lecture 20- mechanical events of the cardiac cycle Flashcards
systole
contraction
diastole
relaxation
during diastole, chambers are
filling with blood
most blood enters ventricles during diastole though the
open AV valves (80%)
during atrial systole, blood is pumped from —- into —- and —-
pumped from ventricles into aorta and pulmonary artery
(20% of blood)
during ventricular systole, blood is pumped from — into — and —
pumped from ventricles into aorta and pulmonary artery
5 stages of the mechanical events of 1 cardiac cycle
- late diastole
- atrial systole
- isovolumic ventricular contraction
- ventricular ejection
- isovolumic ventricular relaxation
late diastole
heart is completely relaxed
-semilunar valves closed
- AV valves open
atrial systole
small amount of blood enters ventricles (15-20%)
-AV valves open bc atria are contracting
isovolumic ventricular contraction
ventricular contraction pushes AV valves closed but not enough force to open semilunar valves
ventricular ejection
-semilunar valves open and blood is ejected
-AV valves close
isovolumic ventricular relaxation
AV valves open/relaxed
–> chambers fill passively
If atrial systole has occurred it would be…
the max volume ventricles can contain
= End diastolic volume
= Max
Ventricular ejection has occured…
residual blood left in the heart after ventricle has contracted
= End systolic volume
= Min
The wiggers diagram displays
pressure in the left ventricle in terms of the electrical and mechanical events of the cardiac cycle
Wiggers: as ventricles contract, there is…
a huge increase in pressure in the left ventricle
Wiggers: why does pressure fall off?
because blood has been ejected from the heart
approx how many mL of blood is the left ventricle ejecting at rest?
70mL
PV relationship: A to A’
passive filling
late ventricular diastole
no increase in pressure
PV relationship: A’ to B
atrial systole (15-20% blood)
incr P, incr V
PV relationship: B
=EDV= 135 mL
PV relationship: B to C
no change in volume
big change in pressure
-ventricles contracted bc not enough pressure to open valves
-isovolumic semilunar valves
PV relationship: C to D
ventricular systole
at C, semilunar open
stroke volume= 70mL at rest/normal
PV relationship: D
ESV= 65mL
= minimum blood left after ventricular systole
PV relationship: D to A
isovolumic ventricular relaxation
- at A, passive filling occurs again
- no change in volume but big change in pressure
PV relationship: A, B, C, D in terms of valves opening and closing
A= mitral valve opens
B= mitral valve closes
C= aortic valve opens
D= aortic valve closes
Stroke volume (SV)
= amount of blood pumped by one ventricle during a contraction
avg resting SV= 70mL/beat (135mL-65mL)
SV= ….-….
end diastolic volume - end systolic volume
Cardiac output (CO)
= volume of blood pumped by one ventricle in a given period of time
avg resting CO= 5L/min
CO= ….x….
HR (beats/min) x SV (mL/beat)
how much blood do we have in our bodies?
5L
your heart pumps all of the blood in your body every single minute
autonomic innervation of the heart: stimulating SA node
-if we add sympathetic input to SA nose= speed up
-if we add parasympathetic input to SA node= slow down
ventricular myocardium ONLY gets — input
sympathetic
chonotropic effect
= autonomic effect on the SA node
-modulation of HR (chronotropic effect)
-parasympathetic or sympathetic
Inotropic effect
= autonomic effect on ventricular myocytes
- modulation of contractility (inotropic effect)
- only sympathetic
in HR increases, contractility…
increases
- contractility increases so SV increases
and therefore CO increases
chronotropic effect: parasympathetic neuron
parasympathetic neuron (ACh on M2 receptor)
-decreases HR
chronotropic effect: sympathetic neuron
sympathetic neuron (NE on beta 1 receptor)
-increases HR
more than 1 heart beat per sec=
+ chronotropic effect
fast?
less than 1 heart beat per second=
Negative chronotropic effect
slow
how is SV modulated?
SV is proportional to contraction force
contraction force is determined by:
1. sarcomere length (approx EDV)
2. contractility of muscle
ideal length for max tension is a skeletal muscle sarcomere=
2 microns
Frank-Starling Curve
the length-tension relationship of the heart
-SV on y axis, EDV on x axis
–> an increase in EDV (EDV prop to length of sarcomere)
–> causes SV to increase
Frank-Starling Law
the heart pumps all the blood returned to the heart (5L)
–> if we stuff in more blood, there will be a more forceful contraction
2 factors that increase EDV
- increased venous return
- decreased HR (more filling time)
as EDV increases, SV…
increases
(increases SV because we increase contractility)
effect of SNS on ventricular contractility
norepinephrine is spit out onto beta 1 receptors
SNS activity of ventricular myocytes, increase in contractility, increased SV
what happens to the Frank Sterling curve with sympathetic input?
it gets “bumped up”
what happens to the Frank Sterling curve with parasympathetic input?
it gets “bumped down”
2 effects of (increased – activity) SNS on myocyte contractility
- increased activity of LTCC (L type calcium channels)
- increased activity of SERCA (Sarcoendoplasmic Reticulum Calcium ATPase)
how does increased activity of the LTCC affect myocyte contractility?
epinephrine/norepinephrine bind to beta 1 receptors, activate cAMP, phosphorylation of voltage gated calcium channels…
opening time increases
increased Ca2+ entry from the ECF
then…
–> Ca2+ is stored in SR and/or eventually released= MORE FORCEFUL CONTRACTION
How does increased SERCA activity affect myocyte contractility?
phospholamban usually inhibits SERCA
epinephrine/norepinephrine binds to beta 1 receptors, activate cAMP, phosphorylation of phospholamban
when phospholamban is phosphorylated it does and does its own thing
SERCA is not inhibited anymore;
increased Ca2+ATPase on SR
then…
–> Ca2+ is stored and/or eventually released= more forceful contraction
–> Ca2+ removed from cytosol faster= shortens Ca-troponin binding time= shorter duration of contraction
adding sympathetic stimulation (such as the SNS example of epinephrine and norepinephrine) would be an example of an —- effect
inotropic effect
