Cpps415 Paet 3

Front 1

Anatomy and flow of blood

Back 1

Right atrium => tricupsid valve => right ventricle => semilunar pulmonic valve => pulmonary artery => left atrium => mitral valve => left ventricle => aortic valve => aorta

Front 2

Preference of nerve innervation

Back 2

Para: sinoatrial node, and atrial muscle

Sympa: atrioventricular node, and both atria and ventricles

Front 3

What are chronotropy, dromotropy, inotropy?

Back 3

Chronotropy: HR

Dromotropy: conduction velocity

Inotropy: contractility

Front 4

Pacemaker AP phases

Back 4

Front 5

Phases of heart contraction

Back 5

_Diastole:

Phase 1 (P wave): atrial systole (AV valve opened, pulmonic and aortic valves closed) => 10% filling blood to ventricle. Increase both atria and ventricle pressure (alpha wave).

*** at the end of phase 1, atria pressure decreases which causes AV valve to partially close (nở ra hút valve đóng lại) => blood in the ventricle reached end-diastolic volume (EDV).

_Systole:

Phase 2: isovolumetric contraction, all valves closed, initiated by QRS complex. Myocardial contraction causes rapid increase in ventricular pressure which forces AV valve to close and creating first heart sound (S1). No blood is ejected or loss yet.

Continued venous return and sudden AV valve closure (bulge) increases atrial pressure (c wave)

Phase 3 (maximal velocity, vessel pressure, maximal outflow): rapid ejection, AV valve remain closed, pulmonic and aortic valve opened. When ventricular pressure exceeds pulmonic and aortic pressure, aortic and pulmonic valve opened.

Phase 4: reduced ejection, aortic and pulmonic valves opened, AV valves remain closed. Associated with T wave, ventricular repolarization. Contraction is getting weaker and decrease in ejection. Although intraventricular pressure is a bit lower than aortic and pulmonic pressure, kinetic energy inertia kepts blood flowing into the aorta and pulmonic artery as well as kept the valves opened.

Phase 5: Isovolumetric relaxation, all valves closed. Aortic and pulmonic valves closed as pressure in the ventricle drop rapidly => second heart sound (S2). Valve closed results in incisura (dicrotic notch) as pressure is slightly increased. No change in blood volume because all valves are closed (end-systolic volume).

Diastole:

Phase 6: rapid filling, AV valves opened, aortic and pulmonic valves closed. AV valves opened due to ventricular pressure drops below atrial puressure. Maximal atrial pressure (v wave) drops rapidly (y wave) as AV valves opened. Third heart sound can result (S3), pathology in adult, normal in children.

Phase 7: reduced filling, AV valves opened, aortic and pulmonary remain closed. Period of ventricular diastasis where passive filling almost complete.

Front 6

Sound in heart contracting cycle

Back 6

S4: in phase 1 atrial systole when blood is pumped to ventricle

S1: in phase 2 beginning of ventricle systole when AV is closed

S2: in phase 5 where all valvea are closed due to ventricle relaxation.

S3: phase 6 during passive filling.

Front 7

Preload

Back 7

Initial stretching of the cardiomyocytes prior to contraction (sarcomere length).

Alternatively measured as EDV.

Front 8

Passive tension dependency

Back 8

Depend on elastic modulus (stiffness) if heart tissue. Khả năng kháng biến dạng => giống như lò xo, sẽ luôn có lực kéo về vị trí đầu (tension) khi bị biến dạng

If elastic modulua is high => high resistance to stretch => high passive tension when stretched.

Front 9

Length tension relationship

Back 9

The higher the preload (stetching of sarcomeres), the higher the active tension (total tension minus passive tension)

However, duration of contraction and time to reach peak tension does not change. Because more rapid fiber shortening (velocity), higher magnitude of shortening, higher rate of active tension development.

Front 10

How to estimate afterload

Back 10

Measuring ventricular wall stress: average tension that each muscle fibre must generate to shorten against ventricular pressure

Front 11

Afterload and velocity

Back 11

The higher the afterload, the lower the velocity of shortening.

Front 12

How to offset decreased velocity caused by increased afterload?

Back 12

By increasing preload (stretching/lengthening of sarcomere).

Front 13

Afterload and preload on velocity

Back 13

Increased afterload: decreases Vmax (maximal speed when there is no load) => muscle connot reach the highest speed.

Increased preload: increases the speed of shortening.

Front 14

Similarity between afterload and preload on ventricular function

Back 14

Both increases isometric active tension (lực thu hồi lại hình dạng ban đầu).

Front 15

Inotropy dependency

Back 15

Not dependent on pre or afterload.

Alter active tension regardless of sarcomere length

Front 16

Effects of increased inotropy. Mechanism

Back 16

Increase Vmax and maximal afterload force can endure.

By increasing the rate of cross-bridge turnovers of actin and myosin filaments

Front 17

Frank-starling curve

Back 17

Stroke volume versus preload

Front 18

Effects of increased inotropy on pressure-volume loop

Back 18

Since increased inotropy enhances ventricular emptying, End systolic volume (ESV) will decrease => pressure-volume loop will expand to the left and the ESPVR (end systolic pressure volume relationship) will shift to the left and become steeper (shift up).

Front 19

Anrep effect

Back 19

Increased inotropy induced by abrupt increased in afterload

Front 20

Bowditch effect

Back 20

Increased inotropy induced by increased HR

Front 21

Cellular mechanisms of increased inotropy

Back 21

1. Increasing calcium influx

2. Increase calcium release by SR

3. Sensitizing troponin C to calcium