Phys 1511 Lecture 31 Systemic Circulation

Front 1

Why is venous blood unstressed volume?

Back 1

Its at low pressure

Front 2

Why is arterial blood stressed volume?

Back 2

it is at high pressure

Front 3

How do we affect the unstressed volume of venous system?

Back 3

Adjust venomotor tone which will decrease capcitance and unstressed volume

Front 4

Why does a pressure volume curve of IVC show a quick increase in volume then a rapid slowing of volume change?

Back 4

Because veins are more collapsable than they are compliant(due to elastic walls) so when volume is full they rapidly lose compliance

Front 5

How does the respiratory pump mechanism work?

Back 5

Central venous pressure decreases due to inspiration\decreased intrathoracic pressure as peripheral venous pressure increases due to peripheral runoff. Causes favorable gradient for venous return

Front 6

What is the ultimate effect of respiratory pump on cardiac performance?

Back 6

Increases EDV\preload and increased SV

Front 7

HOw do we relate CO and venous return?

Back 7

CO is balanced with venous return

Front 8

Why are cardiac and vasculature functions expressed as a function of RAP?

Back 8

Becuase right atrial pressure affects the RV preload and hence the LV preload and ultimate CO

Atrial pressure also affects pressure gradient of venous return

Front 9

How does increased Right atrial pressure affect CO?

Back 9

Increases it because the pressure difference between RA and RV is more so more preload and increased CO

Front 10

How does increased Right atrial pressure affect venous return?

Back 10

Decreases it because it decreases the pressure gradient betwn RA and Peripheral venous system

Front 11

What does the mean systemic pressure represent?

Back 11

The pressure of the Total blood volume if the heart is stopped. It is measured at the point that the venous return is zero( hits x axis) becuase it equals right atrial pressure

Front 12

What does the mean systemic pressure depend on?

Back 12

Total blood volume and vessel capacitance. Affected by capacitance because if vessels are more elastic and want to hold less it will increase the pressure

Front 13

How does the heart restore RAP to equlibrium after an increased volume of venous return?

Back 13

Blood is pumped out of the venous side(RV) to atrial side causing higher SV in LV. Blood being removed from venous side in frank starling fashion returns EDV and hence RAP to normal. Increase EDV increases SV and hence decreases RAP

Front 14

How does increasing inotropicity\contractility affect vasculature function curve?

Back 14

It doesn't, but increasing SV will decrease RAP because less blood left after each contractionH. So CO goes up but at a lower RAP. increasing CO is making it easier to recieve more blood essentially

Front 15

How does decreased contractility\inotropicity affect RAP?

Back 15

Increases it because more blood left in RA and therefor decreases CO

Front 16

In a cardiac\vasculature function curve which one is changed if u affect total blood volume?

Back 16

vascular function curve shifts right

Front 17

How does increasing total blood volume or venomotor tone affect mean systemic pressure?

Back 17

increases it

Front 18

Why do Cardiac output and vasculature function curves shift downward if TPR is increased?

Back 18

Decreased CO because afterload is increased due to slower runoff.
Decreased venous return because less blood returning

Front 19

What are the definitions of chronotropicity, dromotropicity, and inotropicity?

Back 19

Chrono- hear rate\SA node rhythm
Dromo- velocity of conduction through AV node
Inotropicity-contractility

Front 20

Where are B-1 found in the heart?
a-1? B2

Back 20

in the nodal tissues, in vasculature, in coronary tissues

Front 21

What are the primary cholinergic, muscarinic receptors in the heart?

Back 21

M2

Front 22

Are B1 receptors sympathetic of parasympathetic?

Back 22

sympathetic

Front 23

What is the vasculature affect of B2 and a1?

Back 23

B2=Vasodialation
a1=vasoconstriction

Front 24

What is an M2 anatagonist?

Back 24

Atropine

Front 25

What does M2 stimulation cause with regard to cardiac performance?

Back 25

decreased contractility(decreased Ca in phase 1), decreased heart rate(Increase K+ conductance\hyperpolarization in phase 4)

Front 26

What myocardium metabolite level represents interplay in the amount of SNS vs PNS stimulation of the hearts major ANS receptor types?

Back 26

cAMP becuase B1 and M2 receptors increase of decrease amount of adenylate cyclase activity

Front 27

How does acetylcholine affect the amount of NE released and vice versa?

Back 27

postganglionic parasympathetic release Ach which inhibits NE release and vice versa

Front 28

Does sympathetic stimulation of the heart result in more or less cAMP?

Back 28

depends, a1 decreases it and B2 increases it. increased cAMP causes vasodilation

Front 29

What effect does SNS activation have on phase 4 of the pacemaker potentials of the SA node?

Back 29

Increases Na conductance(influx) and causes faster deplolarization of the node, increases HR

Front 30

What effect does PNS stimulation have on phase 4 of the pacemaker potentials of the SA node?

Back 30

Increases K conductance(efflux) which slows funny current depolarization via K-Ach channel

Front 31

What channels are affected by the PNS stimulation of the heart? Function?

Back 31

K+\Ach channel a G-protein coupled channel. Allows K efflux to slow the If current from reaching threshhold, also hyperpolarizes maximum diastolic potential
(sympathetic increases Na conductance to counteract)

Ca channels- decreases conductance, slows upstroke

Front 32

How does ANS stimulation affect dromotropicity?

Back 32

Mostly by affecting Ca influx of the upstroke phase by making it faster(SNS) or slower(PNS)

Front 33

What are the 2 sympathetic affects on inotropicity?

Back 33

Increases Ca conductance which increases Ca-induced-Ca release and Increased Ca uptake via phosphorylation of PLB

Front 34

What are the postganglionic neurotransmitters of each ANS branch in the heart?

Back 34

PNS=ACH
SNS=NE

Front 35

What is enhanced due to positive inotropic effects?

Back 35

Contractile velocity and increased force

Front 36

Are the SNS and PNS tonically active

Back 36

yes

Front 37

How do atropine and propranolol function?

Back 37

Atropine is a M2 antagonist so it inhibits parasympathetic

Propranolol is a B1 antagonist so it inhibts sympathetic