Prolonged Episodes of Hypoxemia in Preterm Infants Undetectable by Cardiorespiratory Monitors

PEDIATRICS ◽  
1995 ◽  
Vol 95 (6) ◽  
pp. 860-863 ◽  
Author(s):  
Christian F. Poets ◽  
Valerie A. Stebbens ◽  
David Richard ◽  
David P. Southall

Objective. To determine whether episodes of prolonged hypoxemia occur without prolonged apneic pauses (≥20 seconds) and without bradycardia (pulse rate, ≤100 beats per minute) in apparently well preterm infants. Methods. Long-term recordings of arterial oxygen saturation as measured by pulse oximetry (SpO2), photoplethysmographic (pulse) waveforms from the oximeter, and breathing movements were performed in 96 preterm infants (median gestational age at birth, 34 weeks; range, 28 to 36 weeks) who were breathing room air. Recordings started at a median age of 4 days (range, 1 to 60 days). Results. During a median duration of recording of 25 hours, 88 episodes in which SpO2 fell to 80% or less and remained there for 20 seconds or longer were identified in 15 infants. The median duration of these prolonged desaturations was 27 seconds (range, 20 to 81 seconds). In 73 episodes (83%), SpO2 continued to fall to 60% or less. Twenty-three desaturations were associated with prolonged apneic pauses and 54 with bradycardia; 19 of these were associated with both apnea and bradycardia. Thirty desaturations (34%; 10 infants) occurred without bradycardia and without prolonged apnea. Conclusions. These results indicate that a proportion of apparently well preterm infants exhibit episodes of severe prolonged hypoxemia unaccompanied by prolonged apneic pauses or bradycardia. Such episodes, therefore, would be difficult to detect if only breathing movements and heart rate are monitored. Indications for the use of oxygenation monitors in preterm infants should be reconsidered.

2021 ◽  
Vol 11 (1) ◽  
pp. 30-36
Author(s):  
Yu. E. Vaguine

According to some literature data, during voluntary long-term breath holding (BH), the heart rate (HR) increases, and according to others, it decreases.Objective: to determine the psychophysiological parameters that cause a change in HR during BH in athletes with different resistance to respiratory hypoxia.Materials and methods: HR at BH was studied in 14 beginner athletes, 15 basketball players and 12 swimmers-divers. Duration of BH was recorded. The HR was recorded on a heart rate monitor. After recording an electrocardiogram, the standard deviation of the duration of cardiac cycles was calculated. The arterial oxygen saturation was measured with a pulse oximeter. The statistically significant values of the correlation coefficient (r) were ≥0.33 with p < 0.05.Results: it was found that out of 41 sportsmen, HR increased by more than 5 % in 4, changed insignificantly in 7 and decreased by less than 5 % in 30. Beginner athletes had tachycardia, and BH was quickly interrupted by an imperative inhalation. The saturation of arterial blood with oxygen did not change and did not affect the change in HR. The decrease in heart rate in swimmers-divers in comparison with the other two groups of people examined was statistically significant (p < 0.05). The duration of BH had a direct correlation (r = 0.5) with bradycardia in these people. The duration of BH caused (r = 0.8) hypoxia, the value of which also directly influenced (r = 0.38) the severity of bradycardia. In addition, the decrease in HR depended on high HR (r = 0.36) and low HR variability (r = 0.38) before BH.Conclusion: tachycardia occurs in beginner athletes who experience discomfort with BH. Bradycardia occurs in sportsmen with a long-term BH setting without discomfort. Sympathicotonia in the prelaunch state predetermines the severity of bradycardia in BH. The duration of BH and the resulting hypoxia provide the occurrence of bradycardia.


2020 ◽  
Vol 91 (10) ◽  
pp. 785-789
Author(s):  
Dongqing Wen ◽  
Lei Tu ◽  
Guiyou Wang ◽  
Zhao Gu ◽  
Weiru Shi ◽  
...  

INTRODUCTION: We compared the physiological responses, psychomotor performances, and hypoxia symptoms between 7000 m and 7500 m (23,000 and 24,600 ft) exposure to develop a safer hypoxia training protocol.METHODS: In altitude chamber, 66 male pilots were exposed to 7000 and 7500 m. Heart rate and arterial oxygen saturation were continuously monitored. Psychomotor performance was assessed using the computational task. The hypoxic symptoms were investigated by a questionnaire.RESULTS: The mean duration time of hypoxia was 323.0 56.5 s at 7000 m and 218.2 63.3 s at 7500 m. The 6-min hypoxia training was completed by 57.6% of the pilots and 6.1% of the pilots at 7000 m and at 7500 m, respectively. There were no significant differences in pilots heart rates and psychomotor performance between the two exposures. The Spo2 response at 7500 m was slightly severer than that at 7000 m. During the 7000 m exposure, pilots experienced almost the same symptoms and similar frequency order as those during the 7500 m exposure.CONCLUSIONS: There were concordant symptoms, psychomotor performance, and very similar physiological responses between 7000 m and 7500 m during hypoxia training. The results indicated that 7000-m hypoxia awareness training might be an alternative to 7500-m hypoxia training with lower DCS risk and longer experience time.Wen D, Tu L, Wang G, Gu Z, Shi W, Liu X. Psychophysiological responses of pilots in hypoxia training at 7000 and 7500 m. Aerosp Med Hum Perform. 2020; 91(10):785789.


Reports ◽  
2021 ◽  
Vol 4 (2) ◽  
pp. 15
Author(s):  
Stephen Malnick ◽  
Waleed Ghannam ◽  
Adam Abu Sharb ◽  
Pavel Alin

The COVID-19 pandemic has affected more than 100 million people worldwide. One of the major presentations is pneumonia. Patients are classified as severe when they have an arterial oxygen saturation of less than 94% on breathing room air. We present a case of a healthy 29-year-old man who had severe COVID-19 pneumonia and responded dramatically to two doses of convalescent plasma. This case underlines the importance of administering the plasma in the first few days of the disease.


2020 ◽  
Vol 14 ◽  
pp. 175346662096302
Author(s):  
Sandra Cuerpo ◽  
Maria Palomo ◽  
Fernanda Hernández-González ◽  
Joel Francesqui ◽  
Nuria Albacar ◽  
...  

Background: Proper adjustment of arterial oxygen saturation (SaO2) during daily activities in patients with interstitial lung disease (ILD) requiring long-term oxygen therapy is challenging. Given the multifactorial nature of the limited exercise tolerance in patients with ILDs, the isolated use of oxygen therapy may not be enough. As demonstrated previously in patients with chronic obstructive pulmonary disease, the use of a noninvasive ventilation (NIV) device combined with oxygen therapy may prevent the falling of oxygen saturation during exercise, due to an improvement of the ventilation–perfusion ratio and a reduction of the respiratory work, thus enhancing exercise tolerance. We sought to assess in patients diagnosed with ILD who are in need of oxygen therapy, the effect of associating an NIV to improve oxygen parameters and the distance covered during the 6 min walking test (6MWT). Methods: We conducted a prospective observational study in patients with ILDs. After a clinical characterization, we performed a 6MWT in two different situations: using a portable oxygen concentrator with the regular flow used by the patient during their daily life activities and afterwards adding the additional support of a NIV. The oxygen saturation parameters were registered with a portable oximeter. Results: We included 16 patients with different ILDs who have oxygen therapy prescribed. The use of NIV associated with oxygen therapy in comparison with the use of oxygen therapy alone showed an increase of the average SaO2 [91% (88–93) versus 88% (86–90%); p = 0.0005] and a decrease in the percentage of time with oxygen saturation <90%: 36% (6–56%) versus 58% (36–77%); p < 0.0001. There were no changes in the 6MWT distance: 307 m (222–419 m) versus 316 m (228–425 m); p = 0.10. Conclusions: In our study the use of a NIV system associated with long-term oxygen therapy during exercise showed beneficial effects, especially improvement of oxygen saturation. The reviews of this paper are available via the supplemental material section.


2020 ◽  
Vol 30 (6) ◽  
pp. 531-540
Author(s):  
Hendrik Kronsbein ◽  
Darius A. Gerlach ◽  
Karsten Heusser ◽  
Alex Hoff ◽  
Fabian Hoffmann ◽  
...  

Abstract Introduction Baroreflexes and peripheral chemoreflexes control efferent autonomic activity making these reflexes treatment targets for arterial hypertension. The literature on their interaction is controversial, with suggestions that their individual and collective influence on blood pressure and heart rate regulation is variable. Therefore, we applied a study design that allows the elucidation of individual baroreflex–chemoreflex interactions. Methods We studied nine healthy young men who breathed either normal air (normoxia) or an air–nitrogen–carbon dioxide mixture with decreased oxygen content (hypoxia) for 90 min, with randomization to condition, followed by a 30-min recovery period and then exposure to the other condition for 90 min. Multiple intravenous phenylephrine bolus doses were applied per condition to determine phenylephrine pressor sensitivity as an estimate of baroreflex blood pressure buffering and cardiovagal baroreflex sensitivity (BRS). Results Hypoxia reduced arterial oxygen saturation from 98.1 ± 0.4 to 81.0 ± 0.4% (p < 0.001), raised heart rate from 62.9 ± 2.1 to 76.0 ± 3.6 bpm (p < 0.001), but did not change systolic blood pressure (p = 0.182). Of the nine subjects, six had significantly lower BRS in hypoxia (p < 0.05), two showed a significantly decreased pressor response, and three showed a significantly increased pressor response to phenylephrine in hypoxia, likely through reduced baroreflex buffering (p < 0.05). On average, hypoxia decreased BRS by 6.4 ± 0.9 ms/mmHg (19.9 ± 2.0 vs. 14.12 ± 1.6 ms/mmHg; p < 0.001) but did not change the phenylephrine pressor response (p = 0.878). Conclusion We applied an approach to assess individual baroreflex–chemoreflex interactions in human subjects. A subgroup exhibited significant impairments in baroreflex blood pressure buffering and BRS with peripheral chemoreflex activation. The methodology may have utility in elucidating individual pathophysiology and in targeting treatments modulating baroreflex or chemoreflex function.


2019 ◽  
Vol 29 (8) ◽  
pp. 1036-1039
Author(s):  
Yoichi Kawahira ◽  
Kyoichi Nishigaki ◽  
Koji Kagisaki ◽  
Takuji Watanabe ◽  
Kazuki Tanimoto

AbstractBackground:In patients with tetralogy of Fallot with the diminutive pulmonary arteries, we sometimes have to give up the complete intra-cardiac repair due to insufficient growth of the pulmonary arteries. We have carried out palliative intra-cardiac repair using a fenestrated patch.Methods:Of all 202 patients with tetralogy of Fallot in our centre since 1996, five patients (2.5%) with the diminutive pulmonary arteries underwent palliative intra-cardiac repair using a fenestrated patch. Mean operative age was 1.8 years. Previous operation was Blalock–Taussig shunt in 4. At operation, the ventricular septal defect was closed using a fenestrated patch and the right ventricular outflow tract was enlarged. Follow-up period was 9.8 ± 2.6 years.Results:There were no operative and late deaths. Fenestration closed spontaneously on its own in four patients 2.7 ± 2.1 years after the intra-cardiac repair with a stable haemodynamics; however, the last patient with the smallest pulmonary artery index had supra-systemic pressure of the right ventricle post-operatively. The fenestration was emergently enlarged. Systemic arterial oxygen saturation was significantly and dramatically increased from 83.5 to 94% after the palliative intra-cardiac repair, and to 98% at the long term. A ratio of systolic pressure of the right ventricle to the left was significantly decreased to 0.76 ± 0.12 at the long term. Now all five patients were Ross classification class I.Conclusion:Although frequent catheter and surgical interventions were needed after the palliative intra-cardiac repair, this repair might be a choice improving quality of life with good results in patients with tetralogy of Fallot associated with the diminutive pulmonary arteries.


Heart ◽  
2020 ◽  
Vol 106 (21) ◽  
pp. 1638-1645
Author(s):  
Alexandra Arvanitaki ◽  
George Giannakoulas ◽  
Helmut Baumgartner ◽  
Astrid Elisabeth Lammers

Eisenmenger syndrome (ES) represents the most severe phenotype of pulmonary arterial hypertension (PAH) associated with congenital heart disease (CHD) and occurs in patients with large unrepaired shunts. Despite early detection of CHD and major advances in paediatric cardiac surgery, ES is still prevalent and requires a multidisciplinary approach by adult CHD experts in tertiary centres. Central cyanosis is the primary clinical manifestation leading to secondary erythrocytosis and various multiorgan complications that increase morbidity and affect quality of life. Close follow-up is needed to early diagnose and timely manage these complications. The primary goal of care is to maintain patients’ fragile stability. Although the recent use of advanced PAH therapies has substantially improved functional capacity and increased life expectancy, long-term survival remains poor. Progressive heart failure, infectious diseases and sudden cardiac death comprise the main causes of death in patients with ES. Impaired exercise tolerance, decreased arterial oxygen saturation, iron deficiency, pre-tricuspid shunts, arrhythmias, increased brain natriuretic peptide, echocardiographic indices of right ventricular dysfunction and hospitalisation for heart failure predict mortality. Endothelin receptor antagonists are used as first-line treatment in symptomatic patients, while phosphodiesterase-5 inhibitors may be added. Due to the lack of evidence, current guidelines do not provide a clear therapeutic strategy regarding treatment escalation. Additional well-designed trials are required to assess the comparative efficacy of various PAH agents and the benefit of combination therapy. Finally, the development of a risk score is of utmost importance to guide clinical therapy.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
R H Boeger ◽  
P Siques ◽  
J Brito ◽  
E Schwedhelm ◽  
E Pena ◽  
...  

Abstract Prolonged exposure to altitude-associated chronic hypoxia (CH) may cause high altitude pulmonary hypertension (HAPH). Chronic intermittent hypobaric hypoxia (CIH) occurs in individuals who commute between sea level and high altitude. CIH is associated with repetitive acute hypoxic acclimatization and conveys the long-term risk of HAPH. As nitric oxide (NO) is an important regulator of systemic and pulmonary vascular tone and asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthesis that increases in hypoxia, we aimed to investigate whether ADMA predicts the incidence of HAPH among Chilean frontiers personnel exposed to six months of CIH. We performed a prospective study of 123 healthy male subjects who were subjected to CIH (5 days at appr. 3,550 m, followed by 2 days at sea level) for six months. ADMA, SDMA, L-arginine, arterial oxygen saturation, systemic arterial blood pressure, and haematocrit were measured at baseline and at months 1, 4, and 6 at high altitude. Acclimatization to high altitude was determined using the Lake Louise Score and the presence of acute mountain sickness (AMS). Echocardiography was performed after six months of CIH in a subgroup of 43 individuals with either good (n=23) or poor (n=20) aclimatization to altitude, respectively. Logistic regression was used to assess the association of biomarkers with HAPH. 100 study participants aged 18.3±1.3 years with complete data sets were included in the final analysis. Arterial oxygen saturation decreased upon the first ascent to altitude and plateaued at about 90% during the further course of the study. Haematocrit increased to about 47% after one month and remained stable thereafter. ADMA continuously increased and SDMA decreased during the study course, whilst L-arginine levels showed no distinct pattern. The incidence of AMS and the Lake Louise Score were high after the first ascent (53 and 3.1±2.4, respectively) and at one month of CIH (47 and 3.0±2.6, respectively), but decreased to 20 and 1.4±2.0 at month 6, respectively (both p<0.001 for trend). In echocardiography, 18 participants (42%) showed a mean pulmonary arterial pressure (mPAP) greater than 25 mm Hg (mean ± SD, 30.4±3.9 mm Hg), out of which 9 (21%) were classified as HAPH (mPAP ≥30 mm Hg; mean ± SD, 33.9±2.2 mm Hg). Baseline ADMA, but not SDMA, was significantly associated with mPAP at month 6 in univariate logistic regression analysis (R = 0.413; p=0.007). In ROC analysis, a cut-off for baseline ADMA of 0.665 μmol/l was determined as the optimal cut-off level to predict HAPH (mPAP >30 mm Hg) with a sensitivity of 100% and a specificity of 63.6%. ADMA concentration increases during long-term CIH. It is an independent predictive biomarker for the incidence of HAPH. SDMA concentration decreases during CIH and shows no association with HAPH. Our data support a role of impaired NO-mediated pulmonary vasodilation in the pathogenesis of high altitude pulmonary hypertension. Acknowledgement/Funding CONICYT/FONDEF/FONIS Sa 09I20007; FIC Tarapaca BIP 30477541-0; BMBF grant 01DN17046 (DECIPHER); Georg & Jürgen Rickertsen Foundation, Hamburg


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