Bradycardia discussion

[Ronin786]

An increased BP in the setting of bradycardia isn't always something to cheer for. Especially if it's not a sinus rhythm.

A) If your HR goes from 100-50, you've just dropped your CO in half. Your SV would have to increase by a factor of two in order to maintain the same CO. Even if it's diastolic dysfunction and you're getting more atrial kick, that's not going to equal 50% of your SV. If your HR goes from 50-40, you've just dropped your CO by another 20%. At some point in time, increased filling time will not result in increased CO.

B) Hypertension with bradycardia isn't necessarily a sign of good perfusion. The body's compensatory response for the diminished CO is extreme vasoconstriction. That good BP could be at the expense of worsening perfusion.

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[chocomorsel]

When you have sepsis induced vasodilation is your preload reduced? Yes
How about rapid AF? Dehydration? Acute blood loss? A combination? Preload reduced. How often do you see those conditions?

Its not as simple as "give more fluid" you have to deliver that fluid from the vasoplegic pulmonary and systemic vascular system to the heart. Have you ever seen someone volume overloaded in sepsis who is hypotensive? Why dont they just give more fluid?

The venoconstriction with neo is greater than the afterload increase, your getting more blood out overall which is why the CO increases in preload dependent situations - which are a LOT of situations, i would argue MOST

In sepsis, we are not just talking about preload problems. We are also often talking about contractility problems.

And in an already weak heart, increasing preload may not necessarily get you increased SV or CO. That preload has to be pumped out effectively by the contractility of the heart. This whole increased preload thing may work well on a patient with a good strong heart since it shifts the Frank Starling curve.

Like you are saying about the overloaded septic patient, increasing both their preload and afterload over a long period of time, without doing anything to augment their contractility is going to lead to worsened symptoms if they have septic cardiopmyopathy. We are not just talking of the few hours we have them in the OR. We all know they need pressors often for days at a time. Of course, not every septic patient has poor contractility.

Just because you increase preload doesn't necessarily mean you increase CO. Maybe intensivists are working under the premise that these septic patients also have cardiomyopathy. Not often the case in everyone but it's not like everyone gets an echo either.

 

[chocomorsel]

The point is you want a reasonable MAP and a reasonable HCT to ensure adequate oxygen delivery to tissues.

Getting fixated on MAP 58 vs 62, Levo vs Neo, or HCT 21 vs 25 and the outrage of the blood bank over such a crime - get over it. Make the vitals look good and make sense for the clinical situation, we should all be good at achieving that.

Dont be scared to give BP medicine or give blood or give pressors which the text book may not agree with to achieve that

I do not think its super important HOW you achieve your desired vital signs when it comes down to such nuances as levo vs neo, Hr 40 vs 60, keep the big picture in mind

But there is evidence that low MAPS do often lead to AKI that we may not see in the OR. So higher is better.
But if you want a HCT of 25, that's your comfort zone and you aren't worried about a transfusion complication, knock yourself out.

Interestingly enough, I was just watching a lecture this morning about transfusion study conducted in severely Anemic kids in East Africa with a HGB of 4-6. Anemia is very common in Africa due to Malaria, and SS and other Hgb diseases. .
Anyway, the restrictive group who didn't get immediate transfusion actually did better overall. As did the kiddos who got lower cc/kg of blood. And giving the same cohort blood when they had a fever increased their mortality. How interesting.

 

[anbuitachi]

But there is evidence that low MAPS do often lead to AKI that we may not see in the OR. So higher is better.
But if you want a HCT of 25, that's your comfort zone and you aren't worried about a transfusion complication, knock yourself out.

Interestingly enough, I was just watching a lecture this morning about transfusion study conducted in severely Anemic kids in East Africa with a HGB of 4-6. Anemia is very common in Africa due to Malaria, and SS and other Hgb diseases. .
Anyway, the restrictive group who didn't get immediate transfusion actually did better overall. As did the kiddos who got lower cc/kg of blood. And giving the same cohort blood when they had a fever increased their mortality. How interesting.

did they discuss why? was it due to transfusion related reactions? AKI? or other?

 

[coffeebythelake]

The point is you want a reasonable MAP and a reasonable HCT to ensure adequate oxygen delivery to tissues.

Getting fixated on MAP 58 vs 62, Levo vs Neo, or HCT 21 vs 25 and the outrage of the blood bank over such a crime - get over it. Make the vitals look good and make sense for the clinical situation, we should all be good at achieving that.

Dont be scared to give BP medicine or give blood or give pressors which the text book may not agree with to achieve that

I do not think its super important HOW you achieve your desired vital signs when it comes down to such nuances as levo vs neo, Hr 40 vs 60, keep the big picture in mind

I want MAP 50-60. I want HR 90-130. I want Fio2 as high as it can be and HCT > 25 at least

What is a reasonable MAP? What is a reasonable HCT? You seem to love phenylephrine (I love using it too) but it isn't a cure-all.
You come up with arbitrary numbers, make blanket statements, try to convince others you are right with non-evidence based medicine, while declaring you are trying to keep the "big picture in mind". Sounds more like you "heard someone do it before" and "that's what I do all the time".

This is the thinking of the surgeon/intensivist. This is the book answer.

Where you trying to make an offhanded remark that your answer is better? If so that is incredibly pretentious

If I have someone under 1 MAC of anesthesia with SBP 160s and a HR of 40, they are getting hydralazine or a nitroglycerin like medication, to achieve both the goals of lowering the SBP and increasing HR.. This combo of HTN and bradycardia could mean an intracranial injury

I'm still waiting for your "big picture" explanation for how giving a cerebral vasodilator like nitroglycerin to a patient with intracranial injury and cushings reflex is going to make things all better.

 

[chocomorsel]

did they discuss why? was it due to transfusion related reactions? AKI? or other?

It was 30 minutes and I may have skipped over about 5-8minutes of it when all the graphs started popping up. I wanted the meat. Don’t remember them discussing AKI or transfusion reactions. But it’s in the NEJM. See if I can find it. They occasionally had to halt the study due blood shortage though.
Amazing how the human body adapts in extreme situation.