Randomised clinical trials in cardiogenic shock in the PCI era
Treatment considerations for patients with AMI-cardiogenic shock
Enrolment data for major randomised cardiogenic shock trials (EuroIntervention 2021; 17: 451-65)
Determination of the Society for Cardiovascular Angiography and Intervention (SCAI) Shock stage using the revised SCAI Shock Classification
Conceptual model showing the overlap between
different states of hemodynamic compromise. Shock is defined by presence of hypoperfusion; most, but NOT ALL, patients will also be hypotensive. Pts w hemodynamic instability who do not meet criteria for shock are labeled as pre-shock
Management algorithm for patients with or at risk for cardiogenic shock (CS) tailored to the Society for Cardiovascular Angiography and Intervention (SCAI) Shock stage
Framework of clinical parameters to follow in patients with heart failure-related cardiogenic shock in the critical care unit
Considerations for invasive hemodynamic assessment in HF-CS
It seems that the most controversial issue is the use of short-term mechanical circulatory support for cardiogenic shock. So, a very recent publication deals with this:
Proposed overview of selection of patients to pVAD based on SCAI shock class A-E
Flowchart to identify and handle potential need for escalation of mechanical circulatory support in patients supported by axial flow pump (AFP)
Flowchart to identify and handle potential need for venting during V-A ECMO support
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IKYK that: i) blood pressure (BP) is the driving force for organ perfusion, but ii) hypotension does not always lead to hypoperfusion
One of my favorite reviews (PMID: 34392972) tries to reconcile the paradox and expand on the topic:
Fact:
Although an abundance of cohort studies have suggested an association between hypotension & unfavorable outcomes, several RCTs have failed to demonstrate consistently improved outcomes from maintaining a higher BP
Back to basics:
Arterial blood pressure is the result of multiple hemodynamic parameters:
When you prepare for the "average" intubation (no cardiac arrest, no active emesis), how do you pre-oxygenate the patient?
In PREOXI, a multicenter, randomized trial conducted in 24 🇺🇸 EDs and ICUs and published in 2024 (PMID: 38869091), 1,301 critically ill adults were randomly assigned to receive preoxygenation with either noninvasive ventilation (NIV) or an oxygen mask (O2M)
Hypoxemia (defined by O2 sat < 85% during the interval between induction of anesthesia & 2 minutes after tracheal intubation) occurred in 9.1% in the NIV group & in 18.5% in the O2M group (difference, −9.4%; 95% confidence interval [CI], −13.2 to −5.6; P<0.001)
For the average RSI - rapid sequence intubation (no cardiac arrest, no active emesis), do you provide bag-mask ventilation between induction and laryngoscopy (I & L)?
RSI flow(s):
In PreVent, a multicenter, randomized trial conducted in 7 academic 🇺🇸 ICUs and published in 2019, 401 critically ill adults were randomly assigned to receive either ventilation with a bag-mask device (BMV) or no ventilation (NoV) between I & L
In a multicenter study of 283 acute heart failure patients, changes in renal filtration markers (cystatin C or creatinine) with aggressive diuresis were not associated with changes in markers of renal tubular injury (NAG, NGAL, or KIM-1)
In this aggressively diuresed population (560 mg iv furosemide -> urine output of 8425 mL over 72h), both worsening renal function & increases in tubular injury biomarkers were not associated with adverse outcomes; rather, there was a trend towards improved outcomes
The data suggested that the small-moderate ⬇️in GFR that commonly occur during aggressive diuresis, colloquially referred to as "bumps in creatinine", may not primarily be a manifestation of renal tubular injury; rather, they represent clinically benign changes in filtration
Ten things that -for no good reason- we don't do in the ICU:
OK, in general a "less is more" approach is reasonable & there is a "rationale" behind many of the following but the truth is that they don't make sense if scrutinized
Here it begins:
1. Holding tube feeds or
any type of nutrition, because the glucose is "high"...
I see it often when I do morning rounds; the tube feeds were held at 2:00 am (and never restarted) because glucose was 400. Obviously, the right approach is to adjust the insulin regimen and keep feeding the patient.
2. Not starting or stopping TPN because the patient is bacteremic/septic...
Does this mean that if a patient cannot be fed enterally and remains bacteremic for 5-7 days (not uncommon scenario in S. aureus bacteremia), she cannot have any caloric intake for a week? 🤷♂️
77 yo patient admitted to the ICU from a nursing home w hyperglycemic-hyperosmotic state & acute kidney injury. On day 6, he spikes a temp 38.3. BP 96/59, HR 110/min. UA suggestive of urinary tract infection. The next day, urine culture grows Enterobacter cloacae
A day later, the blood culture grows Gram (-) rods (eventually proven to be the same bug). The susceptibility profile is:
You discuss with the team about treatment options: