Cardiac output Flashcards
cardiac output
volume of blood each ventricle pumps as a function of time, expressed in litres per minute
in steady state, cardiac output flowing through systemic and pulmonary circulation is the same
cardiac output equation
CO = HR x SV
bpm
volume ejected per ventricle per beat, L/beat
typical cardiac output
CO = 72 bpm x 0.07 L/beat = 5.0 L/min
effect of blood loss on stroke volume and heart rate
stoke volume decreases, heart rate increases
inherent heart rate
100 bpm without nervous or hormonal influences on the SA node
inherent autonomic discharge rate
HR usually higher or lower than this, as SA node is affected by nerves and hormones
effects of nerves on SA node
parasympathetic and sympathetic postganglionic neurons end on the SA node.
activity in parasympathetic neurons (travel within vagus nerve) decreases heart rate
activity in sympathetic neurons increases heart rate
resting heart rate
much more parasympathetic activity to the heart than sympathetic - 70 bpm
sympathetic stimulation
increases slope of pacemaker potential by increasing F-type channel permeability - main current is Na+, so faster depolarisation. causes SA node cells to reach threshold more quickly and the heart rate to increase
parasympathetic stimulation
decreases slope of pacemaker potential due to reduction of inward current
threshold reached more slowly, heart rate decreases
hyperpolarises plasma membranes of SA node cells by increasing permeability to K+. pacemaker potential starts from more negative value (closer to K+)
hormones affecting heart rate
norepinephrine and epinephrine
epinephrine
main hormone secreted by adrenal medulla
increases heart rate
acts on same beta adrenergic receptors in the SA node as the norepinephrine released from neurons
what else is the heart rate sensitive to?
changes in temperature, plasma electrolyte concentrations, other hormones, and adenosine (metabolite produced by cardiac cells)
3 factors affecting changes in force during ejection of stroke volume
changes in EDV (preload)
changes in magnitude of sympathetic nervous system input to the ventricles
changes in afterload (arterial pressure against which ventricles pump)
effect of EDV on stroke volume
increased EDV increases stroke volume
illustrated as a ventricular function curve
Frank-Starling mechanism
length-tension relationship
EDV is a major determinant of how stretched the ventricular sarcomeres are just before contraction - greater EDV, greater stretch and more forceful contraction
difference between length-tension relationship between skeletal and cardiac muscle
normal point for cardiac muscle at rest is not its optimal length for contraction - greater filling causes additional stretching and increases the force of contraction
mechanisms linking changes in muscle length to changes in muscle force
change the overlap of thick and thin filaments
stretching cells toward their optimum length decreases spacing between thick and thin filaments and increases sensitivity of troponin for binding Ca2+ and release from SR
venous return
flow of blood from the veins into the heart
role of Frank-Starling mechanism in maintaining equality of left and right cardiac outputs
increased venous return increases cardiac output by increasing edv and stroke volume
ensures blood doesn’t accumulate in pulmonary circulation