Vascular Hemodynamics Flashcards

1
Q

primary determinant of myocardial oxygen supply

A

coronary blood flow, as determined by vascular resistance

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2
Q

Tx for stable angina

A

first line is medical: reduce myocardial demand w/ beta blockers (lower HR and contractility) and nitrates (reduce preload), also use aspirin and statins to prevent athero and ACS

can move to PCI, improves life but NOT mortality

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3
Q

part of system that regulates MAP

A

arterioles

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4
Q

compliance

A

distensibility of a vessel, determines capacitance

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5
Q

2 components of vascular compliance

A

passive: extracellular matrix like collagen and elastin)
active: smooth muscle tone

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6
Q

venous compliance

A

greater than arteries, will have less pressure for the same volume

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7
Q

regulation of venous compliance

A

a1 adrenergic receptors when activated increase venous tone and decrease venous compliance, increasing venous return to heart (preload)

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8
Q

ateriosclerosis and compliance

A

reduction of vessel compliance in aging, diabetes, chronic HTN, etc by decreasing ECM elasticity

and also from atherosclerosis

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9
Q

functional hyperemia

A

vasodilation in response to increase in metabolic demand, mediated by metabolites such as adenosine, Pi, CO2, H+

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10
Q

main regulator of coronary vascular resistance

A

metabolic control, mainly adenosine, CO2, and H+

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11
Q

describe adenosine nuclear stress test

A

give adenosine which acts as a metabolite vasodilator, healthy vessels will show relatively more perfusion than atherosclerotic ones

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12
Q

how to determine wall tension in vessels

A

Laplace equation, T=Pr/h

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13
Q

in Laplace terms, how do vessels adapt to higher pressures

A

medial hypertrophy, increasing the h variable to lower the tension (chronically this hyaline hypertrophy w/ extracellular matrix, acute is more SMC)

arteries naturally have thicker walls given the higher P and r values as opposed to capillaries

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14
Q

when to Tx AAA?

A

larger than 5.5 cm or growing more than .5 cm a year or symptomatic

rupture is emergent repair

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15
Q

ventricular response to higher blood pressure

A

concentric hypertrophy increases h and reduces r, therefore counteracting the rise in P to avoid super high tension

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16
Q

general features of Marfan syndrome

A

tall, slender, long thin extremities, hyperextensible joints

17
Q

pathophys of Marfan

A

FBN1 fibrillin mutation, disorder of connective tissue

18
Q

CV anomolies of Marfan

A

weakness of thoracic aortic media and proximal dilation, high amount of dissection, and rupture, aortic regurg, CHF

19
Q

describe myocardial oxygen demand

A

highest of any tissue at rest, high metabolism and needs lots of O2, high capillary density but all are perfused so no capillary reserve

20
Q

when are coronary arteries perfused

A

diastole, as myocardium relaxes blood can flow down to/thru myocytes

21
Q

cardio and vascular response to exercise

A

Heart: SNS B1 activation causes increased HR and contractility

Vasculature: B2 activation vasodilates in skeletal muscle, a1 constricts on splanchnic arterioles (dont need abdominal organs)

Local: metabolites cause vasodilation at skeletal muscle arterioles