科研之友
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摘要
Key points A rise in heart rate boosts cardiac output and blood pressure, improves perfusion and oxygen delivery, and speeds recovery during an emergency. Breathing efforts and lung inflation reflexively elevate heart rate during experimental asphyxia, and may rescue (auto resuscitate) an animal from imminent death. We analysed whether this mechanism elevates heart rate when a healthy, sleeping infant is confronted by mild, progressive asphyxia. Term-born infants aged 18 days rebreathed the expired gas for short periods to stimulate breathing and heart rate but not arousal from sleep. We show that a rising CO2 level during asphyxia is much more strongly cardio-acceleratory than either vigorous breathing efforts or lung inflation. This excitatory action of CO2 on the heart develops soon after birth. We suggest that (i) the hypercapnia during asphyxia helps raise heart rate; (ii) excitation by respiratory manoeuvres alone is relatively weak and short lived and may not produce the sustained heart rate rise needed to counteract circulatory depression. Abstract A resumption of, and escalation in, breathing efforts (hyperpnoea) reflexively accelerates heart rate (HR) and may facilitate cardiac and circulatory recovery from apnoea. We analysed whether this mechanism can produce a sustained rise in HR (tachycardia) when a sleeping infant is confronted by mild, rapidly worsening asphyxia, simulating apnoea. Twenty-seven healthy term-born infants aged 18 days rebreathed the expired gas for 90 s during quiet sleep to stimulate breathing and heart rate. To discriminate cardio-excitatory effects of central respiratory drive, lung inflation, hypoxia, hypercapnia and asphyxia, we varied the inspired O2 level and compared temporal changes in response profiles as respiratory sensitivity to hypoxia and asphyxia reset after birth. We demonstrate that asphyxia-induced hyperpnoea and tachycardia strengthen dramatically over the first week with different time courses and via separate mechanisms. Cardiac excitation by hypercapnia improves first, followed by a slower improvement in respiratory hypoxic drive. A rise in CO2 consequently elicits stronger, longer lasting tachycardia than moderate increases in respiratory drive or lung expansion. We suggest that without a strong facilitating action of CO2 on the immature heart, respiratory manoeuvres may be unable to reflexively counteract strong vagal bradycardia. This may increase the vulnerability of some infants to apnoea asphyxia.
- 出版日期2012-12
