Tag Archives: Cardiovascular

Conference Lectures 1/2020

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Obstetrics and Gynecology Emergencies – Dr. Marques

Normal Vaginal Delivery Key Steps

  • Support the perineum to prevent tearing with delivery of the anterior shoulder
  • Upon delivery of the anterior shoulder, provide upward pressure to deliver the newborn
  • Pull only gentle traction when delivering the placenta, to avoid uterine inversion

Post-Partum Hemorrhage

  • Palpate the uterus to feel for inversion or retained products
  • Provide tone by providing suprapubic pressure with an external hand and uterine pressure with an intravaginal hand
  • Oxytocin can be given IM or IV to treat uterine atony

Shoulder Dystocia

  • Leg hyperflexion and abduction at the hips along with suprapubic pressure (McRobert’s Maneuver) can be done if the anterior shoulder cannot be delivered

Breech Delivery

  • This happens in 3-4% of all deliveries
  • Do not pull traction at any time, as this can lead to entrapment in a cervix that is not dilated
  • A pressure against the popliteal fossa can help flex the leg and deliver each leg

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Oral Boards: Sepsis Due to Spontaneous Bacterial Peritonitis – Hugh, Shoff, MD

  • The CMS Core Measures (SEP-1) provide quality measures for providers to follow in sepsis
  • Severe Sepsis is defined as Lactate >2 or organ dysfunction
  • Septic Shock is defined as severe sepsis with hypoperfusion despite fluid resuscitation or lactate>4
  • Within 3 hours of presentation, obtain a lactate, blood cultures prior to broad spectrum antibiotics, and 30cc/kg fluid resuscitation
  • Within 6 hours, lactate must be repeated if >2

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CCU Follow-Up – Phil Giddings, MD

Myocardial bridging- coronary arteries travel deep into myocardium as opposed to laying upon the muscle

The vessels are occluded but when there is demand ischemia it can look like a STEMI

Myocardial bridging is fairly common in the general population, but usually isn’t symptomatic or pathologic.

If it is symptomatic- you could do Ca2+ channel blockers, beta blockers, and even myotomy or CABG if you’re feeling wild.

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Urology Review- Isaac Shaw, MD

Priapism-

  • Normal tumescence- veins constrict so the corpus cavernosum engorges because blood flows in
  • Ischemic= low flow, less venous outflow, rigid, painful
  • Nonsichemic= high flow, more arterial inflow, half rigid
  • (Distinguish w/ a blood gas)
  • Treatment
  • anesthetize by blocking the dorsal nerve of the penis (2 & 10 o’clock) w/o epi
  • then aspirate at 3 or 9 o’clock from the corpus cavernosum
  • Use a phenylephrine stick from Room 9, 100mcg-500mcg Q1-5min

Fournier’s Gangrene

  • polymicrobial
  • assoc w/ DM
  • 22-40% mortality
  • empiric + clindamycin (clinda first because it’s addressing the toxins)

consult surgery before imaging

Paraphimosis

  • foreskin trapped proximal to glans so the tip can get ischemic
  • Treatment: manually reduce, dextrose, lube, may have to incise the dorsal foreskin

Phimosis

  • foreskin can’t be retracted over the glans 2/2 inflammation
  • Treatment in ED: topical steroids with urology follow-up

Urinary Retention

  • often have hesitancy, nocturia, frequency, urgency
  • >200cc PVR
  • d/c w/ Foley à Uro will keep that in for 2 weeks prior to void trial

Renal Stones

  • remember that 10-15% don’t have hematuria
  • CT w/o contrast is still the standard for diagnosis, but some emergent literature exists that US alone is sufficient in young, healthy patients
  • if <5mm, 90% pass; but if >8mm, 5% pass
  • admit for intractable vomiting, pain, urinary extravasation, infection & obstruction

Balanitis

  • Candida on the glans
  • Associated with DM or uncircumcised

Torsion

  • twisted around the spermatic cord
  • if actively torsed, you will NOT have a cremasteric reflex
  • ultrasound 88-100% sensitive because they can torse and untorse
  • consult before imaging

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Breaking Bad News– Frank Woggon, PhD

  • insensitive truth telling can have similar effects as lying
  • goals include gathering info, provide info, support patient, strategy for care
  • keep it simple, no jargon, talk slow, repeat PRN, use neutral language, be honest, allow emotions, consider cultural differences
  • “compassion is the willingness to let yourself be affected by the life and suffering of others”

SPIKES

  • Setting- privacy, sit down, eye contact, turn off pager
  • Perception- don’t combat denial at first, interpret first
  • Invitation- ask how much they want to know first
  • Knowledge- “what I’m about to say is not good,” be direct but not blunt, use their language
  • Empathize- ok to validate the emotions, silence is ok
  • Strategy & Summary- what comes next

GRIEV_ING Protocol

  • Gather the family
  • Resources- call for support
  • Identify yourself & staff, those in the room
  • Educate the family about what happened
  • Verify that the patient died by using that word
  • SPACE- silence is ok, let them have their gut reaction
  • Inquire whether they have questions
  • Nuts & bolts- organ donation, funeral arrangements, personal belongings, etc.
  • Give contact info for f/u questions

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STEMI Mimicks – Frank Shary, MD

OMI= occlusive MI

  • V2 & V3 2mm elev = STEMI; Everywhere else 1mm
  • Wellens: biphasic T wave, they recently had an OMI, symptoms may have gotten somewhat better by the time of the EKG, they need a cath
    • Deep T Wellens- deep and wide
  • LV aneurysm- deep Q wave w/ biphasic T wave, static
  • Sgarbossa criteria- OMI in the setting of LBBB and/or paced rhythm
    • look at vector of QRS and vector of ST segment
    • concordant elevation or depression greater than 1mm
    • discordant greater than 5mm
  • Hyperacute T waves- early into the ischemia, before ST elevation, cath soon because you have potential to save more myocardium, large area under the curve especially in proportion to the QRS complex
    • L circumflex is the vessel most likely to be silent
  • aVR- if it’s the only lead elevated and everywhere else is diffusely depressed, you might have diffuse subendocardial ischemia
    • could be bad triple vessel disease

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Managing the Bleeding Patient Without Blood Products – Chase, PharmD

There are 6 Jehovah’s Witness churches in Louisville

  • Plasma Derivatives are technically not Blood products… so whether or not a patient wants that is up to the individual
  • albumin, clotting factors, PCC, Immunoglobulins (including Rhogam and vaccines)
  • equine Ig and Crofab could also be iffy
  • ECMO, cardiopulmonary bypass, dialysis are allowed generally

Source Control

  • bone wax/putty- use in NES and long bone fx, high infection rate though
  • oxidized regenerated cellulose- ex. Surgicell, promotes rebuilding of proteins to heal & achieve hemostasis, like a mesh
  • gelatin matrix- ex. Floseal, more like a gel
  • there is a powder too but it’s $$$ and causes microemboli so don’t use
  • thombin- apply w/ 4×4’s
  • TXA- derivative of lysine THIS IS NOT A PLASMA DERIVATIVE SO THEY SHOULD BE OK WITH IT, 1g over 10min à another 1g over 8-10 hours
  • have a lower threshold to give TXA since there is a decrease in mortality, even if you wouldn’t have given TXA to a non-Jehovah’s witness

Usable Therapies:

  • Cell Saver
    • blood is collected, washed, centrifuged, returned to patient
    • example indications: AAA, TKA, THA, cardiac surgeries
  • Vitamin K
  • PCC- most efficacious
    • 4 factor is better than 3 factor, but if you try to give 3 factor and then just add Factor VII a la carte, more thromboembolic events
  • FFP- prep time is longer, tonzo volume
  • Adnexanet Alpha- new antidote for rivaroxaban and apixaban, we don’t have that
  • Novo7- directly activates Factor VIII, black box warning for thromboembolic events, no difference in mortality but there was a reduction in transfusions
  • Dabigatran reversal- idarucizumab, dialysis, charcoal
  • Antiplatelet reversal- ASA and Plavix are irreversible, but ticagrelor is reversible
    • DDAVP- indicated for DI, von Willebrand disease, uremic bleeding (renal failure), nocturnal enuresis
    • 0.4mcg/kg over 10min

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Pediatric Environmental Emergencies- Dr. Said

Drowning

  • fresh or salt water doesn’t matter, you’re ruining your surfactant
  • if you are anoxic you get brain damage in 4-6min, irreversible
  • cold temp is only helpful if it happens really quickly
  • outcomes depend on initial resuscitation, degree of pulmonary damage, time submerged
  • poor prognosis- coma, apnea, submersion >9min
  • can try vapotherm for positive pressure, albuterol can treat bronchospasm
  • steroids don’t help
  • goal warming 32C
  • if asymptomatic, obs for 8 hours! Oy vey
  • admit if prolonged submersion, respiratory or neuro symptoms, abnormal CXR

Electrical Injuries

  • lightning strikes carry 30% mortality risk, it causes asystole
  • doesn’t cause renal failure or burns/compartment syndrome
  • thicker tissue less damaged
  • tissue between entry and exit wounds could be more damaged interiorly than it appears
  • AC worse than DC because AC at low voltage causes tetany so you’re holding on longer
  • we use DC for defib, countershock, pacing but you get thrown off
  • oral electrical injury – monitor for progressive edema
  • could have delayed bleeding from labial artery

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EMTALA- Melissa Platt, MD

  • in court, all are case-by-case
  • we have to provide a medical screening exam and treat and stabilize an emergency medical condition
  • transferring physician assumes the risk if the patient crumps en route to accepting hospital

Serial ECGs

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I had a fairly interesting patient back in November 2016 when I was at Jewish.  I had picked up a patient with chief complaint of chest pain after an attending handed me the EKG below.  The patient was being rolled back from triage to a room at the attending’s request. 42yo AAM with history of hypertension, hyperlipidemia, diabetes, sleep apnea and CAD status post CABG in 2008.  The patient was complaining of chest pain that initially started when he was sitting at home watching TV about an hour prior to arrival.  He described the pain as sub-sternal and radiating to his left arm. He had associated SOA, palpitations, and diaphoresis along with the pain. He was also nauseated since the onset of pain.

Pretty classic presentation here in a patient with previous heart disease.  His initial EKG recorded in triage is below:

Upon review, you can appreciate that there may be ST elevation in III.  Also, ST depressions are noted in the precordial leads along with ST changes elsewhere. My question to all of you based upon reviewing this EKG: Would you call this is a STEMI and would you activate the cath lab at this time?

The attending that I was working with at the time didn’t feel that we could definitively call this a STEMI based upon the first EKG.  We examined the patient and collected his history after he was brought back.  After labs were collected, the patient received nitro paste.  Despite the paste, he continued to have pain. After approximately 15 minutes of being in the back, the patient reported that his pain was worsening.  The decision at that time was made to get a repeat EKG.  The repeat EKG is below:

 

So now what are your thoughts? There is obvious ST elevation in the inferior leads.  There are also ST depressions in the precordial leads.  This EKG was taken 34 minutes after the first EKG which was performed in triage.  Through these two EKGs, you can appreciate the evolution of a STEMI.  This patient was emergently taken to the cath lab at that time and underwent left heart cath. He underwent an impella-assisted PCI to his SVG-PDA and was started on dual anti-platelet inhibitors. Following his PCI, he also had an episode of wide-complex rhythm which resolved after receiving amiodarone.

So this patient who was found to have a STEMI on his repeat EKG had presented with an initial EKG that was non-diagnostic for his condition. Did this affect his outcome in any measure? What can we learn from this?

According to a 2013 study conducted by Riley et. al, in a national sample of patients diagnosed as having STEMI (41,560 patients), 11.0% had an initial non-diagnostic ECG. Of those patients, 72.4% had a follow-up diagnostic ECG within 90 minutes of their initial ECG. There did not appear to be clinically meaningful differences in guidelines-based treatment or major inhospital outcomes between patients diagnosed as having STEMI on an initial ECG and those diagnosed on a follow-up ECG.

So, did the additional 30 minute delay in activating the cath lab affect this patient? Likely not. However, what this case reinforces is the importance of a repeat EKG as 11% of these patients likely will not have STEMI on their first EKG.

 

References:

Am Heart J. 2013 Jan;165(1):50-6. doi: 10.1016/j.ahj.2012.10.027. Epub 2012 Nov 21. Diagnostic time course, treatment, and in-hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram: a report from the American Heart Association Mission: Lifeline program. Riley RF1, Newby LK, Don CW, Roe MT, Holmes DN, Gandhi SK, Kutcher MA, Herrington DM.

Poor Lonely Repeat Troponin – posted by Bertolotti and Huecker

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We have noticed more and more this culture in our ED of obtaining an initial ECG, an initial troponin, and then waiting 2 or 3 or 6 hours to obtain a second troponin only and then discharge if negative.

I dove into the literature and wrote this post to address the SECOND ECG AT TIME OF SECOND TROPONIN as part of a rule out strategy for low risk ED patients.

I will not even address the fact that people are not obtaining a 2nd ECG at time 20-30 minutes from the first. This is on UpToDate, in ACC guidelines, in ACEP guidelines. It is simply standard of care to obtain an early, repeat ECG on anyone you remotely suspect of having ACS. I harp on this in lectures and have posted on it before. I also will not be talking about hs-Troponin (high sensitivity troponin). Many articles and FOAMed commentaries have covered hs-Trop, and we do not have this test at UL. So please do not think you can rule out all comers with 1 troponin, because you need the hs-trop to even consider this.

This post relates to the issue of a repeat ECG at time 2hr or 3hr (I am not a 6 hour guy, I like the 2 or 3 hr depending on symptom time frame). Don and I discussed the 2nd ECG phenomenon and he said it is just our culture at UofL, hence inspring our Room9ER post. Well we need to change the culture.

Now I didn’t want Geralds to cherry-pick an article to try to rebut me on this, so I went down a rabbit hole of ACS rule out, nSTEMI, HEARTS, TIMI and cardiac markers.

If your attention span is reaching its limit here is the bottom line:

All rapid rule out tools and their validation studies involve at least a SECOND ECG with the repeat troponin. HEARTS, ACC/AHS guidelines, TIMI-based rule outs, etc.

I was early to drop the CK and CK-MB on initial and repeat marker testing in favor of solely the troponin, but dropping the ECG is irresponsible. And is not evidence-based.

Below are many quotes and a figure, then a letter to the editor, from various sources. It was actually somewhat difficult to find in the methods exactly when or even if a repeat ECG was done. Much of the time, the ECG done at time of 2nd trop was not even the 2nd ECG, as mentioned above. “Serial ECGs” is the rule. It seemed as though the repeat ECG(s) were implied in the study, and that the research question was simply timing a troponin.

 Dr Huecker composed most of this post because Dr Bertolotti is so excited about and diligently preparing for Research Day. 

Enjoy, and please post comments! 

  

— Patients with probable or possible ACS but whose initial 12-lead ECG and cardiac biomarker levels are normal should be observed in a facility with cardiac monitoring (e.g., chest pain unit or hospital telemetry ward), and repeat ECG (or continuous 12-lead ECG monitoring) and repeat cardiac biomarker measurement(s) should be obtained at predetermined, specified time intervals (see Section 2.2.8). (Level of Evidence: B)

— The c-statistic of troponin only was 0.70. With addition of the ECG the c-statistic improved significantly to a value 0.78, with a likelihood ration test p-value of <0.001

— Anderson et al. JACC Vol. 50, No. 7, 2007 ACC/AHA UA/NSTEMI Guideline Revision August 14, 2007:e1–157                                                                                                    If the initial ECG is not diagnostic but the patient remains symptomatic and there is high clinical suspicion for ACS, serial ECGs, initially at 15- to 30-min intervals, should be performed to detect the potential for development of ST-segment elevation or depression. (Level of Evidence: B)

— ACEP (What will be used for or against you in court, as the case may be)

Acute Coronary Syndromes (Non–ST-Segment Elevation – Adult)

Critical Issues in the Evaluation and Management of Adult Patients with Non–ST-Segment Elevation Acute Coronary Syndromes (September 2006)

Complete Clinical Policy on Non–ST-Segment Elevation Acute Coronary Syndromes (PDF)

Scope of Application. This guideline is intended for physicians working in hospital-based emergency departments (EDs) or chest pain evaluation units.

Inclusion Criteria. This guideline is intended for adult patients presenting to the ED with suspected non–ST-segment elevation acute coronary syndromes.

Exclusion Criteria. This guideline is not intended for pediatric patients, patients in cardiogenic shock, or patients with injury on the initial 12-lead electrocardiogram (ECG).

Critical Questions

  1.  Are serial ECGs useful during the ED evaluation of patients with suspected acute coronary syndromes?
  • Level A recommendations. None specified.
  • Level B recommendations.Perform repeat ECG or automated serial ECGs during the ED evaluation of patients in whom the initial ECG is nondiagnostic for injury and who have symptoms consistent with ongoing or recurrent ischemia. No recommendations can be made in regards to the exact timing of repeat ECGs. Studies suggest that 30 to 60 minutes after baseline may be a reasonable time interval for repeat ECG. 
  • Level C recommendations. None specified.

— Letter: Re: “Troponin-negative chest pain”—a diagnostic evasion?

This brief article is well written and I agree the diagnostic label of ‘troponin negative chest pain’ is unhelpful. However the article repeats some common misconceptions which require correction.

Firstly, the article implies that the majority of patients attending hospital with chest pain have an acute coronary syndrome. This is absolutely not the case – in fact most patients with suspected acute coronary syndrome do not have it. (1) Often patients receive a label of acute coronary syndrome and this is later corrected by the cardiology registrar or consultant on call – although by then it may be too late to change the patient’s perception that they have ‘had a heart attack’.

Secondly, there appears to be a misunderstanding of the value of troponin testing. Troponin assays are positive when there has been myocardial necrosis. They do not give any information about the mechanism of myocardial necrosis – a positive troponin can indicate acute coronary syndrome, but may also occur in heart failure, prolonged arrhythmia, sepsis, pulmonary embolism and many other situations. (2)

Similarly, a negative troponin does not absolutely exclude a cardiac cause for symptoms – nor does it mean the patient is necessarily in a low risk group. (3) Patients with unstable angina, dynamic ECG changes, but negative troponin should be considered as having a similar risk of mortality and morbidity to those with a normal ECG but a positive troponin.

Troponin assays should generally be considered a prognostic, not a diagnostic test, and should be used in conjunction with the patients history and ECG – never alone.

 

Chest pain?

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Yesterday, 10 minutes before the end of a very busy shift in the middle of nowhere:
Nurse hand’s me an EKG for the mom of one of our best young medics. Ischemic STD in II, III, aVF, V5, V6. No STE. Maybe some LVH. No other EKG on file, she hasn’t been here before. I get up to see her right away.
In the room is a 50 yo lady in severe distress. BP 250/140. Describes “tearing” L sided CP radiating to her upper back. I ask her if she has a family hx of sudden death or aneurysms, her son says yes. No SOA. No N/V. Lungs are clear. Can’t palpate pulses in her feet. Slightly obese. She is sweating. There isn’t a CT surgeon in this county; I am sweating, too.
The nurse gets CT ready and I start the ball rolling for big IVs, blood, helicopter, etc. She gets dilaudid 1 mg then 0.5 then 0.5 again for pain and hopefully BP control. I tell everyone she’s now the ED’s top priority. The family of another patient grabs me twice in the hallway and asks why their mom, who fell, hasn’t gotten her home dose of lisinopril yet.
~30 minutes from door to imaging – CTAs = no dissection. Great, I have some time. Pain is well controlled now and BP 150s/80s. Repeat EKG w ischemia resolved completely, normal. Hypertensive emergency? She has a bit of a headache so I scan her head because we’re in CT, but it’s not useful due to the residual contrast. Trops, CBC, CMP, urine, tox, etc. all negative. Now looks great and feeling much better. Wants to go home.
Her son, her nurse, and I spend a long time convincing her she needs to stay overnight. She doesn’t want to be admitted, as she’s starting a new job Tuesday and can’t miss it. Eventually, she agrees to stay. Then we have to convince her to be transferred, since ED MD is the only MD in house overnight and she had me straight terrified. Reluctantly, she agrees to the transfer as long as her son will bring her home Monday night, no matter what. Hospitalist at the local mothership accepts readily. At that hospital, she’d had a negative stress 8 months ago and NES had placed her shunt (pseudotumor, she has a lot of headaches); hospitalist will consult cards and NES when she gets in.
I arrive back to work this morning to find out she’d made it upstate only to be transferred again overnight. She’d been flown to a bigger center after repeat CT head demonstrated SAH. She had 2 aneurysms, 1 was bleeding, both were definitively addressed. 24 hours after walking in the door, at the time of this writing, she is extubated and thriving.
Found this article from 1988 with a similar presentation, but I can’t say I’d ever heard of it before. Something else for your differential. Really consider that admission for observation when something seems wrong, even if you don’t know what it is.
Going to change my drawers now.

Just another overdose…..right?

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20 yo M with unknown PMH comes in to room 9 with AMS and tachycardia to the 180s. Per EMS, he had been found down in his apartment, with crack cocaine pipes and other drug paraphernalia around him. He was found to be tachy as mentioned, as well as febrile with a temp of 103 axillary.

When he arrived in room 9, his HR was still in the 170s-180s. Blood pressure normal. He was pale, diaphoretic, and looked sick. He was speaking inappropriate words and would localize pain, GCS 12. Pupils dilated and briskly reactive. Rectal temp 104.1. CXR normal. Started IVF bolus and placed ice packs to the groin and axillae. Also gave Ativan as this was likely a stimulant overdose.

First EKG showed SVT at 180 BPM. After 2L of crystalloid and ativan, a repeat EKG showed sinus tachy at 140. The pt’s mental status was unchanged. The iStat showed a lactate of 13.

The plan was to place a rectal probe and monitor his temp, give him more fluids and Ativan prn, and re-assess later. I thought this was 100% an overdose. No problem.

About 2 hours and who knows how many room 9s later, I go to review his labs. I haven’t heard anything from nursing other than him continuously pulling out his rectal thermometer probe, so all must be well…Turns out he has a WBC of 44,000. Lactate has trended down, but he is still febrile to 102. This is when it hits me that maybe the guy who I’ve been treating for stimulant overdose is actually septic? His CXR and UA were normal, but maybe he has meningitis or encephalitis and that’s the reason for his mental status? Maybe I’m now 2 hours late with ABx?

I suppress the awful feeling in my stomach and go re-evaluate the pt. His mental status is unchanged from when I saw him in room 9. At least now his HR is in the low 100s. Given his mental status and tenuous vital signs, I know this patient is going to have to come in to the MICU. He’s going to need a head CT and an LP to rule out meningitis. I gave him antibiotics and called MICU. They evaluated the patient, and they agreed.

I chart checked the patient the next day. His LP was normal. His mental status improved overnight and he was transferred to the floor. Turns out this actually was likely all tox-related, but I thought it was a good learning point nonetheless. Sometimes it’s convenient to go down the path you’re led to by EMS or by nursing. Not only is it easy, but it’s usually the right path anyway. The stroke buzzer goes off and you immediately get your quick assessment over with so the patient can go to CT and stroke can do their thing. EMS tells you they found the patient in a house with drug paraphernalia, so you run with that.

But it’s important to keep the differential wide open when you first see a patient. At least consider less likely and less obvious possibilities. At some point, you’ll catch something that you otherwise would have missed until it was too late.

Hypotension

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Late 70s year old female with chief complaint of dizziness and fatigue. Patient has a medical history of HTN and recent cataract surgery.  In triage patient was hypotensive with BP of 70\35 and Bradycardic with a heart rate ranging from 55-60, O2 sats 100% on room air and afebrile.

I found the patient to be lethargic. Otherwise her exam was unremarkable with no focal neurologic deficits, cardiac and pulmonary exam unremarkable, and no abdominal pain. Her husband was in the room and states that they were on their way to their grandson’s high school graduation and she began complaining of feeling dizzy and she started to become lethargic. She had not been sick recently and before this morning she was completely at her baseline. To note yesterday her blood pressure was 180/95 when she checked at home so she typically runs high. No new changes to her medications which consisted of metoprolol Succinate 100mg QD and a Baby Aspirin.

As I talked to the husband he went on to explain that she had recently had cataract surgery on her left eye and that this morning she had a follow up appointment with her ophthalmologist. While at the ophthalmologist appointment the doctor said that the pressure in her eye was high and she received some drops in her eye to bring the pressure down but the husband could not remember the name of the drops.

So I started by getting CBC, CMP, TSH, Urine, Chest xray, EKG, Troponin and a head CT to complete my little old lady AMS workup. Obviously the differential diagnosis for AMS in the elderly is vast so I was considering a lot of different possibilities.  While I waited for her results to come back I called her Ophthalmologist that she had seen that morning to see what drops she had received. Ends up she got Alphagan which is an alpha agonist, Trusopt which is a carbonic anhydrase inhibitor, and 3 drops of Timolol. I discussed with him the possibility of the Timolol on top of her morning metoprolol 100mg as potentially causing her hypotension and bradycardia. He stated he had never seen that happen in his 16 yrs of practice but it is theoretically possible. A quick Uptodate search confirmed that hypotension can occur in as many as 10% of patients using Timolol eye drops which to me was a surprisingly high number.

So I’ll go ahead and cut to the good stuff. All of her labs and imaging returned unremarkable and her EKG just showed sinus bradycardia with a rate of 57.  Ultimately she got 2L of Normal Saline and we watched her for about 5 hrs. Throughout her stay her blood pressure steadily increased and at the time of her discharge she was 135/86 with a heart rate of 74 and she was back to her baseline and much more awake.

I thought this was an interesting case as it seems relatively rare for topical eye drops to result in systemic side effects however in the right patient population it can result in severe side effects. A quick literature search brought up multiple case reports of patient’s having symptomatic bradycardia and even syncope resulting from Timolol use.

So definitely something to keep in mind if you have a elderly or frail patient with acute angle glaucoma who is already on beta blocker therapy. Maybe trying other drops first instead of Timolol or at least be sure to make the patient aware of the possibility of side effects including hypotension, bradycardia, fatigue, and even syncope so they know what to watch out for.

Sick PEs

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We had a very ill patient recently. She was found down upstairs visiting her family member. She was calmly altered, not agitated but was in mild distress. Consciousness fluctuated. Tachycardic and hypertensive initially, then had more labile BP and some hypotension.

We had to intubate her due to poor MS and clinical condition. She coded in CT, we placed a central line on the CT table between her noncontrast head CT and her CT chest. We pushed an amp of Epi and ran out of the room for the CT chest. We were worried about dissection and PE in equal amounts. We could not get good cardiac windows on bedside Echo in room 9 prior to the CT.

She continued to intermittently lose her pulse and drop her BP. We confirmed bilat PEs on the CT when we saw NO contrast left her right ventricle. The CT tech noticed first and became worried the patient had no cardiac output (ie pulseless).

We rushed the patient back to room 9 and gave a tPA bolus (50mg) followed by infusion of 40mg. She was on pressors and heparin and improving. Dr Smith accepted her to Jewish for possible EKOS or even ECMO if needed. On arrival to Jewish a few hours later she coded and died.

I was surprised when I found out she had died. Her O2 sat was improving, HR was decreasing, blood pressure was stable (though dependent on pressors). She received a large amount of crystalloid IV which according to some data might not have been optimal management. She also had the following ECG:

FullSizeRender

I think she was infarcting her myocardium. She likely had pulmonary infarction considering her poor oxygenation. She had coded a few times. She had a lot of strikes against her. Her BEST SHOT was going to a place with catheter assisted treatment for PE and ECMO if needed.

I am posting the case to let everyone know:

  1. How to manage sick PE patients (see post below)
  2. To use tPA in massive and in many cases of submassive PE
  3. TRANSFER sick PE patients to Jewish for EKOS/ECMO
  4. The decision to diagnose PE with RV strain on BEDSIDE Echo with no formal Radiologic testing will depend on your attending

This post from EmCrit / PulmCrit is a beautiful summary with potential dogmalysis related to PE management (see take home points below but do read the post).

In addition, here is a nice review article on catheter-based reperfusion treatment for PE with nice references for further reading.

Take home points from the Emcrit post:

  • The only evidence-based intervention that seems to improve mortality in massive PE is thrombolysis.   The primary goal of therapy should be administration of thrombolysis as soon as possible to patients without contraindication.
  • Consider early stabilization of blood pressure using a norepinephrine infusion, administered peripherally if necessary.
  • Volume administration may facilitate dilation of the right ventricle and hemodynamic deterioration.
  • Intubation is very hazardous and should be avoided if possible.   Patients die from cardiovascular collapse, and intubation may worsen this.
  • For a coding PE patient consider 50mg alteplase bolus as well as an infusion of epinephrine.  Patients can do well despite requiring CPR and high dose vasopressor infusions.

Valsartan/sacubitril use likely to increase significantly

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So I just came across that the Valsartan/sacubitril (Entresto) was given a strong class 1 recommendation by the American College of Cardiology for heart failure.  I haven’t seen much of it in med-recs yet, so I just wanted to post a couple of high points that I think we need to know from the ER side. From what I’m reading this drug will start to replace ACE-Inhibitors in the treatment of Class II-IV heart failure. It’s also prescribed in slightly odd dosing in the combination (51 mg/49 mg or 26 mg/24 mg).

Sacubitril is a prodrug that converts to sacubitrilat. Sacubitrilat is responsible for the benefits of this drug as it inhibits the enzyme neprilysin and stops it from degrading atrial/brain natriuretic peptide.

Ultimately the main thing you need to know are the contraindications with other drugs. Basically there are 3: Lithium, ACE-Is, and Aliskiren. Lithium levels have the potential to increase with this drug, while the other 2 can lead to significant hypotension in combination with Valsartan/sacubitril.

Here’s the ACC release: http://www.acc.org/latest-in-cardiology/articles/2016/05/20/11/30/societies-release-focused-update-for-hf-management?wt.mc_id=fb

Would be appreciate if someone with a stronger background in pharmacy or cardiology than I can chime in.

Must-Read Resuscitation

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Folks,

I know I am incessantly encouraging people to follow Dr. Smith’s EKG blog, but the most recent post is too good to not tell you all about. In it, there is a write up of a fantastic resuscitation.

Highlighted in it are double-defibrillation, Head up CPR, hypokalemia bolus dosing, ultrasound for stemi and VFib (!), esmolol bolus for refractory vfib,  cath lab availability and MDM, hypothermia discussion, and prognostics in cardiac arrests.  I mean, this case report has it all, and it is referenced and discussed for our enjoyment.  Read it.

The resuscitation you wish you had run IS HERE!

Read it. I’ll buy you a drink if you do.

Zach

Spice/Heroin Reactions

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So I’ve had to encounter my two sickest patients in the holding area within the past 2 weeks or so. One was a reminder from intern year while looking through spice charts, while the other was an actual patient that I had 3 days ago.

We always tend to take the “Tank” patients lightly and overlook them sometimes. I just want to use this as a warning (especially to the interns) that sick patients can also use heroin/ETOH/Spice, so pick up on the small interactions that don’t go right. I’ll try to present these starting with how their chief complaint lead to the final diagnosis.

Patient 1 (intern year)

  • middle aged male
  • CC: Spice OD, Nausea/Vomiting
  • Final Diagnosis: Subarachnoid Hemorrhage
  • Time to Diagnosis: 7 hours

So this guy presented as a spice reaction. This was before spice became as widely spread as it is now, and no one knew what to expect symptomatically (not that there is ANYTHING that is characteristic to spice anyways).

General story from talking with this guy is that he used spice for the first time that night. No significant past medical history. He was on a first date where everything had been going well. He had borrowed some spice from his friend where he used back at his place after dinner. Soon after he started having nausea and projectile vomiting and was acting ‘goofy.’ At that his date called EMS and the date ended.

Exam:

  • Gen: Fully A&O, slightly odd in that he seems incredibly happy to be here
  • CV: RRR
  • Pulm: CTAB
  • ABD: NT/ND
  • Neuro: CN II-XII intact, motor intact, sensation intact, ambulates without difficulty to bathroom

This man was like most of our intoxicated patients–a sober re-evaluation. At approximately 2 hours he was still vomiting in the ED, so the medical workup was initiated. Due to his odd behavior with vomiting, we got a CMP/CBC/Tox & CT Head. The night continued busy and I almost forgot about him as I waited for results. Ultimately he never got his CT Head due to being uncooperative but I wasn’t told until hours later. He ended up getting Geodon/Ativan in the ED but instead of calming him down he became more agitated and was no longer oriented. Ultimately getting rolled into room9 to be intubated prior to CT and the final diagnosis was made.

Certain forms of spice that lead to agitation also lead to spikes in blood pressure, and there are a few case reports of significant hypertension occurring after spice use. This guy had the unfortunate case of rupturing an aneurysm after using spice likely from a BP spike. I’m honestly not sure if the outcome would have been any different had I reached the diagnosis sooner — he got repetitive Head CTs and ultimately an EVD on hospital day 3. I didn’t really take him seriously even after I ordered a lab workup. This really changed my perspective on patients being held for intoxication. He spent 1.5 months in the hospital (1 month intubated) before being discharged to rehab.

Patient 2 

  • Middle aged white female
  • CC: Heroin OD got Narcan
  • Final Diagnosis: Cardiogenic Shock
  • Time to Diagnosis: 3.5 hours

This case I handled a bit better (I’d hope after 2 years). Story I could get is that this man had a syncopal episode. Received Narcan PTA by EMS and woke up. In the ED the patient adamantly denies heroin use–states he simply passed out. Luckily I got to him before EMS left, and EMS confirmed reports of bystanders stating opiate use.

Exam:

  • Vitals: HR 120, RR 16, O2 96%, BP 80/45, T 98.0
  • Gen: Fully A&O, drowsy
  • CV: tachycardia
  • Pulm: CTAB
  • ABD: NT/ND
  • Neuro: CN II-XII intact, motor intact, sensation intact, ambulates without difficulty to bathroom

My initial thought was that he may need some more narcan or that he received a longer acting opiate. The tachycardia was a wild card and didn’t make much sense with the picture. He remained afebrile and temp recheck, so I wasn’t thinking sepsis much at that time. At this point due to the tachycardia not making sense I ordered labs (and a tox for co-ingestants) and thought his BP/HR would improve with fluids.

I reassessed him after bolus #1 and #2 and neither HR or BP improved. Labs returned with an elevated WBC at 19.6. Opiates positive on top but otherwise were unremarkable. EKG sinus tachycardia. CXR and urine unremarkable. At this point even though I had no fever or source I felt compelled to initiate a septic workup and Lactate returned at 7.9.

I was starting to get lost as why this guy was so unresponsive to fluids and O’Brien and I threw the USN to bedside at this point. Turns out he was in acute systolic failure with an ejection fraction of 11%. No history of CHF and also no signs of volume overload on exam except very mild pulm edema. Troponin peaked at 0.5.

He was admitted by cardiology while they trended his status. He went to the cath lab on hospital day 3 with clean coronary arteries. Ejection fraction improved to 60% by time of discharge. Talking with the team today they are still uncertain of the cause.

These are two cases of sick patients being in the holding area. Hopefully, it serves to remind everyone that any patient can be sick.

The EKG in Palpitations

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Late 20s female w CC of chest discomfort and palpitations, n/v x 1 days. No recent illness, no fever/chills/diarrhea. Says the episodes come on abruptly and last less than a minute. No h/o early cardiac disease or early death in family. Says she feels short of breath with the episodes and her chest feels tight. Denies tunnel vision. Denies syncope but feels like she could pass out. ROS o/w positive for anxiety (grad student). Denies T/ETOH/D. Social history o/w irrelevant. No allergies. Only medicine is OCP. Exam is unremarkable (heart normal, lungs clear, appears well).

What would you order on this young patient with this complaint? How would you document it?

I have recently seen a few charts in this and similar patient presentations that gave me pause. I’ve seen workups from EKG alone to the full cardiac rule-out and everything in between. The only true unifying theme, and I think rightly, the most important test is the EKG (aside from a pregnancy test).

And most of the charts have a documented EKG. Ok. No problem there. Below is an example of a chart documented on a <30yoF patient with Palpitations…

 

Normal_ECG

“NSR, Rate 85, Normal P waves. No S/T wave changes. Normal QTc. No ischemia. No EKG for comparison. “

 

The problem with this? Aside from a few parts, it is mostly irrelevant to the life or limb threatening abnormalities that we are looking for in the EKG. Sure, it will bill just fine, but I worry that there a few among us who aren’t SPECIFICALLY looking at the EKG in the palpitations patient for common causes of palpitations. I mean, really, how many of us see MIs present as palpitations?

 

So what should you look for in an EKG in a palpitations patient?

  1. Rate (tachy or brady or no?)
  2. Blocks
  3. HOCM
  4. Brugada
  5. AVRD
  6. Prolonged QT (cong. QT) or Short QT (why?—AVRD)
  7. WPW
  8. Ischemia

 

Now lets talk about the EKG abnormalities found in each:

HOCM—About 90% of HOCM pts have an abnormal EKG. Remember, these are often young folks, so their ekg should be pristine. The etiology is a hypertrophic septum, so characteristic LVH is seen (V4R wave is “off the chart”), as well as deep, narrow q waves laterally. Occasionally flipped, broad T-waves are seen. There is also an apical variant that shows GIANT TWI in septal and lateral leads… you’ll know it if you see it, it looks grossly abnormal. But HOCM itself can be much more subtle. Look for Q waves and LVH then listen to their heart and refer to cardiology for an echo. Both of the below are pretty obvious, the second one is the GIANT TWI i was talking about. Not a lot of things do that.

time 4 hours HR 84

HypertrophiccardiomyopathyapicalvariantYamaguchisSyndrome

Brugada— 50% familial, most present >20yo but can be seen at birth. In brugada, you’re looking at leads V1-3, looking for a Right bundle branch block and either “coved” (st elevations with long, flat ST-segment that looks like a ski-slalom) or the “saddle type” (which is way less common and looks a lot like, well, a saddle. But remember there is STE there too which makes a side of the saddle, then the T-wave makes the other side of the saddle. This sometimes looks like a STEMI, except in a patient without chest pain and then you notice the saddle shaped concave ST segment and the CC and family history and you can smile because you didn’t activate the cath lab. Also, these patients can have EKGs that show brugada pattern SOMETIMES and not other times. Look for the ski-slope and the saddle. Hop aboard this saddle and you’re going to need a defibrillator, as anti-arrythmics don’t change mortality much….

14_minutes_QRSd_146ms_p_2_Amps_bicarb_axis_167

255v62n11-13145482fig1

This image says there are 3 types. OK, well, that’s true and all but seriously, it’s still a saddle, so you shouldn’t be led astray.

AVRD- What the what? AVRD stands for arrythmogenic right ventricular dysplasia, and basically their RV gets filled up with fat and cartilage during development. This is not so good. These folks may have exertional chest pain (it’s a cardiomyopathy). And, because it’s a structural heart disease, most of them will have EKG abnormalities (~90%). The most specific finding is an EPSILON wave, which is a little puny looking bump after the QRS that looks like a little P wave but is out of place and behind EVERY QRS. These are hard to catch, so you HAVE TO LOOK FOR IT IN PARTICULAR! Also, remember, not every Osborne wave is AVRD (is the patient hypothermic?) Occasionally this will make the QT interval short, but it isn’t reliable. Other, less specific findings are TWI in V1-3 that looks like a juvenile pattern… but remember juvenile pattern should go away when the patient becomes less juvenile. So if they have TWI in percordial leads an they are >20 and have palpitations or syncope… PANIC. No, but really, they probably have AVRD. And the syncope was probably VTACH. But they’re good now, right? Give them a defibrillator too.

avrd_figureone-2

 

Oh, crap. That’s what happens when you send the patient home without looking for AVRD.

 

ARVC

Congenital Prolonged QT-– Ok, so a bit of an update to our usual shortcut “half the R-R rule,” in Academic Emergency Medicine in October 2015, some folks published a retrospective review of some cases of EKGs with prolonged QT and non prolonged QT, and found that our quick half the RR interval thing is about 88% sensitive (r/o prolongation) but only 53% specific. Which ain’t terrible, but its also not super good (12% aren’t ruled out). Of course, what the study failed to highlight but is written and useful is that the ½ RR rule is 100% sensitive (in this study) if the HR was >60. So my take is, if they are brady, calculate it yourself, and if not, 1/2RR is good to go. Which is what I think most of us do anyway. Three cheers for studies confirming our guesses!

Screen Shot 2015-11-08 at 5.44.26 PM
WPW—Not much to say here. You know this. And you damn well should be documenting it. That PR interval is short because your patient is dying for you to find his delta wave.

Wpw

ACS– Well, this is what we do.

Blocks- P before every QRS, QRS after every P. Intervals.

 

So… how should you be documenting these EKGs? With the same attention to the life and limb threatening abnormalities you are looking for on your history (early family death) and exam (murmur?). I can’t say what is right or not, but below is how I would document that EKG on our patient from earlier (NSR, rate 85, No STE/D, No TWI, no definite EKG evidence of WPW/AVRD/CongQT/blocks/HOCM).

Cheers.

 

Images:

https://meds.queensu.ca/central/assets/modules/ECG/Normal_ECG.bmp

http://hqmeded-ecg.blogspot.com/2014/06/history-of-hypertrophic-cardiomyopathy.html

http://www.doctorshangout.com/photo/hypertrophic-cardiomyopathy-apical-variant-yamaguchi-s-syndrome

http://hqmeded-ecg.blogspot.com/2013/05/brugada-pattern-induced-by-tricyclic.html

http://www.revespcardiol.org/imatges/255/255v62n11/grande/255v62n11-13145482fig1.jpg

http://www.geneticheartdisease.org/jpegs/avrd_figureone.jpg

http://www.heartpearls.com/wp-content/uploads/2009/07/ARVC.jpg

http://www.crkirk.com/thumbnail/arrhythmias/images/svt/ECG_WPW.htm

Chest Pain Admission Dilemma

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Hey guys here is an interesting article with actual patient oriented outcomes related to admission for chest pain.

Several take home points:

1. From highest quintile of admission rate to lowest (81% to 38%) the rate of MI and death went up by 3.6 per 1000 and 2.8 per thousand. This correlation implies that when you admit more patients you save lives.

2. It is VERY IMPORTANT to note the patient population. These are Medicare patients with average age of 71 years. So we ARE NOT talking about low risk chest pain ED patients.

3. Even though it looks impressive to save these lives, the NNT or number needed to admit to prevent one MI is 250 and to prevent one death is 333. Thats a lot of admissions. And admitting geriatric patients is often not a good thing for them. May be why the decrease in deaths is less than the decrease in MIs. They were dying because of a hospital acquired infection or deconditioning or something else.

4. It is striking to see how different the practice patterns are at different hospitals regarding admission of a fairly homogenous cohort of patients.

Appreciate any further comments.

EKG Changes in Hyperkalemia

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I have had a couple of good EKG’s in the setting of hyperkalemia that I thought I would share.

The first case is a 68 y/o female with ESRD on dialysis presenting with “back pain”.  Turns out that her back pain was actually chronic and at baseline, but she had missed her last two dialysis appointments.  She denied any chest pain or SOA.  I ended up getting an EKG while waiting on labs.

Initial EKG:

Screen Shot 2015-08-04 at 2.46.53 PM

Previous EKG (~6 months ago)

Feb

 

What says you?  New onset LBBB?  After seeing this we gave Calcium Gluconate and asked one of our wonderful techs to grab a quick iStat as labs were taking forever to result.  Potassium was 6.8.  Gave insulin + D50 and bicarb.  EKG was repeated after Hyperkalemia treatment:

post

Renal consulted for emergent dialysis and medicine admitted.

 

 

Here’s another EKG that I had recently from a DKA patient who had an initial potassium of 7.8:

Hyper-K

 

Here’s a couple of good hyperkalemia resources:

Hyperkalemia EKG Basics

Treatment of Hyperkalemia

Just get a walking O2 sat

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In patients with some suspicion for PE, even with a negative d dimer, I have often ordered a walking O2 sat and HR. This was not really evidence based, but maybe now could be. Below is the abstract for a prospective cohort study of patients known to be with and without PE. Interesting data even if only 114 patients. Cannot get full text yet.

Take home point. Combined sensitivity of HR increase of 10 BPM AND Sat decreased of >/= 2% was 100%.

ie if HR does not go up by 10 or more AND sat does not drop by 2 or more they are very unlikely, based on this small study, to have a PE.

 

 

CJEM. 2015 May;17(3):270-8. doi: 10.1017/cem.2014.45.

Ambulatory vital signs in the workup of pulmonary embolism using a standardized 3-minute walk test.

Amin Q1, Perry JJ1, Stiell IG1, Mohapatra S1, Alsadoon A1, Rodger M2.

Author information

Abstract

OBJECTIVE:

Diagnosing pulmonary embolism can be difficult given its highly variable clinical presentation. Our objective was to determine whether a decrease in oxygen saturation or an increase in heart rate while ambulating could be used as an objective tool in the diagnosis of pulmonaryembolism.

METHODS:

This was a two-site tertiary-care-centre prospective cohort study that enrolled adult emergency department or thrombosis clinic patients with suspected or newly confirmed pulmonary embolism. Patients were asked to participate in a standardized 3-minute walk test, which assessedambulatory heart rate and ambulatory oxygen saturation. The primary outcome was pulmonary embolism.

RESULTS:

We enrolled 114 patients, including 30 with pulmonary embolism (26.3%). A ≥2% absolute decrease in ambulatory oxygen saturation and an ambulatory change in heart rate >10 beats per minute (BPM) were significantly associated with pulmonary embolism. An ambulatory heart rate change of >10 BPM had a sensitivity of 96.6% (95% confidence interval [CI] 83.3 to 99.4) and a specificity of 31.0% (95% CI 22.1 to 45.0) forpulmonary embolism. A ≥2% absolute decrease ambulatory oxygen saturation had a sensitivity of 80.2% (95% CI 62.7 to 90.5) and a specificity of 39.3% (95% CI 29.5 to 50.0) for pulmonary embolism. The combination of both variables yielded a sensitivity of 100.0% (95% CI 87.0 to 100.0) and a specificity of 11.0% (95% CI 6.6 to 21.0).

CONCLUSION:

In summary, our study found that an ambulatory heart rate change of >10 BPM or a ≥2% absolute decrease in ambulatory oxygen saturation from baseline during a standardized 3-minute walk test are highly correlated with pulmonary embolism. Although the findings appear promising, neither of these variables can currently be recommended as a screening tool for pulmonary embolism until larger prospective studies examine their performance either alone or with pre-existing rules.