Neurohormonal Responses to Cardiac Dysfunction Flashcards
heart failure
clinical syndrome defined by the inability of the heart to supply adequate blood flow (cardiac output)
decreased ability to accept or pump blood
is heart failure progressive
yes - does not fail acutely
what does decreased ability to accept blood cause
congestion behind the failed side
L sided HF: congests pulmonary veins and lungs
R sided HF: congests systemic veins and liver/abdomen
what does decreased ability to pump blood cause
low cardiac output
what are 3 common causes of heart failure
- myxomatous mitral valve disease - dogs
- dilated cardiomyopathy (DCM) - dogs
- hypertrophic cardiomyopathy (HCM) - cats
myxomatous mitral valve disease
mitral regurgitation leading to progressive volume overload
is myxomatous mitral valve disease systolic or diastolic dysfunction
systolic
mitral valve leaks fluid from LV to LA during systole –> blood accumulates in LA –> increases EDV and EDP
dilated cardiomyopathy (DCM)
enlarged chamber + thin ventricular walls –> decreased contractility
is DCM systolic or diastolic dysfunction
systolic
unable to contract to eject blood due to eccentric hypertrophy –> increases ESV –> volume overload
hypertrophic cardiomyopathy (HCM)
enlarged/thickened ventricular walls –> decreased filling
is HCM a systolic or diastolic dysfunction
diastolic
thick walls have decreased compliance –> decreases EDV, increases EDP
compensatory mechanisms to CV dysfunction
- frank starling
- sympathetic NS activation
- vasoconstriction
- renal Na + H2O retention
- cardiac hypertrophy
frank starling mechanism
increase in venous return (preload) –> heart fills with more blood –> heart wants to return to same ESV –> must eject more blood –> increased stroke volume
what does the frank starling mechanism require in order to work
functional cardiomyocytes
if dysfunctional cardiomyocytes: preload increases but unable to eject enough blood –> inability to increase SV to compensate
how does disease affect the frank starling curve
FS curve: SV (y axis) vs EDP (x axis)
shifts the curve right and down –> shallow slope in increase of SV as EDP increases
how does the sympathetic nervous system get activated in response to cardiac dysfunction
cardiac dysfunction –> decrease CO –> decrease BP
baroreceptors detect drop in BP and increase SNS stimulation
what are SNS targets, receptors, and effect
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
net effect of sympathetic NS compensation
short term mechanism of maintaining arterial blood pressure and perfusion pressure
can chronic SNS activity become maladaptive
yes
increases MVO2
increases afterload (BP) –> decreases SV
promotes maladaptive hypertrophy
increases Ca –> arrhythmias
desensitizes baroreceptors
how does vasoconstriction contribute to cardiac compensation
low CO triggers vasoconstriction –> increase SVR –> increase BP
is BP during heart failure high, low, or normal
subclinical HF (when compensation works well) –> normal BP
clinical HF (when compensation fails) –> low BP from low CO
cardiogenic shock
hypotension secondary to cardiac disease (poor prognosis)
leads to vasoconstriction to redistribute blood to vital organs; leads to:
- pale MM
- prolonged CRT
- exercise intolerance
is vasoconstriction maladaptive
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
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)
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
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
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
what does atrial enlargement indicate
heart failure
LA enlargement = LHF
RA enlargement = RHF
