Case of the week COW #15

CC: Shortness of breath

HPI: 7 day old female presents to the Emergency Dept. (ED) after being seen earlier in clinic. Mother is rom Nigeria and arrived to the U.S a few weeks prior to delivery. Prenatal care is unclear. Patient was delivered via C-Section at 39 weeks at another nearby hospital. Both mother and baby spent one day in the hospital after delivery being discharged home. Mother states that since last night, the baby appears to “ not breathing right.” She also hasn’t’ been eating much and is crying more often than usual, during which her lips start to turn blue.

Physical Exam:
Obvious respiratory distress, hypoxic on RA, saturating in the middle to low 80’s on NC 3 L
HR 176,   RR 60.    Accuchek 96.
BP: (RA) 69/45    BP (LA) 91/64     BP (LL) 84/64     BP (RL) 71/58

Pertinent Imaging/ECG

ECG in the ED:

Working Diagnosis: Shock secondary to congenital cardiac pathology.

ED/Hospital course:  Patient was admitted to PICU, underwent Echocardiogram and further imaging and was diagnosed with Coarctation of the Aorta. The patient was transferred to Mt. Sinai for operative repair.

Pearls:

  • 7 day olds are terrifying, especially if they are sick.
  • Take a breath! Start with your ABCs.
  • Coarctation of Aorta(CoA) is a congenital aortic narrowing which most commonly occurs at the level of ductus arteriosis. There are Pre-ductal and Post-ductal types. Pre-Ductal CoA is a Truncus dependent lesion and most patients present within 2 weeks of birth once duct closes. Aortic narrowing leads to increased LV function and dilation. Post-ductal are commonly identified in adulthood.
  • Obtain a BP/pulse Ox in all 4 extremities
  • Perform the Hyperoxia test
    • Obtain ABG on RA. Then, apply 100% supplemental oxygen with a NRB for 10-15 minutes. Repeat the ABG on the NRB.
      • On repeat ABG
        If PaO2 > 250mmHg = Lung problem
        If PaO2 < 100mmHg = Congenital Heart Disease
        If PaO2 100-250: Assume the worst situation first
  • You may also apply supplemental oxygen and assess the infant’s response. If saturation increases to at least 5-10%, it’s most likely a Lung problem. If it remains the same, think about Congenital Heart Disease
  • Prostaglandin (pt is less than 4 weeks old typically 1-2 weeks of life) start at 0.05 mcg/kg/min.
  • Dr. Hochman rule #11, call consultants early “don’t be the captain of a sinking ship”
  • Additional medications: Lasix 1 mg/kg if evidence of volume overload.Ductal dependent lesions, pulmonary presentation cyanosis/hypoxia use phenylephrine . If systemic SX, shock, pulmonary congestion on CXR Milrinone (decrease afterload + inotropic support).

The SICK NEONATE!

Case presented by Dr. Daniel Poor

UMEM Emergency Cardiology Symposium PEARLS

View the recorded lectures here: https://livestream.com/UMEmergencyMed/EMCard2018


LBBB and Chest Pain in Acute MI…What Should I Do?

Dr. William Brady – University of Virginia

  • Patients with new LBBB on EKG is not common in the setting of Acute MI (AMI). It is, however, the most common pseudo-infarction pattern.
  • 80% of AMIs with LBBB are not detectable by ECG

Rational approach to AMI in patients with LBBB:

https://pdfs.semanticscholar.org/f80b/9983005179f4718bb1326963c722d4f80e58.pdf


Wonder Women: Exploring the Gender Gap in ACS

Dr. Susanne DeMeester – University of Michigan

  • Average age of women presenting with ACS is 71. This age lags men by about 7-9 years.
  • Women have a higher 1 and 5 year post ACS mortality compared to men
  • 20% of women with acute STEMI on their ECG will have a clean cath
    • Cardiac microvascular dysfunction more common in women
      • Smaller epicardial vessels
      • Increased stiffness
      • Smooth muscle dysfunction
    • Rupture embolic plaque causing STEMI more common in men
    • Coronary vasospasm equal between men and women
  • NSTEMI is more common in women
  • Dyspnea is the most common angina presentation in women and geriatric patients (not chest pain!)
  • Women more likely to complain of chest “discomfort” rather than “chest pain” or “chest pressure”
  • Women have additional risk factors that have a greater association with ACS:
    • Depression, anxiety, psychosocial environment
  • Women with low risk HEART Score have lower risk of 6 week major acute cardiac event (MACE) compared to men (2% vs 6.5%).
  • Women have a smaller degree of ST elevation in acute STEMIs compared to men and are likely to produce lower levels of troponin.
  • Remember the diagnosis of spontaneous coronary artery dissection (SCAD) in the young peripartum woman
    • Risk factors include pregnancy, OCPs, vascular and connective tissue disorders
    • High recurrence rate ~20%
  • Fibrinolytics in ACS – Women are more likely to bleed
  • Women historically have had delays to treatment, and have received non-guideline treatment: Be careful to recognize and appropriately treat ACS in men and women

“Un-Break My Heart”: 2018 NSTEMI Updates

Dr. Tarlan Hedayati – Cook County, Chicago

  • Not all elevated troponin equals ACS
    • PE, dissection, myocarditis, pericarditis
    • History and clinical context are extremely important
  • Some NSTEMIs will have complete vessel occlusion (~25% of the time)
    • These patients are more likely to have higher troponins
  • Main risk factors for ACS: HTN, DM, Hypercholesterolemia (including HDL<40), Family Hx, Tobacco use
    • Others risk factors: Cocaine abuse, HIV/AIDS, ESRD, SLE, RA, stress, exogenous testosterone
  • Clopidogrel (Plavix: pro-drug, needs activation) vs. ticagrelor (Brilinta: works immediately)
    • PLATO trial
      • Lower risk of MACE with Brilinta
      • No difference in bleeding complications between two groups
    • Lovenox vs Heparin
      • No major differences in outcomes
      • Consider using Heparin if patient will be going for upcoming catheterization
  • Three options of NSTEMI management
    • Ischemic guided (conservative management)
      • Wait, trend troponins and serial EKG
      • Better for low risk patients
    • Immediate invasive (Cath ASAP, should be within 1-2 hours)
      • Patients with: refractory angina, recurrent angina, sustained Vtach/Vfib, or those who are clinically or hemodynamically unstable
    • Routine invasive (cath within 24-72 hours)
      • Early (cath within 24 hours)
        • Patients with dynamic EKG changes, new ST depressions or rising troponins
      • Late/delayed (within 72 hours)
        • Patients with DM, CKD/ESRD, LVEF < 40%, CABG/PCI within last 6 months, patients who are post recent MI with chest pain
      • TIMACS study
        • Benefit with early cath only seen with high risk patients

The Crashing Kid

Dr. Mimi Lu – University of Maryland

  • There are 1 million adults with congenital heart defects.
  • 60% of congenital defects are missed on prenatal ultrasounds
  • Clinical findings of pediatric patients with congenital heart defects:
    • Central cyanosis, diastolic murmurs, delayed or difference pulses
    • Hepatomegaly is more common physical exam finding in pediatric patients with CHF (more common than lower extremity edema which is typically seen in adults)
    • Grunting = BAD in children
  • Cyanosis, poor feeding and/or tachypnea in first 7-14 days
    • Think sepsis, sepsis, sepsis (most common cause)
    • But also consider if this is a ductal dependent lesion
      • Typically present within the first 2 weeks of life
      • Hyperoxia test – check ABG on RA à apply 100% FiO2 for 10-15 min à recheck ABG
        • If PaO2 > 150mmHg = Lung problem
        • If PaO2 < 150mmHg = Cardiac problem
      • Quick and dirty hyperoxia test
        • Apply supplemental O2
        • If sats increase at least 5-10% = think Lung problem
        • If sats remain the same = think Cardiac problem
    • Workup
      • EKG – look for hypertrophy, abnormal axis, arrhythmias
      • CXR – look for cardiomegaly or pulmonary edema
        • It can be difficult to appreciate cardiomegaly in neonates (because of thymus, etc.)
        • Get a lateral film and use the anterior tracheal line to help determine if cardiomegaly
          • line parallel to anterior tracheal wall inferiorly to diaphragm – should NOT intersect heart; should NOT be pushed back to “hit” spine above diaphragm
      • Labs
        • BNP literature is weak, but can be considered
    • Initial Management of the Congenital Heart Disease pediatric patient
      • IV fluids – 10cc/kg
      • Maintain SpO2 80-85%
      • Prostaglandin (PGE-1) if considering ductal dependent lesion
        • Dose is 0.1mcg/kg/hr
        • Works within 10-15 minutes
        • Side effects: apnea, hypotension, fever
        • Historically most pts receiving PGE-1 are intubated however recent data supports watch and wait to see how the patients respond, but have RSI equipment ready
          • If transferring the patient to another facility after starting PGE-1 you should secure airway to avoid pt becoming apneic en route
      • Inotropes if shock (did not get into detail on which to use)
      • Furosemide if pulmonary edema (1mg/kg/dose)
      • Make sure to check blood sugar
      • Correct acidosis – early bicarb!
      • Optimize ionized calcium 

Diuretics in Acute Heart Failure: The Dark Side of the Force?

Dr. Peter Pang – Indianapolis EMS

  • Treatment of heart failure has not changed much over the past 40 years
    • Only additions are use of inotropes and nesiritide (recombinant BNP)
  • Patient outcomes have only slightly improved over past 40 years
    • Current data:
      • 75% = 5 yr mortality for patients admitted for CHF
      • 22% = 30 day rehospitalization rate of patients admitted for CHF
      • 8% = 30 day mortality for patients admitted for CHF
  • DOSE trial (2011)
    • No difference in patient outcomes using bolus vs. infusion of Lasix
    • Doubling (2-2.5x) the dose of patients home dose of Lasix ( continuing patients home dose) was associated with better symptom improvement and increased weight change at 72 hours. However there was no difference in mortality, hospital readmission, or ED visit. And there was increased risk of worsening renal failure with the higher dose.
  • Best practice appears to be doubling the oral dose of Lasix. You achieve better sx improvement and better urine output.  You may get a bump in the Creatine but this doesn’t seem to be worrisome as the patients do well.
  • Prospective Cohort Study ~1300 pts.  Loops that were given within 60 mins of arrival have less in Hosp mortality then delayed therapy. This study is suggestive that early therapy may benefit and is at least safe. Will need more studies to duplicate this finding.
  • The addition of captopril to combat the RAA system does not have sufficient evidence out at this time to recommend it.

The Evidence For and Against Epinephrine in CPR

Dr. Corey Slovis – Vanderbilt

  • Epi is a potent alpha and beta agonist
  • The evidence for use of epinephrine in cardiac arrest is weak and incomplete!
    • The case for or against epinephrine in CPR is embarrassingly not based on large randomized double-blind studies
    • Its use stems from a 1968 JAMA study on the use of epi in cardiac arrest of n=15 dogs
    • There is not good objective evidence, in controlled studies, that epinephrine is more effective than placebo
  • “High dose” epinephrine, of more than 1 mg per dose, significantly improves ROSC but not survival to discharge
    • The more you look into the data, the more higher dose of epinephrine looks bad
    • Also, reduced dose of epinephrine appears to offer no benefits
  • Early v. late use of epinephrine in cardiac arrest
    • Use epi as soon as possible (until its effectiveness is proven or disproven)
    • However, if patient is in VF/pVT, data supports waiting for the second shock prior to giving epi (better outcomes when compared to using after the first shock)
  • Try to space your repeat doses of epinephrine by longer intervals, not shorter ones
    • ACLS recommends epinephrine q3-5 min
    • It appears spacing doses out up to 8-10 minutes may be optimal, however this is a violation of current guidelines and no randomized study exists
    • Err on spacing out closer to the q5 minute mark
  • Epi given in shockable rhythms was 1/3 as effective in those patients that did not get epi in a post hoc analysis of a large trial (12% vs 32%)
  • Resuscitation 2018: 2255 pts got low dose epi in out-of-hospital cardiac arrest (0.5 mg).  Reduced dose didn’t cause a difference.
  • There is a London study coming out soon over >8,000 patients comparing epi vs. no epi for OHCA – should provide some useful information for use of epi in cardiac arrest.

Panel Discussion

  • RBBB does not prevent our ability to read an EKG like the LBBB does. You just have to look closely for the st elevation in that it can be more subtle. New RBBB in setting of an acute Mi is a bad prognostic sign.
  • Small group of pts who had pacers were studied with Sgarbossa criteria thus far. Seemed applicable to date. Bigger study by Dr Smith to be out soon that further looks into application of Sgarbossa criteria to paced individuals.
  • No data on continuous drip of epi verses bolus dose epi in cardiac arrest although some centers are doing this.
  • Cardiac Arrest with ROSC + NSTEMI – Should be indication for emergent cath (Also, Arrest with ROSC plus any of following: witnessed arrest with bystander CPR, initial rhythm VF/pVT)

Case of the Week COW #14

Presenting Resident

Traficante

Chief Complaint

Cardiac arrest

Brief HPI

Hispanic male in his mid 30s who presented to the ED as John Doe after he was found unresponsive in the field with cardiac arrest. Unknown downtime. As per EMS endorsement from bystanders, the patient allegedly had a witnessed syncopal episode followed by seizure-like activity after which he became unresponsive. No bystander CPR. EMS arrived at the scene and found him pulseless, CPR started. On ALS arrival patient found to be in PEA. CPR, intubated, epi x 2, bicarb then ROSC achieved. Initial rhythm in ED was sinus tach on monitor. After 5 min in ED patient became bradycardic and went into PEA, compressions started, received epi x 1 w ROSC. Pt then went into wide complex tachycardia on monitor – SVT vs Vtach – pt was cardioverted 200J and given Amiodarone 150mg. Post cardioversion, rhythm changed to afib v aflutter. EKG was obtained after 10 min (below).

Pertinent PE and Vitals

On arrival: BP 81/50; P113; SpO2 95% ambubag 100% FiO2; Temp 37.0; BS 136

PE:
Gen: Unresponsive, intubated, occasional myoclonic jerks
HEENT: 2 cm hematoma right occiput, pupils constricted 1-2 mm b/l and non-reactive CV: tachycardic, s1/s2, no murmurs
Resp: Assisted breathing, good air entry b/l
Abd: Soft, NT
Neuro: GCS 3, has occasional myoclonic jerks

On admission: BP 153/83; P153; SpO2 98% on vent 100% FiO2

Pertinent Labs

ABG done on patient arrival = 6.80/86/253/14; Na+ 133; K+ 4.4, Ca++ 1.04; Glu 246, Lac 8.8, BE -10.2 These were the only labs available at the time of admission.

Pertinent Imaging/EKG

Case d/w Cardio fellow who came to evaluate pt at bedside, decision made to transfer pt directly to cath lab. EKG was repeated after 5 minutes prior to patient being transferred, which is shown below.


Working Diagnosis at time of Disposition

Cardiac Arrest
STEMI – possible LMCA, LAD or Triple vessel dx

ED & Hospital Course

Interventional cardiologist advised immediate transfer to cath lab for diagnostic cath (did not want to wait for CT Head). Cath showed normal coronaries with LVEF 75%.

Patient transferred to the CCU post cath. He was noted to have no brainstem reflexes off sedation. CT Head showed findings c/w anoxic encephalopathy, no bleed. Neuro was consulted who stated patient’s exams and further diagnostic studies were significant for loss of all cortical and brain stem function, consistent with brain death. Patient was pronounced on Day 10 (delay with identifying patient and determining NOK).

Pearls & Takeaways

Is ST-Segment Elevation in Lead aVR Getting Too Much Respect?

Introduction

ECG reading is all about pattern recognition. And this particular pattern of ST-Elevation in aVR with diffuse ST Depression is a very important ECG pattern that you must be able to recognize. But what’s probably more important than being able to recognize the pattern, is understanding what it represents. There appears to be a common misconception that the ST-Elevation in aVR always represents “STEMI”, or acute transmural (full- thickness) ischemia. If this were the case the patient would most likely be dead or at the very least in profound cardiogenic shock. The key to understanding what this pattern represents lies in understanding that the ST-Elevation in aVR is reciprocal to the diffuse ST-Depression – and that this diffuse ST-Depression represents global subendocardial ischemia. So the real question that you must answer is: What is causing the global subendocardial ischemia?

What Else can Cause STE in aVR that Won’t Benefit from Going to the Cath Lab?

Worrisome Diagnoses:

  • –  Thoracic Aortic Dissection
  • –  Massive Pulmonary Embolism
  • –  Massive Gastro Intestinal Hemorrhage

Non-Worrisome Diagnoses:

  • –  Left Bundle Branch Block (LBBB)
  • –  Left Ventricular Hypertrophy (LVH) with Strain Pattern
  • –  Severe Atrial Tachydysrhythmias (i.e. SVT)

It is critical to realize that more often than not the cause is global myocardial strain from a Non-ACS etiology! (profound sepsis, tachycardia, anemia, hypoxemia, etc). In our patient above it may have been because of the SVT he was in during the code in addition to being in Afib w/ RVR at the time of the ECG. It is also very important to understand that in these Non-ACS settings, you can see this pattern with or without underlying coronary artery disease.

But of course it could be ACS. And if it is, then you are dealing with Left Main, Proximal LAD, or even multi-vessel plaque instability. But keep in mind that even if it is ACS you are still dealing with subendocardial and not transmural ischemia.

Take Home Points

    1. STE in aVR Should be Concerning IF you have a patient with:
      1. Worrisome/Concerning Symptoms (Cardiopulmonary Symptoms) AND…
      2. ST-Segment Depression in Several Other Leads

    2. Don’t worry so much about STE 0.5mm or less in lead aVR, because it lacks specificity. Using 1.0mm or greater in lead aVR, has better specificity

    3. Patients with ACS due to LMCA Blockage, Triple Vessel Disease, or Proximal LAD Blockage will look “sick” due to global cardiac ischemia. This narrows the number of patients we would consider activating the cath lab for with STE in aVR.

    4. The key to ECG reading is pattern recognition. The pattern of ST-Elevation of at least 1mm in lead aVR + diffuse ST-Depression with a maximal depression vector towards leads II & V5 is a pattern you must know. It represents global subendocardial ischemia.

    5. When you see this pattern you should divide the differential for the diffuse subendocardial ischemia into two main categories: ACS vs Non-ACS. Do not automatically assume that it is ACS. I have seen this mistake made many times as ACS becomes the focus, at the expense of appropriate resuscitation addressing the underlying cause. It is very important to keep in mind that the etiology is far more likely to be Non-ACS than ACS!

    6. The key to determining the etiology is through history, physical exam, clinical picture, laboratory data, Echo, and vigilant monitoring and frequent reassessment. If you have identified and addressed potentially reversible causes of the ischemia, and the ECG pattern persists then you are dealing with ACS until proven otherwise.

    7. Refrain from using dual-antiplatelet therapy in these patients as there is a high likelihood they will require CABG.

    8. Remember that if this ECG pattern does represent ACS, the ST-Elevation in aVR is not the result of direct injury (or transmural ischemia) and that the ST-Elevation in aVR is reciprocal to the diffuse ST-Depression. Therefore these ACS cases do not represent a clear “STEMI”. However, while there is not great data to guide the timing of cath for these patients, I would advocate going to the cath lab with a much stronger sense of urgency than for other “NSTEMIs”. The reasoning is that ACS is a very dynamic process and without the advantage of optimal medical therapy (a second platelet inhibitor should be withheld) there is a higher chance of the culprit vessel suddenly occluding and evolving to transmural ischemia. If this happens in the Proximal LAD, Left Main, or in the setting of Multi-vessel involvement the myocardial territory in jeopardy is so large that there is a good chance the patient will arrest and die before any reperfusion can be established! If your patient looks sick or has persistent chest pain, they should be going to the cath lab ASAP.

    9. With diffuse subendocardial ischemia, you may not see any wall motion abnormality. Global function can even be normal, although it may be globally depressed as well. A normal bedside echo does not help in:
      1. differentiating the cause of the STE in aVR
      2. ruling out ACS

References: http://hqmeded-ecg.blogspot.com/2018/02/st-elevation-in-avr-with-diffuse-st.html