NR603_week3_quiz study guide
Heart Failure
Heart failure (HF) is a complex syndrome characterized by the inability of the
heart to meet the body's metabolic demands; it is a clinical diagnosis. It results
from any structural or functional cardiac disorder that impairs the ventricle's ability
to fill or to eject blood properly.
Etiology
The etiology of HF can be divided into the following three broad categories:
1.Anatomic or functional abnormalities of the coronary vessels, myocardium,
or cardiac valves, of either sudden or gradual onset
2.Neurohormonal overexpression that causes activation of the adrenergic
nervous system and renin-angiotensin system
3.Extracardiac factors that cause excessive demand on the cardiovascular
system
The most common diseases associated with HF are coronary artery disease,
hypertension, and dilated cardiomyopathies
Cardiomyopathy, the most common cause of HF, is a disease process of the
myocardium that affects the heart's pumping ability. Classification of heart muscle
disease is complex; an expert panel defined cardiomyopathies as “a heterogeneous
group of diseases of the myocardium associated with mechanical and/or electrical
dysfunction that usually (but not invariably) exhibit inappropriate ventricular
hypertrophy or dilatation and are due to a variety of causes that frequently are
genetic. Cardiomyopathies either are confined to the heart or are part of
generalized systemic disorders, often leading to cardiovascular death or
progressive heart failure–related disability.” 5
Cardiomyopathies have been divided into two major groups:
1.Primary (including genetic, nongenetic, and acquired cardiomyopathies)—
confined to the heart muscle
2.Secondary—heart muscle involvement as part of a general or systemic
disease or disorder
Risk Factors.
Many individuals with HF have antecedent hypertension or myocardial infarction
(MI). Other risk factors include coronary artery disease, diabetes, renal disease,
,obesity, smoking, and increasing age.
Pathophysiology
HF is a clinical syndrome characterized by signs and symptoms of volume excess.
Whereas there can be several causes of the HF, common pathophysiologic
mechanisms characterize this important condition. Understanding these
mechanisms is critical to selection of successful therapeutic interventions.
Systolic Dysfunction: Heart Failure with Reduced Ejection Fraction
Systolic dysfunction, which accounts for about half of all HF cases, is a decrease in
both ejection fraction (40% or less) and cardiac output. In systolic dysfunction,
when looking at a hemodynamic model, the three determinants of ventricular
function—preload, contractility, and afterload—are usually altered. Preload is the
degree of myocardial fiber stretch at the end of ventricular filling. When the heart
ejects subnormally, there is an increased volume of blood left in the ventricular
chambers (increased left ventricular end-systolic volume). This excess volume
leads to distention of the ventricles and increased interventricular pressure at the
onset of diastole. Filling must then occur at higher pressures during diastole. At
small increases of volume and pressure, nonfailing myocardial fibers have the
intrinsic property of increasing their force of contraction in an attempt to “revert”
the subsequent volume and pressure conditions of both heart ejection and filling
back to normal. This intrinsic property also enables the heart to maintain cardiac
output during states of pressure or volume overload. However, in the failing heart,
the failing myocardial fibers are both excessively overloaded and stretched beyond
lengths commensurate with the normal reflex-increased force of contraction. This
results in left ventricular remodeling, with dilation and impaired contractility, and
activation of the sympathetic and renin-angiotensin-aldosterone systems. The
ventricular dysfunction in HFrEF is accompanied by a decrease in myocardial
contractility, a reduction in ejection fraction, and often a reduction in stroke
volume and cardiac output. If HF is left untreated, symptoms develop and worsen,
with declining functional capacity, recurrent acute decompensated events, life-
threatening arrhythmias, and pump failure. Effective treatment of HF, primarily
pharmacotherapy, depends on the interruption of left ventricular remodeling and
the pathophysiologic processes that accompany it.
Afterload is the amount of left ventricular wall tension that develops during
,systole; it is determined by both the size of the ventricular chamber and the
dynamic vascular resistance against which the heart contracts. According to
Laplace's law, an increase in the radius of the ventricle results in an increase in
wall tension. Because systolic blood pressure closely approximates afterload, it is a
clinically important indicator of myocardial load or afterload. The LVEF is a
function of afterload and an 557afterload-dependent measure of contractility.
Chronic elevation of cardiac afterload can lead to ventricular enlargement,
reduction in ejection fraction, and reduction in stroke volume and cardiac output.
Several systemic mechanisms exist for the body to compensate for the reduction in
cardiac output. Early on, these compensatory mechanisms serve to increase cardiac
output and tissue perfusion. In the long run, however, they lead to further cardiac
injury and further decompensation. 1
Heart Failure with Preserved Ejection Fraction
The prevalence of HFpEF has increased dramatically. Controversy surrounds the
true cause(s) of HFpEF. One mechanism believed responsible is increased
ventricular stiffness and reduced compliance of the left ventricle, which produces a
rise in cardiac filling pressures during diastole. Left ventricular distensibility is
reduced during part or all of diastole, and filling pressures must increase to
maintain a constant ventricular volume. Whereas filling pressures in the left
ventricle are increased during both rest and exercise, the failure of a normal rise in
cardiac output during exertion results in characteristic symptoms of HF,
particularly dyspnea. The heart attempts to initially compensate for this impaired
distensibility through the “booster” effect of augmented left atrial contraction,
resulting over time in left atrial dilation.
The incidence of HFpEF increases with age and is more prevalent in older adult
women. Recent studies have examined the role of inflammation contributing to
diastolic abnormalities. The most common factors associated with HFpEF are
hypertension, ischemia resulting from coronary artery disease, aortic stenosis, and
infiltrative or restrictive myocardial diseases. 2
Compensatory Mechanisms
Several interrelated compensatory mechanisms attempt to maintain normal
ventricular contractility, ventricular pressures, cardiac output, and blood pressure.
The three primary compensatory mechanisms are increased sympathetic adrenergic
, activity with a resultant increase in circulating neurohormones, neuroendocrine
activation of the renin-angiotensin-aldosterone system, and ventricular remodeling.
In addition, as HF progresses, neurohormonal alterations in peripheral vasculature
and renal function occur. Sodium and water retention through the renal tubules
results in decreased renal perfusion and rising blood urea nitrogen and creatinine
concentrations, broadly called cardiorenal syndrome, which can be chronic or
acute. The same compensatory mechanisms in early and acute stages gradually fail
as HF progresses, and they are responsible for the eventual deterioration in cardiac
function. 1
Sympathetic Adrenergic Activity.
Baroreceptors and chemoreceptors in the heart and vascular system, sensitive to
stretch, pH and CO2, help regulate blood pressure. Cardiac reflexes regulate heart
rate. Abnormalities in both baroreceptor and cardiac reflexes have been
documented in HF. 1 In a healthy heart, stimulation of the baroreceptor reflex
results in activation of the parasympathetic nervous system and inhibition of the
sympathetic nervous system. Heart rate and systemic vascular resistance are
reduced, and normal blood pressure and cardiac output are maintained.
In HF, however, a decrease in cardiac output leads to activation of the
sympathetic nervous system and blunting of the baroreceptor reflex. The result is
an elevation in heart rate, compensating for low cardiac output in an attempt to
maintain perfusion to vital organs. As HF progresses, further depression of the
baroreceptor function leads to greater sympathetic overactivity despite intense
vasoconstriction and volume retention.
Increasing activation of the sympathetic nervous system stimulates release of
catecholamines from cardiac adrenergic nerves and the adrenal medulla; this in
turn causes vasoconstriction in less metabolically active organs (e.g., skin,
kidneys). It results in venoconstriction, which increases preload by increasing
venous return. Catecholamines also affect the cardiac cells, producing an increased
myocardial oxygen demand, myocyte hypertrophy, and tissue necrosis. Progressive
HF occurs as cardiac cells progressively enlarge and die. As a result of sympathetic
activation, plasma norepinephrine levels are elevated. The degree of plasma
norepinephrine elevation correlates with the severity of HF and may be predictive
of mortality, especially in patients with markedly elevated norepinephrine levels. 6 ,
7
Heart Failure
Heart failure (HF) is a complex syndrome characterized by the inability of the
heart to meet the body's metabolic demands; it is a clinical diagnosis. It results
from any structural or functional cardiac disorder that impairs the ventricle's ability
to fill or to eject blood properly.
Etiology
The etiology of HF can be divided into the following three broad categories:
1.Anatomic or functional abnormalities of the coronary vessels, myocardium,
or cardiac valves, of either sudden or gradual onset
2.Neurohormonal overexpression that causes activation of the adrenergic
nervous system and renin-angiotensin system
3.Extracardiac factors that cause excessive demand on the cardiovascular
system
The most common diseases associated with HF are coronary artery disease,
hypertension, and dilated cardiomyopathies
Cardiomyopathy, the most common cause of HF, is a disease process of the
myocardium that affects the heart's pumping ability. Classification of heart muscle
disease is complex; an expert panel defined cardiomyopathies as “a heterogeneous
group of diseases of the myocardium associated with mechanical and/or electrical
dysfunction that usually (but not invariably) exhibit inappropriate ventricular
hypertrophy or dilatation and are due to a variety of causes that frequently are
genetic. Cardiomyopathies either are confined to the heart or are part of
generalized systemic disorders, often leading to cardiovascular death or
progressive heart failure–related disability.” 5
Cardiomyopathies have been divided into two major groups:
1.Primary (including genetic, nongenetic, and acquired cardiomyopathies)—
confined to the heart muscle
2.Secondary—heart muscle involvement as part of a general or systemic
disease or disorder
Risk Factors.
Many individuals with HF have antecedent hypertension or myocardial infarction
(MI). Other risk factors include coronary artery disease, diabetes, renal disease,
,obesity, smoking, and increasing age.
Pathophysiology
HF is a clinical syndrome characterized by signs and symptoms of volume excess.
Whereas there can be several causes of the HF, common pathophysiologic
mechanisms characterize this important condition. Understanding these
mechanisms is critical to selection of successful therapeutic interventions.
Systolic Dysfunction: Heart Failure with Reduced Ejection Fraction
Systolic dysfunction, which accounts for about half of all HF cases, is a decrease in
both ejection fraction (40% or less) and cardiac output. In systolic dysfunction,
when looking at a hemodynamic model, the three determinants of ventricular
function—preload, contractility, and afterload—are usually altered. Preload is the
degree of myocardial fiber stretch at the end of ventricular filling. When the heart
ejects subnormally, there is an increased volume of blood left in the ventricular
chambers (increased left ventricular end-systolic volume). This excess volume
leads to distention of the ventricles and increased interventricular pressure at the
onset of diastole. Filling must then occur at higher pressures during diastole. At
small increases of volume and pressure, nonfailing myocardial fibers have the
intrinsic property of increasing their force of contraction in an attempt to “revert”
the subsequent volume and pressure conditions of both heart ejection and filling
back to normal. This intrinsic property also enables the heart to maintain cardiac
output during states of pressure or volume overload. However, in the failing heart,
the failing myocardial fibers are both excessively overloaded and stretched beyond
lengths commensurate with the normal reflex-increased force of contraction. This
results in left ventricular remodeling, with dilation and impaired contractility, and
activation of the sympathetic and renin-angiotensin-aldosterone systems. The
ventricular dysfunction in HFrEF is accompanied by a decrease in myocardial
contractility, a reduction in ejection fraction, and often a reduction in stroke
volume and cardiac output. If HF is left untreated, symptoms develop and worsen,
with declining functional capacity, recurrent acute decompensated events, life-
threatening arrhythmias, and pump failure. Effective treatment of HF, primarily
pharmacotherapy, depends on the interruption of left ventricular remodeling and
the pathophysiologic processes that accompany it.
Afterload is the amount of left ventricular wall tension that develops during
,systole; it is determined by both the size of the ventricular chamber and the
dynamic vascular resistance against which the heart contracts. According to
Laplace's law, an increase in the radius of the ventricle results in an increase in
wall tension. Because systolic blood pressure closely approximates afterload, it is a
clinically important indicator of myocardial load or afterload. The LVEF is a
function of afterload and an 557afterload-dependent measure of contractility.
Chronic elevation of cardiac afterload can lead to ventricular enlargement,
reduction in ejection fraction, and reduction in stroke volume and cardiac output.
Several systemic mechanisms exist for the body to compensate for the reduction in
cardiac output. Early on, these compensatory mechanisms serve to increase cardiac
output and tissue perfusion. In the long run, however, they lead to further cardiac
injury and further decompensation. 1
Heart Failure with Preserved Ejection Fraction
The prevalence of HFpEF has increased dramatically. Controversy surrounds the
true cause(s) of HFpEF. One mechanism believed responsible is increased
ventricular stiffness and reduced compliance of the left ventricle, which produces a
rise in cardiac filling pressures during diastole. Left ventricular distensibility is
reduced during part or all of diastole, and filling pressures must increase to
maintain a constant ventricular volume. Whereas filling pressures in the left
ventricle are increased during both rest and exercise, the failure of a normal rise in
cardiac output during exertion results in characteristic symptoms of HF,
particularly dyspnea. The heart attempts to initially compensate for this impaired
distensibility through the “booster” effect of augmented left atrial contraction,
resulting over time in left atrial dilation.
The incidence of HFpEF increases with age and is more prevalent in older adult
women. Recent studies have examined the role of inflammation contributing to
diastolic abnormalities. The most common factors associated with HFpEF are
hypertension, ischemia resulting from coronary artery disease, aortic stenosis, and
infiltrative or restrictive myocardial diseases. 2
Compensatory Mechanisms
Several interrelated compensatory mechanisms attempt to maintain normal
ventricular contractility, ventricular pressures, cardiac output, and blood pressure.
The three primary compensatory mechanisms are increased sympathetic adrenergic
, activity with a resultant increase in circulating neurohormones, neuroendocrine
activation of the renin-angiotensin-aldosterone system, and ventricular remodeling.
In addition, as HF progresses, neurohormonal alterations in peripheral vasculature
and renal function occur. Sodium and water retention through the renal tubules
results in decreased renal perfusion and rising blood urea nitrogen and creatinine
concentrations, broadly called cardiorenal syndrome, which can be chronic or
acute. The same compensatory mechanisms in early and acute stages gradually fail
as HF progresses, and they are responsible for the eventual deterioration in cardiac
function. 1
Sympathetic Adrenergic Activity.
Baroreceptors and chemoreceptors in the heart and vascular system, sensitive to
stretch, pH and CO2, help regulate blood pressure. Cardiac reflexes regulate heart
rate. Abnormalities in both baroreceptor and cardiac reflexes have been
documented in HF. 1 In a healthy heart, stimulation of the baroreceptor reflex
results in activation of the parasympathetic nervous system and inhibition of the
sympathetic nervous system. Heart rate and systemic vascular resistance are
reduced, and normal blood pressure and cardiac output are maintained.
In HF, however, a decrease in cardiac output leads to activation of the
sympathetic nervous system and blunting of the baroreceptor reflex. The result is
an elevation in heart rate, compensating for low cardiac output in an attempt to
maintain perfusion to vital organs. As HF progresses, further depression of the
baroreceptor function leads to greater sympathetic overactivity despite intense
vasoconstriction and volume retention.
Increasing activation of the sympathetic nervous system stimulates release of
catecholamines from cardiac adrenergic nerves and the adrenal medulla; this in
turn causes vasoconstriction in less metabolically active organs (e.g., skin,
kidneys). It results in venoconstriction, which increases preload by increasing
venous return. Catecholamines also affect the cardiac cells, producing an increased
myocardial oxygen demand, myocyte hypertrophy, and tissue necrosis. Progressive
HF occurs as cardiac cells progressively enlarge and die. As a result of sympathetic
activation, plasma norepinephrine levels are elevated. The degree of plasma
norepinephrine elevation correlates with the severity of HF and may be predictive
of mortality, especially in patients with markedly elevated norepinephrine levels. 6 ,
7
