GMS6530: HEART FAILURE EXAM QUESTIONS AND ANSWERS
WITH COMPLETE SOLUTIONS VERIFIED LATEST UPDATE
T/F: for heart rate, the primary mechanism involves the autonomic nervous
system
True
heart failure
-inability of the heat to pump sufficient blood to meet the metabolic demands of the body
-reduced efficiency of the heart as a pump
intrinsic cardiac compensatory mechanisms
- when stroke volume decreases = dilation will increase ventricular volume and
hypertrophy will increase ventricular mass
physiologic hypertrophy
-exercise, pregnancy
-cardiomyocytes increase length and width
-balanced enlargement of chambers, walls, and septum
pathologic hypertrophy
-concentric hypertrophy
-cardiomyocytes increase width (vs length)
-wall and septal thickening and loss of chamber area
long term:
, -dilated and eccentric hypertrophy
-cardiomyocytes decrease width (with excessive lengthening)
-loss of wall, septal thickness with large increase in wall tension
maladaptive remodeling
-alteration in dimension/shape/mass in response to hemodynamic stress/injury in
association with neurohormonal activation
-myocyte hypertrophy
-myocyte apooptosis (or necrosis)
-fibroblast proliferation (collagen)
-inflammation
-oxidative stress
inotropic agents
-drugs that stimulate the heart to increase the force of contractions (increase in CO and
SV)
-used in acute way
B-adrenergic receptor agonists
A. epinephrine, isoproterenol (not used clinically)
B. dopamine (D1 > beta > alpha)
C. dobutamine (dopamine derivative)
Dopamine
-beta adrenergic receptor agonist
-higher potency of dopamine receptors
-increased contractility and stroke volume
WITH COMPLETE SOLUTIONS VERIFIED LATEST UPDATE
T/F: for heart rate, the primary mechanism involves the autonomic nervous
system
True
heart failure
-inability of the heat to pump sufficient blood to meet the metabolic demands of the body
-reduced efficiency of the heart as a pump
intrinsic cardiac compensatory mechanisms
- when stroke volume decreases = dilation will increase ventricular volume and
hypertrophy will increase ventricular mass
physiologic hypertrophy
-exercise, pregnancy
-cardiomyocytes increase length and width
-balanced enlargement of chambers, walls, and septum
pathologic hypertrophy
-concentric hypertrophy
-cardiomyocytes increase width (vs length)
-wall and septal thickening and loss of chamber area
long term:
, -dilated and eccentric hypertrophy
-cardiomyocytes decrease width (with excessive lengthening)
-loss of wall, septal thickness with large increase in wall tension
maladaptive remodeling
-alteration in dimension/shape/mass in response to hemodynamic stress/injury in
association with neurohormonal activation
-myocyte hypertrophy
-myocyte apooptosis (or necrosis)
-fibroblast proliferation (collagen)
-inflammation
-oxidative stress
inotropic agents
-drugs that stimulate the heart to increase the force of contractions (increase in CO and
SV)
-used in acute way
B-adrenergic receptor agonists
A. epinephrine, isoproterenol (not used clinically)
B. dopamine (D1 > beta > alpha)
C. dobutamine (dopamine derivative)
Dopamine
-beta adrenergic receptor agonist
-higher potency of dopamine receptors
-increased contractility and stroke volume
