How the Cardiovascular System Fails Flashcards

1
Q

Vessel Wall Compliance = stretchiness

A
  • compliance = change in volume caused by a change in pressure
  • gradient of black lines between corners on delta V against aortic pressure x
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2
Q

Vessel wall compliance —— with age leading to

A
  • decreases
  • pathologies
  • eg: atherosclerosis/calcification
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3
Q

Atherosclerosis

A
  • hardening of the arteries
  • leading cause of heart attacks, strokes and
    peripheral arterial disease
  • refers to the build-up of fats, cholesterol and other substances in and on the artery walls (plaque)
  • which can restrict blood flow
  • plaque can burst, triggering a clot
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4
Q

Laminar flow diagram

A
  • laminar flow
  • slower at edges
  • insert
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5
Q

Is laminar or turbulent flow more likely in not smooth wall arteries? Why?

A
  • turbulent
  • higher velocity
  • low fluid viscosity
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6
Q

What causes turbulent blood flow?

A
  • Junctions (eg: vessel branching)
  • Obstacles (eg: foreign bodies)
  • Mixing (eg: “holes in the heart”)
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7
Q

Structure of the arterial wall diagram

A
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8
Q

Atherosclerosis progression

A
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9
Q

Atherosclerosis: Intimal Plaque:

A
  • fatty streak leads to fibrous plaque leads to calcified plaque leading to plaque rupture
  • can jump from fibrous plaque to plaque rupture
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10
Q

Atherosclerosis: Medial Thinning:

  • effect on compliance
A
  • higher compliance results in adventitial erosion
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11
Q

Two examples of vasodilator substances released by the endothelium

A
  • nitric oxide
  • prostacyclin
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12
Q

Thrombogenic

A
  • liable to provoke blood clotting
  • either via the activation of platelets or the
    activation of the blood clotting cascade or
    activation of both
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13
Q

Endothelial Function and Injury

A
  • local control of vessel tone:
    • local control of perfusion
    • vasodilatation: NO, prostacyclin
  • local control of thrombogenicity:
    • conceals collagen and plaque
      constituents
    • secretes antithrombotic factors (eg:
      prostacyclin)
  • capillary filtration
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14
Q

Plaque

A
  • regions of build-up of fats, cholesterol and
    other substances in and on the artery walls,
    which can restrict blood flow. The plaque
    has a lipid rich core covered by a cap of
    fibrous tissue.
  • the cap of the plaque can rupture revealing
    collagen and lipid
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15
Q

Thrombus

A
  • blood clot
  • this forms here when blood is exposed to
    collagen and lipids, which activate platelets
    and the blood clotting pathways
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16
Q

Myocardial Infarction - coronary thrombosis

A
  • plaque rupture
  • thin cap = vulnerable plaque
  • collagen/lipid exposed increase
    thrombogenicity
  • platelet adhesion
  • clotting system activated
  • occlusion
17
Q

ischaemic cascade

A
18
Q

Starling’s Law

A
19
Q

Heart Failure: Pathophysiology:

A
20
Q

Forces on H2O in capillaries

A
21
Q

Vascular Remodelling

A
  • chronic response to injury
  • change in shape, size and function
  • Pressure overload: narrow valve, hypertension
  • Volume overload: leaky valve
  • myocardial damage eg MI, alcohol, viruses
  • result is hypertrophy and or dilation
  • is initially compensatory and becomes pathological
22
Q

Renin - Angiotensin - Aldosterone System

A
23
Q

Sympathetic Activation:

A
  • low cardiac output activates the sympathetic system
  • increases circulating catecholamines
  • increases contractility: increases cardiac output but
  • increases afterload
  • initially compensatory and becomes pathological
24
Q

Catecholamine Cardiotoxicity

A
  • structural/functional cardio-myocyte
    changes
  • LV dilation and adverse remodelling
  • increased LV systolic dysfunction