Valvular Heart Disease PDF

VALVULAR HEART DISEASE VALVULAR HEART DISEASE OVERVIEW Growing practice – Despite marked decrease in rheumatic heart disease – Aging population – Innovations being made in surgical intervention Variable physiologic and hemodynamic aberrations influenced by anesthetic intervention Natural history of...

VALVULAR HEART DISEASE VALVULAR HEART DISEASE OVERVIEW Growing practice – Despite marked decrease in rheumatic heart disease – Aging population – Innovations being made in surgical intervention Variable physiologic and hemodynamic aberrations influenced by anesthetic intervention Natural history of disease is important to determine: – Timing of intervention – Anesthetic management Maintenance of heart rate/ pacing Inotrope usage Vasodilators/vasoconstrictors PRESSURE-VOLUME LOOPS AFTERLOAD MISMATCH VENTRICULAR COMPLIANCE Acute increases in volume (e.g. acute AI) produce marked increases in LVEDP Chronic change tends to shift the curve to the right such that higher volumes are tolerated In chronic pressure overload there is: – An inverse linear relationship between hypertrophy and compliance – Impaired ventricular relaxation 1 MEASURES OF CONTRACTILITY Contractility = ability to generate force at a given preload Isovolumetric Indices (Vmax, dP/dT) – Relatively insensitive to loading conditions (preload) – Poor reflection of basal contractility Ejection Phase Indices – Directly proportional to preload – Vary inversely with afterload (increase afterload w/out changing preload you would reduce stroke volume) – Unreliable in most valvular disease End Systolic Pressure Volume Relationship (ESPVR) – More precise estimate of contractility – Independent of preload MEASURES OF CONTRACTILITY END SYSTOLIC PRESSURE VOLUME RELATIONSHIP AORTIC STENOSIS AS OVERVIEW In the United States: – Most common cardiac valve lesion – 1-2% of population born with bicuspid valve (prone to stenosis at earlier age vs. tricuspid valve, like middle age) – Marked reduction in rheumatic disease means that disease is now primarily due to: Bicuspid valve Calcification of the valve – Aging population with more concurrent disease, particularly CAD ATHEROSCLEROSIS & AORTIC STENOSIS Early lesion of AS resembles an intimal plaque characteristic of CAD (it’s the same inflammatory process) Coronary calcification correlates highly with aortic valve calcification Identical risk factors – Increased LDL, smoking, HTN, diabetes, increased serum Ca++ and creatinine, male gender 2 AS: SYMPTOMS AND PROGRESSION AS: TIMING OF AVR AS: VOLUME LOOP AORTIC STENOSIS & MYOCARDIAL OXYGEN SUPPLY & DEMAND AS: STRATIFICATION – CONTRACTILE RESERVE Value of prophylactic AVR??? – The most common cause of sudden death in asymptomatic patients with aortic stenosis is? Doing the AVR procedure itself. (asymptomatic leave them alone, symptoms then think about surgery) Concurrent CABG [common] – Unbypassed CAD results in decreased early and late survival following AVR – Concurrent CABG with AVR does not increase perioperatively mortality Increased systolic peak pressure (overcome stenotic valve) Increased chamber stiffness – Importance of atrial systole in LV filling Adequate preload Maintenance of sinus rhythm (need atrial kick) Stroke volume maintained by: – LV hypertrophy – Preload reserve Again, contractility is typically well preserved, and the major threat is sensitivity of the hypertrophied ventricle to ischemia Demand – LV hypertrophy Supply – Increased LVEDP – Arterial Failure of proportionate epicardial coronary enlargement Increased wall: lumen ratio of coronary arterioles 20-30% decrease in capillary density Valve area is calculated AVR will be beneficial if contractility is maintained Group 1 – AV area same, gradient went up, CO went up à benefit from AVR (they have contractile reserve) Group 2 – CO went up, not much gradient or valve area change à benefit from AVR Group 3 – gradient & valve area decreases, CO unchanged à wont benefit from AVR, will die 3 ANESTHETIC MANAGEMENT OF AORTIC STENOSIS PRIMARY GOALS Maintain sinus rhythm (atrial kick) Normal to increased preload Normal to increased afterload (maintain coronary perfusion) AVOID: – Hypotension – Tachycardia – Bradycardia Other Anesthetic Management: Preop sedation (incremental w/ sedation) Oxygen Monitoring o ECG o CVP o PAC o TEE Induction – Narcotics probably ideal, but can be done many ways within the context of the stated goals and severity of disease – Avoid large decreases in SVR Maintenance – Primarily narcotic + nitrous oxide + low-dose volatile Hemodynamic Management – Maintain normal intravascular fluid volume (maybe aggressive?) – Be aggressive in managing hypotension and changes in heart rate Hypotension – Direct acting α agonist (phenylephrine)(want to avoid tachycardia) Tachycardia – Esmolol Bradycardia – Atropine, glycopyrrolate (incremental doses, tachycardia is very devastating) Maintenance of sinus rhythm is critical (atrial kick) AORTIC STENOSIS – OTHER CONSIDERATIONS TRANSCATHETER AORTIC VALVE REPLACEMENT Avoid vasodilators (don’t do it!) Use extreme caution with spinal and epidural anesthesia (particularly epidurals w/ epi – epi cause a drop in SVR as much or greater than a drop from spinal d/t activation of B2 receptors) Patients with aortic stenosis having non-cardiac surgery are at increased risk of MI, CHF, and supraventricular tachyarrhythmias Effective CPR through a stenotic aortic valve is extremely difficult History – First performed in 2002 and indicated for severe AS in a non-operable patient – Resulted in marked improvement in duration and quality of life – Current recommendation of TAVR versus SAVR High-risk patient - TAVR recommended Intermediate risk without anatomic issues – TAVR recommended Low risk – TAVR recommended when these 4 criteria met: – Age > 65 – Feasibility of transfemoral approach – Tri-leaflet valve – No anatomic issues » Adverse aortic root e.g., heavily calcified » Low coronary ostia height (height of the take off of coronary ostia above the valve) » LV outflow tract obstruction 4 TRANSCATHETER AORTIC VALVE REPLACEMENT Approach – Most commonly retrograde trans-femoral (can be done w/ MAC) Contraindications – Severe peripheral vascular disease (d/t emboli risk) – Tortuous vessels – Aortic disease – Other approaches (will be GA) Subclavian Axillary Trans-aortic Carotid others – – – – Vasopressors Defibrillation Bypass (ready access) Pacing – Patients more likely to need pacing: Pre-existing conduction abnormalities – 10 AV Block – Left anterior hemiblock – Right bundle branch block CORE VALVE recipients (more into outflow tract where ---Airway equipment if MAC needs to convert to general TRANSCATHETER AORTIC VALVE REPLACEMENT – VALVE SYSTEMS TRANSCATHETER AORTIC VALVE REPLACEMENT – AVAILABILITY – TRANSCATHETER AORTIC VALVE REPLACEMENT GETA TRANSCATHETER AORTIC VALVE REPLACEMENT MAC Advantages Airway is secure Control of ventilation o Can temporarily stop respiration (motionless field) TEE availability Disadvantages Increased incidence of postop delirium Increased mortality Greater hemodynamic instability When GETA is preferable: High-risk patient Non-transfemoral approach Need for TEE Chronic kidney disease (b/c injecting dye can be problematic to kidneys) Advantages Less hemodynamic instability Faster recovery Avoids intubation and ventilation Monitor of CNS events (primarily embolic, awake patient can ask questions, talk to them) *Reduced postop delirium 15% vs 50% with GETA *Reduced 30-day mortality 2.9% vs 4.1% with GETA Disadvantages Precludes use of TEE Time for conversion to GETA if necessary 5 AORTIC REGURGITATION AORTIC REGURGITATION Origins – Chronic Rheumatic fever, infective endocarditis, connective tissue disorders(e.g. Marfan’s) – Acute Aortic dissection or infective endocarditis Typically, a long, asymptomatic course with: – Gradual increase in regurgitant volume – Progressive ventricular enlargement (largest LV we will ever see) Symptoms – CHF In acute AR symptoms may be refractory to medical management TIMING OF AVR Symptoms correlate poorly with impaired contractility But: Once patients develop LV dysfunction there is a much higher perioperative mortality and an increase in prolonged postoperative heart failure Follow with serial echocardiography with pharmacologic afterload (maybe phenylephrine) enhancement to assess contractility AORTIC REGURGITATION VOLUME LOOP AR: ISCHEMIA Shifted far to the right – SV and EF maintained by using preload reserve No isovolumic diastolic phase because ventricle is backfilling Brief isovolumic systolic phase due to low aortic diastolic pressure Approximately 1/3 of patients will develop angina in the absence of CAD: – Increased myocardial mass – Disproportionate increase in mass relative to increase in coronary blood flow & marked decrease in aortic root pressure (DBP) d/t run off back to ventricle so coronary perfusion pressure is reduced) Problem of intraoperative bradycardia – Prolonged diastolic time Increased regurgitant flow – Rapidly increasing LV diastolic pressure and wall tension (impairs coronary perfusion) Coronary perfusion pressure decreased due to: – Increased diastolic aortic runoff – Increased diastolic LV pressure 6 ANESTHETIC MANAGEMENT OF AORTIC REGURGITATION PRIMARY GOALS Augment forward flow (reduce LV backflow) Increased preload Decreased afterload Avoid – Bradycardia – Myocardial depression Other Anesthetic Management: Monitoring – Ischemia – Pulmonary artery catheter Pacing May be a better patient for Swan but TEE is better if given the option – TEE Induction – Wide variety of acceptable approaches – Avoid bradycardia and increased afterload Maintenance – Dependent on severity of LV dysfunction – Balanced technique vs. primarily opioids – Regional Anesthesia??? (not controllable like IV and also wears off, better off in most cases doing a general anesthetic) MITRAL REGURGITATION ACUTE MITRAL REGURGITATION Acute and chronic forms produce very different outcomes CHRONIC MITRAL REGURGITATION Acute – – – – – Commonly due to papillary muscle dysfunction 20 AMI Sudden increase in preload increases LV contractility Availability of a low-pressure circuit (LA) decreases afterload LA pressure rapidly rises resulting in pulmonary edema and dyspnea Management If mitral apparatus intact reperfusion may be adequate If not, urgent valve repair or replacement is needed Organic – Diseases resulting in distortion, disruption, or destruction of the leaflets or chordal structures E.g., Rheumatic heart disease, endocarditis, connective tissue disorders Functional – Due to altered LV function or geometry in the presence of normal leaflets and chordae E.g., Dilated cardiomyopathy, ischemic changes Pathophysiology – Diastolic filling of LV consists of: Normal LA volume + regurgitant volume ¯ Volume overload of left ventricle ¯ Augmentation of contractility (and maintenance of EF) via: Frank-Starling mechanism Ejection into the relatively low-pressure LA – Over time both LV and LA are dilated – LA wall tension increases such that afterload ~ normal – Ultimately decompensation occurs and patients present with dyspnea and orthopnea 7 CHRONIC MITRAL REGURGITATION - VOLUME LOOP Right shift due to chamber enlargement (eccentric) Brief isovolumic contraction phase due to early ejection of blood into LA EF increased, but not forward flow TIMING OF REPAIR OR REPLACEMENT IN MITRAL REGURGITATION Preoperative EF most accurately predicts: – Long-term survival – Postoperative EF and CHF Predictors of better outcome: – EF > 60% – End-systolic LV diameter < 45 mm – Age less than 75 years If appropriate, repair provides better long-term outcome than replacement, and surgery is being done earlier, with better results. (before significant LV dysfunction) ANESTHETIC MANAGEMENT OF MITRAL REGURGITATION PRIMARY GOALS Augment forward flow Increased preload Decreased afterload Avoid: – Bradycardia – Myocardial depression Other Anesthetic Management Monitoring – PAC Cardiac output Volume trends – Compliance dependent V wave importance? – TEE Induction – Multiple options unless LV dysfunction is severe, in which case an opioid may be preferable – avoid bradycardia Maintenance – Multiple options – Combination of opioid + volatile anesthetic common – N2O controversial – Increased PVR?? Fluid Management – Balance between adequate preload and volume overload, particularly with presence of coexisting mitral stenosis Ventilation – Adjusted to provide adequate time for venous return – Mild hyperventilation preferable to hypoventilation, hypoxia, and acidosis which will elevate right sided pressure 8 MITRAL STENOSIS MITRAL STENOSIS OVERVIEW Most frequently due to rheumatic heart disease – Latency prior to symptoms ~ 20-30 years – Age of onset increasing – Slow progression of disease following onset of symptoms Much more common in females Symptoms: – Dyspnea on exertion – Palpitations (usually 1st complaint, can be new onset of A fib) – CHF Diagnosis made and progression monitored with echocardiography, assessing: Approximately 1/3 of patients with severe disease develop atrial fibrillation LA distention and A Fib increase risk of thromboembolic events Preload reserve is decreased LVEDV and LVEDP are reduced Stroke volume is reduced MITRAL STENOSIS MITRAL STENOSIS VOLUME LOOP MITRAL STENOSIS PROCEDURES AND TIMING ANESTHETIC MANAGEMENT OF MITRAL STENOSIS Patients with severe symptoms or stenosis, or significant pulmonary HTN are operated early (right away) Mild stenosis with few or no symptoms can be managed conservatively Procedures – Percutaneous mitral commissurotomy (PMC) aka Percutaneous balloon valvotomy (risk of emboli) – Open commissurotomy – Valve repair or replacement PRIMARY GOALS Control ventricular rate Normal to increased preload Normal afterload Avoid: – Tachycardia – Pulmonary vasoconstriction Other Anesthetic Management Monitoring – PAC Trends may be useful, but won’t accurately reflect LV volume TEE Sedation – Valuable for avoiding tachycardia, but avoid over sedation leading to hypoventilation Induction – Most are acceptable with the exception of ketamine – Opioid induction if needed – Maintenance – Balanced technique usually with narcotic and low-dose volatile – + Nitrous oxide – concerns with pulmonary HTN 9 MITRAL VALVE PROLAPSE MVP OVERVIEW Affects 1-2.5% of population More commonly in young women Etiology May be related to: Thyrotoxicosis Marfan syndrome SLE Myocarditis Rheumatic disease Definition – Valve leaflet prolapse > 2mm above annulus Things which worsen prolapse (increase LV emptying) – Increased contractility – Decreased SVR – Upright posture § Head up or sitting position for surgery Anesthetic Management – Similar to mitral regurgitation – Maintain adequate intravascular volume HEART MURMURS SOUNDS Systolic Diastolic Aortic Mitral Aortic Stenosis Mitral Regurgitation Aortic Regurgitation Mitral Stenosis Best heard at right 2nd intercostal space Radiation to neck Best heard at apex (5th ICS) Regurg radiation to axilla Stenosis – little radiation ANTICOA GULATION WITH A PROSTHETIC VALVE GUIDELINES General guidelines for patient with a mechanical valve Typically managed with low-dose ASA and a vitamin K antagonist. Desired INR varies but typically >2 – Discontinuing anticoagulation also varies considerably, but “generally”: Discontinue vitamin K antagonist 3-5 days preop Initiate heparin or LMWH when INR falls to subtherapeutic Discontinue heparin day of or day prior to surgery 10 AORTIC STENOSIS PRIMARY GOALS Maintain sinus rhythm (atrial kick) Normal to increased preload Normal to increased afterload (maintain coronary perfusion) AVOID: – Hypotension – Tachycardia – Bradycardia AORTIC REGURGITATION PRIMARY GOALS Augment forward flow (reduce LV backflow) Increased preload Decreased afterload Avoid – Bradycardia – Myocardial depression MITRAL REGURGITATION PRIMARY GOALS Augment forward flow Increased preload Decreased afterload Avoid: – Bradycardia – Myocardial depression MITRAL STENOSIS PRIMARY GOALS Control ventricular rate Normal to increased preload Normal afterload Avoid: – Tachycardia – Pulmonary vasoconstriction Blue – acute AR Green – chronic AR Increased systolic peak pressure (overcome stenotic valve) Increased chamber stiffness – Importance of atrial systole in LV filling Adequate preload Maintenance of sinus rhythm (need atrial kick) Stroke volume maintained by: – LV hypertrophy – Preload reserve Shifted far to the right – SV and EF maintained by using preload reserve No isovolumic diastolic phase because ventricle is backfilling Brief isovolumic systolic phase due to low aortic diastolic pressure Right shift due to chamber enlargement (eccentric) Brief isovolumic contraction phase due to early ejection of blood into LA EF increased, but not forward flow Preload reserve is decreased LVEDV and LVEDP are reduced Stroke volume is reduced 11 12