Intensivist | Internal Medicine Thinking out loud about the ICU Bedside physiology • ICU Pearls • ICU Visuals • occasional hot takes ☕️ 🍩 🥐 🍫

#ICU Visuals #003: The Impella alarms “Suction.” The reflex is to give fluid. But suction is a clue, not a diagnosis. A visual map for troubleshooting #Impella at the bedside ↓ #foamed #foamcc
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Yesterday's post on “#Impella troubleshooting: 10 high-yield ICU pearls #003” is here 👇
#Impella troubleshooting: 10 high-yield ICU pearls #003 The Impella monitor flashes “Suction.” Our knee-jerk reflex says: give a liter of normal saline. But what if volume isn't the problem? The exact same alarm can stem from completely opposite mechanics meaning that treating the alarm instead of the patient can backfire. Here is a step-by-step approach to troubleshooting Impella suction at the bedside: 1️⃣ Suction is a clue, not a diagnosis. Before starting iv fluids, we have to reduce the P-level while we figure out what happened. Then we should build the differential: ? Malposition ? True hypovolemia ? RV failure ? Tamponade ? Excessive support ? Structural obstruction/clot 2️⃣ Check Impella position immediately. Get the probe on the chest early. Is the inlet free in the LV cavity? Is it tangled in the mitral apparatus, grabbing chordae, or hugging the septum? A spinning impeller parked in the wrong spot won't work well, no matter how much volume we give. 3️⃣ Low preload ≠ "give fluid". Hypovolemia? Fluid may help. Severe RV failure? More fluid may dilate the RV, shift the septum to the left, and make LV filling -and suction- worse. Tamponade? Fluid is only a bridge to what the patient actually needs: drainage. Same alarm. Completely different physiology. 4️⃣ Don't forget the RV. The LV can only receive and eject what the right heart delivers. RV failure reduces LV preload, lowers Impella flow, and can trigger suction. Sometimes the “Impella problem” is really an "RV problem". 5️⃣ Read the suction pattern. Diastolic suction can be a clue to inadequate LV filling but it has also been associated with RV dysfunction. Continuous suction will have to make us think systematically through: Loading → Position → Anatomy → Device The waveform gives us clues, but we have to interpret the context. 6️⃣ Suction + dark urine? Think hemolysis. We have to check plasma-free hemoglobin and the rest of the hemolysis markers. But besides staring at the labs, we have to look for malposition, a small underfilled LV, excessive pump speed, or mechanical obstruction. Find the cause of the shear. 7️⃣ Still in shock despite Impella? Step back and ask: ① Is the pump actually delivering effective cardiac output? ② Is there unaddressed vasoplegia or sepsis riding along? ③ Are we over-pumping a dry LV? Cranking up the P-level isn't a fix for vasoplegia. 8️⃣ Is the flow lower than expected? Walk through the sequence: Position → Preload → Afterload → Mechanical hardware Don't jump straight to device escalation when the afterload is sky-high or the inlet is displaced. 9️⃣ CPR can displace the Impella. Chest compressions, coughing, movement, and patient repositioning can displace the catheter. Especially chest compressions can shift hardware. Every single time we get ROSC or complete a code, we have to re-confirm depth and orientation with echocardiography or fluoroscopy before trusting our numbers. 🔟 The core ICU rule. Treat the physiology, not the monitor prompt. "Suction" tells us what the machine is feeling. It is our job is to figure out what is happening. #foamed #foamcc
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#Impella troubleshooting: 10 high-yield ICU pearls #003 The Impella monitor flashes “Suction.” Our knee-jerk reflex says: give a liter of normal saline. But what if volume isn't the problem? The exact same alarm can stem from completely opposite mechanics meaning that treating the alarm instead of the patient can backfire. Here is a step-by-step approach to troubleshooting Impella suction at the bedside: 1️⃣ Suction is a clue, not a diagnosis. Before starting iv fluids, we have to reduce the P-level while we figure out what happened. Then we should build the differential: ? Malposition ? True hypovolemia ? RV failure ? Tamponade ? Excessive support ? Structural obstruction/clot 2️⃣ Check Impella position immediately. Get the probe on the chest early. Is the inlet free in the LV cavity? Is it tangled in the mitral apparatus, grabbing chordae, or hugging the septum? A spinning impeller parked in the wrong spot won't work well, no matter how much volume we give. 3️⃣ Low preload ≠ "give fluid". Hypovolemia? Fluid may help. Severe RV failure? More fluid may dilate the RV, shift the septum to the left, and make LV filling -and suction- worse. Tamponade? Fluid is only a bridge to what the patient actually needs: drainage. Same alarm. Completely different physiology. 4️⃣ Don't forget the RV. The LV can only receive and eject what the right heart delivers. RV failure reduces LV preload, lowers Impella flow, and can trigger suction. Sometimes the “Impella problem” is really an "RV problem". 5️⃣ Read the suction pattern. Diastolic suction can be a clue to inadequate LV filling but it has also been associated with RV dysfunction. Continuous suction will have to make us think systematically through: Loading → Position → Anatomy → Device The waveform gives us clues, but we have to interpret the context. 6️⃣ Suction + dark urine? Think hemolysis. We have to check plasma-free hemoglobin and the rest of the hemolysis markers. But besides staring at the labs, we have to look for malposition, a small underfilled LV, excessive pump speed, or mechanical obstruction. Find the cause of the shear. 7️⃣ Still in shock despite Impella? Step back and ask: ① Is the pump actually delivering effective cardiac output? ② Is there unaddressed vasoplegia or sepsis riding along? ③ Are we over-pumping a dry LV? Cranking up the P-level isn't a fix for vasoplegia. 8️⃣ Is the flow lower than expected? Walk through the sequence: Position → Preload → Afterload → Mechanical hardware Don't jump straight to device escalation when the afterload is sky-high or the inlet is displaced. 9️⃣ CPR can displace the Impella. Chest compressions, coughing, movement, and patient repositioning can displace the catheter. Especially chest compressions can shift hardware. Every single time we get ROSC or complete a code, we have to re-confirm depth and orientation with echocardiography or fluoroscopy before trusting our numbers. 🔟 The core ICU rule. Treat the physiology, not the monitor prompt. "Suction" tells us what the machine is feeling. It is our job is to figure out what is happening. #foamed #foamcc
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News: Yesterday, Tennessee tried to execute #ChristaPike. She survived. Until recently, Tennessee used three drugs for lethal injection: midazolam for sedation, vecuronium for paralysis, and potassium chloride to stop the heart. In 2024, Tennessee switched to pentobarbital alone. The new protocol has a backup plan: if the first set of pentobarbital doesn't work, give a second. Pike received both. More than an hour after the execution started, witnesses could reportedly still hear her breathing and snoring. She was eventually taken to a hospital. Tennessee says that "every step of the protocol was followed". So what happened? IV access? Drug delivery? Preparation? Pharmacokinetics? We don't know. What we do know is that the protocol didn't work. The governor has now stopped Tennessee's remaining execution scheduled for this year and ordered a review. As a physician, I have a hard time reading about IV access, drug protocols and physiologic endpoints when the endpoint we're discussing is deliberately killing someone. Whatever your views on capital punishment, this case deserves a very close look. #medtwitter
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#ICU News: Recarbrio is disappearing from the U.S. market. Not because it failed. Not because of a safety signal. Not because resistant bacteria disappeared. Merck is discontinuing it as part of a portfolio decision. I guess “portfolio decision” is the code name for “not profitable drug.” And that should make every intensivist, ID physician, and pharmacist uncomfortable. Recarbrio is the trade name of imipenem/cilastatin + relebactam. The FDA approved it in 2019 for complicated infections in adults with limited or no alternatives. In 2020, it was approved for hospital- and ventilator-associated bacterial pneumonia. And in 2025, its indication expanded to children ≥ 2 kg. Why did we need it? Because relebactam inhibits important β-lactamases -including KPC and AmpC-helping restore imipenem activity against some extremely difficult Gram-negative infections. And here is where the story gets interesting. Drugs like this are supposed to be used **selectively**. That's good antimicrobial stewardship. But it creates a difficult economic model. Recarbrio launched at roughly $268/vial, summing up to roughly $10,000 for a 10-day course. More recently, wholesale list pricing reached approximately $8,141 for 25 vials, or about $326/vial. Hospitals are supposed to reserve antibiotics like this for patients who truly need them. So the better we steward the antibiotic, the less frequently we use it. And the less frequently we use it, the smaller its commercial market. **That is the antibiotic paradox.** We need new antibiotics to be valuable enough to develop but rarely used enough to preserve their effectiveness. Recarbrio isn't the first warning. And it won't be the last if we continue expecting critical antibiotics to survive on a conventional “sell more doses” business model. One important detail: This does not appear to be a global withdrawal. Recarbrio remains authorized in Europe. So, at least for now, this appears primarily to be a U.S. market exit. Will this leave us defenseless? No. Other agents cover many of the same resistant organisms. But that's not really the point. The point is what happens when we finally develop another weapon against multidrug-resistant bacteria and discover that the economics reward selling antibiotics often, while stewardship requires us to use them rarely. Maybe Merck has a better explanation. I’d genuinely like to hear it. Antibiotic resistance is accelerating. Our antibiotic business model is moving in the opposite direction. #medtwitter #idtwitter #foamed
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#ICU Visuals #002: Cardiogenic shock is not a device problem. It’s a physiology problem. The RIGHT support starts with the RIGHT phenotype. SHOCK → PHENOTYPE → DEVICE → EXIT STRATEGY A visual map of temporary mechanical circulatory support (tMCS) in cardiogenic shock 👇
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Of course, our practice evolves. Five years ago, I had never seen an #Impella placed across a severely stenotic aortic valve. Today, I’ve seen it done more than a few times. Things change...
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🧵 10 HIGH-YIELD ICU PEARLS #002 Temporary Mechanical Circulatory Support in Cardiogenic Shock: I’ve seen patients die despite temporary Mechanical Circulatory Support (tMCS). I’ve seen others die from complications related to it. And I’ve seen several who, in my opinion, are alive today because of it. That has made me a believer in temporary MCS devices but deeply respectful of what happens when we get them wrong. The first rule: Define the shock phenotype before choosing the device. Don’t put the cart before the horse. 1️⃣ Phenotype first LV failure? RV failure? Bi-ventricular failure? Mechanical complication? Obstructive physiology? The “strongest” device isn’t necessarily the right one. PHENOTYPE → DEVICE Not the other way around. 2️⃣ Impella = direct LV unloading Impella moves blood: LV → ascending aorta It reduces LV filling while providing forward flow. The key concept isn’t simply: “More cardiac output.” It’s: "Unload the failing LV". 3️⃣ Think in pressure-volume loops As Impella support increases, the pump assumes more of the work of moving blood forward. The LV PV loop generally shifts leftward: ↓ LV filling pressure/volume ↓ native LV stroke work ↓ pressure-volume area ↓ wall stress A smaller native LV PV loop ≠ less systemic flow. The LV does less work because the pump is doing part of it. That’s LV unloading. 4️⃣ VA-ECMO is different VA-ECMO provides powerful circulatory + respiratory support. But peripheral VA-ECMO can bite you: ↑ LV afterload ↑ LV distension ↑ pulmonary congestion Hemodynamic support ≠ LV unloading. 5️⃣ More support ≠ better support Temporary MCS trades hemodynamic benefit for potential harm: Bleeding. Vascular injury. Hemolysis. Thrombosis. Device complications. And I may be missing some... The goal isn’t the biggest pump. It’s the right level of support for the shock phenotype. 6️⃣ Know DanGer Shock In selected patients with STEMI-related cardiogenic shock, Impella CP + standard care reduced 180-day mortality: 45.8% vs 58.5% (the number needed to treat was 8) But: ⚠️ Safety events: 24.0% vs 6.2% (the number needed to harm was 6) ⚠️ Renal replacement therapy: 41.9% vs 26.7% The lesson isn’t: “Impella saves lives.” It’s: Benefit comes with complications. Patient selection matters. A lot. 7️⃣ Don’t forget the RV An LV support device cannot directly support an isolated failing RV. Impella also needs adequate blood reaching the LV. Ask: Can the RV provide enough preload for effective LV support? Ignore the RV and you may choose the wrong device. 8️⃣ Find the lesion Think beyond “low EF.” Before initiating LV support, ask whether the underlying lesion or physiology makes unloading ineffective or potentially harmful. Find the lesion → understand the physiology → choose the support. Cardiogenic shock is a hemodynamic syndrome, not an EF diagnosis. 9️⃣ Timing matters Escalating vasoactives. Persistent hypoperfusion. Failure to clear lactate. Evolving end-organ dysfunction. Ask: “Is the support actually working?” A better cardiac index ≠ reversal of shock. If lactate isn’t clearing and end-organ dysfunction keeps worsening despite apparently adequate support, ongoing hypoperfusion may still be present. The transition from hemodynamic → hemometabolic shock is ominous and increasingly difficult to reverse. 🔟 Have an EXIT strategy Where are we going? Recovery? Bridge to decision? Durable LVAD Transplant? Another temporary support strategy? Temporary MCS should have a destination. If none is realistic, that matters before support is initiated. After years of watching temporary MCS succeed spectacularly -and fail miserably- my framework has become pretty simple: SHOCK → PHENOTYPE → DEVICE → EXIT STRATEGY Not: SHOCK → BIGGER PUMP #FOAMcc #FOAMed #MedEd
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#ICU Visuals #002: Cardiogenic shock is not a device problem. It’s a physiology problem. The RIGHT support starts with the RIGHT phenotype. SHOCK → PHENOTYPE → DEVICE → EXIT STRATEGY A visual map of temporary mechanical circulatory support (tMCS) in cardiogenic shock 👇
Made with AI
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IMCrit retweeted
🧵 10 HIGH-YIELD ICU PEARLS #002 Temporary Mechanical Circulatory Support in Cardiogenic Shock: I’ve seen patients die despite temporary Mechanical Circulatory Support (tMCS). I’ve seen others die from complications related to it. And I’ve seen several who, in my opinion, are alive today because of it. That has made me a believer in temporary MCS devices but deeply respectful of what happens when we get them wrong. The first rule: Define the shock phenotype before choosing the device. Don’t put the cart before the horse. 1️⃣ Phenotype first LV failure? RV failure? Bi-ventricular failure? Mechanical complication? Obstructive physiology? The “strongest” device isn’t necessarily the right one. PHENOTYPE → DEVICE Not the other way around. 2️⃣ Impella = direct LV unloading Impella moves blood: LV → ascending aorta It reduces LV filling while providing forward flow. The key concept isn’t simply: “More cardiac output.” It’s: "Unload the failing LV". 3️⃣ Think in pressure-volume loops As Impella support increases, the pump assumes more of the work of moving blood forward. The LV PV loop generally shifts leftward: ↓ LV filling pressure/volume ↓ native LV stroke work ↓ pressure-volume area ↓ wall stress A smaller native LV PV loop ≠ less systemic flow. The LV does less work because the pump is doing part of it. That’s LV unloading. 4️⃣ VA-ECMO is different VA-ECMO provides powerful circulatory + respiratory support. But peripheral VA-ECMO can bite you: ↑ LV afterload ↑ LV distension ↑ pulmonary congestion Hemodynamic support ≠ LV unloading. 5️⃣ More support ≠ better support Temporary MCS trades hemodynamic benefit for potential harm: Bleeding. Vascular injury. Hemolysis. Thrombosis. Device complications. And I may be missing some... The goal isn’t the biggest pump. It’s the right level of support for the shock phenotype. 6️⃣ Know DanGer Shock In selected patients with STEMI-related cardiogenic shock, Impella CP + standard care reduced 180-day mortality: 45.8% vs 58.5% (the number needed to treat was 8) But: ⚠️ Safety events: 24.0% vs 6.2% (the number needed to harm was 6) ⚠️ Renal replacement therapy: 41.9% vs 26.7% The lesson isn’t: “Impella saves lives.” It’s: Benefit comes with complications. Patient selection matters. A lot. 7️⃣ Don’t forget the RV An LV support device cannot directly support an isolated failing RV. Impella also needs adequate blood reaching the LV. Ask: Can the RV provide enough preload for effective LV support? Ignore the RV and you may choose the wrong device. 8️⃣ Find the lesion Think beyond “low EF.” Before initiating LV support, ask whether the underlying lesion or physiology makes unloading ineffective or potentially harmful. Find the lesion → understand the physiology → choose the support. Cardiogenic shock is a hemodynamic syndrome, not an EF diagnosis. 9️⃣ Timing matters Escalating vasoactives. Persistent hypoperfusion. Failure to clear lactate. Evolving end-organ dysfunction. Ask: “Is the support actually working?” A better cardiac index ≠ reversal of shock. If lactate isn’t clearing and end-organ dysfunction keeps worsening despite apparently adequate support, ongoing hypoperfusion may still be present. The transition from hemodynamic → hemometabolic shock is ominous and increasingly difficult to reverse. 🔟 Have an EXIT strategy Where are we going? Recovery? Bridge to decision? Durable LVAD Transplant? Another temporary support strategy? Temporary MCS should have a destination. If none is realistic, that matters before support is initiated. After years of watching temporary MCS succeed spectacularly -and fail miserably- my framework has become pretty simple: SHOCK → PHENOTYPE → DEVICE → EXIT STRATEGY Not: SHOCK → BIGGER PUMP #FOAMcc #FOAMed #MedEd
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ICU hot take: A white-out lung is not, by itself, an indication for intubation and bronchoscopy. Intubating someone for a “therapeutic bronch” without first putting an ultrasound probe on the chest should be a federal crime. #POCUS #FOAMcc
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Replying to @IM_Crit_
pneumothorax freaks people out and generally will lead to rapid chest tube insertion. However, an equally voluminous pleural effusion causing respiratory failure often gets ignored. (About once every 1-2 years I'll get an intubated patient in transfer who really just needs a therapeutic thoracentesis.) also, if the white-out is due to atelectasis, this can sometimes respond to BiPAP or CPAP with high mean airway pressures
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ICU Opinion: I have worked in ICUs long enough to have been through plenty of The Joint Commission (TJC, formerly JCAHO) survey weeks. And I have to admit, the longer I do this, the more skeptical I become about how much of the bureaucracy around hospital accreditation actually makes patients safer. I am not against standards. Hospitals need outside scrutiny and TJC has done important work. Medication safety, infection prevention, handoffs and procedural safeguards matter. Outside pressure has helped change practices that needed to change. My problem is when patient safety turns into compliance theater. If you've worked in a hospital during survey week, you know the ritual. Suddenly everyone is worried about where your coffee is sitting. Tape disappears from walls. Doors, ceiling tiles, refrigerators and labels become urgent concerns. At least my beloved ultrasound machine is finally back where it belongs and plugged into the wall! Then administrators who rarely set foot on the unit, and probably haven't visited us since the ribbon-cutting ceremony, show up to remind us about rules that somehow become much more important when the surveyors are in the building. Meanwhile, the ICU is still the ICU. A nurse is titrating three vasopressors, managing CRRT and trying to stop a delirious patient from pulling out his femoral arterial line. Someone is intubating. Another patient is spitting at us and demanding to leave AMA. But please, let's talk about that covered cup. The coffee is actually a good example of the larger problem. Even the famous “TJC says you can't drink at the nursing station” rule isn't that simple. Hospitals can designate safe areas for food and drink based on exposure risk. But by the time a rule works its way through hospital committees, policies and layers of administration, the nuance is often gone. Rules beget rules. Hospitals write policies around standards. Consultants prepare hospitals for surveys. Staff are prepared for the consultants who are preparing everyone for the survey. My work mailbox gets an email every other day warning me about the visit. Eventually, nobody remembers whether a requirement came from CMS, OSHA, TJC, the hospital—or something somebody heard years ago that somehow became hospital law. All of this takes time. So what are we getting in return? A BMJ study of more than 4.2 million Medicare admissions found no significant 30-day mortality associated with accreditation, or for TJC-accredited hospitals compared with other independent accreditors. That doesn't settle whether accreditation works. Mortality is only one outcome. But it should make us question the assumption that more compliance automatically means better care. There is also a part of this system worth being transparent about. Hospitals pay accrediting organizations to evaluate them. TJC has a controlled affiliate, Joint Commission Resources, that provides education and consulting services related to accreditation and quality. That relationship does not by itself mean anything improper is happening. Formal safeguards separate the accreditation and consulting functions to address potential or perceived conflicts of interest. Still, I think it's reasonable to ask how that relationship works and how those safeguards are maintained. To be clear: I don't want to abolish accreditation or leave hospitals to police themselves. My point is simpler: if we're going to ask a nurse or physician to do something in the name of patient safety, we should be able to show that it actually makes patients safer. Every requirement costs something: money, another click in the EHR, another mandatory module or a few more minutes spent on compliance instead of with a patient. We ask for evidence before we do things to our patients. I don't think it's unreasonable to ask for evidence before we make clinicians do things in the name of protecting them. The ICU does not become safer because TJC survey week started. And yes, let the night-shift ICU nurse drink her coffee.
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The return-to-work rules just changed for healthcare workers with respiratory infections. The practical change: Day 4 may now be the EARLIEST return to work but ONLY IF you meet ALL the criteria below. CDC now uses the SAME basic framework for COVID-19, influenza, RSV and several other common respiratory viruses. 🤒 If you're sick: Day 0 = symptom onset. You can return Day 4 or later when: 1. At least 3 days have passed since symptoms started 2. You've been fever-free ≥ 24 h without antipyretics 3. Symptoms are improving 4. You feel well enough to work 😷 When you return: Wear a well-fitting medical mask or respirator through the end of Day 7 and Day 8 is the first possible day without the added masking requirement. And no, you don't automatically need an N95 just because you're returning after an infection. A well-fitting medical mask meets the source-control requirement. Obviously, that doesn't replace PPE. If the patient's isolation precautions or the procedure require an N95, wear an N95. 🦠 Exposed but feeling fine? Generally, NO work restriction. Wear a well-fitting mask or respirator through at least Day 5 after your last exposure and monitor for symptoms for at least 5 days. Also worth noting: CDC doesn't consider simply walking past someone with a cold in the hallway an “exposure.” Proximity, duration, PPE and ventilation matter. Different viruses. Same basic return-to-work framework. There are exceptions, and your hospital's Occupational Health policy may be more restrictive. Now I just need to follow my own advice and stop treating “I feel like crap” as an indication to go to work anyway...
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