Respiratory disorders in pregnancy

doi:10.1017/CBO9780511544552.005

4 - Respiratory disorders in pregnancy

from Section 1 - Cardiovascular and respiratory disorders

Published online by Cambridge University Press: 19 October 2009

John Philip and

Shiv K. Sharma

Edited by

David R. Gambling ,

M. Joanne Douglas and

Robert S. F. McKay

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John Philip: Affiliation:
Associate Professor, Department of Anesthesiology and Pain Management, University of Texas, Southwestern Medical Center, Dallas, TX, USA
Shiv K. Sharma: Affiliation:
Professor, Department of Anesthesiology and Pain Management, Obstetric Division, University of Texas, Southwestern Medical Center, Dallas, TX, USA
David R. Gambling: Affiliation:
University of California, San Diego
M. Joanne Douglas: Affiliation:
University of British Columbia, Vancouver
Robert S. F. McKay: Affiliation:
University of Kansas

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Summary

Adult respiratory distress syndrome

Epidemiology

Adult respiratory distress syndrome (ARDS) is a severe form of acute respiratory failure that can develop following a systemic or pulmonary insult. Adult respiratory distress syndrome is not unique to adults, and in children is known as “acute respiratory distress syndrome”. The incidence of ARDS in pregnancy is variably reported as 1 in 3000 to 1 in 6000 deliveries with mortality as high as 44%.

Etiology

Several disorders can cause ARDS in pregnancy (see Table 4.1). Sepsis, secondary to pyelonephritis, chorioamnionitis, or endometritis, is a common cause of ARDS in pregnancy. Other causes include obstetric hemorrhage, severe preeclampsia, and aspiration. There may be a combination of sepsis, shock, and fluid overload, the latter of which can be exacerbated by tocolytic therapy.

Pathophysiology

Following the initial insult, a number of inflammatory mediators such as tumor necrosis factor and interleukins 1, 6, and 8 are released. Neutrophils are activated to release other mediators such as reactive oxygen (O2) species and proteases. These mediators produce widespread microvascular and alveolar epithelial damage. Microvascular damage leads to increased capillary permeability and subsequent interstitial and alveolar edema. Alveolar damage results in loss of surfactant and subsequent alveolar collapse. Alveolar edema and collapse contribute to ventilation–perfusion (V/Q) mismatching and intrapulmonary shunting with subsequent hypoxemia.

Pulmonary hypertension frequently develops leading to right ventricular (RV) dysfunction which reduces left ventricular (LV) preload and cardiac output (CO). Depressed CO further compromises O2 delivery.

Type: Chapter
Information: Obstetric Anesthesia and Uncommon Disorders , pp. 75 - 100

DOI: https://doi.org/10.1017/CBO9780511544552.005 [Opens in a new window]

Publisher: Cambridge University Press

Print publication year: 2008

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