Pathophysiology of Congestive Heart Failure Flashcards
Braunwald’s Definition of Congestive Heart Failure
The inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body (forward failure)
or
The ability to do so only if the cardiac filling pressures are abnormally high (backward failure)
Major Determinants of Cardiac Performance
Heart Rate
Preload
Afterload
Contractility
Disorders of Impaired Contractility
Myocardial infarction
Ischemic cardiomyopathy
Dilated cardiomyopathy
Disorders of Markedly Increased Afterload
Severe aortic stenosis
Uncontrolled hypertension
Disorders with Impaired Ventricular Relaxation/Decreased Filling
Restrictive cardiomyopathy
Acquired or familial hypertrophic cardiomyopathy
Constrictive pericarditis
Heart Failure with Preserved Ejection Fraction (Diastolic Heart Failure)
Due to decreased diastolic compliance
Stroke volume is reduce and filling pressures are higher
EF is still normal though, makes it difficult to diagnose clinically
Pathophysiology of Right Sided Heart Failure
RV is more compliant than LV (thinner walls, pulmonary vascular resistance is less than systemic)
RV can tolerate larger changes in filling w/o change in pressure
BUT
RV is susceptible to acute changes in Pulmonary Vascular Resistance
Pulmonary disease can cause isolated RV failure
Causes of Right Sided Heart Failure
Cardiac: LV failure, mitral stenosis/regurg, acute MI wtih RV infarction, pulmonic stenosis
Pulmonary parenchymal diseases: COPD, interstitial lung diseases (silicosis, pulmonary fibrosis), ARDS (acute respiratory distress syndrome)
Pulmonary Vascular Diseases: pulmonary embolism, primary pulmonary hypertension
Compensatory Mechanisms to Maintain Cardiac Output in CHF
Frank-starling mechanism (increase in residual volume aka preload which contributes to greater output on next contraction) Autonomic nervous system (baroreceptor response) Renal Compensation (renin-angiotensin-aldosterone system) Ventricular Remodeling
Post-MI Ventricular Remodeling
Any architectural or structural change that occurs after myocardial infarction in either the infarcted or non-infarcted regions of the heart
Alterations in Ventricular Shape and Size Following Acute MI
Acute alterations in ventricular dimensions (seconds)
Infarct expansion (hours-weeks)
**Hypertrophy/dilation of noninfarcted segments (weeks-years)
Eccentric Hypertrophy
Due to volume overload
Ventricular dilation and overall heart enlargement
Sarcomeres added in series
Concentric Hypertrophy
Due to pressure overload
Ventricular wall thickening
Sarcomeres added in parallel
Mechanisms of Post-MI Ventricular Remodeling
Cardiac myocyte hypertrophy Cardiac fibroblast hyperplasia Perivascular and interstital fibrosis Vascular remodeling and angiogenesis Cardiac myocyte apoptosis
Rx of Ventricular Dysfunction
Early recognition of remodeling, because months/years of remodeling will eventually lead to CHF
Remodeling is growth-mediated response and derived from mechanical and local neurohormonal factors
PREVENTING or SLOWING the progression of ventricular remodeling will prevent/delay development of CHF