Congenital Heart Disease In Children: Pitfalls To Avoid

1. “If the patient had CHD, the diagnosis would have been made in utero or prior to leaving the newborn nursery.” Recent studies estimate that greater than 60% of CHD cases are not diagnosed on antenatal ultrasound. Most neonates with CHD are clinically asymptomatic immediately after birth. Even when abnormalities such as a murmur are detected on physical examination, many will not be directly referred to a pediatric cardiologist.

2. “The patient is greater than 1 week old, so the diagnosis cannot be a ductal-dependent CHD. The DA should have closed days ago.” Patients with ductal-dependent cardiac disease, especially ductal-dependent systemic blood flow, may have persistence of DA patency beyond 24 hours of life as a result of increased DA blood flow. Cardiovascular collapse in a child less than 1 month of age should be considered as a CHD with ductal-dependent systemic blood flow until proven otherwise.

3. “The infant is febrile. We should evaluate and treat for sepsis. CHD is not likely.” While sepsis is more common and should be suspected in any neonate presenting to the emergency department with tachypnea, cyanosis, or shock, a diagnosis of CHD should not be excluded based solely on the presence of fever. In fact, the presentation of a patient with CHD may be precipitated by an infectious process.

4. “The blood pressure and SpO2 obtained in triage are normal. I’m reassured.” Infants presenting to the emergency room in distress should have blood pressure and SpO2 measurements performed on the right upper extremity and one lower extremity. A discrepancy between the two extremities is suggestive of CHD.

 

 

Wide Complex Tachycardias

In the June 2008 issue, Drs. Subramanian and Bray discuss the diagnosis and management of wide complex tachycardia in the ED. It is an excellent summary of the available evidence; the article lays out a step-by-step process to approaching this complex problem.

I would just like to add my paradigm, which was created with the thinking that if you have an opportunity to reduce your cognitive load, always take it.

• Unstable is easy–shock
• If they’re stable and the rhythm is fast (>200 bpm), wide, and irregular; assume WPW with antidromic conduction/atrial fibrillation: give procainamide (or if you’re familiar with it, ibutilide)
• If they’re stable with a WCT and none of the above, give amiodarone.
• If it starts to look like TdP or the patient is not getting better, try some Bicarb

They’re you go, basically an acerebrate approach, but you’ll rarely get burned. Now the clever reader may say that this algorithm can be further reduced to shock unstable rhythms and give amio to everyone else and the ACLS guidelines will agree with you. However, there is a small literature out there saying that amiodarone may not be a clever choice for antidromic WPW.

See:
Can J Emerg Med 2005;7(4):262

Certainly not definitive, but makes you think. Perhaps, the authors can comment?

Severe Sepsis

In the May 2008 issue of Emergency Medicine Practice, , Dr. Ethan Booker provides an excellent review of the management of severe sepsis and septic shock. He brings up the value of ScvO2 to diagnose tissue hypoperfusion., even in the face of a good blood pressure and adequate CVP.  The ScvO2 can be obtained by drawing a blood gas from the distal port of your neck central line; make sure to draw up 3-5 ml of blood and discard, before drawing the gas. ScvO2 can detect occult shock in other conditions besides sepsis, though the literature is not as robust. A low ScvO2 (<70) should make you wary that the tissues might not be receiving enough oxygen.

The author points out that the value of CVP as a marker of  inadequate fluid resuscitation is debatable. The study he cites showed very little utility to using CVP for this purpose. However, the population in the study were ICU patients already past their resuscitative phase. The ED population is very different; often, we will get a CVP when the patient is still under-resuscitated. I often obtain CVPs of 1-2 mm HG on patients with severe sepsis and septic shock at the beginning of their treatment. These values almost always indicate the need for fluid resuscitation. Resuscitating from these low levels to the 8-12 recommended in the sepsis guidelines will rarely lead to too much fluid and in fact may under-estimate the volume needs of your patient.Until better measures come to the ED, CVP is essential to treat these patients, even if the set-up of the monitoring equipment is sometimes a hurdle.

rH-APC

Activated protein C is the only drug with FDA approval specifically for treatment of sepsis. Prospective observational studies demonstrated an absolute decrease in the level of activated protein C in some patients with severe sepsis and a subsequent increase in mortality. However, there is much debate as to its efficacy. 

 

What is standard practice in your hospital?  Are you using rH-APC — why or why not?

 

Keep in mind: APC is only FDA approved for patients with an APACHE score greater than 25.  An online APACHE calculator is available at www.mdcalc.com/apacheii.

The use of amiodarone for atrial fibrillation and other tachyarrythmias

………………………………………………………………………………………………………I’ve been perplexed by the increasing number of patients coming in with rapid atrial fibrillation or other tachyarrythmias, in which EMS has started amiodarone. Why amio, when there are other agents that work faster, are easier to mix up and dose, and are safe in pregnancy? It turns out the answer may come down to the nuts and bolts of business and government: many EMS trucks in my area don’t have refrigeration, and the manufacturer of the only room-temperature injectable form of diltiazem recently discontinued it (Biovail’s Cardizem Lyo-ject ). Other injectable diltiazem vials can only be stored at room temperature for a month – so EMTs are turning to amiodarone more often.

As I move through training I’m becoming more aware of how supply and demand sometimes dictate standard of care. One example that comes to mind is how ACLS guidelines changed (partly) in response to the worldwide shortage of bretylium (See pg 41 in the February 2001 edition of JOURNAL OF PHARMACY PRACTICE). Perhaps readers have other good examples, or insight into EMTs’ tendency toward amiodarone? Let us know, in the comments below!

Vagal Maneuvers

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I was impressed to learn the success of vagal maneuvers. They always seemed like something worth trying while waiting for the nurse to draw up meds, and I’ve had a few patients (and an EM colleague with periodic SVT episodes) swear by these techniques. But our readers want evidence, and here it is:

 Vagal Maneuvers (ACC/AHA Class I recommendation for reentry SVT, Level of Evidence B)

Massage of the carotid sinus, having the patient valsalva, and cold-water facial immersion have all been used with varying success in the treatment of SVT.  In a controlled clinical trial of 148 patients, carotid sinus massage, valsalva maneuver, or the combination of carotid sinus massage and valsalva maneuver were successful in terminating nearly 30% of SVTs.⁷¹  A comparison of these techniques for termination of AVRT and AVNRT found that the valsalva maneuver in the supine position was the most effective, with 54% of SVTs successfully treated by this method.  Termination rates were lower with carotid sinus massage (22%) and cold-water facial immersion (17%).⁷²

            It has been suggested that vagal maneuvers are most likely to be successful in terminating the SVT if initiated soon after the arrhythmia starts.⁷³  Sympathetic tone often increases with prolonged duration of the tachydysrhythmias, rendering vagal maneuvers less effective.  Patients should be educated regarding vagotonic methods and instructed to use these methods at the onset of symptoms.

With an important caveat from the Risk Management section –

 

8.   “It was a regular narrow complex tachycardia on the monitor and I couldn’t see any P waves.  While the nurse was pulling adenosine, I figured it couldn’t hurt to try carotid sinus massage.” Do no harm – even a simple vagal maneuver like carotid sinus massage can be disastrous in patients with a history of CVA or presence of a carotid bruit on examination.  To avoid neurologic complications, it’s imperative to get a quick medical history and listen for carotid bruit before initiating carotid sinus massage.  If you want to try a vagal maneuver, ask the patient to valsalva.

71. Lim SH, Anantharaman V, Teo WS, et al. Comparison of treatment of supraventricular tachycardia by Valsalva maneuver and carotid sinus massage. Ann Intern Med. Jan 1998;31(1):30-35. (Prospective; randomized case study; 148 episodes SVT)

72. Mehta D, Ward DE, Wafa S, et al. Relative Efficacy of Various Physical Maneuvers in the Termination of Junctional Tachycardia. Lancet. May 1988;1(8596):1181-1185. (Prospective; 35 patients)

73. Ferguson JD, DiMarco JP. Contemporary management of paroxysmal supraventricular tachycardia. Circulation. Mar 2003;107(8):1096-1099. (Review)

Excerpts above from Singh A, Carnell, J. An Evidence-Based Approach To Supraventricular Tachydysrhythmias. Emergency Medicine Practice. 2008;10.

Supraventricular Tachydysrhythmias

This month’s Emergency Medicine Practice issue on SVT emergencies, written by Drs. Amandeep Singh and Jennifer Carnell of Highland General Hospital, is really a tremendous resource. From pathophysiology to therapy, this issue reflects the latest literature and evidence-based recommendations, and is chock full of figures, tables, and tracings to illustrate the concepts.  I frequently gravitate toward EM Practice’s sections on Risk Management and Cost-Effective Strategies, and this month’s issue has some gems, a few of which are excerpted below:   

1. Avoid routinely sending cardiac enzymes, and avoid admitting patients with SVT for acute coronary syndrome (ACS) evaluation.

While certain forms of SVT (e.g., NPJT) may be associated with ACS/MI, most patients with SVT do not require evaluation for cardiac ischemia.  In fact, ordering cardiac enzymes in all patients with SVT can be a dangerous approach that leads to unnecessary anti-anginal therapy and invasive testing.  Several studies have shown that markers of cardiac ischemia (troponin I) can be elevated but that patients do not have significant coronary artery disease on further evaluation.  Of course, in patients in whom you suspect cardiac ischemia or who have significant risk factors, appropriate evaluation is indicated and may include serial cardiac enzymes and admission.   

5. Minimize unnecessary laboratory testing in young, healthy patients who quickly respond to treatment.  

While hyperthyroidism, electrolyte abnormalities, anemia, and drug/alcohol use have all been associated with SVT, it is unlikely that all of these etiologies need to be investigated in every single patient.  A focused history and physical examination will help guide which, if any, laboratory testing is appropriate.  Additionally, if a patient discloses that he/she abuses drugs or alcohol, a confirmatory test is likely unnecessary.   I remember a conversation on shift with one of my mentors (and prior EM Practice contributor – Scott Weingart, MD – see the July 2007 EM Practice article) about EKG signs of demand ischemia in SVT, and the relevancy of troponin levels. I was pleased to see this edition cite some relevant literature on this vexing issue (references 62 & 63: Redfearn DP, Ratib K, Marshall HJ, et al. Supraventricular tachycardia promotes release of troponin I in patients with normal coronary arteries. Int J Cardiol. Jul 2005;102(3):521-522. [Retrospective case series; 7 patients] Zellweger MF, Schaer BA, Cron TA, et al. Elevated troponin levels in the absence of coronary artery disease after supraventricular tachycardia. Swiss Med Wkly. Aug 2003;133(31-32):439-441. [Case series; 4 patients]). 

To elaborate on this topic, Zellweger et al wrote:  

“Generally speaking, elevated troponin levels are consistent with the diagnosis of acute coronary syndrome and haemodynamically significant coronary artery stenosis. However, it must be borne in mind that troponin results (as also other easily available laboratory variables) need to be interpreted in the context of the patient’s clinical presentation. The TIMI risk score provides a useful tool in the clinical evaluation of patients with elevated troponin levels. In the absence of clinical coronary artery disease, troponin levels may point to minor myocardial injury, as shown by this report on four cases of supraventricular tachycardia (AVNRT).” 

This earlier, small prospective study in a Turkish hospital (Am J Emerg Med. 2001 Jan;19(1):40-2. PMID: 11146016 ) looked explicitly at ST depression in older (45 years and up) patients with paroxysmal SVT. They, too, found the risk of coronary artery disease related to cardiac risk factors: 

“In this study, we detected CAD in 7 of 21 patients (33%) .45 years old who had ST-segment depression during paroxysmal SVT. All patients with significant coronary artery stenosis had evidence of myocardial ischemia on exercise thallium scintigraphy, whereas 6 had had .1-mm ST-segment depression during exercise testing. One patient with isolated left circumflex coronary artery stenosis who developed a thallium defect with redistribution had normal exercise testing. … We failed to identify any electrocardiographic parameter indicative of CAD in patients with ST-segment depression during paroxysmal SVT. The only difference between patients with and without CAD in group I was the coronary risk score, which was higher in those with CAD.”

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