NUR 356 Exam 5 Heart Failure
Congestive Heart Failure - answer A condition resulting from the heart's inability to
pump out all the blood that returns to it; blood backs up in the veins leading to the heart,
causing an accumulation of fluid in various parts of the body
Factors that Affect Cardiac Output - answer Preload
Afterload
Preload - answer Volume of blood in ventricles at end of diastole (end diastolic
pressure). blood coming back to the heart.
Increased in:
Hypervolemia
Regurgitation of cardiac valves
Afterload - answerResistance left ventricle must overcome to circulate blood.
Increased in:
Hypertension
Vasoconstriction
Increased aferload
Increased cardiac workload
Heart Failure Pathophysiology - answerSeen in disease states such as dilated
cardiomyopathy (DCM)
Poor EFs (<35%)
High pulmonary pressures
Biventricular failure
-Both ventricles may be dilated and have poor filling and emptying capacity
Who is at-risk for congestive heart failure? Risk Factors? - answerPrimary causes:
CAD, MI, HTN, Rheumatic HD, Congenital Heart defects, Pulmonary HTN,
Cardiomyopathy, hyperthyroidism, Valvular disorders, and myocarditis.
Precipitating Factors: Anemia, Infection, dysrhythmias, bacterial endocarditis, PE,
Paget's dx, nutritional deficiencies, hypervolemia.
, Heart Failure Compensatory Mechanisms - answerSympathetic nervous system (SNS)
activation
Neurohormonal responses
Ventricular remodeling
Dilation
Sympathetic nervous system (SNS) activation - answerSympathetic nervous system
(SNS) activation is often the first mechanism triggered in low-CO states.
However, it is the least effective compensatory mechanism.
a) In response to an inadequate stroke volume and CO, there is increased SNS
activation, resulting in the increased release of catecholamines (epinephrine and
norepinephrine).
b) This results in increased HR, increased myocardial contractility, and peripheral
vasoconstriction.
c) Initially, this increase in HR and contractility improves CO. However, over time these
factors are harmful as they increase the already failing heart's workload and need for
oxygen. The vasoconstriction causes an immediate increase in preload, which may
initially increase CO. However, an increase in venous return to the heart, which is
already volume overloaded, actually worsens ventricular performance.
As the CO falls, blood flow to the kidneys ________ - answerAs the CO falls, blood flow
to the kidneys decreases.
This is sensed by kidneys as decreased volume. In response, the kidneys release renin,
which converts angiotensinogen to angiotensin I. Angiotensin I is subsequently
converted to angiotensin II by a converting enzyme made in the lungs. Angiotensin II
causes (1) the adrenal cortex to release aldosterone, which results in sodium and water
retention, and (2) increased peripheral vasoconstriction, which increases BP. This
response is known as the renin-angiotensin-aldosterone system (RAAS).
a) Low CO causes a decrease in cerebral perfusion pressure. In response, the posterior
pituitary gland secretes antidiuretic hormone (ADH), also called vasopressin. ADH
increases water reabsorption in the kidneys, causing water retention. As a result, blood
volume is increased in a person who is already volume overloaded.
b) Other factors also contribute to the development of HF. The production of endothelin,
a potent vasoconstrictor produced by the vascular endothelial cells, is stimulated by
ADH, catecholamines, and angiotensin II. Endothelin results in further arterial
vasoconstriction and an increase in cardiac contractility and hypertrophy.
Congestive Heart Failure - answer A condition resulting from the heart's inability to
pump out all the blood that returns to it; blood backs up in the veins leading to the heart,
causing an accumulation of fluid in various parts of the body
Factors that Affect Cardiac Output - answer Preload
Afterload
Preload - answer Volume of blood in ventricles at end of diastole (end diastolic
pressure). blood coming back to the heart.
Increased in:
Hypervolemia
Regurgitation of cardiac valves
Afterload - answerResistance left ventricle must overcome to circulate blood.
Increased in:
Hypertension
Vasoconstriction
Increased aferload
Increased cardiac workload
Heart Failure Pathophysiology - answerSeen in disease states such as dilated
cardiomyopathy (DCM)
Poor EFs (<35%)
High pulmonary pressures
Biventricular failure
-Both ventricles may be dilated and have poor filling and emptying capacity
Who is at-risk for congestive heart failure? Risk Factors? - answerPrimary causes:
CAD, MI, HTN, Rheumatic HD, Congenital Heart defects, Pulmonary HTN,
Cardiomyopathy, hyperthyroidism, Valvular disorders, and myocarditis.
Precipitating Factors: Anemia, Infection, dysrhythmias, bacterial endocarditis, PE,
Paget's dx, nutritional deficiencies, hypervolemia.
, Heart Failure Compensatory Mechanisms - answerSympathetic nervous system (SNS)
activation
Neurohormonal responses
Ventricular remodeling
Dilation
Sympathetic nervous system (SNS) activation - answerSympathetic nervous system
(SNS) activation is often the first mechanism triggered in low-CO states.
However, it is the least effective compensatory mechanism.
a) In response to an inadequate stroke volume and CO, there is increased SNS
activation, resulting in the increased release of catecholamines (epinephrine and
norepinephrine).
b) This results in increased HR, increased myocardial contractility, and peripheral
vasoconstriction.
c) Initially, this increase in HR and contractility improves CO. However, over time these
factors are harmful as they increase the already failing heart's workload and need for
oxygen. The vasoconstriction causes an immediate increase in preload, which may
initially increase CO. However, an increase in venous return to the heart, which is
already volume overloaded, actually worsens ventricular performance.
As the CO falls, blood flow to the kidneys ________ - answerAs the CO falls, blood flow
to the kidneys decreases.
This is sensed by kidneys as decreased volume. In response, the kidneys release renin,
which converts angiotensinogen to angiotensin I. Angiotensin I is subsequently
converted to angiotensin II by a converting enzyme made in the lungs. Angiotensin II
causes (1) the adrenal cortex to release aldosterone, which results in sodium and water
retention, and (2) increased peripheral vasoconstriction, which increases BP. This
response is known as the renin-angiotensin-aldosterone system (RAAS).
a) Low CO causes a decrease in cerebral perfusion pressure. In response, the posterior
pituitary gland secretes antidiuretic hormone (ADH), also called vasopressin. ADH
increases water reabsorption in the kidneys, causing water retention. As a result, blood
volume is increased in a person who is already volume overloaded.
b) Other factors also contribute to the development of HF. The production of endothelin,
a potent vasoconstrictor produced by the vascular endothelial cells, is stimulated by
ADH, catecholamines, and angiotensin II. Endothelin results in further arterial
vasoconstriction and an increase in cardiac contractility and hypertrophy.
