cardiac system 4 Flashcards
cardiac output
the volume of blood ejected by each ventricle each minute
CO through the pulmonary and systemic circulations
is equal
what is CO determined by
heart rate times stroke volume
how is heart rate varied
by altering balance of parasympathetic and sympathetic influence on SA node
parasympathetic stimulation and heart rate
slows it
vagus nerve
sympathetic stimulation and heart rate
speeds it up
cardiac nerve
where are cardio inhibitory and acceletory centres located
in the medulla oblongata
what do cardio inhibitory and acceleratory centres recieve
sensory (chemosensory and baroceptors) and higher (cortex and hypothalamys) input
what does the parasympathetic nerve (vagus) release
acetylcholine that increases permeability of the SA node to potassium
slows closure of K+ channels
decreases AV nodes excitability, lengthens AV ndoal delay
weakens atrial contraction
little to no efffect on ventricular contraction
what does the sympathetic stimualtion of the heart release
norepinephrine has an effect on SA node stimulation
nore decreases time for SA to reach threthold
more frequent AP
speeds spread of AP throughout the cardiac conduction pathways
contractile cells beat more forcefully due to higher ca permeability and enhanced excitation-contraction coupling
effect of parasymp stimulation on SA node
decreases the rate of depolarization to threthold, decreases heart rate
effect of sympth stimulation on SA node
inc the rate of depolarization to threthold, inc heart rate
parasymth on AV node
decreases excitability, inc the AV nodal delay
sympathetic on AV node
inc excitability, dec AV nodal delay
parasympth on ventricular conduction pathway
no effect
sympth on ventricular conduction pathway
inc excitability, hastens conduction thorugh bundle of his and purkinje cells
parasympth on artial muscle
dec contractility, weakens contraction
sympth on artial muscle
inc contractility, strenthens contraction
para on ventricular muscle
no effect
para on adrenal medulla
no effect
para on veins
no effect
symp on ventricular muscle
inc contractility, strengthens contraction
symp on adrenal medulla
proote adrenomedullary secretion of epinephrine, augments sympth actions NS actinos of the heart
symp on veins
increases venous return, inc the strength of cardiac contraction through the frank starling mech
stroke volume
volume of blood ejected by a cardiac ventricle per beat
what influences stroke volume
two types of cotnrols
-intrinsic control of stroke volume determined by ectent of venous return (preload)
-extrinsic control of stoke volume determined by sympathetic activity
what do the two types of control of stroke volume do
increase stroke volume by increasing strength of heart contraction (contractility)
preload
initial stretching of the cardionmycytes prior to contraction and is related to the sarcomere length at the end of diastole (and therefore EDV)
what is the level of filling
essentially the workload imposed on the heart before contraction
contractility
contractility of the heart and realtive effectiveness or strength of the ventricular pump
afterload
the pressure or load that each ventricle has to work against when pumping blood
what are the determinants of stroke volume
preload
contractility
afterload
inc in ventricular preload effect on outflow resistance and afterload
increaes
inc in ventricular preload effect on atrail inotropy
increase
inc in ventricular preload effect on ventricular compliance
increase
inc in ventricular preload effect on venous pressure
increase
inc in ventricular preload effect on inflow resistance
decrease
inc in ventricular preload effect on ventricular inropy
decrease
inc in ventricular preload effect on heart rate
decrease
inc in venous complaince effect on venous pressure
increase
inc in venous blood volume (total blood volmue and venous return) on nevous pressure
increase
sympathetic stimulation of the heart and the frank starling cruve
shifts the curve to the left
