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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

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aortic stenosis non cardiac surgery

Aortic Stenosis & Non-Cardiac Surgery

Stephen R. Ellis, MD

David Warters, MD

slide3
ABG:

7.58/32/472/30/8.2

Na/K 139/3.8

HCT 44

introduction
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.
introduction6
Introduction
  • Aorticstenosiswithout accompanying mitral valve disease is more common in men than in women and very rarely occurs on a rheumatic basis. Instead, isolated AS is usually either congenital or degenerative in origin.
  • The natural history of the disease is of a long asymptomatic latent period followed by the onset of characteristic symptoms (angina, syncope, dyspnea).
etiology
Etiology
  • Degenerative calcific aortic stenosis
    • Mechanical stress over time leads to progressive fibrosis and calcification of a previously normal tri-leaflet valve.
    • Initially, 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.
etiology8
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.
etiology9
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 small round or triangular opening.
    • As a consequence, the rheumatic valve is often regurgitant and stenotic
etiology10
Normal aortic valve.

Congenital aortic stenosis.

Rheumatic aortic stenosis.

Calcific aortic stenosis.

Calcific senile aortic stenosis.

Etiology
classification
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
Pathophysiology
  • The normal aortic valve area (AVA) is 2.6–3.5 cm2 in adults.
  • Hemodynamically significant obstruction occurs as the AVA approaches 1.0 cm2.
  • Increasing obstruction hypertrophy, which allows the LV to maintain a pressure gradient across the valve without dilating or reducing the cardiac output.
pathophysiology13
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
pathophysiology14
Pathophysiology
  • A normal sinus rhythm is beneficial as the left atrial kick accounts for 40% of LV filling.
  • LA hypertrophies secondary to this increased demand on it increased chance of atrial fibrillation.
  • 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, especially when arterial pressure is reduced.
pathophysiology15
Pathophysiology
  • Eventually, cardiac output, stroke volume and therefore pressure gradient across the valve fall.
  • Left ventricular dilatation occurs late in the disease process
pathophysiology16
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
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 symptoms19
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
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 exam21
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 exam22
Assessment - Exam
  • ECHO:
    • Used to assess the anatomy of the aortic valve, grade the stenosis, and assess LV function.
anesthetic management for non cardiac surgery
Anesthetic Management for Non-Cardiac Surgery
  • Careful hemodynamic monitoring is essential:
    • Arterial line
      • Aorticstenosis 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
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 surgery26
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 surgery27
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
Postoperative Management
  • Monitored bed with invasive monitoring, and adequate pain control.
  • Maintain appropriate intravascular filling, blood pressure and sinus rhythm.
references
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