The effect of blood oxygen stores and changes in cardiac output on the rate of fall of arterial oxyhemoglobin saturation during obstructive apnea.
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Animals↗
Biomedical subjects
E C Fletcher
Publications and source records attributed to E C Fletcher.
Central venous O2 saturation and rate of arterial desaturation during obstructive apnea.
We examined the rate of fall of arterial O2 saturation (dSao2/dt) after apnea onset in four spontaneously breathing adult male baboons. We postulated that a lower mixed venous O2 saturation (Svo2) would steepen dSao2/dt by more rapid depletion of alveolar O2. Single isolated (NREP) and five or more sequential repetitive apneas (REP) were created by clamping an indwelling cuffed endotracheal tube at end expiration. Fiberoptic catheters were used for continuous monitoring of Sao2, Svo2, and cardiac output. The mean dSao2/dt for all duration NREP apneas was 0.60%/s. Mean dSao2/dt increased above base line for each consecutive REP apnea and was higher in 60 s than in 45 and 30 s REP apnea series. The increase in dSao2/dt corresponded closely with the fall in preapneic Svo2. Preapneic arterial O2 content fell during successive REP apneas but the maximal decrement from base line (1.3 ml/dl) was much less than the maximal decrement in preapneic mixed venous O2 content of 5.1 ml/dl. Preapneic cardiac output for NREP apneas and nadir cardiac output for REP apneas remained constant. Nadir cardiac output for NREP apneas showed higher values for longer duration apneas. We concluded that dSao2/dt is inversely related to preapneic Svo2.
Airway Obstruction↗
Exercise hemodynamics and gas exchange in patients with chronic obstruction pulmonary disease, sleep desaturation, and a daytime PaO2 above 60 mm Hg.
Nocturnal oxyhemoglobin desaturation (NOD) has been reported in patients with disease of the pulmonary parenchyma and/or chest wall. The resulting hypoxemia could play a role in the development of pulmonary hypertension. We have previously demonstrated a small but statistically significant difference in resting pulmonary artery pressure (Ppa) and pulmonary vascular resistance (PVR) between two groups of patients with COPD of similar age, symptomatology, and degree of pulmonary dysfunction. These two groups were selected only on the basis of the presence or absence of NOD, and all had a mean daytime PaO2 at or above 60 mm Hg. The present study uses exercise to stress the pulmonary circulation of two groups of patients similar to the above. The purpose was to see if exercise can amplify underlying cardiopulmonary hemodynamic differences between NOD and non-NOD subjects. In addition, we attempted to confirm or refute previous studies which claimed that exercise desaturation correlates with NOD. Resting supine, resting upright, and upright exercise cardiopulmonary hemodynamics were measured using an indwelling right heart catheter, and arterial blood and expiratory gases were collected to assess metabolic and other gas exchange parameters. Although both groups showed increase in Ppa during exercise, the increases in systolic Ppa, mean Ppa, and driving pressure were disparately higher in subjects with NOD. Exercise desaturation was not predictive of NOD. The presence of NOD was predictive of a resting PVR greater than 120 dyne.s.cm-5, whereas mean sleep SaO2 and daytime PaO2 were unable to discriminate patients with COPD above or below this level.(ABSTRACT TRUNCATED AT 250 WORDS)
Arteries↗
Pulmonary vascular hemodynamics in chronic lung disease patients with and without oxyhemoglobin desaturation during sleep.
Nonapneic, nocturnal oxyhemoglobin desaturation (NOD) during rapid-eye-movement (REM) sleep has been proposed as a predecessor and possible etiologic factor in the development of pulmonary hypertension in patients both with restrictive and obstructive chronic lung disease. The association between abnormal waking cardiopulmonary hemodynamics and NOD has not been established in patients with mild daytime hypoxemia. Gas exchange, pulmonary function, red cell mass, radionuclide gated cardiac ejection fraction, and supine cardiopulmonary hemodynamics were examined in 36 patients with chronic lung disease. All had a daytime PaO2 greater than 60 mm Hg and REM sleep-related NOD for greater than 5 minutes, to 85 percent or lower. These data were compared to those from 13 subjects with similar symptoms and objective measures of pulmonary dysfunction but without evidence of NOD. Patients with NOD showed more end organ evidence of hypoxemia and more abnormal cardiopulmonary hemodynamics than patients with similar degrees of lung disease but without NOD. The relative role of daytime vs nocturnal hypoxemia in inducing hemodynamic differences between groups cannot be determined from this study.
Heart↗
Recurrence of sleep apnea syndrome following tracheostomy. A shift from obstructive to central apnea.
This report describes an unusual case of severe obstructive sleep apnea and alveolar hypoventilation leading to hypersomnolence and cor pulmonale, which were corrected by tracheostomy. Four years later, after a 22.5-kg weight gain, nocturnal apneas of similar frequency, duration, and depth of desaturation reappeared but were totally central in origin. The central apneas were eliminated with home nocturnal positive-pressure ventilation via cuffed tracheostomy tube. Each time the patient's apneas were corrected (obstructive: tracheostomy; central: mechanical ventilation), daytime alveolar hypoventilation disappeared rapidly. Yearly right heart catheterizations and radionuclide ejection fractions documented pulmonary hypertension and right heart failure, with resolution following tracheostomy and recurrence after appearance of central apneas. The changes in hemodynamic status corresponded to the patient's weight, presence of apnea, daytime alveolar hypoventilation, and treatment of nocturnal oxyhemoglobin desaturation. This case illustrates the theory of a common etiology of both central and obstructive apnea through abnormal respiratory controller gain and points to several roles obesity may play in apnea.
Humans↗
The rate of fall of arterial oxyhemoglobin saturation in obstructive sleep apnea.
During breath holding, correlations have been demonstrated between the rate of fall of arterial oxyhemoglobin saturation (dSaO2/dt) and the following: thoracic gas volume at apnea onset, resting oxygen consumption, preapneic arterial oxyhemoglobin saturation (SaO2) and obesity. A key factor influencing dSaO2/dt is mixed venous oxyhemoglobin saturation (SvO2) as recently demonstrated in an animal model of obstructive apnea. The purpose of the present study was to see if dSaO2/dt was related to SvO2 during sleep in a group of subjects with severe obstructive sleep apnea (OSA) and varying levels of SvO2. Eight OSA subjects were studied during sleep with indwelling arterial and central venous catheters. Continuous SaO2 was measured by ear oximetry while continuous SvO2 was measured through the fiberoptic bundle of a Shaw Opticath catheter. Thirty percent or more of all obstructive apneas were scored for duration, preapneic SaO2, SvO2 and dSaO2/dt. Least squares regression was used to examine the relationship between dSaO2/dt and other measured variables. The dSaO2/dt showed a consistent negative correlation with preapneic SvO2 and was not related to duration. Mean dSaO2/dt during sleep correlated to some degree with the degree of gas exchange (Qva/Qt) abnormality prior to sleep. It is concluded that in humans, SvO2 plays a substantial role in determining dSaO2/dt. Potentially, the presence of gas exchange abnormalities (eg, found in intrinsic lung disease) causing hypoxemia and low SvO2 may steepen dSaO2/dt, lowering the nadir level of apneic desaturation for the same duration of apnea found in a patient with more normal gas exchange.
Humans↗
Accuracy of fiberoptic central venous saturation catheter below 50%.
The fiberoptic central venous flotation catheter has gained widespread clinical acceptance for continuous monitoring of mixed venous oxyhemoglobin saturation. There are obvious research applications to this device, especially in monitoring very low central venous saturations in response to hypoxic challenge and cardiopulmonary exercise testing. However, the accuracy of this device has not been established in such low saturation ranges in humans. This study examines the tracking characteristics of the Opticath (Oximetrix, Mountain View, CA) pulmonary arterial catheter in comparison to simultaneously drawn blood specimens in which oxyhemoglobin saturation was determined by direct spectrophotometric oximetry. The results show that the catheter follows saturation established by bench oximetry quite closely between 50 and 80%, the range most commonly encountered in the clinical setting. However, at saturations below this range, the catheter consistently underestimates direct spectrophotometry. Since accuracy is extremely important for research purposes, two equations that can be used to correct catheter readings for mixed venous saturations less than 50% are presented.
Catheterization, Central Venous↗
Endotracheal mass resulting from a transtracheal oxygen catheter.
A 50 percent or greater savings in oxygen usage and aesthetic benefits leading to increased compliance are reasons for increasing use of the transtracheal catheter for administration of home supplemental oxygen. Minor complications of the procedure are common and include catheter dislodgement, bronchospasm, subcutaneous emphysema, bleeding at the catheter site, as well as hemoptysis and wound infections. Rare complications include retroflexion of the catheter into the upper trachea from coughing, and fracture of the catheter with loss in the trachea. New, improved catheters and detailed descriptions for operator use may reduce the frequency of these complications. This report describes a potentially serious complication of a transtracheal catheter system which resulted despite appropriate use and care of the catheter.
Catheters, Indwelling↗
Urinary catecholamines before and after tracheostomy in patients with obstructive sleep apnea and hypertension.
Obstructive apnea (asphyxia) is accompanied by acute elevation of systemic blood pressure. The usual nocturnal fall in blood pressure seen during sleep in normals may be absent in patients with repetitive apneas, and daytime systemic hypertension is reported to occur in up to 90% of such patients. Increased sympathetic activity in response to repetitive nocturnal episodes of asphyxia could explain the reversal of the diurnal pressure variation but not the daytime systemic hypertension in this setting. We examined diurnal variation in urinary catecholamines in eight subjects with severe apnea before and after tracheostomy. Five obese hypertensive subjects without apnea served as controls. Three urine specimens, two awake (7 a.m. to 3 p.m. and 3 p.m. to 11 p.m.) and one asleep (11 p.m. to 7 a.m.) were collected preoperatively and again 10-14 days postoperatively when the patient was free of pain and signs of stoma infection. All specimens were analyzed for epinephrine, norepineprine, metanephrine, and normetanephrine by liquid chromatography with electrochemical detection. Urinary epinephrine and metanephrine were not different between subjects and controls. Norepinephrine and normetanephrine were significantly higher in apneic subjects pretracheostomy as compared either with controls or with their own values posttracheostomy. Diurnal variation was not seen before or after tracheostomy. Only two of the controls showed significant diurnal variation in norepinephrine. We conclude that the absence of diurnal variation in catecholamines prior to tracheostomy reflects increased nocturnal sympathetic activity. Elevation of daytime norepinephrine and normetanephrine with return to control levels following tracheostomy implies increased sympathetic activity throughout the day.
Adult↗
Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease.
Both obstructive sleep apnea and chronic lung disease can be associated with intermittent or chronic hypoxemia leading to pulmonary hypertension and cor pulmonale. When these problems coexist, it is possible that the cardiopulmonary effects are additive. We hypothesized that hemodynamic disturbances in patients with apnea and lung disease would be more severe than in those with apnea alone, and that hemodynamic improvement should follow apnea cure, but perhaps at a slower rate than in those with apnea alone. To test these hypotheses, we prospectively followed 24 patients with sleep apnea syndrome. They were divided into 3 nonrandomized groups. Nineteen patients had both apnea and lung disease. Nine of these agreed to curative tracheostomy (Group 1). The other 10 subjects (Group 2) refused tracheostomy but accepted noncurative therapies, including nocturnal oxygen (n = 9), uvulopalatopharyngoplasty (n = 2), and protriptyline (n = 4). Five subjects with apnea but without clinically obvious lung disease received tracheostomies (Group 3). Subjects were followed at yearly intervals (mean follow-up, 27.2 months) with radionuclide motion studies and, in 15 of 24 who consented, right heart catheterization. The 3 groups did not vary with respect to age, percent ideal weight, or severity of apnea symptoms. The severity of right-sided hemodynamic dysfunction in the group with apnea but no obvious lung disease was less than that in the 2 groups with lung disease. A substantial decrease in pulmonary artery pressure (p = 0.056) and significant improvement in right ventricular ejection fraction occurred in the tracheostomized group with both apnea and lung disease. Pulmonary vascular resistance decreased in both groups receiving tracheostomy.(ABSTRACT TRUNCATED AT 250 WORDS)
Chronic Disease↗
Nocturnal oxyhemoglobin desaturation in COPD patients with arterial oxygen tensions above 60 mm Hg.
We studied 152 COPD patients with a daytime PaO2 greater than or equal to 60 mm Hg using formal polysomnography (EEG, airflow, respiratory muscle movement, ear oximeter) to detect the presence of nocturnal, nonapneic, oxyhemoglobin desaturation. Nine subjects were disqualified by the unexpected discovery of sleep apnea, as were another eight because they could not sleep in the laboratory setting. Of the remaining 135 subjects, 37 (27 percent) desaturated below a baseline sleep saturation of 90 percent for five minutes or more, reaching a nadir saturation of at least 85 percent. Anthropomorphic, pulmonary function, and historic factors comparing desaturators and nondesaturators failed to separate the groups. Awake PaO2 at rest in the desaturators was significantly lower than in the nondesaturators. The PaCO2 was higher in the desaturators. Reversibility of the desaturation phenomenon was demonstrated in three patients during subsequent polysomnographic studies following periods of clinical improvement. Continuous oxyhemoglobin monitoring during sleep remains the only reliable tool for detecting nocturnal desaturation.
Aged↗
Acute oxygen in patients with sleep apnea and COPD.
Nocturnal oxygen administered to patients with disordered breathing ameliorates hypoxemia. As a result, an important chemical stimulus to arousal is diminished. This could cause prolongation of disordered breathing events, worsen respiratory acidosis, and induce potentially harmful cardiac arrhythmias. The presence of chronic obstructive pulmonary disease (COPD) could further aggravate the situation since such patients may have depressed hypercarbic responses. To test this hypothesis, 20 obese men with sleep apnea and COPD were studied polysomnographically on two nights receiving air on one or oxygen at 4 L/min on the other. Supplemental oxygen increased mean DOB event duration from 25.7 to 31.4 seconds (p less than 0.001), increased end apneic PCO2 from 52.8 to 62.3 mm Hg (p less than 0.025), and decreased mean end apneic pH from 7.34 to 7.28 (p less than 0.001). At the same time, it improved mean sleeping and end-apneic oxygen saturation. The number of ventricular extra-systoles (PVCs) per minute of sleep showed small increases in three subjects while breathing oxygen. Complex ventricular arrhythmias were unaffected by oxygen in five subjects. Oxygen eliminated atrioventricular block in two subjects. We conclude that nocturnal supplemental oxygen does not increase ventricular arrhythmias in the majority of patients with COPD and coexisting disordered breathing events. While the clinical significance of an oxygen associated increase in ventricular extrasystoles in three subjects is unclear, nocturnal monitoring by telemetry or ambulatory recorder should be sufficient to detect such patients.
Adult↗
Bronchogenic carcinoma, massive hemoptysis, and systemic air embolus.
A 57-year-old woman with squamous carcinoma of the right lung (hilum) developed acute massive hemoptysis with syncope and hypotension. Resuscitation was complicated by the development of massive systemic air embolus, and the patient died.
Carcinoma, Bronchogenic↗
Nocturnal oxyhemoglobin desaturation following tracheostomy for obstructive sleep apnea.
Eleven obese men with coexistent obstructive sleep apnea and chronic obstructive pulmonary disease underwent tracheostomy. Nocturnal polysomnography prior to tracheostomy revealed oxyhemoglobin desaturation associated with obstructive apnea. Following surgery, repeated polysomnography was performed to assess the effect of tracheostomy on nocturnal oxygen saturation. Non-apneic desaturation characteristic of that previously described in patients with "type B" chronic obstructive pulmonary disease was noted in six subjects. Oxyhemoglobin saturation in these six fell more than 8 percent below baseline waking and non-rapid-eye-movement (REM) sleep levels. These episodes usually lasted five minutes or longer, occurred almost uniformly during REM sleep, and were acutely ameliorated by low-flow (4 liters per minute) supplemental oxygen. The subjects with REM-associated desaturation did not differ from the subjects without desaturation by preoperative anthropomorphic, blood gas, or pulmonary function criteria. However, subjects with REM-associated desaturation tended to have lower right and left ventricular ejection fractions by pooled gated wall studies. It is concluded that patients with obstructive sleep apnea and chronic obstructive pulmonary disease should be re-evaluated after tracheostomy, since they may be at risk for continued oxyhemoglobin desaturation and progressive right ventricular deterioration despite adequate treatment of their apneic condition.
Humans↗
Undiagnosed sleep apnea in patients with essential hypertension.
The prevalence of sleep apnea was studied in 46 middle- and older-aged men with "essential hypertension." Thirty-four age- and weight-similar normotensive men were also studied. Fourteen hypertensive men and three controls had sleep apnea syndrome, as defined as greater than ten apneas per hour of sleep. Hypertensive men with apnea tended to be more overweight and slightly older than the hypertensive men without apnea, but differences were not statistically significant. Individual men with apnea could not be distinguished by their answers on a questionnaire that elicited symptoms related to apnea. Seven hypertensive men with apnea were treated with protriptyline and one with uvulopalatopharyngoplasty, and apnea index (apneas per hour) decreased by 77% from pretreatment levels while mean blood pressure decreased from 149/95 mm Hg to 139/90 mm Hg. Undiagnosed sleep apnea syndrome may be associated with systemic hypertension in many middle- and older-aged men. In some, sleep apnea syndrome could be the cause of hypertension, and in others it may contribute to hypertension of another cause.
Adult↗
Cardiopulmonary hemodynamics during sleep in subjects with chronic obstructive pulmonary disease. The effect of short- and long-term oxygen.
Some patients with chronic obstructive pulmonary disease (COPD) experience transient arterial hypoxemia (TAH) during rapid eye movement (REM) sleep. To examine the effect of short- and long-term low flow oxygen on TAH associated cardiopulmonary hemodynamics, we recorded pulmonary artery pressure (Ppa) and cardiac output during nocturnal sleep in seven male subjects with COPD. In all of the subjects, parameters were measured breathing room air at baseline time and after eight or more weeks of home supplemental oxygen (15 hours per day, 3 L/min). Five were also studied one full night at baseline time while breathing 3 L/min nasal oxygen. While breathing room air both before and after chronic home oxygen therapy, transient increases in Ppa during TAH were due to increased pulmonary vascular resistance in seven instances, increased cardiac output in four, and increases in both vascular resistance and cardiac output in two. Short-term supplemental oxygen lowered mean sleeping Ppa and eliminated TAH along with its associated hemodynamic changes in four of the five subjects; the fifth did not experience REM sleep. In the six subjects who complied with the eight-week home oxygen protocol, mean sleeping Ppa was significantly reduced (p less than 0.05). In four of these, total pulmonary resistance was lower and cardiac output higher after home oxygen therapy. Short-term supplemental oxygen is useful in correcting REM-associated TAH and in some hypoxemic subjects, reducing mean sleeping Ppa. Sustained reductions in pulmonary vascular resistance after long-term home oxygen therapy may be indicative of improved cardiac and pulmonary vascular status even in subjects showing minimal or no reduction in mean sleeping Ppa.
Cardiac Output↗
Nonapneic mechanisms of arterial oxygen desaturation during rapid-eye-movement sleep.
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Aged↗
Bronchoscopic diagnosis of pulmonary infections. Comparison of protected-specimen brush and cytology brush with lung aspirates.
In a recent study the use of a new plugged double-lumen protected-specimen brush with the flexible fiberoptic bronchoscope was advocated to isolate pathogens in lower respiratory tract infections while avoiding upper respiratory tract contamination. To compare the efficacy of this brush and a standard single-lumen cytology brush in identifying the etiologic agent in lower respiratory tract infections, we studied 18 patients with lung infections. Transthoracic lung aspiration was done in all but two patients in an attempt to identify the specific etiologic agent. In these two cases, cultures of specimens of blood or postmortem lung tissue yielded the causative organism. In 12 patients anaerobic or aerobic bacteria (or both) were identified, whereas one patient had a mixed bacterial and fungal infection. Using the cytology brush and the protected-specimen brush we identified at least one pathogen in 10 of 12 and 10 of 13 cases, whereas both brushes missed one or more causative organisms in 8 of 12 and 8 of 13 cases, respectively. Nonetiologic organisms were found in 8 of 12 cases by the cytology brush and 8 of 13 cases by the protected-specimen brush. Quantitative culture techniques improved the specificity of the brush results in infections where aerobes predominated. Our data show that bronchoscopic cultures of lower respiratory tract infections do not consistently recover the causative agent and are frequently subject to contamination by nonetiologic organisms. There was no difference between the brushes in avoiding contamination.
Adolescent↗