What is a curare cleft?

Receptor Physiology

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In this episode of the FOAMfrat Podcast, we sit down with Joe Hylton, one of the go-to ventilator educators in critical care transport, to break down APRV in a way that actually makes sense. We move beyond surface level explanations and get into how APRV really works, why it is so effective for ARDS and severe hypoxemia, and how volumetric capnography can give you real-time physiologic feedback when titrating mean airway pressure and PEEP. This is not a “set it and forget it” APRV discussion. We dig into the mechanics, the physiology, and the bedside decision making that matters in transport and critical care environments. Topics covered in this episode: • How APRV differs from conventional pressure control ventilation • Why mean airway pressure is the real driver of recruitment • Using flow curves and time constants instead of guesswork • Volumetric CO₂ vs end-tidal CO₂ and why the difference matters • Identifying optimal recruitment and overdistension in real time • How VĊO₂ trends can guide PEEP and pressure adjustments • APRV pitfalls, misconceptions, and when paralysis may still make sense • Practical APRV setup on Hamilton ventilators for transport teams If APRV has ever felt like ventilator voodoo, this episode pulls the curtain back and ties the mechanical settings to what is actually happening at the alveolar and capillary level. Joe brings deep experience from working with Hamilton Medical systems, and the discussion is framed through real-world transport and ICU decision making, including insights relevant to teams like Life Link III and other critical care programs. This episode is ideal for: • Flight paramedics and critical care transport clinicians • ICU nurses and respiratory therapists • Medical directors and educators • Anyone who wants to understand APRV beyond memorized settings 🎧 Listen, learn, and rethink how you approach lung recruitment. Subscribe for more high-yield critical care and EMS education from FOAMfrat.

In this episode of the FOAMfrat Podcast, Dr. Harrison Brookeman joins the discussion to examine methemoglobinemia and the emerging prehospital threat of sodium nitrite ingestion. Often viewed as a rare toxicology concept, this condition is appearing more frequently and can progress rapidly with devastating consequences if it is not recognized early. The episode focuses on what matters most to EMS clinicians in the field: the physiology of methemoglobinemia, why these patients appear profoundly hypoxic despite adequate ventilation, and the classic clue: a pulse oximetry reading that remains fixed around 85 percent regardless of oxygen delivery. The conversation also addresses iatrogenic causes such as benzocaine exposure, expected mental status changes, and why oxygen alone does not correct the problem. Emphasis is placed on prehospital decision-making, including early involvement with poison control, transport destination considerations, and the importance of ensuring these patients are taken to the right facility the first time. This episode is intended to sharpen recognition, improve pattern awareness, and prepare providers for a call that does not follow typical respiratory failure patterns.

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Infants can develop elevated levels of methemoglobin, a form of hemoglobin that can’t carry oxygen. The result is a slate-blue color that doesn’t improve with supplemental oxygen. Instead of obvious respiratory distress, these babies often show up with nonspecific clues like fussiness, poor feeding, or unusual fatigue. One of the big triggers is nitrate exposure, especially when formula is mixed with contaminated well water. Certain medications and rare enzyme deficiencies can do it too. If you see persistent cyanosis with clear lungs, a normal cardiac exam, and an SpO2 that won’t budge, think methemoglobinemia. Early recognition and treatment with methylene blue can be lifesaving. Always keep blue baby syndrome on the radar.