You can read about shock all day. You can memorise the four phenotypes, draw the haemodynamic diagrams, recite the SSC bundles. None of that matters if the first time you see a septic patient transition from warm to cold shock is on a real transport at two in the morning with a 90-minute flight ahead of you. That is what simulation is for. Not to test you. To let you fail safely, recognise the patterns, and build the clinical reasoning that works under pressure. We have built a complete simulation pack for the Shock Module. Five scenarios. Each one comes in two formats: a Relaiti 360 / iSimulate scenario file (.isims) that you can import directly into the app and run as a live vital signs simulation, and a tabletop discussion document (.docx) designed to be worked through as a group with a facilitator. The five scenarios: SHOCK001 — Septic Shock: The Warm-to-Cold Transition. A 72-year-old with urosepsis who starts as textbook warm shock and then transitions to cold shock mid-scenario. The group has to recognise that this is myocardial depression, not fluid overload, and adjust their vasopressor strategy accordingly. The metformin on the medication list forces a discussion about lactate interpretation. SHOCK002 — Cardiogenic Shock: The Post-STEMI Fluid Trap. A 58-year-old anterior STEMI where the sending ED has given a litre of fluid for the low blood pressure. The patient now has elevated JVP, bilateral crackles, and worsening hypotension. The group has to identify that the fluid was the wrong treatment, withhold further volume, and manage the oxygenation spiral from iatrogenic pulmonary oedema. SHOCK003 — Obstructive Shock: Tension Pneumothorax in the Ventilated Patient. A 42-year-old trauma patient, intubated, ICC in situ, stable on departure. Twenty minutes into a fixed-wing transport the ventilator starts alarming. The group works through DOPES, identifies the tension pneumothorax clinically without imaging, and decompresses. The teaching point: positive pressure ventilation converted a simple pneumothorax to tension through a blocked ICC.

Hi Folks, The youtube channel is live, intro uploaded. Watch this space for more.https://www.youtube.com/channel/UCeaULA8__gjkupQ-TX1UfZQ

You are transporting a patient with anaphylactic shock who has received three doses of IM adrenaline 0.5 mg with minimal response. Their MAP is 38 mmHg. Using receptor pharmacology and pharmacokinetics, explain at least three reasons why IM epinephrine may be failing, and describe your complete escalation strategy including route, dose, preparation, adjuncts, and monitoring. To refresh your knowledge on this chekc out the vasopressor pharmacology section out.

I watched a YouTube video recently that changed how I think about ARDS, compliance, and driving pressure. Since diving into the world of critical care , I carried a simple mental model. ARDS was a diffusely stiff lung. Low compliance, hard to inflate, treat accordingly. That picture made sense from the ventilator side. But the CT tells a different story. What looks like a uniformly stiff lung is actually a patchwork. Dependent regions are collapsed or consolidated, while the non-dependent lung remains relatively aerated. Compliance isn't low because everything is stiff. It's low because only a fraction of the lung is actually open. The images that changed this for me were from the same patient, same CT slice, just at different airway pressures. At low PEEP, around 5 cmH₂O, most of the posterior lung is dense and non-aerated. Blood is still flowing through it, but no gas exchange is happening. That's your shunt. What's left is a relatively small anterior portion of lung actually taking the breath. That's the baby lung. Not physically smaller, but functionally reduced. And the ventilator doesn't know that. It's delivering a tidal volume calculated for a full-sized lung, but that volume is concentrating into a much smaller aerated region. That's where the stress lands. At higher pressures, the same lung starts to open. Dependent regions recruit. The functional size increases. The example I'm referencing used pressures around 45 cmH₂O to demonstrate maximal recruitability — that is not a clinical target. The point isn't the number. It's the principle: some of that lung is recruitable, and PEEP is about finding the balance between opening what's closed and overdistending what's already open. In practice, how we find that balance is by watching driving pressure as we titrate PEEP. If driving pressure falls as PEEP increases, the lung is recruiting and compliance is improving. If driving pressure rises, we've likely overdistended the open lung and gone too far. That's your signal to back off.

Hey all, have began to compile exams - check out the Exam centre in the classroom for more info - Exam content is based around the ISBC CCP-FP exams, Ontario Jurusprudence exams and Ontario ACP exams. Happy prepping !