Herz-Kreislauferkrankungen in der Schwangerschaft

1995 
Pregnancy causes substantial changes in the cardiovascular system: cardiac output (40%—50%) and blood volume (40%) increase whereas systemic peripheral resistance and arterial pressure decrease. The rise in progesterone and estrogen levels accompanying pregnancy stimulates the renin-angiotension-aldosterone system. Increased prostaglandin production follows renin activation; simultaneously, the arterial vessels show diminished angiotension sensitivity. The result is pronounced vasodilatation. Heart disease remains the most important nonobstetric cause of maternal death. The physiological changes in the cardiovascular system during pregnancy influence cardiac diseases in different ways. Pregnancy, labor, and delivery appear to be well tolerated in gravidae with an atrial septal defect, ventricular septal defect, and patents ductus arteriosus. Sometimes congestive heart failure occurs and appropriate medical therapy is necessary. Pregnant women with uncorrected cyanotic congenital heart disease (Eisenmenger's syndrome, tetralogy of Fallot) constitute a high-risk group because of right ventricular insufficiency and hypoxic attacks. The consequences for anaesthesia in parturients with congenital heart disease are discussed. The symptoms of acquired mitral or aortic stenosis are aggravated by the physiological changes in the cardiovascular system during pregnancy; the clinical symptoms of valve insufficiency are ameliorated by vasodilatation. Peripartum cardiomyopathy clinically shows similar features to idiopathic dilated cardiomyopathy. The basis of treatment is the same as that of congestive heart failure, with the therapeutic spectrum ranging from diet to heart transplantation. Women with hypertrophic cardiomyopathy tolerate pregnancy, labor, and delivery surprisingly well. Vaginal delivery is possible, but epidural anaesthesia is contraindicated. Hypertensive disorders associated with pregnancy are classified into three groups: chronic, treatment, and preeclamptic hypertension. Whereas chronic and transient hypertension do not affect the outcome of pregnancy appreciably, pre-eclampsia presents a potential danger to mother and fetus. Pre-eclamptic hypertension is accompanied by low cardiac output and plasma volume. An upregulation of angiotension receptors enhances vascular reactivity, with the consequence of high peripheral resistance. For antihypertensive therapy hydralazine, α-methyldopa, and magnesium sulfate are the drugs of choice. A generalised recommendation of anaesthesia for the pre-eclamptic gravida cannot be made because both general and epidural anaesthesia have risks of severe side effects.
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