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出生窒息时的心脏异常。

Cardiac abnormalities in birth asphyxia.

作者信息

Ranjit M S

机构信息

Sri Ramachandra Medical College and Research Institute, Porur, Chennai, Tamil Nadu.

出版信息

Indian J Pediatr. 2000 Jul;67(7):529-32. doi: 10.1007/BF02760486.

Abstract

Cardiac abnormalities in birth asphyxia were first recognised in the 1970s. These include (i) transient tricuspid regurgitation which is the commonest cause of a systolic murmur in a newborn and tends to disappear without any treatment unless it is associated with transient myocardial ischemia or primary pulmonary hypertension of the newborn (ii) transient mitral regurgitation which is much less common and is often a part of transient myocardial ischemia, at times with reduced left ventricular function and, therefore, requires treatment in the form of inotropic and ventilatory support (iii) transient myocardial ischemia (TMI) of the newborn. This should be suspected in any baby with asphyxia, respiratory distress and poor pulses, especially if a murmur is audible. It is of five types (A to E) according to Rowe's classification. Type B is the most severe with respiratory distress, congestive heart failure and shock. Echocardiography helps to rule out critical left ventricular obstructive lesions like hypoplastic left heart syndrome or critical aortic stenosis. ECG is very important for diagnosis of TMI, and may show changes ranging from T wave inversion in one lead to a classical segmental infarction pattern with abnormal q waves. CPK-MB may rise and echocardiogram shows impaired left ventricular function, mitral and/or tricuspid regurgitation, and at times, wall motion abnormalities of left ventricle. Ejection fraction is often depressed and is a useful marker of severity and prognosis. Treatment includes fluid restriction, inotropic support, diuretics and ventilatory resistance if required (v) persistent pulmonary hypertension of the newborn (PPHN). Persistent hypoxia sometimes results in persistence of constricted fetal pulmonary vascular bed causing pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. This causes respiratory tension and right ventricular failure with systolic murmur of tricuspid, and at times, mitral regurgitation. Treatment consists of oxygen and general care for mild cases, ventilatory support, ECMO and nitric oxide for severe cases. Cardiac abnormalities in asphyxiated neonates are often underdiagnosed and require a high index of suspicion. ECG and Echo help in early recognition and hence better management of these cases.

摘要

出生窒息时的心脏异常最早在20世纪70年代被认识到。这些异常包括:(i)暂时性三尖瓣反流,这是新生儿收缩期杂音最常见的原因,若无任何治疗往往会自行消失,除非与暂时性心肌缺血或新生儿原发性肺动脉高压相关;(ii)暂时性二尖瓣反流,这种情况不太常见,常是暂时性心肌缺血的一部分,有时左心室功能降低,因此需要以强心和通气支持的形式进行治疗;(iii)新生儿暂时性心肌缺血(TMI)。在任何有窒息、呼吸窘迫和脉搏微弱的婴儿中都应怀疑有这种情况,尤其是如果能听到杂音时。根据罗伊分类法,它有五种类型(A至E)。B型最为严重,伴有呼吸窘迫、充血性心力衰竭和休克。超声心动图有助于排除诸如左心发育不全综合征或严重主动脉狭窄等严重的左心室梗阻性病变。心电图对TMI的诊断非常重要,可能显示从一个导联的T波倒置到伴有异常Q波的典型节段性梗死模式等各种变化。肌酸磷酸激酶同工酶(CPK-MB)可能升高,超声心动图显示显示左心室功能受损、二尖瓣和/或三尖瓣反流,有时还可见左心室壁运动异常。射血分数常常降低,是严重程度和预后的有用指标。治疗包括限制液体摄入、强心支持、利尿剂以及必要时的通气支持;(v)新生儿持续性肺动脉高压(PPHN)。持续性缺氧有时会导致胎儿肺血管床持续收缩,引起肺动脉高压,进而导致经动脉导管未闭和卵圆孔的右向左分流。这会导致呼吸窘迫和右心室衰竭,并伴有三尖瓣收缩期杂音,有时还伴有二尖瓣反流。轻度病例的治疗包括给氧和一般护理,重度病例则需要通气支持、体外膜肺氧合(ECMO)和一氧化氮治疗。窒息新生儿的心脏异常常常诊断不足,需要高度怀疑。心电图和超声心动图有助于早期识别,从而更好地管理这些病例。

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