Heart Failure. Cardiac Anatomy. Functions of the Heart. Cardiac Cycle/Hemodynamics. Determinants of Cardiac Output. Cardiac Output

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1 Cardiac Anatomy Heart Failure Professor Qing ZHANG Department of Cardiology, West China Hospital Cardiac Cycle/Hemodynamics Functions of the Heart Essential functions of the heart to cover metabolic needs of body tissue (oxygen, substrates) by adequate blood supply to receive all blood coming back from the tissue to the heart Essential conditions for fulfilling these functions normal structure and functions of the heart Adequate filling of the heart by blood Cardiac Output Determinants of Cardiac Output Cardiac output (CO) = heart rate (HR) x stroke vol.(sv) - changes of the heart rate - changes of stroke volume Preload Contractility Afterload Control of HR: - autonomic nervous system - hormonal (humoral) control Control of SV: -preload - contractility -afterload Stroke Volume Cardiac Output Heart Rate 1

2 Cardiac Output What is Heart Failure (HF) 1? Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV) SV = End-diastolic volume (EDV) - End-systolic volume (ESV) Ejection fraction (EF) = SV/EDV = (EDV-ESV)/EDV EDV ESV It is the pathophysiological process in which the heart as a pump is unable to meet the metabolic requirements of the tissue for oxygen and substrates despite the venous return to heart is either normal or increased Causes of the failure: Mechanical abnormalities Myocardial damage Altered cardiac rhythm Mechanical Abnormalities Myocardial Damage Increased pressure load central (aortic stenosis, aortic coarctation...) peripheral (systemic hypertension) Increased volume load valvular regurgitation hypervolemia Obstruction to ventricular filling valvular stenosis pericardial restriction Primary cardiomyopathy myocarditis toxicity (e.g. alcohol) metabolic abnormalities (e.g. hyperthyroidism) Secondary oxygen deprivation (e.g. coronary heart disease) inflammation (e.g. increased metabolic demands) chronic obstructive lung disease Altered Cardiac Rhythm 3 Main Factors Lead to HF Development Ventricular flutter and fibrillation Extreme tachycardia Extreme bradycardia Heart pump function reducing Afterload increase Preload change 2

3 Adaptive Mechanisms in HF Adaptive Mechanisms in HF Frank - Starling mechanism Ventricular hypertrophy increased mass of contractile elements strength of contraction Increased sympathetic adrenergic activity increased HR, increased contractility Incresed activity of R A A system (RAAS) Ventricular Remodeling in HF Maladaptive Mechanisms in HF Jessup M. et al. N Engl J Med 2003;348: What is Heart Failure (HF) 2? Symptoms of HF HF is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood Manifests as Dyspnea and fatigue Limits exercise tolerance Fluid retention Pulmonary congestion and peripheral edema Dyspnea (shortness of breath, SOB) Sen: 66%, Sep: 52% Paroxysmal Noctural Dyspnea (PND) Sen: 33%, Sep: 76% Orthopnea Sen: 21%, Sep: 81% 2013 ACCF/AHAGuideline for the Management of Heart Failure 3

4 Symptoms of HF Symptoms of HF Edema Sen: 23%, Sep: 70% lower extremeties, dependent pitting, not painful other symptoms/signs of HF Fatigue Activity decrease Cough (especially supine) Edema Shortness of breath Epidemiology & Prognosis Epidemiology & Prognosis Lifetime risk of developing HF is 20% 40 years >650,000 new HF cases diagnosed annually HF incidence: 20 per 1,000 for 65 to 69 years, >80 per 1,000 individuals for those >85 years 5.1 million persons have clinically manifest HF Mortality rate for HF about 50% within 5 years HF as primary diagnosis in >1 million hospitalizations 1-month readmission rate of HF at 25% Physician office visits for HF cost $1.8 billion Total cost of HF care exceeds $40 billion Mean cost of HF-related hospitalizations is $23,077 Etiologies of HF Etiologies of HF Coronary artery disease Hypertension Valvular heart disease Cardiomyopathies Dilated (genetic, alcohol, toxic, drugs...idiopathic) Hypertrophic Restrictive Arrhythmia Congenital heart disease Pulmonary disease/cor pulmonale Non-cardiac/systemic Thyroid Anemia Pregnancy 4

5 Conditions Mimicking HF Obesity Chest disease Venous insufficiency Drug-induced ankle swelling Drug-induced fluid retention Hypoalbuminemia Intrinsic renal disease Intrinsic hepatic disease Pulmonary embolic disease Depression/anxiety Severe anemia Thyroid disease Bilateral renal artery stenosis no single diagnostic test for HF Oxford Handbook of Cardiology. 2 nd Edition History and Physical History PMHx of HTN, CAD, DM, thyroid disease, valvular disease, chemotherapy or XRT, PVD, OSA, rheumatic Social history: tobacco, alcohol, illicits Family history: HF, CAD, SCD Functional status (NYHA class) Physical Vitals (admission weight) Cardiopulmonary exam, volume assessment NYHA Functional Class Class I, No limitation of physical activity Class II, Slight limitation of physical activity Symptoms with ordinary level of exertion Class III, Marked limitation of physical activity Symptoms with minimal level of exertion Class IV, Symptoms at rest History and Physical History PMHx of HTN, CAD, DM, thyroid disease, valvular disease, chemotherapy or XRT, PVD, OSA, rheumatic Social history: tobacco, alcohol, illicits Family history: HF, CAD, SCD Functional status (NYHA class) Physical Vitals (admission weight) Cardiopulmonary exam, volume assessment Signs of HF Dyspnea (orthopnea) Edema (pitting, lower part) Neck vein distention/hepatojugular reflex Tachycardia Cardiomegaly S3 gallop Moist rales in lungs Liver enlargement 5

6 Labs: Biochemistry, CBC, Urine analysis 12 lead ECG, CXR Assessment of ventricular function 2D echo with Doppler Other imaging tools if poor echo windows Brain natriuretic peptide (BNP) when appropriate Echocardiography in HF Etiology of HF: valvular, congenital, MI, cardiomyopathy Size of chambers (i.e. ventricular remodeling) LV dysfunction (systolic, diastolic), LA & RV function Real-time hemodynamics Complication of HF: PE, thrombus, functional MR Dyssynchrony Normal Heart on Echocardiography Parasternal Long-axis Apical 4-chamber 6

7 Introduction to BNP Before 2 weeks later 32-aa polypeptide Found in heart ventricles Produced with ventricular stretch and volume Results in vasodilation, natriuresis, diuresis, and reduced preload Increases with worsening heart failure Classification of Recommendation & Level of Evidence Clinical Value of BNP I IIa IIb III In ambulatory patients with dyspnea, measurement of BNP or N-terminal pro-btype natriuretic peptide (NT-proBNP) is useful to support clinical decision making regarding the diagnosis of HF, especially in the setting of clinical uncertainty. I IIa IIb III Measurement of BNP or NT-proBNP is useful for establishing prognosis or disease severity in chronic HF. Clinical Value of BNP Different Forms of HF I IIa IIb III I IIa IIb III BNP- or NT-proBNP guided HF therapy can be useful to achieve optimal dosing of GDMT in select clinically euvolemic patients followed in a well-structured HF disease management program. The usefulness of serial measurement of BNP or NT-proBNP to reduce hospitalization or mortality in patients with HF is not well established. Left vs. right HF Systolic vs. diastolic HF Early vs. late HF Acute vs. chronic HF 7

8 Take Home Messages Part 1 Confirmation/Establishment of HF NYHA functional class? Etiology of HF? Type of ventricular dysfunction (EF)? Fluid retention and perfusion? Risk stratification and prognosis? Indicated for device therapy? HF is a complex clinical syndrome Exercise intolerance & fluid retention SNS & RAAS activation involved Ventricular remodeling as the key process No single diagnostic parameter exists Symptoms + Signs + Lab + Imaging To Be Continued 8