Yellow nail syndrome following thoracic surgery: a new association?

An 80-year-old man presented with the characteristic triad of yellow nail syndrome (chronic respiratory disorders, primary lymphedema and yellow nails) in association with coronary artery bypass graft surgery. Treatment with mechanical pleurodesis and vitamin E resulted in near complete resolution of the yellow nails, pleural effusions, and lower extremity edema. The etiology of the yellow nail syndrome has been described as an anatomical or functional lymphatic abnormality. Several conditions have previously been described as associated with this disease. This is the first report of the association of this syndrome with thoracic surgery.

Treatment of gram-positive nosocomial pneumonia. Prospective randomized comparison of quinupristin/dalfopristin versus vancomycin. Nosocomial Pneumonia Group.

Nosocomial pneumonia is a frequent complication in hospitalized patients. Gram-positive pathogens, particularly Staphylococcus aureus, are responsible for the increasing frequency of nosocomial pneumonia. To evaluate the efficacy and safety of intravenous quinupristin/dalfopristin (Synercid) in the treatment of nosocomial pneumonia caused by gram-positive pathogens we conducted a prospective, randomized, open-label, international, multicenter, comparative clinical trial. Two hundred ninety-eight patients with nosocomial pneumonia were enrolled in 74 active centers in five countries: a subgroup of 171 (87 quinupristin/dalfopristin-treated and 84 vancomycin-treated patients) were evaluable for the major efficacy end points. One hundred fifty received 7.5 mg/kg of quinupristin/dalfopristin every 8 h; 148 patients received 1 g of vancomycin every 12 h. Aztreonam at a dose of 2 g every 8 h could be administered in both groups for coverage of gram-negative organisms, and tobramycin was added for coverage against Pseudomonas aeruginosa. The primary efficacy end point was the clinical response between the seventh and the thirteenth day after the end of treatment in clinically evaluable patients with documented causative pathogen(s) at baseline (bacteriologically evaluable population). Therapy was clinically successful (cure or improvement) in 49 (56.3%) of patients receiving quinupristin/dalfopristin and 49 (58.3%) patients receiving vancomycin (difference, -2.0% [95% CI, -16.8% to 12.8%]) in the bacteriologically evaluable population. Equivalent clinical success rates were also observed in the all-treated population (n = 298), and in the bacteriologically evaluable patients intubated in baseline (39/72 [54%] compared with 36/67 [54%]). The by-pathogen bacteriologic response was similar in both treatment groups, with equivalent clinical success rates for Streptococcus pneumoniae, Staphylococcus aureus, and methicillin-resistant Staphylococcus aureus. Adverse events (venous and nonvenous) were equally distributed between groups; 15.3% of quinupristin/dalfopristin patients and 9.5% of vancomycin patients discontinued therapy because of an adverse clinical event. In this study quinupristin/dalfopristin was shown to be equivalent to vancomycin in the treatment of nosocomial pneumonia caused by gram-positive pathogens. Quinupristin/dalfopristin merits further evaluation for the treatment of nosocomial pneumonia caused by methicillin-resistant S. aureus.

Radiographic evidence of interstitial pulmonary edema after exercise at altitude.

Pulmonary function abnormalities after exercise are suggestive of pulmonary edema; however, radiographic evidence is lacking. Well-trained cyclists were studied to determine whether there is radiographic evidence of pulmonary edema after endurance exercise (cycling distance 5.3-131.5 km) at altitude. Chest radiographs obtained before exercise were coded for later interpretation. Films obtained after exercise were coded with a different number. A total of 74 sets of posteroanterior and lateral films were analyzed by three radiologists for signs of pulmonary edema. Radiographic changes were graded on a three-point scale. An edema score was calculated by summing the score for each individual radiographic finding for each radiologist and an overall edema score representing the mean scores from all three radiologists. The overall edema score increased from 0.8 +/- 1.2 before exercise to 1.8 +/- 1.6 after exercise (P < 0.01). These results suggest that, after prolonged high-intensity exercise at moderate altitude, there is radiographic evidence of early pulmonary edema in some cyclists.

Dyspnea in patients with chronic obstructive pulmonary disease: does dyspnea worsen longitudinally in the presence of declining lung function?

OBJECTIVE: To determine the direction and rate of change in the symptom of dyspnea in patients with chronic obstructive pulmonary disease (COPD) whose lung function has worsened over time. DESIGN: Secondary analysis of a longitudinal data set. SETTING: Outpatient clinic. PATIENTS: Thirty-four medically stable male subjects with chronic obstructive pulmonary disease studied for 5.3 +/- 3.5 years, with a mean reduction in FEV1 over the period studied of 330.9 +/- 288.0 mL. Subjects were 63.3 +/- 5.5 years of age at entry into the study. OUTCOME MEASURES: Dyspnea and functional status scores were obtained using the Pulmonary Functional Status and Dyspnea Questionnaire. RESULTS: There was no significant difference in reports of dyspnea from the beginning to the end of the study, despite significant reductions in lung function. Of all activities studied, dyspnea when raising arms overhead was the only activity showing a relationship to the slope of change in FEV1 %. CONCLUSION: These findings suggest that, although patients with chronic lung disease experience varying degrees of deterioration in lung function longitudinally, there is no evidence that they report worsening of dyspnea in tandem with these physiologic changes. In this study, patient ratings of dyspnea longitudinally were not directly linked to changes in lung impairment.

Dynamics of periodic breathing and arousal during sleep at extreme altitude.

To determine whether nocturnal periodic breathing (PB) at altitude is due primarily to unstable control of ventilation or the inability to maintain stable sleep states, we performed visual and computer analyses of the electroencephalographic and respiratory records of healthy volunteers at simulated altitudes of 4572, 6100 and 7620 m. Transient arousals were associated with < 52% of the apneas identified; thus, the PB cycle was not always associated with transient arousal. Following the termination of oxygen breathing, the reinitiation of PB was not dependent on the occurrence of arousal as the primary event. The transition from apnea to breathing preceded the appearance of arousal by approximately 1 to 4 sec. Ventilatory drive in the breaths immediately following arousal was significantly larger than corresponding control breaths, matched for SaO2. Our findings suggest that altitude-induced PB is unlikely to result from primary fluctuations in state. Arousals promote the development of PB with apnea and help to sustain these episodes, but are not necessary for their initiation.

Carbon dioxide and oxygen partial pressure in expiratory water condensate are equivalent to mixed expired carbon dioxide and oxygen.

This study was to determine whether the PCONCO2 and PCONO2 which collect in the expiratory trap of a ventilator circuit are equivalent to PECO2 and PEO2. Fifty studies were performed in 34 mechanically ventilated male patients. Five milliliters of condensate fluid were collected and PECO2 and PEO2 were measured. Exhaled gases were collected simultaneously with condensate fluid for 5 min in a meteorologic balloon and FECO2 and FEO2 were measured; PECO2 and PEO2 were then calculated. The mean PECO2 was not significantly different from PCONCO2 nor was the PCONO2 significantly different from the condensate PCONO2. There was a high correlation between mixed expired PECO2 and PCONCO2 as well as PEO2 and PCONO2. These data indicate expiratory PCONCO2 and PCONO2 provide a valid reflection of PECO2 and PEO2. The PCONCO2 and PCONO2 measured in a clinical blood gas analyzer are accurate and may be used in calculation of VD/VT and in metabolic assessments.

Operation Everest II: arterial oxygen saturation and sleep at extreme simulated altitude.

Frequent sleep disturbances and desaturation during sleep are common at high altitude, but few data are available from the highest altitudes at which humans are known to sleep. Because sleep fragmentation at low altitude may impair mental function and oxygen deprivation produces lasting central nervous system abnormalities, a better understanding of the severity of sleep disturbances and oxygen desaturation at extreme altitudes is important. The purpose of this study was to determine the severity of sleep disturbance and the extent of arterial oxygen desaturation at extreme simulated altitude. Out of eight healthy male subject volunteers who started, five aged 27.2 +/- 1.5 yr completed the study during 6 weeks of progressive hypobaric hypoxia in a decompression chamber. The men were studied at barometric pressures of 760, 429, 347, 282 mm Hg and following return to 760 mm Hg. All demonstrated frequent nighttime awakenings (37.2 awakenings per subject per night at 282 mm Hg, decreasing significantly to 14.8 on return to sea level, p less than 0.05). Total sleep time decreased from 337 +/- 30 min at 760 mm Hg to 167 +/- 44 min at 282 mm Hg (p less than 0.01). Rapid eye movement (REM) sleep decreased from 17.9% +/- 6.0% of sleep time at sea level to 4.0% +/- 3.3% at 282 mm Hg (p less than 0.01). Sleep continuity as reflected by brief arousals increased from 22 +/- 6 arousals per hour of sleep at sea level to 161 +/- 66 arousals per hour at 282 mm Hg (p less than 0.01). All subjects showed arterial oxygen desaturation proportional to the altitude. The average oxygen saturation (SaO2) was 79% +/- 3% at 429 mm Hg, 66% +/- 6% at 347 mm Hg, and 52% +/- 2% at 282 mm Hg. Sleep stage had only a minimal effect on SaO2 at any altitude. SaO2 was negatively correlated with brief sleep arousals, r = -0.72, p less than 0.01. All subjects demonstrated periodic breathing with apneas throughout much of the night at 347 and 282 mm Hg. These data indicate that sleep quality progressively worsens as SaO2 decreases despite lack of progressive changes in sleep stages at altitude. This study extends previous information on the severity of desaturation during sleep, and suggests that improvements in oxygenation might prove beneficial in restoring consolidated sleep, possibly even improving daytime performance.

Sustained maximal ventilation after endurance exercise in athletes.

Although impaired respiratory muscle performance that persists up to 5 min after exercise is stopped has been demonstrated during exhaustive exercise in normal young men, it is not known whether impaired respiratory muscle function follows endurance exercise to exhaustion in highly trained athletes. To study the effects of exercise on sustained maximal voluntary ventilation immediately after exercise, eight elite cross-country skiers performed a 4-min maximal sustained ventilation (MSV) test before and immediately after exhaustive exercise. Subjects were encouraged to maintain maximal ventilation (VE) throughout the MSV test. To encourage greater effort, rapid visual feedback of VE was provided on a computer terminal along with a target VE based on their 12-s maximum voluntary ventilation (MVV). The subjects (7 males, 1 female) were 18.5 +/- 0.9 yr old (mean +/- SD) and exercised for 62.5 +/- 16.7 min at 77 +/- 5% of their maximum oxygen consumption during which average VE was 106.7 +/- 24.2 l/min BTPS. The mean MVV was 196.0 +/- 29.9 l/min or 107% of their age- and height-predicted MVV. Before exercise the MSV was 86% of the MVV or 176.7 +/- 30.5 l/min, whereas after exercise the MSV was 90% of the MVV or 180.3 +/- 28.9 l/min (P = NS). The total volume of gas expired during the 4-min MSV was 706.7 +/- 121.9 liters before and 721.2 +/- 115.5 liters after exercise (P = NS). In this group of athletes, exhaustive exercise produced no deleterious effects on the ability to perform a 4-min MSV test immediately after exercise.

Changes in cardiac output during sustained maximal ventilation in humans.

To determine the increment in cardiac output and in O2 consumption (Vo2) from quiet breathing to maximal sustained ventilation, Vo2 and cardiac output were measured using an acetylene rebreathing technique in five subjects. Cardiac output and Vo2 were measured multiple times in each subject at rest and during sustained maximal ventilation. During maximal ventilation subjects breathed 5% CO2 to prevent hypocapnia. The increase in cardiac output from rest to maximal breathing was taken as an estimate of respiratory muscle blood flow and was used to calculate the arteriovenous O2 content difference across the respiratory muscles from the Fick equation. Cardiac output increased by 4.3 +/- 1.0 l/min (mean +/- SD), from 5.6 +/- 0.7 l/min at rest to 9.9 +/- 1.1 l/min, during maximal ventilations ranging from 127 to 193 l/min. Vo2 increased from 312 +/- 29 to 723 +/- 69 ml/min during maximal ventilation. O2 extraction across the respiratory muscles during maximal breathing was 9.6 +/- 1.0 vol% (range 8.5 to 10.7 vol%). These values suggest an upper limit of respiratory muscle blood flow of 3-5 l/min during unloaded maximal sustained ventilation.

Work capacity and left ventricular function during rehabilitation after myocardial revascularization surgery.

A prospective randomized trial was conducted to evaluate the effects of exercise-based cardiac rehabilitation after myocardial revascularization surgery (MRS) on work capacity (measured in mets) and left ventricular function as determined from ejection fraction (LVEF). Twenty-eight patients undergoing MRS were randomly assigned to experimental (aerobic exercise, n = 19) or control (muscle relaxation and low-level exercise, n = 9) groups. Patients were studied before surgery (T1) and 2 (T2), 8 (T3), and 24 (T4) weeks after surgery with first-pass radionuclide angiography both while they were at rest and during maximal upright cycle ergometric exercise. Subsets of patients were also studied at T2, T3, and T4 at a standard workload of 75 W, and during maximal exercise 1 year after surgery (T5). Work capacity improved in both groups although significantly more so in the experimental group (3.9, 3.8, 6.0, and 7.3 mets and 3.7, 3.7, 4.9, and 5.7 mets at T1, T2, T3, and T4 in the experimental and control groups, respectively). The differences between groups were significant by T3. Peak exercise LVEF increased significantly in both groups from T1 to T2 then decreased at T3 and remained unchanged through T5. Peak exercise LVEF at T3 to T5 remained significantly above that observed at T1. LVEF responses were not related to the exercise program. During a standard workload, heart rate decreased, blood pressure increased, and LVEF did not change in either group. After conclusion of the formal protocol (T4), work capacity and LVEF did not change for either group throughout an additional 6 months (T5).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of exercise protocol on the left ventricular response to exercise.

The purpose of this study was to determine whether the left ventricular response during exercise radionuclide angiography would be influenced by exercise protocol. One hundred twenty healthy volunteers (aged 18 to 40 years) performed upright bicycle exercise using 1 of 5 protocols. Ejection fraction was measured using first-pass radionuclide angiography. Exercise protocols were as follows: (1) graded exercise (25 W increase every 2 minutes) to fatigue, heart rate greater than 85% of age-predicted maximum, n = 53; (2) graded exercise to 85% of age-predicted maximal heart rate or to fatigue with heart rate less than 85% of age-predicted maximum, n = 26; (3) graded exercise to fatigue, with "exercise" imaging performed immediately after exercise, n = 15; (4) abrupt presentation of a supermaximal work load (400 W), n = 10; (5) graded exercise to a work load of 75 W preceding the abrupt presentation of a supermaximal work load (300 to 400 W), n = 16. Protocols 2 and 3, representing less than maximal stress, yield higher ejection fractions than Protocol 1 and may reduce the sensitivity of exercise radionuclide angiography. Protocols 4 and 5, representing supermaximal stress, yield lower ejection fractions than Protocol 1 and may reduce the specificity of exercise radionuclide angiography. Thus, exercise protocol has a significant influence on the left ventricular response during exercise radionuclide angiography.

Effect of habitual exercise on left ventricular response to exercise.

To evaluate the effects of chronic physical exercise on left ventricular ejection fraction (LVEF) and ejection rate (LVER), radionuclide angiography was performed at rest and during upright-bicycle exercise in 45 healthy men. The subjects varied widely in exercise habits and working capacity. They were divided into three subgroups on the basis of habitual physical activity. Aerobic training was done more than 7, 2-4, and less than 1 h/wk by subgroups of athletes, trained, and untrained men, respectively. The results indicate marked differences in work capacity (298, 233, and 181 W in the athletes, trained, and untrained groups, respectively). Resting LVEF (72, 69, and 68%) and LVER (4.1, 3.4, and 3.6 s-1) were not significantly different among the groups. With maximal exercise, however, small but statistically significant differences in LVEF (75, 69, and 68%; P less than 0.05 athletes vs. trained and athletes vs. untrained) and in LVER (7.5, 6.3, and 5.2 s-1; P less than 0.05 among all groups) were observed. Work capacity was, however, poorly correlated with exercise LVEF (r = 0.18) and LVER (r = 0.47). The results of this study indicate that the enhanced working capacity observed secondary to increases in habitual physical activity can be attributed to differences in LVEF and LVER only in the most general terms. Accordingly the results agree with previous suggestions based primarily on echocardiographic data that the primary cardiac adaptation to exercise is dimensional rather than functional in character.

Diagnostic capabilities of exercise testing soon after myocardial revascularization surgery.

The purpose of this investigation was to compare data on early exercise testing for variables known to be of diagnostic/prognostic value following myocardial infarction in post-myocardial revascularization surgery patients. 70 patients were evaluated soon after surgery, by cardiac catheterization, moderate-intensity treadmill exercise testing, and rest and exercise radionuclide angiography. The results indicated no significant differences among groups with satisfactory and unsatisfactory results by catheterization compared for METs, peak heart rate, double product, ST-segment change, angina pectoris, and dysrhythmias. Significant differences were found among groups when rest and exercise ejection fraction and exercise-induced regional wall motion abnormality were taken into account. It was concluded that the moderate-intensity treadmill exercise test was ineffective in differentiating current cardiac function and arterial/graft status among postmyocardial revascularization surgery patients. Exercise radionuclide angiographic studies were able to identify groups of patients with adequate or inadequate postoperative cardiac catheterization results.

Left ventricular function at rest, peak exercise and postexercise.

To determine whether the temporal sequence of imaging could influence the results of exercise radionuclide angiography, 15 healthy volunteers were studied at rest, during peak bicycle exercise and immediately postexercise using first pass radionuclide angiography. Responses at rest, peak and postexercise included: heart rate (67 to 174 to 170 bpm), double product (7.4 to 31.5 to 27.5 mm Hg X bpm X 10(3)), left ventricular ejection fraction (68 to 69 to 80%) and mean normalized left ventricular ejection rate (3.63 to 6.56 to 8.56 s-1). The results indicate that left ventricular ejection fraction and mean normalized ejection rate were different during exercise and immediately postexercise although heart rate and double product were not. The results indicate that the temporal sequence of imaging is a significant procedural variable in the conduct of exercise radionuclide angiography.

Left ventricular function during sudden strenuous exercise.

Strenuous exercise without warm-up has been shown to produce ischemia-like electrocardiographic (ECG) abnormalities in 60-70% of healthy subjects. These abnormalities appeared to be related to the development of an unfavorable myocardial supply/demand balance and, in chronically instrumented dogs, to transient decreases in coronary blood flow. A mechanism involving subendocardial ischemia has been proposed to explain the response to sudden strenuous exercise (SSE). To determine whether the response to SSE included the development of changes in myocardial pump performance typical of ischemia, left ventricular (LV) function at rest, during graded exercise and during SSE was evaluated in nine young (26.6 +/- 3.4 years), well-trained male volunteers using first-pass radionuclide angiography. During graded exercise, the LV ejection fraction increased from 66.9 +/- 9.4% at rest to 73.0 +/- 7.1% during peak exercise, and the LV ejection rate increased from 3.36 +/- 0.67 sec-1 at rest to 6.58 +/- 1.10 sec-1 during peak exercise. Segmental wall motion was normal in all studies. During SSE, the LV ejection fraction decreased in very subject, from an average 72.2 +/- 8.6% at rst to 57.3 +/- 8.1% during exercise. The LV ejection rate remained relatively constant (3.98 +/- 0.92 sec-1 at rest vs 4.33 +/- 0.74 sec-1 during SSE). No segmental wall motion abnormalities were observed during SSE; however, LV wall motion appeared to be diffusely hypokinetic during SSE. In contrast to previous reports, few ECG abnormalities were observed during SSE. These results support the hypothesis that subendocardial ischemia is an important mechanism in the response to SSE. However, the lack of ECG changes and segmental wall motion abnormalities and the relatively high absolute value of the LV ejection fraction suggest that if subendocardial ischemia occurs during SSE, it is attributable to physiologic rather than pathologic mechanisms.

Fifty years of training and competition in the marathon: Wally Hayward, age 70--a physiological profile.

A 70-year-old South African long-distance runner, holder of his age group's marathon record and former Olympic marathon runner, was studied to determine the effects of 52 years of regular training on functional capacity and health. Maximal treadmill exercise testing revealed no ischaemic ECG abnormalities and an excellent functional capacity (58,6 ml/kg/min). Submaximal testing showed that the subject ran at approximately 86% of maximum aerobic capacity when completing the marathon in his record time. The subject was very lean (13,6% fat) for his age. Muscles contained 82% slow-twitch fibres. Pulmonary function and blood chemical values were within normal limits. Although total cholesterol was somewhat high (247 mg/dl), high-density lipoprotein cholesterol was elevated (53 mg/dl). Twenty-four-hour Holter monitoring revealed no significant ventricular ectopic activity although frequent premature atrial contractions were noted. M-mode echocardiography revealed a normal heart with moderately hypertrophied left ventricular wall thickness. Radionuclide cine angiography showed a normal ejection fraction at rest (69%), followed by a slight drop at maximal exercise (62%). Left ventricular regional wall motion was considered normal at both rest and exercise. He had no significant orthopaedic abnormalities but showed normal flexibility and well-balanced muscular strength. Thickened heel pads were also noted. These results appear to indicate a beneficial effect of habitual physical activity upon the retention of functional capacity with ageing.

The relationship between acute mountain sickness and pulmonary ventilation at 2,835 meters (9,300 ft).

We have demonstrated a small but statistically significant decrease in forced vital capacity and in pulmonary flow rates among 126 persons studied daily for the first three days after arrival at an altitude of 2,835 meters (9,300 ft). Nearly half of these individuals had symptoms attributable to altitude sickness, and those with the most dyspnea and worst headache also showed the greatest changes in pulmonary function studied. We suggest that there is a relationship between the symptoms of altitude sickness and pulmonary function consistent with the appearance of early interstitial or alveolar edema.