SERENITY NOW Posted September 29, 2016 Share Posted September 29, 2016 You, the intrepid EM PA resident, arrive for your Saturday night shift in a busy rural ED. You sit down for all of a minute when you see your first patient being wheeled in by EMS and you get up to meet them at the bedside. They report, "we've got a 78 yo F coming in from home, here for generalized weakness and SOB for the past week or so. Vitals are 142/68, HR 156, Satting 95% on RA. Her son told us she has a history of dementia, DM, heart attack, and "kidney problems." Your quick glance at her and she is awake, somewhat comfortable appearing, stable for now. What else would you like to know from EMS? How do you begin to assess the patient? What are you asking your nursing staff to do in the meantime? Since I am still a new PA resident, I wanted to share this case with the understanding that I still have a lot to learn and may not be able to answer all of your questions. Hopefully the experienced PAs will chime in and we can all work through the best thought-process for this case together. (If the forum newbies don't recognize the "intrepid PA", please search for andersenpa's prior cases. I really enjoyed reading them as a student, and now this is my way of trying to contribute) (UPDATE 2018 ) I have subsequently done more student cases and will continue to do them. To check out my others, click the below links... "stink eye case" / red eye chief complaint "Found down" - More to come! PS - Requests welcomed... if you have a chief complaint you struggle with, let me know and I'll reach back into the memory bank for cases related to those! Link to comment Share on other sites More sharing options...
crossbone2007 Posted September 30, 2016 Share Posted September 30, 2016 Recent surgery? Travel? Smoking? Fever? I'm worried about a PE, or an MI. I would be getting an ECG, CXR, lites, cardiac enzymes, maybe D-dimer. Sent from my VS985 4G using Tapatalk Link to comment Share on other sites More sharing options...
UGoLong Posted September 30, 2016 Share Posted September 30, 2016 A heart rate of 156 for someone of her age isn't really stable. 156/(220-78) = about 110% of max age adjusted heart rate. She can't stay there forever. Sent from my iPad using Tapatalk Link to comment Share on other sites More sharing options...
Administrator rev ronin Posted September 30, 2016 Administrator Share Posted September 30, 2016 (Prodding the MIA eager students to jump in...) What is the relationship of her SBP to her HR, and why does that matter? Link to comment Share on other sites More sharing options...
SERENITY NOW Posted September 30, 2016 Author Share Posted September 30, 2016 Good thoughts so far, team. That tachycardia rule is really good to keep in mind. You ask her the questions but she seems somewhat confused and starts going off on a tangent about how she doesn't like hospitals. Given her history of dementia, you know she may not be able to provide a reliable history, so you ask EMS if her son is coming in, or if they were given any contact information (they give you his phone number). They say their house was rather unkempt, and it didn't seem as if the son was taking too good of care of her. Your nurses get to work on a full set of vitals including temp (afebrile), get IV access, put on cardiac monitor and the EKG Who can interpret this EKG for me? I was lucky enough this past month to work with a great cardiologist who emphasized that there are very few EKGs that are 100% specific/pathognomonic... every ekg finding will have a differential. So, what would your differential for this EKG be? How might you be able to differentiate between the possibilities? Link to comment Share on other sites More sharing options...
fakingpatience Posted September 30, 2016 Share Posted September 30, 2016 Was EMS able to determine if this is her baseline mentation from the son on scene? Did they grab a bag of her meds? Does she pull up in the computer system to obtain a better PMH? Last time she was seen in this hospital system? I'm having trouble getting seeing a bigger picture of the EKG, but from my small look no distinct P waves, rate right at 150 on the nose with the small box method, regular rhythm on the 12 lead at least, narrow QRS intervals, normal enough axis; going with SVT, possibly swayed to think flutter with V2, but the rate is slower than expected for a 1:1, I'd put that far lower on the ddx. Some ST seg. depression but could easily be rate related. Any edema, rales? Does she look ill-kempt? Well nourished? ETA: Can we get a bedside BGL while awaiting more labs? Link to comment Share on other sites More sharing options...
fakingpatience Posted September 30, 2016 Share Posted September 30, 2016 Also, just re-read the title of this post, is she about to go into v-tach/ fib on us?! Link to comment Share on other sites More sharing options...
crossbone2007 Posted September 30, 2016 Share Posted September 30, 2016 Supraventricular tachycardia, most specifically, atrial flutter? Any cardiac murmur? She has a wide pulse pressure. The EKG also kinda looks like tombstones, worried about MI, cardiac enzymes? Sent from my VS985 4G using Tapatalk Link to comment Share on other sites More sharing options...
crossbone2007 Posted September 30, 2016 Share Posted September 30, 2016 What medication is she on? Potassium level? Sent from my VS985 4G using Tapatalk Link to comment Share on other sites More sharing options...
SERENITY NOW Posted September 30, 2016 Author Share Posted September 30, 2016 Excellent thoughts! These were the same thoughts I had as well.... Was EMS able to determine if this is her baseline mentation from the son on scene? Did they grab a bag of her meds? EMS didn't know what her baseline mental status was. You call the son and it appears like aside from the generalized weakness, she is at her baseline mental status of AOx1 and answering questions inappropriately at times. Good to know... we don't have to add altered mental status to our problem list. We don't know her meds. Does she pull up in the computer system to obtain a better PMH? Last time she was seen in this hospital system? Unfortunately no records on her. She typically goes to a different neighboring hospital. I'm having trouble getting seeing a bigger picture of the EKG, but from my small look no distinct P waves, rate right at 150 on the nose with the small box method, regular rhythm on the 12 lead at least, narrow QRS intervals, normal enough axis; going with SVT, possibly swayed to think flutter with V2, but the rate is slower than expected for a 1:1, I'd put that far lower on the ddx. Some ST seg. depression but could easily be rate related. Excellent. This is a regular, narrow complex tachycardia. With a rate of around 150, my mind goes to aflutter with 2:1, but ddx includes SVT, and we've been fooled with a fib / MAT and sinus tach too at times. What would you like to do to differentiate between these? Any edema, rales? Does she look ill-kempt? Well nourished? She is a heavier patient, diminished lung sounds, some leg swelling. Ill-kempt. ETA: Can we get a bedside BGL while awaiting more labs? 182 At this point, your portable CXR is done. You tell her that she has an arrhythmia and out of nowhere she blurts out "my god you better not give me the precordial thump!" Turns out she used to be a big fan of medical TV shows, yet ironically hates the hospital... No VT/VF.... yet...! Link to comment Share on other sites More sharing options...
crossbone2007 Posted September 30, 2016 Share Posted September 30, 2016 That does not look good. My God! That looks like takotsubo cardiomyopathy! Heart failure? Sent from my VS985 4G using Tapatalk Link to comment Share on other sites More sharing options...
crossbone2007 Posted September 30, 2016 Share Posted September 30, 2016 Had she been under a lot of stress, death in the family? Combining the CXR with the EKG makes it look more like takotsubo. Could be tamponade but the EKG does not match the senario Sent from my VS985 4G using Tapatalk Link to comment Share on other sites More sharing options...
SERENITY NOW Posted September 30, 2016 Author Share Posted September 30, 2016 No death or stress in the family. I've only seen a couple cases of takotsubo and they both came in with very crazy STEMIs on ekg and were only diagnosed after clean coronaries and echo. This was not one of those cases. I wouldn't let the CXR throw you off the common things quite yet. I can definitely see some cardiomegaly, but with portable AP CXRs the heart will always look bigger than what it actually is... this didn't look too terribly big to me. So we have a somewhat stable patient with a regular, narrow complex tachycardia at a rate of 150 with the differential for this listed above. Where do you go from here? Link to comment Share on other sites More sharing options...
crossbone2007 Posted September 30, 2016 Share Posted September 30, 2016 The heart seems to occupy more than 65% of the chest. I understand that it is portable. I was thinking of TCM because of the tombstones look of the EKG and the size of the heart. But would need an Echo to confirm. I might be wrong though. Sent from my VS985 4G using Tapatalk Link to comment Share on other sites More sharing options...
crossbone2007 Posted September 30, 2016 Share Posted September 30, 2016 Anything unusual finding on physical exam? Narrow complex tachycardia, stable patient, next step I would do vagal maneuver, if unsuccessful, then adenosine Sent from my VS985 4G using Tapatalk Link to comment Share on other sites More sharing options...
Deanj59 Posted September 30, 2016 Share Posted September 30, 2016 Recent surgery? Travel? Smoking? Fever? I'm worried about a PE, or an MI. I would be getting an ECG, CXR, lites, cardiac enzymes, maybe D-dimer. Sent from my VS985 4G using Tapatalk While PE is a good thought in any pt. with dyspnea and tachycardia this patient is hypertensive. Obstructive processes like PE increase right ventricular pressure, pushing the septum of the heart to the left and reducing left ventricular filling and systolic BP. Doesn't mean this is not a PE, but just keep that physio in mind because it would be a less likely also with a 95% SpO2. Not 100% sure on this case thus far but have my ideas. I would point out the precordial leads at something to look at more...I'll let the students continue to reply though. Link to comment Share on other sites More sharing options...
Administrator rev ronin Posted September 30, 2016 Administrator Share Posted September 30, 2016 [...] maybe D-dimer. As a bit of an aside, what is a D-dimer going to tell you in a 78 year old patient? What levels are you going to be looking for? Link to comment Share on other sites More sharing options...
newton9686 Posted September 30, 2016 Share Posted September 30, 2016 D-dimer is basically worthless in this patient. Also where the physical exam guys? I would like to know if lung fields are clear, any bruits, heart sounds, vascular status and a neurological exam. Given that the patient is 78, diabetic with possible delirium, I would like to do a genital exam looking for signs of a UTI due to propensity for yeast infections in DM pts. I am interested in K levels as well after looking at that EKG. Link to comment Share on other sites More sharing options...
UGoLong Posted September 30, 2016 Share Posted September 30, 2016 Hard to read such a little EKG. A rate of 150 is atrial flutter with 2:1 response until proven otherwise. Also inferior and anterolateral ischemic changes that could be because of the rate. I'd like to see a V4R lead too, given how many inferior changes have right-sided involvement. Again, it would be easier if I was looking at the patient. I agree that it's unlikely to be a significant pe with such a good spo2. Sent from my iPad using Tapatalk Link to comment Share on other sites More sharing options...
SERENITY NOW Posted September 30, 2016 Author Share Posted September 30, 2016 D-dimer is basically worthless in this patient. Also where the physical exam guys? I would like to know if lung fields are clear, any bruits, heart sounds, vascular status and a neurological exam. Given that the patient is 78, diabetic with possible delirium, I would like to do a genital exam looking for signs of a UTI due to propensity for yeast infections in DM pts. Patient is obese. Diminished lung sounds. No bruits. Difficult to assess JVD. S1, S2, no murmurs. 2+ peripheral pulses. Lower extremities obese but still with some pitting edema. AOx1, lucid, answers questions but not necessarily appropriately (though reportedly at baseline), strength and sensation nl symmetric UE and LE. I did not do a genital exam to evaluate for signs of a UTI, but the UA was negative. I am interested in K levels as well after looking at that EKG. Okay, initial lab results come back: CBC: 8 > 10 / 39 < 173 BMP: 142 / 4.8 / 102 / 27 / 27 / 1.9 Mag: 2.2 Phos: 4 VBG: 7.34 / 47 Lactate: high normal (we have different range from most hospitals) UA: negative Okay, so we agreed with crossbones and we went ahead with vagal maneuvers. Even though we tried the "latest and greatest" vagal maneuver (see below), we were not able to convert the patient. The research-supported most successful vagal maneuver: https://www.ncbi.nlm.nih.gov/pubmed/?term=26314489 Randomized 433 patients with SVT to one of the following:“Modified” Valsalva maneuver: patient sitting up performs Valsalva using a syringe to maintain 40 mm Hg for 15 sec and then placed supine with passive leg raise immediately after procedure (see video) “Standard” Valsalva maneuver: patient sitting up performs Valsalva using a syringe to maintain 40 mm Hg for 15 sec while maintaining upright position 43% of the patients in modified Valsalva group versus 17% in the standard technique achieved sinus rhythm at one minute yielding an absolute risk reduction of 26.2% (p<0.001) with a number needed to treat of about 4 (3.8) So our next step was adenosine. Remember this is a unique drug to give. Always look out for WPW before considering this. Warn the patient that its going to feel very uncomfortable, you have to have a decent-bore proximal IV, have arm elevated, push it fast followed by a saline push so that it makes it to the heart quickly. It has a very short half life, so you better have the EKG machine running! Here is what we saw... (FYI all of these images are not the actual images but representative for HIPPA reasons) 10 seconds after the adenosine was pushed, the patient went back into the rapid rhythm again. So, it should be pretty clear at this point that the patient has aflutter with RVR. What would you all like to do at this point? What are the main management points you have to consider in patients with afib/flutter? Is rhythm control/conversion the goal for this patient, or just rate control? Agree with above that there are some ST segment changes concerning for perhaps rate related ischemia. What medications would you like to give to facilitate these goals? Link to comment Share on other sites More sharing options...
jk5142 Posted September 30, 2016 Share Posted September 30, 2016 I would want to try and lower possibility of AMI on the differential, while simultaneously managing/working up AFlutter. -cardiac biomarkers -additional labs (didn't see Ca levels), PT/INR -additional history/chart review to help determine likely duration, new onset, etc of the AFlutter as she's probably seen a cardiologist with history of CAD s/p MI in the past. -get TEE -would probably try to use electrical cardioversion rather than pharmocological (per the cardiologist I rotated with, AFib tends to respond better to pharmacological agents (BB, CCB, etc) while AFlutter responds better to DCC) *don't really know how to read CXR -but is there some widening of the mediastinum, + tracheal deviation there? Link to comment Share on other sites More sharing options...
SERENITY NOW Posted September 30, 2016 Author Share Posted September 30, 2016 I would want to try and lower possibility of AMI on the differential, while simultaneously managing/working up Aflutter. Good thoughts. Always think about a fib/flutter (especially new onset) as more of a symptom and try to find the underlying cause. -cardiac biomarkers - troponin comes back .06 (very mildly elevated, often seen in tachyarrhythmias and scoffed by cardiologists because its not necessarily a reflection of acute plaque rupture/ACS -- the inpatient team can wait for the trends!) -additional labs (didn't see Ca levels), PT/INR - normal -additional history/chart review to help determine likely duration, new onset, etc of the AFlutter as she's probably seen a cardiologist with history of CAD s/p MI in the past. She has not been to our hospital before, so no records. You call the son and he doesn't remember a history of any heart arrhythmia. -get TEE - generally we don't get this in the ED, but good thought for inpatient workup. -would probably try to use electrical cardioversion rather than pharmocological (per the cardiologist I rotated with, AFib tends to respond better to pharmacological agents (BB, CCB, etc) while AFlutter responds better to DCC). You are absolutely right... our cardiologist explained it like this: in general, a fib is easily rate controlled, but hard to rhythm control, as opposed to aflutter which is harder to rate control, but easy to rhythm control/cardiovert. However, I personally haven't seen any stable patients electrically cardioverted in the ED even for aflutter. I'd imagine its because A) they're stable so its not time critical, and B) we generally don't try to rhythm control in the ED, especially in a case like this where sx have been going on for an unknown period of time (>48hrs) with risk of clot/embolism. We generally will anti coagulate with heparin and will rate control the patient with IV medications (cardizem is our favorite), especially in this case where there is some concern for symptomatic tachycardia and possible rate related ischemia. Then we admit the patient to cardiology for the full etiology workup (full lytes, tsh, echo, ischemic, etc), anticoagulation bridging, consideration of rhythm control and transitioning to PO rate control. So, we went ahead and did our standard routine. Started the heparin, gave cardizem weight based dosing .25 mg/kg which required 2 doses and then a drip to achieve adequate rate control within about 30 minutes. The patient reported that she felt better, vital signs remained normal, repeat EKG did not show any more ischemic signs, and all was good. Called up to the CCU (because she is requiring a drip to maintain rate control) admitting resident who accepted the patient without issue. Nice job team! Time to move on to the next patient... Link to comment Share on other sites More sharing options...
SERENITY NOW Posted September 30, 2016 Author Share Posted September 30, 2016 ***Paging intrepid PA*** About 30 minutes later, the nurse comes running up to you - "Hey, I was about to take her upstairs but she doesn't look so good!" You go to evaluate her and she is now pale, only arousing to physical stimuli. You repeat vitals and note BP 67/43 HR 96 RR 24 pulse ox 84% on 5L. You look at cardiac monitor and see that she is still in rate controlled aflutter, so no change there. What do you do now? In general, how do you approach the acutely decompensated/shocky/hypotensive patient? What are the general categories of shock states, how would you apply them to form a ddx relevant to this case? How do you distinguish between the general shock states quickly and at the bedside? What can you do to empirically treat her in the meantime? precordial thump?! Link to comment Share on other sites More sharing options...
jk5142 Posted October 1, 2016 Share Posted October 1, 2016 Primary survey -airway/breathing: is she protecting her airway (i'd consider putting her on HFNC while preparing for possible intubation) -circulation: check pulse to ensure she's perfusing, look for any clues (acrocyanosis, peripheral plethora, heart/lung sounds), and give her a small 250ml bolus of NS and check response -Check her drips/meds: make sure she didn't inadvertently get a big dose of the dilt, NTG etc -stop the dilt drip if it hasn't already Shock -cardiogenic possibly acute decompensated HF -distributive (include neurogenic from embolus or bleed) -hypovolemic (acute gi bleed) -obstructive (pe, tamponade) Bedside US to look at the IVC, LV function, tamponade *Hope that the patient responds to HFNC and fluid bolus -Cardiology comes down soon Link to comment Share on other sites More sharing options...
SERENITY NOW Posted October 1, 2016 Author Share Posted October 1, 2016 Very nice approach jk5142! You hit the majority of things to consider Primary survey -airway/breathing: is she protecting her airway (i'd consider putting her on HFNC while preparing for possible intubation). She is protecting her airway. Agree with high flow NRB for now. While intubation is definitely something to consider, remember that RSI meds and then positive pressure ventilation is really hard on a patient in shock - it will worsen most of their hemodynamics and they often crump. Thats why many EM providers are recommending "resuscitation sequence intubation" RSI , or "resuscitate before you intubate", especially in this case where the primary issue seems to be cardiovascular shock as opposed to a primarily respiratory issue. -circulation: check pulse to ensure she's perfusing, look for any clues (acrocyanosis, peripheral plethora, heart/lung sounds), and give her a small 250ml bolus of NS and check response. she has weak pulses, has pale extremities, clear heart, and now you can hear crackles on exam. your 250 cc bolus does not help. -Check her drips/meds: make sure she didn't inadvertently get a big dose of the dilt, NTG etc. -stop the dilt drip if it hasn't already - excellent. Shock -cardiogenic - possibly acute decompensated HF -distributive (include neurogenic from embolus or bleed) I'd also add sepsis as a possibility since its so common, and we often see reactionary tachyarrhythmias like afib/flutter in response to sepsis as well. -hypovolemic (acute gi bleed) -obstructive (pe, tamponade) One of the easiest bedside exams that you can do to help narrow which type of shock is occurring is just by putting your hands on the patients extremities. If a patient is hypotensive with warm extremities, its likely one of the distributive varieties (sepsis, anaphylaxis, neurogenic etc). If they have cold extremities, its likely hypovolemic vs obstructive vs cardiogenic. In this case, the patient has cool extremities, delayed cap refill, pale appearing -- all consistent with the latter shock states with high systemic vascular resistance -- we can tentatively take off distributive / sepsis for now. You then assess overall volume status and she appears volume overloaded... pitting leg edema, now with crackles on the lungs. If she looked dry, you could check a quick hemmoccult to ensure no GIB since you did just start them on heparin, but this probably isn't needed in our case. Bedside US to look at the IVC, LV function, tamponade. I like that you are going for the ultrasound... it really shines in cases like this, where you don't have time to wait lab tests to come back. This can help us again to keep narrowing down our categories of shock. Checking for the IVC is a great way to ddx hypovolemic (small collapsible ivc) from cardiogenic/obstructive (large noncollapsible ivc). In this case, you see an IVC that is 3cm and noncollapsible -- We can now take hypovolemic off the ddx. You should be aware that recent studies have not shown there to be great / linear predictive values of IVC to CVP, BUT considering we are using it more as a "is it one extreme or the other" in conjunction with physical exam, I think the vast majority of EM providers accept it in this use. So you make your way to do a quick focused echocardiogram, quickly rule out effusion, and then you use a very simple tool to confirm your gestault and you see this: This is the "E-point Septal Separation", or the EPSS -- basically its a measure of how much the mitral valve moves, and in a low EF, the heart is barely pumping and it won't move much, resulting in an increased distance/separation from the septum. Our patient's EPSS is 2.37, probably in the EF of 10-15% range. So, we know that this patient is in cardiogenic shock. At this point, we know that giving the patient more fluids will probably just hurt them (fall off the other end of the frank starling curve), so we have to go to inotropes like dobutamine to temporize the shock as we sort through things. So, what happened exactly? Why is this patient in cardiogenic shock? Can we offer a more targeted therapy in addition to the empiric therapy / inotropes? Was there a mistake made, and if so, what could we have done to avoid it? Link to comment Share on other sites More sharing options...
Recommended Posts
Archived
This topic is now archived and is closed to further replies.