Diagnosis Treatment of Heart Failure

Diagnosis & Treatment of Heart Failure Jason M. Lynch, RN, BSN, BA, CCRN Director Cardiac Cath Lab & Cardiovascular Diagnostic Services St. John’s Mercy Medical Center Contact Information • Office: 314-251-7911 • Pager: 314-510-8628 • E-Mail: Jason.Lynch@mercy.net Heart Failure • General term used to describe several types of cardiac dysfunction that results in the inadequate perfusion of tissues • Left vs. Right • Left = Congestive Heart Failure (CHF) • Right = Cor Pulmonale • Systolic vs. Diastolic A Growing Problem Annual Incidence Prevalence Annual Mortality 250,000 U.S. 400,000 5.0 million Europe 580,000 6.5 million 300,000 A Medical Challenge Compliance • 50% have three or more co-morbidities • Average of six medications • 78% had at least two admissions per year • Only 10% completed their annual prescription regimen • One-third never refilled any heart failure prescription Co-morbid Disorders • Hypertension (HTN) • Coronary Artery Disease (CAD) • Peripheral Vascular Disease (PVD) • Diabetes NYHA Classification Heart failure functional status assessment Class I Class II Class III Moderate symptomatic heart failure with less than ordinary exertion Class IV Symptomatic heart failure at rest Asymptomatic Mild symptomatic heart failure heart failure ejection fraction with ordinary (EF) <40% exertion Direct Causes of Heart Failure • Myocardial abnormalities • Hemodynamic overload • Ventricular filling abnormalities – Aortic or mitral valve disease • • • • Ventricular dyssynchrony Changes in cardiac rhythm Cardiomyopathy Pulmonary emboli Aggravating Factors Medications New heart disease Myocardial ischemia • • • • • Pregnancy Arrhythmias (AF) Infections Thromboembolism Hyper/hypothyroidism • Endocarditis • Obesity • Hypertension • Physical activity • Dietary excess Hemodynamics Cardiac Output • The amount of blood pumped by each ventricle/minute – Cardiac output = HR X SV CO Cardiac output (ml/min) = HR Heart rate (beats/min) X SV Stroke volume (ml/beat) Factors Affecting Cardiac Output Factors Affecting Heart Rate • Autonomic Nervous System – Sympathetic Stimulus increases BP, HR, & renal perfusion Fear Factor • Parasympathetic Nervous System – stimulation decreases BP & HR Feed and breed Factors Effecting Stroke Volume Preload -Stretch of ventricles prior to contraction Volume Venous Tone Factors Effecting Stroke Volume Afterload - Pressure that the ventricle that must be overcome prior to ventricular ejection Resistance Contractility • Frank-Starling Law: – The fundamental principle of cardiac behaviour which states that the force of contraction of the cardiac muscle is proportional to its initial length. The energy set free at each contraction is a simple function of cardiac filling. When the diastolic filling of the heart is increased or decreased with a given volume, the displacement of the heart increases or decreases with this volume. Frank-Starling Law Curve Physiology of Heart Failure Pathogenesis of Heart Failure Myocardial Insult Myocardial Dysfunction Reduced System Perfusion Sympathetic System Activation Renin-Angiotensin-Aldosterone System Activation Altered Gene Expression Apoptosis Remodeling Hypertension • ↑afterload causes ↑resistance to LV emptying • ↑work load of heart • ↑oxygen consumption • ↑ventricular hypertrophy • ↑ventricular remodeling Myocardial Injury • • • • MI = most common cause Myocarditis Cardiomyopathies Myocardial ischemia results in process of ventricular remodeling • Leads to progressive myocyte contractile dysfuntion over time Cardiac Output Falls • ↓contractility results in ↓ CO • LVEDP ↑ from ↓ contractility, fluid overload, renal failure, mitral valve disease • Rising LVEDP ↑CO to a point, but eventually leads to dysfunction (FrankStarling Law) The Vicious Cycle Continues… • ↓CO results in ↓renal perfusion • ↓renal perfusion activates the ReninAngiotensin-Aldosterone System • Baroreceptors in the central circulation detect ↓in perfusion • Body says “I must be low on volume!” • Sympathetic nervous system causes secretion of catecholamines • ↑vasoconstriction and secretion of ADH which leads to fluid retention Role of Catecholamines • Sympathetic nervous system activation initially compensates for ↓CO by ↑HR and PVR • Cause direct toxicity to myocardium – Induction of myocyte apoptosis – Myocardial remodeling – Facilitation of arrhythmias Renin-Angiotensin-Aldosterone System Let’s Keep it Simple! Myocardial Infarction ↓Contractility ↓EF ↑LVEDV ↓Renal Perfusion ↑Renin and Angiotensin ↑ Preload ↑ Afterload Renal Failure Hypertension Types of Heart Failure Systolic vs. Diastolic Heart Failure Hypertrophic Cardiomyopathy Diastolic Heart Failure • Can occur alone or along with systolic heart failure • Isolated diastolic heart failure – Pulmonary congestion despite a normal CO – Accounts for 25-40% of all cases of left heart failure – More common in women – ↓compliance of LV & abnormal relaxation – ↑LVEDP – Pulmonary edema LV Diastolic Dysfunction • The LV does not fill appropriately – Myocardial ischemia or necrosis – LV hypertrophy (Hypertrophic cardiomyopathy) – Constriction of myocardium or pericardium • Pericardial tamponade • Restrictive cardiomyopathy – Hypertension – Valvular disease: • Aortic stenosis, mitral regurgitation or stenosis LV Systolic Dysfunction • LV failure results in increased pressure in LA, pulmonary veins, & capillaries • Pulmonary congestion results in: – Hemoptysis – Decreased oxygen saturation – Low PaO2 – Tachycardia • Further diminishes stroke volumes Causes of Diastolic Failure • HTN induced myocardial hypertrophy with ventricular remodeling Right Sided Heart Failure • RV failure causes increased RV pressures, which is transmitted to the RA and systemic veins – Decreased RV output leads to decreased LV filling. – Decreased LV filling leads to diminished stroke volume Making the Diagnosis Assessing Heart Failure Clinical Manifestations of Left Heart Failure • Result of pulmonary vascular congestion and inadequate systemic perfusion • Dyspnea • Orthopnea • Frothy sputum • Fatigue • ↓Urine output • Edema Physical Examination Findings in Left Heart Failure • Pulmonary edema – Cyanosis – Rales – Pleural effusions • Hypotension • S3 gallop • Evidence of underlying CAD or HTN Physical Examination in Diastolic Heart Failure • Dyspnea on exertion • Fatigue • Evidence of pulmonary edema – Rales on auscultation – Pleural effusions – Worsens with increased HR • Evidence of underlying CAD, HTN or valvular disease • S3 • Tachypnea • Decreased LOC • Decreased PO2 Right Sided Heart Failure Clinical Findings • • • • • • • • • • • Fatigue Anorexia N/V Peripheral edema Cachexia Increased CVP, JVD Ascites Hepatomegaly Diagnostic findings: RV hypertrophy Hepatic jugular reflex Decreased BP Assessing for JVD Making the Diagnosis Suspected Heart Failure because of SYMPTOMS and/or SIGNS Assess presence of CARDIAC DISEASE by ECG, X-Ray or BNP (if available) NORMAL No Heart Failure Tests abnormal VENTRICULAR FUNCTION Imaging by ECHO-Doppler, Nuclear angiography or MRI if available NORMAL No Heart Failure Tests abnormal Heart Failure: Systolic / Diastolic Identify etiology, evaluate severity, choose therapy Initial/On-Going Evaluation • Identify heart disease • Assess functional capacity (NYHA, 6 min walk, …) • Assess volume status: (edema, rales, jugular, hepatomegaly, body weight, CVP) • Lab assessment: routine: electrolytes, renal function. Repeat ECHO, Tx only if significant changes in functional status • Assess prognosis Prognosis 50 40 <30 Post MI n=196 Cardiac Mortality 30 % 20 10 0 20 31-35 36-45 46-53 54-60 >60 30 40 50 60 70 80 LVEF Did you say BNP? • Natriuretic Peptides – Brain – Atrial • Hormone secreted primarily by the ventricles in response to increased “stretch” and volume • ↑levels in CHF • Useful in differentiating CHF from COPD • Direct relation to NYHA Class, prognosis and LVEDP Role of BNP Correlation of CHF & BNP Treatment of Heart Failure Treatment Objectives ↑Survival ↑Exercise capacity ↓Morbidity ↑Quality of life ↓Neurohormonal changes ↓Progression of CHF ↓Symptoms Treatments • Prevention. Control of risk factors • Life style • Treat etiologic cause / aggravating factors • Drug therapy • Personal care. Team work • Revascularization if ischemia causes HF • ICD (Implantable Cardiac Defibrillator) • Ventricular resynchronization • Ventricular assist devices • Heart transplant • Artificial heart All Selected patients Stevenson Hemodynamic Classification Stable or Unstable? Chronic or Acute? Treatment of Acute Onset of Left Heart Failure • Often results from myocardial ischemia • Oxygen • Reduce preload – Morphine – Nitrates • Inotropic drugs – Dopamine – Dobutamine • ACE inhibitors & diuretics • PTCA • IABP Pharmacological Treatments • • • • • • Diuretics ACE Inhibitors Beta Blockers Digoxin Natrecor Aldosterone Inhibitors Diuretics Thiazides Cortex Inhibit active exchange of Cl-Na in the cortical diluting segment in the ascending loop of Henle Potassium Sparing Inhibit reabsorption of Na in the distal convoluted tubule Medulla Loop of Henle Loop Diuretics Inhibit exchange of Ca-Na-K in the thick segment of the ascending loop of Henle Collecting tubule Diuretics Indications • Symptomatic HF, with fluid retention – – – – – – Edema Dyspnea Rales Jugular distension Hepatomegaly Pulmonary edema (CXR) AHA / ACC HF guidelines 2001 ESC HF guidelines 2001 Loop Diuretics Initial Maximum • Bumetanide • Furosemide • Torsemide 0.5 to 1.0 / 12-24h 20 to 40 / 12-24h 10 to 20 / 12-24h 10 / day 400 / day 200 / day • Monitor serum K+ & Mg+ levels • Strict I/O • Monitor weight daily ACE Inhibitors VASOCONSTRICTION ALDOSTERONE VASOPRESSIN SYMPATHETIC Angiotensinogen RENIN PROSTAGLANDINS Kininogen tPA Kallikrein Angiotensin I BRADYKININ A.C.E. ANGIOTENSIN II Inhibitor Kininase II Inactive Fragments ACE Inhibitors Clinical Effects • Improve symptoms • Reduce remodeling progression • Reduce hospitalization • Improves survival ACE-i Mortality Studies 0.7 0.6 Placebo p< 0.001 Probability 0.5 of Death 0.3 0.2 0.1 0.4 p< 0.002 Enalapril 0 0 1 2 3 4 5 6 7 8 9 10 11 12 CONSENSUS N Engl J Med 1987;316:1429 Months ACE-i Dosing Guidelines Initial Captopril Enalapril Fosinopril Lisinopril Quinapril Ramipril 6.25 / 8h 2.5 / 12 h 5 to 10 / day 2.5 to 5.0 / day 10 / 12 h 1.25 to 2.5 / day Maximum 50 / 8h 10 to 20 / 12h 40 / day 20 to 40 / day 40 / 12 h 10 / day ACE Inhibitors • • • • Captopril Enalapril Rimapril Benzapril ACE-I Adverse Effects • • • • • • • Hypotension (1st dose effect) Worsening renal function Hyperkalemia Cough Angioedema Rash Neutropenia Natrecor (Nesiritide) • • • • • • Use in acutely decompensated CHF Recombinant BNP Promotes arterial and venous dilation Reduces PCWP Promotes diuresis May aid in the reduction of intravascular volume • Weight based • Available only in IV form • SBP should be >90 mm Hg prior to initiation Natrecor Dosing Other Pharmacological Agents Used in Heart Failure • Beta blockers • Antiarrhythmic agents • Inotropes – Dobutrex – Milrinone – Inamrinone Digoxin Na-K ATPase Na+ K+ Na+ Ca++ K+ Na+ Myofilaments Ca++ CONTRACTILITY Digitalis Method of Action Blocks Na+ / K+ ATPase => Ca+ + • Inotropic effect • Natriuresis • Neurohormonal control - Plasma Noradrenalin - Peripheral nervous system activity - RAAS activity - Vagal tone - Normalizes arterial Baroreceptors Digitalis Indications • When no adequate response to • ACE-i + diuretics + betablockers (AHA / ACC Guidelines 2001) • In combination with ACE-i + diuretics • If symptoms persist (ESC Guidelines 2001) • AF, to slow AV conduction • Dose 0.125 to 0.250 mg / day Digitalis Clinical Effects • Improve symptoms • Modest reduction in hospitalization • Does not improve survival Digitalis Contraindications • Digoxin toxicity • Advanced A-V block without pacemaker • Bradycardia or sick sinus without PM • PVC’s and VT • Marked Hypokalemia • W-P-W with atrial fibrillation Vasodilators VENOUS Nitrates Molsidomine Venous Vasodilatation MIXED Calcium antagonists a-adrenergic Blockers ACE-I, ARBs K+ channel activators Nitroprusside Arterial Vasodilatation ARTERIAL Minoxidil Hydralazine Nursing Interventions Nursing Interventions • Administer oxygen • Position to facilitate breathing and decrease preload • Strict I & O • Daily weight • 2 lbs in a day or 3-5 lbs in a week significant fluid retention • Every 2.2 lbs of weight gain associated with 1liter volume • Promote adequate nutrition • Fluid & sodium restriction Patient Education Topics • Cessation of smoking • Weight gain • Dietary modifications • Medications • Pathophysiology of disease process Core Measures • Discharge Instructions • Evaluation of LV Function • Use of ACE-I for LV systolic dysfunction • Smoking cessation education • Data available to public • http://www.hospitalcompare.hhs.gov/ Non-Pharmacological Treatments Theory Behind Cardiac Resynchronization • In the normal heart, the heart's lower chambers (ventricles) pump at the same time and in sync with the heart's upper chambers (atria) • When a patient has heart failure, often times the right and left ventricles do not pump together (dysynchrony). • When the heart's contractions become out of sync, the walls of left ventricle (LV) do not contract at the same time. • The heart has less time to fill with blood and is not able to pump enough blood out to the body. This eventually leads to an increase in heart failure symptoms Issues Associated with Heart Failure Sinus node • Sub-optimal contribution of atrial systole • Limited filling period • Mitral regurgitation AV node Issues Associated with Heart Failure Issue II–delayed ventricular activation Sinus node AV node Conduction block • Delayed lateral wall contraction • Disorganized ventricular contraction • Decreased pumping efficiency Cardiac Resynchronization Therapy • Biventricular Pacemakers • Leads are implanted through a vein into the right atrium (RA) and right ventricle (RV) and into the coronary sinus (CS) vein to sense and pace the left ventricle (LV). This helps the heart beat in a more balanced way • Traditional pacemakers are used to treat slow heart rhythms. • Pacemakers use one or two leads to sense and pace the right atrium (RA) right ventricle (RV), or both, to maintain a good heart rate and keep the atrium and ventricle working together. This is called AV Synchrony. Biventricular Pacemakers • Biventricular pacemakers use a third lead. • When the atrium senses and contracts, both ventricles are paced to contract at the same time, causing the walls of the left ventricle (the septal and free walls) to contract "in synch" • The end result is improved cardiac function • Take a 15 Minute Break! Cardiomyopathies • Etiology of Myocarditis: – Inflammation of myocardium as a response to invading organism, chemical or drugs • • • • • Viral: related to Coxsackie B and enteroviruses or HIV Bacterial, fungal, protozoa Autoimmune: antibodies against myosin Toxins: heavy metals or drugs Pregnancy is a predisposing factor – – – – Infectious organism colonizes myocardium Interstitial fibrosis and myofibril necrosis Decreased CO and contractility Decreased LV function and heart failure Findings in Myocarditis • Flu like symptoms up to 6 wks prior to onset of heart failure • Rash, fever and/or cold symptoms • Chest pain • Dyspnea, rales, exercise intolerance, weakness, fatigue, myalgia • Hypotension • Pericardial friction rub, mitral or tricuspid regurgitation murmurs Diagnostic Testing Myocarditis • Elevated sedimentation rate, CKMB, WBC • Tachycardia or bradycardia • Do not generally develop BBB • CXR may show normal cardiac silhouette or cardiomegaly • Echo may show LV systolic dysfunction, wall motion abnormalities, mitral or tricuspid insufficiency, diastolic filling abnormalities Treatment of Myocarditis • Antipyretics • Sodium and fluid restrictions • Activity restrictions • Oxygen therapy • Vasodilators, ACE inhibitors • May require valve replacement surgery, ICD and or pacemaker implantation Dilated Cardiomyopathy • Etiology: – Significant ventricular dilation with minimal hypertrophy – Enlargement of all or select chambers – Impaired systolic and diastolic function • • • • Decreased CO, SV, EF Compensatory increase in HR may be seen Heart failure refractory to treatment Associated with malignant ventricular dysrhythmias – OFTEN ASSOCIATED WITH DEATH – Viral – Idiopathic – Alcoholism (most common) Clinical Findings Dilated Cardiomyopathy • Symptoms of left and right-sided heart failure Treatment Dilated Cardiomyopathy • Na and fluid restriction • ACE inhibitors, B-blockers, diuretics, antidysrhythmic drugs • Anticoagulation with EF < 30% • AICD implantation • Heart transplant Hypertrophic Cardiomyopathy • Significant increase in myocardial mass with decreased chamber size – Diastolic dysfunction: • • • • Impaired diastolic filling Decreased ventricular compliance Increased EDVP without increased EDV LV and septal hypertrophy result in enlarged silhouette with decreased chamber size Etiology Hypertrophic Cardiomyopathy • Mitral insufficiency and papillary muscle dysfunction are common • Familial occurrence Diagnosis and Treatment Hypertrophic Cardiomyopathy • CXR shows pulmonary venous congestion and enlarged cardiac silhouette • EKG: LV hypertrophy, dysrhythmias, P mitrale, Q waves in inferior/lateral leads • Echo: septal thickening, asymmetrical LV wall thickness, decreased dimensions of LV chamber and or mitral insufficiency • B-Blockers, CCB, diuretics, antidysrhythmic agents, pacemaker, ICD • MVR Restrictive Cardiomyopathy • Least common • Loss of ventricular compliance due to fibrosis that interferes with the ability of the heart to contract effectively and results in diastolic dysfunction • Etiology: – – – – Amyloidosis Radiation Sarcoidosis Idiopathic Restrictive Cardiomyopathy Clinical Findings • • • • • Reduced chamber size Rigid but not thickened ventricles Right and left-sided failure Elevated PCWP & PAD Dyspnea, orthopnea, exercise intolerance Peripheral edema, ascites Normal BP RV heave S3 & S4 heart sounds A-Fib • • • • • Case Study • 62 y/o white female who presents to ER by private vehicle c/o increasing dyspnea x 3 days. Initially the pt only had SOB w/ exertion, but now is symptomatic at rest. Also reports PND, nausea and fatigue. Denies c/o CP or sx of pneumonia Case Study • CC: – SOB • PMH: – + for hx of CAD. s/p PTCI. + HTN + hyperlipidemia – Current Medications: • Diltiazem, lovastatin, ASA, HCTZ, SL NTG Case Study • Physical Exam: – Moderate distress w/ obvious air hunger. • • • • • Tele: A-Fib rate = 126 BP: 196/100 Chest Exam reveals rales 2/3 up bilaterally SpO2: 89% on .50 VM 2+ pitting edema bilaterally • 12-Lead EKG: – Non-suggestive of AMI – LV hypertrophy Case Study What next? Questions? YOU are the next Superstars of St. John’s Mercy Medical Center