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:* Increase in resting [[heart rate]] by 10 to 15 beats per minute is observed during the first and second trimester suggesting an initial increase in [[venous return]].<ref name="pmid2705548">{{cite journal |author=Robson SC, Hunter S, Boys RJ, Dunlop W |title=Serial study of factors influencing changes in cardiac output during human pregnancy |journal=[[The American Journal of Physiology]] |volume=256 |issue=4 Pt 2 |pages=H1060–5 |year=1989 |month=April |pmid=2705548 |doi= |url=http://ajpheart.physiology.org/cgi/pmidlookup?view=long&pmid=2705548 |accessdate=2012-04-17}}</ref> Higher rates of increase in [[heart rate]] is observed with multiple gestation.
:* Increase in resting [[heart rate]] by 10 to 15 beats per minute is observed during the first and second trimester suggesting an initial increase in [[venous return]].<ref name="pmid2705548">{{cite journal |author=Robson SC, Hunter S, Boys RJ, Dunlop W |title=Serial study of factors influencing changes in cardiac output during human pregnancy |journal=[[The American Journal of Physiology]] |volume=256 |issue=4 Pt 2 |pages=H1060–5 |year=1989 |month=April |pmid=2705548 |doi= |url=http://ajpheart.physiology.org/cgi/pmidlookup?view=long&pmid=2705548 |accessdate=2012-04-17}}</ref> Higher rates of increase in [[heart rate]] is observed with multiple gestation.
:* [[Blood pressure]] remains relatively unchanged when measured in the left lateral recumbent position.


:*Several factors influence the changes observed in [[cardiac output]] during pregnancy. Serial hemodynamic measurements performed in supine position are erroneous secondary to the [[IVC|inferior vena caval]] compression by the enlarging uterus which subsequently decreases the [[venous return]] from the lower extremities. Therefore, owing to the caval compression, [[cardiac output]] has shown to decline in supine position whereas increases in the left lateral position.<ref name="pmid14341106">{{cite journal |author=KERR MG |title=THE MECHANICAL EFFECTS OF THE GRAVID UTERUS IN LATE PREGNANCY |journal=[[The Journal of Obstetrics and Gynaecology of the British Commonwealth]] |volume=72 |issue= |pages=513–29 |year=1965 |month=August |pmid=14341106 |doi= |url= |accessdate=2012-04-17}}</ref><ref name="pmid4368892">{{cite journal |author=Metcalfe J, Ueland K |title=Maternal cardiovascular adjustments to pregnancy |journal=[[Progress in Cardiovascular Diseases]] |volume=16 |issue=4 |pages=363–74 |year=1974 |pmid=4368892 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/0033-0620(74)90028-0 |accessdate=2012-04-17}}</ref>
:*Several factors influence the changes observed in [[cardiac output]] during pregnancy. Serial hemodynamic measurements performed in supine position are erroneous secondary to the [[IVC|inferior vena caval]] compression by the enlarging uterus which subsequently decreases the [[venous return]] from the lower extremities. Therefore, owing to the caval compression, [[cardiac output]] has shown to decline in supine position whereas increases in the left lateral position.<ref name="pmid14341106">{{cite journal |author=KERR MG |title=THE MECHANICAL EFFECTS OF THE GRAVID UTERUS IN LATE PREGNANCY |journal=[[The Journal of Obstetrics and Gynaecology of the British Commonwealth]] |volume=72 |issue= |pages=513–29 |year=1965 |month=August |pmid=14341106 |doi= |url= |accessdate=2012-04-17}}</ref><ref name="pmid4368892">{{cite journal |author=Metcalfe J, Ueland K |title=Maternal cardiovascular adjustments to pregnancy |journal=[[Progress in Cardiovascular Diseases]] |volume=16 |issue=4 |pages=363–74 |year=1974 |pmid=4368892 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/0033-0620(74)90028-0 |accessdate=2012-04-17}}</ref>
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:*Precipitation of [[heart failure|high cardiac output failure]] may be observed in a few patients secondary to the shunting of blood to the placenta where it may pass from arterioles to venules bypassing the capillaries.
:*Precipitation of [[heart failure|high cardiac output failure]] may be observed in a few patients secondary to the shunting of blood to the placenta where it may pass from arterioles to venules bypassing the capillaries.


====Blood pressure====
===IV. Blood pressure===
:* arterial pressure begins to fall during the first trimester reaches a nadir in mid pregnancy and returns toward pregestational levels before term.
:*Arterial blood pressure begins to fall during the first trimester, reaching a nadir during the mid trimester (usually 100 mmHg below baseline) and returns toward pre-gestational levels before term.<ref name="pmid2178537">{{cite journal |author=Pitkin RM, Perloff JK, Koos BJ, Beall MH |title=Pregnancy and congenital heart disease |journal=[[Annals of Internal Medicine]] |volume=112 |issue=6 |pages=445–54 |year=1990 |month=March |pmid=2178537 |doi= |url= |accessdate=2012-04-17}}</ref><ref name="pmid8373615">{{cite journal |author=Weiss BM, Atanassoff PG |title=Cyanotic congenital heart disease and pregnancy: natural selection, pulmonary hypertension, and anesthesia |journal=[[Journal of Clinical Anesthesia]] |volume=5 |issue=4 |pages=332–41 |year=1993 |pmid=8373615 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/0952-8180(93)90130-7 |accessdate=2012-04-17}}</ref>
:* because [[diastolic blood pressure]] decreases substantially more than [[systolic blood pressure]], the [[pulse pressure]] widens.
 
:* reduction [[blood pressure]] is caused by a decline in [[systemic vascular resistance]] due to reduce vascular tone. This is mediated by gestational hormone activity, increased circulate levels of [[prostaglandins]] and [[atrial natriuretic peptides]], as well as [[Nitric oxide|endothelial nitric oxide]]. Increased heat production by the developing fetus small and the creation of a lower resistance circulation in the uterus also play a role.
:*[[Wide pulse pressure|Widened pulse pressure]] is present because there is a substantial reduction in the [[diastolic blood pressure]] greater than the [[systolic blood pressure]].
:* supine hypotensive syndrome of pregnancy: occurs in 11% of women.  Associated with [[weakness]], [[lightheadedness]], [[nausea]], [[dizziness]] and even [[syncope]]. This is often explained by acute occlusion of the [[inferior vena cava]] by the enlarged uterus. Symptoms usually subside when the supine position is abandoned.
 
:*Drop in [[blood pressure]] is caused by a decline in [[systemic vascular resistance]] secondary to reduced vascular tone.<ref name="pmid6869444">{{cite journal |author=Willcourt RJ, King JC, Queenan JT |title=Maternal oxygenation administration and the fetal transcutaneous PO2 |journal=[[American Journal of Obstetrics and Gynecology]] |volume=146 |issue=6 |pages=714–5 |year=1983 |month=July |pmid=6869444 |doi= |url= |accessdate=2012-04-17}}</ref><ref name="pmid3826166">{{cite journal |author=Shime J, Mocarski EJ, Hastings D, Webb GD, McLaughlin PR |title=Congenital heart disease in pregnancy: short- and long-term implications |journal=[[American Journal of Obstetrics and Gynecology]] |volume=156 |issue=2 |pages=313–22 |year=1987 |month=February |pmid=3826166 |doi= |url= |accessdate=2012-04-17}}</ref> This is mediated by gestational hormone activity, increased circulating levels of [[prostaglandins]] and [[atrial natriuretic peptides]],<ref name="pmid9853271">{{cite journal |author=Chapman AB, Abraham WT, Zamudio S, Coffin C, Merouani A, Young D, Johnson A, Osorio F, Goldberg C, Moore LG, Dahms T, Schrier RW |title=Temporal relationships between hormonal and hemodynamic changes in early human pregnancy |journal=[[Kidney International]] |volume=54 |issue=6 |pages=2056–63 |year=1998 |month=December |pmid=9853271 |doi=10.1046/j.1523-1755.1998.00217.x |url=http://dx.doi.org/10.1046/j.1523-1755.1998.00217.x |accessdate=2012-04-17}}</ref> as well as [[Nitric oxide|endothelial nitric oxide]].<ref name="pmid3191059">{{cite journal |author=McFaul PB, Dornan JC, Lamki H, Boyle D |title=Pregnancy complicated by maternal heart disease. A review of 519 women |journal=[[British Journal of Obstetrics and Gynaecology]] |volume=95 |issue=9 |pages=861–7 |year=1988 |month=September |pmid=3191059 |doi= |url= |accessdate=2012-04-17}}</ref><ref name="pmid577983">{{cite journal |author=Selzer A |title=Risks of pregnancy in women with cardiac disease |journal=[[JAMA : the Journal of the American Medical Association]] |volume=238 |issue=8 |pages=892–3 |year=1977 |month=August |pmid=577983 |doi= |url= |accessdate=2012-04-17}}</ref>
 
:* [[Blood pressure]] remains relatively unchanged when measured in the left lateral recumbent position. However, '''''supine hypotensive syndrome of pregnancy''''' occurs in approximately 11% of pregnant women and is often associated with [[weakness]], [[lightheadedness]], [[nausea]], [[dizziness]] and even [[syncope]]. Acute compression of the [[inferior vena cava]] by the gravid uterus is the possible explanation for this syndrome. Symptoms usually subside when the supine position is abandoned.
 
===V. Respiratory rate===
:* Increased [[respiratory rate]] is present secondary to increased abdominal pressure and accompanying elevation of the diaphragm.
:* Increased [[respiratory rate]] subsequently lowers carbon dioxide tension.
 
===VI. Gastrointestinal changes===
:* Reduced [[gastric emptying]] secondary to reduced gastrointestinal motility is observed during pregnancy.


====Increased respiratory rate====
:* An incompetent gastro-oesophageal sphincter leads to [[GERD|gastro-oesophageal reflux]] with increased risk of aspiration of gastric contents into the trachea.
:* secondary to increased abdominal pressure, elevation of the diaphragm.
:* lowers carbon dioxide tension.


====Gastrointestinal changes====
:* Intra-gastric pressure increases during late trimester.<ref>Jevon P, Raby M. Physiological and anatomical changes in pregnancy relevant to resuscitation. In: O'Donnell E, Pooni JS, editors. Resuscitation in Pregnancy. A practical approach. Oxford: Reed Educational and Professional Publishing Ltd.; 2001. p. 10-16.</ref>
:* [[Gastric emptying]] is slower – in pregnancy women have reduced gastrointestinal motility.
:* An incompetent gastro-oesophageal sphincter leads to gastro-oesophageal reflux with greater danger of aspiration of gastric contents into the trachea.
:* Increased intragastric pressure in late pregnancy<ref>Jevon P, Raby M. Physiological and anatomical changes in pregnancy relevant to resuscitation. In: O'Donnell E, Pooni JS, editors. Resuscitation in Pregnancy. A practical approach. Oxford: Reed Educational and Professional Publishing Ltd.; 2001. p. 10-16.</ref>


====Other changes in pregnancy====
===VII. Other changes in pregnancy===
:* Flared ribs.
:* Flared ribs.
:* Breast hypertropy<ref name="Morris"> Morris S, Stacey M. Resuscitation in pregnancy. BJM 2003;327:1277-1279.</ref> (may impede effective resuscitation).
:* Breast hypertropy which may impede effective resuscitation.<ref name="Morris"> Morris S, Stacey M. Resuscitation in pregnancy. BJM 2003;327:1277-1279.</ref>


==Physiology of Labor and Delivery==  
==Physiology of Labor and Delivery==  

Revision as of 18:26, 17 April 2012

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I. Pre-existing Cardiac Disease:
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III. Cardiomyopathy:
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IV. Cardiac diseases that may develop During Pregnancy:
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Lakshmi Gopalakrishnan, M.B.B.S. [3]

Effect of Pregnancy on Maternal Physiology

I. Hormonal Changes

Increased progesterone levels

Increased estrogen levels

  • Elevated estrogen levels may increase myocardial contractility.

Increased renin and aldosterone levels

II. Plasma volume expansion

  • Plasma volume expansion starts as early as 6-weeks of gestation and is increased to approximately 40-45% by the mid trimester.
  • Plasma volume expansion → hemodilution → anemia
  • Despite the development of anemia, the total red cell mass is not decreased because the rate of rise in plasma volume is more than rate of rise in red cell mass. This occurs until 30-week of gestation and is referred to as the physiologic anemia of pregnancy.
  • The hematocrit may drop to 33-38%.
  • Higher increase in blood volume may be prevalent among multigravidas.
  • An increase in atrial natriuretic peptide levels is observed in response to changes in intravasular volume.[1]

III. Cardiac output

  • Approximately 50% increase in cardiac output is observed which is required to well oxygenate the fetus.
  • The increase in cardiac output begins as early as the 5th week of gestation and steadily increases up to 24th week of gestation following which it plateaus.[2][3]
  • Increase in resting heart rate by 10 to 15 beats per minute is observed during the first and second trimester suggesting an initial increase in venous return.[2] Higher rates of increase in heart rate is observed with multiple gestation.
  • Several factors influence the changes observed in cardiac output during pregnancy. Serial hemodynamic measurements performed in supine position are erroneous secondary to the inferior vena caval compression by the enlarging uterus which subsequently decreases the venous return from the lower extremities. Therefore, owing to the caval compression, cardiac output has shown to decline in supine position whereas increases in the left lateral position.[4][5]
  • Precipitation of high cardiac output failure may be observed in a few patients secondary to the shunting of blood to the placenta where it may pass from arterioles to venules bypassing the capillaries.

IV. Blood pressure

  • Arterial blood pressure begins to fall during the first trimester, reaching a nadir during the mid trimester (usually 100 mmHg below baseline) and returns toward pre-gestational levels before term.[6][7]
  • Blood pressure remains relatively unchanged when measured in the left lateral recumbent position. However, supine hypotensive syndrome of pregnancy occurs in approximately 11% of pregnant women and is often associated with weakness, lightheadedness, nausea, dizziness and even syncope. Acute compression of the inferior vena cava by the gravid uterus is the possible explanation for this syndrome. Symptoms usually subside when the supine position is abandoned.

V. Respiratory rate

  • Increased respiratory rate is present secondary to increased abdominal pressure and accompanying elevation of the diaphragm.
  • Increased respiratory rate subsequently lowers carbon dioxide tension.

VI. Gastrointestinal changes

  • Reduced gastric emptying secondary to reduced gastrointestinal motility is observed during pregnancy.
  • An incompetent gastro-oesophageal sphincter leads to gastro-oesophageal reflux with increased risk of aspiration of gastric contents into the trachea.
  • Intra-gastric pressure increases during late trimester.[12]

VII. Other changes in pregnancy

  • Flared ribs.
  • Breast hypertropy which may impede effective resuscitation.[13]

Physiology of Labor and Delivery

  • The work of labor may increase the cardiac output by 60% over the baseline level.
  • Immediately following delivery, the uterus contracts and delivers a sudden bolus of 500-750 cc of blood to the circulatory system which may result in pulmonary edema in the patient with heart disease.

Hemodynamic effect of Cesarean Section:

To avoid the hemodynamic changes assocaited with vaginal delivery, cesarean section is frequently recommended for women with cardiovascular disease. This form of delivery can also be associated with hemodynamic fluctuations related to intubation, analgesic as well as anesthetic use. There can be a greater extent of blood loss as well as relief of caval compression.

Hemodynamic changes Postpartum:

There can be a temporary increase in venous return immediately after delivery due to relief of caval compression in addition to blood shifting from the contracting uterus into the systemic circulation. This change and effective blood volume occurs despite blood loss during delivery and can result in a substantial rise in ventricular filling pressures, stroke volume, and cardiac output that may lead to clinical deterioration.

Both heart rate and cardiac output returned to prelabor values by one hour after delivery and the blood pressure and stroke volume at 24 hours after delivery.

Hemodynamic adaptation of pregnancy persists postpartum and gradually returns to prepregnancy values within 12-24 weeks after delivery.

Fetal Physiology

  • Uterine blood flow increases by a factor of 50 during pregnancy.
  • The uterine blood vessels remain dilated throughout pregnancy.
  • Transfer of oxygen across the placenta is flow-limited.
  • Fetal oxygen tension is normally quite low (30 to 40 mmHg).
  • Supplemental oxygen to the mother is quite effective in increasing fetal oxygen, particularly with fetal distress.
  • Normal fetal pH is 7.35. Fetal scalp pHs <7.25 are abnormal.
  • Labor can precipitate fetal distress because during uterine contractions, uterine blood flow is nearly occluded.
  • In a mother with cyanosis, it is easier for problems to arise during labor because of the reduced reserve in oxygen delivery.
  • With contractions, there may normally be a reduction or deceleration in the fetal heart rate, but this rapidly returns to normal.
  • In fetal distress, the decelerations are later in the contraction and persist, i.e. late decelerations.
  • Fetuses do not die suddenly during labor, and there are many minutes or hours of fetal distress before death so that there is time to intervene.
  • Placing the mother in the left lateral recumbent position and oxygen will relieve many cases of fetal distress.
  • Fetal monitoring should be used in the presence of maternal heart disease, cardiac surgery, cardioversion.

References

  1. ↑ 1.0 1.1 1.2 Chapman AB, Abraham WT, Zamudio S, Coffin C, Merouani A, Young D, Johnson A, Osorio F, Goldberg C, Moore LG, Dahms T, Schrier RW (1998). "Temporal relationships between hormonal and hemodynamic changes in early human pregnancy". Kidney International. 54 (6): 2056–63. doi:10.1046/j.1523-1755.1998.00217.x. PMID 9853271. Retrieved 2012-04-17. Unknown parameter |month= ignored (help)
  2. ↑ 2.0 2.1 2.2 Robson SC, Hunter S, Boys RJ, Dunlop W (1989). "Serial study of factors influencing changes in cardiac output during human pregnancy". The American Journal of Physiology. 256 (4 Pt 2): H1060–5. PMID 2705548. Retrieved 2012-04-17. Unknown parameter |month= ignored (help)
  3. ↑ Robson SC, Hunter S, Moore M, Dunlop W (1987). "Haemodynamic changes during the puerperium: a Doppler and M-mode echocardiographic study". British Journal of Obstetrics and Gynaecology. 94 (11): 1028–39. PMID 3322367. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  4. ↑ KERR MG (1965). "THE MECHANICAL EFFECTS OF THE GRAVID UTERUS IN LATE PREGNANCY". The Journal of Obstetrics and Gynaecology of the British Commonwealth. 72: 513–29. PMID 14341106. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  5. ↑ Metcalfe J, Ueland K (1974). "Maternal cardiovascular adjustments to pregnancy". Progress in Cardiovascular Diseases. 16 (4): 363–74. PMID 4368892. Retrieved 2012-04-17.
  6. ↑ Pitkin RM, Perloff JK, Koos BJ, Beall MH (1990). "Pregnancy and congenital heart disease". Annals of Internal Medicine. 112 (6): 445–54. PMID 2178537. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  7. ↑ Weiss BM, Atanassoff PG (1993). "Cyanotic congenital heart disease and pregnancy: natural selection, pulmonary hypertension, and anesthesia". Journal of Clinical Anesthesia. 5 (4): 332–41. PMID 8373615. Retrieved 2012-04-17.
  8. ↑ Willcourt RJ, King JC, Queenan JT (1983). "Maternal oxygenation administration and the fetal transcutaneous PO2". American Journal of Obstetrics and Gynecology. 146 (6): 714–5. PMID 6869444. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  9. ↑ Shime J, Mocarski EJ, Hastings D, Webb GD, McLaughlin PR (1987). "Congenital heart disease in pregnancy: short- and long-term implications". American Journal of Obstetrics and Gynecology. 156 (2): 313–22. PMID 3826166. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  10. ↑ McFaul PB, Dornan JC, Lamki H, Boyle D (1988). "Pregnancy complicated by maternal heart disease. A review of 519 women". British Journal of Obstetrics and Gynaecology. 95 (9): 861–7. PMID 3191059. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  11. ↑ Selzer A (1977). "Risks of pregnancy in women with cardiac disease". JAMA : the Journal of the American Medical Association. 238 (8): 892–3. PMID 577983. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  12. ↑ Jevon P, Raby M. Physiological and anatomical changes in pregnancy relevant to resuscitation. In: O'Donnell E, Pooni JS, editors. Resuscitation in Pregnancy. A practical approach. Oxford: Reed Educational and Professional Publishing Ltd.; 2001. p. 10-16.
  13. ↑ Morris S, Stacey M. Resuscitation in pregnancy. BJM 2003;327:1277-1279.


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