Pregnancy
Medical > Therapy > Special situations
Pregnancy
During pregnancy, physiologic cardiovascular and pulmonary changes seriously affect the diseased pulmonary circulation and the right heart (1). Due to the enlargement of the abominal contents with an upward displacement of the diaphragm, there is a progressive decline in expiratory reserve volume and residual volume by 7 % and 22 %, respectively, which results in a reduction in functional residual capacity by 10 % to 25 % close to term (1, 2). Overall, no significant changes in FEV1 are observed. There is marked increase in minute ventilation up to 40 % (3). This is mainly achieved by an elevated tidal volume (+50 %), and less by an increase in respiratory rate (+10 %). As a result, alveolar ventilation rises by up to 60 %, and PaCO2 and plasma bicarbonate levels decrease to 28-32 mmHg and 18-21 mEq/L (3). While sitting, PaO2 decreases only by about 5 mmHg by the third trimester. The respective decline in the supine position is about 13 mmHg. The alveolar to arterial oxygen gradient increases within the normal limit from 14 to 20 mmHg. As a consequence of hyperventilation, dyspnea may occur already in the first or second trimester, and is reported in up to 76 % of healthy pregnant women (4, 5).
Most relevant to pregnant women with pulmonary hypertension (PH) are the cardiovascular changes during pregnancy and parturition (6). Generally spoken, pregnancy represents a high-volume, low-resistance state characterized by a more than 20 % increase in cardiac output (CO) by 2 months, and by 30-40 % by the late second and early third trimester. The increase in CO is mainly due to an increase in stroke volume by 30 %, and to a lesser extent in heart rate, which increases by 10-15 beats per minute. Intermittent compression of the inferior vena cava might inhibit venous return and cause an abrupt large fall in CO and serious systemic hypotension (7). In addition to the direct cardiovascular effects associated with pregnancy, there is an increase in blood volume by about 35 % caused mainly by an augmentation in plasma volume (+50 %), and to a lesser extent in red blood cell volume (+20 %) (8). This results in a hemodilution, e. g. a fall in hematocrit by 15 %. During delivery, pain and apprehension further increase in CO by 45 %. Each uterine contraction results in an auto transfusion resulting in additional rises in blood volume and CO by 10-25 %. After delivery, relief of caval compression and another auto transfusion form the placental sinusoids cause an increase in CO by up to 80 %.
Hence, pregnancy in patients with PH carries an extremely high risk of morbidity and mortality for the mother, and to a lesser extent for the child. Fifteen years ago, PH and pregnancy has been called a lethal combination (9). In a comprehensive survey, Weiss et al. found an overall mortality rates related to pregnancy and delivery ranging from 30 % in IPAH, to 36 % in Eisenmenger’s Syndrome, and 56 % in other forms of PH such as APAH and CTEPH (10). On the contrary, despite about one fifth of the children were delivered before 32 weeks, neonatal death was relatively low with 11 %, 13 %, and 12 %, respectively. Except 3 Eisenmenger patients who died during pregnancy, all fatalities occurred within 35 days after delivery. Almost all patients died indirectly or directly because of PH. Risk factors for fatal outcome were late diagnosis of PH, late hospital admission (risk increasing by 9 % with each week of pregnancy), severity of PH, and delivery by cesarean section. The latter risk factor, however, most probably was largely due to a bias because more severe cases were more probable to undergo operative delivery.
Since even very recent series of highly experienced centers report a mortality of 36 % (11), it can be concluded that pregnancy should strongly be discouraged in patients with PH. Effective birth control is therefore of paramount importance. Vasectomy in the male partner or barrier methods are the most recommended options. There is no consensus if oral contraception is feasible in patients with PH. Nowadays, the majority of PH specialists feel that birth control pills are acceptable in this situation. Preparations with the lowest amount of estrogen are recommended. Potential interactions with bosentan have to be considered, and additional barrier methods are advocated. Pregnant women should be motivated for therapeutic abortion. The same anesthetic considerations apply in this context. The use of prostaglandin F2 is prohibited because, in contrast to prostaglandin E, it induces pulmonary vasoconstriction (12).
In women not willing to undergo therapeutic abortion, delivery has to be meticulously planned (11, 13). It is a highly interdisciplinary undertaking, which should be performed only in experienced tertiary referral centers. Scheduled cesarean section is now mostly recommended. It can be planned during the day, and the risks of acute hemodynamic changes during vaginal delivery and the potentiality of an urgent cesarean section can be avoided (14). Regional anesthesia using a combined spinal-epidural procedure with incremental epidural doses is the preferred method (14, 15). To circumvent compression of the inferior vena cava a left lateral position is recommended. Monitoring with right heart catheterization is necessary in most cases, especially in severe PH. However, there may be an increased risk of pulmonary artery rupture (16, 17). As for other operative procedures in patients with PH, scheduled hospitalization in an ICU ward one day before the intervention, installation of a comprehensive monitoring and if needed optimization of vasoactive therapy should be strongly considered. Since most fatalities occur several days up to one month after delivery (13), ICU treatment including invasive hemodynamic monitoring should be continued for at least 14 days postoperatively.
In patients with overt right heart failure, the situation has to be stabilized in an ICU. Careful general anesthesia with intubation, mechanical ventilation, invasive hemodynamic monitoring and sophisticated vasoactive drug therapy is necessary in these patients. Extracorporeal membrane oxygenation should be available at any time.
References:
1. Elkus R, Popovich J, Jr. Respiratory physiology in pregnancy. Clin Chest Med 1992;13:555-565.
2. Milne JA. The respiratory response to pregnancy. Postgrad Med J 1979;55:318-324.
3. Pereira A, Krieger BP. Pulmonary complications of pregnancy. Clin Chest Med 2004;25:299-310.
4. Contreras G, Gutierrez M, Beroiza T, Fantin A, Oddo H, Villarroel L, Cruz E, Lisboa C. Ventilatory drive and respiratory muscle function in pregnancy. Am Rev Respir Dis 1991;144:837-841.
5. Milne JA, Howie AD, Pack AI. Dyspnoea during normal pregnancy. Br J Obstet Gynaecol 1978;85:260-263.
6. Abbas AE, Lester SJ, Connolly H. Pregnancy and the cardiovascular system. Int J Cardiol 2005;98:179-189.
7. Kunzel W. (Physiopathology and clinical aspects of the vena cava occlusion syndrome). Gynakologe 1984;17:106-114.
8. Pitkin RM. Nutritional support in obstetrics and gynecology. Clin Obstet Gynecol 1976;19:489-513.
9. Roberts NV, Keast PJ. Pulmonary hypertension and pregnancy - a lethal combination. Anaesth Intensive Care 1990;18:366-374.
10. Weiss BM, Zemp L, Seifert B, Hess OM. Outcome of pulmonary vascular disease in pregnancy: a systematic overview from 1978 through 1996. J Am Coll Cardiol 1998;31:1650-1657.
11. Bonnin M, Mercier FJ, Sitbon O, Roger-Christoph S, Jais X, Humbert M, Audibert F, Frydman R, Simonneau G, Benhamou D. Severe pulmonary hypertension during pregnancy: mode of delivery and anesthetic management of 15 consecutive cases. Anesthesiology 2005;102:1133-1137.
12. Dagher E, Dumont L, Chartrand C, Blaise G. Effects of PGE1 in experimental vasoconstrictive pulmonary hypertension. Eur Surg Res 1993;25:65-73.
13. Weiss BM, Hess OM. Pulmonary vascular disease and pregnancy: current controversies, management strategies, and perspectives. Eur Heart J 2000;21:104-115.
14. Slomka F, Salmeron S, Zetlaoui P, Cohen H, Simonneau G, Samii K. Primary pulmonary hypertension and pregnancy: anesthetic management for delivery. Anesthesiology 1988;69:959-961.
15. Fan SZ, Susetio L, Wang YP, Cheng YJ, Liu CC. Low dose of intrathecal hyperbaric bupivacaine combined with epidural lidocaine for cesarean section--a balance block technique. Anesth Analg 1994;78:474-477.
16. Weeks SK, Smith JB. Obstetric anaesthesia in patients with primary pulmonary hypertension. Can J Anaesth 1991;38:814-816.
17. Barash PG, Nardi D, Hammond G, Walker-Smith G, Capuano D, Laks H, Kopriva CJ, Baue AE, Geha AS. Catheter-induced pulmonary artery perforation. Mechanisms, management, and modifications. J Thorac Cardiovasc Surg 1981;82:5-12.
Back to > Medical > Therapy > Special situations
Pregnancy
During pregnancy, physiologic cardiovascular and pulmonary changes seriously affect the diseased pulmonary circulation and the right heart (1). Due to the enlargement of the abominal contents with an upward displacement of the diaphragm, there is a progressive decline in expiratory reserve volume and residual volume by 7 % and 22 %, respectively, which results in a reduction in functional residual capacity by 10 % to 25 % close to term (1, 2). Overall, no significant changes in FEV1 are observed. There is marked increase in minute ventilation up to 40 % (3). This is mainly achieved by an elevated tidal volume (+50 %), and less by an increase in respiratory rate (+10 %). As a result, alveolar ventilation rises by up to 60 %, and PaCO2 and plasma bicarbonate levels decrease to 28-32 mmHg and 18-21 mEq/L (3). While sitting, PaO2 decreases only by about 5 mmHg by the third trimester. The respective decline in the supine position is about 13 mmHg. The alveolar to arterial oxygen gradient increases within the normal limit from 14 to 20 mmHg. As a consequence of hyperventilation, dyspnea may occur already in the first or second trimester, and is reported in up to 76 % of healthy pregnant women (4, 5).
Most relevant to pregnant women with pulmonary hypertension (PH) are the cardiovascular changes during pregnancy and parturition (6). Generally spoken, pregnancy represents a high-volume, low-resistance state characterized by a more than 20 % increase in cardiac output (CO) by 2 months, and by 30-40 % by the late second and early third trimester. The increase in CO is mainly due to an increase in stroke volume by 30 %, and to a lesser extent in heart rate, which increases by 10-15 beats per minute. Intermittent compression of the inferior vena cava might inhibit venous return and cause an abrupt large fall in CO and serious systemic hypotension (7). In addition to the direct cardiovascular effects associated with pregnancy, there is an increase in blood volume by about 35 % caused mainly by an augmentation in plasma volume (+50 %), and to a lesser extent in red blood cell volume (+20 %) (8). This results in a hemodilution, e. g. a fall in hematocrit by 15 %. During delivery, pain and apprehension further increase in CO by 45 %. Each uterine contraction results in an auto transfusion resulting in additional rises in blood volume and CO by 10-25 %. After delivery, relief of caval compression and another auto transfusion form the placental sinusoids cause an increase in CO by up to 80 %.
Hence, pregnancy in patients with PH carries an extremely high risk of morbidity and mortality for the mother, and to a lesser extent for the child. Fifteen years ago, PH and pregnancy has been called a lethal combination (9). In a comprehensive survey, Weiss et al. found an overall mortality rates related to pregnancy and delivery ranging from 30 % in IPAH, to 36 % in Eisenmenger’s Syndrome, and 56 % in other forms of PH such as APAH and CTEPH (10). On the contrary, despite about one fifth of the children were delivered before 32 weeks, neonatal death was relatively low with 11 %, 13 %, and 12 %, respectively. Except 3 Eisenmenger patients who died during pregnancy, all fatalities occurred within 35 days after delivery. Almost all patients died indirectly or directly because of PH. Risk factors for fatal outcome were late diagnosis of PH, late hospital admission (risk increasing by 9 % with each week of pregnancy), severity of PH, and delivery by cesarean section. The latter risk factor, however, most probably was largely due to a bias because more severe cases were more probable to undergo operative delivery.
Since even very recent series of highly experienced centers report a mortality of 36 % (11), it can be concluded that pregnancy should strongly be discouraged in patients with PH. Effective birth control is therefore of paramount importance. Vasectomy in the male partner or barrier methods are the most recommended options. There is no consensus if oral contraception is feasible in patients with PH. Nowadays, the majority of PH specialists feel that birth control pills are acceptable in this situation. Preparations with the lowest amount of estrogen are recommended. Potential interactions with bosentan have to be considered, and additional barrier methods are advocated. Pregnant women should be motivated for therapeutic abortion. The same anesthetic considerations apply in this context. The use of prostaglandin F2 is prohibited because, in contrast to prostaglandin E, it induces pulmonary vasoconstriction (12).
In women not willing to undergo therapeutic abortion, delivery has to be meticulously planned (11, 13). It is a highly interdisciplinary undertaking, which should be performed only in experienced tertiary referral centers. Scheduled cesarean section is now mostly recommended. It can be planned during the day, and the risks of acute hemodynamic changes during vaginal delivery and the potentiality of an urgent cesarean section can be avoided (14). Regional anesthesia using a combined spinal-epidural procedure with incremental epidural doses is the preferred method (14, 15). To circumvent compression of the inferior vena cava a left lateral position is recommended. Monitoring with right heart catheterization is necessary in most cases, especially in severe PH. However, there may be an increased risk of pulmonary artery rupture (16, 17). As for other operative procedures in patients with PH, scheduled hospitalization in an ICU ward one day before the intervention, installation of a comprehensive monitoring and if needed optimization of vasoactive therapy should be strongly considered. Since most fatalities occur several days up to one month after delivery (13), ICU treatment including invasive hemodynamic monitoring should be continued for at least 14 days postoperatively.
In patients with overt right heart failure, the situation has to be stabilized in an ICU. Careful general anesthesia with intubation, mechanical ventilation, invasive hemodynamic monitoring and sophisticated vasoactive drug therapy is necessary in these patients. Extracorporeal membrane oxygenation should be available at any time.
References:
1. Elkus R, Popovich J, Jr. Respiratory physiology in pregnancy. Clin Chest Med 1992;13:555-565.
2. Milne JA. The respiratory response to pregnancy. Postgrad Med J 1979;55:318-324.
3. Pereira A, Krieger BP. Pulmonary complications of pregnancy. Clin Chest Med 2004;25:299-310.
4. Contreras G, Gutierrez M, Beroiza T, Fantin A, Oddo H, Villarroel L, Cruz E, Lisboa C. Ventilatory drive and respiratory muscle function in pregnancy. Am Rev Respir Dis 1991;144:837-841.
5. Milne JA, Howie AD, Pack AI. Dyspnoea during normal pregnancy. Br J Obstet Gynaecol 1978;85:260-263.
6. Abbas AE, Lester SJ, Connolly H. Pregnancy and the cardiovascular system. Int J Cardiol 2005;98:179-189.
7. Kunzel W. (Physiopathology and clinical aspects of the vena cava occlusion syndrome). Gynakologe 1984;17:106-114.
8. Pitkin RM. Nutritional support in obstetrics and gynecology. Clin Obstet Gynecol 1976;19:489-513.
9. Roberts NV, Keast PJ. Pulmonary hypertension and pregnancy - a lethal combination. Anaesth Intensive Care 1990;18:366-374.
10. Weiss BM, Zemp L, Seifert B, Hess OM. Outcome of pulmonary vascular disease in pregnancy: a systematic overview from 1978 through 1996. J Am Coll Cardiol 1998;31:1650-1657.
11. Bonnin M, Mercier FJ, Sitbon O, Roger-Christoph S, Jais X, Humbert M, Audibert F, Frydman R, Simonneau G, Benhamou D. Severe pulmonary hypertension during pregnancy: mode of delivery and anesthetic management of 15 consecutive cases. Anesthesiology 2005;102:1133-1137.
12. Dagher E, Dumont L, Chartrand C, Blaise G. Effects of PGE1 in experimental vasoconstrictive pulmonary hypertension. Eur Surg Res 1993;25:65-73.
13. Weiss BM, Hess OM. Pulmonary vascular disease and pregnancy: current controversies, management strategies, and perspectives. Eur Heart J 2000;21:104-115.
14. Slomka F, Salmeron S, Zetlaoui P, Cohen H, Simonneau G, Samii K. Primary pulmonary hypertension and pregnancy: anesthetic management for delivery. Anesthesiology 1988;69:959-961.
15. Fan SZ, Susetio L, Wang YP, Cheng YJ, Liu CC. Low dose of intrathecal hyperbaric bupivacaine combined with epidural lidocaine for cesarean section--a balance block technique. Anesth Analg 1994;78:474-477.
16. Weeks SK, Smith JB. Obstetric anaesthesia in patients with primary pulmonary hypertension. Can J Anaesth 1991;38:814-816.
17. Barash PG, Nardi D, Hammond G, Walker-Smith G, Capuano D, Laks H, Kopriva CJ, Baue AE, Geha AS. Catheter-induced pulmonary artery perforation. Mechanisms, management, and modifications. J Thorac Cardiovasc Surg 1981;82:5-12.
Back to > Medical > Therapy > Special situations
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SSPH Research Prize 2012
Deadline for submission: April 30, 2012
Further information
Symposium "pulmonal-arterielle Hypertension im Kindesalter"
Donnerstag, 10. Mai 2012, 16.00-18.00, Bern
Further information:
5th International Congress of the Swiss Society of Pulmonary Hypertension (SSPH)
28.-29. September 2012, Thun, Congress Hotel Seepark Thun
Informationen: www.imk.ch/sgph2012
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