UMEM Educational Pearls - Cardiology

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.

A few pearls regarding pacing a patient with an unstable bradycardia:

If the patient has an implanted pacemaker (which isn't working properly), the transcutaneous pacing pads should be placed at least 10 cm away from the implanted PM pulse generator.

Placement of a transvenous pacemaker is absolutely contraindicated if the patient has a prosthetic tricuspid valve.

Neither transcutaneous or transvenos pacing is likely to work in the setting of severe acidosis or severe hypothermia. Severely hypothermic patients, in fact, have very irritible myocardial tissue and therefore attempts at pacing may produce ventricular dysrhythmias.

Atypical presentations of ACS in the elderly are common.
Only 40% of patients > 85yo present with chest pain. Dyspnea is the most common presenting complaint in these patients. Other atypical presentations include isolated nausea, vomiting, diaphoresis, or syncope.

The presence of an atypical presentation is not reassuring in terms of prognosis. Patients presenting atypically have a 3-fold higher in-hospital mortality (13% vs. 4%). This doesn't even include the patients that are inadvertently discharged home because of failure to diagnose ACS.

Although CHF is usually associated with low cardiac output, "high output failure" can occur as well. In this condition, cardiac output is normal or even high but not high enough to meet markedly elevated metabolic demands of the heart in certain conditions. Those conditions include: severe anemia, thyrotoxicosis, lartge arteriovenous sunts, Beriberi, and Paget disease of the bone.

The T-wave in lead V1 is usually inverted or flat. When the T-wave is upright, especially if it is tall (taller than the T-wave in lead V6), be worried about cardiac ischemia...especially if the large upright T-wave is a new finding compared to prior ECGs.

LVH, LBBB, and misplaced precordial leads are the other causes of tall upright T-waves in lead V1. In the absence of any of these three conditions, worry about ischemia.

Marriott described this finding many years ago and refers to it as "loss of precordial T-wave balance."

Recent  studies have identified that a significant cause of morbidity and mortality in women, elderly, and patients with renal failure is the failure to consider renal insufficiency in dosing certain anticoagulants and anti-platelet medications, resulting in bleeding complications. Medications should be based on creatinine clearance, NOT SERUM CREATININE. When the creatinine clearance is < 30 mL/min, the dose of any renally-excreted medications should be decreased.

For example, an 85 yo woman that is 110 lbs and has a serum creatinine of 1.2 (sounds normal!) actually has a creatinine clearance < 30, which means that she has relative renal insufficiency. Her dosages of medications (e.g. enoxaparin) should be adjusted for this.

 Creatinine clearance can easily be calculated via computer programs that you can "google" (e.g. just google "creatinine clearance calculation"). If you enter the patient's gender, age, weight, and serum creatinine, the programs will calculate the value for you.

New onset atrial fibrillation is rarely the sole manifestation of myocardial infarction. In other words, in the absence of accompanying chest pressure, dyspnea, diaphoresis, or other anginal equivalents, a rule-out ACS workup in not supported by the literature and is not cost-effective.

The two exceptions to the statement above are elderly and diabetic patients, in whom subtle presentations of ACS are common with or without atrial fibrillation.

In the treatment of an acute ST-elevation MI, there are three major signs of successful reperfusion:

1. T-wave inversion within the first 4 hours. If the T-wave inversions occur beyond 4 hours, it's uncertain.
2. Resolution of the STE by at least 70% in the lead with maximal STE.
3. Development of a "reperfusion arrhythmia," most notably accelerated idioventricular rhythm (AIVR), which looks like V.Tach but the rate is only 60-120. Remember, V.Tach should have a rate > 120.

Persistent pain/symptoms OR absence of STE resolution by 90 minutes warrants strong consideration of rescue angioplasty.

• "Small" = less than 10 mm of echo-free space (anterior plus posterior)
• "Moderate" = 10-20 mm
• "Severe" = > 20 mm.