Female, 40y old, works as a waiter in a bar.

Past Medical History:
Raynaud disease since 3 y, previous subclavian artery thrombosis (treated with stenting).
No previous hospital admissions.
No medications.

Recent Medical History:
Intermittent fever since a week, worsening dispnoea.
A few hours before, admitted to the E.R. with dispnea, hypotension, mottled skin, acrocianosys.

ECG: Atrial Fibrillation, suspected anterior STEMI (V1-V4 ST elevation)
Chest X-Ray: bilateral pleural effusion, pulmonary congestion
BGA: pH 7.42, PaCO2 22mmHg, PaO2 205, HCO3- 14.3, Lactates 4.4 mMol/L
Biochemistry: Mild elevation in myocardial enzymes; WBC 13160 /mm3, D-Dimer 1000 mcg/ml
Transferred to the Coronary Care Unit. You are the hospital Medical Emergency Team
called to attend the lady due to further hemodynamic deterioration

These are the available vital parameters at your arrival:

The patient is clearly in a profound state of shock. Septic shock, Massive pulmonary embolism, and Myocardial Infarction with severe systolic dysfunction or mechanical complications are considered in the differential.

High dosage epinephrine i.v. infusion (0.3 mcg/Kg/min) is initiated, and a FoCUS exam yields the following findings:

Q: According to the shown Apical 4 Chamber (A4Ch), Parasternal short axis (PSAX), and subcostal Inferior Vena cava (SIVC) views, what is the overall FoCUS pattern? What is the pathophysiology underpinning this shock state?

A: FoCUS findings speak to a dramatic acute biventricular dysfunction, without remarkable signs of chronic cardiac disease (no major dilatation or hypertrophy of the LV, no hypertrophy of the RV, no dilatation of the atria), absence of pericardial effusion, caval plethora.
The pathophysiology of shock is cardiogenic, i.e. biventricular failure. Septic shock is ruled out due to the absence of a hyperdynamic pattern and the presence of systemic venous congestion (not expected in non volume resuscitated septic shock at presentation).
Massive pulmonary embolism is ruled out based on the absence of acute cor pulmonale.

The patient is quickly transferred to the ICU, invasive arterial pressure monitoring is established, and intubated, with increasing vasopressor support. She is finally put under hemodynamic mechanical support with peripherally inserted V-A ECMO:

Please note in the video clip how the aortic valve does not open (Parasternal long axis view, PLAX), due to poor LV contractility and insufficient LV unloading. Also note in the subcostal inferior vena cava view (SIVC) the presence of the ECMO venous cannula.

Subsequent coronary angiography and endomyocardial biopsy finally ruled out coronary artery disease, and allowed a lupus-associated myocarditis to be diagnosed.