Cardiac disease in pregnancy pathophysiology: Difference between revisions

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{{Cardiac disease in pregnancy}}
{{Cardiac disease in pregnancy}}
{{CMG}}; {{AOEIC}} {{CZ}}
{{CMG}}; {{AOEIC}} {{CZ}}; {{AC}}; {{LG}}


==Physiology of Labor and Delivery==  
==Overview==
*Hemodynamics are altered substantially during labor and delivery secondary to [[anxiety]], [[pain]], and [[contractions|uterine contractions]].  Oxygen consumption increases threefold, and [[cardiac output]] rises progressively during [[labor]] owing to increases in both [[stroke volume]] and [[heart rate]]. [[Blood pressure]] is higher in the lateral position. Both the [[systolic blood pressure|systolic]] and [[diastolic blood pressure]] increase markedly during [[uterine contractions]] with a greater augmentation during the second stage. The form of anesthesia impacts the [[blood pressure]]. <br>
There are significant hemodynamic changes associated with pregnancy that begin early, reach their peak during the second trimester, and persist through delivery.  These changes include a 40% increase in blood volume expansion, reductions in both the [[systemic vascular resistance]] and [[pulmonary vascular resistance]], a 30% rise in [[cardiac output]] and little change in the [[blood pressure]].  These changes can have a significant impact on both the mother and the fetus, particularly when there are maternal cardiac disorders.
==Pathophysiology==
===Effect of Pregnancy on Maternal Physiology===
====I. Hormonal Changes====
=====Increased Progesterone Levels=====
:*During early stages of pregnancy, prior to full placentation, [[progesterone]] is produced by the [[corpus luteum]].
:*Increased progesterone  decreases smooth muscle tone which decreases the [[systemic vascular resistance]] ([[SVR]]).<ref name="pmid9853271">{{cite journal| author=Chapman AB, Abraham WT, Zamudio S, Coffin C, Merouani A, Young D et al.| title=Temporal relationships between hormonal and hemodynamic changes in early human pregnancy. | journal=Kidney Int | year= 1998 | volume= 54 | issue= 6 | pages= 2056-63 | pmid=9853271 | doi=10.1046/j.1523-1755.1998.00217.x | pmc= | url= }} </ref>


*By the time of delivery the [[cardiac output]] has increased by 50%, the [[plasma volume]] has increased by 40% and the [[red cell mass]] has increased by 25 to 30%. <br>
=====Increased Estrogen Levels=====
:* Elevated estrogen levels may increase myocardial contractility.<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=Am J Physiol | year= 1989 | volume= 256 | issue= 4 Pt 2 | pages= H1060-5 | pmid=2705548 | doi= | pmc= | url= }} </ref>


*The work of labor may increase the [[cardiac output]] by 60% over the baseline level. <br>
=====Increased Renin and Aldosterone Levels=====
:*[[Peripheral vasodilation]] subsequently causes [[vasodilation|renal vasodilation]] and activation of the [[renin-angiotensin-aldosterone system]],<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> which results in:
:::*Increased sodium and water retention.
:::*Compensation for the decreased [[systemic vascular resistance]].
:*Increased [[renin]] and [[aldosterone]] levels are caused by increased [[estrogen]]


*During the second stage of [[labor]] the patient is on her back there is [[venous stasis]], [[heart rate]] increases to greater than 120/min and the [[blood pressure]] may be more than 150 mm Hg. <br>
====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-weeks of gestation and is referred to as the '''''physiologic anemia of pregnancy'''''.
:*The [[hematocrit]] may drop to 33-38%.<ref name="pmid5621454">{{cite journal| author=Lund CJ, Donovan JC| title=Blood volume during pregnancy. Significance of plasma and red cell volumes. | journal=Am J Obstet Gynecol | year= 1967 | volume= 98 | issue= 3 | pages= 394-403 | pmid=5621454 | doi= | pmc= | url= }} </ref>
:*A greater increase in [[blood volume]] may be observed among multigravidas.<ref name="pmid5621454">{{cite journal| author=Lund CJ, Donovan JC| title=Blood volume during pregnancy. Significance of plasma and red cell volumes. | journal=Am J Obstet Gynecol | year= 1967 | volume= 98 | issue= 3 | pages= 394-403 | pmid=5621454 | doi= | pmc= | url= }} </ref>
:*An increase in [[atrial natriuretic peptide]] levels is observed in response to changes in intravasular volume.<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>


*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.
====III. Cardiac Output====
:*There is a higher volume of more dilute blood to circulate.<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=Am J Physiol | year= 1989 | volume= 256 | issue= 4 Pt 2 | pages= H1060-5 | pmid=2705548 | doi= | pmc= | url= }} </ref>
:* There is approximately a 50% increase in [[cardiac output]] which is required to oxygenate the fetus.
:* The increase in [[cardiac output]] begins as early as the 5<sup>th</sup> week of gestation and steadily increases up to the 24<sup>th</sup> week of gestation after which time it plateaus.<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><ref name="pmid3322367">{{cite journal |author=Robson SC, Hunter S, Moore M, Dunlop W |title=Haemodynamic changes during the puerperium: a Doppler and M-mode echocardiographic study |journal=[[British Journal of Obstetrics and Gynaecology]] |volume=94 |issue=11 |pages=1028–39 |year=1987 |month=November |pmid=3322367 |doi= |url= |accessdate=2012-04-17}}</ref>


===Hemodynamic effect of Cesarean Section:===
:* The initial increase in [[cardiac output]] is attributed to an increase in [[stroke volume]], whereas during late trimesters, it is attributed to an increase in [[heart rate]] and a reduction in [[systemic vascular resistance]].<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>
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:===
:* 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.
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.
:*Several factors influence the changes observed in [[cardiac output]] during pregnancy.  Serial hemodynamic measurements performed in the supine position may be erroneous secondary to the compression of the [[IVC|inferior vena caval]] by the enlarging uterus which subsequently decreases the [[venous return]] from the lower extremities. Therefore, owing to the caval compression, [[cardiac output]] has been shown to decline in the supine position whereas the [[cardiac output]] 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>


Hemodynamic adaptation of pregnancy persists postpartum and gradually returns to prepregnancy values within 12-24 weeks after delivery.
:*Precipitation of [[heart failure|high cardiac output failure]] may be observed in some patients secondary to the shunting of blood within the [[placenta]] where it may pass from [[arterioles]] to [[venules]] bypassing the [[capillaries]].


==Effect of Pregnancy on Maternal Physiology==
====IV. Blood Pressure====
:*Arterial blood pressure begins to fall during the first trimester, reaching a nadir during the mid trimester (usually 10 mm Hg 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>


====Corpus uteum produces progesterone====
:*A [[Wide pulse pressure|widened pulse pressure]] is present because there is a more substantial reduction in the [[diastolic blood pressure]] when compared with the [[systolic blood pressure]].
:* increased [[progesterone]] → decreased smooth muscle tone → therefore decreased [[systolic vascular resistance]].
:* later in pregnancy the placenta produces progesterone.


====Increased estrogen levels====
:*A drop in the [[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>
:* may increase contractility of heart.


====Increased renin and aldosterone levels caused by increased estrogen====
:* The [[blood pressure]] remains relatively unchanged when measured in the left lateral recumbent position. However, the '''''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 a possible explanation for this syndrome.  Symptoms usually subside when the patient changes from the supine position.<ref name="pmid19781045">{{cite journal| author=Almeida FA, Pavan MV, Rodrigues CI| title=The haemodynamic, renal excretory and hormonal changes induced by resting in the left lateral position in normal pregnant women during late gestation. | journal=BJOG | year= 2009 | volume= 116 | issue= 13 | pages= 1749-54 | pmid=19781045 | doi=10.1111/j.1471-0528.2009.02353.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19781045  }} </ref>
:* enhances Na and water retention.  
:* compensates for the decreased [[systemic vascular resistance]].
:* by the middle trimester, [[plasma volume]] is increased by 40 to 45%.
:* hemodilution → [[anemia]], but total [[red cell mass]] is not decreased. Rate of rise in volume is more rapid than rate of rise in red cell mass. This occurs until week 30 and is referred to as the physiologic [[anemia]] of pregnancy. The hematocrit can be as low as 33% to 38%.
:* starts as early as 6 weeks.
:* greater increase in [[blood volume]] among multigravidas.


====Cardiac output increases by 50%====
====V. Respiratory Rate====
:* have a higher volume of more dilute blood to circulate.
:* An increased [[respiratory rate]] is present secondary to increased abdominal pressure and accompanying elevation of the diaphragm.
:* need well oxygenated blood to circulate to the fetus.
:* An increased [[respiratory rate]] subsequently lowers the carbon dioxide tension.
:* begins to rise at 5<sup>th</sup> week, and [[cardiac output]] increases until week 24 at which time it plateaus.
:* resting [[heart rate]] increases by 10 to 15 beats per minute. Pregnancy with multiple fetuses is associated with even more rapid heart rates.
:* [[blood pressure]] remains relatively unchanged when measured in the left lateral recumbent position.
:* hemodynamics measured in the supine position are erroneous because the uterus compresses the IVC decreasing the return from the lower extremities. Therefore may have syncope when a gravid stands up from a supine position.
:* keep in mind that much of the blood is shunted to the placenta where it may pass from arterioles to venules bypassing the capillaries. May precipitate [[heart failure|high cardiac output failure]] in some women.
:* cardiac output increases in the lateral position and declines in the supine position owing to caval compression by the gravid uterus.
:* the increase in [[cardiac output]] in early pregnancy is due to an increase in [[stroke volume]] early on, but in the third trimester it is due to an increase in [[heart rate]].


====Increased respiratory rate====
====VI. Gastrointestinal Changes====
:* secondary to increased abdominal pressure, elevation of the diaphragm.
:* Reduced [[gastric emptying]] secondary to reduced gastrointestinal motility is observed during pregnancy.
:* lowers carbon dioxide tension.


====Blood pressure====
:* An incompetent gastro-oesophageal sphincter leads to [[GERD|gastro-oesophageal reflux]] with an increased risk of aspiration of gastric contents into the [[trachea]].
:* arterial pressure begins to fall during the first trimester reaches a  nadir in mid pregnancy and returns toward pregestational levels before term.
:* 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.
:* 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.


====Gastrointestinal changes====
:* Intra-gastric pressure increases during the last 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. Hematologic Changes in Pregnancy====
:*There is an increase in [[clotting factor]] concentration
:*There is an increase in platelet adhesiveness
:*There is a decrease in [[fibrinolysis]] and [[protein S]] activity
:*As a result of all of the above, there is an increased risk of thormbosis and embolism
====VIII. 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>


==Fetal Physiology==
===Physiology of Labor and Delivery===
====Hemodynamic Changes During Labor and Delivery:====
*Hemodynamics are altered substantially during labor and delivery secondary to increased sympathetic tone caused by [[anxiety]], [[pain]], and [[contractions|uterine contractions]].


* Uterine blood flow increases by a factor of 50 during pregnancy <br>
*These changes include:
* The uterine blood vessels remain dilated throughout pregnancy <br>
::*Oxygen consumption increases by threefold.
* Transfer of oxygen across the placenta is flow-limited. <br>
::*[[Cardiac output]] rises progressively during [[labor]] owing to an increase in both [[stroke volume]] and [[heart rate]]. The work of labor has also shown to increase [[cardiac output]] by 60% over the baseline.
* Fetal oxygen tension is normally quite low (30 to 40 mmHg) <br>
::*[[Blood pressure]] is higher in the left lateral position. During [[uterine contractions]], a marked increase in both the [[systolic blood pressure|systolic]] and [[diastolic blood pressure]] is observed with a greater augmentation during the second stage of labor.  The form of anesthesia impacts the [[blood pressure]].<ref>PRITCHARD JA. CHANGES IN THE BLOOD VOLUME DURING PREGNANCY AND DELIVERY,  Anesthesiologyvolume 26, pages 393–9, 1965.</ref>
* Supplemental oxygen to the mother is quite effective in increasing fetal oxygen, particularly with [[fetal distress]]. <br>
*During the second stage of [[labor]], an increase in [[venous stasis]], [[heart rate]] ''(greater than 120 beats/min)'' and [[blood pressure]] ''(more than 150 mmHg)'' is observed.<ref name="pmid290123">{{cite journal| author=Kjeldsen J| title=Hemodynamic investigations during labour and delivery. | journal=Acta Obstet Gynecol Scand Suppl | year= 1979 | volume= 89 | issue=  | pages= 1-252 | pmid=290123 | doi= | pmc= | url= }} </ref>
* Normal fetal pH is 7.35. Fetal scalp pHs <7.25 are abnormal. <br>
 
* Labor can precipitate [[fetal distress]] because during uterine contractions, uterine blood flow is nearly occluded. <br>
*By the time of delivery, [[cardiac output]] has increased by 50%, the plasma volume has increased by 40% and the red cell mass has increased by 25% to 30%.
* In a mother with [[cyanosis]], it is easier for problems to arise during labor because of the reduced reserve in oxygen delivery. <br>
 
* With contractions, there may normally be a reduction or deceleration in the fetal heart rate, but this rapidly returns to normal. <br>
*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 patients with [[coronary heart disease]].
* In fetal distress, the decelerations are later in the contraction and persist, i.e. late decelerations. <br>
 
* 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. <br>
====Hemodynamic effects of Cesarean Section:====
* Placing the mother in the left lateral recumbent position and oxygen will relieve many cases of fetal distress. <br>
*To avoid the hemodynamic changes associated with [[vaginal delivery]], [[cesarean section]] is frequently recommended for women with cardiovascular disease.
* Fetal monitoring should be used in the presence of maternal heart disease, cardiac surgery, cardioversion. <br> <br>
 
*[[Cesarean section]] is also associated with hemodynamic fluctuations that are related to [[intubation]], [[analgesia]] and the choice of [[anesthesia]]. Most common form of anesthesia used is [[epidural]] which significantly reduces pain but is also associated with significant [[peripheral vasodilation]] and subsequent [[hypotension]].
 
*[[Cesarean section]] is associated with greater extent of [[blood loss]] as well as provides relief of [[IVC|caval]] compression.<ref name="pmid15762965">{{cite journal| author=Tihtonen K, Kööbi T, Yli-Hankala A, Uotila J| title=Maternal hemodynamics during cesarean delivery assessed by whole-body impedance cardiography. | journal=Acta Obstet Gynecol Scand | year= 2005 | volume= 84 | issue= 4 | pages= 355-61 | pmid=15762965 | doi=10.1111/j.0001-6349.2005.00489.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15762965  }} </ref>
 
====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.<ref name="pmid5761774">{{cite journal| author=Ueland K, Hansen JM| title=Maternal cardiovascular dynamics. II. Posture and uterine contractions. | journal=Am J Obstet Gynecol | year= 1969 | volume= 103 | issue= 1 | pages= 1-7 | pmid=5761774 | doi= | pmc= | url= }} </ref>
 
*Effective increase in [[venous return]] and [[blood volume]], despite the blood loss occurred during delivery, results in a substantial increase in ventricular filling pressures, [[stroke volume]], and [[cardiac output]] that may lead to clinical deterioration.
 
*Both [[heart rate]] and [[cardiac output]] return to pre-gestational values by an hour after delivery. However, it takes about 24-hours for the [[blood pressure]] and [[stroke volume]] to return to baseline.
 
*Hemodynamic adaptation of pregnancy persists postpartum and gradually returns to pre-gestational 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==
==References==
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Latest revision as of 20:48, 29 July 2020

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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]; Anjan K. Chakrabarti, M.D. [3]; Lakshmi Gopalakrishnan, M.B.B.S. [4]

Overview

There are significant hemodynamic changes associated with pregnancy that begin early, reach their peak during the second trimester, and persist through delivery. These changes include a 40% increase in blood volume expansion, reductions in both the systemic vascular resistance and pulmonary vascular resistance, a 30% rise in cardiac output and little change in the blood pressure. These changes can have a significant impact on both the mother and the fetus, particularly when there are maternal cardiac disorders.

Pathophysiology

Effect of Pregnancy on Maternal Physiology

I. Hormonal Changes

Increased Progesterone Levels
Increased Estrogen Levels
  • Elevated estrogen levels may increase myocardial contractility.[2]
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-weeks of gestation and is referred to as the physiologic anemia of pregnancy.
  • The hematocrit may drop to 33-38%.[3]
  • A greater increase in blood volume may be observed among multigravidas.[3]
  • An increase in atrial natriuretic peptide levels is observed in response to changes in intravasular volume.[1]

III. Cardiac Output

  • There is a higher volume of more dilute blood to circulate.[2]
  • There is approximately a 50% increase in cardiac output which is required to oxygenate the fetus.
  • The increase in cardiac output begins as early as the 5th week of gestation and steadily increases up to the 24th week of gestation after which time it plateaus.[2][4]
  • 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 the supine position may be erroneous secondary to the compression of the inferior vena caval by the enlarging uterus which subsequently decreases the venous return from the lower extremities. Therefore, owing to the caval compression, cardiac output has been shown to decline in the supine position whereas the cardiac output increases in the left lateral position.[5][6]

IV. Blood Pressure

  • Arterial blood pressure begins to fall during the first trimester, reaching a nadir during the mid trimester (usually 10 mm Hg below baseline) and returns toward pre-gestational levels before term.[7][8]
  • The blood pressure remains relatively unchanged when measured in the left lateral recumbent position. However, the 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 a possible explanation for this syndrome. Symptoms usually subside when the patient changes from the supine position.[13]

V. Respiratory Rate

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

VI. Gastrointestinal Changes

  • Reduced gastric emptying secondary to reduced gastrointestinal motility is observed during pregnancy.
  • Intra-gastric pressure increases during the last trimester.[14]

VII. Hematologic Changes in Pregnancy

  • There is an increase in clotting factor concentration
  • There is an increase in platelet adhesiveness
  • There is a decrease in fibrinolysis and protein S activity
  • As a result of all of the above, there is an increased risk of thormbosis and embolism

VIII. Other Changes in Pregnancy

  • Flared ribs.
  • Breast hypertropy which may impede effective resuscitation.[15]

Physiology of Labor and Delivery

Hemodynamic Changes During Labor and Delivery:

  • Hemodynamics are altered substantially during labor and delivery secondary to increased sympathetic tone caused by anxiety, pain, and uterine contractions.
  • These changes include:
  • By the time of delivery, cardiac output has increased by 50%, the plasma volume has increased by 40% and the red cell mass has increased by 25% to 30%.

Hemodynamic effects of Cesarean Section:

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.[19]
  • Hemodynamic adaptation of pregnancy persists postpartum and gradually returns to pre-gestational 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 1.3 Chapman AB, Abraham WT, Zamudio S, Coffin C, Merouani A, Young D; et al. (1998). "Temporal relationships between hormonal and hemodynamic changes in early human pregnancy". Kidney Int. 54 (6): 2056–63. doi:10.1046/j.1523-1755.1998.00217.x. PMID 9853271.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Robson SC, Hunter S, Boys RJ, Dunlop W (1989). "Serial study of factors influencing changes in cardiac output during human pregnancy". Am J Physiol. 256 (4 Pt 2): H1060–5. PMID 2705548.
  3. ↑ 3.0 3.1 Lund CJ, Donovan JC (1967). "Blood volume during pregnancy. Significance of plasma and red cell volumes". Am J Obstet Gynecol. 98 (3): 394–403. PMID 5621454.
  4. ↑ 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)
  5. ↑ 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)
  6. ↑ Metcalfe J, Ueland K (1974). "Maternal cardiovascular adjustments to pregnancy". Progress in Cardiovascular Diseases. 16 (4): 363–74. PMID 4368892. Retrieved 2012-04-17.
  7. ↑ 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)
  8. ↑ 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.
  9. ↑ 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)
  10. ↑ 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)
  11. ↑ 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)
  12. ↑ 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)
  13. ↑ Almeida FA, Pavan MV, Rodrigues CI (2009). "The haemodynamic, renal excretory and hormonal changes induced by resting in the left lateral position in normal pregnant women during late gestation". BJOG. 116 (13): 1749–54. doi:10.1111/j.1471-0528.2009.02353.x. PMID 19781045.
  14. ↑ 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.
  15. ↑ Morris S, Stacey M. Resuscitation in pregnancy. BJM 2003;327:1277-1279.
  16. ↑ PRITCHARD JA. CHANGES IN THE BLOOD VOLUME DURING PREGNANCY AND DELIVERY, Anesthesiologyvolume 26, pages 393–9, 1965.
  17. ↑ Kjeldsen J (1979). "Hemodynamic investigations during labour and delivery". Acta Obstet Gynecol Scand Suppl. 89: 1–252. PMID 290123.
  18. ↑ Tihtonen K, Kööbi T, Yli-Hankala A, Uotila J (2005). "Maternal hemodynamics during cesarean delivery assessed by whole-body impedance cardiography". Acta Obstet Gynecol Scand. 84 (4): 355–61. doi:10.1111/j.0001-6349.2005.00489.x. PMID 15762965.
  19. ↑ Ueland K, Hansen JM (1969). "Maternal cardiovascular dynamics. II. Posture and uterine contractions". Am J Obstet Gynecol. 103 (1): 1–7. PMID 5761774.


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