Cardiac Physiology Question

[RxBoy]

Assuming someone has a normal heart, normal coronaries... We know:

Oxygen Delivery:
Arterial DaO2= Q x CaO2 x 10 [N=1000 mL/min]
Venous DvO2= Q x CvO2 x 10 [N=775 mL/min]
Given:
Oxygen carrying capacity
CaO2 = (hgb x SaO2 x 1.38) + (PaO2x0.003) [N=20 mL/dL]
CvO2 = (hgb x SvO2 x 1.38) + (PaO2x0.003) [N=15 mL/dL]

Oxygen Delivery:
VO2 = DaO2-DvO2
Reducing Equation:
VO2 = Q x (SaO2-SvO2) x Hgb x 13.8 [N=200-250 mL/min]

Extraction Ratio:
(CaO2-CvO2)/CaO2 x 100 (N=25%)

So.... VO2 = Q x (SaO2-SvO2) x Hgb x 13.8
My question is this, utilizing maximum oxygen extraction (I believe 50%)... At what level can the heart increase the cardiac output (Q) before oxygen delivery needs to be increased?

Stated another way, at what point can your Q increase to make up for decreased Hgb until oxygen delivery becomes dependent on hgb?

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[urge]

My question is this, utilizing maximum oxygen extraction (I believe 50%)... At what level can the heart increase the cardiac output (Q) before oxygen delivery needs to be increased?

Stated another way, at what point can your Q increase to make up for decreased Hgb until oxygen delivery becomes dependent on hgb?

Level 9. Point C.

 

[RT2MD]

Level 9. Point C.

While I know it's not helpful, it almost made me spit my drink all over my keyboard... I'm a little sleep deprived right now...

 

[RxBoy]

NM found it myself... Thank you Marino.

50% SvO2
10% hematocrit is the magic number.

Cardiac Output
The influence of anemia on circulatory blood flow is described at the end of Chapter 1.
The hematocrit is the principal determinant of blood viscosity (see Table 1.2 in Chapter
1), and thus a decrease in hematocrit will decrease the viscosity of blood. According to
the Hagen–Poiseuille equation shown below, a decrease in viscosity (µ) will result in an
increase in circulatory blood flow (Q) as long as the pressure gradient along the
circulation (?P) and the dimensions of the blood vessels (r for radius
P.664
and L for length) remain constant. (This equation is described in detail in Chapter 1.)
A decrease in blood viscosity augments cardiac stroke output by reducing ventricular afterload.
Anemia can also be accompanied by activation of the sympathetic nervous system
(4,12), which will augment cardiac output by increases in both myocardial contractility and
heart rate. However, this response is not prominent, and thus tachycardia is not a
prominent finding in anemia (at least at rest) (4).
When considering the isolated effects of anemia on cardiac output, the blood volume
should be normal or unchanged (this condition is referred to as isovolemic anemia). The
changes in cardiac output associated with progressive, isovolemic anemia are shown in
Figure 1.8 (Chapter 1). Note that the increase in cardiac output is proportionally much
greater than the decrease in hematocrit. This response is attributed to the
flow-dependency of blood viscosity; i.e., an increase in blood flow (cardiac output) will
decrease blood viscosity. Thus, anemia decreases blood viscosity, which then increases
cardiac output, which then decreases blood viscosity, and so on. Ketchup is another fluid
with a flow-dependent viscosity, so if you can picture what happens when you pour
ketchup (the flow is sluggish at first, then increases as you continue to pour), you will get
the idea. Blood viscosity is described at the end of Chapter 1.
In addition to the global changes in cardiac output, anemia can preferentially increase
flow in the cardiac and cerebral circulations, and decrease flow in the splanchnic
circulation (5). This will have a protective effect on myocardial and cerebral metabolism in
the presence of anemia.
Peripheral Oxygen Extraction
The effects of progressive isovolemic anemia on systemic oxygen transport is
summarized in the graphs in Figure 36.3 (17). The initial decrease in hematocrit is
accompanied by a decrease in systemic oxygen delivery (DO2), and this is
counterbalanced by an increase in O2 extraction (SaO2 2 SvO2). The reciprocal changes
in DO2 and O2 extraction keep the VO2 constant (VO2 = DO2 × O2 extraction). However,
when the hematocrit falls below 10%, the increase in O2 extraction is no longer able to
match the decreasing DO2, and the VO2 begins to fall. The decrease in VO2 is a sign of
dysoxia (defined in Chapter 2 as oxygen-limited aerobic metabolism), and is
accompanied by an increase in lactate production. The point at which the VO2 begins to
fall is thus the threshold for tissue dysoxia, and it usually occurs when the O2 extraction
reaches a maximum level of 50 to 60%. This means that an O2 extraction (SaO2 2 SvO2)
that is 50% or higher is a sign of inadequate tissue oxygenation.View Figure
Figure 36.3 The effects of progressive
isovolemic anemia on oxygen delivery
(DO2), oxygen extraction ratio (O2ER),
oxygen uptake (VO2), and blood lactate
levels in experimental animals. (From
Wilkerson DK, Rosen AL, Gould SA, et
al. Oxygen extraction ratio: a valid
indicator of myocardial metabolism in
anemia. J Surg Res
1987;42:629–634.Full
TextBibliographic Links)
P.665
Thus, because of the compensatory changes in cardiac output and peripheral O2
extraction, progressive anemia will not impair tissue oxygenation until the hemoglobin
and hematocrit reach dangerously low levels. In the results of the animal study shown in
Figure 36.3, the hematocrit had to fall below 10% (corresponding to a hemoglobin
concentration of 3 g/dL) before tissue oxygenation was compromised. The experimental
animals in this study were anesthetized and breathing pure oxygen (which could favor
tolerance to severe anemia), but similar results have been reported in awake animals
breathing room air (18). The lowest hemoglobin or hematocrit that is capable of
supporting tissue oxygenation in humans in not known, but one study of isovolemic
anemia in healthy adults showed that hemoglobin levels of 5 g/dL had no deleterious
effects on tissue oxygenation (19)

 

[RT2MD]

NM found it myself... Thank you Marino.

Does that really answer your question? I admit that I'm just a 2nd year med student, so please feel free to correct me as needed.

I thought that you were asking about how increased blood flow could maintain an adequate level of oxygen delivery in the setting of anemia. I understand how decreased hematocrit results in the viscosity being lowered, which lowers afterload, which increases output, but the part of your post that said:

The effects of progressive isovolemic anemia on systemic oxygen transport is summarized in the graphs in Figure 36.3 (17). The initial decrease in hematocrit is accompanied by a decrease in systemic oxygen delivery (DO2), and this is counterbalanced by an increase in O2 extraction (SaO2 2 SvO2). The reciprocal changes in DO2 and O2 extraction keep the VO2 constant (VO2 = DO2 × O2 extraction). However, when the hematocrit falls below 10%, the increase in O2 extraction is no longer able to match the decreasing DO2, and the VO2 begins to fall.

Just makes me think this: Basically there is a built in "safety net" in oxygen delivery, due to the fact that - normally - there is so much more oxygen delivered than is extracted, but if you hit a crit of 10%, then you have run out of your "safety net" and you aren't going to be delivering enough O2 to support aerobic metabolism. This part doesn't seem to address flows at all ... at least the way that I understood it.

Did I misunderstand you initial question, or am I not getting the point of your posting here? Honestly, at this point it could easily be either... I'm not firing on all cylinders!

Thank you in advance.

 

[RxBoy]

Does that really answer your question? I admit that I'm just a 2nd year med student, so please feel free to correct me as needed.
Thank you in advance.

I asked at what point can your Q increase to make up for decreased Hgb until oxygen delivery becomes dependent on hgb?

Q (or cardiac output) increases due to decreased viscosity in the setting of isovolumic anemia (replacing lost blood with fluid). I was wondering at what state can this increased CO with the compensatory increase of ERO2 maintain a steady VO2. This was the answer:

Its not a simple multiple of CO (I originally didn't realize there were other variables like viscosity) but basically to a point where you dilute the hct to 10%. At that point regardless of how much extra volume/inotropes you give (to increase CO), the VO2 is completely dependent on Hgb.

Clinically: Using Hgb during blood loss is a inferior trigger point for transfusion. A more reliable trigger is to increase the CO using volume until SvO2 approaches 50% (maximum extraction). At that point the body has exhausted the compensatory extraction ratio and oxygen content will only be increased with transfusion.

Conversely, transfusing too early will actually hinder your CO.

 

[RxBoy]

.

 

[RT2MD]

I asked at what point can your Q increase to make up for decreased Hgb until oxygen delivery becomes dependent on hgb?

Q (or cardiac output) increases due to decreased viscosity in the setting of isovolumic anemia (replacing lost blood with fluid). I was wondering at what state can this increased CO with the compensatory increase of ERO2 maintain a steady VO2. This was the answer:

Its not a simple multiple of CO (I originally didn't realize there were other variables like viscosity) but basically to a point where you dilute the hct to 10%. At that point regardless of how much extra volume/inotropes you give (to increase CO), the VO2 is completely dependent on Hgb.

Clinically: Using Hgb during blood loss is a inferior trigger point for transfusion. A more reliable trigger is to increase the CO using volume until SvO2 approaches 50% (maximum extraction). At that point the body has exhausted the compensatory extraction ratio and oxygen content will only be increased with transfusion.

Conversely, transfusing too early will actually hinder your CO.

Oh, ok. I think that I was making your question more difficult than it actually was.

What you are really saying is that, in the event of a decreased Hgb, as long as you replace fluid (up to a point) to maintain isovolemia (and therefore output), the tissues are still able to undergo aerobic metabolism b/c there is still adequate oxygen content in the arterial blood. In addition the lower viscosity of the blood also will help increase cardiac output. Also, if you transfuse too early, you can actually hinder your CO due to increased viscosity/after load. Using a venous saturation to guide your transfusion threshold is the way to do it. Is that *somewhat* correct? Does that mean that you (anesthesiologists in general) are frequently drawing SvO2s on patients with large amounts of blood loss to guide transfusion therapy?

I know that when we had ECMO patients, we had a sat monitor on the venous side as an indicator of oxygen delivery... you know, SvO2 goes down = a decrease in o2 delivery. Either a pump problem, increased metabolic needs, or a membrane problem. Having one of those monitors on a patient without extra corporeal circulation might be a bit difficult, though!

I realize that the threshold for transfusion has decreased - allowing for more severe anemia in some cases before transfusion takes place... but the point on viscosity counteracting increased O2 carrying capacity seems backwards to me. I would think that the increase in Hgb, and therefore O2 carrying capacity would make up for an increased viscosity causing lower CO at a moderately lowered Hgb (like around 9 or so, for example)... I know that a Hgb of 9 doesn't necessarily show need for transfusion, though. I guess that's one of those things that will seem counter intuitive to me.

Thanks for the discussion, by the way... I love the level of phys knowledge that anesthesiologist need to have. I just think of that whenever somebody tells me "How can you be interested in anesthesia?!?!?! It's so... BORING." I just smile and reply "To some people it might seem that way... but it's not!"

 

[RxBoy]

Oh, ok. I think that I was making your question more difficult than it actually was.

Is that *somewhat* correct? Does that mean that you (anesthesiologists in general) are frequently drawing SvO2s on patients with large amounts of blood loss to guide transfusion therapy?

Nice to spark your interest. You are absolutely correct except there are still some anesthesiologists who follow Hgb which really is a very poor indicator of tissue oxygenation.

Hgb is just a concentration (g/dL) so for example if someone had a hgb of 9 and bleed out 1 liter and instantly after you drew a hgb, your hgb will still be 9 g/dL. Its only after renin-angiotensin-aldostorone activation that hgb concentration will drop (without fluid rescitation) as your extravascular fluid shifts to the intravascular compartment. This could take 6 hours! So the more important parameter is to increase CO first. So in the example above, if someone losses a liter during surgery and 1 hour later the hgb has not budged, you actually have done a very poor job resuscitating (the patient needs fluid).

SvO2 is a much better marker. One way to measure svo2 is with a pulmonary catheter (swan ganz), it can continuously measure svO2 however highly invasive. A much easier approach is to sample a venous gas from a central line (ScVO2) and compare that to your pulse ox (an estimate of SaO2). Although ScVO2 is not a true SVO2, the change is very little (+/- 5% depending on anesthetized vs. awake). So I send off a ScVO2 all the time when I have acute hemorrage and want to know my tissue oxygenation status. I sometimes send off a lactic acid as well. ABGs should not be used to guide fluid management, they should be used to guide hypoxia/ hypercaria or acid/base. VBGs (particularly SvO2) are much more useful for tissue oxygenation.

SvO2 is a little tricky with sepsis though. In severe sepsis it actually increases. This due to the relationship.
VO2 = DO2 x ER
And sepsis is odd because it doesn't effect your oxygen delivery but rather your oxygen extraction. The theory is that bacterial toxins inhibit mitochondrial oxygen utilization. Therefore because the body is unable to use oxygen, the SvO2 increases so the tissue oxygenation suffers even with a normal oxygen delivery. Cyanide poisoning does something similar.

BTW no idea where that graph I included above went so I am reattaching:

 

[RT2MD]

Awesome, thanks so much for the reply!

 

[periopdoc]

Just wanted to say that I am really enjoying this thread.

to RxBoy.

-pod

 

[jetproppilot]

Oh, ok. I think that I was making your question more difficult than it actually was.

What you are really saying is that, in the event of a decreased Hgb, as long as you replace fluid (up to a point) to maintain isovolemia (and therefore output), the tissues are still able to undergo aerobic metabolism b/c there is still adequate oxygen content in the arterial blood. In addition the lower viscosity of the blood also will help increase cardiac output. Also, if you transfuse too early, you can actually hinder your CO due to increased viscosity/after load. Using a venous saturation to guide your transfusion threshold is the way to do it. Is that *somewhat* correct? Does that mean that you (anesthesiologists in general) are frequently drawing SvO2s on patients with large amounts of blood loss to guide transfusion therapy?

I know that when we had ECMO patients, we had a sat monitor on the venous side as an indicator of oxygen delivery... you know, SvO2 goes down = a decrease in o2 delivery. Either a pump problem, increased metabolic needs, or a membrane problem. Having one of those monitors on a patient without extra corporeal circulation might be a bit difficult, though!

I realize that the threshold for transfusion has decreased - allowing for more severe anemia in some cases before transfusion takes place... but the point on viscosity counteracting increased O2 carrying capacity seems backwards to me. I would think that the increase in Hgb, and therefore O2 carrying capacity would make up for an increased viscosity causing lower CO at a moderately lowered Hgb (like around 9 or so, for example)... I know that a Hgb of 9 doesn't necessarily show need for transfusion, though. I guess that's one of those things that will seem counter intuitive to me.

Thanks for the discussion, by the way... I love the level of phys knowledge that anesthesiologist need to have. I just think of that whenever somebody tells me "How can you be interested in anesthesia?!?!?! It's so... BORING." I just smile and reply "To some people it might seem that way... but it's not!"

Nicely done man. Both posts.

 

[jetproppilot]

Nice to spark your interest. You are absolutely correct except there are still some anesthesiologists who follow Hgb which really is a very poor indicator of tissue oxygenation.

Hgb is just a concentration (g/dL) so for example if someone had a hgb of 9 and bleed out 1 liter and instantly after you drew a hgb, your hgb will still be 9 g/dL. Its only after renin-angiotensin-aldostorone activation that hgb concentration will drop (without fluid rescitation) as your extravascular fluid shifts to the intravascular compartment. This could take 6 hours! So the more important parameter is to increase CO first. So in the example above, if someone losses a liter during surgery and 1 hour later the hgb has not budged, you actually have done a very poor job resuscitating (the patient needs fluid).

SvO2 is a much better marker. One way to measure svo2 is with a pulmonary catheter (swan ganz), it can continuously measure svO2 however highly invasive. A much easier approach is to sample a venous gas from a central line (ScVO2) and compare that to your pulse ox (an estimate of SaO2). Although ScVO2 is not a true SVO2, the change is very little (+/- 5% depending on anesthetized vs. awake). So I send off a ScVO2 all the time when I have acute hemorrage and want to know my tissue oxygenation status. I sometimes send off a lactic acid as well. ABGs should not be used to guide fluid management, they should be used to guide hypoxia/ hypercaria or acid/base. VBGs (particularly SvO2) are much more useful for tissue oxygenation.

SvO2 is a little tricky with sepsis though. In severe sepsis it actually increases. This due to the relationship.
VO2 = DO2 x ER
And sepsis is odd because it doesn't effect your oxygen delivery but rather your oxygen extraction. The theory is that bacterial toxins inhibit mitochondrial oxygen utilization. Therefore because the body is unable to use oxygen, the SvO2 increases so the tissue oxygenation suffers even with a normal oxygen delivery. Cyanide poisoning does something similar.

BTW no idea where that graph I included above went so I am reattaching:

Nice thread dude. Thank you.

 

[RxBoy]

Just wanted to say that I am really enjoying this thread.

to RxBoy.

-pod

Nice thread dude. Thank you.

Thanks guys. Having periopdoc the CT specialist compliment me is a honor. And of course JPP compliments speaks for itself.

 

[RT2MD]

Nicely done man. Both posts.

Thanks, man... but the bigger props to RxBoy (who is undoubtedly much busier than I, yet still took the time to have that discussion).

SDN Anesthesia rocks.