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Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094On-line version ISSN 1806-907X

Rev. Bras. Anestesiol. vol.56 no.6 Campinas Nov./Dec. 2006 



Anesthesia and obstructive sleep apnea*


Anestesia y apnea obstructiva del sueño



Charles MachadoI; Américo Massafuni Yamashita, TSAII; Sonia Maria Guimarães Pereira TogeiroIII; Dalva PoyaresIV; Sérgio TufikV

IAnestesiologista e Especialista em Biologia e Medicina do Sono – UNIFESP
IIChefe de Disciplina de Anestesiologia, Dor e Medicina Intensiva – UNIFESP
IIIDoutora em Pneumologia, Responsável pelo Curso de Especialização em Medicina do Sono – UNIFESP
IVDoutora em Ciências, Neurologista e Professora Afiliada da Disciplina de Medicina e Biologia do Sono – UNIFESP
VChefe da Disciplina de Biologia e Medicina do Sono – UNIFESP

Correspondence to




BACKGROUND AND METHODS: Maintaining the patency of the upper airways is fundamental to anesthesia and patients with obstructive sleep apnea (OSA). During anesthesia and while a person is sleeping, the tonus of the pharyngeal muscles is reduced. It is important to identify patients with OSA to prevent risks in the perioperative period. The objective of this report was to present a revision of the relationship between OSA and anesthesia regarding planning of anesthesia, stressing the importance of identifying the obstructive sleep apnea hypopnea syndrome (OSAHS).
CONTENTS: OSAHS is caused mainly by total or partial pharyngeal collapse, which may cause a reduction in hemoglobin saturation and cardiovascular complications. The main predisposing factors include male gender, obesity, and cranial and orofacial characteristics. It is diagnosis by its clinical and polysomnographic characteristics, which also determine its severity. Patients with severe OSAHS may present problems during tracheal intubation and sedation, and may be more susceptible to hypoxia and hypercapnia, even in the presence of normal lungs. The authors discuss the importance of diagnosing and treating OSAHS before surgeries in order to reduce the anesthetic risk.
CONCLUSION: Prior diagnosis and treatment of OSAHS with continuous positive pressure in the upper airways may reduce perioperative complications and influence the anesthetic and postanesthetic management.

Key Words: DISEASES, Obstructive Sleep Apnea; VENTILATION, continuous positive airway pressure.


JUSTIFICATIVA Y OBJETIVOS: El mantenimiento de la permeabilidad de las vías aéreas superiores (VAS) es fundamental para la anestesia y para pacientes con apnea obstructiva del sueño (AOS). Durante los de los estados, ocurre una reducción del tono de la musculatura faríngea. Identificar pacientes con AOS es importante para prevenir riesgos durante el período perioperatorio. El objetivo de este trabajo fue el de presentar una revisión sobre la relación entre AOS y anestesia, teniendo en cuenta la planificación de la anestesia, enfatizando la importancia de la identificación del síndrome de la apnea e hipopnea obstructiva del sueño (SAHOS).
CONTENIDO: La SAHOS se da principalmente por colapso total o parcial de la faringe pudiendo llevar a la disminución en la saturación de la oxihemoglobina y complicaciones cardiovasculares. Los principales factores de predisposición son el sexo masculino, obesidad, características del cráneo y orofaciales. Su diagnóstico es clínico y del gráfico de poli sueño, lo que también cuantifica la gravedad de la AOS. Los pacientes con SAHOS especialmente acentuada, pueden presentar problemas durante la intubación traqueal y la sedación pudiendo estar más susceptibles para la incidencia de hipoxia e hipercapnia, incluso con los pulmones normales. Los autores discuten la importancia del diagnóstico previo y el tratamiento de la SAHOS con la intención de reducir el riesgo anestésico.
CONCLUSIONES: El diagnóstico y tratamiento previo de la SAHOS con presión positiva continua en las VAS pueden reducir complicaciones perioperatorias e influenciar la conducta anestésica y en la recuperación postanestésica.




Maintaining the patency of the upper airways is a concern of anesthesiologists and other physicians managing sleep disorders. The tonus of the pharyngeal muscles is decreased during sleep and this reduction is even more accentuated during anesthesia, increasing the possibility of upper airways obstruction and consequent hypoxia and hypercapnia. Patients with obstructive sleep apnea (OSA) are more susceptible to those changes, especially when under the added effects of drugs used for sedation during general anesthesia 1. Besides, patients with airways that are difficult to manage during anesthesia, with or without tracheal intubation, or during the immediate postoperative period, probably have OSA. Those correlations are clinically important because identifying patients with OSA may help prevent accidents secondary to difficult intubations and improve care in the immediate postoperative period with positive pressure ventilation.

The objective of this study was to present a revision of the relationship between OSA and anesthesia regarding planning the anesthesia, stressing the importance of identifying the obstructive sleep apnea syndrome (OSAS).



Obstructive sleep apnea, also known as obstructive sleep apnea hypopnea syndrome (OSAHS) is characterized by increased respiratory effort due to the occlusion the of upper airways, which can be complete (apnea) or partial (hypopnea). According to the American Academy of Sleep Medicine (AASM), those respiratory events are defined by the polysomnographic recordings and based on the severity of the reduction of the respiratory flow, its repercussion in oxyhemoglobin saturation, and in sleep fragmentation. Thus, there is absence of airflow in obstructive sleep apnea, while there is a reduction of airflow (independent of the severity, as long as it is associated with a 3% or greater reduction in oxygen saturation or with brief awakenings in hypopnea 2. Those events should last for at least 10 seconds.

It is estimated that it has an incidence of 4% in men and 2% in women 3. Episodes of apnea and hypopnea during sleep cause brief awakenings that can be observed on the electroencephalogram (EEG) with the consequent dilating muscular activity of the airways, which prevents prolonged hypoxemia 4,5. These brief awakenings also contribute to the hyperactivity of the autonomous nervous system, which is one of the mechanisms responsible for hypertension in these individuals. The clinical spectrum of the disease varies from mild to severe, including symptoms such as: snoring, respiratory pauses, according to a third part, nocturnal choking, somnolence during the day, hypertension, nocturia, impotence, cognitive impairment, besides the predisposition for accidents at work and motor vehicle accidents 2,6-8. Polysomnography during the night is the main diagnostic method for respiratory disturbances; it provides a continuous record of the electroencephalogram (EEG), mental electromyography (EMG), and electro-oculography (EOG). In addition, oronasal airflow, thoraco-abdominal movements, and pulse oxymetry are also recorded 2. The Wisconsin Sleep Cohort Study, among others, determined that the number of obstructive respiratory events per hour of sleep, also called the apnea-hypopnea index (AHI), was related to an increase in the cardiovascular comorbidity. Five to 15 obstructive respiratory events is considered mild apnea, 15 to 30 is moderate apnea, and above 30 is severe apnea 2-9.



The anatomic region between the posterior pharynx and the larynx does not have bone or cartilage and, therefore, is prone to obstruction 1. The muscles in this area are responsible for maintaining the upper airways open while an individual is awake. However, when a person falls asleep or is under the influence of drugs used routinely in anesthesia that inhibit the central nervous system (CNS), there is decreased sensitivity of the chemoreceptors in the brain stem and of the cortical drive to the pharyngeal muscles, favoring the collapse of the upper airways in this region. The decreased activation of the pharyngeal muscles has two important consequences. First, due to the turbulent airflow caused by the decreased caliber of the upper airways, there is a vibration in the pharyngeal structures, which is perceived as snoring. Second, due to the Bernoulli effect, the upper airways may have a tendency for a partial (hypopnea) or complete (apnea) collapse 10.

Structurally, the upper airways may follow the Starling's resistor model (Figure 2), in which flow through a collapsible segment (pharynx) depends on how the upstream (nasal cavity) and downstream (trachea) pressures relate to the pressure exerted by the soft tissues of the pharynx. Using this model, one can observe three states: 1. Upstream and downstream pressures exceed the pressure in the collapsible segment of the pharynx and the airflow varies according to the pressure gradient, according to the Poiseuille's equation; 2. The pressure in the collapsible segment is greater than the downstream (tracheal) pressure, but is smaller than the upstream (nasal cavity) pressure, and the airflow is determined by the pressure gradient between the nasal cavity and the collapsible segment (pharynx); and 3. The pressure exerted by the pharyngeal tissue is greater than the upstream (nasal cavity) pressure and, therefore, the critical pressure for closure of the collapsible segment (pharynx) is the pressure in the pharynx. These states can be observed both during sleep and anesthesia 11-13.






Several factors make the upper airways prone to obstruction during sleep or anesthesia. As a rule, the causes of pharynx collapse include a reduction in its caliber or increased complacency of the pharyngeal tissues, increased pressure of the tissues surrounding the upper airways, and increased negative pressure inside the upper airways 1.

The changes in the upper airways that make them collapsible follow three main elements: 1. According to Laplace's law, the pressure necessary to maintain the upper airways open increases as the radius decreases; 2. The change in caliber necessary to close the upper airways is smaller if their caliber is already reduced; 3. Resistance to airflow associated with narrowing of the upper airways requires that a more negative intraluminal air pressure be generated during inspiration.

Characteristics, such as male gender, age, obesity, increased cervical circumference, macroglossia, retrognathic mandible, maxillary constriction, intraluminal abnormalities (for example, tumors, tonsilar hypertrophy, nasal septal deviation), neuromuscular diseases, genetic syndromes, like Down and Pierre-Robin syndromes, endocrine diseases, such as hypothyroidism and acromegaly, are associated with OSA 1.

Disease expression is usually multifactorial, demanding a detailed history and physical exam. Laboratory and diagnostic imaging exams can be useful in detecting anatomic and metabolic changes that contribute to OSA.

Central obesity can trigger or exacerbate the disease due to fat accumulation in the upper airways, besides changing pulmonary volumes; 60% to 70% of the patients with OSA are obese. The incidence of OSA in patients with morbid obesity is 12 to 15 times higher than in the general population. Due to the androgenic fat pattern associated with the action of male hormones in the neuromuscular activity of the upper airways and respiratory muscles, the risk of OSA in middle aged men is two to three times greater when compared with women in the same age Group. There is evidence that menopause is a risk factor for OSA, since the differences between men and women decrease with aging 14-16.

Other risk factors for OSA include alcohol and benzodiazepines, dorsal decubitus, family history of sleep apnea, stroke, smoking, and history of snoring.



Several sings and symptoms can be observed in patients with OSA. Snoring, usually loud and intermittent, and often associated with 20- to 30-second respiratory pauses, unnoticed by the patient and usually reported by his/her partner, followed by reanimating awakenings or snoring, is the most prevalent among the nocturnal symptoms in adult patients 17. Among diurnal symptoms, excessive somnolence is frequent, and may be classified as mild, moderate, and severe. Mild somnolence occurs during activities that demand little attention (for example, watching TV); moderate somnolence occurs during medium-attention activities (for example, meetings, classes); severe somnolence occurs during activities requiring a lot of attention (for example, driving, eating) 2. Some studies demonstrate that the incidence of car accidents in patients with OSA is twice or three times greater than in the general population 18.



Repeated episodes of apnea during the night in patients with OSA produce hypoxia and hypercapnia associated with sympathetic activation, endothelial vascular dysfunction, increased oxidative stress and platelet aggregation, and metabolic imbalance, all of which have been implicated in the genesis and pathophysiology of cardiovascular diseases 19.

Epidemiological studies demonstrated that OSA is a cause of hypertension, independent of age, body mass index (BMI), gender, and alcohol intake or smoking 20,21 and demonstrated the relationship between the severity of the respiratory sleep disturbance and the increase in blood pressure. The recent recommendations of the VII Joint National Committee (JNC) for prevention, detection, and treatment of hypertension place OSA as the first on the list of identifiable causes of hypertension 22.

OSA produces acute hypoxemia, hypercapnia, sympathetic activation, and variations in blood pressure that can predispose to myocardial ischemia. Chronically, these events can promote endothelial dysfunction, activation of inflammation, changes in clotting mechanisms, and release of vasoactive substances, such as endothelin-1, a potent vasoconstrictor, that might be associated with the genesis of hypertension 23-29.

Obstructive sleep apnea was identified in the Sleep Heart Study as an independent risk factor for coronary artery disease 30,31. In patients with OSA and coronary artery disease, the increased oxidative stress is associated with increased levels of soluble circulating adhesion molecules, such as intracellular adhesion molecule-1 (ICAM-1) and the vascular cellular adhesion molecule-1 (VCAM-1) 32,33.

It has been demonstrated that hypoxia stimulates the production of angiogenic substances, such as the vascular endothelial growth factor (VEGF) 34. Plasma concentration of VEGF is increased in patients with OSA, correlating with the number of episodes of apnea and the degree of nocturnal hypoxemia, decreasing with treatment with Continuous Positive Airway Pressure (CPAP). However, there is no direct evidence that increased levels of VEFG induces angiogenesis in OSA 35,36.

Data from the Sleep Heart Health Study indicate a strong association between the severity of OSA and congestive heart failure (CHF), with a greater risk in those patients with an apnea or hypopnea index above 11 events per hour 37. Obesity, in men, and age, in women, also contribute to increase the risk 38. The increased knowledge about the pathophysiology of congestive heart failure led to the recognition that asymptomatic diastolic dysfunction frequently precedes symptoms of CHF and that many individuals are asymptomatic, even in the presence of important left systolic dysfunction, often with an ejection fraction below 40 39.

Hypoxemia, fluctuation in the levels of catecholamines, elevation of arterial blood pressure at night, and sustained hypertension during the day, may predispose to hypertensive cardiac failure. Systolic dysfunction can be induced by cytokines released by the inflammatory activation present in OSA, as well as by the increased post-load and left ventricular transmural pressure caused by the increased intrathoracic negative pressure during episodes of apnea 40,41. Thus, evidence indicates that OSA is a risk factor for cardiovascular disease.



Due to the anesthetic complications in individuals with OSA, anesthesiologists should be familiar with this sleep disorder. In the general population, one in five adults have OSA and approximately 10% of the population undergoes diagnostic or surgical procedure under general anesthesia each year 42. A few studies demonstrated that 13% to 24% of the patients with OSA are difficult to intubate, and 8% of them need to be intubated when awake 50. Increased neck circumference, elevated Mallampati index, and craniofacial skeletal alterations are indicators of a difficult intubation. It is estimated that a considerable number of those patients are undiagnosed. There are no studies defining the real risk of anesthesia and sedation in patients with OSA. It is known that the depressing effects of anesthesia and sedation cause relaxation of the upper airways and change the arousal response to hypoxic and hypercarbic stimuli, but the aggravating or triggering effects of anesthesia and sedation on OSA are still to be determined. There is evidence that OSA can contribute to the perioperative morbidity and mortality, especially in procedures in the head and neck, which can reduce the caliber of the upper airways by postoperative edema, presence of nasal tubing (such as nasogastric tube), or intraluminal obstruction (hematoma) 43-47. Likewise, pain caused by an upper abdominal surgery or surgery affecting the rib cage can affect ventilation. Dorsal decubitus in patients prone to OSA who underwent surgical procedures favor this condition.

These patients should be identified during the preoperative evaluation whenever possible. However, sings and symptoms can be discrete and do not indicate the diagnosis of OSA 48,49. Sometimes the anesthesiologist suspects the diagnosis of OSA in the surgical room, during the surgery. Snoring or obstruction of the upper airways after the premedication, difficulty during the tracheal intubation or maintaining the upper airways open during the anesthesia, or high respiratory obstruction in the postoperative recovery period, suggest the possibility of OSA. Thus, the anesthesiologist should stimulate investigating these patients for OSA.



Whenever there is the possibility a patient has OSA, a polysomnographic study should be done to identify the severity of the apnea and, when indicated, determine the ideal titulation of CPAP, the treatment of choice for those patients. As a rule, the patient should be treated with CPAP for 4 to 6 weeks before the surgery in order to reduce edema of the upper airways and the clinical complications of the disease. In severe cases in which the patient does not tolerate CPAP or the treatment has not been effective, one should consider a tracheotomy 50,51. Pre-anesthetic and intraoperative medications can exacerbate the obstruction in patients with OSA. Therefore, one should be careful when using them or avoid them altogether whenever possible; when they have to be administered, it is necessary to monitor oxygen saturation and benzodiazepines antagonists should be readily available 1.

The choice of anesthetic technique depends on the experience of the anesthesiologist, type and site of the surgery, the severity of OSA, and availability of monitoring and trained personnel in the postanesthetic recovery unit to care for this type of patient. Factors that contribute to the development of postoperative complications include: surgeries in the upper abdomen, head, and neck; increased duration of the anesthesia (equal or greater than three hours); long-acting neuromuscular blockers; and emergency surgeries 52.

In surgeries with general anesthesia, one should prefer short-acting agents for anesthesia induction and maintenance 1.

Regional blocks, such as epidural or subarachnoid blocks, can be an option.

Potential problems in the intra- and postoperative periods keeping the upper airways open and regarding the suppression of the arousable response associated with general anesthesia can be avoided with regional techniques. The benefits of the continuous epidural block can be prolonged to the immediate postoperative period, decreasing pain and the need for analgesics 1.

Due to the potential risk of a difficult intubation in these patients, it is advisable to have auxiliary devices available, such as bronchofibroscopy and laryngeal mask, and the anesthesiologist should know how to manage a difficult airway. One should be careful when extubating these patients, which should be done when they are fully awake, with a positive gag reflex for protection of the upper airways. Postoperative pain should be properly controlled because it can increase oxygen consumption and reduced oxygenation in a patient with OSA. One should prefer locoregional anesthesia and nonsteroidal anti-inflammatories, avoiding opioids. Patients with severe OSA, AHI greater than 30 per hour, and oxihemoglobin saturation lower than 80% should be transferred to an Intensive Care Unit. Continuous Positive Airway Pressure can be restarted immediately after extubation, in the postanesthetic recovery unit. One should not treat hypoxemia in these patients with oxygen supplementation only, since it inhibits the arousable response, increases retention of carbon dioxide, and masks a probable obstruction 10.

Patients with OSA have a higher risk of complications related to anesthesia. These are related to difficult intubation, worsening upper airways obstruction, and increased awakening threshold caused by the anesthetics and analgesics, especially opioids that cause respiratory depression.

The anesthesiologist must follow a protocol that includes early diagnosis or the identification of risk factors for this condition, the choice of the most adequate anesthesia technique, and individualized postoperative management. Treatment with CPAP should be encouraged in the pre- and postoperative periods in patients with OSA, since it is effective in controlling complications related to this condition and those related to the anesthesia.



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Correspondence to:
Dr. Charles Machado
Rua Azambuja, 1.089
H.C.C. Renaux Azambuja
83530-902 Brusque, SC

Submitted for publication 26 de janeiro de 2006
Accepted for publication 07 de agosto de 2006



* Received from Departamento de Psicobiologia da Universidade Federal de São Paulo (UNIFESP) e Serviço de Anestesiologia do Hospital Cônsul Carlos Renaux (SHCCR), São Paulo, SP

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