In Action!!! Physiology. Ventricular Hypertrophy ANESTHETIC MANAGEMENT OF THE PATIENT WITH VALVULAR HEART DISEASE

Transcription

1 ANESTHETIC MANAGEMENT OF THE PATIENT WITH VALVULAR HEART DISEASE Physiology In Action!!! Peggy Contrera, MSN, CRNA CWRU/CC School of Nurse Anesthesia Department of Cardiothoracic Anesthesia Cleveland Clinic Health System 1 2 Anesthetic Management of Valvular Heart Disease Abnormal pressure and volume loads Structural and functional mechanisms of compensation Events that signal the limits of compensation (dysrhythmias, CHF) Secondary complications (endocarditis or emboli) Factors affecting blood flow across the valve 1. Valve Area Stenotic lesions fixed Regurgitant lesions variable based on loading conditions (preload and afterload) 2. Square root of the hydrostatic pressure gradient across the valve 3. Duration of flow whether systole or diastole Goals Stenotic lesions maximize or enhance transvalvular flow Regurgitant lesions minimize regurgitant transvalvular flow 3 4 Ventricular Function Ventricular Hypertrophy Systolic Function Ability to contract and generate a force against an afterload Directly related to contractility which is independent of changes in preload and afterload Cardiac output however, does change based on preload and afterload ESV/ESP Diastolic Function Ability to relax and accept preload EDP/EDV Directly related to compliance Both systolic and diastolic function require energy and can be compromised by ischemia! 5 6

2 Ventricular Hypertrophy Concentric Hypertrophy: Occurs with pressure overload Parallel replication of sarcomeres wall thickness (volume constant) Wall tension = P x R/2h. Laplace's Law Eccentric Hypertrophy Occurs with volume overload Results in an chamber size (heart dilates) The Cardiac Cycle and The Pressure -Volume Loop Phase 1: Diastolic Filling Phase 2: Isovolumetric Contraction Phase 3: Systolic Ejection Phase 4: Isovolumetric Relaxation Systole C F (phases 2 & 3) Diastole F C (phases 1 & 4) ESV EDV SV 7 8 Pressure -Volume Relationships ESPVR Reflects Contractility Preload Afterload Compliance (EDPVR) Contractility (ESPVR) EF Systolic Dysfunction Diastolic Dysfunction 9 10 Alterations in Preload and Afterload Systolic (ESPVR) and Diastolic Dysfunction (EDPVR) 11 12

3 All Valvular Defects Each Valve Defect 13 Etiology Natural History Anatomy Pathophysiology Pressure-Volume Relationship Murmur Anesthetic Considerations Homodynamic Goals Monitoring Anesthetic Technique Treatment of Untoward Events Surgical Options 14 Aortic Stenosis Etiology of Aortic Stenosis Most serious valvular defect Carries the highest risk of sudden death AS is present in 40% of pt w/ CAD Independently risk of MI 2.4 fold Perioperative mortality is 11% w/ critical AS Congenital Unicuspid (90% have AI) Bicuspid Tricuspid Acquired Calcified (most common esp. w/ age age) Rheumatic Causes of AS as a Function of Age Natural History Long Asymptomatic Period Rx w/ statins and ACE inhibitors Survival 5 years after onset of ANGINA* 3 years after onset of SYCOPE 2 years after onset of CHF* Sudden Death! From Passik CS, Ackermann DM, Pluth JR, Edwards WD: Temporal changes in the causes of aoertic stenosis: A surgical patholologic study of 645 cases. Mayo Clin Proc 62;119, ***Caution when using nitrates to treat angina or CHF**** 18

4 Anatomy of AS VALVE AREA (cm 2 ) GRADIENT (mm Hg) Normal : 3 0 Mild (Stage 1) > Moderate (Stage 2) Severe (Stage 2) < 1.0 >40 Critical (Stage 3) < 0.75 Jet Flow > 4.5 m/sec or an 0.3 m/sec/year or LV EF < 50% Pathophysiology of Aortic Stenosis Aortic Stenosis Obstruction to LV Ejection Pressure Gradient Created Across the Valve Chronic LV Pressure Overload Parallel Replication of Sarcomeres 19 Concentric LV Hypertrophy 20 Pathophysiology of AS Concentric Hypertrophy (normal chamber size) Decreased Compliance LVEDP Reliance on atrial kick (40% of LVEDV) CO and EF are initially normal (don t t let this fool you!) Very Vulnerable to Ischemia Demand d/t muscle mass and wall tension Supply d/t diastolic time and LVEDP HR can be disastrous Maintaining diastolic BP is essential CPR is often ineffective Acute AS the Pressure -Volume Loop Pressure Gradient Across the Valve 23 24

5 Physical Findings Mid systolic Ejection murmur RSB, 2nd ICS ECG LVH ECG: LVH Monitoring A-Line: Slow upstroke pulsus tardus Late peak w/ loss of the dicrotic notch causing a narrow pulse pressure pulsus parvus PAP waveform Great beat to beat respiratory variation Echo: Narrowed orifice (causing jet) LVH Homodynamic Goals HEMODYNAMIC GOALS P- Full: adequate intravascular volume to fill noncompliant ventricular chamber Preload Need increased preload to fill noncompliant LV. A- Already elevated, but relatively fixed; coronary perfusion pressure must be maintained C- Usually not a problem; inotropes may be helpful preinduction in end-stage AS with hypotension R- Not too slow ( ( CO), not too fast (ischemia) Rhy- Sinus!! Cardioversion if hemodynamic crash from supraventricular dysrhythmia MVO2- Ischemia is an ever-present risk; tachycardia and hypotension must be avoided 27 Heart Rate Contractility SVR PVR Slow Normal Sinus Maintain Maintain Avoid extremes of HR. Decreased CO with very slow HR, ischemia with fast HR. Maintain Sinus Rhythm. Usually not a problem; inotropes may be helpful preinduction in end-stage aortic stenosis with hypotension. Afterload is elevated, but relatively fixed; coronary perfusion pressure must be maintained. Avoid hypotension. PA pressures remain relatively normal until end-stage aortic stenosis. 28 Anesthetic Technique Surgical Options Regional Maintain filling pressure Keep diastolic BP up Adequate pain control (avoid tachycardia) General Etomidate and primary narcotic technique Low dose inhalation Junctional rhythm is a distinct disadvantage 29 Repair: rarely possible Replacement: Bioprosthesis Porcine( pig valve) or Bovine (cow pericardium sewn on frame) No anticoagulation Lasts years Mechanical Require anticoagulation Careful antibiotic prophylaxis Lasts a lifetime Other Options Homografts (cadaver valves) Ross Procedure (Pulmonary Valve placed in Aortic Position) Percutaneous AVR 30

6 Hypertrophic Cardiomyopathy (HCM) HOCM AKA: HOCM: Hypertrophic Obstructive Cardiomyopathy IHSS: Idiopathic Hypertrophic Subaortic Stenosis HCM HCM- Medical Management Etiology: Genetic (mutation of the B-myacinB heavy chain) Most common genetically transmitted CVD Leading Cause of Death in Athletes < 35 Natural History LVH in septum, apex and midventrical (> 30 mm) Not all patients are at equal risk, family hx of sudden death or documented obstruction are risk Sx include: syncope, dyspnea, palpitations, PND, CHF, fatigue MR causes LA enlargement making the patient prone to A-fibA Sx worsen with HR, preload, hypotension, PPV, and peep Obstruction is worse with MR caused by SAM ( systolic anterior motion of the mitral valve) 33 Medications- Beta blockers to control HR and outflow obstruction Ca channel blockers to improve ventricular filling and ischemia Disopyramide to contractility Amiodarone for atrial dysrhythmias Procedures- Ethanol ablation of septal perforators AICD Asynchronous RV prexcitation biventricular pacing 34 Septal Myectomy Hemodynamic Goals in HOCM 35 36

7 HOCM: HEMODYNAMIC GOALS Preload Heart Rate Contractility SVR PVR Decreased Decreased Maintain preload reduces the gradient across LVOT. Avoid hypovolemia. Decreased HR reduces oxygen demand of thickened myocardium. May also allow time for adequate LV filling. Decreased contractility reduces gradient across LVOT. Beta- blockade is beneficial. afterload reduces the gradient across LVOT. Thickened myocardium requires increased diastolic BP. Usually not a problem. 37 SAM Intraoperative transesophageal echocardiography images demonstrating systolic anterior motion of the anterior mitral valve leaflet (upper right panel) and an interleaflet gap (lower left panel) through which a jet of mitral regurgitation (lower right panel) is centrally directed into the left atrium 38 Aortic Insufficiency Etiology of AI Congenital: (rarely an isolated lesion) Acquired: Acute Infective endocarditis Dissections of the thoracic aorta d/t Marfan s or thoracic trauma Chronic RHD is the most common cause Aortic root annuloaortectasia from Aging Chronic HTN Connective tissue disorders Appetite suppressant meds (fenfluramine( fenfluramine) Natural History of AI Anatomy: AV Incompetence Acute Sudden LV failure Pulmonary congestion Systemic hypotension Chronic Long asymptomatic period (20 years) Regurgitant flow volume overload. Volume overload SV HTN Pressure Overload. Progressive eccentric hypertrophy of LV When failure finally occurs, damage is irreversible LV function is both an early and late predictor of mortality after AVR Survival after sx begin is years 41 Classification Grade Mild Moderate Severe (wide open) Regurgitant Fraction < 40% 40-60% >60% Symptoms Minimal Dyspnea & CHF Angina, CHF, Irreversible LV dysfunction 42

8 Pathophysiology of Aortic Regurgitation Backward flow of blood from aorta into LV (Diastolic) Rapid fall of aortic pressure during diastole SV (Frank-Starling Mechanism) Peak systolic pressure increased because of increased SV ejected into aorta LV volume and pressure LA pressure pulmonary venous pressure Pulmonary edema diastolic pulse pressure wall-tension produces eccentric hypertrophy Pressure Volume Relationship Classic Murmur of AI Decrescendo 2 nd ICS RSB Homodynamic Goals P- Normal - Full: adequate intravascular volume to fill compliant ventricle A- Reduction beneficial with vasodilators or anesthetics; Increases augment regurgitant flow C- Usually adequate AORTIC REGURGITATION: HEMODYNAMIC GOALS Preload Heart Rate Because of increased LV volumes, need increased preload to maintain forward flow. Avoid hypovolemia. HR reduces diastolic time and reduces regurgitant fraction. Also raises diastolic BP and decreases LVEDP. R- Modest tachycardia reduces ventricular volume, raises aortic diastolic pressure Contractility Maintain Must be maintained. Rhy- Usually sinus MVO2- Not usually a problem 47 SVR PVR Decreased Maintain Afterload reduction is helpful in improving forward flow. PA pressures remain relatively normal except in patients with end- stage disease. 48

9 Monitoring Anesthetic Management ECG A-line: Rapid upstroke with low dicrotic notch Wide pulse pressure ( mmhg) Double peaked (biferiens( biferiens) Bounding CVP PA Catheter (giant V wave on wedge trace) TEE Grade regurgitant fx Assess adequacy of repair or replacement 49 Regional Anesthesia Afterload reduction reduces regurgitant fx and enhances forward flow Maintain intravascular volume General Anesthesia Use agents that maintain or elevate HR Potent agents are OK Etomidate/Narcotic technique good for poor LVF Maintain intravascular volume 50 Surgical Options Mitral Stenosis Indications: All symptomatic patients Asymptomatic patients with LV fx Options: Repair with annuloplasty ring or valvular plication Replace with mechanical or biologic valve Experimental percutaneous AV replacement Etiology Natural History Congenital Acquired Rheumatic Fever (2 x s as frequent in women) Sometimes after radiation of the chest from breast or other CA Rheumatoid Arthritis, lupus or carcinoid syndrome Stenosis begins 2 yrs after RHD 20 yr asymptomatic Sx begin in 40 s- 50 s Heart failure is most common presentation 40% develop a-fiba Sx develop w/pregnancy, anemia, infection 53 54

10 Anatomy of MS Pathophysiology of MS VALVE AREA (cm 2 ) Normal : 4-6 SYMPTOMS LV fx usually maintained (15% LV dysfunction) PG = (Cardiac Output) 2 Diastolic Filling Time Mild (Stage 1) with exercise Moderate (Stage 2) mild exertion onset of a-fiba Severe (Stage 3) < 1.0 at rest A-fib PG (2 o rapid HR) pulmonary edema Pulmonary HTN (80%) 5-15 x s In PVR V/Q mismatches (reversal in normal apex to base perfusion gradient) Pathophysiology of Mitral Stenosis Obstruction to LA emptying Decreased LV filling LA pressure LA size Pulmonary edema pulmonary venous pressure Atrial fibrillation pulmonary artery pressure RV overload Pressure Volume Relationships Pressure Volume Loop 59 60

11 Murmur MS Hemodynamic Goals MS P- Enough to maintain flow across stenosis A- Avoid RV afterload (pulmonary vasoconstrictors)? inotropes for systemic hypotension C- LV usually OK until after CPB; right ventricle may be impaired if there is long-standing pulmonary hypertension R- Slow to allow time for ventricular filling Diastolic rumbling murmur Heard best at the apex Rhy- Often atrial fibrillation; control ventricular response MVO2- Not a problem 61 CPB- Vasodilators may help post CPB RV failure; control of ventricular response may be difficult 62 Hemodynamic Goals Monitoring Avoid Tachycardia Continue/Administer meds that control HR Treat new onset A fib aggressively (control ventricular rate) Avoid Exacerbations of PHT Avoid hypoxia, hypercarbia and acidosis Avoid N 2 O Avoid trendelenburg position Rx PHT w/ hypocapnia, NTG, and Nitric Oxide Watch for RV failure and consider Milrinone Maintain adequate intravascular volume Treat hypotension with volume (vasoconstrictors can worsen PHT) Early use of inotropes if needed EKG A-line Pa Cath PCWP or LAP will be > LVEDP With tachycardia, LAP while LVEDP TEE Check adequacy of repair Check for leaks Check for regurgitation after commissurotomy Anesthetic Technique Surgical Options Regional Caution d/t residual anticoagulation Avoid hypotension. Position for adequate ventilation Maintain intravascular volume General Consider Etomidate/narcotic technique for PHT or severe LV Inhalation agents OK except N 2 O Avoid agents that HR Maintain intravascular volume Commissurotomy-fused leaflets are separated Decalcification Replacement with bioprosthetic or mechanical valve If full sternotomy- Maze or Pulmonary Vein Isolation to treat A-fibA Left atrial appendage ligation or resection A-fib treated with radiofrequency (heat) ablation or cryotherapy (freeze) ablation 65 66

12 Mitral Insufficiency or Regurgitation Etiology of MR Congenital-rare Acquired- both acute and chronic RHD- rare Most commonly encountered valve lesion Mitral Valve Prolapse (MVP) Most common cause 15% will develop chronic MR Chronic LVH w/ annular dilation (eccentric hypertrophy) MVP Myxomatous degeneration Fenfluramine appetite suppression Acute Papillary muscle dysfunction Ruptured chordea tendinea (most often d/t ischemia) Bacterial endocarditis Natural History Anatomy: MV Incompetence Variable Long asymptomatic period w/ eccentric hypertrophy of LA and LV Sx of forward heart failure develop (fatigue, weakness) Dysfunction is significant if EF is 50% Classification Mild (stage 1) Moderate (stage 2) Severe (stage 3) Grade Regurgitant Fraction < 30% 30-60% >60% Symptoms Minimal Fatigue, weakness, CHF CHF, Irreversible LV dysfunction Pathophysiology Chronic MR LV volume load eccentric hypertrophy Regurgitant volume determined by atrial/ventricular pressure gradient Ventricular size directly correlates with annulus size Vasodilators may improve hemodynamics ( ( LV size) Patients with sx have underlying LV dysfunction Acute MR LAP and PAP pulmonary edema and RHF In Acute MI w/ MR ischemia is usually present and survival is poor 71 72

13 Pathophysiology of Mitral Regurgitation Backward flow of blood from LV to LA (Systolic) Pressure Volume Relationship Left atrial enlargement LA volume and pressure LV filling ( LVEDV) pulmonary venous pressures SV Pulmonary edema Blood ejected into aorta Pressure Volume Loop in Chronic MR Murmur (Pansystolic or Holosystolic) Hemodynamic Goals In MR Hemodynamic Considerations Mild Tachycardia Low SVR (peripheral venodilation) Exception: : in patients with MVP who have redundant leaflets because higher HR and Low SVR will cause more obstruction to flow 77 78

14 Monitoring Monitoring Anesthetic Anesthetic Technique Technique EKG RegionalRegional- benefits from afterload General Inhalation/STP is OK for normal LV Etomidate/Narcotic for impaired LV A-line CVP PA CathCath- classic giant V wave TEE Surgical Surgical Options Options Mini Mitral Valve Repair Repair (Cosgrove Ring for Annuloplasty) Annuloplasty) Robotically Assisted MV repair or replacement Percutaneous mitral valve repair (E(E- Valve) Repair flail leaflet, Chordae or papillary muscle Replacement with biologic or mechanical valve If Full Sternotomy: Maze or PV Isolation for A-fib Thanks for Your Attention A Pleasure and a Privilege! 83