Biomedical Engineering 403

Vascular Diseases & Section Review

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Reading for Today:

Chapter 12 in Berne & Levy .

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Howdy Folks!

For those of you who are curious to review the copious list of topics that were explicated by the intrepid students who indulged in the extra credit project, click here!

This is what happened in class today (12-5-97).

As usual, all of this is in outline format with hypertext, so if you want to review the specifics, or if you have any questions on a specific topic, click the hypertext for that topic.

Today's topic:

MYSTERY TOPIC

Consequently, we'll discuss:

Many of these topics are incomplete.
They should be completed when the extra credit projects are turned in.

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Dr. Schechtman's Notes!

These are Dr. Schechtman's very own notes for this lecture.

I hope you find them helpful.



15
Vascular Disease

Hypertension--factor in stroke, CHF, MI, peripheral vascular disease,
renal failure
Essential Hypertension--no apparent cause, more common, runs in families,
more common in men and in blacks
Secondary Hypertension--only ~5%.  Usually if you correct the underlying
medical condition, it fixes itself.

problems--	causes heart to work harder,
		damages inner layer of blood vessels, 
		a factor in atherosclerotic buildup

By definition > 90 diastolic or 150 systolic

Lack of patient compliance with diet and drug schedules is problem because
patients feel fine.  So physician has to “sell” the patient on the
importance of treating high BP.

Treatment of Hypertension

Intensive sodium restriction can get good results, but poor patient
compliance because must be very restrictive, which is expensive (buy
special bread, etc.), time-consuming, and unpleasant.

Always look for a primary cause of secondary hypertension before
implementing therapy.

Step 1.	A diuretic lowers BP by reducing plasma volume.  Well-tolerated
and sufficient treatment for some 	hypertensives.

Step 2.	Beta-blocker (contraindicated in CHF)  reduces cardiac output and
vascular resistance.

Step 3.	Arteriolar vasodilator

If none works, reevaluate possibilities for secondary hypertension.

Stroke
	Thrombosis--clotting blocks already narrow artery
	Embolism--a bit of arterial wall, plaque, or small blood clot is
carried in the bloodstream until it becomes 		wedged in a place
where it obstructs blood flow
	Hemorrhage--
		Aneurysm--a dilation of a segment of blood vessel
			Potential Problems--
				can burst and cause loss of blood flow to
an area and/or hemorrhaging
				can press on neighboring organs or nerves
				can cause turbulent flow leading to clot
formation

Effects and prognosis depend on  
	brain location
	size of area damaged by ischemia
	extent of damage exerted by increased cranial pressure
	TPA

Transient Ischemic Attack--temporary obstruction of an artery
	Causes transient loss of vision, paralysis, confusion, etc.
depending on location; may forebode a major stroke
	Anticoagulant therapy used to prevent subsequent events and/or a
major stroke

Hemorrhage and Shock--

Compensatory mechanisms for blood loss are so fast and so effective, that
in all but rare instances, donating half a 	liter of blood has no
noticeable effect.  Provide time for restoration of fluid over a few hours
and the 	somewhat slower regeneration of proteins and blood cells.

Acute Compensatory responses to blood loss
	Increased peripheral resistance includes reduced blood flow to
kidneys and thus reduced urine output
	Symptoms:
		cool skin from cutaneous vasoconstriction
		rapid pulse and sweating are direct effects increased
sympathetic activity
		sunken features result of tissue dehydration secondary to
absorption of extracellular fluid
		intense thirst, dry mouth, and scanty urine reflect
attempt to replenish lost fluid
		increased respiratory activity may occur, when oxygen
supply drops and chemoreceptors kick in


Irreversible Shock--	Caused by metabolic effects and anoxia
			Products of tissue damage are released including
histamine and adenosine, which cause
vasodilation (positive feedback loop)
			The reduction in tissue blood flow that follows an
intense vasoconstriction leads, with 				time, to
tissue hypoxia and local accumulation of metabolic end products
(including histamine and adenosine).  The vasoactive metabolites
eventually reach 				a level where they
override the vasoconstrictor effect of sympathetic stimulation.
This permits capillary beds to fill with blood at the expense of arterial
blood 				volume.  Finally lack of tissue perfusion,
cell damage, and death follow.



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A Copy of Today's Overhead Images:

Figure 1

Figure 1

Figure 2

Figure 2

Figure 3

Figure 3

Figure 4

Figure 4

Figure 5

Figure 5

Figure 6

Figure 6

Figure 7

Figure 7

Figure 8

Figure 8

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Or, Jump to Lesson Number:

respiratory
1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11 | 12 | 13 | 14 | 15 | Exam #1
auditory
17 | 18 | 19 | 20 | 21 | 22 | 23 | 24 | 25 | 26 | Exam #2
cardiovascular
28 | 29 | 30 | 31 | 32 | 33 | 34 | 35 | 36 | 37 | 38 | 39 | 40 | 41 | 42 | Exam #3

No!
Please don't make me go to any of those pages!
I want to go somewhere completely different!

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