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Year : 2018  |  Volume : 7  |  Issue : 1  |  Page : 20-24

Cardiovascular involvement in birth asphyxia

1 Department of pediatrics, Pravara Institute of Medical Sciences, Ahmednagar, Maharashtra, India
2 Department of Pediatrics, Sir Ganga Ram Hospital, New Delhi, India

Date of Web Publication6-Feb-2018

Correspondence Address:
Dr. Rohit Vohra
Sir Ganga Ram Hospital, 22/2A, Tilak Nagar, New Delhi - 110 018
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jcn.JCN_80_17

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Background: Asphyxia before, during, or after birth is an important cause of perinatal mortality and morbidity. The newborn infant who does not breathe at birth suffers from oxygen lack, carbon dioxide excess, and fall in blood pH. Although the fetal and neonatal myocardium seems to be resistant to hypoxia, heart failure is commonly seen after perinatal asphyxia. We performed this study to determine the incidence of cardiovascular insult in birth asphyxia. Materials and Methods: This is a prospective, observational, hospital-based study carried out on 152 asphyxiated neonates admitted in Neonatal Intensive Care Unit (NICU) of Rural Medical College of Pravara Institute of Medical Sciences, Loni, Ahmednagar, Maharashtra, from September 2013 to August 2015. Results: Cardiovascular involvement was seen in 48 (32%) of the infants who had birth asphyxia. Cardiovascular dysfunction most commonly manifested by the use of inotropes (32%) followed by abnormal echocardiography (27%), electrocardiography (ECG) changes (13%), and elevated creatinine kinase-MB (14.5%). Out of the 48 neonates who had cardiovascular system (CVS) dysfunction, 28 children survived till hospital discharge. Conclusions: CVS dysfunction is present in significant proportion of neonates following asphyxia injury and neonates with cardiovascular dysfunction have a poor outcome.

Keywords: Birth asphyxia, creatine kinase-MB, cardiovascular system, inotropes

How to cite this article:
Singh V, Vohra R, Bansal M. Cardiovascular involvement in birth asphyxia. J Clin Neonatol 2018;7:20-4

How to cite this URL:
Singh V, Vohra R, Bansal M. Cardiovascular involvement in birth asphyxia. J Clin Neonatol [serial online] 2018 [cited 2022 May 19];7:20-4. Available from: https://www.jcnonweb.com/text.asp?2018/7/1/20/224814

  Introduction Top

Perinatal asphyxia remains an important cause of neonatal mortality, morbidity, and late sequelae, especially in a developing country. The focus in perinatal asphyxia is mostly on the brain, due to hypoxic-ischemic encephalopathy causing mortality or morbidity with sequelae in a large number of cases. Other organ systems also suffer the consequences of hypoxic-ischemic insult but are often overlooked. Target organs of perinatal asphyxia are the brain, heart, lungs, kidneys, gut, and bone marrow. The most frequent abnormalities involving kidneys (50%) followed by CNS (28%), cardiovascular system (CVS) (25%), and pulmonary system (23%). Thus, there is evidence of multiorgan system dysfunction in the immediate neonatal period.[1]

Although the fetal and neonatal myocardium seems to be resistant to hypoxia,[2] heart failure was the main recognized manifestation of myocardial dysfunction after perinatal asphyxia.[3] Thus, the incidence of severe heart damage is low although less severe manifestations of heart involvement may be frequent.[4] A murmur suggestive of atrioventricular value insufficiency, electrocardiographic abnormalities characteristic of myocardial ischemia or both were found in 29% of the infants who were suspected to have cardiac involvement.[5] Other recognized complications include cardiogenic shock and hypotension, functional tricuspid incompetence secondary to acute cardiac dilation, arrhythmia, and myocardial ischemia that may be diagnosed from electrocardiogram.

However, the incidence of histologically proven myocardial ischemic damage after perinatal asphyxia seems to be greater than could be anticipated on clinical grounds, the true incidence of mild myocardial ischemia might be underestimated if pathological studies are not performed.[6] We performed this study to determine the incidence of cardiovascular dysfunction in birth asphyxia.

  Materials and Methods Top

Study design

This was a prospective, observational, hospital-based study.

Data collection

All asphyxiated newborns delivered at Pravara Institute of Medical Sciences, Loni, from September 2013 to August 2015 who had features of birth asphyxia with Apgar score of ≤7 at 5 min and/or umbilical cord arterial pH of <7.2 at birth or/and required more than 1 min of positive pressure ventilation before sustained respiration or the need for mechanical ventilation at birth were included in the study.

Neonates born before 37 weeks of gestation, or born outside Pravara Institute of Medical Sciences, Loni, or with congenital anomalies or with early-onset sepsis were excluded from study.

Approval from the institutional ethics committee and written consent was taken from all parents before inclusion of their child in the study.

A detailed history was taken and examination performed at the time of admission to NICU. The neonatal clinical course was followed up to 14 days of birth. The data so obtained was recorded. Natal history was taken to find out the mode of delivery and indications for interventions, if any. Complications during and before labor were noted.

All births were attended and resuscitated by the pediatricians. For resuscitation, the Neonatal Resuscitation Protocol of American Academy of Pediatrics 2010 was followed.[7] Postnatal history was obtained regarding birth asphyxia and for details of resuscitation measures done at birth, Apgar score at 1 and 5 min was assessed.

Gestational age in completed weeks was assessed on the basis of mother's last menstrual period and confirmed where ever necessary by routine early antenatal ultrasonography (USG) examination. In cases where ever last menstrual period (LMP) was not available, and antenatal USG was not done, then gestational age was assessed by Modified Ballard Scoring system.[8]

All biochemical samples were taken on admission. Special investigation like echocardiography (ECHO) was done at Department of Radiology at Pravara Institute of Medical Sciences, Loni. Daily follow-up of the patient was done, and overall progress was monitored till the discharge from NICU or death of the baby.

Cardiac evaluation

Every infant was examined for the presence of heart murmur, dysrhythmias, cyanosis, increase in respiratory distress with systemic hypotension, and signs of shock (abnormal peripheral pulses, reduced peripheral pulsation evident by prolonged capillary refill time >3 s.). Any infant who continue to have signs of systemic hypoperfusion even after fluid boluses up to 40 ml/kg were started on inotropic support.

Twelve-lead serial ECGs were recorded in all asphyxiated neonates in first 72 h of life to look for transient myocardial ischemia. Infants with ECG changes of grade 1 or 2 were diagnosed to have mild, whereas those with changes of grades 3 or 4 were considered to have severe injuries. The grading was done as per criteria defined by Jedeikin et al.[9]

  • Grade 1: Flat or inverted T waves on 1 or 2 limb leads AVR
  • Grade 2: Flat or inverted T-waves in 3 or more leads except AVR
  • Grade 3: Flat or inverted T-waves in 3 or more leads and either ST depression or elevation >2 mm in at least two chest leads or >1 mm in at least two standard leads, or a Q-wave abnormality of duration >0.02 s or amplitude >25% of R wave in one anterior or three related chest leads
  • Grade 4: Presence of classical segmental infarction with abnormal Q-wave and markedly elevated ST segment or complete left bundle branch block.

Creatinine kinase-MB (CK-MB) isoenzyme levels were estimated at 8 h and 24 h life in all neonates. A value of more than 92.6 U/L at 8 h and 60 U/L at 24 h were taken as high. In cases with persistent murmurs and other abnormal findings, an ECHO was carried out.[10]

Statistical analysis

Values have been expressed as mean ± standard deviation. The data were compiled and analyzed using descriptive statistics using Student's t-test. The P < 0.05 was considered to be statistically significant.

  Results Top

Total 152 asphyxiated babies were included in the study. In this study, out of 152 neonates, 84 were male and 68 female. About 55.17% of our patients were delivered by vaginal delivery, whereas 38% of them were delivered by cesarean section, 4.88% by ventouse, and 1.95% by forceps.

Cardiovascular involvement was seen in 48 (32%) of the infants who had birth asphyxia. In this study, cardiovascular dysfunction most commonly manifested by the use of inotropes (32%) [Table 1] followed by abnormal ECHO (27%), ECG changes (13%), and elevated CK-MB (14.5%) [Figure 1].
Table 1: Cardiovascular system involvement in form of use of inotropes in perinatal asphyxia

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Figure 1: Cardiovascular system involvement in cases of perinatal asphyxia

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We found that 32% asphyxiated newborns required inotropic support on day 1 of life, however, on 3rd day, only 21% of asphyxiated cases required inotropic support. The number of newborns requiring inotropes decreased over next few days and only 4% of newborns required inotropes by 5-7 days of life (P < 0.0001).

In this study, 14 (9.2%) cases had grade I ECG changes as per criteria defined by Jedeikin [Figure 2]. Only 2 (1.3%) cases had grade II and grade III changes. CK-MB enzyme levels was significantly high on first 12 h of life and gradually comes to normal over 72 h [Table 2]. CK-MB enzymes are significantly raised in 23 (15%) asphyxiated neonates on first 12 h of life [Figure 3]. However, CK-MB values normalized in majority of neonates by 72 h by applying Chi-square for trend test; these values are statistically significant as P < 0.0001.
Figure 2: Cardiovascular system involvement in the form of abnormal electrocardiography in perinatal asphyxia

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Table 2: Cardiovascular system involvement in form of raised creatine kinase-MB in perinatal asphyxia

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Figure 3: Creatinine kinase-MB profile of neonates in perinatal asphyxia

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Most common echocardiographic findings were persistent pulmonary hypertension (PPHN) which was seen in 20 neonates followed by patent ductus arteriosus (PDA) [Table 3]. Out of the 48 neonates who had CVS dysfunction, 28 children survived till hospital discharge while 20 children died (42%).
Table 3: Echocardiographic patterns in asphyxiated neonates

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  Discussion Top

In the present study, cardiovascular involvement was there in 32% of neonates [Table 4]. This was similar to the results obtained by Perlman et al.[4] Martín-Ancel et al.,[11] and Goodwin et al.[12] in their study. Other studies noted variable results.
Table 4: Cardiovascular system involvement in various studies

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In the present study, cardiovascular dysfunction most commonly manifested by the use of inotropes (32%).

Use of inotropic support

In the present study, 32% of the neonates required inotropic support while in the study conducted by Shah et al.,[13] 62% of the neonates required inotropes. Hankins et al.[14] noted inotrope requirement in 61% neonates. Shankaran Seetha [15] noted hypotension in 7% study neonates. 4% neonates required inotropes in the study conducted by Martín-Ancel et al.[11]


In the present study, abnormal ECG was noted in 13% of the neonates. Among these, 9.2% had grade I myocardial ischemic changes (as per Jedeikin criterion), 1.3% of neonates had grades II and III myocardial ischemic changes (as per Jedeikin criterion) each. In the study by Agrawal et al.[16] in 2012, ECG changes were observed in 76.7% neonates; 41.3% of whom had Grade I, 28.2% had Grades II and III each, and 2.1% had grade IV abnormalities. Rajakumar et al.[17] reported ECG changes in almost similar percentage (73.3%) of cases. The most common finding in their study was “T”-wave inversion (36.7%) followed by “T”-wave flattening (33.3%), which is equivalent, to grade 1 ECG change. These ECG abnormalities indicate myocardial ischemia due to birth asphyxia in neonates.

Elevated creatinine kinase-MB

In the present study, elevation of CK-MB was in 14.5% of neonates. Our result is in agreement with the study by Hankins et al.[14] They have noted elevated CK-MB values in 17% neonates. Similar interpretation was also given by Primhak et al.[9] who studied serial electrocardiogram and CK-MB in term infants and found that CK-MB was associated with myocardial injury in asphyxiated infants. Omokhodion et al.[18] concluded that specificity of CK-MB as a marker of myocardial injury in asphyxiated newborns is possible remains uncertain.


In the present study, most common ECHO finding was pulmonary hypertension followed by PDA. In a study by Masyur et al.[19] in 2009, the most common cardiac abnormality found in asphyxiated neonates was PDA, followed by atrial septal defect, tricuspid regurgitation, and pulmonary hypertension.

Association between meconium aspiration and PPHN are well known in clinical practice. In this study, we have a large group of neonates who had meconium aspiration syndrome. This could be a reason for most common finding of PPHN.

Mortality with cardiovascular involvement

In the present study, 42% neonates died with cardiovascular dysfunction. In the study by Shah et al.,[13] death or adverse outcomes were seen in 64% of those with cardiovascular involvement.

  Conclusions Top

CVS dysfunction is present in significant proportion of neonates following asphyxia injury and neonates with cardiovascular dysfunction have a poor outcome. Early screening and aggressive support of cardiovascular system may help to improve outcome in neonates with asphyxia injury.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Neil M, Ben S. Birth asphyxia. In: Forfar and Arneil's Textbook of Paediatrics. 6th ed. New York, USA: Churchill Livingstone; 2003. p. 197-201.  Back to cited text no. 1
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Rowe RD, Izukawa T, Mulholland HC, Bloom KR, Cook DH, Swyer PR, et al. Nonstructural heart disease in the newborn. Observations during one year in a perinatal service. Arch Dis Child 1978;53:726-30.  Back to cited text no. 3
Perlman JM, Tack ED, Martin T, Shackelford G, Amon E. Acute systemic organ injury in term infants after asphyxia. Am J Dis Child 1989;143:617-20.  Back to cited text no. 4
Dijxhoorn MJ, Visser GH, Fidler VJ, Touwen BC, Huisjes HJ. Apgar score, meconium and acidaemia at birth in relation to neonatal neurological morbidity in term infants. Br J Obstet Gynaecol 1986;93:217-22.  Back to cited text no. 5
Donnelly WH, Bucciarelli RL, Nelson RM. Ischemic papillary muscle necrosis in stressed newborn infants. J Pediatr 1980;96:295-300.  Back to cited text no. 6
Agarwal R, Paul VK, Deorari AK. Ghai Essential Pediatrics. Ch 8. CBS Publisher and Distributors pvt limited; 2013. p. 124-83.  Back to cited text no. 7
Mohan PV, Pai PM. Renal insult in asphyxia neonatorum. Indian Pediatr 2000;37:1102-6.  Back to cited text no. 8
Jedeikin R, Primhak A, Shennan AT, Swyer PR, Rowe RD. Serial electrocardiographic changes in healthy and stressed neonates. Arch Dis Child 1983;58:605-11.  Back to cited text no. 9
Pesce MA. Reference ranges for laboratory tests and procedures. In: Kliegman RM, Behrman RE, Jenson HB, Stanton BF, editors. Nelson Textbook of Pediatrics. 18th ed., Ch. 715. Philadelphia: W. B. Saunders; 2007. p. 2943-54.  Back to cited text no. 10
Martín-Ancel A, García-Alix A, Gayá F, Cabañas F, Burgueros M, Quero J, et al. Multiple organ involvement in perinatal asphyxia. J Pediatr 1995;127:786-93.  Back to cited text no. 11
Goodwin TM, Belai I, Hernandez P, Durand M, Paul RH. Asphyxial complications in the term newborn with severe umbilical acidemia. Am J Obstet Gynecol 1992;167:1506-12.  Back to cited text no. 12
Shah P, Riphagen S, Beyene J, Perlman M. Multiorgan dysfunction in infants with post-asphyxial hypoxic-ischaemic encephalopathy. Arch Dis Child Fetal Neonatal Ed 2004;89:F152-5.  Back to cited text no. 13
Hankins GD, Koen S, Gei AF, Lopez SM, Van Hook JW, Anderson GD, et al. Neonatal organ system injury in acute birth asphyxia sufficient to result in neonatal encephalopathy. Obstet Gynecol 2002;99:688-91.  Back to cited text no. 14
Reddy S, Dutta S, Narang A. Evaluation of lactate dehydrogenase, creatine kinase and hepatic enzymes for the retrospective diagnosis of perinatal asphyxia among sick neonates. Indian Pediatr 2008;45:144-7.  Back to cited text no. 15
Agrawal J, Shah GS, Poudel P, Baral N, Agrawal A, Mishra OP, et al. Electrocardiographic and enzymatic correlations with outcome in neonates with hypoxic-ischemic encephalopathy. Ital J Pediatr 2012;38:33.  Back to cited text no. 16
Rajakumar PS, Vishnu Bhat B, Sridhar MG. et al. Electrocardiographic and echocardiographic changes in perinatal asphyxia. Indian J Pediatr 2009;76:261.  Back to cited text no. 17
Omokhodion SI, Losekoot TG, Jaiyesimi F. Serum creatine kinase and creatine kinase-MB isoenzyme activities in perinatally asphyxiated newborns. Eur Heart J 1991;12:980-4.  Back to cited text no. 18
Masyur M, Amir I, Putra ST, Tumbelaka AR. Echocardiographic patterns in asphyxiated neonates. Paediatr Indones 2009;49:214-8.  Back to cited text no. 19


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2], [Table 3], [Table 4]

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