Heart Failure and Cardiomyopathies Student Notes PDF

HEART FAILURE AND CARDIOMYOPATHIES NRAN 80413 SPRING 2024 RON ANDERSON, M.D. 1 HEART FAILURE Definition Inability of the heart to fill with (diastolic failure) or eject (systolic failure) enough blood to meet tissue oxygen requirements Epidemiology Systolic heart failure – More common in males at an...

HEART FAILURE AND CARDIOMYOPATHIES NRAN 80413 SPRING 2024 RON ANDERSON, M.D. 1 HEART FAILURE Definition Inability of the heart to fill with (diastolic failure) or eject (systolic failure) enough blood to meet tissue oxygen requirements Epidemiology Systolic heart failure – More common in males at an earlier age due to the increased incidence of ischemic heart disease Diastolic heart failure – Higher incidence in elderly women due to increases in hypertension, obesity(and associated diabetes) following menopause 2 ETIOLOGY OF HEART FAILURE Systolic heart failure Decreased ejection fraction due to: – Ischemic injury – Dilated cardiomyopathy – Chronic volume overload » Aortic or mitral regurgitation – Chronic pressure overload » Long-standing hypertension » Aortic stenosis 3 MECHANISMS OF SYSTOLIC HEART FAILURE SNS Activation RAAS 4 ETIOLOGY OF HEART FAILURE Diastolic heart failure Due to decreased distensibility of the ventricle May exist independently or along with systolic HF Incidence increases with age Most common causes: – Long-standing hypertension – Ischemic heart disease – Aortic stenosis – Mechanism Impaired relaxation due to decreased Ca++ uptake by the sarcoplasmic reticulum and delayed transport of Ca++ out of the myocyte 5 SYSTOLIC vs DIASTOLIC 6 LEFT vs RIGHT HEART FAILURE Left heart failure LVEDP LA Pressure Pulmonary Venous Congestion Symptoms – Dyspnea, orthopnea, PND Right heart failure Right Heart Pressures Systemic Venous Congestion Symptoms – Peripheral edema, hepatomegaly 7 PRESSURE OVERLOAD HYPERTENSION AORTIC STENOSIS LV FRANK-STARLING RELATIONSHIP VOLUME OVERLOAD MITRAL REGURG AORTIC REGURG ISCHEMIA / INFARCTION MYOCARDIAL INFLAMMATORY DISEASE D Y S F U N C T I O N SNS ACTIVATION HUMORAL-MEDIATED RESPONSE RAAS MYOCARDIAL REMODELING THE PRIMARY PATHOPHYSIOLOGIC CHANGE LEADING TO DEVELOPMENT AND PROGRESSION OF HEART FAILURE ALTERED INOTROPY HEART RATE RESTRICTED DIASTOLIC FILLING AFTERLOAD 8 COMPENSATORY MECHANISMS IN LV DYSFUNCTION Frank-Starling Relationship Venous blood is shifted centrally, increasing preload Increased LVEDV and LVEDP increaseswall tension and subsequently stroke volume SNS Activation Venous constriction shifts blood centrally Arteriolar constriction maintains coronary and cerebral circulations at the expense of other organs Decreased renal blood flow activates RAAS High plasma NE levels produce: – Down-regulation of β-adrenergic receptors – Necrosis of myocytes leading to remodeling 9 COMPENSATORY MECHANISMS IN LV DYSFUNCTION Humoral-mediated response Vasoconstriction results from: – – – – – Activation of the SNS Activation of the RAAS Parasympathetic withdrawal Endothelial dysfunction High circulating levels of vasopressin and inflammatory mediators Myocardium attempts to compensate by increasing secretion of ANP and BNP Increased cardiac expression of ACE and Angiotensin II in the failing heart 10 CHANGES IN INOTROPIC STATE, HEART RATE, AND AFTERLOAD Inotropic state Sympathetic stimulation attempts to counter the decreased contractility of the failing ventricle Afterload Increased due to sympathetic stimulation and the subsequent arteriolar vasoconstriction Heart rate In systolic heart failure the heart rate is elevated to compensate for inability to increase stroke volume In diastolic heart failure the heart rate must be controlled to avoid further decreases in ventricular filling 11 MYOCARDIAL REMODELING The result of the bodies compensatory mechanisms to maintain cardiac output Most commonly a result of ischemic injury ACE Inhibitors effective in reversing the remodeling process 12 KAPLAN A VICIOUS CYCLE Mechanical Disadvantages Created by LV Remodeling LV DYSFUNCTION INITIAL COMPENSATORY INSULT MECHANISMS MYOCARDIAL REMODELING Increased wall stress Afterload mismatch Episodic subendocardial ischemia Increased O2 utilization Sustained hemodynamic overloading Increasing activation of compensatory mechanisms 13 PRESSURE OVERLOAD HYPERTENSION AORTIC STENOSIS LV FRANK-STARLING RELATIONSHIP VOLUME OVERLOAD MITRAL REGURG AORTIC REGURG ISCHEMIA / INFARCTION MYOCARDIAL INFLAMMATORY DISEASE D Y S F U N C T I O N SNS ACTIVATION HUMORAL-MEDIATED RESPONSE RAAS MYOCARDIAL REMODELING THE PRIMARY PATHOPHYSIOLOGIC CHANGE LEADING TO DEVELOPMENT AND PROGRESSION OF HEART FAILURE ALTERED INOTROPY HEART RATE RESTRICTED DIASTOLIC FILLING AFTERLOAD 14 HEART FAILURE Hemodynamic consequences Decreased cardiac output Increased LVEDP Peripheral vasoconstriction Sodium and water retention Decreased tissue oxygen delivery Widened arterial-venous oxygen gradient 15 SIGNS AND SYMPTOMS OF HEART FAILURE Dyspnea Increased work of breathing due to increased lung water Orthopnea Secondary to increased venous return in the recumbent position Fatigue and weakness Inadequate oxygen supply during work Anorexia, nausea, abdominal pain Liver congestion and prerenal azotemia Confusion, insomnia, worsening dementia Inadequate cerebral oxygen delivery 16 PHYSICAL EXAM IN HEART FAILURE LV Failure Tachypnea Basilar rales Tachycardia S3 RV or Biventricular Failure Jugular venous distention Peripheral edema 17 DIAGNOSTIC TESTING AND PROCEDURES BNP levels < 100 pg/ml gives a 90% negative predictive value 100 – 500 pg/ml - intermediate probability >500 pg/ml gives a 90% positive predictive value BUN / creatinine Prerenal azotemia Liver function tests Mild elevations to more severe derangements ( PT) Chest Xray Echocardiography 18 CLASSIFICATION OF HEART FAILURE New York Heart Association – Class I Ordinary physical activity does not cause symptoms – Class II Symptoms occur with ordinary exertion – Class III Symptoms occur with less than ordinary activity – Class IV Symptoms occur at rest 19 ACC/AHA CLASSIFICATION SYSTEM STAGE DESCRIPTION EXAMPLES A High risk for developing HF. No structural or functional disorders of the heart. No symptoms of HF. HTN, CAD, Diabetes mellitis,hx of RHD or alcohol abuse, family hx of cardiomyopathy B Structural heart disease strongly associated with HF. No symptoms of HF. LVH or fibrosis, LV dilation or decreased contractility, asymptomatic valvular dz, previous MI Structural heart disease with prior or current symptoms of HF. Dyspnea or fatigue due to LV dysfunction, asymptomatic currntly but being treated for prior symptoms of HF C D TREATMENT Frequent or prolonged Advanced structural heart disease. Marked symptoms of HF at rest despite hospitalization for HF, awaiting transplant, or in hospice care maximal medical therapy. 20 ADAPTED FROM ACC/AHA MANAGEMENT OF HEART FAILURE Short-term goals Symptom relief – Decrease congestion – Increase tissue perfusion Long-term goals Slow or reverse ventricular remodeling 21 MANAGEMENT OF HEART FAILURE HINES 22 MANAGEMENT OF HEART FAILURE Lifestyle modifications useful in preventing or delaying the progression of heart failure Smoking cessation Healthy diet with moderate sodium restriction Weight control Exercise Moderate alcohol consumption Glycemic control 23 INHIBITION OF THE RAAS ACE Inhibitors Promotes vasodilation Reduces salt and water reabsorption Decreases ventricular remodeling Promotes “reverse remodeling” Decrease morbidity and mortality in any stage of HF Angiotensin II receptor blockers Recommended in those unable to tolerate ACE Inhibitors Similar efficacy to ACE Inhibitors Consider alternative pathways of angiotensin production KAPLAN 24 EFFECTS OF ANGIOTENSIN II ON ANGIOTENSIN RECEPTORS AT1 RECEPTOR Increased salt and water reabsorption Vasoconstriction AT2 RECEPTOR Natriuresis Vasodilation Release of bradykinin and nitric oxide Inhibition of cell growth Inhibition of apoptosis Catecholamine release Cell growth and proliferation of cardiovascular tissue Cardiomyocyte hypertrophy Fibroblast proliferation Extracellular matrix deposition 25 ALDOSTERONE ANTAGONISM Spironolactone – Opposes effects of sodium and water retention, hypokalemia, and ventricular remodeling – Decreased mortality in late stage HF 26 KAPLAN BETA-BLOCKERS IN HF Useful in reversing the harmful effects of SNS activation Result in improved ejection fraction and decreased ventricular remodeling Shown to reduce morbidity and mortality 27 KAPLAN BETA-BLOCKERS IN HF 28 KAPLAN OTHER TREATMENT IN HF Diuretics Can rapidly decrease circulatory congestion and reduce LVEDP Digitalis Used when patients remain symptomatic despite ACEIs, beta-blockers, and diuretics Enhance inotropy Decrease activation of SNS and RAAS – Via restoration of normal baroreceptor function Vasodilators Decreased resistance to LV ejection and increase venous capacitance Statins Morbidity and mortality reduced due to anti-inflammatory and lipid lowering effects Anticytokines and endothelin receptor antagonists 29 OTHER TREATMENT IN HF Ivabradine (Corlanor) – Blockade of HCN channel responsible for cardiac pacemaker (If) current – Produces a dose-dependent reduction in heart rate – Results Reduces risk of hospitalization for heart failure No reduction in cardiovascular death or MI – Reference trials SHIFT BEAUTIFUL SIGNIFY 30 OTHER TREATMENT IN HF Sacubitril/Valsartan (Entresto) – Sacubitril – a prodrug neprilysin inhibitor Neprilysin responsible for breakdown of ANP, BNP, CNP – Valsartan – ARB which blocks the AT1 receptor – Results Sacubitril/valsartan versus Enalapril – 20% reduction in CV death, hospitalization for HF, 30-day readmission – 16% reduction in all-cause mortality – Reference trial PARADIGM-HF SGLT-2 Inhibitors – May be useful in HF with preserved EF 31 MANAGEMENT OF DIASTOLIC HF 32 KAPLAN MANAGEMENT OF ACUTE HF Traditional therapy Diuretics Vasodilators Inotropes IABP Surgical intervention Newer therapy Exogenous BNP Calcium sensitizers – levosimendan (Semdax) – Increases contractility and produces arterial dilation without increasing diastolic dysfunction Nitric oxide synthase inhibitors 33 PREDICTORS OF POOR PROGNOSIS IN HEART FAILURE Increased BUN and creatinine Hyponatremia Hypokalemia Severely depressed EF High levels of endogenous BNP Severely limited exercise tolerance Presence of multifocal PVCs 34 MECHANICAL ASSIST DEVICES (LVAD) KAPLAN 35 36 MECHANICAL ASSIST DEVICES TandemHeart Impella MYOCARDIAL RESTRAINT DEVICES Seem to slow the progression of ventricular dilation Offer no benefit in the already dilated and remodeled ventricle 37 ANESTHETIC MANAGEMENT OF PATIENT WITH NON-PULSATILE VAD General – Avoidance of chest compressions – Cautery Bipolar vs unipolar and dispersive electrode placement Monitoring – Blood pressure Arterial line – Oxygenation Cerebral oximetry – TEE 38 HYPOTENSION WITH A NONPULSATILE LVAD Common causes RV failure Decreased preload » Both of these first two will result in underfilling of the LV and may create a suction event with a constant flow LVAD Increased afterload Management Increase fluid volume Reduce LVAD flow rate Low-dose vasopressin Avoid increased PVR 39 ANESTHETIC MANAGEMENT OF HF Preoperative medications Beta-blockers ACE Inhibitors Diuretics ARBs Digoxin Continue +/+/+/Continue Laboratory Electrolytes BUN/creatinine LFTs ECG Echocardiogram 40 ANESTHETIC MANAGEMENT OF HF Induction Opioids desirable if HF is severe, otherwise many choices are acceptable Maintenance As above Ventilation Positive pressure ventilation + PEEP may be useful in decreasing pulmonary venous return and congestion Monitoring Dependent on extent of surgery and severity of disease Regional anesthesia Decreases in afterload may be beneficial, although not that predictable 41 CARDIOMYOPATHIES HYPERTROPHIC DILATED PERIPARTUM SECONDARY WITH RESTRICTIVE PHYSIOLOGY 42 HYPERTROPHIC CARDIOMYOPATHY Most common genetic cardiovascular disorder Incidence 1/500 Autosomal dominant Presents at any age Pathological features Myocardial hypertrophy Left ventricular outflow tract obstruction (LVOT) Anterior movement of mitral valve with systole Mitral regurgitation Diastolic dysfunction Myocardial ischemia Dysrythmias 43 HYPERTROPHIC CARDIOMYOPATHY Signs and symptoms Angina Fatigue Syncope Tachydysrhythmias Heart failure Treatment Beta-blockers Ca++ channel blockers Amiodarone AICD Septal myomectomy 44 ANESTHETIC MANAGEMENT OF HYPERTROPHICCARDIOMYOPATHY GOOD Mild decreases in contractility Volatiles Increased preload Maintained afterload Sinus rhythym BAD Sympathetic stimulation Pain Anxiety Post op shivering Decreased preload PPV / PEEP Abdominal insufflation Hypovolemia Vasodilation 45 DILATED CARDIOMYOPATHY Characteristics LV or biventricular dilation Systolic dysfunction Normal ventricular wall thickness Most common cardiomyopathy 3rd most common cause of heart failure #1 indication for cardiac transplant 46 DILATED CARDIOMYOPATHY Treatment As described for chronic heart failure Anticoagulation due to risk of thromboembolism from hypokinetic, enlarged chambers Prognosis 5 year mortality = 50% in symptomatic patients Anesthetic Management As described for heart failure 47 TAKOTSUBO (APICAL BALLOONING) Temporary loss of contractility in apical LV Most often stress related Females >> males Occurs in the absence of CAD – But presents as chest pain and dyspnea Treatment is supportive – Negative inotropes – IABP in some cases 48 PERIPARTUM CARDIOMYOPATHY Features Dilated cardiomyopathy Occurs from 3rd trimester to ~ 5 months postpartum Etiology unclear Viral Abnormal immune response to pregnancy Response to hemodynamic changes of pregnancy Symptoms Dyspnea, fatigue, peripheral edema Treatment Diuretics, vasodilators, digoxin ACE Inhibitors are teratogenic Prognosis Up to 50% mortality 49 RESTRICTIVE CARDIOMYOPATHY Etiology Due to systemic diseases which produce myocardial infiltration – – – – Amyloidosis Hemochromatosis Sarcoidosis Carcinoid Pathophysiology Infiltration produces increased stiffness of the ventricle with decreased compliance and diastolic dysfunction Systolic function typically normal Symptoms Those of heart failure in the absence of cardiomegaly 50 RESTRICTIVE CARDIOMYOPATHY Treatment Similar to that of diastolic heart failure Prognosis Very poor Anesthetic management goals Maintenance of sinus rhythm Avoid bradycardia Maintain fluid status and venous return 51 SOURCES Anesthesia and Coexisting Disease. Hines, Marschall. 8th Edition. 2022 Kaplan’s Cardiac Anesthesia. Kaplan. 7th Edition. 2016 Miller’s Anesthesia. Miller. 9th Edition. 2020 52