attenuated by the increased buffering capacity available. A “chicken and egg” question then becomes important: is CO2 retention secondary to an underlying ventilatory control abnormality in these patients, or is the diminution in ventilatory sensitivity merely secondary to chronic CO2 retention? Although this question remains unanswered, some evidence suggests that hereditary factors may be important and that CO2 retention is more likely to develop in patients with a genetically lower respiratory sensitivity.
Whatever the answer to this question, there is a clinically important corollary to this depression in CO2 sensitivity, irrespective of the cause of CO2 retention. When O2 is administered to the chronically hypoxemic and hypercapnic patient, PCO2 may rise even further. Three factors account for this wellrecognized clinical event: changes in minute ventilation, changes in ventilation-perfusion matching, and the Haldane effect. To understand this phenomenon, each of these factors should be appreciated. The easiest factor to understand is the change in minute ventilation. If a patient is hypoxemic, low PaO2 is sensed by the peripheral chemoreceptors, causing stimulation of the respiratory center. When supplemental oxygen is given and the patient is no longer hypoxemic, this stimulation abates. This was previously thought to be the sole explanation for the rise in PCO2 seen in hypoxic, hypercapnic patients who were given supplemental oxygen. However, it now is known that hypoxic drive and a decrease in ventilation play only a small role in the frequently observed increase in PCO2 occurring in this situation. More important is a worsening of ventilation-perfusion matching. Recall that alveolar hypoxia results in decreased perfusion to the hypoxic lung segments, an effect that is mediated through hypoxic vasoconstriction of those pulmonary arterioles supplying hypoxic alveoli. However, administration of supplemental O2 may alleviate alveolar hypoxia in these poorly ventilated regions, thus inhibiting the compensatory localized vasoconstriction. Ventilation-perfusion mismatch becomes more marked in the absence of hypoxic vasoconstriction, leading to less efficient elimination of CO2 and increased levels of PCO2. The third factor contributing to the rise in PCO2 is the Haldane effect, in which deoxygenated hemoglobin has a higher affinity for CO2 (see Chapter 1). When supplemental oxygen is administered, the more oxygenated hemoglobin has a lower affinity for CO2, leading to enhanced release of CO2 from hemoglobin into plasma and a higher PCO2.
Administration of O2 to the chronically hypoxemic and hypercapnic patient may elevate PCO2.
Significant elevations in PCO2 on administration of supplemental O2 to the chronically hypercapnic patient can generally be prevented by avoiding excessive concentrations of supplemental O2 beyond those needed to raise oxygen saturation to approximately 90% to 94%. In the presence of significant hypoxemia, the clinician should not withhold supplemental O2 from patients who have chronic hypercapnia, because significant hypoxemia poses a greater risk than a further increase in PCO2. Nevertheless, such patients usually are given relatively limited amounts of supplemental O2 to minimize the degree of further hypercapnia. In the hospital setting, oxygen can be administered via noninvasive positive-pressure ventilation, which generally attenuates any hypercapnia that may develop.
Sleep apnea syndrome
Sleep apnea is a common disorder in which patients have repetitive episodes of apnea (cessation of breathing) during sleep that lead to gas exchange abnormalities and disruption of normal sleep architecture. In subjects older than 50 years, studies estimate the prevalence of moderate to severe sleep
apnea to be 17% in men and 9% in women. Obesity is a strong risk factor for sleep apnea, and the prevalence of sleep apnea increases with higher body mass indices.
A period of more than 10 seconds without airflow is considered to constitute an apneic episode, and patients with this syndrome often have hundreds of such episodes during the course of a night’s sleep. The term hypopnea is used to describe a reduction in airflow of 50% or more without the complete cessation of airflow implied by the term apnea. Because episodes of apnea and hypopnea commonly coexist, the broader term sleep apnea–hypopnea syndrome is sometimes used.
Types
Sleep apnea syndrome is commonly divided into two types, obstructive and central, depending on the nature of the episodes. In addition, some patients have a mixture of the two types. Obstructive sleep apnea (OSA), which is much more common, is characterized by transient collapse and obstruction of the pharyngeal airway that prevents inspiratory airflow. Inspiratory muscles are still active during the obstructive episodes, but initiation of airflow is unsuccessful due to the obstruction. Some degree of decreased upper airway muscle tone and narrowing occurs in all people during sleep, but in patients with OSA this reaches the point of airway occlusion.
In contrast, central sleep apnea (CSA) is characterized by apneas due to lack of respiratory efforts— that is, there is no signal from the respiratory center to initiate inspiration. Hence, no respiratory muscle activity can be observed when airflow ceases. CSA is rare in the general population but commonly seen in patients with heart failure, where Cheyne-Stokes breathing is grouped under CSA. Some patients may have episodes of apnea that have features of both central and obstructive apnea, a condition called mixed apnea. Typically, such episodes start without ventilatory effort (central apnea), but upper airway obstruction occurs when ventilatory effort resumes (obstructive apnea). Because OSA is more common than CSA, the focus here is on the clinical features, pathophysiology, and treatment of obstructive apnea, with only a brief discussion of CSA.
Categories of sleep apnea syndrome:
1.Obstructive
2.Central
3.Mixed
Clinical features
Patients with sleep apnea syndrome may seek medical consultation because of (1) symptoms or signs that they or their partner have noticed during a night’s sleep, (2) daytime hypersomnolence, or (3) complications that arise from the repetitive apneic episodes. During sleep, patients with OSA are often noted to have loud snoring and may have obvious snorting, gasping, and agitation as a result of trying to breathe against the obstructed airway. They also may have violent movements during periods of obstruction. The sleep partner may report being hit or injured due to these violent movements. On awakening, patients often report a severe headache, presumably related to cerebral vasodilation associated with derangements in gas exchange that occur during the apneic episodes. However, it is important to note that many patients, especially those with milder cases, will not report any problems to their physician. Symptoms may be noted only when the physician specifically inquires about sleep issues.
With such a disordered pattern of sleep, patients are effectively sleep deprived and, not surprisingly, frequently are somnolent during normal waking hours. Even though the patient is in bed and “asleep,” only
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the lighter phases of sleep are entered, and adequate amounts of the deeper restorative phases of sleep are not achieved because of repeated “microarousals.” The degree of daytime hypersomnolence can be debilitating and even dangerous. Patients may fall asleep while driving, eating, or working, or during a variety of other usual daytime activities. Patients may appear to have a psychiatric disorder, partially because of their extreme hypersomnolence and partially because of psychological changes that have presumably resulted from their disease. Inability to concentrate and depression are common symptoms.
Clinical features of sleep apnea syndrome:
1.Disordered respiration during sleep
2.Daytime hypersomnolence
3.Morning headaches
4.Cardiovascular complications
Secondary cardiovascular complications are associated with OSA and are believed to be mediated in part by increased sympathetic nervous system activity. OSA is a risk factor for systemic hypertension, pulmonary arterial hypertension, coronary artery disease, atrial fibrillation, heart failure, and stroke. Treatment of OSA is associated with improved blood pressure control in patients with systemic hypertension. Atrial fibrillation is strongly associated with OSA, and during the episodes of apnea, patients may have a variety of other cardiac conduction disturbances, although they rarely are life threatening. As a result of multiple episodes of hypoxemia at night, pulmonary hypertension can result, and unexplained cor pulmonale may be the presenting clinical problem.
Pathophysiology
During the past 3 decades, a great deal has been learned about the pathogenesis and risk factors leading to OSA. Normally, inspiration is characterized by contraction of the diaphragm, resulting in negative airway pressure accompanied by increased activity of upper airway muscles acting to keep the pharynx patent.
The genioglossus muscle is particularly important in this regard because it prevents the tongue from falling against the posterior pharyngeal wall and occluding the pharynx.
In patients with OSA, structural and functional factors often work together to allow the upper airway to close during inspiration. In most patients, an excess of soft tissue in the upper airway, often as a consequence of obesity, reduces the size of the pharyngeal opening. During sleep, particularly rapid eye movement sleep, loss of activity of the upper airway muscles results in inspiratory collapse of the soft tissues and obstruction of the upper airway. Airflow eventually resumes after each episode of obstruction as the patient arouses (although these microarousals often are not evident to the patient), when activity of the upper airway muscles is restored and when the airway temporarily becomes patent. However, as the patient falls asleep again, upper airway muscle activity is again lost, and the cycle repeats itself. Because of the importance of structural factors contributing to a small upper airway, patients who are obese or who have a small jaw (micrognathia), a large tongue, or large tonsils are at particular risk for OSA.
In contrast, CSA can be further characterized as one of two subtypes: hyperventilation-associated and hypoventilation-associated. The former type is more common and frequently seen in heart failure. The pathophysiology is similar to that of Cheyne-Stokes respiration, with ventilatory instability leading to both episodic overshooting (hyperventilation) and periods of apnea. The latter, on the other hand, is seen in patients with chronic hypoventilation, usually in the setting of CNS disease, neuromuscular disease, or severe pulmonary disease.
In CSA, during an episode of central apnea, monitoring of chest wall motion reveals no movement,
corresponding to cessation of airflow and a fall in O2 saturation (Fig. 18.2A). With OSA, chest wall and abdominal movement can be detected during an ineffective attempt to move air through the obstructed airway. Airflow measured simultaneously is found to be absent (tidal volume = 0), and O2 saturation drops, often to profoundly low levels (see Fig. 18.2B). When O2 saturation drops significantly during sleep, disturbances in cardiac rhythm can occur, and elevation of pulmonary artery pressure may be seen as a consequence of hypoxia-induced pulmonary vasoconstriction.
FIGURE 18.2 Examples of recordings in sleep apnea syndrome. A, Central sleep
apnea. Absence of abdominal, rib cage, and sum movements are associated with a
small fall in arterial oxygen saturation. B, Obstructive sleep apnea. Apneas at
beginning and midportion of recording are marked by absence of sum movements
(VT) despite respiratory efforts. When diaphragm contracts and upper airway is obstructed during attempted inspiration, abdomen moves out (upward on tracing)
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while rib cage moves inward (downward). Each apnea shown is associated with
marked fall in O2 saturation and is terminated by three deep breaths. ABD, abdominal movement; O2 Sat, O2 saturation; RC, rib cage; VT, tidal volume (monitored as sum of rib cage and abdominal movements). Source: (From Tobin, M.
J., Cohn, M. A., & Sackner, M. A. (1983). Breathing abnormalities during sleep.
Archives of Internal Medicine, 143, 1221–1228. Copyright 1983, American
Medical Association.)
Treatment
The first-line therapy used in most patients with OSA is continuous positive airway pressure, commonly called CPAP. A mask connected to an air compressor is placed over the nose or the full face of the patient at bedtime. The compressor maintains positive pressure in the upper airway throughout the respiratory cycle, thus providing a pneumatic splint to prevent the airway from collapsing. For patients who are obese, an attempt at significant weight loss is recommended. Although weight loss can sometimes dramatically improve the number and severity of apneic episodes, long-term weight reduction is difficult for most patients to maintain, making other forms of therapy necessary. In all patients, respiratory depressants, including alcohol and sedative-hypnotic drugs, should be avoided because they may worsen OSA. An alternative but less effective form of therapy involves nocturnal use of an oral appliance to maintain the tongue and/or the jaw in a relatively anterior position. This mechanical form of therapy facilitates airway patency by keeping the tongue away from the posterior pharyngeal wall.
Nasal or full-face mask CPAP is often applied at night to patients with OSA to prevent upper airway closure.
Because CPAP and oral appliances are so often effective, other forms of therapy now are used less frequently. Nevertheless, surgical modes of therapy may be beneficial in selected patients. For example, some patients are treated by a surgical procedure called uvulopalatopharyngoplasty, which involves removal of redundant soft tissue in the upper airway. Because the procedure is not without a risk of complications, this surgery is generally reserved for patients who cannot tolerate CPAP.
A newer surgical technique called hypoglossal nerve stimulation requires surgical implantation of a neurostimulator device that can be turned on before sleep. Electrical impulses from the device activate the hypoglossal nerve to in turn stimulate the protrusion muscles of the tongue and maintain patency of the lower pharyngeal airway.
Rare patients with particularly severe obstructive apnea whose disease is refractory to other forms of therapy can be treated with a tracheostomy, which involves placement of a tube in the trachea to allow air to bypass the site of upper airway obstruction. Despite the drastic nature of tracheostomy as a form of treatment, for patients who have failed other treatment, the therapeutic response can be quite significant. Patients may have a dramatic reversal of symptoms and a striking improvement in their lifestyle, which previously was limited by intractable daytime sleepiness.
In patients with CSA, treatment is primarily focused on addressing the underlying disease. In the appropriate clinical setting, respiratory stimulants, an electrical implanted phrenic nerve pacemaker to stimulate the diaphragm, or mechanical ventilation, either noninvasive via a face mask or invasive via a tracheostomy tube, may all be considered.