Aortic Stenosis & Non-Cardiac Surgery

Aortic Stenosis & Non- Cardiac Surgery Stephen R. Ellis, MD David Warters, MD

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 ABG: – 7.58/32/472/30/8.2– Na/K 139/3.8– HCT 44

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Introduction  Aortic stenosis derives its position as the most important valvular lesion because of its potential for sudden death (15–20%), and because of the inability to obtain adequate systemic perfusion by external cardiac massage during a cardiac arrest.

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Introduction  Aortic stenosis without accompanying mitral valve disease is more common in men than in women and very rarely occurs on a rheumatic basis. Instead, isolated AS is usual y either congenital or degenerative in origin.  The natural history of the disease is of a long asymptomatic latent period fol owed by the onset of characteristic symptoms (angina, syncope, dyspnea).

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Etiology  Degenerative calcific aortic stenosis – Mechanical stress over time leads to progressive fibrosis and calcification of a previously normal tri- leaflet valve. – Initial y, this process is seen as sclerosis. – It is an early form of the disease that can progress to stenosis. – associated with many of the risk factors for coronary artery disease – diabetes, hypercholesterolaemia, smoking and hypertension.

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Etiology  Congenital bicuspid aortic valve – Bicuspid aortic valve is the most common congenital cardiac malformation ( 2% of general population). – abnormal valve structure – two rather than three leaflets – leads to turbulent flow, which, in turn, can produce fibrosis, calcification and orifice narrowing secondary to trauma. – commonly produces symptoms in the fourth to sixth decades of life. – accounts for 50% of patients <70 yr requiring aortic valve surgery for stenosis but only 25% of those >70 yr.

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Etiology  Rheumatic AS – results from adhesions and fusions of the commissures and cusps – There is vascularization of the leaflets of the valve ring– This leads to retraction and stiffening of the free borders of the cusps. – Calcific nodules develop on both surfaces, and the orifice is reduced to a smal round or triangular opening. – As a consequence, the rheumatic valve is often regurgitant and stenotic

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Etiology A. Normal aortic valve. B. Congenital aortic stenosis. C. Rheumatic aortic stenosis. D. Calcific aortic stenosis. E. Calcific senile aortic stenosis.

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Classification  Mild AS – AVA 1.2-1.8cm2, mean gradient 12-25 mmHg  Moderate AS – AVA 0.8-1.2cm2, mean gradient 40-50 mmHg  Severe AS – AVA <0.8cm2, mean gradient > 50 mmHg

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Pathophysiology  The normal aortic valve area (AVA) is 2.6–3.5 cm2 in adults.  Hemodynamical y significant obstruction occurs as the AVA approaches 1.0 cm2.  Increasing obstruction hypertrophy, which al ows the LV to maintain a pressure gradient across the valve without dilating or reducing the cardiac output.

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Pathophysiology  However, over time the hypertrophied ventricle becomes increasingly stiff, diastolic dysfunction with a reduced compliance.  This is transmitted to the pulmonary circulation pulmonary edema

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Pathophysiology  A normal sinus rhythm is beneficial as the left atrial kick accounts for 40% of LV fil ing.  LA hypertrophies secondary to this increased demand on it increased chance of atrial fibril ation.  Major alterations of myocardial oxygen supply and demand occur.  The ventricle becomes – very sensitive to changes in preload – dependent on the maintenance of sinus rhythm – susceptible to ischemia, especial y when arterial pressure is reduced.

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Pathophysiology  Eventual y, cardiac output, stroke volume and therefore pressure gradient across the valve fal .  Left ventricular dilatation occurs late in the disease process

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Pathophysiology  There is a direct relationship b/w the aortic valve area and the flow across the valve.  Blood flow is not significantly impeded until the aortic valve area is < 0.5-0.7 cm2

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Pathophysiology

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Assessment – Symptoms  As stated the three cardinal signs of AS are – angina, syncope, and dyspnea.  Angina – occurs as oxygen demand from the hypertrophied LV outstrips the supply – Initial symptom in 50-70% of pts  Syncope – etiology unclear– Initial symptom in 15-30% of pts

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Assessment – Symptoms  Dyspnea – pulmonary congestion, CHF Symptoms that develop late in AS, and reflect inc pulmonary HTN – exertional dyspnea, orthopnea, PND, pulmonary edema

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Assessment – Exam  Arterial pulse is slow rising, and of low volume  Carotid thrill Precordial thrill with leaning forward during expiration  Late systolic murmur (2nd intercostal space at base of heart)

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Assessment – Exam  EKG: – LVH – present in ~ 85% of pts– T-wave inversion & ST depression as hypertrophy becomes worse – AV and intraventricular blocks can be seen

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Assessment – Exam  ECHO: – Used to assess the anatomy of the aortic valve, grade the stenosis, and assess LV function.

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Assessment – Exam  ECHO:

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Anesthetic Management for Non- Cardiac Surgery  Careful hemodynamic monitoring is essential: – Arterial line  Aortic stenosis produces a fixed obstruction to left ventricular ejection that results in reduced stroke volume and an arterial pressure waveform that rises slowly (pulsus tardus) and peaks late in systole  Pulsus parvus (narrow pulse pressure) – CVC, or large bore PIVs– Swan-Ganz? Absolutely not, as the potential for it to precipitate arrhythmias is too high. – TEE is appropriate if available

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Anesthetic Management for AS & Non-Cardiac Surgery  Avoid systemic hypotension – leads to myocardial ischemia, and then decreased contractility and a vicious cycle ensues. – vasoconstrictors must be at hand – consider an infusion from the beginning – treat hypotension aggressively  Maintain sinus rhythm – sinus tachy decreases diastolic time for myocardial perfusion – sinus brady limits CO in pts with fixed stroke volume

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Anesthetic Management for AS & Non-Cardiac Surgery  Treat arrhythmias promptly Contractility – Stroke volume is maintained with a heightened contractile state  Maintain adequate intravascular volume to ensure ventricular filling – b/c of dec LV compliance and inc LVEDP & LVEDV, preload augmentation is needed for a normal stroke volume

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Anesthetic Management for AS & Non-Cardiac Surgery  GA vs Regional: – successful use of spinal and epidural have been reported. – Can use combined lumbar plexus and sciatic PNB for hips – GA is safe, as long as care is taken to maintain blood pressure and sinus rhythm  Narcotic-based technique is often used

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Postoperative Management  Monitored bed with invasive monitoring, and adequate pain control.  Maintain appropriate intravascular filling, blood pressure and sinus rhythm.

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References  Brown , J et al. Aortic Stenosis and Non-Cardiac Surgery. Continuing Education in Anaesthesia, Critical Care & Pain 2005 5(1):1-4  Hensley F, Martin DE, Gravlee GP. A Practical Approach to Cardiac Anesthesia, 3rd ed. Philadelphia: LWW, 2003:303-309  Miller, RD. Anesthesia, 5th ed. Philadelphia: Churchill Livingstone, 2000: 1770- 1771  Miller, RD. Anesthesia, 6th ed. Philadelphia: Churchill Livingstone, 2000: 1954- 1957  Braunwald. Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia: WB Saunders, 2001:1671-1680

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