Neurohormonal Responses to Cardiac Dysfunction

Question 1

heart failure

Answer 1

clinical syndrome defined by the inability of the heart to supply adequate blood flow (cardiac output)

decreased ability to accept or pump blood

Question 2

is heart failure progressive

Answer 2

yes - does not fail acutely

Question 3

what does decreased ability to accept blood cause

Answer 3

congestion behind the failed side

L sided HF: congests pulmonary veins and lungs
R sided HF: congests systemic veins and liver/abdomen

Question 4

what does decreased ability to pump blood cause

Answer 4

low cardiac output

Question 5

what are 3 common causes of heart failure

Answer 5

1. myxomatous mitral valve disease - dogs
2. dilated cardiomyopathy (DCM) - dogs
3. hypertrophic cardiomyopathy (HCM) - cats

Question 6

myxomatous mitral valve disease

Answer 6

mitral regurgitation leading to progressive volume overload

Question 7

is myxomatous mitral valve disease systolic or diastolic dysfunction

Answer 7

systolic

mitral valve leaks fluid from LV to LA during systole –> blood accumulates in LA –> increases EDV and EDP

Question 8

dilated cardiomyopathy (DCM)

Answer 8

enlarged chamber + thin ventricular walls –> decreased contractility

Question 9

is DCM systolic or diastolic dysfunction

Answer 9

systolic

unable to contract to eject blood due to eccentric hypertrophy –> increases ESV –> volume overload

Question 10

hypertrophic cardiomyopathy (HCM)

Answer 10

enlarged/thickened ventricular walls –> decreased filling

Question 11

is HCM a systolic or diastolic dysfunction

Answer 11

diastolic

thick walls have decreased compliance –> decreases EDV, increases EDP

Question 12

compensatory mechanisms to CV dysfunction

Answer 12

1. frank starling
2. sympathetic NS activation
3. vasoconstriction
4. renal Na + H2O retention
5. cardiac hypertrophy

Question 13

frank starling mechanism

Answer 13

increase in venous return (preload) –> heart fills with more blood –> heart wants to return to same ESV –> must eject more blood –> increased stroke volume

Question 14

what does the frank starling mechanism require in order to work

Answer 14

functional cardiomyocytes

if dysfunctional cardiomyocytes: preload increases but unable to eject enough blood –> inability to increase SV to compensate

Question 15

how does disease affect the frank starling curve

Answer 15

FS curve: SV (y axis) vs EDP (x axis)

shifts the curve right and down –> shallow slope in increase of SV as EDP increases

Question 16

how does the sympathetic nervous system get activated in response to cardiac dysfunction

Answer 16

cardiac dysfunction –> decrease CO –> decrease BP

baroreceptors detect drop in BP and increase SNS stimulation

Question 17

what are SNS targets, receptors, and effect

Answer 17

heart (B1) : increase chrono/dromo/ino/lusitropy
arterioles (a1): vasoconstriction to inc. BP
veins (a1): vasoconstriction to inc. venous return and preload –> inc. CO via frank starling
kidney (B1): renin release –> RAAS activation –> vasoconstriction and Na/H2O reabsorption –> inc. blood volume and BP

Question 18

net effect of sympathetic NS compensation

Answer 18

short term mechanism of maintaining arterial blood pressure and perfusion pressure

Question 19

can chronic SNS activity become maladaptive

Answer 19

yes
increases MVO2
increases afterload (BP) –> decreases SV
promotes maladaptive hypertrophy
increases Ca –> arrhythmias
desensitizes baroreceptors

Question 21

how does vasoconstriction contribute to cardiac compensation

Answer 21

low CO triggers vasoconstriction –> increase SVR –> increase BP

Question 22

is BP during heart failure high, low, or normal

Answer 22

subclinical HF (when compensation works well) –> normal BP

clinical HF (when compensation fails) –> low BP from low CO

Question 23

cardiogenic shock

Answer 23

hypotension secondary to cardiac disease (poor prognosis)

leads to vasoconstriction to redistribute blood to vital organs; leads to:
- pale MM
- prolonged CRT
- exercise intolerance

Question 24

is vasoconstriction maladaptive

Answer 24

yes - causes increased venous return and increased BP –> increased preload and afterload –> increased demand on pump –> decreased CO

vasoconstrictors (NE, epi, aldosterone) are toxic - cause hypertrophy and fibrosis

Question 25

what are the kidney’s mechanisms of compensation during cardiac failure

Answer 25

stimulate RAAS to increase blood volume and BP

mediators: ANG II, aldosterone, ADH

inhibits diuretic pathways (natriuretic peptides)

Question 26

how does RAAS become maladaptive

Answer 26

as RAAS gets stimulated, negative feedback is lost

RAAS tries to increase BP, but as cardiac disease progresses, BP continues to drop –> constantly sets back the set point for RAAS stimulation –> constitutive stimulation

Question 27

effects of chronic RAAS stimulation

Answer 27

chronic increase blood volume –> increase venous return –> increase preload –> overwhelms vein reservoirs (decreased compliance from vasoconstriction) –> the increase in blood volume goes directly to RA –> congestion and edema/effusion

Question 28

what are the main clinical signs of heart failure

Answer 28

edema and effusion

can manifest first as exercise intolerance

LHF: pulmonary edema
RHF: hepatic congestion, ascites, pleural effusion, peripheral edema

Question 29

what does atrial enlargement indicate

Answer 29

heart failure

LA enlargement = LHF
RA enlargement = RHF