiac dysrhythmias are treated with standard advanced cardiac life support protocols, unless severe, metabolic acidosis is treated with sodium bicarbonate. Treatment with sodium bicarbonate is controversial as acidosis may increase tissue oxygen availability. Treatment of acidosis may only need to consist of oxygen therapy. The delayed development of neuropsychiatric impairment is one of the most serious complications of carbon monoxide poisoning. Brain damage is confirmed following MRI or CAT scans. Extensive follow up and

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supportive treatment is often required for delayed neurological damage. Outcomes are often difficult to predict following poisoning, especially patients who have symptoms of cardiac arrest, coma, metabolic acidosis, or have high carboxyhemoglobin levels. One study reported that approximately 30% of people with severe carbon monoxide poisoning will have a fatal outcome.

Treatment for Methemoglobinemia

Methemoglobinemia can be treated with supplemental oxygen and methylene blue[4] 1% solution (10 mg/ml) 1 to 2 mg/kg administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state.

This is achieved by providing an artificial electron acceptor (such as methylene blue, or flavin) for NADPH methemoglobin reductase (RBCs usually don't have one; the presence of methylene blue allows the enzyme to function at 5x normal levels. The NADPH is generated via the hexose monophosphate shunt.

Diaphorase II normally contributes only a small percentage of the red blood cells reducing capacity but is pharmacologically activated by exogenous cofactors, such as methylene blue, to 5 times its normal level of activity. Genetically induced chronic low-level methemoglobinemia may be treated with oral methylene blue daily. Also, vitamin C can occasionally reduce cyanosis associated with chronic methemoglobinemia but has no role in treatment of acute acquired methemoglobinemia.

BIBLIOGRAPHY

http://en.wikipedia.org/wiki/CPRhttp://en.wikipedia.org/wiki/Mechanical_ventilationhttp://en.wikipedia.org/wiki/Artificial_ventilationhttp://en.wikipedia.org/wiki/Intubationhttp://en.wikipedia.org/wiki/Oxygen_concentratorhttp://en.wikipedia.org/wiki/Sleep_apnea#Treatmenthttp://en.wikipedia.org/wiki/Acclimatizationhttp://en.wikipedia.org/wiki/Altitude_traininghttp://en.wikipedia.org/wiki/Carbon_monoxide_poisoning#Treatmenthttp://en.wikipedia.org/wiki/Methemoglobinemia#Treatment

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