Lecture 17 Flashcards
When does ventricular diastole begin?
With the closure of the semilunar valves. The pulmonary semilunar valve and the aortic semilunar valve.
What happens after the closure of the semilunar valves?
There is iso-volumetric relaxation, this will end as soon as the pressure in the atria exceed the ventricle pressure. Rapid filling phase will occur once the AV valves open. It is then followed by a phase of slowed filling (determined by HR), finally atrial systole terminates the period of ventricular diastole and the cycle begins again.
Describe diastolic filling?
You can measure the pressure changes in the LV via a balloon catheter. As LV volume increases then so does LV pressure (non-linear). Myocytes are relaxed and at long length.
Describe systolic relationship between LV volume and pressure?
There is a linear relationship, so as LV volume increases so does pressure.
Describe pressure-volume loops?
During passive filling there is a slight increase in pressure (and increase in volume). During the isovolumetric contraction there is a big increase in pressure, with the opening of the valves there is ejection volume will decrease during this phase.
What are the four determinants of ventricular performance?
- Preload - degree of filling (EDV) and stretch of muscle before contraction.
- After load - pressure at which valve opens and pressure against which ventricle contracts.
- Inotropic state.
- Heart rate.
Describe the effect of preload?
Look at the LV EDV to get a measure of preload or the change in pressure.
Describe the effect of after load?
If we increase after load then the mycoytes must produce an increased pressure when the ventricles contract. Need to consider the wall stress on the mycoytes (which is dependent on Law of La Place - tension is proportional to the P r). In hypertrophy there is increased heart wall thickness (due to increased myocyte size), this will increase the wall stress. During systemic hypertension there is an increased after load.
Describe the effect of increased chronotropy?
The force of contraction increases as HR increases (as HR increases SV decreases). At low heart rates the R-R interval is long, as HR increases R-R interval drops. The diastolic interval (time for ventricular filling) is decreasing with increasing heart rate. High heart rates SV is decreased due to reduced filling time in general.
Describe the balancing of R and L sides of the heart?
Both sides of the heart pump the same volume over time (what enters the heart must leave the heart) - any changes that occur that affect R and L side of the heart need to effect both sides of the heart not just one side of the heart. Something that increases afterlaod dramatically may take a few beats for the R side of the heart to adjust as well. Increase in after load means the LV needs to pump harder to achieve the same SV.
What happens when there is an increase in after load?
If there is an increase in MAP (pressure in the aorta) this will increase LV after load, so decreases LV volume (SV). The RV continues pumping, accumulation of volume in the lungs, this will increase the stretch of the capacitance circuit, which will increase the pressure to the LV so that the next beat EDV is increasing. SV reaches a new steady state. This regulation is occurring through our daily lives.
What are the assessments of ventricular performance?
- Ejection fraction.
- Peak dP/dt - a heart that i functioning well will have a high rate of change of pressure with time.
- End-systolic PV relation.
- Ventricular function curves.
Describe ejection fraction?
Fraction of the CO or the fraction of the blood in the ventricle that is ejected during contraction. The change in EDV - ESV over the EDV (the fraction of blood ejected with one contraction). This can be determined from echocardiography or MRI data. Normal EF for LV is 55-65% at rest and during exercise (when HR has increased and strength of contraction) EF is 85%. Depressed contractility your EF will be
Describe maximum rate of rise in ventricular pressure?
When dP/dt is positive it is during the increase in LV pressure and negative during relaxation. You want a high peak dP/dt and negative during relaxation (because relaxation is a slower process - uptake of calcium - than the release of calcium).
Describe ESPVR?
IF there is a positive inotropic stimulus (increase the force of contraction - stretch of beta-adrenergic stimulation) then the ESPVR line is shifted to the left. In heart disease where the mycoytes are unable too develop sufficient force during contraction, then the line is shifted to the right.
