I know you know them, but let’s remind ourselves of some additional basic hemodynamic "secrets":
16. Volume status is a nebulous term, but I don’t foresee stop using it anytime soon
17. The ultimate goal of hemodynamic management is adequate tissue perfusion (TP). TP may suffer even if the macrohemodynamic markers look good. This scenario is called “hemodynamic incoherence”. Sadly,
we don’t have yet a widely available, clinically useful, research-supported tool to monitor TP; it is the next frontier…
PS: Will it be capillary refill time?
18. Several patients with pulmonary edema don’t suffer from “excess total fluid volume”; they are actually “euvolemic”, but a sympathetic system surge leads to increased arterial tone (increased afterload) & fluid redistribution. Therefore, diuretics are not the answer;
non-invasive ventilation and afterload reduction are more helpful (and faster!)
I will rephrase: some patients with pulmonary edema can be treated without diuretics...
19. A patient can be at the same time both fluid-responsive and fluid intolerant. Sorry… 🤷♂️
20. Volume responsiveness is biventricular volume responsiveness; the left ventricle can eject only what it receives. Right ventricular failure is an important cause of insufficient left ventricular preload...
21. A hyperdynamic LV (“kissing” papillary muscles) on echo is not necessarily a sign of hypovolemia & should not reflexively trigger iv fluid bolus. Give yourself 1 mg of iv epinephrine and see what happens in your LV. Actually: don’t do it!
22. Right- and left-sided filling pressures may be discordant. A patient may have a wedge of 8 mmHg and a CVP of 20 mmHg or the other way around…
23. A patient can have venous congestion without any sign of peripheral edema. At all..
24. Patients on vasopressors can still receive diuretics for the right reason and with the appropriate monitoring!
25. When managing a patient with venous congestion: Diuretic drips are not more effective than diuretic boluses
Bonus info: there is no magical ingredient in bumetanide (Bumex in 🇺🇸)!
26. There is not such a thing as “max dose” vasopressors
This 👇is from a case earlier today:
27. The right ventricle is not important until it is!
28. LV outflow tract obstruction (LVOTO) should be suspected in any patient with shock refractory to vasopressors/inotropes, especially if you dial up the inotropes and the patient gets worse!
29. LVOTO and stress-cardiomyopathy are quite common in Critical Care; more common than you think! Please use #pocus
30. Hemodynamic monitors do not improve patient outcomes; sensible therapeutic interventions based on a combination of data points (including the ones provided by monitors) can improve outcomes
#foamed #foamcc #meded #MedTwitter
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I know you know them, but let’s remind ourselves of some basic hemodynamic "secrets":
1. Pressure ≠ volume, even though volume can affect pressure
2. CVP (central venous pressure) is not a marker of “volume status” since it can be affected by non-volume related disorders (eg, tricuspid regurgitation/stenosis, pericardial pressure etc)
Elderly 👴 w interstitial🫁disease was admitted -on NIV- from the ED to StepDown unit w "pneumonia": bil infiltrates/low-grade fever. PF ratio 140. Since I was in the ICU, I asked how he looked. Reply: needs high FiO2 but pulls good tidal volumes
When I saw him:
This is not an uncommon scenario: a "low" expired tidal volumes (Vt) makes the staff worried during NIV initiated for hypoxemic respiratory failure but a "high" Vt (even if accurately measured) is left unabated...
In fact, high Vt during NIV has been associated with NIV failure and poor outcomes
The American Thoracic Society (ATS) updated its recommendations on some aspects of the diagnosis and management of community-acquired pneumonia (CAP)
This guideline update focuses only on immunocompetent adult patients with a standard diagnosis of CAP
It addresses four clinically relevant questions:
The guideline underwent peer review by 16 experts (4 from ATS; 11 from Infectious Diseases Society of America (IDSA). It Is not clear to me why IDSA did not approve it. I copy from the supplement: "The IDSA chose to withdraw rather than approve the final version of the guideline"
Have you ever managed a septic patient & ordered antibiotics to be given stat only to discover hours later that they were still infusing? If yes, stay tuned
Among several controversies in sepsis management, the early administration of antibiotics
is one of the least debatable ones. Time is life in sepsis!
Even though it's hard to believe that every hr of delay in antibiotics ⬆️ mortality by 8% (this is a different topic...), it's one of my pet peeves when it takes for ever to give antibiotics to a septic shock patient
The most commonly ordered combination in 🇺🇸 hospitals (EDs/ICUs) is piperacillin-tazobactam (Zosyn in 🇺🇸) + vancomycin (V). If the usual practice is followed, giving a dose of Zosyn & a dose of vanco can take close to 3 hours. This should not be the case!
Is there anything regarding UGIB that has not been already done, studied or tweeted about? Not much, but all of the following are things I witnessed happening (or not happening…) in two UGIB cases I recently saw in the ICU
Here it begins:
1. If a patient does not have an obvious UGIB as in the clip above, she has just presented with melena & it is still unclear if this is due to upper or lower GIB, a quick & dirty trick is to check the blood urea nitrogen/creatinine (BUN/creat) ratio. There are various published
cut-offs in the literature (don’t sweat about them…) but, in general, a ratio of >30 suggests UGIB. This is due to the small bowel absorption/digestion of blood protein which is subsequently metabolized to urea. There are confounding factors, but the trick usually works well