Heart Failure and Cardiomyopathies PDF

HEART FAILURE AND CARDIOMYOPATHIES HEART FAILURE ETIOLOGY OF HEART FAILURE Definition – Inability of the heart to fill with (diastolic failure) or eject (systolic failure) enough blood to meet tissue oxygen requirements (about 1% of population over 65 years old have HF) Epidemiology – Systolic heart...

HEART FAILURE AND CARDIOMYOPATHIES HEART FAILURE ETIOLOGY OF HEART FAILURE Definition – Inability of the heart to fill with (diastolic failure) or eject (systolic failure) enough blood to meet tissue oxygen requirements (about 1% of population over 65 years old have HF) Epidemiology – Systolic heart failure o More common in males at an earlier age due to the increased incidence of ischemic heart disease – Diastolic heart failure o Higher incidence in elderly women due to increases in hypertension, obesity (and associated diabetes) following menopause (LV can’t relax to fill, its stiffà results in LVH & failure of lusitrophy) Systolic heart failure (aka HF w/ reduced EF) – Decreased ejection fraction due to: o Ischemic injury o Dilated cardiomyopathy o Chronic volume overload § Aortic or mitral regurgitation o Chronic pressure overload § Long-standing hypertension § Aortic stenosis MECHANISMS OF SYSTOLIC HEART FAILURE - Ron says ignore SNS activation à RAAS à ETIOLOGY OF HEART FAILURE Diastolic heart failure (preserved ejection fraction) – Due to decreased distensibility of the ventricle (can’t effectively fill) – May exist independently or along with systolic HF – Incidence increases with age – Most common causes: (pressure overload à LVH) o Long-standing chronic hypertension o Ischemic heart disease o Aortic stenosis Mechanism – Impaired relaxation due to decreased Ca++ uptake by the sarcoplasmic reticulum and delayed transport of Ca++ out of the myocyte SYSTOLIC vs DIASTOLIC Systolic – pump out a lower EF Diastolic – they have preserved EF, they can pump out whatever blood was in the ventricle, but there isn’t much blood in the ventricle 1 Insults LEFT vs RIGHT HEART FAILURE Compensatory Mechanisms - Most common cause of Right HF? Left HF COMPENSATORY MECHANISMS IN LV DYSFUNCTION COMPENSATORY MECHANISMS IN LV DYSFUNCTION CHANGES IN INOTROPIC STATE, HEART RATE, AND AFTERLOAD MYOCARDIAL REMODELING -skip picture Frank-Starling Relationship – Venous blood is shifted centrally, increasing preload (d/t SNS activation) – Increased LVEDV and LVEDP increases wall tension & subsequently stroke volume (but increases workload on the failing heart leading to hypertrophy/remodeling) SNS Activation – Venous constriction shifts blood centrally – Arteriolar constriction maintains coronary & cerebral circulations potentially at the expense of other organs (like kidneys) – Decreased renal blood flow activates RAAS – High plasma NE levels produce: o Down-regulation of β-adrenergic receptors (resistant to endogenous catecholamines) o Necrosis of myocytes leading to remodeling Humoral-mediated response – Vasoconstriction results from: o Activation of the SNS o Activation of the RAAS o Parasympathetic withdrawal o Endothelial dysfunction (decreased nitric oxide) o High circulating levels of vasopressin and inflammatory mediators – Myocardium attempts to compensate by increasing secretion of ANP and BNP (vasodilation, naturesis) – Increased cardiac expression of ACE and Angiotensin II in the failing heart (acts on AT1 receptor à leads to remodeling of the heart) 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 (low EF) – In diastolic heart failure the heart rate must be controlled to avoid further decreases in ventricular filling (need adequate time to fill) 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 (or ARBS if can’t tolerate ACE) 2 A VICIOUS CYCLE Mechanical Disadvantages Created by LV Remodeling – Increased wall stress – Afterload mismatch – Episodic subendocardial ischemia – Increased O2 utilization – Sustained hemodynamic overloading – Increasing activation of compensatory mechanisms Insults Compensatory Mechanisms HEART FAILURE HEART FAILURE Hemodynamic consequences – Decreased cardiac output – Increased LVEDP – Peripheral vasoconstriction – Sodium and water retention – Decreased tissue oxygen delivery (d/t decreased CO) – Widened arterial-venous oxygen gradient (in periphery, heart O2 extraction is maximal all the time) SIGNS AND SYMPTOMS OF HEART FAILURE -acute HF is THE most ominous predictor of a bad outcome – can you climb a flight of stairs w/out getting SOB? PHYSICAL EXAM IN HEART FAILURE Dyspnea – Increased work of breathing due to increased lung water Orthopnea – Secondary to increased venous return in the recumbent/lying down position (nonproductive cough) Fatigue and weakness – Inadequate oxygen supply during work (can be difficult to assess MET level, sedentary lifestyle in a lot of people & can be difficult to assess) Anorexia, nausea, abdominal pain – Liver congestion and prerenal azotemia (increased nitrogen secondary to urea) Confusion, insomnia, worsening dementia – Inadequate cerebral oxygen delivery LV Failure – Tachypnea – Basilar rales – Tachycardia – S3 (sudden deceleration of blood from LA to LV) RV or Biventricular Failure – Jugular venous distention – Peripheral edema 3 DIAGNOSTIC TESTING AND PROCEDURES CLASSIFICATION OF HEART FAILURE ACC/AHA CLASSIFICATION SYSTEM 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 – On Entresto, you can’t use BNP levels b/c impairs breakdown, so level is inaccurate BUN / creatinine – Prerenal azotemia Liver function tests – Mild elevations to more severe derangements ( á PT) Chest Xray (useful but lags behind acute clinical symptoms) Echocardiography (gold standard but not needed every time) 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 Treatment: A – preventive, ACE/ARB B – prevention, ACE/ARB, maybe BB C – ACE/ARB, diuretics, digoxin, BB D – all the above, mechanical, etc. - don’t memorize Anyone with those risk factors for HF should be started on an ACE inhibitor unless they have a contraindication, then start/switch to ARB. ACE inhibitors are the initial mainstay first line drug to slow the progression of heart failure. MANAGEMENT OF HEART FAILURE 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 4 INHIBITION OF THE RAAS EFFECTS OF ANGIOTENSIN II ON ANGIOTENSIN RECEPTORS 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 AT1 RECEPTOR (AGII formed in heart acts primarily on AT1 receptors)(Ron says “bad” ones) Increased salt and water reabsorption Vasoconstriction Catecholamine release Cell growth and proliferation of cardiovascular tissue (remodeling) – Cardiomyocyte hypertrophy – Fibroblast proliferation – Extracellular matrix deposition AT2 RECEPTOR (Ron says good ones in HF, oppose remodeling) Natriuresis Vasodilation Release of bradykinin and nitric oxide (vasodilatory) Inhibition of cell growth (reverse remodeling) Inhibition of apoptosis ALDOSTERONE ANTAGONISM Spironolactone – Opposes effects of sodium and water retention, hypokalemia, & ventricular remodeling – Decreased mortality (30% â) in late-stage HF BETA-BLOCKERS IN HF Useful in reversing the harmful effects of SNS activation (usually 2nd line drug) Result in improved ejection fraction and decreased ventricular remodeling Shown to reduce morbidity and mortality (significantly) 5 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 (á) inotropy – Decrease activation of SNS and RAAS o Via restoration of normal baroreceptor function Vasodilators – Decreased resistance to LV ejection (âSVR in systolic HF patient) and increase venous capacitance (but would be a bad idea in diastolic HF) Statins – Morbidity and mortality reduced due to anti-inflammatory and lipid lowering effects Anticytokines and endothelin receptor antagonists Ivabradine (Corlanor) – Blockade of HCN (hyperpolarization nucleotide gated chloride channels) - channel responsible for cardiac pacemaker (If) current – Produces a dose-dependent reduction in heart rate – Results o Reduces risk of hospitalization for heart failure o No reduction in cardiovascular death or MI (just keeps the out of the hospital as often) Reference trials o SHIFT o BEAUTIFUL o SIGNIFY Sacubitril/Valsartan (Entresto) – Sacubitril – a prodrug neprilysin inhibitor o Neprilysin responsible for breakdown of ANP, BNP, CNP – Valsartan – ARB which blocks the AT1 receptor – Cannot use BNP for accurate measurement – need to get NT-proBNP level (N-terminal prohormone of brain natriuretic peptide) – Results o Sacubitril/valsartan versus Enalapril – 20% reduction in CV death, hospitalization for HF, 30-day readmission – 16% reduction in all-cause mortality – Reference trial o PARADIGM-HF (stopped early d/t overwhelming positive results) SGLT-2 Inhibitors – May be useful in HF with preserved EF MANAGEMENT OF DIASTOLIC HF -Diastolic HF is difficult to treat, overall try to treat most patients most at risk early - skip chart Treat patients early who are most at risk: HTN, old, DM 6 MANAGEMENT OF ACUTE HF PREDICTORS OF POOR PROGNOSIS IN HEART FAILURE - sick ppl do worse J MECHANICAL ASSIST DEVICES (LVAD) Traditional therapy – Diuretics – Vasodilators – Inotropes – IABP – Surgical intervention Newer therapy – Exogenous BNP – Calcium sensitizers – levosimendan (Semdax) o Increases contractility & produces arterial dilation without increasing/worsening diastolic dysfunction – Nitric oxide synthase inhibitors Increased BUN and creatinine (renal insufficiency) Hyponatremia Hypokalemia Severely depressed EF High levels of endogenous BNP (implies severe HF) Severely limited exercise tolerance Presence of multifocal PVCs Risks are infection, bleeding, thrombosis MECHANICAL ASSIST DEVICES MYOCARDIAL RESTRAINT DEVICES Seem to slow the progression of ventricular dilation Offer no benefit in the already dilated and remodeled ventricle ANESTHETIC MANAGEMENT OF PATIENT WITH NON-PULSATILE VAD General – Avoidance of chest compressions – Cautery Bipolar vs unipolar and dispersive electrode placement (place pad so current doesn’t cross path of the mechanical device)(bipolar is better) Monitoring – Blood pressure Arterial line (may be difficult to place A line) – Oxygenation Cerebral oximetry (will give you an idea of perfusion of MCA) – TEE (echo would be best) 7 HYPOTENSION WITH A NON-PULSATILE LVAD ANESTHETIC MANAGEMENT OF HF ANESTHETIC MANAGEMENT OF HF Common causes – RV failure – Decreased preload o 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 (maintain fluid volume) – Reduce LVAD flow rate – Low-dose vasopressin – Avoid increased PVR Preoperative medications – Beta-blockers à Continue – ACE Inhibitors à Continue (deal with hypotension if it develops) – Diuretics à Continue – ARBs à Continue (deal with hypotension if it develops) – Digoxin à Continue Laboratory – Electrolytes – BUN/creatinine – LFTs (sometimes) – ECG – Echocardiogram (not always necessary) 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 (not ideal in isolated diastolic HF patient) Monitoring – Dependent on extent of surgery and severity of disease Regional anesthesia – Decreases in afterload may be beneficial, although not that predictable (Ron - don’t do it with the intention of dropping their afterload) CARDIOMYOPATHIES HYPERTROPHIC CARDIOMYOPATHY 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 “SAM” (results in LVOT) – Mitral regurgitation – Diastolic dysfunction – Myocardial ischemia (likely d/t ventricular hypertrophy to overcome LVOT) – Dysrhythmias 8 HYPERTROPHIC CARDIOMYOPATHY ~ S&S, TREATMENT HYPERTROPHIC CARDIOMYOPATHY ~ ANESTHETIC MANAGEMENT - Primary goal is to minimize left ventricular outflow tract obstruction so avoid SNS stimulation Signs and symptoms – Angina – Fatigue – Syncope – Tachydysrhythmias – Heart failure Treatment – Beta-blockers (slow HR & á diastolic perfusion/filling time) – Ca++ channel blockers (reduce ischemia, improve diastolic filling) – Amiodarone (for tachydysrhythmias) – AICD – Septal myomectomy (remove tissue blocking the tract) GOOD (avoid excessive SNS, so avoid Ketamine) Mild decreases in contractility (but could be problematic if they have LVOT, so don’t decrease SVR too much, they need to be able to perfuse coronary’s) – Volatiles Increased preload Maintained afterload Sinus rhythm (need to fill LV) BAD Sympathetic stimulation – Pain – Anxiety – Post op shivering Decreased preload – PPV / PEEP – Abdominal insufflation (like w/ deep NMB, it can be useful to â insufflation pressures ) Hypovolemia Vasodilation DILATED CARDIOMYOPATHY DILATED CARDIOMYOPATHY ~ CHARACTERISTICS DILATED CARDIOMYOPATHY ~ TREATMENT, PROGNOSIS, ANESTHETIC MANAGEMENT Characteristics – LV or biventricular dilation (may produce regurg b/c valves don’t close together, too big) – Systolic dysfunction – Normal ventricular wall thickness (eccentric hypertrophy) Most common cardiomyopathy (don’t confuse it w/ hypertrophic b/c that one’s genetic) 3rd most common cause of heart failure #1 indication for cardiac transplant 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 9 TAKOTSUBO TAKOTSUBO (APICAL BALLOONING) Temporary loss of contractility in apical LV (typically only lasts a couple months) Most often stress related (broken heart syndrome, stress induced cardiomyopathy) Females >> males Occurs in the absence of CAD – But presents as chest pain and dyspnea Treatment is supportive – Negative inotropes, maybe beta blockade – IABP in some cases PERIPARTUM CARDIOMYOPATHY PERIPARTUM CARDIOMYOPATHY - often times these patients are anticoagulated, before placing a block you may need labs! 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 – NO ACE Inhibitors à they are teratogenic Prognosis – Up to 50% mortality (often during post-partum period) RESTRICTIVE CARDIOMYOPATHY RESTRICTIVE CARDIOMYOPATHY RESTRICTIVE CARDIOMYOPATHY SUICIDE LV – Ron may ask Etiology – Due to systemic diseases which produce myocardial infiltration o Amyloidosis o Hemochromatosis o Sarcoidosis o Carcinoid Pathophysiology – Infiltration produces increased stiffness of the ventricle with decreased compliance and diastolic dysfunction (resembles tamponade almost, can’t fill the heart) – Systolic function typically normal Symptoms – Those of heart failure in the absence of cardiomegaly Treatment – Similar to that of diastolic heart failure (transplant usually avoided b/c will just re-damage the new heart) Prognosis – Very poor Anesthetic management goals – Maintenance of sinus rhythm (need filling) – Avoid bradycardia (stroke volume is likely fixed, bradycardia could produce acute HF) – Maintain fluid status and venous return (stay on top of blood loss, minimize PEEP) After opening/repair of the aortic valve, the reduction in gradient across the aortic valve allows the LV to really contract & mid-cavitary collapse of the LV & the LV can/t eject. Abrupt hemodynamic collapse after PCI or TAVR. Treatment is VOLUME, not Inotropes 10