heart failure Flashcards
(39 cards)
congestive heart failureCHF p
inability of heart to pump blood at a rate to meet the needs of active tissues, or needs to via an elevated filling pressure
Common and recurrent condition with a poor prognosis , l
CHF pathogenesis
Usually results from a SLOW developing intrinsic deficit in contraction, but occasionally occurs acutely
Mechanisms: abnormal load presented to heart (acutely fluid overload MI or valve dysfunction) (chronically- ischemic heart disease, dilated cardiomyopathy, HTN)
Impaired Ventricular filling: Acutely (pericarditis, tampanode), Chronically (restrictive cardiomyopathy, severe left Ventricular hypertrophy)
Obstruction due to valve stenosis (chronic rheumatic valve disease mitral valve)
CHF characterization
Systolic vs diastolic dysfunction
Systolic dysfunction: progressive deterioation of cardiac contractile funciton (Ischemia, pressure volume overload, dilated cardiomyopathy)
Diastolic dysfunction (inability of heart to relax, expand and fill sufficiently during diastole) (massive left ventricular hypertrophy, amyloidosis, myocardial fibrosis, constrictive pericarditis)
Compensatory mechanisms
Frank starling mechanism- increased preload dilation (increased end diastolic filling volume) sustains cardiac performance by enhancing contractility (lengthens fibers contract more forcibly), results in increased wall tension and increase oxygen requirements
Neurohumoral systems: release of NE by cardiac nerves increases heart rate, myocardial contractility and vascular resistance, RAAS system increases Na and water resorption, increases cardiac output and increased vasoconstriction, release of ANP (secreted from atrial myocytes when atrium is dilated, causing vasodilation, diuresis)
Cardiac hypertrophy: increases load occuring over weeks to monthes, increased number of sarcomeres, no hyperplasia
patterns of hypertrophy
Reflect the nature of stimulus
Pressure overload: concentric hypertrophy (HTN and aortic stenosis)
volume overload: hypertrophy accompanied by dilatation (mitral or aortic regurgitation)- eccentric hypertrophy
Cardiac hypertrophy and CHF
sustained cardiac hypertrophy often evolves to cardiac failure
Increased myocyte size results in decreased capillary density, increased intercapillary distance and increased fibrous tissue
higher cardiac oxygen consumption
Altered gene expression and roteins
Loss of myocytes due to apoptosis
LVH (hypertrophy) independent risk factor for sudden death
Left sided heart failure
effects primarily due to progressive damming of blood within the pulmonary circulation and diminished peripheral blood pressure and flow
Causes: ischemic heart disease, HTN, aortic and mitral valve disease, non ischemic myocardial disease (cardiomyopathies, myocarditis_
Clinical effects and morphology (LVH and often dilation, often result in mitral valve insufficiency) Secondary enlargement of left atrium –> atrial fibrillation–> stagnant blood in atrium–> thrombus embolic stroke
Left HF clinical effects on lung
increased pressure in pulmonary veins which is transmitted to capillaries and arteries
Pulmonary congestion and edema, heart failure cells, dyspnea, orthopnea (dyspnea when recumbent) and paroxysmal nocturnal dyspnea)
When supine, venous return increases and dipharagms elevate Rales on exam
Left sided HF kidneys and brain
Kidneys: decrease renal perfusion activats RAAS–> increased blood volume, if perfusion deficit is severe–> prerenal azotemia (impaired kidney function due to low perfusion)
Brain: cerebral hyposia and encephalopathy
Right sided heart failure
Effects are primarily due to engorgement of systemic and potral venous systems
Causes: Secondary to left-sided failure, usually, pulmonary HTN, primary myocardial disease, tricuspid or pulmonary valvular disease
R HF on heart, liver portal system, kidneys, brain, lungs
Heart: right ventricle responds to the increased workload with hypertrophy and often dilatation
Liver: elevated pressure in the portal vein leads to congestive hepatosplenomegaly, cardiac cirrhosis, ascites
Kidneys: congestion, fluid retention, peripheral edema, azotemia (more marked with right heart failure than left)
Brain: venous congestion and hypoxic encephalopathy
Lung: pleural and pericardial effusion, atelectasis, peripheral edema (at ankle and presarcal), eventual anasarca (generalized massive edema)
Heart failure left vs Right
Left: pulmonary congestion and edema prominent, kidneys have reduced perfusion, fluuid retention, azotemia less prominent, Brain: reduced perfusion, cerebral hypoxia and encephalopathy
right: Systemic and portal venous congestion (hepatosplenomagaly, peripheral edema, pleural effusion, ascites), kidneys: congesiont fluid retention and azotemia more prominent, brain: venous congestion, hypoxia and encephalopathy
Heart failure
State in which the heart cant pump blood at a rate sufficient to meet the requirements of metabolizing tissues, or only able to do so if the cardiac filling pressures are really high
Inadequate perfusion–> retention of fluid
Heart failure pathophysiology
CVD that impairs ventricular contractility, increases afterload, impairs relaxation and filling
HF due to abnormal emptying (systolic dysfunction), filling (diastolic dysfunction)
Pts categorized according to ejection fraction : reduced EF, or preserved EF
Heart failure with reduced ejection fraction
Ventricle has diminished capacity to eject blood because of impaired contractility or pressure overload
Loss of contractility may result from : destruction of myocytes, abnormal myocyte function, fibrosis
With pressure overload ejection is impaired by increased resistance to outflow
Heart failure wiht preserved ejection fraction
usually demonstrate abnormalities in diastolic function, impaired early relaxation and or increased stiffness
Acute ischemia, hypertrophy, fibrosis, restrictive cardiomyopathy, pericardial diseases
Right sided heart failure
RV highly compliant
Susceptible to failure with a sudden increase in afterload
Right sided heart failure that results froma primary pulmonary Process
Cardiac causes: Left sided heart failure, pulmonic valve stenosis, right ventricular infarction
Pulmonary parenchymal disease: Chronic obstructive pulmonary disease, interstitial lung disease, chronic lung infection
Pulmonary vascular diseases: pulmonary embolism, pulmonary arteriolar hypertension
Compensatory mechanisms of HF
Helps to maintain perfusion of vital organs Neurohormanal activation (increase in RAAS, SNS and antidiuretic hormone
hypertrophy and remodeling- compensatory process that develops overtime, increases stiffness,
Natriuretic Pepetides
ANP- atrial natriuretic peptide, released from atrial cells in response to stretch
BNP- B, type natriuretic peptide, produced by ventricular myocardium in response to hemodynamic stress (HF, MI)
Oppose actions of other hormone systems (promote exrection of sodium and water, produce vasodilation, inhibit renin secretion
Serum BNP level = HF, degraded by neprilysin
Precipitating factors
Symptomatic for extended periods (increased metabolic demands, increased ciculating volume, increase in afterload, impaired contractility, failure to take prescribed HF meds, slow HR
Symptoms of HF
Left sided: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue
Right sided: peripheral edema, right upper quadrant discomfort- hepatic enlargement
Physical: diaphoresis, tachycardia, tachypnea, pulmonary rales, loud P2, S3
Jugular venous distenstion (hepatomegalu, peripheral edema
Classification of HF
Class 1 mild (cardiac disease, no limitation in physical activity)
Class 2 mild (slight limitation of physical activity, dyspnea and fatigue with moderate exertion)
Class 3 moderate (limitation of physical activiity, dyspnea with minimal exertion), comfort only at rest
Class 4 severe : sever limitation of activity, symptoms present ar rest
Prognosis
45-60% death rate in 5 yrs
Treatment of HF with reduced ejection fraction
Diuretics, Inhibitors of RAAS (ace inhibitor, angiotensin blocker, aldosterone antagonist), B blockers, vasodilators, positive inotropic agents, HR reducing agents
Positive inotropes- Digoxin (glycoside, increase contraction and stroke volume, increases vagal tone slows HR), Secondary effects (decrease HR, arterial and venous dilation, decreased venous pressure, Blocks Na K ATpas) 36 hour half life, orally absorben, renal elimination
SE- low therapy, GIT, visual, neuro, muscular, cardiac
Doesnt prolong survival
