Cardiovascular Alterations in the Parturient Undergoing Cesarean Delivery With Neuraxial Anesthesia

Katherine W Arendt; Jochen D Muehlschlegel; Lawrence C Tsen

Disclosures

Expert Rev of Obstet Gynecol. 2012;7(1):59-75. 

In This Article

Delivery of the Fetus

Fetal delivery is associated with dramatic hemodynamic changes. As the uterus is evacuated, aortocaval compression is relieved and an autotransfusion of uterine blood occurs as the uterine muscle involutes to a contracted state. This increase in cardiac preload typically results in an increase in CO through an increase in both HR and SV. A decrease in SVR can result in an unchanged MAP.[40,96,101] These hemodynamic alterations are believed to exist for approximately 10 min[40] prior to resolution to predelivery values. The increase in CO at the time of fetal delivery varies significantly, with a range of less than 10%,[98] to as much as 61% (from baseline) and 140% (from post-block values).[66] The latter values were originated in a study where uterine displacement was not used, likely exaggerating the removal of uterine aortocaval compression upon delivery.

Contribution of Blood Loss

The mean blood loss during CD of a singleton fetus historically was estimated to be as high as 1 l,[102] but more recently (using a hemoglobin extraction test before and after cesarean) has been found to be approximately 440 ml with a wide range of variability (135–1000 ml).[103] Additional blood loss can result from peripartum bleeding, uterine atony or injury, or placental abnormalities. Blood loss and resuscitation can significantly affect hemodynamic values. Blood loss reduces circulating volume, most often resulting in decreased preload, stroke volume, CO and MAP. In healthy parturients, MAP may remain normal until over 1500 ml of blood are lost, making hypotension a late sign of hemorrhage.[104] When blood loss is replaced with crystalloid or colloids sufficient to maintain normovolemia, decreased blood viscosity and anemia can result in increased CO. A healthy parturient may tolerate such physiologic alterations as long as red cell mass maintains adequate oxygen-carrying capacity to the tissues.

Contribution of Uterotonic Agents

Uterotonic agents administered to prevent blood loss immediately after delivery affect maternal hemodynamics. Oxytocin has a direct relaxation effect on vascular smooth muscle, causing a decrease in systolic and diastolic blood pressure related in part to the dose and rate of administration.[105] Consequently, it has been recommended that anesthesia providers administer oxytocin in smaller amounts, which have proven to be efficacious for restoring uterine tone, and not as a bolus dose.[106]

A recent case series used pulse wave analysis (PulseCO system, LiDCO Ltd, Cambridge, UK) to follow MAP, SVR and CO in six cesarean deliveries.[101] Upon administration of 5 units of oxytocin, a decrease in MAP was associated with a decrease in SVR and an increase in CO, SV and HR. Interestingly, a different study showed that a second bolus of oxytocin 5 units produced hemodynamic effects as well, but to a lesser degree than the initial bolus.[107] It is possible that the sympathetic blockade of neuraxial anesthesia may exacerbate the decrease in SVR associated with oxytocin administration.[108]

Methylergonovine maleate (Methergine®), a sympathomimetic α-agonist, causes intense venous and arterial vasoconstriction that can result in significant hemodynamic effects. As such, this agent should be used with caution in parturients with preexisting hypertension, pregnancy-induced hypertension or preeclampsia. Moreover, because such cardiovascular effects are frequently related to the route and speed of administration, intramuscular administration is recommended. Even intramuscular administration, however, can cause an elevation in SBP in 20% of recipients with a duration of several hours.[109]

Carboprost tromethamine (15-methyl prostaglandin F2α or Hemabate®) is a uterotonic agent that causes systemic vasodilation, which may result in hypotension and a reflex elevation in HR. More concerning, Hemabate can cause both arterial and venous pulmonary circulation vasoconstriction with elevations in pulmonary arterial pressure and wedge pressure, and an overall change in the pattern of regional pulmonary blood flow.[19] Consequently, Hemabate is administered intramuscularly in an attempt to mitigate these side effects. There is currently little data as to the hemodynamic effects of misoprostol (Cytotec®), a synthetic E1 prostaglandin analogue that can be administered rectally or buccally to produce uterine contractions.

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