When flow dyssynchrony occurs in VC modes, the first reaction is often to increase the flow rate. Reasonable… but it often fails! Why? Maybe because any fixed (or fixed decelerating) flow can have trouble matching the patient effort at all stages of inspiration. Example:
Here the flow starvation occurs in the latter part of the breath, not the start, creating a biphasic appearance to the flow curve. What if we simply increase the flow?
It’s no better! Now flow is probably too high at the start (initial flow overshoot as evidenced by the steep pressure spike)… but still inadequate at the end. Also, the pressure spike and resulting short I-time contributes to some double triggers.
Solution? Switch to a variable-flow mode, ie with a pressure limit (PC, PS). Flow now can change during the breath to match the curve of effort.
Start with increasing the flow in VC, but with significant effort, this is usually what you’ll need!
A patient suffers STEMI causing biventricular failure, including severe RV infarct. An Impella is placed, and they arrive in the ICU from the cath lab. You see the following. (This arterial line is functioning.)
In this case, the Impella is completely decompressing the LV and taking over its output. There is NO pulsatility to the arterial flow — only laminar flow from the Impella. Can you think of any implications of this for the immediate resuscitation?
1. PULSE oximetry will not function. Absorption or reflection oximetry relies on detecting pulsatility to differentiate arterial blood from other blood and tissues (that’s why it gives you a pleth). You will need to rely on blood gases.
Michae Levy on refractory VF: resuming immediate compressions after a defibrillation shock may in some cases induce refibrillation after initial (unnoticed) ROSC, due to the mechanical stimulus. #CCPRFSummit2021
Double sequential defibrillation may work, but just changing the vector (moving pads) may work as well.
Daniel Dante Yeh: In first 7 days of critical illness., hypocaloric (<70%) nutrition should be used, can advance to 80-100% after day 3. Use indirect calorimetry if you can. #CCC50
Use high-protein, hypocaloric feeding in obese patients to preserve lean mass while not overfeeding. If 30-50 BMI use 11-14 kcal/kg actual bodyweight, if BMI >50 use 22-25 kcal/kg of ideal bodyweight.
Generally use normal protein goals for kidney failure. If on CRRT, however, need to account for loss of aminos in the membrane, may be ~15-17%.
John Teerlink: Cardiac calcitropes (catecholamines, PDE3 inhibitors) increase contractility, ischemia, arrhythmias, mortality. We use them anyway because it's what we've got. #CCC50
OPTIME-CHF: Milrinone for CHF exacerbation when NOT requiring inotropes. No clinical benefit but trend for more MI/death and significant increase in arrhythmias and hypotension.
OptimaCC: epi vs norepi in cardiogenic shock in MI: no difference in change in cardiac index, but discontinued for harm in epi group (tachycardia and increase in refractory shock). So maybe use norepi?
Xavier Monnet: CNPN doesn't work for fluid responsiveness because it ignores the shape of the Starling curve, which varies by patient. You can't get the intersection of two lines if you don't know one of them. #CCC50
"Mini" fluid challenge (100-150ml) avoids as much overload if it proves negative, but requires very sensitive markers of cardiac output. Maybe pulse counter analysis...
PPV, SVV Uses the respiratory cycle as an intrinsic fluid challenge. Automatically measured by some bedside monitors. No good in arrhythmias, spontaneous breathing, low lung compliance or tidal volumes (eg ARDS), so only works out in about 20% of ICU patients.