UMEM Educational Pearls - By Amal Mattu

NOTE THE CORRECTION TO THIS PEARL BELOW:

If a patient with an implantable cardioverter defibrillator needs to receive a paralytic for rapid sequence intubation, succinylcholine alone is not the best choice. The muscle fasciculations sometimes produced by succ can cause enough electrocardiographic artifact that inappropriate discharges of the ICD can occur.

Therefore, giving defasciculating doses of a paralytic before administering succ is recommended. Alternatively, use a nondepolarizing paralytic. Give 'em the rock!
Yet another reason to go with rocuronium.

AM

Dr. Ron Walls and colleagues emailed me about the pearl above, which was adapted from an article in AJEM [McMullan J, Valento M, Attari M, Venkat A. Care of the pacemaker/implantable cardioverter defibrillator patient in the ED. Am J Emerg Med 2007;25:812-822.]

The authors of the AJEM article reference another article for the statement [Stone KR, McPherson CA. Assessment and management of patients with pacemakers and implantable cardioverter defibrillators. Crit Care med 2004;32(4)Suppl:S155-S165.]. The CCM article actually states that SCH-induced fasciculations may cause artifact which may cause problems with some pacemakers, not ICDs. So it appears that there is no reported problem in using SCH in patients with ICDs. Sorry for the confusion.

Pulsus paradoxus (exaggerated decrease in BP during inspiration) > 10 mm Hg is a physical exam finding that is often considered diagnostic of cardiac tamponade. The sensitivity of the finding, based on pooled studies, is actually only 82% and specificities are reported as low as 70%. In other words, the presence of the PP does not guarantee the presence of tamponade, and (more importantly) the absence of PP does not rule it out.

Conditions that can mask the presence of PP include hypotension, pericardial adhesions, aortic regurgitation, atrial septal defects, and RVH.

Conditions that can produce a PP in the absence of tamponade include severe COPD, CHF, mitral stenosis, massive PE, severe hypovolemic shock, obesity, and tense ascites.

The bottom line...when you are considering the diagnosis of tamponade, get the bedside ECHO. Don't hang your hat (and the patient's life!) on a pulsus paradoxus.

Here's a nice, simple pearl for cardiogenic shock:
"A normal ECG virtually rules out shock due to myocardial infarction."

Essentially, even though MI may be associated with a normal ECG in approximately 5-8% of cases, if a patient has cardiogenic shock due to MI, the ECG will ALWAYS be abnormal.

Gowda RM, Fox JT, Khan IA. Cardiogenic shock: basics and  clinical considerations. Int J Cardiol 2008;123:221-228.

Amal

Cardiogenic shock associated with LV outflow obstruction is managed best without the use of vasoconstrictive agents and vasopressors. Ideally, patients should be treated with IVF and beta blockade. Alpha agonists (e.g. ISO) can also be added.

Typical vasopressors may actually worsen LV outflow obstruction in these patients.

Right ventricular (RV) dysfunction in the setting of acute MI accounts for only 5% of cases of cardiogenic shock but carries nearly the same mortality as LV shock. Shock due to RV dysfunction is usually treated by aggressive volume loading with IVF. However...

In some cases of RV dysfunction, RV end-diastolic pressure can be very high, resulting in shiftng of the invterventricular septum into the LV cavity, which in turn decreases LV filling and cardiac output. Aggressive fluid resuscitation in these patients may actually further worsen RV pressures, leading to further reductions in cardiac output. These patients should instead be treated early with vasopressors.

How do you tell if your patient needs aggressive fluid resuscitation or early vasopressors? Bedside ultrasound can be the answer...if you find marked distension of the RV, go with early vasopressors. If the RV appears normal in size (smaller than LV), go with the IVF.

And of course early revascularization is critical as well.

(adapted from: Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation 2008;117:686-697.)

Just a reminder, after a recent case of a patient that had a large AMI the day after a negative dobutamine stress test...

Neither stress testing nor coronary angiography are definitive for ruling out unstable/vulnerable plaques. If the HPI for your patient is very concerning, don't obviate your concern just because of a recent negative stress test or angiography. These tests are good at identifying large occlusions, but they tell us nothing about recent rupture or about composition of the plaques, and we now know that it is the composition that determines plaque instability. Size doesn't always matter...

Adenosine should never be used in the setting of a wide complex regular tachycardia as a diagnostic maneuver. Adenosine will convert some types of VT, and this may mislead the health care provider into thinking that the WCT is an SVT. The electrophysiology literature is rife with reports of "adenosine-sensitive VT," and these patients are often young and without prior history of CAD...the very patients that we'd most be inclinded to assume have SVT.

The bottom line is that one should always assume that a regular WCT (without obvious evidence of sinus tachycardia) is VT, and treat the tachydysrhythmia as such.

The 5 most important factors at predicting the presence of ACS in a patient presenting with chest pain (in order of importance):
1. nature of anginal symptoms (i.e. the HPI)
2. prior history of CAD
3. male gender
4. older age
5. increasing number of traditional risk factors

Notice this means that the MOST important factor is the HPI...the OLDCAAAR. If the patient has a concerning HPI, NEVER drop your concerns just because the patient is young or has minimal other risk factors.

The ACC/AHA just recently published a "Focused Update" of their guidelines for management of ST-elevation MI. Amongst the changes:

Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI who receive thrombolytics.

Clopidogrel 300-600 mg orally should be added to aspirin in patients that are going for PCI for STEMI. This is listed as a Class I intervention, although the level of evidence is rated "C." In other words, it is judged to be definitely helpful though based on not-so-robust evidence (you figure that one out!).

Glycoprotein receptor antagonists can also be added (Class IIa, level of evidence B).

[I personally believe there is better evidence for the GP2B3A inhibitors than for clopidogrel, but there is a general push for more and more guideline writers to support clopidogrel. The number of writers for these ACC/AHA guidelines who have affiliations with the drug companies, including the ones that manufacture clopidogrel (Plavix), is tremendous; the list of disclosures is listed at the back of the document. Nevertheless, people tend to want to follow guidelines, and the boards will test you on this stuff so it is worth knowing.]

[Also for the record, if I have a STEMI, here's what I want: 162 mg ASA (not 325 mg), unfractionated heparin (not enoxaparin), abciximab/ReoPro (not eptifibitide/Integrilin) in the cath lab (not in the ER), and quick PCI; if I can't get the PCI within 60 minutes (not 90, but 60 minutes!), give me either tenectaplase or retaplase (not tPA) + 162 mg ASA + UFH; if I have a lot of pain that is not responding to NTG, give me dilaudid or fentanyl (not morphine)...and some Bailey's on ice; add oral BBs, ACEIs, and a statin at the 24 hour mark, NOT any earlier (early BBs only if I have Bailey's-resistant hypertension). Thanks.]

Amal

 

Recent literature (Collins, et al, Ann Emerg Med, Jan 2008; and Cotter, et al, Am Heart J, Jan 2008) confirms something that we've been talking about for YEARS....more than 50% of patients presenting with acute cardiogenic pulmonary edema are not fluid overloaded, but rather have fluid mis-distributed into the lungs. Management should focus on fluid re-distribution rather than diuresis. Use of diuretics in these patients is associated with worsening renal function, which is a significant predictor of in-hospital mortality.

The best patients to use diuretics on are patients with slow progression of dyspnea, lower extremity edema, and weight gain over days-weeks. In the absence of a history of this slow progression, don't go crazy with the diuretics!

Aspirin is the only NSAID that should be used in the acute treatment and also the in-hospital management of patients with STEMI or NSTEMI/unstable angina, even if the patient is chronically managed on other NSAIDs. The use of any of the non-ASA NSAIDS, both nonselective as well as COX-2 selective agents, in these patients is associated with increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture. Their use should be discontinued immediately at the time of admission.

Transient ST-segment depression during rapid atrial fibrillation is of uncertain clinical significance (much as is true for ST segment depression in SVTs). A recent study indicates that ST-segment depression in rapid AFib is not consistently associated with positive stress testing or occlusions on cardiac catheterization.

On the other hand, if the ST-segment depression persists after the rate is controlled, then there should be greater concern.

[Androoulakis A. J Am Coll Cardiol 2007;50:1909-1911.]

In the setting of an ACS, the minimum dose of ASA that should be given is 162 mg. Chewing provides antiplatelet effects slightly faster than simply swallowing, though the difference is probably not clinically significant. Enteric coated aspirin, however, clearly takes longer to work and should therefore be avoided in patients with ACS.

A dose of 325 mg does not appear to provide any further benefit beyond the 162 mg dose, though there might be a slightly higher bleeding rate. Despite that the 2005 PCI guidelines recommend a dose of 325 mg as the initial dose for patients with ACS if they are not chronically taking ASA. Otherwise, 162 mg is sufficient.

Adenosine should be used with great caution in patients with wide complex tachycardia for two major reasons:
1. Adenosine should never be used as  diagnostic maneuver to decide whether someone has ventricular tachycardia vs. SVT. Adenosine is well-reported to convert certain types of VT.
2. If the WCT is irregular, this may be atrial fibrillation with WPW, in which case adenosine is well-known to produce ventricular fibrillation.

Here's a pearl for everyone that is "enjoying" the holidays with friends...friends named Jack Daniels, Remy Martin, and Louis XIII, among others.

It's fairly well-known that light-moderate alcohol intake is associated with reductions in cardiovascular death and nonfatal MI and also a reduction in the development of heart failure. In case you've ever wondered exactly what a "drink" is and what "moderate" intake are, here are some definitions:
a. In the U.S., a standard alcohol "drink" is 1.5 oz or a "shot" of 80-proof spirits or liquor, 5 oz of wine, or 12 oz of beer.
b. "Moderate" drinking is no more than 1 drink per day for women and 2 per day for men.
c. "Binge" drinking is > 4 drinks on a single occasion for men or > 3 for women within 2 hours.

Although some studies suggest that wine (esp. red) has an advantage over other types of alcohol, other studies (including ones we've reviewed in the cardiology update series) indicate that the type of alcohol doesn't matter. Good news for many of our patients!

What do you do if a patient with an AICD presents to the ED with a shock? 

If the patient receives a single shock and is otherwise asymptomatic and fine, there is probably no need for intervention (or even an ED visit). For the patient in the ED, monitor them and discuss with their cardiologist. Consider checking some labs, but emergent pacer evaluation is not generally necessary (unless there are other concerning issues--abnormal rhythms on monitor, complaints of lightheadedness and preceding chest pain, etc.). You should manage and treat the patient for other symptoms and signs, but not for the shock itself.

If the patient received multiple shocks, however, device interrogation is generally required. Also search for the underlying cause--ischemia, electrolyte abnormalities, etc. Bear in mind that most of the time, multiple shocks are later deemed to be inappropriate (device error).

Post-shock ECG will likely show ST segment changes but they normalize within 15 minutes.

15-20% of the time there will be some TN-I elevation for up to 24 hours due to a shock.

Women are more likely to present with atypical presentaitons for ACS.

Women are more likely to present without chest pain, but instead with middle or upper back pain, neck pain, jaw pain, dyspnea, vomiting, indigestion, weakness/fatigue, loss of appetite, cough, or palpitations than men.

Rheumatic heart disease (RHD) has traditionally been considered the most common underlying condition predisoposing to infective endocarditis. While RHD is still common in developing countries, its prevalence has declined and "mitral valve prolapse is now the most common underlying condition in patients with infective endocarditis."

(from AHA Guideline on Prevention of Infective Endocarditis, Circulation, October 9, 2007)

The standard dose for adenosine in treating SVT is 6 mg given as a rapid IV push. The dose should be immediately followed by a saline flush and works best if the drug is administered through a good, proximal (e.g. antecubital) IV line.

A few points:

1. The initial dose of adenosine should be reduced to 3 mg if the dose is administered through a central line, if the patient has a transplanted heart, or if the patient is taking carbamazepine or dipyridimole.
2. The initial dose of adenosine should be increased to 9-12 mg if the patient is taking theophylline or large doses of caffeine.
3. ALWAYS warn the patient that he/she will experience 5-10 seconds of chest pressure, warmth, dyspnea, and perhaps a feeling of "impending doom" as the adenosine kicks-in, and reassure the patient that the sensation will resolve. Failure to warn the patient of these symptoms may result in the patient refusing to ever take the medication again...plus it's just plain cruel to not warn the patient.