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Aortic stenosis (AS) presents a challenge to anesthesia professionals. It has been classified as the most important valvular lesion in patients presenting for noncardiac surgery because it has a high prevalence in the older population, a significant potential for sudden death, and high perioperative morbidity.1 People with AS often have little or no cardiac reserve, and may not tolerate the stress response associated with surgery. Anesthesia may also produce hemodynamic changes that can be disastrous in the presence of severe AS. Patients with AS are at a higher risk for developing cardiac complications, including myocardial infarction, heart failure, and ventricular arrhythmias. A report by Kertai et al indicated that the degree of stenosis is proportional to the level of cardiac risk.2
A 77 year old, 80kg, 173 cm, female presented to the operating room for an angiogram of the right lower extremity and right femoral to below-knee popliteal bypass with cryopreserved saphenous vein. The surgery was performed secondary to critical limb ischemia from an occluded superficial femoral artery. She was already status post bypass and multiple percutaneous interventions, which were unsuccessful with opening the superficial femoral artery and her femoral-popliteal bypass.
The patient's past medical history included hypertension, hyperlipidemia, CVA, and peripheral vascular disease. Upon physical assessment in the preoperative area, lungs were clear to auscultation bilaterally. Cardiac auscultation revealed a distinct systolic murmur that radiated to the neck. Medications included amlodipine, aspirin, cilostazol, enoxaparin, ramipril, alendronate and warfarin. Patient stated she had a history of postoperative nausea and vomiting (PONV) following surgery in June 2010.
In response to the murmur, a 2D echocardiogram was ordered in the preoperative area. The echocardiogram revealed left ventricular hypertrophy, severe aortic valve stenosis with an area of 0.8 cm2, aortic insufficiency, moderate mitral regurgitation, and an ejection fraction of 20%. In the preoperative area, an 18G peripheral intravenous catheter and a 20G arterial catheter were placed in her left radial artery for continuous blood pressure monitoring.
The patient was brought to the operating room and transferred to the operating table. ASA monitors were applied and the patient's vital signs were stable. The patient was pre-oxygenated with 100% FiO2 for approximately 3 minutes. The patient was then induced with lidocaine 60 mg IV, propofol 50 mg IV, in addition to mask inhalation of sevoflurane, followed by succinylcholine 80 mg IV. Vital signs remained stable throughout induction and a 7.0 OETT was placed at 21 cm. After induction the patient was maintained on sevoflurane with an end-tidal concentration of 2.0%. After induction, a double lumen central venous catheter was placed in the right internal jugular vein for continuous central venous pressure (CVP) monitoring. Famotidine 20 mg IV, dexamethasone 8 mg IV, and ondansetron 4 mg IV were given as prophylaxis, given her history of PONV. In response to a decrease in blood pressure, a norepinephrine drip was initiated at 2 mcg/min and titrated to blood pressure response. The patient tolerated the surgery well and was discharged home 3 days later.
Aortic stenosis results in obstruction to left ventricular emptying secondary to a reduced valve area. This in turn leads to left ventricular hypertrophy, which generates a greater pressure during systole, forcing blood past the mechanical obstruction. Thus, cardiac output is maintained as well as left ventricular end-diastolic volume. Consequently, the patient remains asymptomatic for a prolonged period of time despite the systolic pressure gradient between the left ventricle and the peripheral arterial system. Over time, the chronic pressure overload placed on the left ventricle results in concentric hypertrophy, reducing the compliance of the left ventricle (LV) and its ability to dilate. As ventricular compliance decreases, passive filling of the ventricle during diastole is decreased.3 The hypertrophied LV requires high filling pressures (left ventricular end-diastolic pressure [LVEDP]) to accommodate adequate preload and to sustain adequate CO.1 As a result, ventricular filling becomes increasingly dependent upon the blood volume provided by the atrial kick. (Noncardiac surgery in patients with AS - Up to Date, May 2010)
Concentric hypertrophy reduces coronary reserve and makes the patient more susceptible to ischemia in the presence of increased myocardial oxygen demand. Left ventricular hypertrophy increases intraventricular systolic pressure and nearly eliminates systolic coronary flow. Diastolic subendocardial blood flow also decreases as a result of a decrease in transmural pressures. For this reason, perfusion pressures must remain elevated to provide adequate myocardial blood flow.3 In addition, decreases in systemic vascular resistance can result in systemic hypotension and decreased coronary perfusion secondary to the fixed obstruction of the left ventricular outflow tract.4 (Noncardiac surgery in patients with AS - Up to Date, May 2010)
The main causes of AS are senile calcification, rheumatic heart disease, congenital abnormalities, and infective endocarditis. Senile calcification of a tricuspid aortic valve (AV) is often seen in patients older than 70 years of age. Using transthoracic Doppler echocardiography in a population sample of randomly selected men and women between the ages of 75 and 86 years of age, critical AS (valve area < 0.8 cm2) had a prevalence of 2.9%. Women may be affected more frequently than men. A bicuspid AV may be found in 1-2% of the population. A congenital bicuspid AV typically becomes calcified and stenotic earlier in life than a tricuspid AV, with symptoms of aortic regurgitation developing as early as 20 to 40 years of age.1 AS is usually detected during physical examination with the presence of a low systolic ejection murmur that is heard over the right second intercostal space. Other findings may include a soft S2 during auscultation due to a lack of or a delay of aortic valve closure and the arterial pulse described as "parvus and tardus," best heard in the carotid artery.5 Echocardiography is the gold standard for confirming diagnosis and determining the severity of stenosis. It is noninvasive and provides superior information on the morphologic features and motion of the aortic valve.
The aortic valve area and the aortic pressure gradient are the two most commonly used values to determine the severity of stenosis. These parameters can be obtained with echocardiography and cardiac catheterization. A normal aortic valve area is 3-4 cm2. Mild aortic stenosis is characterized by > 1.5 cm2 and moderate aortic stenosis has a valve area of 1.0-1.5 cm2. Severe AS is defined as a valve area <1 cm2 and a pressure gradient of more than 50 mmHg.6 Patients with mild to moderate AS are usually asymptomatic. This is mainly due to the hypertrophied left ventricle compensating for the increased pressure gradient. Clinical signs and symptoms in patients with severe AS (valve area of < 1 cm2) include dyspnea on exertion, shortness of breath, angina pectoris, syncope and arrhythmia. Angina is the initial symptom in 50-75% of patients, with only 25-50% having coronary artery disease. Syncope is the initial symptom in 15-30% of patients and is usually caused by exercise-induced vasodilation in the presence of a fixed cardiac output. Symptoms of AS imply a progression of the disease and a need to consider therapy.1,7
Aortic stenosis and noncardiac surgery
Recently, Kertai2 et al found that patients with a pressure gradient greater than 40 mmHg have 6.8 times the risk for cardiac complications, while patients with a gradient greater than 25 mmHg have 5.2 times the risk. The report also indicated that the degree of stenosis is proportional to the level of risk. Patients with a pressure gradient of 25 to 49 mmHg had a 15% complication rate, whereas patients with a gradient of more than 50 mm Hg had a 30% complication rate.2
There is little research supporting one anesthetic management technique over the other. Most of the literature regarding this subject is related to case reports. However, some authors of anesthesia textbooks suggest that general anesthesia is a preferable technique over regional anesthesia because there is greater control over blood pressure.8,9
The chronic pressure overload experienced in AS leads to concentric hypertrophy which reduces the compliance of the left ventricle. The ventricle is then increasingly dependent upon the blood volume contributed by the atrial kick. The concentric hypertrophy also decreases coronary reserve, making the patient more susceptible to ischemia in situations where myocardial oxygen demand is increased. Additionally, because of the fixed obstruction of the left ventricular outflow tract, decreases in SVR can result in systemic hypotension and ischemia from reduced coronary perfusion.4 ( Noncardiac surgery in patients with AS, Up-to-date, May 2010)
Maintenance of normal sinus rhythm is important because the atrial kick may provide up to 40 percent of ventricular filling. This is of particular importance in a left ventricle with decreased compliance. Arrhythmias can also have adverse hemodynamic effects. In particular, atrial fibrillation with rapid ventricular response can be very dangerous. The loss of the atrial kick and associated tachycardia will decrease coronary perfusion, which is dependent upon an acceptable diastolic time interval.4 (Noncardiac surgery in patients with AS, Up-to-date, May 2010)
First and foremost, a favorable outcome in patients with aortic stenosis undergoing surgery is related to the anesthesia provider's knowledge of the severity of the AV disease. Therefore, a thorough preoperative assessment is essential, followed by appropriate anesthetic management. Premedication in patients with AS can be problematic as it may oversedate the patient and lead to hypotension and decreased cerebral perfusion pressure (CPP). However, undersedation may lead to an anxious, tachycardic patient who is prone to myocardial ischemia. All patients should receive supplemental oxygen in the preoperative holding area.
The main goals for anesthetic management in patients with AS involve maintaining an adequate systemic vascular resistance (SVR; afterload), cardiac output (CO), a relatively slow heart rate (HR) and sinus rhythm. Tachycardia must be avoided because it decreases diastolic filling time, shortens systolic ejection time and therefore decreases CO, leading to a vicious cycle that may lead to sudden hemodynamic decompensation and cardiac arrest. Additionally, blood flow across the stenotic AV is fixed, and severe bradycardia (HR < 40) will result in low CO. According to Mittnacht et al, the ideal HR is likely between 60 and 70 beats per minute.1 This allows for adequate diastolic filling, thus providing sufficient CO.
Patients with AS can experience major decreases in CO and blood pressure with even minor changes in HR, preload, and afterload. Therefore, it is prudent to employ invasive arterial blood pressure monitoring before the induction of anesthesia. Central venous catheters offer the advantage of access to the central circulation for venous pressure monitoring and administration of pressors and inotropes as needed.10
In mixed AV lesions (AS and AR), the stenotic lesion is more concerning. However, slightly higher HRs can be tolerated if severe AR coexists with AS. It is important to maintain sinus rhythm as arrhythmias are poorly tolerated. It is recommended that a defibrillator be present in the operating room and pads be placed on the patient prior to positioning if easy access is not available during the surgery. In the unstable patient with supraventricular tachyarrhythmias, cardioversion is considered the first line therapy. However, in the stable patient, a therapeutic maneuver such as vagal stimulation or adenosine can be attempted. If the underlying rhythm is identified, treatment of supraventricular tachyarrhythmias usually consists of beta-adrenergic blockers, amiodarone, or cardioversion, depending on the rhythm. In patients that have impaired cardiac function (identified as an ejection fraction (EF) < 40%), or a ventricular tachycardia that cannot be ruled out, amiodarone is the drug of choice. A slow heart rate should be treated with the most predictable increase in HR to avoid tachycardia that may lead to sudden hemodynamic decompensation or ischemia. Treatments to consider should include anticholinergics, a - and b - adrenergic agonists, or atrioventricular sequential pacing.
Patients with AS are very sensitive to preload and proper fluid management must be initiated prior to induction. SVR must be maintained at all times which is why it is questionable to perform neuraxial anesthesia because of the risk of a sympatholytic response. If a neuraxial technique is chosen, it is recommended that it be an epidural technique because it allows for incremental dosing and therefore a sudden decrease in SVR can be avoided. It is also recommended that frequent blood pressure monitoring and vasopressor agents are available if implementing a neuraxial technique.11 As mentioned earlier, some authors consider the presence of severe AS as a contraindication for the use of spinal or epidural anesthesia.8
General anesthesia, along with adequate monitoring, provides the best hemodynamic control. Etomidate, midazolam, and opioids are good choices but should be titrated to effect. Neuromuscular blockers with favorable hemodynamic profiles include vecuronium and cisatracurium. Ketamine, pancuronium, and rocuronium may increase HR and may be poorly tolerated in the patient with severe AS. Thiopental should also be avoided as it decreases preload and contractility. Similarly, propofol may reduce contractility and afterload which results in hypotension and therefore is relatively contraindicated with severe AS.
Many different anesthetic techniques can be used as long as preload, afterload, HR, and contractility are monitored to avoid adverse hemodynamic responses. It is recommended that all anesthetics be titrated with attention to maintaining SVR and CO. Hypotension should be treated immediately with an a-agonist such as phenylephrine being the agent of choice. The goal is to maintain CPP, so that the heart is not exposed to irreversible ischemia. Pure a-agonists are the preferred vasoconstrictor agents because they do not cause tachycardia, and therefore the CPP is increased and diastolic filling time is maintained without causing an increase in oxygen demand. It is important to note that overly aggressive treatment of hypotension can be harmful and lead to excessively high arterial pressures with a significant increase in left ventricular wall tension, increases in oxygen demand, decreases in myocardial perfusion, and may cause ischemia in the hypertrophied LV of patients with AS.1
Aortic stenosis and valvular lesions present a host of potential difficulties during perioperative care for noncardiac surgery. A thorough understanding of the pathophysiology along with its implications in the perioperative period is essential in preventing undesirable outcomes. Patients with AS require a careful and thorough preoperative evaluation with excellent optimization and planning. In addition, aggressive intraoperative monitoring must be employed, with rigorous hemodynamic control that must be continued into the postoperative period. As the population continues to age, we can expect to treat many more of these patients with valvular lesions, making it more crucial than ever to be prepared for their treatment.