Case Study
A 29-year-old gravida 2, para 1 woman at 34 weeks’ gestation presented to the maternity center in labor. She had no previous medical history other than a cesarean delivery for early-onset preeclampsia during her previous pregnancy. In this pregnancy, she developed increasing dyspnea over the 3 days prior to admission. The cardiotocograph (CTG) indicated variable decelerations, and the obstetrician requested emergency operative delivery. Although the patient was tachycardic (heart rate 112 beats/min) and hypertensive (blood pressure 185/110 mmHg), with sparse crackles audible in the lower chest zones bilaterally, there was no known contraindication to neuraxial anesthesia. A standard spinal anesthetic (bupivacaine 9 mg and fentanyl 10 µg in 2 ml volume) was administered with 500 ml of colloid coload. After rapid onset of a T4 sensory block to cold sensation, the obstetrician proceeded with a lower segment cesarean delivery. Shortly after delivery, the patient’s blood pressure fell from 150/95 to 85/40 mmHg, with worsening tachycardia (heart rate 130 beats/min).
As per routine practice, multiple titrated 50- to 100-µg boluses of phenylephrine were administered. Unexpectedly, the blood pressure and tachycardia did not improve, arterial oxygen desaturation was noted, and the patient became progressively more tachypneic, with the respiratory rate approaching 30 breaths/min. After preoxygenation, a rapid-sequence induction with etomidate and suxamethonium was performed, and the trachea was intubated. Rapid arterial oxygen desaturation occurred during intubation. Frank pulmonary edema was recognized when pink frothy sputum was seen in the endotracheal tube, and inotropic support and diuretic therapy using an epinephrine infusion and furosemide boluses were started. The patient was admitted to the obstetric high-dependency-care unit. Point-of-care transthoracic echocardiography (TTE) showed severe systolic heart failure (ejection fraction 15 percent). After 2 days of ventilation with positive end-expiratory pressure (PEEP) and a combination of inotrope and diuretic therapy, the patient was extubated. Echocardiography showed an improved ejection fraction of 30 percent with residual diastolic dysfunction, and full recovery was documented within 1 month.
Key Points
Hypotension is a frequent complication of spinal anesthesia in healthy women. Typically, this develops in response to reduction in sympathetic outflow below the upper level of the block, with early-onset arteriolar dilatation and a decreased systemic vascular resistance, together with some degree of venodilatation.
Prevention is most commonly achieved through coloading with IV fluids, and correction of hypotension by administration of phenylephrine.1 However, not all hypotension during spinal anesthesia is due to the above-listed effects (Table 31.1).
Increasing understanding of the cardiovascular effects of preeclampsia has lead to the appreciation of the varying pathologies that can occur in this disease.2 In particular, ventricular hypertrophy in response to hypertension may result in decreased diastolic compliance and ultimately diastolic heart failure.
Recent research has shown that patients with uncomplicated severe hypertension are less susceptible to spinal hypotension. In these patients, the usual response is mild afterload reduction.3 Acute, rapid progression of hypertension, the rapid hemodynamic shifts during labor and delivery, and/or liberal fluid management may provide the tipping point from compensated to uncompensated cardiac failure.
The obstetric anesthetist should be prepared to recognize and manage these complications.
Table 31.1 Recognition and Management of Hypotension during Spinal Anesthesia for Cesarean Delivery
| Hemodynamic changes | Causes | Recommended management |
|---|---|---|
| Hypotension, increased heart rate | Decreased systemic vascular resistance and some venodilatation: | Phenylephrine |
| ||
| Hypotension, bradycardia | Preload reduction: Bezold-Jarisch or inverse Bainbridge reflex | Anticholinergic; consider ephedrine |
| Severe persistent hypotension | Undiagnosed hypovolemia | Fluids and inotropes if necessary |
| Undiagnosed cardiac disease: | ||
| ||
| Cardiorespiratory collapse | High motor block | Full cardiopulmonary resuscitation |
| Anaphylaxis | ||
| Amniotic fluid embolism | ||
| Sepsis |
Discussion
Intrathecal anesthesia results in blockade of sympathetic innervation below the upper level of the spinal block. The resulting vasodilatation has a twofold effect. First, arteriolar dilatation dramatically reduces systemic vascular resistance to blood flow. Second, there is some increase in venous capacitance, effectively distributing the blood volume into a larger space and so directly reducing blood pressure. The increase in venous capacitance can be reduced by the administration of an IV fluid bolus at the time of onset of spinal anesthesia. This practice is referred to as coloading. Various studies have explored the value of crystalloid and colloid solutions, as well as the appropriate volume to be administered. While practices differ widely throughout the world, most practitioners are comfortable with administrating approximately 10–20 ml/kg of a crystalloid solution.
Techniques that attempt to improve venous return and limit aortocaval compression reduce, but do not prevent, spinal hypotension. Work done in the past 10 years suggests that early arteriolar dilatation is the major contributor to hypotension; this is usually accompanied by a partial compensatory increase in heart rate and cardiac output.4 Therefore, pure alpha agonists are the logical choice to restore baseline heart rate, blood pressure, systemic vascular resistance, and cardiac output. Phenylephrine has been studied extensively in this role. It is easily titrated in small aliquots or by continuous infusion and may improve fetal biochemistry and outcomes.5 Ephedrine has also been commonly used. Its action is twofold: direct beta-adrenergic receptor agonism and delayed, indirect alpha-adrenergic effects by increasing the activity of norepinephrine at the postsynaptic alpha receptors. Because most patients with spinal hypotension respond with a reflex tachycardia, the beta-adrenergic stimulation is unnecessary.
Typically, for cesarean delivery, a spinal level of at least the T5 dermatome to pinprick and temperature is desirable.6 Should spinal blockade extend above T4, progressive blockade of the cardiac accelerator fibers (T1–T4) may limit the tachycardic response to hypotension, although the baroreceptor reflex is usually well maintained. Occasionally, reflex bradycardia in response to spinal anesthesia may necessitate anticholinergic therapy.7 The prophylactic use of anticholinergic agents to counter phenylephrine-induced bradycardia is not recommended.8
Preeclampsia is a life-threatening complication of pregnancy with a complex, incompletely understood etiology.2 The pathognomonic hypertension has recently been shown through TTE to result in one of two patterns of cardiac dysfunction. This may be categorized by ventricular hypertrophy and diastolic dysfunction (heart failure with preserved ejection fraction) or occasional progression to severe systolic dysfunction and frank heart failure (heart failure with reduced ejection fraction).9 In the former instance, whereas the hypertrophied ventricle is able to maintain adequate ejection and thereby systolic function the reduction in compliance reduces diastolic filling. This diastolic dysfunction is often clinically subtle and unrecognized until decompensation due to disease progression or effects of anesthesia. In the latter instance, systolic heart failure occurs as a consequence of the inability of the hypertrophied ventricle to maintain adequate ejection. The recognition and correct management of these subtypes are essential in the avoidance of adverse outcomes. While rapid cardiac decompensation is an uncommon consequence of spinal anesthesia and cesarean delivery, understanding the pathophysiology is essential in the management of these rare events.
The importance of diastolic function in the etiology of cardiac failure cannot be underestimated. Typically, preeclampsia represents a hyperdynamic state with increased contractility, left ventricular hypertrophy, raised systemic vascular resistance, and diastolic dysfunction.10 This produces abnormalities of left ventricular diastolic filling. The heart becomes progressively more dependent on atrial contraction to ensure adequate ventricular filling. The gradual increase in left ventricular end-diastolic pressure probably contributes to the development of pulmonary edema.
The incidence in preeclampsia of progression to heart failure with reduced ejection fraction is unknown; one previous paper described systolic heart failure in 4 of 16 patients with pulmonary edema.11 Recognition of the cause of cardiac dysfunction (whether diastolic or systolic) is essential for the safe management of these patients.2
The vast majority of cases of uncomplicated severe preeclampsia with isolated diastolic dysfunction develop minimal spinal hypotension, and cardiac output is well maintained (Figure 31.1). Such spinal hypotension responds rapidly to conventional vasopressor therapy using phenylephrine, in preference to excessive fluid administration.12 However, a poor or paradoxical response should prompt the obstetric anesthesiologist to search rapidly for an alternative cause. Volume overload will frequently be signaled by worsening respiratory function, desaturation, and the development of pulmonary edema. Failure of adequate contractile function and ejection should respond better to inotropic agents than to the use of phenylephrine, which as a pure alpha agonist increases afterload and may in this condition impair maternal cardiac output to a clinically significant extent. In the event that a patient continues to deteriorate despite the use of phenylephrine, undiagnosed cardiac dysfunction should be suspected, and inotropic agents such as epinephrine should be used. In the emergency setting, the obstetric anesthesiologist should follow the ABC approach, providing supportive care. Supplemental oxygen, rapid tracheal intubation, ventilation, and administration of adrenergic agents take precedence over the exact diagnosis and etiology.
