Cardiac Output and HR

[DrMasochist]

---

Members don't see this ad.

I have some conflicting information concerning CO and HR.
My initial understanding was:

increase in HR = increase available Ca++ (Treppe/staircase) = incr. contractility ----> larger CO (CO= SV x HR)

But I also understand that great increases HR also mean less time for diastolic filling. So does this mean that an incr. HR increases contractility but because there is less time to fill the ventricle, the two factors negate each other, and thus, CO is not greatly affected?

After watching one of the Kaplan videos on CO (physiology), I believe it was Dr. Kudrath who said HR has very little effect on CO. He then proceeded to show a graph which showed changes in HR giving the same CO and only extremely low or high HRs affecting the CO. But I think he failed to make the distinction that the graph does not include exercise or sympathetic stimulation.

 

[Yope]

Even though increases in HR increase contractility, preload is the biggest contributor to cardiac output. For the reasons you discussed, at super high HRs there isn't enough time between contractions and end diastolic volume is low.

 

[IntelInside]

I was under the impression that increasing HR will decrease CO because of the decrease in SV which will occur due to decreased filling, although minutely

 

[Yope]

Gradually increasing HR will increase overall intracellular calcium due to repeated calcium release from the sarcoplasmic reticulum in cardiac myocytes. Overall contractility will increase, so CO will increase.

But a huge jump in HR will decrease SV due to decreased filling time as you mentioned.

 

[nickolas]

Cardiac output increases as HR increases, period.
Only above the maximum HR for a given age does cardiac output begin to drop. (and I think only really old patients can enter this zone under sympathetic stimulation)

Just consider stress echo. Dobutamine is administered iv and EF (ejection fraction) is not supposed to drop. For a given heart EFxHR=cardiac output.

Implying that a nervous but healthy individual has a heart rate of 100bpm with an EF below 40% at rest (it has to be like that if he has 65% EF at 60bpm) is, well, stupid.

 

[nkhan]

I have some conflicting information concerning CO and HR.
My initial understanding was:

increase in HR = increase available Ca++ (Treppe/staircase) = incr. contractility ----> larger CO (CO= SV x HR)

But I also understand that great increases HR also mean less time for diastolic filling. So does this mean that an incr. HR increases contractility but because there is less time to fill the ventricle, the two factors negate each other, and thus, CO is not greatly affected?

After watching one of the Kaplan videos on CO (physiology), I believe it was Dr. Kudrath who said HR has very little effect on CO. He then proceeded to show a graph which showed changes in HR giving the same CO and only extremely low or high HRs affecting the CO. But I think he failed to make the distinction that the graph does not include exercise or sympathetic stimulation.

For sure during excercise CO increases (due to catecholamines, local factors vasodilation-->increase Q etc.) so there will be an overall increase in CO (along with the increased HR contributing directly) during excercise and increased HR. At some point there is a maximum HR (220-age) so even if you approach this the decrease in SV should override (with increased return etc.) the increase in CO due to exercise.

 

[nickolas]

Cardiac output increases as HR increases, period.
Only above the maximum HR for a given age does cardiac output begin to drop. (and I think only really old patients can enter this zone under sympathetic stimulation)

Just consider stress echo. Dobutamine is administered iv and EF (ejection fraction) is not supposed to drop. For a given heart EFxHR=cardiac output.

Implying that a nervous but healthy individual has a heart rate of 100bpm with an EF below 40% at rest (it has to be like that if he has 65% EF at 60bpm) is, well, stupid.

I stand corrected. Cardiac output is not altered and EF remains about stable. End diastolic volume decreases.
(at least that is what my prof. in cardiology tells me)