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Journal Article
Review
Maternal cardiac haemodynamics in severe pre-eclampsia complicated by acute pulmonary oedema: A review.
Journal of Maternal-fetal & Neonatal Medicine 2017 December
AIM: To establish alterations in maternal cardiac haemodynamics and function using electrocardiography and echocardiography in severe pre-eclampsia complicated by acute pulmonary oedema.
METHODS: An extensive literature search including any research articles, randomised control trials, observational study, case report or expert or consensus statement pertaining to severe pre-eclampsia, eclampsia, hypertensive crises of pregnancy, pulmonary oedema, maternal cardiac haemodynamics, Holter monitoring and maternal echocardiography was done. Electronic search strategies included searching the MEDLINE, EMBASE, Cochrane Library and Pubmed databases.
RESULTS: Toxic substrates from a chronically ischaemic placenta and elevated maternal cathecolamines leads to widespread elevated systemic vascular resistance, endothelial cell damage and increased left ventricular afterload all of which combine to result in left ventricular hypertrophy with impaired ventricular filling reflected as significant diastolic dysfunction, increased left ventricular end systolic and end diastolic volumes, increased left ventricular stroke work, myocardial ischaemia and resultant ventricular arrhythmias, in particular ventricular tachycardia. These factors could lead to cardiac failure in severe pre-eclampsia, either in combination or in independently of each other depending on the magnitude of the angiogenic imbalances, degree of elevated systemic vascular resistance, degree of impaired myocardial relaxation and diastolic filling anomalies, gene-environment interaction and degree of possible pre-existing or potential cardiovascular dysfunction.
CONCLUSION: Comprehensive maternal echocardiographic and electocardiographic assessment should be incorporated in the work-up of severe pre-eclampsia to stratify these cases, to enable clinicians to choose the appropriate acute hypertensive drug therapy and plan optimal management pathways.
METHODS: An extensive literature search including any research articles, randomised control trials, observational study, case report or expert or consensus statement pertaining to severe pre-eclampsia, eclampsia, hypertensive crises of pregnancy, pulmonary oedema, maternal cardiac haemodynamics, Holter monitoring and maternal echocardiography was done. Electronic search strategies included searching the MEDLINE, EMBASE, Cochrane Library and Pubmed databases.
RESULTS: Toxic substrates from a chronically ischaemic placenta and elevated maternal cathecolamines leads to widespread elevated systemic vascular resistance, endothelial cell damage and increased left ventricular afterload all of which combine to result in left ventricular hypertrophy with impaired ventricular filling reflected as significant diastolic dysfunction, increased left ventricular end systolic and end diastolic volumes, increased left ventricular stroke work, myocardial ischaemia and resultant ventricular arrhythmias, in particular ventricular tachycardia. These factors could lead to cardiac failure in severe pre-eclampsia, either in combination or in independently of each other depending on the magnitude of the angiogenic imbalances, degree of elevated systemic vascular resistance, degree of impaired myocardial relaxation and diastolic filling anomalies, gene-environment interaction and degree of possible pre-existing or potential cardiovascular dysfunction.
CONCLUSION: Comprehensive maternal echocardiographic and electocardiographic assessment should be incorporated in the work-up of severe pre-eclampsia to stratify these cases, to enable clinicians to choose the appropriate acute hypertensive drug therapy and plan optimal management pathways.
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