lecture 14: cardiac cycle

Question 1

cardiac cycle phases

Answer 1

contraction (systole) —> produces the pressure
relaxation (diastole)

Question 2

mechanical events in cardiac cycle

Answer 2

two pumps that work together (R and L), ventricles contract at the same time; atria contract at the same time
blood moves through the circulatory system from areas of higher to areas of low pressure
always have a driving force, usually a pressure gradient between 2 compartments

Question 3

pressure volume curves

Answer 3

can do it for any chamber, normally done for L ventricle since its pushing blood to tissues
L ventricle never completely empty
limit the PV loop
can talk with phases of contraction too like with skeletal muscle
PICTURE/DIAGRAM IN NOTES

1. ventricles and atria relaxed (DIASTOLE)
   —-blood enters L atrium, coming back from lungs with oxygenated blood
   —–L atrium full of blood and exerting pressure/force on walls of atrium
2. pressure higher in L atria than L ventricle = passive ventricular filling phase
   —-mitral valve opens, still in diastole (no contraction yet), gravity helps move blood into ventricle
   ——70-75% of blood entering ventricle happens during this phase
3. L atrium CONTRACTS = active ventricular filling phase
   —-ejects remaining 25-30% of blood into L ventricle
   —-ventricle in diastole but atrium in systole
   —-slight increase in pressure because blood is entering L ventricle
   —–end of diastole/relaxation phase of ventricle (EDV)
4. isovolumetric contraction phase
   —–no change in volume, pressure increase with contraction of ventricle
   —–atria now in diastole
   —–bottom to top systole/contraction, blood catches back of mitral valve flaps and forces them to close
   —–completely sealed chamber of ventricle
5. pressure in L ventricle higher than in aorta
   —-ventricle contraction and full of blood
   —–aortic semilunar valve opens, L ventricle keeps increasing pressure but volume is decreasing, being ejected into aorta
6. ventricle still contracting but pressure starts decreasing
   —–slowly pressure decreases, less force of fluid against walls of ventricle
7. isovolumic relaxation phase
   —-ventricle enters diastole again with very little blood volume
   —–blood in aorta, pressure higher than in L ventricle which is relaxing
   —–blood will try to back up from high to low pressure but catch flaps of aortic semilunar valve, cause them to close
   —-pressure decrease with relaxation, volume not changing due to sealed chamber

Question 4

EDV

Answer 4

end diastolic volume
max volume each ventricle has in cardiac cycle
step 3 of pressure volume curve
in mL/beat
determined by venous return

Question 5

ESV

Answer 5

end systolic volume
minimum amount of blood ventricle will have in cardiac cycle at the end of contraction phase

Question 6

diastolic BP

Answer 6

same as AFTERLOAD
minimum pressure that the ventricle needs to generate to cause aortic semilunar valve to open and eject blood in aorta and shorten
pressure in L ventricle matches pressure in aorta
ventricle not actively ejecting blood into it yet
reached tension/pressure needed to generate shortening of muscle
if not —-> ventricle cannot shorten, isometric contraction —> death, no blood in tissue

Question 7

systolic BP

Answer 7

maximum pressure in aorta in cardiac cycle
ventricle has maximum contraction generated

Question 8

stroke volume

Answer 8

width of pressure volume loop
amount of blood pumped/ejected by one ventricle during a contraction (mL/beat)
EDV - ESV = SV
can change from beat to beat
related to the force generated by cardiac muscle during contraction

1. volume increase with blood during ventricular diastole
2. EDV reached, both have max volume
3. eject blood into aorta and pulmonary arteries, volume decreases
   —–amt of blood ejected = SV
   —-calculate for each ventricle
4. end of contraction, ventricles have reached ESV

Question 9

first heart sounds (S1)

Answer 9

vibrations following closures during ventricular systole of the AV valves (tricuspid and mitral, happen at the same tiem)
“Lub”

Question 10

ausculation

Answer 10

listening to the heart through the chest wall using a stethoscope

Question 11

second heart sounds (S2)

Answer 11

vibrations generated by closing of the semilunar valves (aortic and pulmonic, aortic closes slightly before)
closing marks beginning of diastole, ventricles relax
“Dup”

Question 12

heart sounds

Answer 12

should not hear anything between S1 and S2
listen for murmurs
can have S3 or S4 but they may be pathological

Question 13

preload

Answer 13

EDV or end diastolic volume
load muscle feels when relaxed
stretch muscle —> cause cardiac muscle in ventricles to
more blood filling, more stretch

Question 14

afterload

Answer 14

minimum pressure in the aorta or diastolic BP
muscle generates tension with contraction of the ventricle until it overcomes the load and starts to shorten
if it cant overcome threshold —-> cant open aortic SL valve, aortic pressure is higher, L ventricle cannot eject blood or shorten
—-isometric contraction

Question 15

phases of the cardiac cycle

Answer 15

isometric —-> isovolumic contraction and relaxation
isotonic

Question 16

isovolumic contraction

Answer 16

isometric, muscle not shortening
pressure change
right before afterload

Question 17

isovolumic relaxation

Answer 17

isometric
pressure decrease but volume has no change
right after ESV

Question 18

cardiac passive tension curve

Answer 18

very steep and to the left of the total tension curve

Question 19

cardiac active tension curve

Answer 19

not much of a plateau like with skeletal muscle

Question 20

passive tension curve with skeletal muscle

Answer 20

generated by stretch
elastic elements
relaxed

Question 21

active tension curve with skeletal muscle

Answer 21

muscle contracts
forms crossbridges
tension

Question 22

total tension curve for skeletal muscle

Answer 22

2.1 micrometers for sarcomere at rest
add passive and active at middle of curve

Question 23

cardiac total tension curve

Answer 23

add passive and active right away
basically linear
1. resting sarcomere length is 1.6 micrometer start for curve compared to 2.1 for skeletal muscle, shorter
—–cardiac muscle is stiffer, more connective tissue
——stretch cardiac muscle a bit, immediately get pretty big passive tension, passive tension is starting left of the curve
2. change in length immediately generates passive tension
—-slope of curve tension
—-passive tension increase more and faster than in skeletal muscle

Question 24

Frank-Starling Law

Answer 24

intrinsic regulation
any change in length is a change in total tension
more stretch of cardiac muscle = more speed and force of contraction that cardiac muscle can generate
inherent property of the heart
sensitivity to Ca increases with cardiac stretch = same amount of Ca but able to bind more of it to generate contraction
muscle fiber length determined by blood volume at the beginning of contraction (EDV)
increase in stretch of ventricular wall = increase in stroke volume
SV increase with EDV/preload increase

Question 25

different preloads (change in stretch)

Answer 25

isotonic contraction
constant total tensions (measure change in length)
increase PRELOAD = increase SHORTENING, stretch of muscle
change weight hung from muscle at rest
faster contraction too
same afterload!
generate passive tension
cause muscle to contract more forcefully/with more tension when forming crossbridges (active tension)

Question 26

increased preload

Answer 26

force of contraction is larger
due to Frank Starling law
eject larger stroke volume
afterload doesnt change
EDV increase

Question 27

venous return

Answer 27

how much blood from venous circulation is returning to the heart
~60% of blood is in venous circulation (like a volume reservoir)
determines EDV
increases with EDV increase

Question 28

what affects venous return

Answer 28

1. skeletal muscle pump —> most veins go between skeletal muscle, every time you move the muscle contracts and squeezes the veins
   —-pump has a valve that prevents backflow, only way blood can go back up is through the path to the heart
   —–always move even on bedrest to prevent edema, if not then you cant return enough blood to heart and then to tissue
2. respiratory pump —> every time you take a breath you release a little pressure from the vena cavae with thoracic cavity expansion
   —-veins help to move blood to the heart
3. sympathetic innervation of veins —> contract veins, adrenergic receptors take in NE that is released and bind causing vasoconstriction of smooth muscle which decreases lumen of veins
   —– decrease lumen, blood goes back to heart, cannot go back due to valves

Question 29

inotropic state

Answer 29

regulated by ANS/sympathetic control of Ca concentration
increase in contractility or force of contraction
increase in the speed of contraction
increase in Ca concentration
positive or negative

Question 30

positive inotropy

Answer 30

increases contractility
more Ca release from SR into cytosol
generate more force of contraction
increase in slope
pressure volume curve increased more to the left
larger SV

Question 31

negative inotropy

Answer 31

decrease in contractility
decrease Ca influx from ECF and ER
lower force of contraction
steeper slope

Question 32

factors that influence stroke volume

Answer 32

related to force generated by cardiac muscle during contraction
1. length of muscle fiber
—–depends on stretch, EDV, more sensitive to Ca
——longer muscle fiber and sarcomere when contraction begins = greater the tension developed (up to a maximum)
2. contractility of the heart
—-ability of cardiac muscle fibers to contract at any given fiber length
—-if more Ca coming in = + inotropic event
—–function of Ca interaction with contractile filaments
—-regulated by sympathetic NS

Question 33

different afterloads

Answer 33

increase in afterload = DECREASE in force of contraction = DECREASE in SV
constant preload
less shortening of the muscle until it reaches a maximum tension
cannot contract outside of the total tension curve
isotonic reaction (measure how much a muscle shortens)
muscle needs to contract and generate enough tension to overcome afterload and shorten
heaviest afterload —-> cannot overcome it, no muscle shortening, isometric contraction

Question 34

active tension > total tension

Answer 34

muscle cannot shorten
decrease force of contraction

Question 35

example of increased afterload

Answer 35

increase in total peripheral resistance
blood vessels are clogged
harder for ventricle to eject blood, contract less
need more force of contraction to overcome afterload
starts to atrophy due to strain –> decreased amount of blood and stretch —> hypertension
decreased total tension, decreased SV, smaller than normal loop

Question 36

pressure volume loop

Answer 36

PICTURE NEAR END OF SLIDES

A. opening of mitral valve and beginning of ventricular filling
B. EDV/preload, closure of mitral valve
isovolumic contraction between
C. beginning of systole, opening of aortic semilunar valve, afterload
Systolic BP here (peak)
D. EDV, closure of aortic semilunar valve

Diastole —-> DAB
Systole —–> BCD
SV : volume ejected from C to D

Question 37

cardiac output

Answer 37

volume of blood pumped by one ventricle in a period of time
HR (beats/min) x SV (mL/beat)
average = 5 L/min
L ventricle to whole body, R ventricle only goes to lungs
both ventricles have the same value BUT the pressure is different
L. pressure is much higher (~120 mmHg) and R. pressure (~25 mmHg)
indicates how efficiently the heart is working as a pump