The FlightBridgeED Podcast

In this episode of the FlightBridgeED MDCast, Dr. Mike Lauria explores the role of intra-aortic balloon pumps (IABPs) in managing cardiac dysfunction and cardiogenic shock, with a particular focus on critical care transport. The discussion begins with a review of cardiogenic shock physiology, emphasizing the dangerous cycle of declining cardiac output, reduced coronary perfusion, worsening myocardial function, and progressive end-organ dysfunction. While intra-aortic balloon pumps have historically been used to support patients in cardiogenic shock, their relatively limited ability to increase cardiac output makes them less effective in profound or rapidly deteriorating shock. However, they may still provide meaningful support in select populations, including patients with acute decompensated heart failure, mitral regurgitation, or temporary myocardial dysfunction following cardiac surgery or coronary intervention. The episode explains the fundamental mechanism of intra-aortic balloon counterpulsation, which relies on precisely timed balloon inflation and deflation to improve cardiovascular performance. Positioned within the descending thoracic aorta, the balloon inflates during diastole, increasing diastolic aortic pressure and improving coronary artery perfusion. Immediately before systole, the balloon rapidly deflates, reducing left ventricular afterload and myocardial oxygen demand while modestly increasing stroke volume and cardiac output. Although these physiological benefits are well established, large clinical trials have not demonstrated a consistent mortality benefit in patients with cardiogenic shock. Nevertheless, IABPs remain commonly encountered in critical care transport because of their availability, relative simplicity, and potential usefulness as temporary support or a bridge to more definitive therapies. Dr. Lauria emphasizes a systematic approach to bedside assessment, beginning with the patient's overall clinical condition before evaluating the device itself. Transport clinicians should assess hemodynamics, oxygenation, perfusion, and other critical interventions before examining balloon pump function. Device assessment includes confirming appropriate diastolic augmentation, evaluating assisted end-diastolic pressure, verifying catheter position on chest radiography, and inspecting the insertion site for bleeding or catheter migration. Proper inflation and deflation timing are essential because incorrect timing can increase ventricular workload or reduce coronary perfusion. Although modern IABP consoles generally manage timing effectively through automated triggering, clinicians should still recognize abnormalities and understand their physiological consequences. The discussion concludes with complications and operational considerations associated with transporting patients receiving IABP support. Significant concerns include vascular access hemorrhage, limb ischemia, balloon rupture, helium loss, and complete device malfunction. Blood appearing within the helium tubing is particularly concerning because it may indicate balloon rupture and requires immediate intervention according to device-specific protocols. Transport teams must also ensure adequate battery capacity and helium reserves, particularly during air medical transport, where altitude changes can increase helium consumption through system recalibration. Careful patient positioning, prevention of excessive hip and knee flexion, and protection of the catheter insertion site are essential. Ultimately, safe IABP transport requires a solid understanding of counterpulsation physiology, consistent patient-centered assessment, familiarity with equipment operation, and early recognition of potentially life-threatening complications. Key Points Counterpulsation improves coronary perfusion and reduces cardiac workload. Balloon inflation during diastole increases coronary perfusion pressure, while rapid deflation before systole reduces left ventricular afterload and myocardial oxygen demand. IABPs provide modest circulatory support and are not appropriate for every case of cardiogenic shock. They typically increase cardiac output by approximately 0.5–1 L/min and may be most useful in select patients requiring temporary support while myocardial function recovers or definitive treatment is arranged. Effective assessment begins with the patient, not the machine. Clinicians should evaluate hemodynamic stability, oxygenation, and peripheral perfusion before confirming appropriate balloon augmentation, deflation, catheter position, and vascular access integrity. Bleeding, limb ischemia, balloon rupture, and device malfunction are major transport complications. Frequent access-site inspections, distal pulse assessments, and monitoring for blood in the helium tubing are essential for identifying complications before they become life-threatening. Transport preparation must account for equipment limitations and patient movement. Adequate battery reserves, supplemental helium, secure catheter placement, and appropriate patient positioning are critical, particularly during air transport when altitude-related recalibration can increase helium consumption.

In this episode of the FlightBridgeED MDCast, Dr. Mike Lauria explores the role of Impella devices in managing cardiogenic shock, with a particular focus on critical care transport. Impella devices provide temporary mechanical circulatory support (MCS) for patients experiencing severe cardiac dysfunction. They are commonly used as a bridge to recovery, high-risk cardiac interventions, surgical procedures, heart transplantation, or further clinical decision-making. The episode reviews the progression of cardiogenic shock, emphasizing how decreased cardiac output, inadequate coronary perfusion, and compensatory vasoconstriction can create a dangerous cycle of worsening myocardial function, pulmonary congestion, and multiorgan failure. The Impella is a percutaneous microaxial blood pump that moves blood directly from the left ventricle into the aorta, providing three major physiological benefits: increased cardiac output, left ventricular unloading, and improved coronary perfusion. By reducing ventricular pressure, volume, and wall stress, the device decreases myocardial oxygen demand while improving systemic circulation. Dr. Lauria also discusses the evolving evidence supporting Impella use, highlighting the landmark DanGer Shock trial. This randomized study demonstrated a significant reduction in six-month mortality among selected patients with acute myocardial infarction complicated by cardiogenic shock who received early Impella CP support. However, these benefits must be weighed against complications such as major bleeding, limb ischemia, and device-related problems. A substantial portion of the discussion focuses on the practical assessment and management of patients receiving Impella support during transport. Dr. Lauria emphasizes that clinicians must assess the patient before focusing on the device, evaluating hemodynamic stability, respiratory status, perfusion, and signs of ongoing ischemia. Device assessment includes reviewing the automated Impella controller, confirming appropriate aortic and ventricular pressure waveforms, evaluating motor current oscillations, and monitoring pump flow and purge pressures. Particular attention must be directed toward the vascular access site, where catheter movement can result in significant hemorrhage, and toward the affected extremity for evidence of compromised distal perfusion. Other important complications include device malposition and suction events, which may result from inadequate preload, right ventricular failure, or improper catheter positioning. The episode concludes with considerations for safely transporting patients supported by Impella devices, including power management, equipment accessibility, patient positioning, and emergency response. Transport teams must ensure adequate battery reserves, secure the controller where it remains visible and accessible, protect the catheter and vascular access site, and minimize excessive patient movement. Although patients with Impella support can undergo conventional resuscitation, cardiac arrest requires additional attention to pump settings and potential device displacement. Ultimately, successful Impella transport requires an understanding of cardiogenic shock physiology, familiarity with device function, careful patient assessment, and proactive recognition of complications. Key Points Impella devices provide temporary mechanical circulatory support. They serve as a bridge to myocardial recovery, definitive cardiac interventions, transplantation, or further clinical decision-making in patients with significant cardiac dysfunction. Impella support improves cardiovascular physiology through three primary mechanisms. The device increases cardiac output, unloads the left ventricle to reduce myocardial workload, and improves coronary perfusion. The DanGer Shock trial demonstrated a mortality benefit in a carefully selected population with myocardial infarction-related cardiogenic shock. Patient assessment takes priority over device assessment. Transport clinicians should evaluate hemodynamics, oxygenation, perfusion, and clinical stability while monitoring pump flow, pressure waveforms, motor current, and purge system performance. Bleeding, limb ischemia, device malposition, and suction events are critical complications. Vascular access sites require frequent inspection, distal perfusion must be monitored, and abnormal device waveforms or alarms should prompt immediate evaluation. Safe transport requires meticulous equipment and patient management. Teams must maintain reliable electrical power, ensure the controller remains accessible, protect the insertion site from movement or compression, and be prepared to perform resuscitation while accounting for the Impella device.

What begins as respiratory distress quickly spirals into a critical care nightmare. In this episode of the FlightBridgeED Podcast, Eric Bauer is joined by Kari Young to break down a challenging case that tests clinical reasoning, airway management, and ventilatory decision-making under pressure. Together, they walk through the patient's presentation, discuss the DASH-1A airway assessment, and explore the critical decision-making process behind when, and when not to intubate. From there, they examine the differential diagnosis, review the interventions that can either halt, or accelerate the hypoxic spiral, and highlight common pitfalls, evidence-based strategies, and practical pearls that every EMS, flight, and critical care clinician can apply on their next respiratory emergency. Whether you're preparing for certification, sharpening your critical thinking, or simply enjoy learning through real-world cases, this is an episode you won't want to miss. Because sometimes the nightmare isn't the airway, it's recognizing the spiral before it's too late.

In this compelling episode of the FlightBridgeED Podcast, Eric Bauer is joined by Kari Young, Advanced Practice Paramedic and educator, for another installment of The Nightmare Series. Together, they dissect a complex critical care case where the obvious diagnosis was only the beginning. What initially appeared to be a straightforward presentation quickly evolved into a diagnostic minefield involving diabetic ketoacidosis (DKA), end-stage renal disease (ESRD), pneumonia, sepsis, acute respiratory failure, hypoxemia, and acute encephalopathy. Throughout the discussion, Eric and Kari walk listeners through the clinical presentation, differential diagnosis, decision-making process, and the cognitive biases that can lead providers to anchor on a single diagnosis while overlooking other life-threatening conditions. Filled with practical teaching points, evidence-based discussion, and real-world lessons, this episode challenges clinicians to think beyond the first diagnosis and embrace a more comprehensive approach to critically ill patients. Whether you're an EMT, paramedic, flight clinician, nurse, or physician, The Nightmare Series: The Diagnostic Minefield will sharpen your clinical reasoning and remind you that sometimes the sickest patients aren't suffering from one disease, but several, all at once.

This episode of the FlightBridgeED podcast focuses on post-cardiac arrest care during critical care transport, particularly for crews moving patients from outside or critical access hospitals to higher levels of care. Dr. Mike Lauria frames the post-ROSC patient around a simple mental model: help the heart, hunt for the cause, sustain the brain, and then provide all the other good critical care support needed during transport. While not all post-arrest patients are the same, this framework helps crews prioritize the problems most likely to affect survival and neurologic outcome. The first priority is stabilizing the cardiovascular system. After ROSC, crews should consider securing a definitive airway, especially if the patient is stable enough to safely exchange a supraglottic airway for an endotracheal tube. Perfusion should be optimized with a MAP goal around 65, cautious fluid administration, and early use of vasopressors when needed. Norepinephrine is presented as a reasonable first-line pressor, with epinephrine added when there is evidence of poor contractility or a need for inotropic support. The episode also emphasizes the usefulness of arterial lines, repeat EKGs, and point-of-care ultrasound when available, while cautioning against delaying transport for interventions that are not essential. A major theme is that crews must continue to search for the cause of the arrest even after ROSC. The H’s and T’s still matter, and transport teams may have access to critical information that can disappear during the handoff chain. Speaking directly with family, bystanders, or the sending team can uncover symptoms or events that change the patient’s trajectory. The episode also highlights the risk of re-arrest, noting that pads should stay on, ACLS medications should remain immediately available, and crews should stay alert for reversible causes, worsening shock, recurrent ventricular arrhythmias, or signs that the patient may need more urgent cardiac intervention. The final major priority is protecting the brain from secondary injury. Luria emphasizes normothermia, avoiding fever, maintaining perfusion, avoiding both hypoxia and hyperoxia, and targeting normal or high-normal CO2 rather than rapidly overcorrecting ventilation. Sedation should be minimized when possible so the receiving team can obtain a meaningful neurologic exam, while still treating pain, agitation, ventilator asynchrony, or unsafe movement. The episode closes with the “ALIVE-12” checklist: Airway secure, Look at the heart, Inotrope/pressor support, Ventilate safely, End-tidal CO2 monitoring, and a 12-lead ECG after enough time has passed for better diagnostic accuracy. Key Points • Post-cardiac arrest transport can be organized around four priorities: help the heart, hunt for the cause, sustain the brain, and provide good supportive critical care. • A MAP around 65 is generally an appropriate perfusion goal; higher blood pressure targets have not clearly shown benefit. • Norepinephrine is a reasonable first-line pressor, with epinephrine added when inotropic support is needed. • Repeat 12-lead EKGs matter; an ECG immediately after ROSC may be misleading, so repeating around 8–10 minutes and again later can improve diagnostic accuracy. • Brain protection means avoiding hypotension, fever, hypoxia, hyperoxia, and hypocapnia while minimizing unnecessary sedation.

This episode of the FlightBridgeED podcast focuses on acute decompensated left heart failure, especially in the transport setting. Dr. Mike Lauria frames these patients through the lens of the SCAI cardiogenic shock spectrum, with special attention to the earlier A and B stages that can be easy to underestimate. While the crashing, hypotensive cardiogenic shock patient often gets immediate attention, the episode emphasizes that patients with early decompensated heart failure may look “stable” because their blood pressure is still normal or high, even while they are beginning to slide toward shock. The case centers on a 58-year-old man with coronary artery disease, hypertension, diabetes, atrial fibrillation, and known reduced ejection fraction who stops taking his antihypertensives and diuretics while traveling. After some dietary indiscretion and worsening fluid overload, he presents with dyspnea, hypoxia, pulmonary edema, crackles, pedal edema, and increased work of breathing. Although he is not hypotensive, his clinical picture suggests acute decompensated left ventricular failure with early cardiogenic shock physiology. Point-of-care ultrasound, chest X-ray, BNP, and clinical exam all support the diagnosis, but the episode stresses that crews often do not need to wait for labs to recognize a patient who is clearly congested and deteriorating. Management focuses on reducing the burden on the failing left ventricle while supporting oxygenation and ventilation. In a hypertensive patient with pulmonary edema, nitroglycerin is highlighted as a key therapy because it reduces afterload and helps improve forward flow. Non-invasive positive pressure ventilation, whether CPAP or BiPAP, is presented not just as respiratory support but as hemodynamic support: by increasing intrathoracic pressure, it reduces venous return, decreases pulmonary congestion, and lowers the relative afterload faced by the left ventricle. The episode also emphasizes that crews should raise EPAP/PEEP when the goal is increasing mean airway pressure, and should coach anxious patients through NIV rather than reflexively sedating them. Volume management and inotropic support round out the treatment strategy. If the patient is volume overloaded and not hypotensive, loop diuretics are appropriate, especially for longer transports, and doses should be meaningful rather than overly timid. If ultrasound or clinical assessment suggests reduced cardiac output despite adequate or elevated blood pressure, low-dose dobutamine may help improve forward flow. However, if the patient begins to transition from SCAI stage B into stage C cardiogenic shock, crews should reassess immediately: stop vasodilators, consider vasopressors or epinephrine, continue positive pressure ventilation when appropriate, repeat the ECG, and communicate the deterioration clearly to the receiving team. Key Points • Acute decompensated heart failure can represent early cardiogenic shock even when the patient is not hypotensive. • Hypertensive pulmonary edema is often an afterload problem; nitroglycerin can be a powerful tool to reduce afterload and improve forward flow. • CPAP and BiPAP are not just oxygenation tools; they also provide hemodynamic support for a failing left ventricle. • Avoid sedating patients simply because they are anxious on NIV; coach them, start with tolerable pressures, and increase support as they adjust. • If a heart failure patient deteriorates from SCAI stage B to stage C, reassess the cause, stop vasodilators, consider pressors/inotropes, repeat the ECG, and update the receiving facility.

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