The Cardiac Cycle Flashcards
3 basic evens of the cardiac cycle
- LV contraction,
- LV relaxation,
- LV filling.
The cardiac cycle phases- LV contraction
- Isovolumic contraction ( b )
- Maximal ejection ( c )
The cardiac cycle phases- LV relaxation
- Start of relaxation and reduced ejection ( d )
- Isovolumic relaxation ( e )
- Rapid LV filling and LV suction ( f )
- Slow LV filling (diastasis) ( g )
- Atrial booster ( a ).
Ventricular contraction: Systole
Wave of depolarisation arrives,
Opens the L-calcium tubule, {ECG: Peak of R},
Ca2+ arrive at the contractile proteins,
LVp rises > LAp:
MV closes: M1 of the 1st HS, first heart sound
LVp rises (isovolumic contraction) > Aop,
AoV opens and Ejection starts.
Ventricular relaxation: Diastole
LVp peaks then decreases.
Influence of phosphorylated phospholambdan, cytosolic calcium is taken up into the SR.
“phase of reduced ejection”.
Ao flow is maintained by aortic distensibility.
LVp < Ao p, Ao. valve closes, A2 of the 2nd HS.
“isovolumic relaxation”, then “MV opens”.
Ventricular filling
LVp < LAp, MV opens, Rapid (E) filling starts.
Ventricular suction (active diastolic relaxation), may also contribute to E filling (esp. ex. ?S3).
Diastasis (separation): LVp=LAp, filling temporarily stops.
Filling is renewed when A contraction (booster), raises LAp creating a pressure gradient.(path, S4)
Physiologic systole
Isovolumic contraction
Maximal ejection
Cardiologic systole
From M1 to A2
Only part of isovolumic contraction (includes maximal and reduced ejection phases)
Physiologic diastole
Reduced ejection
Isovolumic relaxation
Filling phases
Cardiologic Diastole
A2 to M1 interval (filling phases included)
Preload
is the load present before LV contraction has started
Volume of blood in the LV which streches the cardiac myocytes before LV contraction. Load present before LV contraction has started (EDV).
Afterload
is the load after the ventricle starts to contract
Pressure the LV must overcome to eject blood during contraction
Starling’s Law of the heart
Starling 1918: Within physiologic limits, the larger the volume of the heart, the greater the energy of its contraction and the amount of chemical change at each contraction
The more the ventricles fill, the harder they contract
Higher end diastolic volume= myocytes stretch= increase in strength of contraction= increase in cardiac output
•LV filling pressure: is the difference between LAp and LV diastolic pressure
•The relationship reaches a plateau
The Force-Length Interaction & Starling’s law
The force produced by the skeletal muscle declines when the sarcomere is less than the optimal length (Actin’s projection from Z disc “1micrometre” X 2).
In the cardiac sarcomere, at 80% of the optimal length, only 10% of the maximal force is produced
All or none principal
The cardiac sarcomere must function near the upper limit of their maximal length (LMAX) = 2.2 micrometer.
The physiologic LV volume changes are affected when the sarcomere lengthens from 85% of LMAX to LMAX
Steep relationship: length-dependent activation.
Frank and Isovolumic contraction
The heart can, during the cycle, increase and decrease the pressure even if the volume is fixed.
Increasing diastolic heart volume, leads to increased velocity and force of contraction (Frank 1895).
This is the positive inotropic effect.
Ino: Fibre (Greek); tropus: move (Greek).
Contractility (inotropic state)
the state of the heart which enables it to increase its contraction velocity, to achieve higher pressure, when contractility is increased (independent of load)
The pressure-volume loop reflects contractility in the end-systolic pressure volume relationship, while compliance is reflected at the end diastolic pressure volume relationship
Force of contraction and the change in fibre length - how hard the heart pumps.
When muscle contracts myofibrils stay the same length but the sarcomere shortens - force of heart contraction that is independent of sarcomere length
Elasticity
Is the myocardial ability to recover its normal shape after removal of systolic stress.
Compliance
is the relationship between the change in stress and the resultant strain.(dP/dV)
How easily the heart chamber expands when filled with blood volume
Diastolic distensibility
is the pressure required to fill the ventricle to the same diastolic volume.
Isometric vs. Isotonic contraction
Iso = the same (Greek),
Metric = length (Greek),
Tonic = contractile force (Greek),
The force-velocity curve may be a combination of initial isometric conditions followed by isotonic contraction.
The isometric conditions can be found during isovolumic contraction, isotonic contraction is totally impossible in the heart, given the constantly changing load.
Total Peripheral Resistance
Total resistance to flow in systemic blood vessels from beginning of aorta to vena cava - arterioles provide the most resistance
Stroke volume
Volume of blood ejected from each ventricle during systole
SV = end diastolic volume - end systolic volume
Cardiac cycle is 72 bpm
0.3 secs- systole
0.5 secs- diastole
Systole – Ventricular Contraction and blood ejection
Diastole – Ventricular relaxing and blood filling.
Unless clearly states atrial systole etc
Basic 3 events
LV contraction
-Isovolumic contraction
-Maximal ejection
LV relaxation
-Start of relaxation and reduced ejection
-Isovolumic relaxation
-Rapid LV filling and LV suction
-Slow LV filling (diastasis)
-Atrial booster (systole)
LV filling
Ventricular contraction- Systole
1) Wave of depolarisation arrives at AV node
2) Ventricular walls contract
3) Pressure in ventricles > pressure in atria
4) AV valves close (first heart sound)
5) Isovolumic contractions (during isovolumic contraction/relaxation – all valves are closed)
6) Pressure in ventricles > aorta/pulm arteries
7) Semi lunar valves open and ejection begins
Ventricular relaxation- Diastole
1) Once pressure aorta > ventricles, semi-lunar valves close – 2nd heart sound
2) Isovolumetric ventricular relaxation
3) Pulmonary veins/SVC/IVC are filling atria (forming pressure gradient between ventricles)
4) Pressure in atria > ventricles
5) AV valves open and blood passively flows into ventricles (80%)
Atrial systole- Ventricular filling
1) As ventricle refill, pressure in atria and ventricles are equalising ( DIASTASIS- slows down flow into ventricles from atria)
2) Firing of SA node, causing atrial depolarisation (P wave) to increase flow into ventricles
3) When the pressure in atria = ventricles, rapid ejection starts
4) AV n is delaying the stimuli from the SA node to allow full ventricular filling and full atrial emptying
