Various permutations of assessing a central venous pressure surrogate (e.g. size and phasicity of the inferior and/or superior vena cavae), cardiac structure/function,  pulmonary parenchymal/pleural features and major extra-thoracic vessels and surrounding anatomy form the basis of most sonographic protocols utilized in shock. Analysis of the abovementioned afforded us the following information to guide decision-making at bedside:

• while lung sliding was reduced bilaterally it was universally present throughout each lung zone examined
  • argues against a tension pneumothorax as the source of the hemodynamic instability ⁵
•  the left ventricle had a normal global systolic function with no evidence of significant regional wall motion abnormalities
  • argues against acute LV failure as the precipitant
    • of note, acute aortic and mitral regurgitation cannot be readily excluded using this schema, as both often feature a hyperdynamic LV ⁵
• bilateral lung rockets usually suggestive of elevated LAP and raises the question of cardiogenic (i.e. left sided) etiologies to the shock state
  • however, their presence is expected in severe manifestations of COVID-19 pneumonia, and are therefore of marginal use in this regard
• the absence of a pericardial effusion makes tamponade as the proximate cause of shock unlikely 
• when present, end-systolic left ventricular obliteration is consistent with decreased ventricular filling secondary to decreased total (or stressed) intravascular volume or the vasoplegia of e.g. early septic shock ⁴
  • best appreciated from the parasternal short axis, which demonstrated a normal left ventricular end diastolic area (by visual estimate)
• septal flattening as a consequence of right ventricular volume and/or pressure overload results in a diminution of LV preload
  • its presence, therefore, implies some degree of hemodynamic significance
  • dilation of the right ventricle virtually ubiquitous in circulatory collapse due to massive pulmonary emboli

CT has far superior test characteristics to transthoracic echocardiography (bedside or formal) in the diagnosis of pulmonary embolism; in the absence of profound instability e.g. peri-arrest it should be sought expeditiously.

Shock with evidence of acute cor pulmonale in this patient was likely multifactorial, with major contributions from alveolar overdistension and VQ mismatch likely. Optimization of oxygenation (higher extrinsic PEEP) volume (diuresis), and respiratory mechanics (reduction in dynamic hyperinflation or "auto-PEEP") occurred over the following hours, with subsequent improvement in clinical status.