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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From: Cardiovascular Hemodynamics. An Introductory Guide. Arman T. Askari, Adrian W. Messerli. Springer International Publishing; 2019
CVP waveform (note: there is generally an electromechanical delay of ~ 80 msec between the atrial depolarization of the P wave & the pressure deflection of atrial systole represented by the "a" wave)
Intracardiac pressure waveforms derived from the pulmonary artery catheter
ICU stories (common): Middle-aged pt w hx of COPD was brought to the ED by EMS after SOB x 2 days. No fever or chest pain. Very quickly after ED arrival, he was intubated. CXR showed hyperinflated, “COPD” lungs. Here depicted in two images:
Post-intubation ABGs showed:
BP dropped post-intubation to 55/40; propofol was started & then discontinued due to hypotension. iv fluids (2L Lactate Ringer's) were started & patient was brought to the ICU w SBP in upper 80s. Re-institution of propofol led again to hypotension. What would be the next step?
ICU pictorials: A patient was admitted for "weakness". Unimpressive vitals / phys exam / labs. A few days later because of temp 101 F, a fever w/u was initiated. Due to "SOB", a CT chest angio was done:
👆Massive saddle PE extending in both sides w evidence of R heart strain
It seems that the textbook 👆 uses a sodium correction factor of < 1.0 mEq/L for every 100 mg/dL of Glu above 100 or applies the correction starting from a higher Glu level (probably 200 mg/dL?)
ICU stories (last night): A patient had been admitted w pneumonia / intubated / on norepi 0.12. At 01:00 am, the nurse notifies you that urine output is 5-10 cc/hr for the previous 3 hours. BP is 99/44, HR 90, CRT 3 sec. You take the US in patient's room to see what's happening.
What POCUS finding(s) is/are likely to explain the oligo-anuria in the shortest amount of time?
If you (and the patient) are lucky, you may find this: