N5315 - Advanced Pathophysiology -
Cardiomyopathies and Heart Failure (Lecture) |
Questions with Answers Verified 100% Correct
A decrease in contractility in the left ventricle will lead to a decrease in stroke volume, decrease
in cardiac output, an increase in left ventricular end diastolic volume (preload) - ✔✔What is
the first step of ventricular remodeling?
Causes a dilation of the ventricle and further compromises contraction and cardiac output -
✔✔What happens as preload increases over time?
Further pathological deterioration of the myocytes - ✔✔What does ventricular remodeling
lead to?
Some pathologic insult to the myocardium which causes damage that leads to dysfunction -
✔✔What is ventricular remodeling initially triggered by?
Baroreceptor activation and renin angiotensin aldosterone system activation -
✔✔Myocardial systolic dysfunction and low cardiac output triggers what 2 processes?
Baroreceptors in left ventricle, aortic arch and carotid sinus detect low cardiac output (low BP)
and notify medulla which in turn stimulates SNS. SNS stimulates release of catecholamines
epinephrine and norepinephrine, causing vasoconstriction and leads to increased after load,
increased BP and increased HR. This increases work load of heart and causes hypertrophy and
dilation of left ventricle and further impairs contractility - ✔✔What is the baroreceptor
activation process?
RAAS is activated by decreased renal blood flow. End result is release of angiotensin II and
aldosterone. Angiotensin II causes vasoconstriction, which increases after load, BP and
contributes to worsening of left ventricular hypertrophy, dilation and worsening contraction.
, Aldosterone enhances renal sodium retention and thereby water. This increases after load
again contributing to worsening of left ventricular hypertrophy, dilation and worsening
contraction. - ✔✔What is the RAAS activation process?
Beta blockers are given to block effects of catecholamines on the heart. ACE Inhibitors and
ARBS are given to block effects of RAAS. These medications prevent progression of heart
failure, remodeling and may improve systolic function. They also decrease mortality. -
✔✔What medication is given to patients with HFrEF and why?
Pulmonary edema secondary to back up of blood and high pressures into the pulmonary
circulation; may experience edema from sodium and water retention - ✔✔What are the
clinical manifestations of HFrEF?
Presence of pulmonary congestion in the setting of normal left systolic EF, stroke volume and
cardiac output - ✔✔HFpEF is characterized by what?
More common in women - ✔✔HFpEF is more common in what population?
HTN-induced hypertrophy or myocardial ischemia which result in remodeling - ✔✔HFpEF is
most commonly caused by what?
Inability of the myocytes to actively pump calcium from cytosol which impairs ventricular
relaxation - ✔✔Pathologically, HFpEF results from what?
In left or right side of the heart - ✔✔HFpEF can happen where?
The filling of the ventricle results in increased LVEDP - ✔✔What does the defect in relaxation
on HFpEF lead to?
Cardiomyopathies and Heart Failure (Lecture) |
Questions with Answers Verified 100% Correct
A decrease in contractility in the left ventricle will lead to a decrease in stroke volume, decrease
in cardiac output, an increase in left ventricular end diastolic volume (preload) - ✔✔What is
the first step of ventricular remodeling?
Causes a dilation of the ventricle and further compromises contraction and cardiac output -
✔✔What happens as preload increases over time?
Further pathological deterioration of the myocytes - ✔✔What does ventricular remodeling
lead to?
Some pathologic insult to the myocardium which causes damage that leads to dysfunction -
✔✔What is ventricular remodeling initially triggered by?
Baroreceptor activation and renin angiotensin aldosterone system activation -
✔✔Myocardial systolic dysfunction and low cardiac output triggers what 2 processes?
Baroreceptors in left ventricle, aortic arch and carotid sinus detect low cardiac output (low BP)
and notify medulla which in turn stimulates SNS. SNS stimulates release of catecholamines
epinephrine and norepinephrine, causing vasoconstriction and leads to increased after load,
increased BP and increased HR. This increases work load of heart and causes hypertrophy and
dilation of left ventricle and further impairs contractility - ✔✔What is the baroreceptor
activation process?
RAAS is activated by decreased renal blood flow. End result is release of angiotensin II and
aldosterone. Angiotensin II causes vasoconstriction, which increases after load, BP and
contributes to worsening of left ventricular hypertrophy, dilation and worsening contraction.
, Aldosterone enhances renal sodium retention and thereby water. This increases after load
again contributing to worsening of left ventricular hypertrophy, dilation and worsening
contraction. - ✔✔What is the RAAS activation process?
Beta blockers are given to block effects of catecholamines on the heart. ACE Inhibitors and
ARBS are given to block effects of RAAS. These medications prevent progression of heart
failure, remodeling and may improve systolic function. They also decrease mortality. -
✔✔What medication is given to patients with HFrEF and why?
Pulmonary edema secondary to back up of blood and high pressures into the pulmonary
circulation; may experience edema from sodium and water retention - ✔✔What are the
clinical manifestations of HFrEF?
Presence of pulmonary congestion in the setting of normal left systolic EF, stroke volume and
cardiac output - ✔✔HFpEF is characterized by what?
More common in women - ✔✔HFpEF is more common in what population?
HTN-induced hypertrophy or myocardial ischemia which result in remodeling - ✔✔HFpEF is
most commonly caused by what?
Inability of the myocytes to actively pump calcium from cytosol which impairs ventricular
relaxation - ✔✔Pathologically, HFpEF results from what?
In left or right side of the heart - ✔✔HFpEF can happen where?
The filling of the ventricle results in increased LVEDP - ✔✔What does the defect in relaxation
on HFpEF lead to?
