Hypoxia and the heart.

Davies, SW; Wedzicha, JA

doi:10.1136/hrt.69.1.3

Cited by 37 publications

(7 citation statements)

References 47 publications

(8 reference statements)

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“…Hypoxia is associated with increased renin and catecholamine levels but the effects of neurohormonal activation on central ventilatory control are unknown.2026 Captopril may similarly improve cardiac function and respiratory gas exchange by reducing hypoxic vasoconstriction of systemic and pulmonary vessels. 26 The role of nasal continuous positive airway pressure in patients with heart failure has yet to be defined, with conflicting data from several small studies. [28][29][30] It is unclear why continuous positive airway pressure should be effective in central apnoea, although it has been suggested that by increasing functional residual capacity arterial oxygen and carbon dioxide concentrations increase.2 This would stabilise the respiratory system to the effects of hypocapnia, reducing both periodic breathing and Cheyne-Stokes respiration.…”

Section: Discussionmentioning

confidence: 99%

Effects of captopril and oxygen on sleep apnoea in patients with mild to moderate congestive cardiac failure.

Walsh

Andrews²,

Starling³

et al. 1995

Heart

140

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Objectives-To determine the effects of captopril and oxygen on sleep quality in patients with mild to moderate cardiac failure.Design-An open observational study. Patients-12 patients with New York Heart Association class II-III heart failure were studied at baseline. 9 of these patients were then examined at the end of 1 month of treatment with captopril; 9 of the patients were separately assessed during a single night of supplementary oxygen.Main outcome measures-Sleep patterns by polysomnography, overnight oximetry, and subjective sleep assessment using visual analogue scores. Results-Abnormal sleep was present in all baseline studies. Complete polysomnograms after treatment with captopril were obtained in 8 patients. Light sleep (stages 1 and 2) was reduced (mean (SEM) 61%(8)% to 48%(6)% actual sleep time, P < 0.05) but slow wave (stages 3 and 4) and REM (rapid eye movement) sleep increased (25%(6)% to 31%(5)%, 14%(2)% to 21%(5)% actual sleep time, P < 0.05). Apnoeic episodes (242(59) to 118(30), P < 0-05), desaturation events (171(60) to 73(37), P < 0.05), and arousals (33(5) to 18(3) P < 0.01) were reduced. Visual analogue scores of sleep quality increased 49(5) to 69(5), P < 0.01). Complete polysomnograms were obtained in 7 patients treated with oxygen. Light sleep duration was reduced (55% (7)% to 42%(5)% actual sleep time, P < 0 05) and slow wave sleep increased (30%(5)% to 38%(6)% actual sleep time, P < 0.05). REM sleep duration was not significantly different. Total arousals (33(6)% to 20(2) P < 0.05), desaturation events (140(33) to 38(10), P < 0.01), and apnoeic episodes (212(53) to 157(33), P < 0.05) were reduced. Visual analogue scores of sleep quality were unchanged. Conclusions-Captopril and oxygen may improve sleep quality and reduce nocturnal desaturation in patients with mild to moderate cardiac failure. Improved sleep quality could explain the reduction in daytime symptoms seen after treatment in patients with chronic heart failure. (Br Heart3' 1995;73:237-241)

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Section: Discussionmentioning

confidence: 99%

Effects of captopril and oxygen on sleep apnoea in patients with mild to moderate congestive cardiac failure.

Walsh

Andrews²,

Starling³

et al. 1995

Heart

140

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“…Clinical practice does not normally include the administration of oxygen beyond the first 24 h postoperatively and this raises the question about the significance of episodic hypoxaemia in patients with ischaemic heart disease. The effect of hypoxaemia on the heart has been discussed in a number of recent editorials [ 2 4 ] but surprisingly little is known about the effects of hypoxaemia on the diseased heart, although it is suggested that sleep-related hypoxaemia may precipitate potentially serious arrhythmias [2]. The role of hypoxaemia in precipitating myocardial ischaemia and infarction is controversial.…”

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confidence: 99%

The effect on the heart of hypoxaemia in patients with severe coronary artery disease

et al. 1996

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SummaryThe aim of the study was to examine the effect of Key wordsHypoxia. Heart; ischaemia, coronary occlusion.Smokers and overweight patients may have ischaemic heart disease and following upper abdominal or thoracic surgery such patients usually have prolonged and profound postoperative hypoxaemia [ 11. The worst hypoxaemia is often on the second and third nights but can be maximal on the fourth. In these circumstances, profound oxygen desaturation (Sao? < 80%) can occur without being noticed and may last for several hours, almost invariably when the patient falls asleep. Clinical practice does not normally include the administration of oxygen beyond the first 24 h postoperatively and this raises the question about the significance of episodic hypoxaemia in patients with ischaemic heart disease. The effect of hypoxaemia on the heart has been discussed in a number of recent editorials [ 2 4 ] but surprisingly little is known about the effects of hypoxaemia on the diseased heart, although it is suggested that sleep-related hypoxaemia may precipitate potentially serious arrhythmias [2]. The role of hypoxaemia in precipitating myocardial ischaemia and infarction is controversial. It has been proposed that in susceptible patients some episodes of postoperative myocardial infarction and cardiac failure are caused by hypoxaemia and that oxygen therapy would therefore be beneficial [3]. However, an editorial in the Lancet [4] claimed that there is insufficient evidence that postoperative oxygen therapy either reduces the amount of ischaemia in patients with coronary artery disease or improves outcome.In an extensive review of peri-operative morbidity, Mangano [5] pointed out that the incidence of postoperative myocardial infarction in the general population is low (0.1-0.7%). However, the risk of postoperative myocardial infarction increases for those who have suffered a previous infarct (1.9-7.7%) and the rate is very much higher, up to 37%, in those who have had an infarction within the previous 3 months. The mortality from postoperative myocardial infarction is considerable (36-70%) [5]. Knorring [6] showed that 87% of the postoperative infarctions occurred during the first 3 postoperative days with a peak incidence on the second day. In another study by Rao et al. [7], 89-100% of reinfarctions occurred within the first 3 postoperative days, with a peak incidence on the third postoperative day, 50% of these being silent infarctions. It is tempting to speculate that this temporal relationship between myocardial infarction and hypoxaemia may indicate that postoperative hypoxaemia is a causative factor.Factors associated with significantly increased postoperative reinfarction rates include: pre-operative hypertension, intra-operative hypotensive episodes and non-cardiac thoracic or upper abdominal operations of more than 3 h H

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“…Focusing on a specific exposure is a strength that helps elucidate our understanding of a driver of physiologic effects in flight. Altitude-induced hypoxia is known to acutely increase heart rate, stroke volume, and coronary blood flow but it does not appear to cause arrhythmias unless the ascent results in acute mountain sickness 26 . Heart rate, stroke volume, and coronary blood flow do gradually decrease to pre-ascent levels over a period of 2 to 10 days 26 .…”

Section: Discussionmentioning

confidence: 99%

Impact of simulated flight conditions on supraventricular and ventricular ectopy

Meyer

Mordukhovich

Coull

et al. 2023

Sci Rep

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Though billions of passengers and crew travel by air each year and are exposed to altitude equivalents of 7000–8000 feet, the health impact of cabin oxygenation levels has not been well studied. The hypoxic environment may produce ectopic heartbeats that may increase the risk of acute in-flight cardiac events. We enrolled forty older and at-risk participants under a block-randomized crossover design in a hypobaric chamber study to examine associations between flight oxygenation and both ventricular (VE) and supraventricular ectopy (SVE). We monitored participant VE and SVE every 5 min under both flight and control conditions to investigate the presence and rate of VE and SVE. While the presence of VE did not differ according to condition, the presence of SVE was higher during flight conditions (e.g. OR ratio = 1.77, 95% CI: 1.21, 2.59 for SVE couplets). Rates of VE and SVE were higher during flight conditions (e.g. RR ratio = 1.25, 95% CI: 1.03, 1.52 for VE couplets, RR ratio = 1.76, 95% CI: 1.39, 2.22 for SVE couplets). The observed higher presence and rate of ectopy tended to increase with duration of the flight condition. Further study of susceptible passengers and crew may elucidate the specific associations between intermittent or sustained ectopic heartbeats and hypoxic pathways.

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Hypoxia and the heart.

Cited by 37 publications

References 47 publications

Effects of captopril and oxygen on sleep apnoea in patients with mild to moderate congestive cardiac failure.

Effects of captopril and oxygen on sleep apnoea in patients with mild to moderate congestive cardiac failure.

The effect on the heart of hypoxaemia in patients with severe coronary artery disease

Impact of simulated flight conditions on supraventricular and ventricular ectopy

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