Transcript Cardiac Cycle: diastole Phase

A heartbeat is a two-part pumping action that takes about
a second.
This part of the two-part pumping phase (the longer of the
two) is called diastole.
Diastole begins as the ventricles start to relax. Soon the
pressures within the aorta and pulmonary artery exceed
ventricular pressures, causing the semilunar valves to
close (B2 murmur).
As the ventricular pressure falls below the atrial pressure
the AV valves open and the ventricles fill with blood. The
ventricles fill to about 80% of capacity prior to contraction
of the atria, the last event in diastole.
Atrial contraction forces the final 20% of the enddiastolic volume (the volume of blood that exists in the
ventricles at the end of diastole) into the ventricles. / SA node
contracts
Summary of Diastole:
pulmonary and aortic valves close
Ventricles relax => isovolumic relaxation
AV valves open
ventricles fill (about 80% of capacity) => inflow
atria contract (ventricles fill another 20%)
Contraction reaches AV node…
Cardiac Cycle: diastole Phase
The second part of the pumping phase begins
when the ventricles are full of blood.
The electrical signals from the SA node travel
along a pathway of cells to the ventricles,
causing them to contract. This is called systole.
As the ventricles start to contract, the
ventricular pressure soon exceeds the atrial
pressure, causing the AV valves to close (B1
murmur).
As the ventricles continue to contract, the
ventricular pressure exceeds the arterial
pressures causing the semilunar valves open.
Blood is forcefully ejected out of the ventricles
and into the aorta and pulmonary artery.
Summary of Systole :
AV valves close
ventricles contract => isovolumic contraction
aortic and pulmonary valves open
blood is ejected => ejection phase
atria relax and fill with blood
Cardiac Cycle: Systole Phase
Plan: Evaluation of the cardiac performance
• On the cellular « scale »
–
–
–
–
–
muscular cells and cardiac myocytes
myofibril / « Sarcomere »
proteins: actin / myosin
role of Ca++
=> « cell’s performance »
• Laws and principles of haemodynamic:
– Poiseuille or Darcy
– Starling : preload and post load
– «heart’s performance »
• On the scale of the organ: the heart
– Cardiac cycle
– Relation pressure-volume
– The regulation of the cardiac output
Physiology (1)
All muscles derive from paraxial mesoderm.
The three types of muscle (skeletal, cardiac and
smooth) have significant differences. However, all
three use the movement of actin against myosin to
create contraction.
Cardiac muscle is a type of involuntary striated
muscles found in the walls of the heart, specifically
the myocardium.
Cardiac and smooth muscle contractions are
stimulated by internal pacemaker cells which
regularly contract, and propagate contractions to
other muscle cells they are in contact with.
Muscle is mainly composed of muscle cells. Within
the cells are myofibrils; myofibrils contain
sarcomeres, which are composed of actin and
myosin.
muscle cell or
Muscle / Fasicle / Fiber (cell) / Fibril / sarcomere
muscle
fiber or cell
myofibrils
sarcomere
Physiology (2)
Myofibrils are cylindrical organelles. They are found
within muscle cells or fibers.
They are bundles of actomyosin filaments that run
from one end of the cell to the other and are
attached to the cell surface membrane at each end.
The filaments of myofibrils, or myofilaments,
consist of two types, thick and thin.
Thin filaments consist primarily of the
protein actin, coiled with nebulin filaments.
Thick filaments consist primarily of the
protein myosin, held in place by titin filaments.
The filaments are organized into repeated subunits
along the length of the myofibril.
These subunits are called sarcomeres.
The sarcomere is the “functional” basic unit of
contraction.
1:Axon / 2:neuromuscular junction /
3:muscle cell / 4:myofibril
sarcomere
sarcomere
sarcomere
Physiology (3)
Cardiac muscle requires extracellular calcium
ions for contraction to occur. Like skeletal
muscle, the initiation and upshoot of the
action potential in ventricular muscle cells is
derived from the entry of sodium ions across
the sarcolemma in a regenerative process.
Once the intracellular concentration of
calcium increases, calcium ions bind to the
protein troponin, which initiates contraction
by allowing the contractile proteins, myosin
and actin to associate through cross-bridge
formation.
Sliding filament model of muscle contraction
relaxed
contracted
Shortening of 1 µm / sarcomere
If 10 5 sarcolemma (striated muscle)
=> Shortening of 10cm
myosin
actin filament
Neuromuscular junction
for the next presentation…
In contrast to skeletall muscle, cardiac muscle
requires extracellular calcium ions for
contraction to occur.
Like skeletal muscle, the initiation and
upshoot of the action potential in ventricular
muscle cells is derived from the entry of
sodium ions across the sarcolemma in a
regenerative process. However, an inward flux
of extracellular calcium ions through type
calcium channels sustains the depolarization
of cardiac muscle cells for a longer duration.
Once the intracellular concentration of
calcium increases, calcium ions bind to the
protein troponin, which initiates contraction
by allowing the contractile proteins, myosin
and actin to associate through cross-bridge
formation.
Poiseuille or Darcy’s law / (Ohm)
– ∆P = Q x Rv / (Flow = Pressure/Resistance )
• ∆P => Mean gradient pressure
– ∆Ps = PAo – POD
– ∆Pp = PAP – PVP
– Qs = SV x Hr
(SV=> Stroke Volume = EDV – ESV )
After birth: « serial circulation »
without shunt => Qs=Qp
=> pressures in aorta and PA depend on Resistances
Before birth: « parallel circulation »
With shunts => Pao = PAP / Qs ≠ Qp
Rp are high => Qp is low
Rs are low (placenta) => Qs is high
Frank-Starling law
•
•
The Frank-Starling law of the heart states that the greater the volume of blood
entering the heart during diastole (end-diastolic volume), the greater the volume
of blood ejected during systolic contraction (stroke volume).
This allows the cardiac output to be synchronized with the venous return, arterial
blood supply and humeral length[1] without depending upon external regulation to
make alterations.
•
As the heart fills with more blood than usual, the force of the muscular
contractions will increase.
•
The stretching of the muscle fibres increases the affinity of troponin C for calcium,
causing a greater number of cross-bridges to form within the muscle fibers; this
increases the contractile force of the cardiac muscle.
•
The force that any single muscle fiber generates is proportional to the initial
sarcomere length (known as preload), and the stretch on the individual fibers is
related to the end-diastolic volume of the ventricle.
TA
Toum
TA
Toum
Parameter Values
• End-diastolic volume (EDV)
120 ml
• End-systolic volume
(ESV)
50 ml
• Stroke volume
(SV)
70 ml
290 l / hour
7 056 l / day
2 575 440 l / year
180 280 800 l / 70 years
• Ejection fraction
(Ef)
58%
• Heart rate
•
• Cardiac output
(HR)
70 bpm
(CO)
4.9 L/mn
• Cardiac index
(CI)
2,5 -3,5 l/mn/m2
End systolic volume (afterload volume)
Pressure
mm Hg
Starling law
Contractility
140
Systolic phase
Ejection phase
Closure of the aortic valves
80
Opening of the aortic valves
SV (35ml)
Isometric relaxation
30
Isometric contraction
Compliance
Opening of the AV valves
10
Closure of the AV valves
Filling
10
Diastolic phase
40
50
100
End diastolic volume (preload volume)
Volume ml
the cardiac performance
Regulation of cardiac output
the rate of contraction can be changed by
nervous or hormonal influences, exercise and
emotions. For example, the sympathetic
nerves to heart accelerate heart rate and the
vagus nerve decelerates heart rate.
Qs = SV x Hr
(SV=> Stroke Volume = EDV – ESV )
Evaluation of and for the « teacher » !
• How do you define a muscular fiber and a sarcomere ?
• Explain the mechanism of shortening of a muscle fiber ?
• What is the Starling’s law ?
• What happens during the isovolumic relaxation concerning
the heart’s valves ?
• Define the « compliance » of the heart
• How many liters does the heart pump during one year ?
(bonus)
Physiopathology