Neurohormonal Responses to Cardiac Dysfunction Flashcards

1
Q

heart failure

A

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

decreased ability to accept or pump blood

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2
Q

is heart failure progressive

A

yes - does not fail acutely

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3
Q

what does decreased ability to accept blood cause

A

congestion behind the failed side

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

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4
Q

what does decreased ability to pump blood cause

A

low cardiac output

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5
Q

what are 3 common causes of heart failure

A
  1. myxomatous mitral valve disease - dogs
  2. dilated cardiomyopathy (DCM) - dogs
  3. hypertrophic cardiomyopathy (HCM) - cats
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6
Q

myxomatous mitral valve disease

A

mitral regurgitation leading to progressive volume overload

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7
Q

is myxomatous mitral valve disease systolic or diastolic dysfunction

A

systolic

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

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8
Q

dilated cardiomyopathy (DCM)

A

enlarged chamber + thin ventricular walls –> decreased contractility

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9
Q

is DCM systolic or diastolic dysfunction

A

systolic

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

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10
Q

hypertrophic cardiomyopathy (HCM)

A

enlarged/thickened ventricular walls –> decreased filling

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11
Q

is HCM a systolic or diastolic dysfunction

A

diastolic

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

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12
Q

compensatory mechanisms to CV dysfunction

A
  1. frank starling
  2. sympathetic NS activation
  3. vasoconstriction
  4. renal Na + H2O retention
  5. cardiac hypertrophy
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13
Q

frank starling mechanism

A

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

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14
Q

what does the frank starling mechanism require in order to work

A

functional cardiomyocytes

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

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15
Q

how does disease affect the frank starling curve

A

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

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

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16
Q

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

A

cardiac dysfunction –> decrease CO –> decrease BP

baroreceptors detect drop in BP and increase SNS stimulation

17
Q

what are SNS targets, receptors, and effect

A

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

18
Q

net effect of sympathetic NS compensation

A

short term mechanism of maintaining arterial blood pressure and perfusion pressure

19
Q

can chronic SNS activity become maladaptive

A

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

20
Q
A
21
Q

how does vasoconstriction contribute to cardiac compensation

A

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

22
Q

is BP during heart failure high, low, or normal

A

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

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

23
Q

cardiogenic shock

A

hypotension secondary to cardiac disease (poor prognosis)

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

24
Q

is vasoconstriction maladaptive

A

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

25
Q

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

A

stimulate RAAS to increase blood volume and BP

mediators: ANG II, aldosterone, ADH

inhibits diuretic pathways (natriuretic peptides)

26
Q

how does RAAS become maladaptive

A

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

27
Q

effects of chronic RAAS stimulation

A

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

28
Q

what are the main clinical signs of heart failure

A

edema and effusion

can manifest first as exercise intolerance

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

29
Q

what does atrial enlargement indicate

A

heart failure

LA enlargement = LHF
RA enlargement = RHF