Cerebral oxygenation in highlanders with and without high-altitude pulmonary hypertension.

NEW FINDINGS: What is the central question of this study? Cerebral hypoxia impairs cognitive function and exercise performance and may result in brain damage. Residents at high altitude, in particular those with high-altitude pulmonary hypertension, are prone to hypoxaemia due to the exposure to reduced barometric pressure and impaired pulmonary gas exchange. Whether highlanders have a reduced cerebral oxygenation has not been studied. What is the main finding and its importance? We found that despite a reduced arterial oxygen saturation, healthy highlanders and even those with pulmonary hypertension have a similar cerebral oxygenation to healthy lowlanders, suggesting that compensatory mechanisms protect long-term residents at high altitude from cerebral hypoxia. Abstract High-altitude pulmonary hypertension (HAPH), a chronic altitude-related illness, causes hypoxaemia and impaired exercise performance. We evaluated the hypothesis that haemodynamic limitation and hypoxaemia in patients with HAPH are associated with impaired cerebral tissue oxygenation (CTO) compared with healthy highlanders (HH) and lowlanders (LL). We studied 36 highlanders with HAPH and 54 HH at an altitude of 3250 m, and 34 LL at 760 m. Mean(±SD) pulmonary artery pressures were 34(±3), 22(±5) and 16(±4) mmHg, respectively (P < 0.05, all comparisons). The CTO was monitored by near-infrared spectroscopy along with pulse oximetry (peripheral arterial oxygen saturation, SpO2) during quiet breathing of room air (RA) and oxygen for 20 min each, and during hyperventilation with RA and oxygen, respectively. In HAPH, HH and LL breathing RA, SpO2 was 88(±4), 92(±2) and 95(±2)%, respectively (P < 0.001, all comparisons), and CTO was similar in the three groups, at 68(±3), 68(±4) and 69(±4)%, respectively (n.s., all comparisons). Breathing oxygen increased SpO2 and CTO significantly more in HAPH than in HH and LL. Hyperventilation (RA) did not reduce CTO in HAPH but did in HH and LL; hyperventilation (oxygen) increased CTO in HAPH only. Highlanders with and without HAPH studied at 3250 m had a similar CTO to healthy lowlanders at 760 m even though highlanders were hypoxaemic. The physiological response to hyperoxia and hypocapnia assessed by cerebral near-infrared spectroscopy suggests that healthy highlanders and even highlanders with HAPH effectively maintain an adequate CTO. This adaptation may be of particular relevance because adequate cerebral oxygenation is essential for vital brain functions.

High altitudes and partial pressure of arterial oxygen in patients with chronic obstructive pulmonary disease - A systematic review and meta-analysis.

IMPORTANCE: Prior study in healthy subjects has shown a reduction of partial pressure of arterial oxygen (PaO2) by -1.60 kPa/kilometre of altitude gain. However, the association of altitude-related change in PaO2 and altitude-related adverse health effects (ARAHE) in patients with chronic obstructive pulmonary disease (COPD) remain unknown. OBJECTIVE: To provide an effect size estimate for the decline in PaO2 with each kilometre of altitude gain and to identify ARAHE in relation to altitude in patients with COPD. www.crd.york.ac.uk/prospero: CRD42020217938. DATA SOURCES: A systematic search of PubMed and Embase was performed from inception to May 30, 2023. STUDY SELECTION: Peer-reviewed and prospective studies in patients with COPD staying at altitudes >1500 m providing arterial blood gases within the first 3 days at the target altitude. DATA EXTRACTION AND SYNTHESIS: Aggregate data (AD) on study characteristics were extracted, and individual patient data (IPD) were requested. Estimates were pooled using random-effects meta-analysis. MAIN OUTCOME AND MEASURES: Relative risk estimates and 95 % confidence intervals for the association between PaO2 and altitude in patients with COPD. RESULTS: Thirteen studies were included in the AD analysis, of which 6 studies (222 patients, 45.2 % female) provided IPD, thus were included in the quantitative analysis. The estimated effect size of PaO2 was -0.84 kPa [95 %CI, -0.92 to -0.76] per 1000 m of altitude gain (I2=65.0 %, P < 0.001). In multivariable regression analysis, COPD severity, baseline PaO2, age and time spent at altitude were predictors for PaO2 at altitude. Overall, 37.8 % of COPD patients experienced an ARAHE, whereas older age, female sex, COPD severity, baseline PaO2, and target altitude were predictors for the occurrence of ARAHE (area under ROC curve: 0.9275, P < 0.001). CONCLUSIONS AND RELEVANCE: This meta-analysis, providing altitude-related decrease in PaO2 and risk of ARAHE in patients with COPD ascending to altitudes >1500 m, revealed a lower altitude-related decrease in PaO2 in COPD patients compared with healthy. However, these findings might improve patient care and facilitate decisions about initiating preventive measures against hypoxaemia and ARAHE in patients with COPD planning an altitude sojourn or intercontinental flight, i.e. supplemental oxygen or acetazolamide.

Acclimatization improves submaximal exercise economy at 5533 m.

We tested whether the better subjective exercise tolerance perceived by mountaineers after altitude acclimatization relates to enhanced exercise economy. Thirty-two mountaineers performed progressive bicycle exercise to exhaustion at 490 m and twice at 5533 m (days 6-7 and day 11), respectively, during an expedition to Mt. Muztagh Ata. Maximal work rate (W(max)) decreased from mean ± SD 356 ± 73 watts at 490 m to 191 ± 49 watts and 193 ± 45 watts at 5533 m, days 6-7 and day 11, respectively; corresponding maximal oxygen uptakes (VO2max ) were 50.7 ± 9.5, 26.3 ± 5.6, 24.7 ± 7.0 mL/min/kg (P = 0.0001 5533 m vs 490 m). On days 6-7 (5533 m), VO(2) at 75% W(max) (152 ± 37 watts) was 1.75 ± 0.45 L/min, oxygen saturation 68 ± 8%. On day 11 (5533 m), at the same submaximal work rate, VO(2) was lower (1.61 ± 0.47 L/min, P < 0.027) indicating improved net efficiency; oxygen saturation was higher (74 ± 7%, P < 0.0004) but ratios of VO(2) to work rate increments remained unchanged. On day 11, mountaineers climbed faster from 4497 m to 5533 m than on days 5-6 but perceived less effort (visual analog scale 50 ± 15 vs 57 ± 20, P = 0.006) and reduced symptoms of acute mountain sickness. We conclude that the better performance and subjective exercise tolerance after acclimatization were related to regression of acute mountain sickness and improved submaximal exercise economy because of lower metabolic demands for non-external work-performing functions.

Effect of 5 weeks of oral acetazolamide on patients with pulmonary vascular disease: A randomized, double-blind, cross-over trial.

BACKGROUND: The carbonic anhydrase inhibitor acetazolamide stimulates ventilation through metabolic acidosis mediated by renal bicarbonate excretion. In animal models, acetazolamide attenuates acute hypoxia-induced pulmonary hypertension (PH), but its efficacy in treating patients with PH due to pulmonary vascular disease (PVD) is unknown. METHODS: 28 PVD patients (15 pulmonary arterial hypertension, 13 distal chronic thromboembolic PH), 13 women, mean±SD age 61.6±15.0 years stable on PVD medications, were randomised in a double-blind crossover protocol to 5 weeks acetazolamide (250mg b.i.d) or placebo separated by a ≥2 week washout period. Primary endpoint was the change in 6-minute walk distance (6MWD) at 5 weeks. Additional endpoints included safety, tolerability, WHO functional class, quality of life, arterial blood gases, and hemodynamics (by echocardiography). RESULTS: Acetazolamide had no effect on 6MWD compared to placebo (treatment effect: mean change [95%CI] -18 [-40 to 4]m, p=0.102) but increased arterial blood oxygenation through hyperventilation induced by metabolic acidosis. Other measures including pulmonary hemodynamics were unchanged. No severe adverse effects occurred, side effects that occurred significantly more frequently with acetazolamide vs. placebo were change in taste (22/0%), paraesthesia (37/4%) and mild dyspnea (26/4%). CONCLUSIONS: In patients with PVD, acetazolamide did not change 6MWD compared to placebo despite improved blood oxygenation. Some patients reported a tolerable increase in dyspnoea during acetazolamide treatment, related to hyperventilation, induced by the mild drug-induced metabolic acidosis. Our findings do not support the use of acetazolamide to improve exercise in patients with PVD at this dosing. GOV IDENTIFIER: NCT02755298.

Sleep apnea in school-age children living at high altitude.

INTRODUCTION: Among adults, sleep apnea is more common in highlanders than in lowlanders. We evaluated the sleep apnea prevalence in children living at high altitude compared to age-matched low-altitude controls. METHODS: Healthy children, 7-14 y of age, living at 2500-3800m in the Tien Shan mountains, Kyrgyzstan, were prospectively studied in a health post at 3250m. Healthy controls of similar age living at 700-800m were studied in a University Hospital at 760m in Bishkek. Assessments included respiratory sleep studies scored according to pediatric standards, clinical examination, medical history, and the pediatric sleep questionnaire (PSQ, range 0 to 1 with increasing symptoms). RESULTS: In children living at high altitude (n = 37, 17 girls, median [quartiles] age 10.8y [9.6;13.0]), sleep studies revealed: mean nocturnal pulse oximetry 90% (89;91), oxygen desaturation index (ODI, >3% dips in pulse oximetry) 4.3/h (2.5;6.7), apnea/hypopnea index (AHI) total 1.7/h (1.0;3.6), central 1.6/h (1.0;3.3), PSQ 0.27 (0.18;0.45). In low-altitude controls (n=41, 17 girls, age 11.6y [9.5;13.0], between-groups comparison of age P=0.69) sleep studies revealed: pulse oximetry 97% (96;97), ODI 0.7/h (0.2;1.2), AHI total 0.4/h (0.1;1.0), central 0.3/h (0.1;0.7), PSQ 0.18 (0.14;0.31); P<0.05, all corresponding between-group comparisons. CONCLUSIONS: In school-age children living at high altitude, nocturnal oxygen saturation was lower, and the total and central AHI were higher compared to children living at low altitude. The greater score of sleep symptoms in children residing at high altitude suggests a potential clinical relevance of the nocturnal hypoxemia and subtle sleep-related breathing disturbances.

Echocardiography and extravascular lung water during 3 weeks of exposure to high altitude in otherwise healthy asthmatics.

Background: Asthma rehabilitation at high altitude is common. Little is known about the acute and subacute cardiopulmonary acclimatization to high altitude in middle-aged asthmatics without other comorbidities. Methods: In this prospective study in lowlander subjects with mostly mild asthma who revealed an asthma control questionnaire score >0.75 and participated in a three-week rehabilitation program, we assessed systolic pulmonary artery pressure (sPAP), cardiac function, and extravascular lung water (EVLW) at 760 m (baseline) by Doppler-echocardiography and on the second (acute) and last day (subacute) at a high altitude clinic in Kyrgyzstan (3100 m). Results: The study included 22 patients (eight male) with a mean age of 44.3 ± 12.4 years, body mass index of 25.8 ± 4.7 kg/m2, a forced expiratory volume in 1 s of 92% ± 19% predicted (post-bronchodilator), and partially uncontrolled asthma. sPAP increased from 21.8 mmHg by mean difference by 7.5 [95% confidence interval 3.9 to 10.5] mmHg (p < 0.001) during acute exposure and by 4.8 [1.0 to 8.6] mmHg (p = 0.014) during subacute exposure. The right-ventricular-to-pulmonary-artery coupling expressed by TAPSE/sPAP decreased from 1.1 by -0.2 [-0.3 to -0.1] mm/mmHg (p < 0.001) during acute exposure and by -0.2 [-0.3 to -0.1] mm/mmHg (p = 0.002) during subacute exposure, accordingly. EVLW significantly increased from baseline (1.3 ± 1.8) to acute hypoxia (5.5 ± 3.5, p < 0.001) but showed no difference after 3 weeks (2.0 ± 1.8). Conclusion: In otherwise healthy asthmatics, acute exposure to hypoxia at high altitude increases pulmonary artery pressure (PAP) and EVLW. During subacute exposure, PAP remains increased, but EVLW returns to baseline values, suggesting compensatory mechanisms that contribute to EVLW homeostasis during acclimatization.

Corrigendum: Echocardiography and extravascular lung water during 3 weeks of exposure to high altitude in otherwise healthy asthmatics.

[This corrects the article DOI: 10.3389/fphys.2023.1214887.].

Visuomotor performance at high altitude in COPD patients. Randomized placebo-controlled trial of acetazolamide.

Introduction: We evaluated whether exposure to high altitude impairs visuomotor learning in lowlanders with chronic obstructive pulmonary disease (COPD) and whether this can be prevented by acetazolamide treatment. Methods: 45 patients with COPD, living <800 m, FEV1 ≥40 to <80%predicted, were randomized to acetazolamide (375 mg/d) or placebo, administered 24h before and during a 2-day stay in a clinic at 3100 m. Visuomotor performance was evaluated with a validated, computer-assisted test (Motor-Task-Manager) at 760 m above sea level (baseline, before starting the study drug), within 4h after arrival at 3100 m and in the morning after one night at 3100 m. Main outcome was the directional error (DE) of cursor movements controlled by the participant via mouse on a computer screen during a target tracking task. Effects of high altitude and acetazolamide on DE during an adaptation phase, immediate recall and post-sleep recall were evaluated by regression analyses. www.ClinicalTrials.gov NCT03165890. Results: In 22 patients receiving placebo, DE at 3100 m increased during adaptation by mean 2.5°, 95%CI 2.2° to 2.7° (p < 0.001), during immediate recall by 5.3°, 4.6° to 6.1° (p < 0.001), and post-sleep recall by 5.8°, 5.0 to 6.7° (p < 0.001), vs. corresponding values at 760 m. In 23 participants receiving acetazolamide, corresponding DE were reduced by -0.3° (-0.6° to 0.1°, p = 0.120), -2.7° (-3.7° to -1.6°, p < 0.001) and -3.1° (-4.3° to -2.0°, p < 0.001), compared to placebo at 3100 m. Conclusion: Lowlanders with COPD travelling to 3100 m experienced altitude-induced impairments in immediate and post-sleep recall of a visuomotor task. Preventive acetazolamide treatment mitigated these undesirable effects.

Markers of cardiovascular risk and their reversibility with acute oxygen therapy in Kyrgyz highlanders with high altitude pulmonary hypertension.

BACKGROUND: High altitude pulmonary hypertension (HAPH), a chronic altitude related illness, is associated with hypoxemia, dyspnea and reduced exercise performance. We evaluated ECG and pulse wave-derived markers of cardiovascular risk in highlanders with HAPH (HAPH+) in comparison to healthy highlanders (HH) and lowlanders (LL) and the effects of hyperoxia. METHODS: We studied 34 HAPH+ and 54 HH at Aksay (3250m), and 34 LL at Bishkek (760m), Kyrgyzstan. Mean pulmonary artery pressure by echocardiography was mean±SD 34±3, 22±5, 16±4mmHg, respectively (p<0.05 all comparisons). During quiet rest, breathing room air or oxygen in randomized order, we measured heart-rate adjusted QT interval (QTc), an ECG-derived marker of increased cardiovascular mortality, and arterial stiffness index (SI), a marker of cardiovascular disease derived from pulse oximetry plethysmograms. RESULTS: Pulse oximetry in HAPH+, HH and LL was, mean±SD, 88±4, 92±2 and 95±2%, respectively (p<0.05 vs HAPH+, both comparisons). QTc in HAPH+, HH and LL was 422±24, 405±27, 400±28ms (p<0.05 HAPH+ vs. others); corresponding SI was 10.5±1.9, 8.4±2.6, 8.5±2.0m/s, heart rate was 75±8, 68±8, 70±10 bpm (p<0.05, corresponding comparisons HAPH+ vs. others). In regression analysis, HAPH+ was an independent predictor of increased QTc and SI when controlled for several confounders. Oxygen breathing increased SI in HH but not in HAPH+, and reduced QTc in all groups. CONCLUSIONS: Our data suggest that HAPH+ but not HH may be at increased risk of cardiovascular mortality and morbidity compared to LL. The lack of a further increase of the elevated SI during hyperoxia in HAPH+ may indicate dysfunctional control of vascular tone and/or remodelling.

Disability and survival in Duchenne muscular dystrophy.

BACKGROUND: Duchenne muscular dystrophy (DMD) leads to progressive impairment of muscle function, respiratory failure and premature death. Longitudinal data on the course of physical disability and respiratory function are sparse. OBJECTIVES: To assess prospectively physical impairment and disability, respiratory function and survival in patients with DMD over several years to describe the course of the disease with current care. METHODS: In 43 patients with DMD, aged 5-35 years, yearly assessments of physical disability by the Duchenne muscular dystrophy physical Impairment and Dependence on care (DID) score, ranging from 9 (no disability) to 80 (complete dependence), and forced vital capacity (FVC), were obtained over a mean time interval of 5.4 (SD 2.1) years. RESULTS: DID scores were correlated with age according to a hyperbolic function (f = 85.3 x age/(10.05+age), R = 0.62, p<0.0001). FVC declined exponentially with age (f = 139.1 x exp(-0.08 x age), R = 0.52, p<0.0001). Mean age at which patients lost their ambulation was 9.4 (SD 2.4) years and they became dependent on an electric wheelchair at 14.6 (4.0) years. Age at the beginning of assisted ventilation was 19.8 (3.9) years, Three patients died during the observation period. The estimated probability of survival to age 30 years was 85% (median survival was 35 years). CONCLUSIONS: Our detailed observations of the progression of physical disability, dependence on care and respiratory impairment in patients with DMD from childhood to adult life is valuable for predicting the clinical course with current medical care. Compared with historical data, survival has improved considerably.

Children at high altitude have less nocturnal periodic breathing than adults.

Although children commonly travel to high altitudes, their respiratory adaptation to hypoxia remains elusive. Therefore, in the present study respiratory inductive plethysmography, pulse oximetry (S(p,O(2))) and end-tidal CO(2) tension (P(ET,CO(2))) were recorded in 20 pre-pubertal children (aged 9-12 yrs) and their fathers during 1 night in Zurich (490 m) and 2 nights at the Swiss Jungfrau-Joch research station (3,450 m) following ascent by train within <3 h. In children, mean+/-sd nocturnal S(p,O(2)) fell from 98+/-1% at 490 m to 85+/-4 and 86+/-4% at 3,450 m (nights 1 and 2, respectively); P(ET,CO(2)) decreased significantly from 37+/-6 to 32+/-3 and 33+/-4 mmHg (3,450 versus 490 m). In adults, changes in nocturnal S(p,O(2)) and P(ET,CO(2)) at 3,450 m were similar to those in children. Children spent less time in periodic breathing at 3,450 m during night 1 and 2 (8+/-11 and 9+/-13%, respectively) than adults (34+/-24 and 22+/-17%, respectively), and their apnoea threshold for CO(2) was lower compared with adults (27+/-2 and 30+/-2 mmHg, respectively, both nights). S(p,O(2)), P(ET,CO(2)) and time in periodic breathing at altitude were not correlated between children and their fathers. In conclusion, children revealed a similarly reduced nocturnal O(2) saturation and associated hyperventilation at high altitude as adults but their breathing pattern was more stable, possibly related to a lower apnoea threshold for CO(2).

Periodic whole body acceleration: a novel therapy for cardiovascular disease.

BACKGROUND: Periodic whole body acceleration in the spinal axis (pGz) applied by a motion platform is a novel treatment modality that induced endothelial nitric oxide release into the circulation of animals, healthy subjects and patients with inflammatory diseases during single treatment sessions in previous studies. We hypothesized that patients with advanced arteriosclerotic diseases who are not candidates for a surgical intervention would clinically benefit from repeated pGz treatments over several weeks through improvement of endothelial function. PATIENTS AND METHODS: 11 patients, 5 men (37 to 71 y) with stable ischemic heart disease, LVEF < 35%, NYHA stage > II, and 6 patients (51 to 83 y, 1 woman) with intermittent leg claudication, Fontaine stage II, were enrolled after optimization of pharmacological therapy. PGz was applied for 40 min, 5 days/week during 5 weeks. Quality of life (SF-36 questionnaire), exercise performance, and endothelial function were assessed at baseline, during the treatment period, and 4 weeks after discontinuation of pGz. RESULTS: PGz was well tolerated. In heart failure paitents, pGz therapy improved quality of life, increased 6 min walking distance by a mean +/- SE of 105 +/- 24 m, and improved postischemic skin hyperemia (p < .05 in all instances). In 4 of 6 patients with intermittent claudication, quality of life, treadmill walking distance and post-ischemic skin hyperemia improved with pGz therapy (p < .05). Four weeks after discontinuation of pGz, most therapeutic effects had vanished in both patient groups. CONCLUSIONS: In patients with severe heart failure and with leg claudication who remain symptomatic despite maximal medical therapy and who were not candidates for surgery, periodic acceleration applied over several weeks improved quality of life and exercise capacity. The clinical benefits appear to be mediated through improved endothelial function.

Impact of physical activity on cardiovascular risk factors in IDDM.

OBJECTIVE: To study the impact of physical activity on glycemic control and plasma lipids [HDL cholesterol (HDL-C), HDL-C subfractions, triglycerides, lipoprotein(a)], blood pressure, weight, and abdominal fat and to determine the necessary short-term adaptations in diabetes management during intensive endurance training in patients with IDDM. RESEARCH DESIGN AND METHODS: Well-controlled subjects with IDDM (n = 20; HbA1c = 7.6%) engaged in a regular exercise program over a period of 3 months involving endurance sports such as biking, long-distance running, or hiking. Subjects were instructed to exercise at least 135 min per week. If baseline activity exceeded this level, subjects were to increase further their physical activity as much as possible and record the type and time of such activity. RESULTS: During the 3-month intervention, physical activity increased from 195 +/- 176 to 356 +/- 164 min (mean +/- SD) per week (P < 0.001). Physical fitness as assessed by VO2max increased from 2,914 +/- 924 to 3,092 +/- 905 ml/min (P < 0.001), and insulin sensitivity increased significantly (steady-state plasma glucose [SSPG] decreased from 10.5 +/- 4.8 to 7.0 +/- 3.3 mmol/l; P < 0.01). Subsequently, LDL cholesterol decreased by 14% (P < 0.05), and HDL and HDL3-C subfraction increased by 10 (P < 0.05) and 16% (P < 0.05), respectively. Systolic and diastolic blood pressure decreased significantly from 127 +/- 9 to 124 +/- 8 (P < 0.05) and from 80 +/- 5 to 77 +/- 5 mmHg (P < 0.01), respectively. Resting heart rate decreased from 63 +/- 6 to 59 +/- 7 bpm (P < 0.01). Waist-to-hip circumference ratio decreased from 0.882 +/- 0.055 to 0.858 +/- 0.053 (P < 0.001), body weight decreased from 70.7 +/- 10.4 to 68.7 +/- 10.2 kg (P = 0.003), with a consequent decrease in body fat from 21.9 +/- 8.2 to 18.0 +/- 6.3% (P < 0.001) and an increase in lean body mass from 54.9 +/- 12.2 to 56.8 +/- 11.0 kg. These effects occurred independently of glycemic control. The overall frequency of severe hypoglycemic episodes was reduced from 0.14 to 0.10 per patient-year during the study period. CONCLUSIONS: This study shows that increasing physical activity is safe and does not result in more hypoglycemic episodes and that there is a linear dose-response between increased physical activity and loss of abdominal fat and a decrease in blood pressure and lipid-related cardiovascular risk factors, with a preferential increase in the HDL3-C subfraction.

Time-varying signal analysis to detect high-altitude periodic breathing in climbers ascending to extreme altitude.

This work investigates the performance of cardiorespiratory analysis detecting periodic breathing (PB) in chest wall recordings in mountaineers climbing to extreme altitude. The breathing patterns of 34 mountaineers were monitored unobtrusively by inductance plethysmography, ECG and pulse oximetry using a portable recorder during climbs at altitudes between 4497 and 7546 m on Mt. Muztagh Ata. The minute ventilation (VE) and heart rate (HR) signals were studied, to identify visually scored PB, applying time-varying spectral, coherence and entropy analysis. In 411 climbing periods, 30-120 min in duration, high values of mean power (MP(VE)) and slope (MSlope(VE)) of the modulation frequency band of VE, accurately identified PB, with an area under the ROC curve of 88 and 89%, respectively. Prolonged stay at altitude was associated with an increase in PB. During PB episodes, higher peak power of ventilatory (MP(VE)) and cardiac (MP(LF)(HR) ) oscillations and cardiorespiratory coherence (MP(LF)(Coher)), but reduced ventilation entropy (SampEn(VE)), was observed. Therefore, the characterization of cardiorespiratory dynamics by the analysis of VE and HR signals accurately identifies PB and effects of altitude acclimatization, providing promising tools for investigating physiologic effects of environmental exposures and diseases.

Thoracocardiographic-derived left ventricular systolic time intervals.

Thoracocardiography noninvasively estimates left ventricular performance by recording ventricular volume curves with inductive plethysmography. We studied timing of these curves to evaluate their potential to accurately track systolic time intervals in comparison with standard methods. Thoracocardiographic left ventricular volume curves, carotid pressure pulses determined by applanation tonometry, the phonocardiogram and ECG were recorded simultaneously in ten normal subjects at various body positions achieved with a tilt table. An equation was derived to predict preejection period from onset of ejection in thoracocardiographic curves. Ventricular ejection time was calculated as total electromechanical systole obtained by phonocardiography minus preejection period. The equation was validated prospectively in 31 measurements in critically ill patients. In normal subjects, the interval ECG Q wave to ejection onset in thoracocardiographic curves correlated well with preejection period from applanation tonometry and phonocardiography (r = 0.92; standard error of estimate (SEE), 8 ms; p < 0.001). Thoracocardiographic curves showed a delay that varied with body position according to the regression equation: delay = 40 ms + 10 x sine (tilt angle) (where r = 0.62; SEE, 7 ms; p < 0.001). Application of this equation in the prospective study in patients revealed close agreement in systolic time intervals from thoracocardiography and simultaneous applanation tonometry plus phonocardiography, respectively. The mean difference +/- SD between methods in preejection periods was 3 +/- 7 ms and in the ratios of preejection period to left ventricular ejection time, 0.02 +/- 0.05. Trends of changes in systolic time intervals were identical for the two methods. We conclude that thoracocardiography combined with phonocardiography provides accurate systolic time intervals when corrected for a position-dependent delay of its waveforms.

Pulmonary hypertension five years after left pneumonectomy for adenoid cystic carcinoma.

We report the findings in a patient with shortness of breath due to pulmonary hypertension five years after left pneumonectomy. Mediastinal recurrence of an incompletely resected and slowly growing adenoid cystic carcinoma of the left main bronchus had encased the right main pulmonary artery.

Noninvasive measurement of central venous pressure by neck inductive plethysmography.

Bedside estimation of the height at which the internal jugular veins collapse, referenced to a standard hemodynamic location, theoretically reflects central venous pressure. This method has never been demonstrated as accurate when compared to invasive CVP measurements because of the great clinical skills and time required to visually identify the internal jugular venous waveform. Since the principles of the bedside method are sound, we utilized them in conjunction with the neck inductive plethysmograph, a device which has the capability of recording internal jugular venous and carotid arterial waveforms. The respiratory distortion of these vascular waveforms was eliminated by employing a digital bandpass filter, making it easy to identify the venous and arterial waveforms on the videoscreen of a personal computer. The upper torso was positioned while observing the videoscreen until the vascular waveform was seen as a mixed arteriovenous waveform, signifying intermittent internal jugular venous collapse. The height of the internal jugular vein above the phlebostatic axis was obtained by external measurement and recorded as CVPni in cm H2O. In 43 patients, 86 percent of CVPni (NIP) values fell within 20 percent CVPi (invasive catheter measurements) over a range of CVP from 0 to 19 cm H2O. In an additional seven patients, CVPi was greater than the height that the upper torso could be elevated and an arterial waveform could not be obtained. Here, CVPni was recorded as the value at least exceeding the value measured. In two other patients, obstruction of an internal jugular vein gave spuriously low values of CVPni. Our study indicates that this new neck inductive plethysmographic method is accurate compared to invasive catheter measurements of CVP and should serve as a safe, noninvasive alternative in situations where such measurements are required.

Bilateral volume reduction surgery for diffuse pulmonary emphysema by video-assisted thoracoscopy.

UNLABELLED: We prospectively studied the surgical aspects, functional results, and complications of video-assisted bilateral thoracoscopic volume reduction surgery in patients with severe diffuse pulmonary emphysema. METHODS: Fifteen men and five women with a mean age of 64 years (range 42 to 78 years) whose daily activity was substantially impaired by severe airflow obstruction and hyperinflation underwent thoracoscopic volume reduction surgery. The prospective preoperative assessment and postoperative assessment at 3 months included (1) pulmonary function studies, (2) grading of dyspnea, and (3) exercise performance; pulmonary function tests were also performed immediately before discharge from the hospital. RESULTS: There was no perioperative mortality. All patients left the hospital after a median stay of 15 days (6 to 27 days). Only seven patients had a prolonged chest tube drainage time (>7 days). At 3 months the mean (+/- standard deviation) forced expiratory volume in 1 second had improved by 42% (+/-3.8%), from 0.80 L (+/-0.23) to 1.09 L (+/-0.28) (p < 0.001); residual volume had decreased from 5.8 L (+/-1.5) to 4.4 L (+/-1.0) (p < 0.001). Shortly before discharge the forced expiratory volume in 1 second was already 1.10 L (+/-0.26). The median 12-minute walking distance increased from 495 m (35 to 790 m) to 688 m (175 to 1035 m) (p < 0.001) and the mean maximal oxygen consumption from 10 ml/kg per minute (+/-2.5) to 13 ml/kg per minute (+/-2.3) (p < 0.0005). The patients reported a substantial relief of dyspnea with a mean decrease in the Medical Research Council score from 3.4 to 1.8.

Coronary artery disease in patients undergoing lung volume reduction surgery for emphysema.

OBJECTIVES: Most patients with severe pulmonary emphysema referred for lung volume reduction surgery (LVRS) have a long-standing history of cigarette smoking. Coronary artery disease (CAD) predisposes to perioperative cardiac complications. Since symptoms and signs of myocardial ischemia are often absent in patients with severe ventilatory impairment even during exercise, we investigated the prevalence of CAD in candidates for LVRS by angiography. DESIGN: We prospectively studied the prevalence of CAD by angiography and assessed the CAD risk factor profile in 41 candidates for LVRS (26 men, 15 women; mean age, 66+/-6.8 years; range, 52 to 76 years), who had no current symptoms or a history of myocardial ischemia. RESULTS: In six patients (15%), asymptomatic but significant coronary lesions (> 70% stenosis) were detected. In five patients, these findings altered the clinical management. Patients with CAD had significant higher cholesterol levels, tended to have smoked more, and had more often additional vascular risk factors. CONCLUSIONS: We found a high prevalence of angiographically significant but clinically silent CAD in this particular population of heavy smokers with advanced emphysema.