The FlightBridgeED Podcast

This episode provides an overview of cardiogenic shock and explains why it remains such a major problem despite decades of progress in treating acute coronary syndromes. Dr. Mike Lauria notes that while STEMI and other ACS outcomes have improved dramatically with better systems, PCI, and modern cardiac care, mortality from cardiogenic shock has stayed stubbornly high. A central theme is that cardiogenic shock is becoming more common, especially among more medically complex patients with chronic heart failure and prior cardiac disease, and that critical care transport teams are increasingly encountering these patients because so many require transfer to higher-level centers. 
A major focus of the episode is the modern framework for thinking about shock, especially the SCAI stages A through E, which describe cardiogenic shock as a spectrum rather than a simple yes-or-no diagnosis. Dr. Lauria emphasizes that this shared language helps clinicians identify patients earlier, communicate severity more clearly, and escalate care before they progress into multi-organ failure. Dr. Lauria argues that early recognition, rapid team-based decision-making, and transfer to experienced shock centers are some of the most promising ways to improve outcomes, particularly because late interventions often fail once the patient has already tipped into severe end-organ injury. 
From a transport perspective, the episode frames care around recognition, resuscitation, and retrieval. Clinicians are encouraged to identify deterioration early, support perfusion by maintaining MAP, optimize oxygenation and ventilation, think carefully about volume status, add inotropic support when needed, and pay close attention to whether existing mechanical circulatory support is truly sufficient. Just as importantly, Dr. Lauria stresses the logistical and systems side of transport: moving quickly but safely, anticipating equipment and oxygen needs, and advocating for the patient to reach the right destination the first time, especially if advanced support such as Impella or ECMO may soon be needed. 
Key points
 Cardiogenic shock remains a high-mortality condition even though outcomes for acute coronary syndromes have improved substantially. 
 It is increasingly common, especially among complex patients with chronic heart failure and prior cardiac disease. 
 The SCAI shock stages (A-E) provide a practical shared language for identifying severity and guiding escalation of care. 
 Early recognition, shock teams, and transfer to experienced cardiogenic shock centers may improve outcomes by preventing delayed intervention. 
 For transport teams, priorities include supporting MAP, optimizing oxygenation/ventilation, considering volume status and inotropy, checking device adequacy, and getting the patient to the right place quickly and safely.

This episode is an overview of acute right heart failure, with a strong emphasis on why the right ventricle is so vulnerable and why clinicians often miss its role in critically ill patients. Dr. Mike Lauria explains that, unlike the left ventricle, the RV is designed to pump against a low-pressure, high-compliance pulmonary circulation. That makes it especially sensitive to sudden increases in afterload, whether from pulmonary embolism, pulmonary hypertension, ARDS, sepsis, or other cardiopulmonary stressors. The result is that RV dysfunction can develop quickly and become a major driver of shock in transport, emergency, and ICU patients. 
A major theme of the episode is the “RV spiral of death”: as RV afterload rises, the right ventricle dilates, pumps less effectively, and begins to impair left ventricular filling by bowing into the septum. This lowers cardiac output, worsens systemic perfusion, and reduces blood flow to the RV itself, which further weakens the ventricle and accelerates hemodynamic collapse. The transcript also reviews practical clues that can help identify RV failure, especially in transport, including CT evidence of an enlarged RV, bedside echo findings such as septal flattening, an increased RV:LV ratio, reduced TAPSE, tricuspid regurgitation, and a dilated vena cava. 
Management is organized around a practical resuscitation framework: maintain systemic blood pressure, optimize preload, reduce RV afterload, improve contractility, and address the underlying cause. Dr. Lauria discusses norepinephrine as a first-line vasopressor, warns that extra fluid is often not helpful and may make things worse, and stresses the importance of correcting hypoxia and hypercapnia to reduce pulmonary vascular resistance. Inhaled pulmonary vasodilators, low-dose inotropes such as epinephrine or dobutamine, and avoiding unnecessary positive-pressure ventilation are all highlighted as useful strategies, while definitive therapy depends on the cause, such as thrombolysis for PE or disease-specific treatment for pulmonary hypertension. 
Key points
 The right ventricle is built for a low-pressure system and does not tolerate sudden increases in afterload well. 
 Acute RV failure is commonly triggered by PE, pulmonary hypertension, ARDS, sepsis, and other causes of increased pulmonary vascular resistance. 
 The RV spiral of death occurs when RV dilation, reduced LV filling, and worsening RV perfusion compound each other and drive shock. 
 Useful bedside clues include RV enlargement, septal flattening, abnormal RV:LV ratio, reduced TAPSE, tricuspid regurgitation, and a dilated IVC. 
 Management focuses on supporting MAP, being cautious with fluids, reducing RV afterload, adding inotropy when needed, and treating the underlying cause.

This week’s FAST Replay is a double feature! Two talks that tackle high-stakes medicine from completely different angles, but with the same underlying theme: thinking differently when the usual approach isn’t enough.

First up, Brittany Bernardoni takes us into the rapidly evolving world of Extracorporeal Cardiopulmonary Resuscitation (ECPR). From the limitations of conventional CPR to the growing use of ECMO in cardiac arrest, this session explores what may become the next major leap forward in resuscitation care. Brittany walks through the physiology, patient selection, timing, and the real-world programs already bringing ECPR directly to patients in the field.
Then, Elizabeth Garcher dives into one of the most intimidating areas in prehospital and critical care medicine: pregnancy-related emergencies. This talk focuses on “errors of omission.”  The treatments clinicians hesitate to give because of fear of harming the baby, even when delaying care, can seriously harm both patients. From airway changes and hypertensive emergencies to eclampsia, DKA, blood products, and seizure management, this session is packed with practical pearls and critical reminders for managing pregnant patients in the field.
Two completely different topics. Two incredibly practical talks.
One common thread: understanding the physiology well enough to act decisively when it matters most.

We’re continuing our FAST Replay series, bringing you full sessions recorded live from past FAST conferences as we build toward FAST26: Austin. This episode features Jeff Jarvis and covers a wide range of topics that directly address how we practice in EMS.
From trauma care to airway to cardiac arrest, this session walks through current position statements and evolving recommendations, including:
 Blood product use in trauma 
 How to approach traumatic (circulatory) arrest 
 Pneumothorax and chest decompression decisions 
 Postpartum hemorrhage and hypertension management 
 Airway timing and first-pass success 
 And where some of our long-standing practices don’t hold up to the evidence 
More than anything, this talk highlights a core idea: not everything we do in EMS is built on strong evidence, and we need to be willing to question and refine our approach as new data emerge.
FAST26 is coming to Austin this year on May 27 - 29, 2026. We are co-locating with EMS World Live, bringing together the entire EMS community with FAST26: Austin and EMS World Live Austin, giving you the very best of every possible aspect from basics to critical care to administration!
👉 Learn more or grab your spot at https://fbefast.com

This episode focuses on the critically ill patient with pulmonary arterial hypertension (PAH) and explains why this subgroup is especially dangerous in emergency and transport medicine. Dr. Mike Lauria distinguishes PAH from the broader label of “pulmonary hypertension,” emphasizing that elevated pulmonary pressures can come from several very different disease processes, but group 1 PAH is a rare intrinsic disease of the pulmonary arteries that creates fixed resistance to blood flow. Over time, this chronic increase in pulmonary vascular resistance places an enormous burden on the right ventricle, which may initially compensate but can eventually dilate and fail, especially when stressed by infection, hypoxia, medication interruption, or other acute illness. 
A major theme of the episode is that right ventricular failure is the central problem when these patients decompensate. Dr. Lauria reviews how rising RV afterload leads to RV dilation, reduced RV output, impaired LV filling, worsening cardiac output, and eventual shock. He also highlights an important practical pearl: many PAH patients depend on specialized outpatient therapies such as endothelin receptor antagonists, PDE-5 inhibitors, and especially continuous prostacyclin infusions like epoprostenol or treprostinil. Abrupt interruption of these medications can trigger rebound pulmonary hypertension and rapid deterioration, making continuation of home therapy a critical part of transport and ICU management. 
Management is framed around supporting the failing RV while avoiding interventions that can worsen hemodynamics. The speaker recommends maintaining MAP, usually with norepinephrine, carefully managing preload, and recognizing that this is one of the few shock states where patients may need both vasopressors and diuresis. The episode strongly warns against aggressive fluid loading, stresses the importance of correcting hypoxia and hypercapnia, and supports use of inhaled pulmonary vasodilators such as nitric oxide or epoprostenol in the right setting. It also cautions that intubation is particularly dangerous in PAH because induction and positive-pressure ventilation can sharply worsen RV function and precipitate cardiovascular collapse. 
Key points
 The episode distinguishes group 1 pulmonary arterial hypertension from the broader and more nonspecific category of pulmonary hypertension. 
 PAH is dangerous because it creates fixed pulmonary vascular resistance, which can eventually cause right ventricular failure and shock. 
Medication interruption, especially stopping continuous prostacyclin infusions, can cause rebound pulmonary hypertension and sudden collapse. 
 Management focuses on supporting the RV: maintain MAP, avoid unnecessary fluids, optimize oxygenation and ventilation, and consider inhaled pulmonary vasodilators. 
Intubation is high risk in these patients because positive pressure and induction can worsen RV afterload and trigger hemodynamic collapse.