20% normally). LVEDP is often elevated, causing symptoms of pulmonary congestion despite normal LV contractility. LVEDP values that are normal may, in fact, represent a patient who is hypovolemic.
Diagnosis
As mentioned, a long latency period exists (
40–50 years) during which obstruction increases gradually and the pressure load on the myocardium increases while the patient remains asymptomatic. Patients with advanced AS may begin to have angina, syncope, and signs of CHF. They also have a characteristic systolic murmur, best heard in the second right intercostal space, which transmits sound to the neck. Cardiac catheterization will give vital information about intracavitary pressures, the gradient across the aortic valve, and contractility. In patients with calcific AS, echocardiography often shows thickening and calcification of the aortic valve and decreased mobility of the valve leaflets. The incidence of arrhythmias leading to severe hypoperfusion accounts for syncope and the increased incidence of sudden death in patients with AS.
Treatment
When significant symptoms develop, most patients die without surgical treatment within 2 to 5 years. Percutaneous transluminal valvuloplasty may be an alternative to surgery, but restenosis usually occurs within 6 to 12 months.
Anesthetic considerations
The goals of anesthesia management include maintaining hemodynamic stability without causing significant alterations in compensatory mechanisms. Anesthetic management of patients with AS should focus on the following hemodynamic factors:
General anesthesia is the preferred technique for major surgical procedures involving patients with AS because of the ability to manipulate hemodynamic parameters, especially DBP.
Central neural blockade (spinal or epidural) must be used with extreme caution because precipitous reductions in blood pressure associated with a sympathectomy decrease SVR. Epidural anesthesia offers the advantage of a slower onset of vasodilation. A high dermatome level sensory block causes greater vasodilation or hypotension and is contraindicated in those with moderate to severe AS.
Monitoring and premedication
In addition to standard intraoperative monitoring, complete invasive monitoring may be required for patients with AS, even for routine procedures. Any significant change in basic hemodynamic variables (i.e., heart rate, heart rhythm, LVEDV, coronary perfusion pressure [CPP]) can rapidly cause irreversible myocardial deterioration. The complexity of hemodynamic monitoring modalities depends on the physical status of the patient, the severity of AS, the extent of the surgical procedure, and the ability of the anesthesia provider to use and interpret hemodynamic values.
Absolute criteria for intraoperative invasive monitoring for patients with AS are controversial. However, clinical judgment, experience, and the ability to appropriately use a PA catheter must be considered before implementation.
Maintenance of anesthesia
Commonly used induction agents can be used as long as profound hypotension is avoided. Tracheal intubation can be performed with any of the available muscle relaxants. However, caution must be exercised to avoid histamine release because this situation can dramatically increase the heart rate. Anesthetic maintenance can be accomplished with the use of a volatile agent in conjunction with nitrous oxide, opiates, or both. The adverse cardiovascular effects of the volatile agents must be considered before these drugs are used. Higher concentrations of inhaled agent result in greater degrees of myocardial depression and vasodilation. Volatile agents must be used with extreme caution because the myocardial depressant effect can be deleterious in patients with impaired ventricular function. The use of high-dose opioid-based agents (fentanyl, 50–100 mcg/kg, or sufentanil, 5–30 mcg/kg) is an alternative anesthetic approach that may help achieve cardiovascular stability by not causing a significant amount of myocardial depression. A combination of inhaled agents and narcotics has been used safely to provide anesthesia for patients with AS. Despite the anesthetic technique that is chosen, immediate and aggressive treatment of adverse changes that occur in heart rate and rhythm, SVR, blood pressure, and LVEDV is paramount if successful anesthetic outcomes are to be achieved in patients with AS.
Aortic insufficiency
Incidence and prevalence
Aortic insufficiency, also known as AI, can be classified as acute or chronic and as primary or secondary, depending on the cause. Primary chronic AI is caused by rheumatic valvular disease and almost always involves the mitral valve to some degree. Primary acute AI usually is caused by infective endocarditis, which is caused by direct damage to the valve cusps. Acute secondary (functional) AI results from aortic root dissection caused either by trauma or aneurysm and results in a mechanical and functional impairment of functional aortic valve closure.
Pathophysiology
The major hemodynamic aberration related to AI occurs during diastole. A portion of the blood volume that is ejected from the LV into the aorta regurgitates backward into the ventricle because of incomplete closure of the aortic valve. AI causes LV volume overload. Chronic ventricular overload causes eccentric ventricular hypertrophy and chamber dilation. The degree of regurgitation depends on three factors: the diastolic time available for regurgitation to occur, the diastolic pressure gradient between the aorta and the LV, and the degree of incompetence of the aortic valve.
Diagnosis
Most patients with chronic AI remain asymptomatic for 10 to 20 years. When symptoms develop, exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea are the principal complaints. Diastolic murmur is often auscultated at the left sternal border. Angina is a late and ominous symptom.
In acute AI, patients develop sudden clinical manifestations of cardiovascular collapse, weakness, severe dyspnea, and hypotension. Chronic AI is recognized by its characteristic diastolic murmur (best heard in the second intercostal space, right sternal border), widened pulse pressure, decreased diastolic pressure, and bounding peripheral pulses.
Treatment
Arterial blood pressure should be decreased to reduce the diastolic gradient for regurgitation using afterload reduction via arterial vasodilators and ACE inhibitors. Early surgery is indicated for patients with acute AI because medical management is associated with a high mortality rate. Patients with chronic AI should undergo surgery before irreversible ventricular dysfunction occurs.
Anesthetic considerations
The goals for anesthesia management are to increase forward flow and decrease the degree of regurgitation and therefore should focus on the following hemodynamic factors:
