Lecture 22 Flashcards

1
Q

Heart failure

A

despite adequate venous return, CO is insufficient to meet tissue demands at rest or on physical exertion

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2
Q

Signs of heart failure(3)

A

poor exercise tolerance
shortness of breath
cool extremities

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3
Q

early compensated heart failure

arterial BP falls->

A

destimulated baroreceptors->inc sympathetic activity->inc catecholamines into blood stream

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4
Q

Early compensated heart failure
alpha 1 receptors bind

beta 1 receptors bind

A

->vasoconstriction (arterial)-> inc TPR->inc workload of heart

in myocardium and lead to inc HR and force of contraction->inc workload of the heart

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5
Q

early compensated heart failure

how to increase preload/afterload(arrows)

A

inc sympathetic stimulation->hypothalamus secrete ADH->fluid retention in kidneys->inc blood volume and BP->inc preload and afterload->increased work on failing heart

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6
Q

chronically high levels of circulating neuroendocrine hormones (catecholamines, renin, angiotensin, aldosterone) leads to

A

affecting myocardium directly->structural remodeling long term

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7
Q

early compensated heart failure

reduced perfusion to skeletal muscle(2)

A

atrophy of muscle fibers(cachexia)

exercise intolerance

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8
Q

Chronic activation of SNS(2)

A

dec baroreceptor sensitivity- maintained sympathetic drive even when MAP is normal
down regulation of Beta receptors in the heart-dec capacity of heart to respond to sympathetic stimulation

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9
Q

Cardiac hypertrophy(4)

A

dec mitochondria density-dec energy supply
dec inotropy-weak heart
stiff heart
inc risk of arrythmias

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10
Q

Counter regulatory mechanisms in heart failure(2)

A

atrial naturetic peptide

prostaglandins- antagonize vasoconstrictive effects of angiotensin (to protect kidney)

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11
Q

Volume overload leads to

A

eccentric hypertrophy

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12
Q

Eccentric hypertrophy
response to what
what occurs
end stage

A

response to elevated ventricular end diastolic pressures
ventricular dilation occurs as new sarcomeres are added in series to existing sarcomeres
not enough overlap of actin and myosin

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13
Q

pressure overload leads to

A

concentric hypertrophy

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14
Q

concentric hypertrophy
due to
what occurs
end stage

A

due to chronic pressure overloads (afterload)
ventricular chamber radius may not change, but wall thickness greatly inc as new sarcomeres are added in parallel
capable of generating greater forces and higher pressures

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15
Q

Changes in cardiac parameters in heart failure (4)

A

dec contractility
dec SV
dec exercise tolerance
inc HR- sympathetic NS response to fall in BP

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16
Q

dec contractility in end stage eccentric hypertrophy leads to

A

inc ESV

17
Q

dec filling in concentric hypertrophy leads to

A

dec EDV