Tag Archives: cardiology

Conference Notes 08/30/23

Posted on by
Reply

Emergency Management of Dentition and Midface

  • Dentoalveolar trauma can include fractures, avulsions, displacement of teeth
  • An avulsed tooth is only viable within one hour, however, even outside of this window it is still worth replacing the tooth. In some cases, they may then get a root canal with dentistry
  • Alveolar fractures need timely treatment or risk poor cosmetic outcome and infection
  • Most oral abscesses can be drained in the ED with close dental follow-up
  • The need to obtain CT is dependent on the full clinical picture. If pt has significant RFs for deep space infection or cancer, it may warrant a face CT
  • Trismus sometimes can be confused with guarding due to pain. Can be worthwhile to provide analgesia and reassess
  • Buccal and canine space infections can present with significant facial swelling. These should be assessed with CT, drainage should occur from within the oral cavity near the involved tooth, not through the skin of the face
  • Radiology reads will frequently indicate Ludwig’s, however, this is often overread. True Ludwig’s is a surgical emergency. Can cause significant airway compromise
  • As a general approach to anesthetic for oral abscesses, should first infiltrate around the abscess, then can attempt direct injection
  • Inferior alveolar N blocks can be challenging due to surrounding vessels as well as the parotid gland that can be inadvertently damaged

Anti-Arrhythmics

  • Among the sodium channel blockers, they are divided into IA, IB and IC. Procainamide is the common IA, Lidocaine is a IB and Flecanide is IC
  • Class II antiarrhythmics are the beta blockers
  • Class III antiarrhythmics are K channel blockers. Amiodarone is the most common example
  • Class IV antiarrhythmics are the Ca channel blockers
  • Beta-blockers and calcium channel blockers should be used with caution in the setting of CHF exacerbation given their negative inotropic effects
  • Amiodarone has both rate and rhythm-control properties
  • Ibutilide and procainamide are the safest medications to give in the setting of WPW
  • Dr Huecker: Can also consider adding magnesium to any of the aforementioned therapies

Infective Endocarditis

  • Defined by the Modified Duke Criteria
  • Most commonly caused by Staph species
  • Don’t forget about pseudomonal coverage in those with prosthetic valves
  • Valves are at high risk of infection given their lack of robust vasculature as well as the turbulent flow around them
  • IE cases are increasing due to both increased IVDU as well as increased prosthetics being placed
  • The average age of IE is now >65. Majority will require surgical intervention
  • Recall Osler nodes, Janeway lesions, splinter hemorrhages, Roth spots/ conjunctival petechiae
  • IVDU leads to right-sided IE
  • When IE is diagnosed don’t forget to get blood cx from 3 separate sites
  • Empirically give Vancomycin. Add on pseudomonal coverage if pt has a prosthetic valve
  • The biggest RF for IE is prior IE
  • Undomiciled patients are at increased risk of IE due to Bartonella species given flea exposure

Ultrasound in the Unstable Patient

  • CXR sensitivity for edema/ effusions is low
  • Ultrasound has good sensitivity in confirming ETT placement
  • Palpating pulses during ACLS has poor sensitivity/ specificity, another area where ultrasound can be helpful, in addition to checking for reversible causes of a patient’s arrest
  • Ultrasound can be used to find the CO plus the SVR, which together can be very valuable information when resuscitating an undifferentiated shock/ SOA/ hypotensive patient

Conference Notes For 08/09/2023

Posted on by
Reply

Infective Endocarditis Lightning Lecture

  • Pathophysiology: Usually starts with an insult to the endothelium, leading to formation of sterile vegetations. Then, an episode of transient bacteremia may seed an infection to these pre-existing vegetations
  • Infected vegetations often embolize, leading to a wide range of symptoms and secondary effects
  • Prevalence is as high as 10-15% in those who abuse IV drugs
  • The Modified Duke Criteria is used for diagnosis
  • When you suspect IE, three blood cultures from three different sights should be drawn
  • Antibiotic selection varies depending on native or prosthetic valve

Pericarditis and Myocarditis Lightning Lecture

  • Myocarditis is inflammation of the muscle cells of the heart. Can be acute, subacute or fulminant
  • Wide range of etiologies including viral/ bacterial infections and autoimmune diseases
  • Can lead to dilated cardiomyopathy and heart failure
  • Up to 80% of cases of pericarditis have an idiopathic etiology. Other causes include infections, radiation, Dressler’s syndrome
  • Pericarditis can lead to effusions/ adhesions, leading to constrictive pericarditis or even tamponade
  • Pericarditis does have some characteristic EKG findings. Important to differentiate from a STEMI

Pediatric Congenital Heart Disease

  • CHD is the most frequently occurring birth defect
  • Cyanotic lesions- think the “Five T’s” plus pulmonary atresia
  • When you’re concerned about a ductal-dependent lesion, don’t hesitate to give prostaglandins; biggest side effect is apnea, which can be managed
  • First two things to get when a newborn presents with suspicion of a CHD: All four extremity BPs and preductal+ postductal O2 sats
  • First two things to do during a suspected tet-spell: Squat/ knees to chest and give O2
  • If a baby is tachycardic, try to address potential secondary causes before giving adenosine

EKGs

  • When interpreting EKGs, especially early on you need to be systematic
  • A “significant” Q wave will be > 1/3rd the height of the R wave
  • When you see STD, you should be asking yourself “where is the STE?”
  • Most important factor to consider when evaluating for ischemia is the history, don’t get caught up too much on risk factors or lack thereof
  • Hyperacute T waves are broad-based, become asymmetric as the J point begins to elevate
  • Convex STE is very specific for ischemia
  • Don’t forget to get serial EKGs when there’s any suspicion; If you’re repeating troponin, you should also repeat EKGs. Don’t be afraid to get a quick repeat in 15-20 minutes when they’re actively in chest pain and you’re concerned

R3 Procedure Sim: Pericardiocentesis + Transvenous Pacing

  • Pericardiocentesis has three different approaches. No consensus on which is best
  • If performing the parasternal approach be careful to avoid the thoracic artery
  • Major indications for transvenous pacing include unstable bradycardia, sick sinus syndrome with pauses or failure to pace with the transcutaneous approach
  • RIJ is the preferred approach for floating a transvenous pacer

Prolonged QT

Posted on by
Reply

58 yo F presents to the ED for cough, chest pain, and fatigue for 1wk. She has sharp, atypical sounding chest pain. But she is 58 and has risk factors: HTN, HLD, 0.5ppd smoker x48yrs. Better get an EKG.

Prolonged QT EKG

Initial EKG

Awesome, no STEMI. Done with EKG right? Hope you didn’t miss that really long QT interval.

First, how do we measure the QT?

QTc imageWe usually talk about QTc rather than just the QT. This is because the QT interval varies depending on the HR. Using a correction equation standardizes the interval so it can be interpreted regardless of the HR. The EKG computer does give a calculation of the QTc, because we are obviously not hand calculating this on every patient. You should compare what the computer calculates to your gestalt when you review the EKG. If there are any concerns or discrepancies, you should hand calculate the QTc. MDCalc has an easy to use calculator. Above is the Bazett’s formula, which seems to be the most commonly used. Other formulas do exist. QTc is considered prolonged if > 440ms in men or > 460ms in women.

Next, why do we care?

ecg_hypokalaemia_torsades

This is the start of Polymorphic VT. There are several things that can cause this rhythm. Long QT is one possible cause. When Polymorphic VT is caused by a prolonged QT we give it a special name, torsades de pointes. The mechanism behind this is demonstrated on the above EKG. As the QT interval becomes more prolonged, there is a higher chance for an R-wave to hit on just the right part of the T-wave and cause this rhythm. QTc > 500ms seems be associated with higher risk.

So what causes prolonged QT?

Many things can cause prolonged QT. The most common etiologies are electrolyte abnormalities and drugs. Hypokalemia, hypomagnesemia, and hypocalcemia are well known to cause prolonged QT. Potassium and calcium are included on the CMP but don’t forget about magnesium. Drugs are also a big cause of prolonged QT. The list of drugs is long. Probably too long to memorize. However, there are some common medications and medication classes that you should know. The big classes are, Antiarrhythmics (like Amiodarone), Antihistimines (like Diphenhydramine), Macrolides (like Erythromycin), Antipsychotics (like Haloperidol), and TCAs (like Amitriptyline). This is not a complete list, just some highlights. If you really want to know if a specific medication is associated with prolonged QT, www.crediblemeds.org is a good source.

Other causes worth mentioning are structural heart disease, cardiac ischemia, and stroke. Some people do have Congenital Long QT Syndrome, but this should not be the leading diagnosis in the ED. Also those people are still at high risk for developing Polymorphic VT.

How did our patient do?

Her medications were reviewed and she was not on any of the most common offenders. Then routine labs came back. Unremarkable, except for K of 2.9! Repeat EKG after potassium repletion.

Normal EKG

EKG after K repletion

 

References:

  • www.uptodate.com
  • http://lifeinthefastlane.com/ecg-library/basics/qt_interval/
  • http://hqmeded-ecg.blogspot.com/2013/10/polymorphic-ventricular-tachycardia.html
  • bjsm.bmj.com/content/43/9/657/F3.large.jpgamp

Interesting case from the weekend – thoughts?

Posted on by
1

Hey guys, I was hoping to get your input on an interesting case I had at Kosair over the weekend.

16 yo F (6 ft, 150 lb…so basically an adult) with a PMH of depression, self injury, and prior suicide attempt presents after ingesting citalopram 40 mg x 90 pills (her prescription, just filled 2 days ago) and concerta 10 mg x 8-9 pills (her brother’s). Patient had been at a party the night before, admitted to EtOH.  Parents found out about the party the morning of admission and they had a big fight, took away car keys, etc. Patient decides to retaliate by swallowing pills, doesn’t tell anyone. Parents find her altered about 10:30, at Kosair at 11:40. Best guess is ingestion occurred sometime around 9-9:30am.  Had one seizure at home per family, and one en route per EMS. Generalized, tonic-clonic, brief.

Initial exam shows a drowsy but arousable patient. Answers orientation questions x3. Initial vitals show HR 147, BP 135/70, RR 25, 93% on some oxygen (can’t remember if NC or nonrebreather). Patient denies CP, palpitations, SOB, abd pain, N/V, weakness/numbness.  4mm, PERRL. MAE equally. Old self injury scars noted on wrists bilaterally. Exam otherwise unremarkable.

We start IVs, get her on a non-rebreather, get IV fluids going. Agree that charcoal seems like a bad idea with her mental status and seizures. Mom has shown up, and as we’re getting some additional history from her, respiratory is placing EKG leads. I’ve talked to poison control. Then, about 20 minutes into her stay, she seizes again. We bag her through the seizure, again generalized tonic-clonic, and just as we’re pushing 2 mg of IV Ativan she comes out of it. She appears post-ictal, but is maintaining her airway. We load her with Keppra, and as I glance at the monitor behind the attending’s head, I notice that her rhythm has changed and she looks like she’s got a wide QRS. We confirm she still has good pulses, still out of it mentally, and since she’s already connected to the EKG leads we grab one (time stamp 12:04):

EKG 1

By the time we get this printed off (!!!!) she appears to have spontaneously converted back to sinus on the monitor. But woah, holy wide QRS/long QT batman! As the attending and I are pouring over the first EKG we get another one immediately (time stamp 12:08):

EKG 2

Thankfully, the QRS appears to have normalized, but we’ve still got a loooong QT, one of the things poison control definitely told us to look out for. Having seen a few similar ingestions at University, I suggest it’s time for bicarb. The attending wants to confirm and we quickly call poison control back, they agree and suggest starting a bicarb gtt, with pH goal of 7.45-7.55.  Now we look back at the monitor and she’s throwing a ton of PVCs, captured here on EKG #3 (time stamp 12:12):

EKG 3

At this point, we opt to push an amp of bicarb while we’re waiting for pharmacy to tube up the bicarb gtt. I have to say, we see it start to work pretty darn quickly. The PVCs slow down, and her rate really starts to head back towards normal. We get an iStat (shot me down when I suggested one earlier), and a few minutes after we’ve pushed the bicarb we get an initial pH of 7.15, pCO2 of 51.5, HCO3 of 18, BE -11, and AG of 21. Electrolytes were WNL. By this time we also know her pregnancy is negative, and her serum tox is negative, no acetaminophen/salicylates on board.  At this point, we talk about intubation as the patient’s mental status is still waxing/waning and she’s breathing shallowly with brief periods of apnea, almost like an opiate overdose. Attending wants to hold off, so I go off to call the PICU resident…and end up having to hang up the conversation halfway through when he changes his mind.

So we intubate her (finally got a peds tube…in an adult), the bicarb gtt comes up from pharmacy, they’re cleaning the PICU bed her, the last EKG looks 1000x better, and all’s well that ends well (time stamp 13:08):

EKG 6

So I’m curious to see what your all’s suggestions/thoughts are on this case.  Looking back at that first EKG, how would you classify it? We’ve got a wide complex, monomorphic tachycardia that to me looks like sustained V tach (with a pulse).  The long QT doesn’t surprise me, but this rhythm does as you’d typically you’d worry about it devolving into Torsades, but that’s not what this is.

Looking back, things I would have done differently:  get a temperature sooner/order a total CK (serotonin syndrome could have been a factor and we don’t have a recorded temp until she’d almost 2 hours into her stay, no one ever ordered a CK), intubate sooner, loading her with keppra when she hit the door after 2 witnessed seizures, maybe could have prevented the 3rd?

Also, if you’re curious, I found this “Toxicology Conundrum” on LITFL that specifically discusses citalopram overdose. Has some good info, citalopram is definitely one of the more potent SSRIs, and QT prolongation is dose dependent and can be seen after ingesting >600 mg (this chick took 3.6 GRAMS). Seizures are also fairly rare, only seen in 2-3% of cases.

Reasons not to get into prison fights…

Posted on by
4

Middle aged male transferred from an OSH, accepted by ENT for a mandible fracture.

The patient is incarcerated, and was involved in an “altercation” with other inmates. The incident occurred around 2PM; but he didn’t report any of his pain to the guards until 10PM.  On arrival at the OSH he had multiple contusions to his face/head, lacerations over his hands, and obvious dental trauma.  The patient was also complaining of chest pain – he stated that another inmate had slammed him in the chest with his knee. Despite his age, the patient has a history of previous MI in 2011, cathed at U of L with no stents placed. Takes a baby aspirin, no other meds and no other PMH.

At this point, the patient is about 10 hours out from the incident. Work-up at the OSH with the following: neg CT head and CXR. CT face with a mandible fracture. Labs notable for WBC 17.8, Hgb 14.3, platelet 373, normal coags, normal electrolytes, BUN/Cr 14.0/1.1. Total CK 213 (55-170 normal), troponin <0.012, CKMB  1.66 (0 – 3.38 normal), myoglobin 271.8 (0-121 normal).  Tox screen negative. EKG is as follows:

OSH EKG

His hand lacerations were repaired and he was started on Augmentin for a human bite. ENT accepted, and the patient was transferred to U of L, arriving about 6 AM. Dental was consulted on arrival and splinted his teeth. By 9 AM ENT had evaluated the patient and admitted him to the floor, planning for surgical intervention.

The patient was an ED floor hold, and around 2PM began complaining of worsening chest pain. ENT was paged and ordered an EKG and a set of cardiac enzymes, coming down to re-eval the patient. His EKG now looked like this:

1410 EKG

Enzymes came back with CK total 5024, CKMB 303, and troponin 44.1. Cardiology was consulted and ordered a stat echo and started the patient on ACS protocol. The echo showed an EF of 30%, an akinetic mid/distal anferoseptum and an akinetic apex. Cards initially thought that this was consistent with stress cardiomyopathy in the setting of trauma, but couldn’t rule out cardiac ischemia due to direct cardiac trauma. They planned to treat medically and cath in the morning.

Throughout the evening, he developed worsening ST elevation in his lateral leads and his troponin continued to rise, up to 67.0 by midnight.

0308 EKG

The on call cath attending at Jewish was consulted and by about 3AM the decision was made to transfer the patient to Jewish for a cath first thing in the morning.

Final result: 100% LAD occlusion, secondary to direct cardiac trauma.

Definitely rare injury, but one to keep in the back of your mind, especially as it can occur in previously healthy, relatively young patients. Of note, these can have delayed presentations, up to several days. Typically occur after MVA, but there are several cases reports occurring after crush injuries, being hit in the chest by a soccer/rugby ball, and my personal favorite, one listed as “struck in the chest by an umbrella tip.”