CONGESTIVE HEART FAILURE

Congestive Heart FailureInadequate pump function of the heart, which leads to congestion resulting from fluid in the lungs and peripheral tissues, is a common end result of many cardiac disease processes.

Left Ventricular Failure

CLINICAL PRESENTATIONBreathlessness (Dyspnea) : Orthopnea, Paroxysmal nocturna dyspneaHemoptysisChest painFatiqueNocturiaConfusion

Breathlessness (Dyspnea) : Orthopnea, Paroxysmal nocturna dyspneaRise in pulmonary capillary pressures as a consequence of elevated left ventricular and atrial pressures Causes fluid to move into the interstitial spaces of the lung (pulmonary edema)

EtiologyInappropriate workloads placed on heart, such as volume overload or pressure overloadRestricted filling of the heartMyocyte lossDecreased myocyte contractility

Hemodynamic Changes Systolic DysfunctionIsovolumic systolic pressure curve of the pressure-volume relationship is shifted downwardThis reduces stroke volume reduces cardiac output

To maintain cardiac output, heart respond with three compensatory mechanisms: First, increased return of blood to the heart (preload) can lead to increased contraction of sarcomeres (Frank-Starling relationship).In the pressure-volume relationship, the heart operates at a' instead of a, and stroke volume increases,

Second, increased release of catecholamines can increase cardiac output by both increasing the heart rate and shifting the systolic isovolumetric curve to the left

Finally, cardiac muscle can hypertrophy and ventricular volume can increase, which shifts the diastolic curve to the right.Although each of these compensatory mechanisms can temporarily maintain cardiac output, each is limited in its ability to do so, and if the underlying reason for systolic dysfunction remains untreated, the heart ultimately fails.

Diastolic DysfunctionIn diastolic dysfunction, the position of the systolic isovolumic curve remains unchanged (contractility of the myocytes is preserved).The diastolic pressure-volume curve is shifted to the left, with an accompanying increase in left ventricular end-diastolic pressure and symptoms of congestive heart failure

NEUROHUMORAL CHANGESInitially, increased activity of the adrenergic system and the renin-angiotensin system provides a compensatory response that maintains perfusion of vital organs. Over time these changes can lead to progressive deterioration of cardiac function.Increased sympathetic activity occurs early in the development of heart failure.

Elevated plasma norepinephrine levels cause increased cardiac contractility and an increased heart rate that initially help maintain cardiac output. Continued increases lead to increased preload (as a result of venous vasoconstriction) and afterload (from arterial vasoconstriction), which can worsen heart failure.

Reduced renal blood pressure stimulates the release of renin and increases the production of angiotensin II.Both angiotensin II and sympathetic activation cause efferent glomerular arteriolar vasoconstriction, which helps maintain the glomerular filtration rate despite a reduced cardiac output.Angiotensin II stimulates aldosterone synthesis, which leads to sodium resorption and potassium excretion by the kidneys.

A vicious circle is initiated as continued hyperactivity of the renin-angiotensin system leads to severe vasoconstriction, increased afterload, and further reduction in cardiac output and glomerular filtration rate.

Heart failure is associated with the release of cytokines and other circulating peptides. The interleukins (ILs) and tumor necrosis factor- (TNF- ) are the two major groups of cytokines that may have an important pathophysiologic role in heart failure.TNF- appears to have an important role in the cycle of myocyte hypertrophy and cell death (apoptosis)IL-1 may accelerate myocyte hypertrophy.

CELLULAR CHANGESdelivery of Ca2+ to the contractile apparatus and reuptake of Ca2+ by the sarcoplasmic reticulum are slowed.levels of 1 adrenergic receptors are slightly increased myocardial hypertrophysignificant -adrenergic receptor desensitization as a result of chronic sympathetic activation.

Right Ventricular Failure

PatophysiologyPatients with isolated right ventricular failure (pulmonary hypertension, cor pulmonale) can have a mechanical reason for left ventricular failureWhen right ventricular pressure increases relative to the left, the interventricular septum can bow to the left and prevent efficient filling of the left ventricle, which may lead to pulmonary congestion.

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