Advertisement

Cardiac Disease in Pregnancy

  • T. A. Thomas
Conference paper

Abstract

Pregnancy converts the normal female’s cardiovascular system into a hyperdynamic, vasodilated, hypervolaemic, hypercoagulable and hypo-osmolar state. Increases occur in circulating blood volume and cardiac output which sustains placental blood flow and function. The increases in blood volume, together with the enhanced coagulability, provide a reserve capacity which compensates for the acute blood loss which occurs at delivery and minimises its effect. The additional demands that pregnancy makes on the heart make the parturient vulnerable to cardiac failure. When congenital or acquired cardiac disease is present the risk of heart failure, dysrhythmias and ischaemia are all increased. Aorto caval compression occurs quite commonly during the later stages of pregnancy, especially during the final trimester. Compression of the vena cava will cause a decrease in venous return and pre load. Compression of the aorta can potentially increase peripheral resistance and after load. A decrease in venous return combined with an increased systemic vascular resistance in the presence of cardiac disease will add to the risk of the heart being unable to cope with the demands of pregnancy and may precipitate sudden decompensation. In addition to this already complex set of changes it must be remembered that normal pregnancy is associated with a decrease in colloid osmotic pressure which makes the formation of both peripheral and pulmonary oedema more likely.

Keywords

Pulmonary Hypertension Cardiac Disease Ischaemic Heart Disease Pulmonary Vascular Resistance Regional Anaesthesia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Kerr MG, Scott DB, Samuel E (1964) Studies of the inferior vena cava in late pregnancy. Brit Med J 1:532–533PubMedGoogle Scholar
  2. 2.
    Lees MM, Scott DB, Kerr MG et al (1967) The circulatory effects of recumbent postural change in late pregnancy. Clin Sci 32:453–465PubMedGoogle Scholar
  3. 3.
    Abitbol MM (1977) Aortic compression and uterine blood flow during pregnancy. Obstet Gyn 50:562–570Google Scholar
  4. 4.
    Kinsella SM, Whitwam JG, Spencer JAE (1990) Aortic compression by the uterus: Identification with the Finapres digital arterial pressure instrument. Br J Obstet Gyn 97:700–705CrossRefGoogle Scholar
  5. 5.
    Busch RL (1992) Cardiac disease. In: Ostheimer GW (ed) “Manual of Obstetric Anaesthesia” 2nd edn. Churchill Livingstone, New York, 276–291Google Scholar
  6. 6.
    Department of Health, Welsh Office, Scottish Office, Home and Health Department, Department of Health and Social Security Northern Ireland HMSO (1994) Report on Confidential Enquiries into Maternal Deaths in United Kingdom 1988–1990, 106–111Google Scholar
  7. 7.
    Department of Health, Welsh Office, Scottish Office, Home and Health Department, Department of Health and Social Security Northern Ireland HMSO (1991) Report on Confidential Enquiries into Maternal Deaths in United Kingdom 1985–87, 95–102Google Scholar
  8. 8.
    Department of Health, Welsh Office, Scottish Office, Home and Health Department, Department of Health and Social Security Northern Ireland HMSO (1996) Report on Confidential Enquiries into Maternal Deaths in United Kingdom 1991–93, 109–120Google Scholar
  9. 9.
    Carvalho JCA (1966) Cardiac disease. In: Van Zundert A, Ostheimer GW (eds) Pain relief and anesthesia in obstetrics. Churchill Livingstone, New York, 547–557Google Scholar

Copyright information

© Springer-Verlag Italia 1997

Authors and Affiliations

  • T. A. Thomas

There are no affiliations available

Personalised recommendations