Heart Failure Nursing Certification Questions
and verified answers.
Causes of heart failure - ANS CAD - most common
HTN
MI
Valvar disease
Genetic disease (i.e. Duchene muscular dystrophy, certain hypertrophic
cardiomyopathies)
Congenital abnormalities (i.e. tricuspid atresia, septal defects)
Per partum cardiomyopathy
Infiltrative CMO (i.e. amyloidosis, sarcoidosis, hemochromatosis)
Infection/inflammatory processes (i.e. viral myocarditis, Chagas disease)
Metabolic disorders (i.e. hyperthyroidism, DM)
Toxins (alcohol, chemotherapy radiation therapy illicit drugs)
Arrhythmias
heart failure (HF) - ANS condition in which there is an inability of the heart to pump
enough blood through the body to supply the tissues and organs with nutrients and
oxygen
contributing factors of ventricular remodeling - ANS Neurohormal activation
Dysregulation of the immune system
Alterations in the extracellular matrix ("scaffolding" that hold myocardial cells in
alignment)
Neurohormal activation - ANS SNS (stimulation of b-adrenergic receptors by
epi/notepad)
RAAS (release of renin, angiotensin II, and aldosterone) Natriuretic peptides (BNP
elevated and release d/t increase stretch/stress)
Vasopressin (anti-diuretic hormone)
Endothelin (myocardial ET stimulated by hypoxia, ischemia, and neurohormones)
What receptors does the SNS release? - ANS B-adrenergic
Chrono tropism - ANS increased heart rate
Inotropes - ANS increased contractility
Preload - ANS degree of stretch of the cardiac muscle fibers at the end of diastole.
Diuretics decrease preload. Ventricular end diastolic pressure is increased in a failing
heart. Determining factor for pre-load is venous return and circulating volume
Afterload - ANS the amount of resistance to ejection of blood from the ventricle.
Antihypertensive decrease after load. This is reflective of aortic pressure for left
,ventricle and pulmonary artery pressure for the right ventricle. As afterload increases,
cardiac output decreases. As arterial pressure increases afterload increases.
Cardiac Output (CO) - ANS HR x SV. The amount of blood ejected by the left ventricle
with each contraction. Normal is 4-8/minute. Decreased cardiac output, require
shedding of blood and peripheral vasoconstriction to perfuse vital organs
vascular resistance - ANS The arterial resistance to blood flow that must be over, come
to push blood from the heart through the circulatory system
Vasoconstriction increases vascular resistance
Vasodilation decreases vascular resistance
Systemic Vascular Resistance (SVR) - ANS The resistance the left ventricle must
overcome to pump blood through the systemic, or peripheral circulation, often used as a
clinical index of left ventricular afterload
Pulmonary Vascular Resistance (PVR) - ANS The resistance of the right ventricle must
overcome to pump blood through the vasculature of the lungs; 0.25-1.6
Angiotensin II - ANS vasoconstrictor, increases blood pressure by stimulating kidneys to
retain more water and by releasing aldosterone--which stimulates Na retention and K
release and causes myocardial fibrosis
Decreased renal perfusion causes what to be released? - ANS Renin
Natures is - ANS excretion of sodium in the urine
BNP - ANS biomarker for increase cardiac wall stretch/stress. It is secreted when there
is cardiac wall stretch and stress
BNP levels - ANS <100--low likelihood HF
100-300--suggest HF present, but not definite
>300 indicates mild HF
>600 indicates moderate HF
>900 indicates severe HF
When is vasopressin released? - ANS when circulating plasma volume is low, when the
body needs to conserve water, under filling/reduced via high pressure baroceptors in
the carotid and aorta arch
When are nature tic peptides produced? - ANS ventricle wall stress/stretch
Baroreceptors - ANS Cells that are sensitive to blood pressure changes
What does vasopressin do? - ANS raises blood pressure and inhibits urine formation
(Vasopressin is also known as ADH or antidiuretic hormone)
,Retains water
Increases peripheral vascular resistance (PVR)
Increases arterial BP by vasoconstriction
Increase central venous pressure (CVP)
--elevated levels lead to congestion and hyponatremia
when is endothelium released? - ANS hypoxia, ischemia, neurohormone receptors
(notepad, vasopressin, and angiotensin II), and inflammation
what kind of inotropic effect does endothelium have in a failing heart? - ANS negative. it
does stimulate contraction in all other smooth muscles
what does increased endothelium lead to - ANS progression of LV dysfunction and
secondary to palm HTN. it can lead to LV remodeling, hypertrophy, fibroblast
proliferation
What do pro-inflammatory cytokines do (i.e. tumor necrosis factor (TFN) and interleukin
(IL)? - ANS cause inflammation, negative inotropic effect, abnormalities in cardiac
metabolism, myocardial remodeling, cardio myocyte hypertrophy, apoptosis, necrosis
what does an increase in fibroblasts do to cardiac extracellular matrix? - ANS increases
the proteins in the myocardium leading to fibrosis, myocardial stiffening, impaired
ventricular relaxation/contraction
what is a fibroblast - ANS a cell in connective tissue that produces collagen and other
fibers?
what is the main principle behind Here? - ANS neurohormoal activation
what is the main principle behind Hope? - ANS inflammation
Heart failure with preserved ejection fraction (Hope) - ANS Diastolic heart failure. Can
be caused by HTN. Caused by a stiffening of the left ventricle, which leads to the
inability of the left ventricle to relax/fill properly during diastole. The EF is normal, >50%.
When the heart cannot fill properly, the extra fluid that the heart cannot accommodate
back up and heart failure symptoms occur. Furthermore, an inadequate amount of blood
is pumped out of the left ventricle into the systemic circulation and low cardiac output
can occur.
What is the most common cause of diastolic heart failure? - ANS HTN
Heart failure with reduced ejection fraction (Here) - ANS Heart failure with a left
ventricular ejection fraction <40%. When the EF it's below normal, it is difficult for the
heart to meet the demands of the body and symptoms of heart failure occur.
What is the most common cause of systolic heart failure? - ANS ischemic heart disease
, Hope, borderline - ANS EF 41-49%
Biventricular Heart Failure - ANS Inability of both ventricles to pump, blood, effectively.
Backward failure: secondary to decreased contractility, fluid buildup, and passive
engorgement of systemic veins.
Forward failure: blood flow is compromised, secondary to inadequate, cardiac output,
resulting in decreased perfusion divide organs
Increase venous pressure in heart failure causes what - ANS Sodium and water
retention and edema
Central Venous Pressure (CVP) - ANS 0-5 mmHg; the pressure of blood in the vena
cava, near the right atrium of the heart
Reflects the amount of blood returning to the heart
CVP is a good approximation of right atrial pressure, which is a major determinant of
right ventricular end diastolic volume.
Used to estimate preload
Right ventricular pressure - ANS Systolic 15-30 mmHg
Diastolic 0-5 mmHg
Left ventricular pressure - ANS Systolic: 100-140 mmHg
Pulmonary artery pressure - ANS Systolic: 15-30 mmHg
Diastolic: 4-12 mmHg
Pulmonary Capillary Wedge Pressure (PCWP) - ANS 6-15 mmHg
Provides an indirect measure of left atrial pressure
Pulmonary edema is reflective of PCWP >25
Dyssynchrony of contraction - ANS Delay in electrical activation between the right and
left ventricles often due to a bundle branch block, and which one ventricle contracts
prior to the other, leading to a decreased EF
Frank-Starling Law - ANS The greater the stretch, the stronger is the heart's contraction.
This increased contractility results in an increased volume of blood ejected. Excessive
preload exhausts this mechanism, and eventually no longer increases cardiac output.
As the heart undergoes remodeling, it becomes less what shape - ANS Less elliptical
and more spherical (from a football to a basketball shape)
Pulmonary arterial hypertension, versus pulmonary venous hypertension - ANS in
pulmonary arterial hypertension unfavorable RV remodeling leads to progressive failure
of the right ventricle resulting in decrease LV output. In pulmonary venous hypertension
an elevation in the LV pressure leads to an increase in the LA pressure which leads to
and verified answers.
Causes of heart failure - ANS CAD - most common
HTN
MI
Valvar disease
Genetic disease (i.e. Duchene muscular dystrophy, certain hypertrophic
cardiomyopathies)
Congenital abnormalities (i.e. tricuspid atresia, septal defects)
Per partum cardiomyopathy
Infiltrative CMO (i.e. amyloidosis, sarcoidosis, hemochromatosis)
Infection/inflammatory processes (i.e. viral myocarditis, Chagas disease)
Metabolic disorders (i.e. hyperthyroidism, DM)
Toxins (alcohol, chemotherapy radiation therapy illicit drugs)
Arrhythmias
heart failure (HF) - ANS condition in which there is an inability of the heart to pump
enough blood through the body to supply the tissues and organs with nutrients and
oxygen
contributing factors of ventricular remodeling - ANS Neurohormal activation
Dysregulation of the immune system
Alterations in the extracellular matrix ("scaffolding" that hold myocardial cells in
alignment)
Neurohormal activation - ANS SNS (stimulation of b-adrenergic receptors by
epi/notepad)
RAAS (release of renin, angiotensin II, and aldosterone) Natriuretic peptides (BNP
elevated and release d/t increase stretch/stress)
Vasopressin (anti-diuretic hormone)
Endothelin (myocardial ET stimulated by hypoxia, ischemia, and neurohormones)
What receptors does the SNS release? - ANS B-adrenergic
Chrono tropism - ANS increased heart rate
Inotropes - ANS increased contractility
Preload - ANS degree of stretch of the cardiac muscle fibers at the end of diastole.
Diuretics decrease preload. Ventricular end diastolic pressure is increased in a failing
heart. Determining factor for pre-load is venous return and circulating volume
Afterload - ANS the amount of resistance to ejection of blood from the ventricle.
Antihypertensive decrease after load. This is reflective of aortic pressure for left
,ventricle and pulmonary artery pressure for the right ventricle. As afterload increases,
cardiac output decreases. As arterial pressure increases afterload increases.
Cardiac Output (CO) - ANS HR x SV. The amount of blood ejected by the left ventricle
with each contraction. Normal is 4-8/minute. Decreased cardiac output, require
shedding of blood and peripheral vasoconstriction to perfuse vital organs
vascular resistance - ANS The arterial resistance to blood flow that must be over, come
to push blood from the heart through the circulatory system
Vasoconstriction increases vascular resistance
Vasodilation decreases vascular resistance
Systemic Vascular Resistance (SVR) - ANS The resistance the left ventricle must
overcome to pump blood through the systemic, or peripheral circulation, often used as a
clinical index of left ventricular afterload
Pulmonary Vascular Resistance (PVR) - ANS The resistance of the right ventricle must
overcome to pump blood through the vasculature of the lungs; 0.25-1.6
Angiotensin II - ANS vasoconstrictor, increases blood pressure by stimulating kidneys to
retain more water and by releasing aldosterone--which stimulates Na retention and K
release and causes myocardial fibrosis
Decreased renal perfusion causes what to be released? - ANS Renin
Natures is - ANS excretion of sodium in the urine
BNP - ANS biomarker for increase cardiac wall stretch/stress. It is secreted when there
is cardiac wall stretch and stress
BNP levels - ANS <100--low likelihood HF
100-300--suggest HF present, but not definite
>300 indicates mild HF
>600 indicates moderate HF
>900 indicates severe HF
When is vasopressin released? - ANS when circulating plasma volume is low, when the
body needs to conserve water, under filling/reduced via high pressure baroceptors in
the carotid and aorta arch
When are nature tic peptides produced? - ANS ventricle wall stress/stretch
Baroreceptors - ANS Cells that are sensitive to blood pressure changes
What does vasopressin do? - ANS raises blood pressure and inhibits urine formation
(Vasopressin is also known as ADH or antidiuretic hormone)
,Retains water
Increases peripheral vascular resistance (PVR)
Increases arterial BP by vasoconstriction
Increase central venous pressure (CVP)
--elevated levels lead to congestion and hyponatremia
when is endothelium released? - ANS hypoxia, ischemia, neurohormone receptors
(notepad, vasopressin, and angiotensin II), and inflammation
what kind of inotropic effect does endothelium have in a failing heart? - ANS negative. it
does stimulate contraction in all other smooth muscles
what does increased endothelium lead to - ANS progression of LV dysfunction and
secondary to palm HTN. it can lead to LV remodeling, hypertrophy, fibroblast
proliferation
What do pro-inflammatory cytokines do (i.e. tumor necrosis factor (TFN) and interleukin
(IL)? - ANS cause inflammation, negative inotropic effect, abnormalities in cardiac
metabolism, myocardial remodeling, cardio myocyte hypertrophy, apoptosis, necrosis
what does an increase in fibroblasts do to cardiac extracellular matrix? - ANS increases
the proteins in the myocardium leading to fibrosis, myocardial stiffening, impaired
ventricular relaxation/contraction
what is a fibroblast - ANS a cell in connective tissue that produces collagen and other
fibers?
what is the main principle behind Here? - ANS neurohormoal activation
what is the main principle behind Hope? - ANS inflammation
Heart failure with preserved ejection fraction (Hope) - ANS Diastolic heart failure. Can
be caused by HTN. Caused by a stiffening of the left ventricle, which leads to the
inability of the left ventricle to relax/fill properly during diastole. The EF is normal, >50%.
When the heart cannot fill properly, the extra fluid that the heart cannot accommodate
back up and heart failure symptoms occur. Furthermore, an inadequate amount of blood
is pumped out of the left ventricle into the systemic circulation and low cardiac output
can occur.
What is the most common cause of diastolic heart failure? - ANS HTN
Heart failure with reduced ejection fraction (Here) - ANS Heart failure with a left
ventricular ejection fraction <40%. When the EF it's below normal, it is difficult for the
heart to meet the demands of the body and symptoms of heart failure occur.
What is the most common cause of systolic heart failure? - ANS ischemic heart disease
, Hope, borderline - ANS EF 41-49%
Biventricular Heart Failure - ANS Inability of both ventricles to pump, blood, effectively.
Backward failure: secondary to decreased contractility, fluid buildup, and passive
engorgement of systemic veins.
Forward failure: blood flow is compromised, secondary to inadequate, cardiac output,
resulting in decreased perfusion divide organs
Increase venous pressure in heart failure causes what - ANS Sodium and water
retention and edema
Central Venous Pressure (CVP) - ANS 0-5 mmHg; the pressure of blood in the vena
cava, near the right atrium of the heart
Reflects the amount of blood returning to the heart
CVP is a good approximation of right atrial pressure, which is a major determinant of
right ventricular end diastolic volume.
Used to estimate preload
Right ventricular pressure - ANS Systolic 15-30 mmHg
Diastolic 0-5 mmHg
Left ventricular pressure - ANS Systolic: 100-140 mmHg
Pulmonary artery pressure - ANS Systolic: 15-30 mmHg
Diastolic: 4-12 mmHg
Pulmonary Capillary Wedge Pressure (PCWP) - ANS 6-15 mmHg
Provides an indirect measure of left atrial pressure
Pulmonary edema is reflective of PCWP >25
Dyssynchrony of contraction - ANS Delay in electrical activation between the right and
left ventricles often due to a bundle branch block, and which one ventricle contracts
prior to the other, leading to a decreased EF
Frank-Starling Law - ANS The greater the stretch, the stronger is the heart's contraction.
This increased contractility results in an increased volume of blood ejected. Excessive
preload exhausts this mechanism, and eventually no longer increases cardiac output.
As the heart undergoes remodeling, it becomes less what shape - ANS Less elliptical
and more spherical (from a football to a basketball shape)
Pulmonary arterial hypertension, versus pulmonary venous hypertension - ANS in
pulmonary arterial hypertension unfavorable RV remodeling leads to progressive failure
of the right ventricle resulting in decrease LV output. In pulmonary venous hypertension
an elevation in the LV pressure leads to an increase in the LA pressure which leads to
