Aortic Stenosis & Non- Cardiac Surgery Stephen R. Ellis, MD David Warters, MD
ABG: – 7.58/32/472/30/8.2– Na/K 139/3.8– HCT 44
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.
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).
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.
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.
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
Etiology A. Normal aortic valve. B. Congenital aortic stenosis. C. Rheumatic aortic stenosis. D. Calcific aortic stenosis. E. Calcific senile aortic stenosis.
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
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.
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
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.
Pathophysiology Eventual y, cardiac output, stroke volume and therefore pressure gradient across the valve fal . Left ventricular dilatation occurs late in the disease process
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
Pathophysiology
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
Assessment – Symptoms Dyspnea – pulmonary congestion, CHF Symptoms that develop late in AS, and reflect inc pulmonary HTN – exertional dyspnea, orthopnea, PND, pulmonary edema
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)
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
Assessment – Exam ECHO: – Used to assess the anatomy of the aortic valve, grade the stenosis, and assess LV function.
Assessment – Exam ECHO:
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
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
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
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
Postoperative Management Monitored bed with invasive monitoring, and adequate pain control. Maintain appropriate intravascular filling, blood pressure and sinus rhythm.
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