How the Cardiovascular System Fails Flashcards
Vessel Wall Compliance = stretchiness
- compliance = change in volume caused by a change in pressure
- gradient of black lines between corners on delta V against aortic pressure x
Vessel wall compliance —— with age leading to
- decreases
- pathologies
- eg: atherosclerosis/calcification
Atherosclerosis
- 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
Laminar flow diagram
- laminar flow
- slower at edges
- insert
Is laminar or turbulent flow more likely in not smooth wall arteries? Why?
- turbulent
- higher velocity
- low fluid viscosity
What causes turbulent blood flow?
- Junctions (eg: vessel branching)
- Obstacles (eg: foreign bodies)
- Mixing (eg: “holes in the heart”)
Structure of the arterial wall diagram
Atherosclerosis progression
Atherosclerosis: Intimal Plaque:
- fatty streak leads to fibrous plaque leads to calcified plaque leading to plaque rupture
- can jump from fibrous plaque to plaque rupture
Atherosclerosis: Medial Thinning:
- effect on compliance
- higher compliance results in adventitial erosion
Two examples of vasodilator substances released by the endothelium
- nitric oxide
- prostacyclin
Thrombogenic
- liable to provoke blood clotting
- either via the activation of platelets or the
activation of the blood clotting cascade or
activation of both
Endothelial Function and Injury
- 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)
- conceals collagen and plaque
- capillary filtration
Plaque
- 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
Thrombus
- blood clot
- this forms here when blood is exposed to
collagen and lipids, which activate platelets
and the blood clotting pathways
Myocardial Infarction - coronary thrombosis
- plaque rupture
- thin cap = vulnerable plaque
- collagen/lipid exposed increase
thrombogenicity - platelet adhesion
- clotting system activated
- occlusion
ischaemic cascade
Starling’s Law
Heart Failure: Pathophysiology:
Forces on H2O in capillaries
Vascular Remodelling
- 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
Renin - Angiotensin - Aldosterone System
Sympathetic Activation:
- low cardiac output activates the sympathetic system
- increases circulating catecholamines
- increases contractility: increases cardiac output but
- increases afterload
- initially compensatory and becomes pathological
Catecholamine Cardiotoxicity
- structural/functional cardio-myocyte
changes - LV dilation and adverse remodelling
- increased LV systolic dysfunction