Full flexion of the hips and knees in the supine position to treat an episode of acute hypotension and pulseless electrical activity in a patient with severe aortic stenosis

Abstract

This is a case report of a 77-year-old man with severe symptomatic aortic stenosis who underwent removal of an impacted ureteral stone under general anesthesia. During emergence from general anesthesia, his legs were lowered from lithotomy position, resulting in sudden hypotension with progression to pulseless electrical activity. The legs were raised and placed into full flexion of the hips and knees. This maneuver was temporally related to a return of spontaneous circulation and full recovery. Possible mechanisms for this effect are discussed.

Sudden and severe hypotension in the presence of severe aortic stenosis (AS) is associated with severe morbidity and mortality due to an acute loss of diastolic blood pressure (BP) distal to the aortic valve, which leads to a sudden decrease in coronary perfusion pressure (CPP). This case describes a patient with severe AS who had an acute decompensation associated with sudden lowering of the legs from the lithotomy position and a unique treatment that proved to be successful in reversing his symptoms.

CASE REPORT

A 77-year-old man with symptomatic severe AS with a valve area of 0.7 cm² underwent treatment in the lithotomy position for correction of severe obstructive uropathy. The procedure was felt to be sufficiently urgent that it should proceed prior to surgically addressing his severe AS. He had an uneventful general anesthetic (desflurane, fentanyl, and rocuronium with phenylephrine) with standard American Society of Anesthesiologists monitoring and a preoperatively placed radial arterial catheter. The patient remained stable throughout the surgery on moderate doses of phenylephrine for support of preload and afterload. However, during emergence from anesthesia, his legs were abruptly lowered from the high lithotomy position, and he immediately experienced profound hypotension with a dramatic drop in his systolic BP that had been previously stable (from 130–140 to 50–60 mm Hg). The acute decompensation was presumed to be due to the patient’s severe AS and a sudden drop in CPP. The patient’s BP was unresponsive to a 160 mg intravenous bolus of phenylephrine and continued to worsen over the next 30 seconds until his arterial line tracing was flat and he became pulseless despite a normal sinus rhythm on his electrocardiogram (pulseless electrical activity). Chest compressions were initiated with only minimal improvement seen on the arterial line waveform.

It was recognized within 30 seconds that the patient’s acute decompensation had occurred when the legs were lowered from the lithotomy position, likely resulting in an acute drop in the preload, systemic vascular resistance, and diastolic BP. The surgeons were asked to raise the legs and bring the knees to the chest (full flexion of the hips and knees). The patient had immediate return of spontaneous circulation, and his systolic BP immediately recovered to levels of >100 mm Hg. Concurrent crystalloid infusion combined with infusions of phenylephrine and norepinephrine were employed to maintain systolic BP > 110 mm Hg, and the knee to chest position was maintained for the next 5 minutes. The leg position was then slowly relaxed to a normal lithotomy position. The patient remained stable, and his legs were then brought down from the lithotomy position to the supine position slowly over a 3-minute period while intravenous fluids and vasopressor agents were titrated to maintain systolic BP >110 mm Hg. The patient emerged from anesthesia without any further difficulty and without cardiac or neurologic sequelae. No further episodes of cardiovascular instability were encountered, and vasopressor support was able to be discontinued approximately 25 minutes later when the patient was stable and had met extubation criteria.

DISCUSSION

Patients with symptomatic severe AS are dependent upon adequate preload and diastolic BP to maintain adequate CPP, measured just distal to the stenotic aortic valve and defined as diastolic BP minus left ventricular end-diastolic pressure. Sudden or profound hypotension can lead to acute cardiac decompensation as CPP becomes inadequate. Resultant myocardial ischemia leads to worsening diastolic and systolic function, potentially decreasing cardiac output and increasing left ventricular end-diastolic pressure. Once initiated, this process can lead to a vicious, self-perpetuating feedback loop in which worsening hypotension and increasing left ventricular end diastolic pressure lead to ever-worsening myocardial ischemia and rapid hemodynamic collapse. Additionally, standard cardiopulmonary resuscitation with external chest compressions often has reduced effectiveness for patients with AS.

Goals in anesthetic management of severe AS revolve around maintaining adequate preload and diastolic BP. Full flexion of the hips and knees may provide improved conditions for patients in hypotensive crisis due to severe AS by a number of potential mechanisms. The raising of the legs causes a rapid infusion of blood from the peripheral to the central circulation passively by gravity, thereby acutely increasing preload.¹ In addition, the crimping of the femoral arterial vasculature by this maneuver may increase diastolic BP and CPP by decreasing arterial capacitance.^2,3 The additional action of pushing the legs into the chest may add the benefits of increasing the tissue pressure in the legs, thereby further emptying the venous blood supply, much like an Esmarch bandage used in surgery to achieve exsanguination of an extremity.⁴ Furthermore, the increased tissue pressure decreases venous capacitance, further increasing preload and afterload. Finally, the pressure of the thighs pressed against the abdominal compartment may also result in improved CPP and cerebral blood flow, as reported in descriptions of abdominal counterpulsation during external cardiopulmonary resuscitation.^5,6 These five mechanisms combined may explain our patient’s immediate and drastic recovery from hypotensive pulseless electrical activity.

It is conceivable that this maneuver can allow the valuable moments needed to make adjustments in vasopressor therapy and intravascular volume in order to interrupt the downward spiral of hypotension and low CPP that can be lethal in patients with severe AS. Interestingly, this maneuver shares similarities with the squatting maneuver in patients with tetralogy of Fallot, which shares many physiologic goals with severe AS.²

The sudden infusion of blood from the lower extremities to the central circulation, decreased arterial and venous capacitance, and increased systemic vascular resistance that results from partial occlusion of the femoral arteries by this maneuver can assist to rapidly increase preload and systemic vascular resistance for a patient population that has increased morbidity and mortality due to severe AS.

Further research is needed to fully evaluate the hemodynamic effects of full flexion of the knees and hips while in the supine position in the presence of severe AS. Given the high morbidity and mortality of this patient population which is in extremis related to sudden low preload and afterload, this noninvasive measure warrants further consideration.