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

Neuraxial Anesthesia Onset: Spinal

Spinal anesthesia is the most common anesthetic employed for elective CD. It provides a rapid, symmetrical, dense motor and sensory block, and allows the parturient to be awake for the birth of her baby. However, the hemodynamic changes that occur with the induction of spinal anesthesia are common and often profound.

Contribution of Arterial & Venous Peripheral Resistance

When spinal anesthesia is administered for CD, a rapid onset block of the lumbosacral and thoracic dermatomes occurs. The resulting preganglionic sympathetic blockade of the thoracic spine likely leads to relatively unopposed parasympathetic tone in the vasculature and, as a result, arterial and venous dilation. In general, it is thought that the level of the sympathectomy extends two to six dermatomal levels above the sensory block when measured by skin temperature changes.[59] Some experts have held that the hemodynamic effects of this relative sympathectomy on venodilation supersedes that of arterial dilation, because 75% of the body's blood is contained within the venous system and the arteries maintain greater autonomous tone.[60] As a consequence, overcoming the loss in preload has historically been an important strategy in maintaining CO when treating post-spinal hypotension. However, the observation that neither prehydration nor co-loading can reliably prevent hypotension following neuraxial blockade[46–49] underscores that the role of venodilation may have been historically overemphasized. Furthermore, it has been suggested that if CO is maintained, total peripheral resistance should decrease by only 15–18% in normovolemic healthy patients, even with a relative sympathectomy.[60] However, data from parturients undergoing spinal anesthesia for CD have demonstrated a decrease (from baseline) in SVR in the range of 26–31%,[40,52,61] begging the question of whether arterial vasodilation plays a greater role than previously anticipated. Finally, more recent studies specifically looking at the arterial circulation[41,62,63] have led experts to believe that it is possible that the role of preload in spinal hypotension has been overemphasized,[64] and "in the fluid replete parturient undergoing elective cesarean delivery, moderate spinal hypotension (20% decrease from baseline) primarily reflects decreased systemic vascular resistance".[65]

Contribution of Cardiac Output Variability

There is a wide variation in CO alterations when the spinal block is being established (Table 2). Using a dye dilution technique, Ueland et al. demonstrated a 35% decrease in CO when a spinal anesthetic was performed (tetracaine 7–10 mg with epinephrine 200 mcg) without prehydration, and the pregnant patient placed in the supine position.[66] By contrast, utilizing the beat-to-beat CO measurements provided by bioimpedance, Tihtonen et al. observed an immediate 11% increase in CO when 10 ml/kg colloid prehydration was given, hyperbaric bupivacaine 12–13.5 mg was administered, the patient was positioned in left uterine displacement, and a mean ephedrine dose of 0.53 mg/kg was provided.[40] The prehydration, left uterine displacement and ephedrine used in the latter study could have resulted in the CO differences observed. However, other studies utilizing both bioimpedance and LiDCO measurement techniques have confirmed this immediate increase in CO observed after induction of spinal anesthesia, even when phenylephrine, and not ephedrine, is administered.[41,63] Other factors that affect CO include, but are not limited to, prehydration, maternal positioning during and after the block, height and density of the block, presence of hypertensive disorders of pregnancy, gestational age, the number of gestations, the presence of labor, the prophylactic or therapeutic use of vasoactive substances, and the complex system of vascular tone and reactivity unique to each individual woman.

Direct and indirect cardiac output measurements are infrequently performed during a typical cesarean delivery. Instead, fetal heart rate activity is often correlated to a range of noninvasive blood pressure measurements to give an indication of the adequacy of uteroplacental blood flow. Following the removal of fetal heart rate monitors for skin sterilization of the abdomen, systolic blood pressure (SBP) is typically maintained within 20% of baseline values, or above a SBP of 100 mmHg (a common research definition of hypotension). Hypotension is typically poorly tolerated in parturients, often resulting in nausea, vomiting and lightheadedness. Spinal-induced hypotension in parturients undergoing CD is frequent, with reported incidences ranging from 17 to 95%.[51,67] The associated maternal and fetal morbidity and mortality associated with hypotension have investigators seeking clinically feasible and reliable ways to predict which parturients are at greatest risk.[68–70] Maternal HR variability as a measure of autonomic nervous system activity appears promising in predicting hypotension risk.[71–74]

The most effective strategies for prevention of spinal-induced hypotension include prehydration with a sufficient amount of colloid[51] or co-loading with sufficient crystalloid,[45] positioning the parturient for surgery in the left uterine displacement position,[75] using a lower dose of intrathecal bupivacaine,[63,76–78] and administering prophylactic vasoactive agents such as ephedrine or phenylephrine.[63,79,80] Each of these strategies will be reviewed, with their relative efficacy summarized (Box 1).

Contribution of Block Height

One factor affecting hemodynamic changes at the onset of spinal anesthesia is block height. Typically, the higher the thoracic level of intrathecal block, the greater the hemodynamic effect.[81] The height of a spinal block is associated with the dose and baricity of the local anesthetic. Doses of bupivacaine ranging from 4.5 to 15 mg intrathecal bupivacaine have been described as adequate for CD, but the higher doses have resulted in greater decreases in arterial blood pressure in both nonpregnant[82] and pregnant patients.[83]

To maintain adequate blood pressure for uteroplacental blood flow, multiple studies have sought to evaluate the lowest dose of intrathecal local anesthetic that can provide adequate anesthesia for CD.[63,76,78,84,85] An excellent review of such studies has been previously published.[86] The addition of opioids allows for lesser intrathecal local anesthetic dosing, and often lesser hemodynamic effects, while still allowing for adequate anesthesia.[84] The data comparing hyperbaric to isobaric bupivacaine are confounding; for example, hyperbaric (vs isobaric) bupivacaine 6.6 mg combined with sufentanil 3.3 mcg demonstrated lesser hemodynamic effects.[87] Alternatively, a similar study showed no differences in hemodynamic changes when hyperbaric versus isobaric bupivacaine 9 mg, combined with fentanyl 20 mcg, were used.[88]

Contribution of Heart Rate

Some studies indicate limited HR changes as a result of spinal anesthesia.[40,52,61,89] However, it is not uncommon to initially see an increase in HR with induction of spinal anesthesia.[63] This is likely from preservation of the baroreceptor response and the initial dilation of vasculature associated with spinal anesthesia. Subsequently, if the sympathetic block travels high enough, HR slowing may occur with a reduction in sympathetic output from the cardioaccelerator fibers located at the T1 through T4 levels. Because achieving a T4 sensory level is frequently the goal for CD anesthesia, a sympathetic blockade of the cardioaccelerator fibers may occur. However, significant bradycardia occurs in less than 2% of all cases.[90] Because CO is the product of HR and SV, it is important to note that as HR decreases, CO may also decrease, depending on whether alterations in SV can compensate for the change. This may be especially relevant during the onset of neuraxial anesthesia because venodilation results in decreased preload and an inability to increase SV to compensate for a decreased HR.

Significant bradycardia may be a cause of cardiac arrest under spinal anesthesia in otherwise healthy patients.[91–93] Although these cases may result from cardioaccelerator fiber blockade, other cardiac mechanisms are more likely responsible. A sudden decrease in preload activates intrinsic cardiac receptors such as baroreceptors in the right atrium, mechanoreceptors in the left ventricle, or receptors in cardiac pacemaker cells leading to a decrease in HR; this mechanism is supported by the observation that HR decreases in transplanted hearts after spinal anesthesia.[94]

In summary, the effect of intrathecal local anesthetic on HR most often depends upon the height of the block; blocks extending to the first through fourth thoracic sympathetic spinal levels affect the cardiac acceleration fibers and potentially cause bradycardia. A study has shown that increased doses of intrathecal hyperbaric bupivacaine increase the likelihood of bradycardia.[76]

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