CV overeview Flashcards

1
Q

small arteries and arterioles

A
  • relatively large proportion of vascular smooth muscle
  • highly innervated
  • major site of resistance
  • regulate arterial blood pressure
  • regulate flow to capillaries/tissue
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2
Q

capillaries

A
  • endothelial tubes
  • no smooth muscle
  • regulate permeability
  • exchange fluid, nutrients, electrolytes, hormones, CO2, waste
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3
Q

venules

A
  • no smooth muscle
  • no innervation
  • function to collect blood from capillaries
  • participate in blood-tissue exchange
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4
Q

veins

A
  • limited smooth muscle
  • sometimes innervated
  • low resistance to flow
  • high capacitance
  • conduct blood, reservoir, regulate blood volume distribution
  • constriction increases return and CO while decreasing the volume in circulation
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5
Q

pulse pressure

A
  • systolic-diastolic
  • decreases in smaller vessels due in part due to hydraulic filtering
  • can increase with decreased compliance and increasing stroke volume
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6
Q

arterial compliance

A

-change in volume over change in pressure

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7
Q

Blood pressure equation

A
  • change in pressure (input minus output)
  • delta P=R (resistance to flow) xQ (flow)
  • MABP=TPR x CO
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8
Q

vascular resistance

A
  • changes can be due to smooth muscle contraction or changes in hematocrit
  • changes are due to vessel diameter changes or viscosity changes
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9
Q

influence of vessel internal radius on resistance

A
  • inversely proportional to r^4
  • small changes in radius, have large impact on resistance
  • regulated mostly by VSM
  • thickening of the walls because of remodeling, atherosclerosis and inflammation can increase resistance
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10
Q

influence of blood viscosity on vascular resistance

A

-polycythemia (increased hematocrit) would have an increase in vascular resistance

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11
Q

laminar versus turbulent flow

A
  • normal resting conditions provide laminar flow
  • turbulent flow is most often seen in aorta and arterial branch points
  • in laminar, highest velocity is in the middle, lowest is on the sides of the tube
  • eddy currents can occur at branch points
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12
Q

Reynold’s number and turbulence

A
  • flow become turbulent at higher reynolds numbers
  • takes into account fluid density, vessel diameter, mean flow velocity, fluid velocity
  • turbulent flow predicted when vessel is large, blood velocity is high, and blood viscosity is low
  • can be seen in exercise, cardiac valve stenosis, occlusion
  • causes heart murmurs and vascular bruits
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13
Q

regulation of vascular resistance

A
  • sympathetic nervous system
  • hormones
  • VSM tone
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14
Q

neural control of vascular resistance

A
  • SNS
  • NE released from varicosities
  • binds to adrenergic receptors to elicit VSM contraction
  • withdrawal of sympathetic tone leads to relaxation
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15
Q

hormonal control of vascular resistance

A
  • catecholamines, angiotensins, arginine vasopression
  • can be a stress response, can be present in disease states
  • can bind to endothelial cell membrane or directly to VSM membranes
  • can cause release of vasoactive factors from the endothelium
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16
Q

enothelial control of vascular resistance

A
  • vasoactive factors that provide regulation mechanisms
  • both dilatory and constrictive factors
  • gap junctions between VSM and endothelial cells for electric and chemical messages to pass
17
Q

autoregulation on vascular resistance

A
  • change to keep constant blood flow when there are changes in arterial pressure
  • dilation when pressure decreases, constriction when pressure increases
  • explained by myogenic response
18
Q

myogenic mechanism

A
  • arterial constriction in response to distending force exerted by increasing transmural pressure
  • fall in transmural pressure elicits dilation
  • helps maintain basal vascular tone
19
Q

metabolic regulation of vascular resistance

A
  • increases blood flow to delivery oxygen to hypoxic tissue

- can result from increased metabolic activity or decreased oxygen availability

20
Q

flow (CO)

A
  • product of stroke volume and heart rate
  • both are regulated by sympathetic and parasympathetic
  • SV can be altered by changes in myocardial performance through an intrinsic mechanism (Starling)