Biomedical Engineering 403

Cardiac Pacemakers and an Introduction to the Autonomic Control of the Heart

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Reading for Today:

Chapters 1 and 3 in Berne & Levy .

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Howdy Folks!

This is what happened in class today (10-8-97).

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.



2
Cardiac Pacemakers,
Introduction to Autonomic Control

Sinoatrial Node and Atrioventricular Node--cells do not contract, but
serve only to generate electrical activity.  Functions as the pacemaker,
determining rate.

At rest,  pacemaker cells look pretty much like other cells.

Pacemaker Potential  (Depolarization procedes at a slow steady pace until
threshold is attained and AP is triggered)

The action potential is much slower than that of other cells, because
nodal cells lack fast sodium channels so AP is generated solely by iCa,
the slow inward current of Calcium ions.

The slow speed of this action potential allows cardiac cells to contract
and at least partially relax, before they contract again, thereby making
it impossible for the heart muscle to go into sustained contraction, in
which it could not pump.

Ionic Currents contributing to diastolic depolarization of pacemaker cells
        1.      if   --an inward Na+ current caused by hyperpolarization
(the more negative the membrane                potential, the greater the
activation of if)--flow of Na+ ions into cell responsible for spontaneous
potential decay.  The slope of this decay determines HR.
        2.      iCa --an inward Ca++ current (becomes active when membrane
potential depolarizes to approx              threshold potential; T-type
Ca++ channels activate at this transmembrane potential; the Ca++ influx
accelerates depolarization, which then leads to AP.  Thus decreasing
external Ca++ concentration                or blocking Ca++ channels can
diminish amplitude of AP and slow pacemaker rate.
        3.      iK --an outward K+ current is responsible for repolarizing
the cell after the AP.  It continues at a            slower rate through
early phase of depolarization for next cycle. 

The fastest pacemaker cell becomes the pacemaker for the heart,
determining heart rate.  Because the cells in the Sinus node reach
threshold before the cells of the AV Node, a Sinus Node cell is always the
pacemaker in healthy people.  AV Node can take over if Sinus Node is
damaged.

Overdrive suppression--caused by overworking Sodium/Potassium Pump
Sinus Node Recovery Time
Sick Sinus Syndrome > syncope

Intrinsic HR > 100 bpm

(Pacemaker rate temperature-sensitive)

Discharge frequency of pacemaker cells may be modified by a change in:
        1.      the rate of depolarization
        2.      the threshold potential
        3.      the resting potential


Autonomic Control of Pacemaker Cells

Increased symp activity to SA node speeds up heart--tachycardia
Increased parasymp activity to SA node slows down heart--bradycardia
Obviously PS dominates at rest

Vagus Nerve Efferents from Dorsal Motor Nucleus and Nucleus Ambiguus
        Post-gangliotic Cells are on the heart itself (most near SA node
and AV conduction tissue)
Sympathetic Pathways
        Emerge from C6 to T5 of spinal cord
        Synapse in the Stellate Ganglia, then join with parasympathetic
pathways to heart

Sympathetic:
Adrenergic neurotransmitters increase all three currents, but augment if
and iCa more than iK, thus increasing  the slope of the diastolic
depolarization. In addition to those contributed by sympathetic nerves to
the heart,         circulating catecholamines have similar effects.
Effects are slower than parasympathetic (cannot exert         beat-to-beat
control, like vagus).  Sympathetic effects decay slowly as most NE is
reuptaken into terminals     (remainder carried into bloodstream)

Parasympathetic:
Acetylcholine hyperpolarizes the cells by opening choline-sensitive K+
channels, and also depresses if and iCa  currents.  It also slows the
slope because of its effect on if.  ACh effects very rapid effect, and
lots of     cholinesterase in SA (and AV) node means effects are very
short-lasting.  

Sympathetic and Parasympathetic systems --Push/Pull (reciprocal)
relationship
        Changes in HR usually due to changes in both symp and parasymp
activation:
        In exercise--increased symp and reduced PS



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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

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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!

BME 403 Pages maintained by the T.A., Douglas Miles.