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

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
what are the kidney's mechanisms of compensation during cardiac failure
stimulate RAAS to increase blood volume and BP mediators: ANG II, aldosterone, ADH inhibits diuretic pathways (natriuretic peptides)
26
how does RAAS become maladaptive
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
effects of chronic RAAS stimulation
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
what are the main clinical signs of heart failure
edema and effusion can manifest first as exercise intolerance LHF: pulmonary edema RHF: hepatic congestion, ascites, pleural effusion, peripheral edema
29
what does atrial enlargement indicate
heart failure LA enlargement = LHF RA enlargement = RHF