SCCM Resource Library-Case Presentation: Current Opinions in Shock Monitoring

Video Transcription

Hello. My name is Dr. Saras Chandra Vallabha Josula. I'm an interventional and critical care cardiologist at the Wake Forest University School of Medicine in North Carolina. I'm  here to talk to you about a case presentation as a part of the session entitled Current Opinions in Shock Monitoring. These are my disclosures. None of these are relevant to  today's case presentation. So our patient was a 71-year-old female who was transported by the EMS for unresponsiveness. The call was activated by the family who found her  down and they reported that she's been worseningly feeling worse with fatigue and leg swelling  for the past four days. End route from home to the ED, she was placed on a non-rebreather because she wasn't satting the greatest. Her only history was some lung disease and  history of tobacco abuse. These are pertinent skin findings on her legs when she came in  through the ED. As you can see, a lot of swelling, blistering, erythema, and generalized speed leutema too. On exam, her vitals were she was tachycardic, hypotensive, systolics of  the 50s to 60s, not satting very well on room air, and breathing pretty rapidly. And she wasn't particularly awake. She was only moving extremities to noxious stimuli. Her  rhythm was irregularly regular. Her cap refill was okay. So because, and she had 2 plus pitting  edema like we talked about. This is her ECG. As you can see, this is largely sinus tachycardia.  I'm finding it really tough to appreciate the P waves. There may be atrial fibrillation or flutter that's very well organized, but nothing dramatic. No major ST segment elevations,  no major arrhythmias. So in the ED, she was first entetrically intubated, airway was secured,  and she was put on continuous mandatory ventilation. She was pan-cultured, obviously very high  suspicion for sepsis given those leg wounds and overall presentation. Start on broad spectrum  antibiotics was lined and tubed appropriately. These were the first set of labs that came back from the ED. Hemoglobin, hematological panel in general was okay. Her potassium was  high, which was confirmed on recheck. It wasn't a hemolyzed sample. She was in acute kidney injury. Cardiac biomarkers showed high B-type nitritic peptide. She was acidotic, largely  metabolic, or largely respiratory. I mean, her lactate was only 1.3. So she was treated appropriately with norepinephrine for presumed septic shock, calcium gluconate, insulin D50,  Lasix, amiodarone, sodium zirconium, cyclostilastate, but essentially treated for hypokalemia. She  was treated for hypokalemia, pressors, broad spectrum antibiotics. This is an echocardiogram.  Oh, they're all out of order, but I'm going to play them for you. Okay. So unfortunately, this is a virtual recording. I'm going to interpret for them for you. Ideally, I would  have loved to have a live audience to discuss this with. But as you can see, she has biventricular  decrease in function. Her right side appears to be somewhat generous in the short axis view. She's globally hypokinetic on the left. No single segment is particularly hypokinetic,  the best I can tell. This is her valve assessment. As you can see, there's moderate to severe MR. The color is rather prominent. This is a tricuspid valve, and you can see severe  tricuspid regurgitation. Even though you don't see a very prominent jet, this is a rapid equalization of pressure. This is her CAT scan, not much in the way of lung disease,  chronic changes, some left lateral, left pleural effusion on the lower lobes here, but otherwise no major, you know, crazy findings on the CT scan. So in the ICU, due to, because  her RV was slightly enlarged, there was no clear understanding of whether it was acute or chronic.  She did have some lung disease in outpatient, but we don't know. We didn't have prior echocardiograms,  and her creatinine was three, so we couldn't send her to the CAT scanner with contrast. We ended up treating her empirically with an heparin infusion. Because she had biventricular  failure and with high filling pressures and echo, we decided to diurese her, put her on vasopressors  and inotropes to help get fluid off, and the serial lactate and SAVO2 monitoring.  So these are time trends of her creatinine. As you can see, she started three-ish and came down  rather rapidly with diuresis, confirming our suspicion that this was, at least in part,  cardiorrhenal syndrome. And these are her, these are snapshots of her volume status. As you can  see, she was significantly volume up on day one, where she was treated for sepsis, presumed sepsis  with the fluid resuscitation, and then, but gradually we got it off in the subsequent two days and nearly a liter and a half negative here or nearly half a liter here.  Her high INS was because she was getting, if I remember right, she was getting amiodarone because she went into AFib-RVR, which we kind of suspected when we first saw her.  So a couple of days of good diuresis, improvement in renal function, I said, you know what, let's take her down to the lab, let's do a left and right heart CAT, see what's,  what the filling pressures are, see she where she is, what the etiology for this is.  So, like I said, she developed AFib-RVR, she needed to be cardioverted a couple of times.  Her oxygenation or respiratory status overall was improving. So we took her down for elective  left and right heart CAT. She was also on a touch of epinephrine at that point, but all other ways  for active medications. These are her hemodynamics. Again, unfortunately, due to the absence of live  interaction, I'm going to interpret them for you. Her right atrial pressures and vent pressures were both high, suggesting biventricular involvement. PA pressures were only modestly  elevated, again, probably secondary left heart disease. Central pressures, aortic pressures were  okay. For central venous oxygen saturation in the RA and PA were great, which essentially shows that  she's getting, going in the right direction. Her cardiac output or cardiac index was 1.8 on  epinephrine, so still low. This is an important parameter, CPO, which is essentially MAP times  cardiac output divided by 451. So less than 0.6 tells us that the LV isn't doing its job. PAPI,  which is pulmonary artery pulsatility index, which is systolic pulmonary artery pressure minus  diastolic pulmonary artery pressure divided by mean RA pressure. Again, less than 1 tells us  that the right ventricle isn't doing its job. So here, essentially, the left ventricle was doing  okay-ish. The right ventricle wasn't doing its job as well, which we kind of knew from  the echocardiogram too. So this is a coronary angiogram. I know many of you are not cardiologists  in this group, so I just wanted to show it to you. This is the LAD. This is the left circumflex.  This view, you're essentially looking at the left circumflex, and largely looks okay. This is a cranial view of the LAD. As you can see, there's a tight mid-LAD stenosis here where  I'm circling with my mouse. So 19.599% occlusion, but there's still good flow. And this is the right  coronary artery, which for the large part looks okay. So because she was cardiogenic shock, definitely not acute MI, but cardiogenic shock, we decided to revascularize that  mid-LAD stenosis. These pictures are all out of order, but before we did that, now knowing she has LV failure, knowing her RV wasn't doing the greatest, we put in a balloon  pump because she was already doing reasonably well on the epinephrine. As you can see, we went in through the right groin, put in a 40cc balloon pump, ending at the right level.  We just flowed that to position. So here we wired, ballooned, and stented the LAD. This is the end result. It looked great, good flow, good stent expansion. Obviously,  we did all the right things like iversing this and sizing it one-to-one with the vessel and other things that are technically important to ensure that you have a good PCI result.  So we did that, took her back to the ICU. Initially, she was doing great with the IABP, and especially because she has MR, which again is a very important indication for  interiortic balloon pump, one of the last few remaining indications. She responded tremendously to this, decongested her lungs, peed out extensively with the Lasix infusion. Her  cardiac index went up as high as 3 to 3.5, which is near normal or really good. And her  ventilator requirements improved. But suddenly, post-procedure day two, so by now she was about  five days in the hospital, she started having worsening shock. Her urine output declined despite vasoactive medications, furosemide. And that is a red flag because when somebody  is doing really, really well and suddenly dips, you have to start thinking what caused this dip.  It's important to know that not all shocks are made alike. So we started norepinephrine,  added some vasopressin. The PA catheter just in time stopped working and refused to transduce.  We tried to reposition it at the bedside. It didn't work. So now we have no assessment of  her hemodynamic situation. So she has started having peripheral vasodilatation. She started,  for somebody with cardiogenic shock, she started getting warm in the extremities, which is rare,  and essentially should point you in the direction of an alternate etiology or mixed cardiogenic and  septic shock. This is a graph of all her vitals. Obviously, I'm not expecting you to read through  this. But what I want to highlight is her fever curves. Gradually, her temperatures are going up  102, 104. She developed AFib-RBR here. As you can see, her pulse rates are pretty high,  which preceded this fever curve. And then she was better controlled amyotrone, but her pressure  started tanking. So essentially, she got better and then suddenly got worse. And that's the  temporal course that I wanted to show you. Like I said, the fever curve, the AFib-RBR were the  highlights. So we repeated an echocardiogram at this time. Like I said, our PA catheter wasn't  working. But these are two slides I wanted to show you. One, her right ventricle is far more generous here than it was on the initial echocardiogram. Her mitral valve is leaking  back quite a bit. But comparing apples to oranges, but it probably looks better compared to the  original echocardiogram that we got at admission. This is a tricuspid regurgitation jet. If you see  a TR jet like this, a triangular, that means there's a rapid equalization of pressures across.  TR is much worse than you can ever imagine on color Doppler. So she went down for a repeat right heart cath, because prior PA catheter stopped transducing. Now here, as you can see,  are the pressures up, which pressures are up? They're about the same, but her cardiac index is still 1.8. Papi cardiac power output is relatively unchanged. So most things were  relatively unchanged, but she was clinically doing worse. So then you start suspecting that  this is not a central hemodynamic problem. Then you start wondering if this is a peripheral problem,  which sure it was. But given all that is going on, essentially with now with biventricular failure,  you wanted to give her the best shot at cardiogenic shock survival. So the IBP wasn't doing his job. So she actually got upgraded to biventricular impeller assistance. So this is  the echocardiogram after impeller. So here you can see this is the impeller shaft in the LV  outflow tract coming into the left ventricle, to the left ventricle with the left side impeller.  Here you see the impeller shaft and the shadowing of the right side impeller. This is the echo  after the impeller placement. And despite the impeller, her LV is not doing a whole lot. This  septal flattening and the septum being pushed towards the left ventricle, suggesting that  the right ventricular pressure volumes are high. This is severe, severe tricuspid regurgitation  through the tricuspid valve. These color changes here, this, you know, splash of rainbow colors is  because of the impeller catheter being across the tricuspid valve. So like I said, she received  biventricular support, impeller CP, impeller RP, went back to the ICU. As you can see, her urine  output declined. Pay attention to the small number in parentheses. Essentially it's ml per kg per  hour, and she's really like single digit cc's per hour. That's what I wanted to highlight.  She continued to be oliguric, worsening temperatures. At this point, she'd been pan-cultured already. They grew klebsiella in the blood, developed multi-organ failure. At this  point was on the cusp of needing dialysis, and then that's when family stepped in and said, I  think we don't want to prolong this any further. We transitioned her to comfort care, and then she  passed peacefully with the family at the bedside. Thank you for your time. The reason I wanted to  bring this case is this is a critical care forum. It's not a cardiology forum, so cardiogenic shock  is not the only shock we see. And as a critical care cardiologist, I've worn both hats, and I see  it from both sides. Shock can come in many ways and shapes and forms, sometimes often in different  patients, but sometimes in the same patient. So it's always important to have a holistic approach  to shock, understand what alternate etiologies there might be, and then hopefully this will be a good segue into the subsequent talks of this session. Thank you all for your time,  and I look forward to questions that you might have. Thank you.

Video Summary

Dr. Saras Chandra Vallabha Josula, an interventional and critical care cardiologist, presented a case of a 71-year-old female with unresponsiveness and worsening symptoms over the past four days. The patient had swelling, blistering, erythema, and generalized edema on her legs. She had tachycardia, hypotension, and was not breathing well. Initial labs showed high potassium, acute kidney injury, and high B-type nitritic peptide. She was treated for septic shock with norepinephrine, broad spectrum antibiotics, and other medications. An echocardiogram showed biventricular decrease in function and moderate to severe mitral and tricuspid regurgitation. Coronary angiogram revealed a mid-LAD stenosis, which was revascularized. The patient initially responded well to treatment but suddenly worsened with declining urine output and peripheral vasodilation. Repeat echocardiogram showed worsening right ventricular involvement. The patient was placed on biventricular impeller support but continued to decline and eventually passed away. The case highlights the importance of considering alternate etiologies and taking a holistic approach to shock.

Asset Subtitle

Cardiovascular, Procedures, 2022

Asset Caption

Hemodynamics in patients with shock are often complex and can change rapidly as the course of disease evolves and as therapies are initiated. Close monitoring of patients with shock is clearly important, but precisely how to do this remains a subject of great controversy. Years ago, invasive hemodynamic monitoring was common and even routine in some settings, but over time less invasive options have evolved. It remains uncertain whether something has been lost in this shift.

Meta Tag

Content Type Presentation

Knowledge Area Cardiovascular

Knowledge Area Procedures

Knowledge Level Intermediate

Knowledge Level Advanced

Learning Pathway Cardiothoracic Critical Care

Membership Level Select

Tag Shock

Tag Monitoring

Tag Cardiothoracic Critical Care

Year 2022

Keywords

Dr. Saras Chandra Vallabha Josula

interventional and critical care cardiologist

septic shock

biventricular decrease in function

mid-LAD stenosis

	Society of Critical Care Medicine 500 Midway Drive Mount Prospect, IL 60056 USA Phone: +1 847 827-6888 Fax: +1 847 439-7226 Email: support@sccm.org	Contact Us About SCCM Newsroom Advertising & Sponsorship DONATE	MySCCM LearnICU Patients & Families Surviving Sepsis Campaign Critical Care Societies Collaborative	GET OUR NEWSLETTER
© Society of Critical Care Medicine. All rights reserved. \| Privacy Statement \| Terms & Conditions The Society of Critical Care Medicine, SCCM, and Critical Care Congress are registered trademarks of the Society of Critical Care Medicine.