Cardiovascular Physiology Lecture 5

Front 1

what is the mechanism of adrenergic influence upon cardiac cellular functions?

Back 1

epinephrine from adrenal medualla or norepinephrine from sympathetic neurons binds B1 receptors on myocardial contractile cell that activates cAMP second messenger system that phophorylates 2 paths for 3 mechanisms for 2 results: more forceful contraction (iontropic) and shorter duration of contraction (chronotropic)

Front 2

the adrenergic affect of phosphorylating voltage gated CA++ channels results in what?

Back 2

open time increases, increasing Ca++ entry from the extracellular fluid that causes increases in Ca++ stores in SR and increases Ca++ released through Ca++ induced Ca++ release, causing more forceful contractions

Front 3

the adrenergic affect of phosphorylating phospholamban results in what?

Back 3

increasing Ca++-ATPase activity of SR, resulting in increasing stores in SR and increasing Ca++ released through Ca++-induced Ca++ release causing more forceful contraction AND Ca++ removed from cytosol faster and time of Ca-troponin binding shorter creating shorter duration of contraction

Front 4

what is the mechanism of cholinergic influence upon cardiac cellular functions?

Back 4

acetylcholine affect G-protein with inhibits cAMP second messenger system (preventing phosphorylation)

Front 5

how does the central cardioinhibitory center sends inhibitory impulese to the SA and AV nodes via what?

Back 5

the vagus nerve

Front 6

what does the central cardioinhibitory center send via the vagus nerve?

Back 6

inhibitory impulses to the SA and AV nodes

Front 7

the vagus nerve sends inhibitory impulses to the SA and AV nodes from what?

Back 7

the central cardioinhibitory center

Front 8

what type of impulses does the central cardioinhibitory center send ote the SA and AV nodes via the vagus nerve?

Back 8

inhibitory impulses

Front 9

what is the only nervous system input that influences cardiac function?

Back 9

autonomic nervous system

Front 10

what do autonomic neurotransmitters do to the intrinsic myocardial electrical events?

Back 10

modulate but do not initiate

Front 11

what is the adrenergic affect on the AV nodal function on slow conduction velocity (AV delay)?

Back 11

shortens delay

Front 12

what is the cholinergic affect on the AV nodal function on slow conduction velocity (AV delay)?

Back 12

lengthens delay

Front 13

what is the adrenergic affect on the AV nodal function on long refractory period?

Back 13

shortens - ventricles keep pace at increased sinus HR

Front 14

what is the cholinergic affect on the AV nodal function on long refractory period?

Back 14

lengthens

Front 15

what is the adrenergic affect on the AV nodal function on spontaneous depolarization to threshold as an auxiliary pacemaker (slower than SA)?

Back 15

faster depolarization

Front 16

what is the cholinergic affect on the AV nodal function on spontaneous depolarization to threshold as an auxiliary pacemaker (slower than SA)?

Back 16

slower depolarization

Front 17

where are sympathetic, adrenergic neurons distributed in the heart?

Back 17

all cardiac cells

Front 18

all cardiac cells receive what type of ennervation?

Back 18

sympathetic, adrenergic neurons

Front 19

what does activation of B1-adrenergic receptors lead to?

Back 19

action potentials that are of greater magnitue and velocity (faster, shorter duration) and stronger, quicker contractions

Front 20

what does stimulation of B1-adrenergic receptors cause?

Back 20

increased number of Ca++ channels open, increasing amount of extracellular Ca++ entering the cardiac myocites

Front 21

Ca++ is the primary triggering influence for what during the plateau phase?

Back 21

cardiac muscle depolarization

Front 22

what does increased intracellular Ca++ do to membrane potential?

Back 22

makes it more positive

Front 23

More positive membrane potential does what to the action potential?

Back 23

shortens the duration because the more positive the membrane potential is in the plateau phase, the sooner the slow K+ channels open and lead to repolarization

Front 24

B1-adrenergic receptor stimulation leads to AP's that are what?

Back 24

greater amplitude and shorter duration that propagate more quickly from cell-to cell and causes muscle to contract more vigorously (positive inotropic affect)

Front 25

what is positive inotropic affect?

Back 25

more vigorous muscle contractions

Front 26

A shorter AP refractory period facilitates what?

Back 26

a higher HR

Front 27

parasympathetic, cholinergic influences are generally opposite of what affect?

Back 27

sympathetic adrenergic

Front 28

parasympathetic, cholinergic influences are limited to where?

Back 28

the SA node, AV node, and atrial myocardium

Front 29

cardiac arrhythmias arise as the result of what?

Back 29

abnormalities of impulse generation or abnormalities of impulse conduction

Front 30

organic disease of the intrinsic conduction system can be the underlying cause of what?

Back 30

arrhyhmia

Front 31

extrinsic influence upon the activity of the intrinsic conduction system or the contractile myocardium can lead to what?

Back 31

arrythmia

Front 32

any disruption of normal sinus rhythm (NSR) renders the heart what?

Back 32

as a less efficient pump

Front 33

what does NSR stand for?

Back 33

normal sinu rhythm

Front 34

what is the major clinical relevance of any arrhythmia?

Back 34

the negative impace upon cardiac output, a hemodynamic consideration

Front 35

what are the relevant generic concepts that apply to any given disturbance of normal cardiac rate and rhythm from a clinical perspective?

Back 35

location, frequency, and timing