Spinal anesthesia is the most widely used anesthetic for cesarean delivery performed in the United States and the United Kingdom.1,2 While generally considered safe, recognized adverse effects in both parturient and nonparturient populations include hypotension, arrhythmia, and cardiac arrest.3–5 Published cases of arrhythmia most frequently involve first-degree atrioventricular (AV) block. We describe a patient in whom third-degree AV block occurred during spinal anesthesia for cesarean delivery. Although our patient was healthy and suffered no morbidity, there is a trend toward increasing maternal age and congenital heart disease in adulthood. Parturients may therefore present with cardiac disease in increasing numbers. The consequences of this arrhythmia may be more severe in those with comorbid cardiac disease.
The patient reviewed the case report and gave written permission for publication.
A 34-year-old woman G2P1001 (weight 83 kg, height 1.57 m) was scheduled for an elective repeat cesarean delivery at 39.6 weeks of gestation. Her previous cesarean delivery was uneventful and performed secondary to an arrest of cervical dilation in the setting of preeclampsia under epidural anesthesia. This pregnancy was without medical complications. Her medical history was significant for 2 isolated episodes of syncope as a teenager, occurring in the setting of prolonged periods of standing. Both were sudden and not preceded by symptoms. Preoperative clinical evaluation was unremarkable, and hematological and biochemical investigations were normal. Spinal anesthesia for cesarean delivery was discussed, and the patient agreed.
She received routine premedication with 30 mL oral sodium citrate. Standard American Society of Anesthe siologists monitors were applied. Her baseline arterial blood pressure was 122/86 mm Hg and SpO2 was 100% while breathing room air. The initial electrocardiograph (ECG) displayed sinus rhythm with normal PR interval at a rate of 69 bpm. Before the regional anesthetic, the patient received 750 mL Ringer’s lactate solution through an 18-gauge IV cannula. With the patient in the sitting position, a 25-gauge Whitacre spinal needle was introduced at the L4-L5 interspace. When the free flow of cerebrospinal fluid was confirmed, 12 mg hyperbaric 0.75% bupivacaine, 10 mcg fentanyl, and 200 mcg preservative-free morphine were injected intrathecally. The patient was immediately positioned supine while manually using left uterine displacement. As per institutional practice, an infusion of phenylephrine was started at 25 mcg/min. She was given supplementary oxygen via facemask at 6 L/min. Four minutes after injection, her arterial blood pressure decreased to 83/41 mm Hg. Her heart rate remained stable at 64 bpm. The phenylephrine infusion was increased to 50 mcg/min, and a bolus of 160 mcg phenylephrine was administered IV. The patient complained of dizziness and nausea. Over the following minute, bradycardia was observed, and the ECG showed worsening bradyarrhythmia that progressed from sinus to Mobitz type I and finally to third-degree AV block at 29 bpm, Figure 1. The patient appeared pale and diaphoretic and complained of worsening lightheadedness, nausea, and now headache. Her legs were raised to improve venous return; lateral uterine displacement was verified, and ephedrine 10 mg and atropine 0.4 mg were given IV. Over the next 4 minutes, there was an increase in heart rate to 56 bpm, arterial blood pressure to 196/84 mm Hg, the phenylephrine infusion was discontinued, and sinus rhythm was restored. Over the next 5 minutes, her blood pressure returned to 101/59 mm Hg. The patient’s dizziness, nausea, and physical appearance improved; however, headache persisted.
Sensory test to pinprick revealed a bilateral T4 level. The patient was reassured, and cesarean delivery was performed. Approximately 40 minutes after the administration of spinal anesthesia, a healthy baby girl, weighing 3520 g, was delivered with normal Apgar scores of 8 and 9 at 1 and 5 minutes, respectively. Third-degree AV block did not reappear during the remainder of the operation. The patient was monitored with a single lead rhythm strip for 24 hours postoperatively, and cardiology was consulted given her history of syncope. A postoperative 12-lead ECG and transthoracic echocardiogram were normal. The cardiology service did not recommend further treatment.
AV block is defined as a delay or interruption in the conduction of an electrical impulse from the atria to the ventricles secondary to an anatomical or functional impairment of the cardiac conduction system. The arrhythmia ranges from first- to third-degree blockade, with classification based on the location of the AV conduction delay. Previous descriptions of the arrhythmia during spinal anesthesia mostly detail first-degree block, with 2 mechanisms generally discussed. The first is unopposed vagal tone secondary to sympathetic blockade of the cardiac accelerator fibers arising from the first 4 thoracic spinal segments.6 The second is a consequence of decreased venous return and manifested as the Bezold–Jarisch reflex.7
The classic Bezold–Jarisch reflex is inhibitory and occurs from the mechanical or chemical stimulation of receptors located in the inferoposterior wall of the left ventricle. Stimulation increases activity through nonmyelinated afferent C fibers and leads to increased parasympathetic activity, producing bradycardia, systemic vasodilation, and hypotension. A decrease in left ventricular diastolic volume normally inhibits these receptors. However, a vigorous contraction around an underfilled ventricle can lead to a paradoxical increased activity, promoting bradycardia and hypotension.7,8
There were several possible mechanisms for bradycardia and third-degree AV block in our patient. A paradoxical reflex relating to decreased venous return is certainly possible, because bradycardia followed the onset of systemic hypotension. Resuscitation with anticholinergic, adrenergic, and α-agonist drugs, presumably resulting in increased venous return, led to an increase in heart rate. Despite the use of phenylephrine before the event, first as a low-dose infusion and then as a bolus, a drug-induced baroreceptor-mediated reflex bradycardia seems unlikely. Noninvasive arterial blood pressure measurements, at 1-minute intervals before and after spinal anesthesia, clearly demonstrated first a trend toward worsening hypotension after insertion, later followed by bradycardia, a faint pulse, and unmeasurable noninvasive blood pressure readings. While one may argue that without an intra-arterial catheter, an unmeasured episode of hypertension precipitating reflex bradycardia is conceivable; it is unlikely that this was missed given the frequency of noninvasive measurements. After the administration of multiple vasopressor drugs, hypertension occurred only with recovery from the event.
High sympathetic blockade may have also contributed to hemodynamic instability. Sympathetic blockade to the T1 dermatome can occur with a sensory block as low as T7, because it has been shown that sympathetic blockade lies cephalad to sensory blockade and with a differential of up to 6 segments.9 It is plausible that there was a T9 sensory level at the onset of the event, corresponding with a sympathetic block to the T3 dermatome.
Her history of preeclampsia may also be relevant because preeclampsia survivors have an increased risk of cardiac disease and those with early severe preeclampsia appear with earlier disease.10 In fact, a history of preeclampsia may identify those at increased risk for cardiac events compared with those with healthy pregnancies.10 We therefore consider that hypotension from the spinal anesthetic may have unmasked nonocclusive coronary artery disease. An ischemic AV node as a consequence of right coronary ischemia could have then led to third-degree AV nodal block.
In the parturient, increased blood volume, oxygen demand, and a relatively fixed stroke volume in the last trimester of pregnancy mean that maintenance of heart rate is crucial to ensure adequate cardiac output and end-organ perfusion, which includes the fetoplacental unit.11
Treatment of third-degree AV nodal block includes discontinuing AV nodal blocking drugs, treatment with atropine if the QRS complex remains narrow, temporary transcutaneous or transvenous pacing, and perhaps permanent pacemaker implantation. We propose maintaining left uterine displacement to avoid aortocaval compression, decreased venous return, and hypotension, raising the legs to promote redistribution of peripherally pooled venous blood back to the central circulation, and avoiding the head-down position because it has not sufficiently been shown to improve hypotension after spinal anesthesia.12,13 Use of ephedrine and even dilute epinephrine should be considered. However, caution is advised with epinephrine because it may result in uterine vasoconstriction, decreased uterine blood flow, and fetal anoxia.14 Ephedrine may result in fetal acidosis secondary to its β effects.15
Our patient suffered no morbidity. However, with the trend of advanced maternal age, parturients may be presenting in increasing numbers with cardiac disease.16 Investigations have shown that complications of preexisting medical conditions appear to be the fastest rising category of maternal death.10 Also, several reports indicate that advancing maternal age is strongly associated with near-miss morbidity/mortality.10,17 An awareness of third-degree AV nodal block and a familiarity with a treatment algorithm is required because the consequence may be more severe in those with comorbid cardiac disease.
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