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Aortal stricture ( AS ) presents a challenge to anesthesia professionals. It has been classified as the most of import valvular lesion in patients showing for noncardiac surgery because it has a high prevalence in the older population, a important potency for sudden decease, and high perioperative morbidity.1 Peoples with AS frequently have small or no cardiac modesty, and may non digest the emphasis response associated with surgery. Anesthesia may besides bring forth hemodynamic alterations that can be black in the presence of terrible AS. Patients with AS are at a higher hazard for developing cardiac complications, including myocardial infarction, bosom failure, and ventricular arrhythmias. A study by Kertai et al indicated that the grade of stricture is relative to the degree of cardiac risk.2

Case Summary

A 77 twelvemonth old, 80kg, 173 centimeter, female presented to the operating room for an angiogram of the right lower appendage and right femoral to below-knee popliteal beltway with cryopreserved saphenous vena. The surgery was performed secondary to critical limb ischaemia from an occluded superficial femoral arteria. She was already position station beltway and multiple transdermal intercessions, which were unsuccessful with opening the superficial femoral arteria and her femoral-popliteal beltway.

The patient ‘s past medical history included high blood pressure, lipemia, CVA, and peripheral vascular disease. Upon physical appraisal in the preoperative country, lungs were clear to auscultation bilaterally. Cardiac auscultation revealed a distinguishable systolic mutter that radiated to the cervix. Medicines included amlodipine, acetylsalicylic acid, cilostazol, enoxaparin, Altace, Fosamax and Coumadin. Patient stated she had a history of postoperative sickness and emesis ( PONV ) following surgery in June 2010.

In response to the mutter, a 2D echocardiogram was ordered in the preoperative country. The echocardiogram revealed left ventricular hypertrophy, terrible aortal valve stricture with an country of 0.8 cm2, aortal inadequacy, moderate mitral regurgitation, and an expulsion fraction of 20 % . In the preoperative country, an 18G peripheral endovenous catheter and a 20G arterial catheter were placed in her left radial arteria for uninterrupted blood force per unit area monitoring.

The patient was brought to the operating room and transferred to the operating tabular array. ASA proctors were applied and the patient ‘s critical marks were stable. The patient was pre-oxygenated with 100 % FiO2 for about 3 proceedingss. The patient was so induced with lidocaine 60 milligram IV, propofol 50 milligram IV, in add-on to dissemble inspiration of sevoflurane, followed by succinylcholine 80 milligram IV. Vital marks remained stable throughout initiation and a 7.0 OETT was placed at 21 centimeter. After initiation the patient was maintained on sevoflurane with an end-tidal concentration of 2.0 % . After initiation, a dual lumen cardinal venous catheter was placed in the right internal jugular vena for uninterrupted cardinal venous force per unit area ( CVP ) monitoring. Famotidine 20 milligram IV, Decadron 8 milligram IV, and ondansetron 4 milligram IV were given as prophylaxis, given her history of PONV. In response to a lessening in blood force per unit area, a norepinephrine trickle was initiated at 2 mcg/min and titrated to blood force per unit area response. The patient tolerated the surgery good and was discharged place 3 yearss subsequently.


Aortal stricture consequences in obstructor to go forth ventricular emptying secondary to a reduced valve country. This in bend leads to go forth ventricular hypertrophy, which generates a greater force per unit area during systole, coercing blood past the mechanical obstructor. Therefore, cardiac end product is maintained every bit good as left ventricular end-diastolic volume. Consequently, the patient remains symptomless for a drawn-out period of clip despite the systolic force per unit area gradient between the left ventricle and the peripheral arterial system. Over clip, the chronic force per unit area overload placed on the left ventricle consequences in homocentric hypertrophy, cut downing the conformity of the left ventricle ( LV ) and its ability to distend. As ventricular conformity lessenings, inactive filling of the ventricle during diastole is decreased.3 The enlarged LV requires high filling force per unit areas ( left ventricular end-diastolic force per unit area [ LVEDP ] ) to suit equal preload and to prolong equal CO.1 As a consequence, ventricular filling becomes progressively dependent upon the blood volume provided by the atrial boot. ( Noncardiac surgery in patients with AS – Up to Date, May 2010 )

Concentric hypertrophy reduces coronary modesty and makes the patient more susceptible to ischemia in the presence of increased myocardial O demand. Left ventricular hypertrophy additions intraventricular systolic force per unit area and about eliminates systolic coronary flow. Diastolic subendocardial blood flow besides decreases as a consequence of a lessening in transmural force per unit areas. For this ground, perfusion force per unit areas must stay elevated to supply equal myocardial blood flow.3 In add-on, decreases in systemic vascular opposition can ensue in systemic hypotension and decreased coronary perfusion secondary to the fixed obstructor of the left ventricular outflow tract.4 ( Noncardiac surgery in patients with AS – Up to Date, May 2010 )


The chief causes of AS are doddering calcification, arthritic bosom disease, inborn abnormalcies, and morbific endocarditis. Senile calcification of a tricuspid aortal valve ( AV ) is frequently seen in patients older than 70 old ages of age. Using transthoracic Doppler echocardiography in a population sample of indiscriminately selected work forces and adult females between the ages of 75 and 86 old ages of age, critical AS ( valve country & lt ; 0.8 cm2 ) had a prevalence of 2.9 % . Women may be affected more often than work forces. A bicuspid AV may be found in 1-2 % of the population. A inborn premolar AV typically becomes calcified and stenosed earlier in life than a tricuspid AV, with symptoms of aortal regurgitation developing every bit early as 20 to 40 old ages of age.1 AS is normally detected during physical scrutiny with the presence of a low systolic expulsion mutter that is heard over the right 2nd intercostal infinite. Other findings may include a soft S2 during auscultation due to a deficiency of or a hold of aortal valve closing and the arterial pulsation described as “ parvus and tardus, ” best heard in the carotid artery.5 Echocardiography is the gilded criterion for corroborating diagnosing and finding the badness of stricture. It is noninvasive and provides superior information on the morphologic characteristics and gesture of the aortal valve.

The aortal valve country and the aortal force per unit area gradient are the two most normally used values to find the badness of stricture. These parametric quantities can be obtained with echocardiography and cardiac catheterisation. A normal aortal valve country is 3-4 cm2. Mild aortal stricture is characterized by & gt ; 1.5 cm2 and moderate aortal stricture has a valve country of 1.0-1.5 cm2. Severe AS is defined as a valve country & lt ; 1 cm2 and a force per unit area gradient of more than 50 mmHg.6 Patients with mild to chair AS are normally symptomless. This is chiefly due to the hypertrophied left ventricle counterbalancing for the increased force per unit area gradient. Clinical marks and symptoms in patients with terrible AS ( valve country of & lt ; 1 cm2 ) include dyspnoea on effort, shortness of breath, angina pectoris, faint and arrhythmia. Angina is the initial symptom in 50-75 % of patients, with merely 25-50 % holding coronary arteria disease. Syncope is the initial symptom in 15-30 % of patients and is normally caused by exercise-induced vasodilation in the presence of a fixed cardiac end product. Symptoms of AS imply a patterned advance of the disease and a demand to see therapy.1,7

Aortal stricture and noncardiac surgery

Recently, Kertai2 et Al found that patients with a force per unit area gradient greater than 40 mmHg have 6.8 times the hazard for cardiac complications, while patients with a gradient greater than 25 mmHg have 5.2 times the hazard. The study besides indicated that the grade of stricture is relative to the degree of hazard. Patients with a force per unit area 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

Anaesthetic Management

There is small research back uping one anaesthetic direction technique over the other. Most of the literature sing this topic is related to instance studies. However, some writers of anesthesia text editions suggest that general anaesthesia is a preferred technique over regional anaesthesia because there is greater control over blood pressure.8,9

The chronic force per unit area overload experienced in AS leads to concentric hypertrophy which reduces the conformity of the left ventricle. The ventricle is so progressively dependent upon the blood volume contributed by the atrial boot. The homocentric hypertrophy besides decreases coronary modesty, doing the patient more susceptible to ischemia in state of affairss where myocardial O demand is increased. Additionally, because of the fixed obstructor of the left ventricular outflow piece of land, decreases in SVR can ensue in systemic hypotension and ischaemia from reduced coronary perfusion.4 ( Noncardiac surgery in patients with AS, Up-to-date, May 2010 )

Care of normal fistula beat is of import because the atrial boot may supply up to 40 per centum of ventricular filling. This is of peculiar importance in a left ventricle with reduced conformity. Arrhythmias can besides hold inauspicious hemodynamic effects. In peculiar, atrial fibrillation with rapid ventricular response can be really unsafe. The loss of the atrial boot and associated tachycardia will diminish coronary perfusion, which is dependent upon an acceptable diastolic clip interval.4 ( Noncardiac surgery in patients with AS, Up-to-date, May 2010 )

First and first, a favourable result in patients with aortal stricture undergoing surgery is related to the anaesthesia supplier ‘s cognition of the badness of the AV disease. Therefore, a thorough preoperative appraisal is indispensable, followed by appropriate anaesthetic direction. Premedication in patients with AS can be debatable as it may oversedate the patient and lead to hypotension and reduced intellectual perfusion force per unit area ( CPP ) . However, undersedation may take to an dying, tachycardic patient who is prone to myocardial ischaemia. All patients should have auxiliary O in the preoperative keeping country.

The chief ends for anaesthetic direction in patients with AS involve keeping an equal systemic vascular opposition ( SVR ; afterload ) , cardiac end product ( CO ) , a comparatively slow bosom rate ( HR ) and sinus beat. Tachycardia must be avoided because it decreases diastolic filling clip, shortens systolic expulsion clip and therefore lessenings CO, taking to a barbarous rhythm that may take to sudden hemodynamic decompensation and cardiac apprehension. Additionally, blood flow across the stenosed AV is fixed, and terrible bradycardia ( HR & lt ; 40 ) will ensue in low CO. Harmonizing to Mittnacht et Al, the ideal HR is likely between 60 and 70 beats per minute.1 This allows for equal diastolic filling, therefore supplying sufficient CO.

Patients with AS can see major lessenings in CO and blood force per unit area with even minor alterations in HR, preload, and afterload. Therefore, it is prudent to use invasive arterial blood force per unit area monitoring before the initiation of anaesthesia. Central venous catheters offer the advantage of entree to the cardinal circulation for venous force per unit area monitoring and disposal of vasoconstrictors and inotropes as needed.10

In assorted AV lesions ( AS and AR ) , the stenosed lesion is more refering. However, somewhat higher HRs can be tolerated if terrible AR coexists with AS. It is of import to keep sinus beat as arrhythmias are ill tolerated. It is recommended that a defibrillator be present in the operating room and tablets be placed on the patient prior to positioning if easy entree is non available during the surgery. In the unstable patient with supraventricular tachyarrhythmias, cardioversion is considered the first line therapy. However, in the stable patient, a curative manoeuvre such as pneumogastric stimulation or adenosine can be attempted. If the underlying beat is identified, intervention of supraventricular tachyarrhythmias normally consists of beta-adrenergic blockers, Cordarone, or cardioversion, depending on the beat. In patients that have impaired cardiac map ( identified as an expulsion fraction ( EF ) & lt ; 40 % ) , or a ventricular tachycardia that can non be ruled out, Cordarone is the drug of pick. A slow bosom rate should be treated with the most predictable addition in HR to avoid tachycardia that may take to sudden hemodynamic decompensation or ischaemia. Treatments to see should include anticholinergics, a – and b – sympathomimetic agonists, or auriculoventricular consecutive tempo.

Patients with AS are really sensitive to preload and proper unstable direction must be initiated prior to initiation. SVR must be maintained at all times which is why it is questionable to execute neuraxial anaesthesia because of the hazard of a sympatholytic response. If a neuraxial technique is chosen, it is recommended that it be an extradural technique because it allows for incremental dosing and therefore a sudden lessening in SVR can be avoided. It is besides recommended that frequent blood force per unit area monitoring and vasopressor agents are available if implementing a neuraxial technique.11 As mentioned earlier, some writers consider the presence of terrible AS as a contraindication for the usage of spinal or extradural anesthesia.8

General anaesthesia, along with equal monitoring, provides the best hemodynamic control. Etomidate, Versed, and opioids are good picks but should be titrated to consequence. Neuromuscular blockers with favourable hemodynamic profiles include vecuronium and cisatracurium. Ketamine, pancuronium, and rocuronium may increase HR and may be ill tolerated in the patient with terrible AS. Thiopental should besides be avoided as it decreases preload and contractility. Similarly, propofol may cut down contractility and afterload which consequences in hypotension and therefore is comparatively contraindicated with terrible AS.

Many different anaesthetic techniques can be used every bit long as preload, afterload, HR, and contractility are monitored to avoid inauspicious hemodynamic responses. It is recommended that all anaesthetics be titrated with attending to keeping SVR and CO. Hypotension should be treated instantly with an a-agonist such as phenylephrine being the agent of pick. The end is to keep CPP, so that the bosom is non exposed to irreversible ischaemia. Pure a-agonists are the preferable vasoconstrictive agents because they do non do tachycardia, and hence the CPP is increased and diastolic filling clip is maintained without doing an addition in oxygen demand. It is of import to observe that excessively aggressive intervention of hypotension can be harmful and lead to overly high arterial force per unit areas with a important addition in left ventricular wall tenseness, additions in O demand, decreases in myocardial perfusion, and may do ischaemia in the enlarged LV of patients with AS.1


Aortal stricture and valvular lesions present a host of possible troubles during perioperative attention for noncardiac surgery. A thorough apprehension of the pathophysiology along with its deductions in the perioperative period is indispensable in forestalling unwanted results. Patients with AS require a careful and thorough preoperative rating with first-class optimisation and planning. In add-on, aggressive intraoperative monitoring must be employed, with strict hemodynamic control that must be continued into the postoperative period. As the population continues to age, we can anticipate to handle many more of these patients with valvular lesions, doing it more important than of all time to be prepared for their intervention.

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