1. Normal - Rest
- In the normal heart at resting level of activity, if the myocardial contractile status is maintained and a sufficient stroke volume sufficient to supply the body while walking is required, then preload would have to increase from point A to A' (1)
- Frank-Starling mechanism
2. Normal - Exercise
- Cardiac contractility is increased due to sympathetic activation.
- In this condition, to raise the cardiac
performance from rest to walking,
preload needs to rise from point Bo to
B; this is a smaller increase in preload
(2) compared with the normal-rest condition (1).
- Requires less EDV
- In reality, however, our cardiac performance point goes from point A to point B. This is a decrease in the required preload to produce such a level of performance.
- This difference (A -> B) represents the importance of myocardial contractile
status in development of the stroke volume. If the increase in contractility is coupled with an increase in preload, the ultimate level of performance will be very high, a normal response based on the Frank-Starling mechanism.
3. Heart Failure Exercise
- a much greater increase preload would be required to bring ventricular performance from the resting to the walking level, from point C to point C'
- cannot increase contractility, so must increase stretch to increase stroke volume
- If heart failure is severe enough,
contractility may not increase.
- On the contrary, due to peripheral sympathetic activation, the effect of afterload now is big enough to have an effect on stroke volume. The EDV-SV
curve may not change at all or even further shifted to the right (3'). In these individuals, the requirement for increasing preload can be so big that it goes beyond the maximal point on
the Frank-Starling relationship, after which there will be severe increases in pulmonary capillary pressure and pulmonary edema will ensue.
4. severe, fatal myocardial depression
- contractile status of the myocardium is so low that without pharmacological intervention, the heart will not be able
to provide a sufficient stroke volume for the body even at rest.
Normally in the human heart, peak contractile force at a fixed muscle length (isometric contraction) increases and a peak is reached at about 150 to 180 stimuli/min.
In situ, the optimal heart rate is not only the rate that would give maximal mechanical performance of an isolated muscle strip, but is also determined by the need for adequate time for diastolic filling.
In normal humans, it is not possible to attach exact values to the heart rate required to decrease rather than increase cardiac output or to keep it steady.
Pacing rates of up to 150 beats/min can be tolerated, whereas higher rates cannot because of the development of AV block.
In contrast, during exercise, indices of LV function still increase up to a maximum heart rate of about 170 beats/min, presumably because of enhanced contractile function and peripheral vasodilation.
In patients with severe left ventricular hypertrophy, the critical heart rate is between 100 and 130 beats/min, with a decrease in LV function at higher rates.
With atrial tachycardia of a higher rate, blood pressure, cardiac output and coronary flow fell more markedly, then blood pressure and cardiac output rose to or toward control level, remaining below control level with higher rates of tachycardia, whereas the coronary flow rose to or above control level and only exceptionally remained below control level.
Ventricular tachycardia had essentially the same effects as atrial tachycardia, but a ventricular tachycardia of a given rate had the same quantitative effect as an atrial tachycardia of a higher rate.