USMLERx Question Discussion Thread

[mrmandrake]

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Hey guys,

I'm currently going through USMLERx with my classes and there are some issues I have with some of their questions. There really isn't any place to discuss these concerns so maybe we can discuss them here.

First question I have:
QID: 5033

USMLERx says the initial management of cardiac tamponade is IV fluids. I was thinking pericardiocentesis. Is the general consensus for IV fluids first?

Plenty more to come after this ...

 

[StIGMA]

Maybe check http://emedicine.medscape.com/ or uptodate.com first for these clinical questions that no-one at this level could have fruitful discussions about.

In general, you do NON-INVASIVE interventions before invasive interventions. Tamponade = decreased cardiac output. Increase fluids = more cardiac output. Stabilization before interventions = good.
http://emedicine.medscape.com/article/152083-treatment

 

[jaguar1]

I agree with you. IV fluids seems counter intuitive obviously because if given more fluids to increase stroke volume, the heart will simply be squished more by the fluids around it. pericardiocentesis is what I would think would be better and then treating the underlying cause of what caused the tamponade while replenishing fluids back if required!

Hey guys,

I'm currently going through USMLERx with my classes and there are some issues I have with some of their questions. There really isn't any place to discuss these concerns so maybe we can discuss them here.

First question I have:
QID: 5033

USMLERx says the initial management of cardiac tamponade is IV fluids. I was thinking pericardiocentesis. Is the general consensus for IV fluids first?

Plenty more to come after this ...

 

[unsung]

Hey guys,

I'm currently going through USMLERx with my classes and there are some issues I have with some of their questions. There really isn't any place to discuss these concerns so maybe we can discuss them here.

First question I have:
QID: 5033

USMLERx says the initial management of cardiac tamponade is IV fluids. I was thinking pericardiocentesis. Is the general consensus for IV fluids first?

Plenty more to come after this ...

Good idea to start a thread (as long as others contribute and keep it alive 😀). I'm not using USMLERX at this point. But, I might start it this winter break..

As for your Q, first thing that comes to my mind is, tamponade is
sort of like hypertrophic cardiomyopathy in that if there's decreased blood volume, there's a great chance of really low cardiac output (sudden death?)

Sort of like the same reasoning for why you wouldn't want to give diuretics to a person with HOCM.

So with tamponade, there's a similar danger 'cuz of the heart is basically being "squeezed" and prevented from filling as well. In which case, starting an IV and maintaining adequate volume prevents immediate heart failure/death.

Does that make any sense? 😕 It sort of does in my head..

 

[NoWayOut]

I haven't started Rx either but am planning to in a few days.
It does make a lot of sense though to give fluids if you think about it.
As some have commented here, it is an issue of cardiac output being low.
If you give fluids, then you increase the preload on the heart which will allow greater sacromere stretch against the force of pericadial tamponade pushing the heart inwards. That way maybe, it would be able to compensate somewhat for the loss in stroke volume.

 

[mrmandrake]

From UpToDate:

Early tamponade with only mild hemodynamic compromise may be treated conservatively, with careful monitoring, serial echocardiographic studies, avoidance of volume depletion, and therapy aimed at the underlying cause.

Tamponade with overt hemodynamic compromise requires urgent removal of pericardial fluid, which produces a rapid and dramatic improvement in cardiac and systemic hemodynamics [4] . Among patients with dyspnea, symptomatic improvement is common after pericardiocentesis, even if a few clinical or echocardiographic signs of tamponade persist [30]. Volume expansion with agents such as blood, plasma, dextran, or saline may be used, but only as a temporizing measure [21].

The question in USMLERx described a patient in cardiogenic shock. I would argue that this constitutes "overt hemodynamic compromise" and that USMLERx is wrong. Surgery is the way to go IMHO.

Remember that USMLERx questions are written by students so I think it would be a good idea to get together to discuss any issues we have with them.

 

[StIGMA]

I think the point of the question is that while pericardiocentesis is the definitive therapy, it is important to improve the patient's condition before this, which can be done by giving the heart more fluid to pump and restoring what may be lost from the tamponade. It is very quick and easy to hang a bag of fluid, while prepping a patient for pericardiocentesis will take a bit of time. So you hang the fluid while everything else can be set up. It is not definitive, but it is done first.

 

[mrmandrake]

Hey guys, quick question. USMLERx has this to say about COX-2 vs COX-1 inhibitors:

COX-2 inhibitors selectively decrease PGI2, leaving the action of TxA2 unopposed. This could well result in increased cerebrovascular and cardiovascular events due to the tonic, unopposed prothrombotic action of TxA2.

I have never heard of this before. As far as I know, COX-1 just found more in the GI tract or something like that. I never heard of COX-2 inhibitors not affecting the synthesis of TxA2. I couldn't find a reference to this information in UpToDate either. Anyone have anything to add?

 

[StIGMA]

Just from my lecture notes (dont have time to find a better source):

COX 1 is mostly constitutive in cells and involved in housekeeping functions (so when it is inhibited you get side effects). It produces TXA2, PGI2, PGE2.

COX 2 is mostly upregulated by inflammatory stimuli (it is inducible, not constitutive). It produces PGI2/PGE2 for inflammation.

The COX2 inhibitors also inhibit COX1 but to a far lesser extent. So why is TXA2 "unopposed"? I have no idea...

From (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1336714/):
The Biology
McAdam and colleagues have shown that the COX-1 antagonist ibuprofen causes a marked reduction in thromboxane A2 synthesis (as represented by the urinary metabolite 11-dehydrothromboxane B2). COX-2 inhibitors have a more modest effect on thromboxane A2 production. In contrast, they exhibit varying inhibitory effects on synthesis. When the biological effects are considered collectively, COX-2 inhibitors shift the balance toward preserved thromboxane A2 effects (platelet aggregation/vasoconstriction) and away from the protective effects attributable to prostacyclin (which include platelet inhibition, vasodilation, and resistance to inflammation).

Apparently COX2 affects thromboxane production, but compared to the effect on prostacyclins, the relative increase in thromboxanes leads to more cardiovascular effects. I think Rx is using poor phrasing... ie: thromboxanes are not "unopposed" just at a relative increase.

 

[kmed0]

I think it's mostly related to the fact that COX-2 is inducible while COX-1 is not. Because platelets do not have nuclei, they will only carry the constitutive COX-1 which is primarily responsible (in platelets) for making TXA2. Production of PGI2 is largely mediated by COX-2 from endothelial cells.

COX-2 inhibitors will thus prevent endothelial production of prostacyclin but not prevent platelet production of TXA2 --> tendency for platelets to aggregate --> hypercoagulable state

 

[mrmandrake]

Hey guys,

I came across a question in USMLERx that required you to know the normal reference ranges for total iron binding capacity and serum haptoglobin in order to make a diagnosis of anemia of chronic disease and rule out an autoimmune hemolytic anemia. Both of these lab values were not given on the "lab values" button.

Is this something I need to commit to memory for the boards? It's an easy question if I had the values in my head.

 

[dozitgetchahi]

Just from my lecture notes (dont have time to find a better source):

COX 1 is mostly constitutive in cells and involved in housekeeping functions (so when it is inhibited you get side effects). It produces TXA2, PGI2, PGE2.

COX 2 is mostly upregulated by inflammatory stimuli (it is inducible, not constitutive). It produces PGI2/PGE2 for inflammation.

The COX2 inhibitors also inhibit COX1 but to a far lesser extent. So why is TXA2 "unopposed"? I have no idea...

From (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1336714/):
The Biology
McAdam and colleagues have shown that the COX-1 antagonist ibuprofen causes a marked reduction in thromboxane A2 synthesis (as represented by the urinary metabolite 11-dehydrothromboxane B2). COX-2 inhibitors have a more modest effect on thromboxane A2 production. In contrast, they exhibit varying inhibitory effects on synthesis. When the biological effects are considered collectively, COX-2 inhibitors shift the balance toward preserved thromboxane A2 effects (platelet aggregation/vasoconstriction) and away from the protective effects attributable to prostacyclin (which include platelet inhibition, vasodilation, and resistance to inflammation).

Apparently COX2 affects thromboxane production, but compared to the effect on prostacyclins, the relative increase in thromboxanes leads to more cardiovascular effects. I think Rx is using poor phrasing... ie: thromboxanes are not "unopposed" just at a relative increase.

This is all correct - in fact, Goljan uses the "unopposed" phrasing in one of his lectures.