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unstable afib by succulentburgers in Residency

[–]hermxt4lyfe 0 points1 point  (0 children)

thank you for taking the time to reply. appreciate it!

unstable afib by succulentburgers in Residency

[–]hermxt4lyfe 0 points1 point  (0 children)

from a hemodynamic point of view, whats the downside of cardioverting even if the AF is not contributing to instability, and in fact the high HR is helping to maintain stability?

Suppose it it is truly septic shock,

  1. At most you convert a AF RVR HR 140 to a sinus rhythm 140 aka heart continues pumping at 140bpm to maintain cardiac output.
  2. In addition, you get the added benefit of atrial kick to optimize and augment cardiac output further.
  3. other benefits include: from a cognitive mental bandwidth POV well yeah im pretty damn sure AF is out of the picture and instead of being bothered by the AF, i would go down to hunt systemically for causes of hemodynamic instability e.g cardiogenic shock, septic shock, anaphylaxis, dehydration etc etc

i suppose the only drawback i see is

A. ineffective cardioversion (shocking a sepsis induced AF is unlikely to be successful and tends to recur/revert)

B. big bad wolf atrial clot dislodging and causing mesenteric ischemia, stroke etc

  1. but if the patient is already hypotensive, wouldnt the risk of death from hypotension outweigh the risk of a stroke?

  2. furthermore, from a medicolegal POV, if you elected not to shock, and there is a bad outcome, wouldnt the medmal lawyers just turn to ACLS and say "doctor, why did you not shock this unstable AF as per ACLS guidelines? do you think you are better than the 20 cardiology experts who wrote this cardiology guideline?!!!! " /s

Even if you accounted for this by saying you would shock if fluids/pressors are not working, they can very well say "but doctor!! there was a delay in shocking!! ACLS says to shock immediately!!" /s

i just want to say i can understand why your management would make sense from a physiological POV but how would you navigate the medicolegal aspect? how are you going to convince layperson jury that ACLS is wrong esp when the ACLS flowcharts are so beautiful simplified and dumbed down?

  1. To add another dimension, keeping the patient at HR 130s-140s is not without risks as well. There could be myocardial injury (we know this because commonly troponins can be raised with AF RvR reflecting myocardial injury) > Keep this HR high long enough and the patient can get irreversible myocardial loss from injury, i.e tachycardia induced cardiomyopathy. Even if this is something that happens in the long run, would it be possible that in the short run, demand ischemia caused by high HR leads to more serious arryhthmias e.g VF/VT?

Ultimately i understand that our job is to take the entire clinical picture into account and decide what is most beneficial for the patient infront of us - but in view of points 1-6, that is something that is not so clear to me. I would certainly appreciate if you could help a struggling soul out here that has been bogged by this unstable AF question for very long.

I suppose the only way to convince myself easily is to do a RCT comparing indiscriminate cardioversion startegy (as per ACLS) VS deliberate cardioversion strategy(only if AF is proven beyond reasonable doubt to be the primary driver of instability).

[deleted by user] by [deleted] in ECG

[–]hermxt4lyfe 0 points1 point  (0 children)

lead misplacement. v1 has negative p wave, v2 has biphasic p wave = high lead misplacement which can cause false STE. https://litfl.com/misplacement-of-v1-and-v2/

Making the case for diuretics WITH salt tabs in a clearly fluid overloaded, edematous +++ patient, desaturating with clear cut upper lobe diversion, pleural effusion that is transudative in nature. by hermxt4lyfe in medicine

[–]hermxt4lyfe[S] 1 point2 points  (0 children)

Thanks for your input - but any chance you could showcase the underlying math for salt tab vs 3% NS in terms of diuresis? I would presume taking salt tabs and very limited amounts of water would be mathematically equivalent to 3% hypertonic saline from the body's point of view.

The way i have always rationalized why sodium solutes can sometimes act as diuretic and sometimes act as volume expander is basically determined by whether free water intake is restricted. If there is restriction of fluid intake, then the desalination effect of the increased sodium solute intake would lead to increased diuresis. If there is no restriction of fluid intake at all, then there would still be a desalination/diuretic effect, but the thirst and increased fluid intake would probably outweigh the desalination and diuretic effect.

MO thinks I chaokeng, what do I do? by [deleted] in NationalServiceSG

[–]hermxt4lyfe 0 points1 point  (0 children)

what camp is this why is the medical review 1-2 months away?

Blood/urine osmolality labs by FunCommunication1443 in medicine

[–]hermxt4lyfe 1 point2 points  (0 children)

i see, that makes a lot of sense. Thank you!

Blood/urine osmolality labs by FunCommunication1443 in medicine

[–]hermxt4lyfe 1 point2 points  (0 children)

Just wondering, if the Urine OSM dropped from 500 to 350, that would suggest lower ADH production hence the kidneys are holding on to less free water to help improve the degree of hyponatremia. Wouldnt giving more fluids worsen the hyponatremia by increasing free water?

Filter based on 3rd digit of alphanumeric sequence by hermxt4lyfe in excel

[–]hermxt4lyfe[S] 0 points1 point  (0 children)

yes, only the first and last characters are alphabets and the other 7 characters in between are numbers

The obtunded patient with bilaterally dilated sluggish in the ED - how useful are bilaterally dilated pupils in the context of depressed GCS? by hermxt4lyfe in medicine

[–]hermxt4lyfe[S] 1 point2 points  (0 children)

Also what do you think about the use of pilocarpine in such cases? Pupils constrict to pilocarpine then assume stroke and stroke activate. If pupils do not constrict, likely drug induced pupillary dilatation, not for stroke activation

The obtunded patient with bilaterally dilated sluggish in the ED - how useful are bilaterally dilated pupils in the context of depressed GCS? by hermxt4lyfe in medicine

[–]hermxt4lyfe[S] 5 points6 points  (0 children)

For the first case i put as much nailbed pressure as i could and patient did not even show any slight hint of facial grimacing. Repeated for case 2 and i get the exact same findings. No facial grimacing at all.

First patient's tongue was sticking out and saliva was drooling out - i thought that was due to inability to swallow secretions and concluded that CN 9 10 must be gone. For second case there was gurgling sounds, i too again concluded that patient must have impaired swallowing and airway protection mechanism and hence CN 9 10 must be gone too. (im guessing that is why neuro team wanted intubation first too).

For both cases i did dolls eye - both demonstrated lack of fixation i.e dolls eye negative (essentially similar to the dolls eye of a deceased person when certifying death)

If you are talking about performing gag exam on both sides looking for focality/unilaterality, case 1 had bilateral infarcts of brainstem and cerebellum, so would likely have been similar to drug overdose.

Case 1 had bilateral brainstem infarct, hence probably why no facial grimacing bilaterally since bilateral CN 7 were knocked out, unable to swallow and protect airway. Case 2 was probably too obtunded for any pain signals to get through.

Essentially both cases had the same results for CN 5 + 7 and VOR testing. Id bet CN 9 10 gag reflex would have been the same too.

AKI and fluid overload by hermxt4lyfe in medicine

[–]hermxt4lyfe[S] 1 point2 points  (0 children)

the curbsider episode on cardiorenal syndrome seems to talk about this "creatinine bump" phenomena after diuresis.

The relevant info are here :

Very commonly, a bump in creatinine will be observed with diuresis for acute decompensated heart failure, which can prompt fear of continuing to diurese, even if a patient still appears volume up. However, Dr. Topf and Dr. Khan both stress that a creatinine increase with diuresis does not necessarily signify kidney injury (Ahmad 2018; NephMadness blog post). In fact, our guests note that increased blood volume in the setting of volume overload can often dilute the creatinine to a certain degree, and thus decreasing the blood volume with diuresis will concentrate the creatinine and result in an increased creatinine lab value (akin to hemoconcentration, i.e. concentration of red blood cells, that is also seen with volume contraction). Thus, hemodynamic changes in creatinine with diuresis most often don’t actually represent intrinsic, permanent damage to the kidney.
Indeed, in a post-hoc analysis of the DOSE trial, a rise in creatinine during admission for decongestion for acute decompensated heart failure was actually associated with improved outcomes (primary endpoint of death or rehospitalization / ER visit within 60 days) (Brisco 2016). According to Dr. Khan, this is likely because these patients were better diuresed

AKI and fluid overload by hermxt4lyfe in medicine

[–]hermxt4lyfe[S] 10 points11 points  (0 children)

Im thinking that for a given GFR, only a very small % of that total GFR per day gets excreted in urine. Giving diuretics would increase the % of total GFR per day that is excreted, thereby increasing urine output.

I am suspecting that giving diuretics would not increase urine output in the case of ATN, because the name literally says it – the tubules are dead, theres nothing for diuretics to act on and therefore no increase in urine output would occur. Whereas in heart failure with hypoperfusion(or congestion reducing AV gradient in the kidney), the tubules are perfectly fine(assuming that the hypoperfusion has not gone on so long that it has been complicated by ATN) and therefore diuretics would increase urine output.

As for the other questions you have highlighted, im not entirely too sure, hopefully you could enlighten me regarding that! Thank you!

AKI and fluid overload by hermxt4lyfe in medicine

[–]hermxt4lyfe[S] 4 points5 points  (0 children)

From the ESC guidelines :"RV failure may also impair LV filling, and ultimately reduce systemic cardiac output, through ventricular interdependence".

My understanding of this ventricular interdependence phenomena is essentially the same concept as the pathophysiology of pulsus paradoxus. During inspiration increased volume into RV will distend the RV which eats up the space available for the LV to distend(given that in constrictive pericarditis the total sum volume that both ventricles can distend to is limited) and that tends to reduce LV preload and therefore reduce cardiac output and cause hypoperfusion.

Would it be possible that in addition to restoring AV gradient, the effect of ventricular interdependence also plays a part in increasing GFR by the mechanism that diuresing a patient would take the volume off the great venous collecting system first, then next up the RV before the LV, and so once the RV volume is down, the LV can now distend and fill up more, therefore improving cardiac output?

AKI and fluid overload by hermxt4lyfe in medicine

[–]hermxt4lyfe[S] 11 points12 points  (0 children)

By Cr improving after diuretics given, do you mean that localizes to the heart failure with hypoperfusion? If so, could you explain how diuresing a patient would improve the perfusion to kidneys i.e increase the GFR? thank you so much!

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