Cardiology Pearls

In NSTE ACS, this thrombus is usually only partially occlusive but may cause intermittent downstream myocardial ischemia or downstream microvascular infarction due to microemboli (JEM, Vol. 36, pg. 162).

NSVT terminates spontaneously without hemodynamic compromise. Sustained VT lasts > 30 seconds, requires an intervention for termination or produces severe hemodynamic compromise or syncope before terminating spontaneously

It indicates critical stenosis high in the LAD coronary artery (JEM, In Press, 5/26/10).

Increasing literature is supportive of the idea of electrically cardioverting new-onset atrial fibrillation (onset < 48 hours). The traditional concerns are that (1) cardioversion doesn't work well with atrial fibrillation and that (2) you will induce an embolic event. The literature actually indicates that both of these concerns are not true. The success rate of electrically cardioverting new-onset atrial fibrillation is actually >90% and the risk of embolism is < 1% (Burton, Ann Emerg Med). Many EDs already utilize such protocols that recommend routine cardioversion for these patients and discharge after a brief observation period.

In coming years, fueled by issues pertaining to hospital overcrowding and cost containment, we'll all be seeing more and more papers and guidelines recommending early electrical cardioversion, so if you aren't comfortable with the idea....you will be!

Only 40%, as compared with 77% of non-STEMI patients younger than 65 years (Annals of EM, In Press, Online 7/12/10).

ST elevation in lead aVR in such a patient is strongly suggestive of WPW-related narrow complex tachycardia (AJEM, Vol. 24:864).

1.Both entities cause Q-waves and STE that can be concave or convex upwards. However, aneurysms shouldn't cause reciprocal depression, whereas a true STEMI often does.

2. Serial ECGs and old ECGs are helpful. The aneurysm shouldn't change from a recent ECG or with serial testing, but STEMI ECGs often do, even over the course of 1-2 hours. Look for any changes in ST segments, T-wave morphology changes, or development of Q-waves.

3. Aneurysms are almost always associated with STE in the anterior leads (because most aneurysms involve the anterior wall). STEMI can involve anterior, lateral, or inferior wall.

4. Aneurysms are almost always associated with Q-waves, whereas STEMI may not (yet) have Q-waves.

• -U waves (produces appearance of long QT), especially in the precordial leads
• -Ventricular ectopy (PVCs typically)
• -ST segment depression or downward sagging, especially in the precordial leads
• -Note that the sagging ST segments that terminate in large U-waves end up producing biphasic T-waves; these have the mirror image appearance of Wellens waves

A greater ST elevation in lead III than lead II is often indicative of a right coronary artery occlusion manifesting as an RV infarct (Mayo Clin Proc, 8/10, pg. e52).

There are multiple reasons for ST-segment elevation, the most important of which is acute myocardial infarction. However, because the treatment difference between MI vs. other more benign causes is so important, one should keep in mind the following factors that strongly point toward the diagnosis of MI:

1. The presence of ST-segment depression in any lead aside from aVR or V1

2. ST elevation that is horizontal or convex upwards (like a tombstone)

3. ST or T-wave morphologies that change over time with serial testing

4. ST changes compared to old ECGs

5. The development of Q-waves

6. ST elevation that follows coronary anatomy (e.g. limited to inferior leads, anterior leads, or lateral leads)

-Short QT (e.g. QTc < 400 msec)

-ST-segment depression

• Prolonged QT
• Tidbit: Note that hyperkalemia is often associated with hypocalcemia, and as a result, hyperkalemic patients often have a prolonged QT, but it's not the hyperkalemia that prolongs the QT, it's the hypocalcemia

Orthodromic SVT: narrow regular tachycardia, looks just like a routine SVT, treat just like any other SVT (AV nodal blockers work fine)

Antidromic SVT: wide regular tachycardia, looks just like VTach, treat like VTach (amiodarone, procainamide, shock; lidocaine won't work, though won't harm either)

Atrial fibrillation: very different!! irregularly irregular, morphologies of the QRS complexes vary between narrow and wide, some areas may have rates as high as 250-300/min, MUST avoid all AV nodal blockers (which includes adenosine, CCBs, BBs, digoxin, amiodarone); treat with procainamide or sedation+cardioversion

Acute use of cocaine increases risk of acute MI due to:

• -Tachydysrhythmias
• -Vasospasm
• -Increased platelet aggregation.

24-fold increased risk

6% of patients presenting with cocaine-chest pain rule in for acute MI.

The delta wave reflects the segment of ventricular myocardium that depolarizes earlier than anticipated because AV accessory conduction is faster than AV node conduction

(Am J EM, 9/09, pg. 880).

Such findings are attributed to cocaine metabolites, which persist in the circulation for up to 24 hours and may caused delayed or recurrent coronary vasoconstriction

(Circulation, Vol. 117, pg. 1897).

Stage 1 – diffuse PR depression and diffuse ST segment elevation with reciprocal changes.

Stage 2 – ST segment normalization and T wave flattening with decreased amplitude.

Stage 3 – T wave inversion.

Stage 4 – Return to baseline

(AJEM, 2010;28:364).

17-18% of cases of syncope are attributable to arrhythmias

1. Abnormal ECG (odds ratio 8.1)

2. History of CHF (odds ratio 5.3)

• 3. Age older than 65 (odds ratio 5.4)
• Sarasin, et al. Academic Emergency Medicine 2003

Ischemia can be caused by septic emoboli. In addition, large vegetations on valve cusps can occlude the coronary ostium

(Am J of EM 2010;28:364).

The extent of plaque rupture is the critical factor. Generally, a large plaque rupture will generate a large thrombus of sufficient size to completely occlude the artery and cause STEMI

(Am J EM, Vol. 26, pg. 212).

Occlusion of the proximal right coronary artery is typically the culprit lesion (Mayo Clin Proc, 8/10, pg. e52).

1. ST segment depression, typically in leads V1-V32.

2. Upright T-waves in leads V1-V33.

3. Development of tall R-waves (R > S in amplitude) in V1-V3 over the course of a few hours (this is analogous to Q-waves forming in the posterior portion of the ventricle)

Approximately 4% of acute MIs will present as an isolated posterior MI (AKA "true posterior MI").

These are easily misdiagnosed as simply anterior ischemia because of the ECG findings. However, the distinction is critically important because posterior STEMI is now considered an indication for immediate reperfusion (PCI or lytics), whereas anterior ischemia is not.

Early on, you may not be able to rely on the presence of tall R-waves to help you. Therefore, it's best to simply do the following: whenever you find ST-segment depression in leads V1-V3, always repeat the ECG using posterior leads (simply place a couple of the V leads on the left mid-back area). These leads will "look" directly at the posterior heart. If those leads show ST elevation, the diagnosis is posterior STEMI. If those leads don't show ST elevation, you can then make the diagnosis of simply anterior ischemia and hold off on immediate PCI or lytics.

Many emergency physicians are not aware of current ACC recommendations to start at a higher energy level, such as 200 J for biphasic waveform devices (Ann of EM, In Press, Online 9/23/10).

A greater ST elevation in lead III than lead II is often indicative of a right coronary artery occlusion manifesting as an RV infarct

(Mayo Clin Proc, 8/10, pg. e52)

1. ST-segment depression, typically in leads V1-V32.

2. Upright T-waves in leads V1-V3.

3. Development of tall R-waves (R > S in amplitude) in V1-V3 over the course of a few hours (this is analogous to Q-waves forming in the posterior portion of the ventricle)

An isolated posterior MI ("true posterior MI") can be easily misdiagnosed as isolated anterior ischemia. The distinction is critically important because posterior STEMI is an indication for immediate reperfusion therapy, whereas anterior ischemia is not.

Early on, tall R-waves may not be present to help make the diagnosis of a posterior MI. Therefore, whenever ST-segment depression in leads V1-V3 is found, it is always best to repeat the ECG using posterior leads, which will "look" directly at the posterior heart. If these leads show ST elevation, the diagnosis is posterior STEMI. If these leads do not show ST elevation, the diagnosis is simply anterior ischemia and immediate PCI/thrombolysis is not indicated.

Ventricular arrhythmias occurring immediately after cocaine use result from the local anesthetic (sodium channel) effects on the myocardium.

• These arrhythmias may respond to the administration of sodium bicarbonate
• (Circulation, Vol. 117, pg. 1897).

Approximately 2/3 of such patients spontaneously convert to NSR wtihin 2-3 days

(JEM, Articles in press, Online 7/16/10).

• The sensitivity of ECG is less likely to be diagnostic in patients with left circumflex lesions
• (Mayo Clin Proc, 3/10, pg. 284).

1. BER is ONLY allowed to have STE that is concave upwards. If you ever see STE that is convex upwards (like a tombstone) or horizontal, it MUST be a STEMI.

2. BER should not have ST-segment depression, except maybe in aVR and V1. If there is ST depression in any of the other 10 leads, it is almost definitely a STEMI.

3. If you see STE in the inferior leads, compare the STE in lead II vs. lead III. If the STE in lead III is greater than the STE in lead II, it rules out BER....gotta be STEMI.

• 4. STE from BER is usually maximal in the mid precordial leads. You CAN have STE in the inferior leads with BER also, but you really shouldn't have STE isolated to the inferior leads. In other words, BER can have (1) STE in the precordial leads alone, or (2) STE in the precordial + inferior leads, but it should never have STE isolated to the inferior leads, and also the STE in the precordial leads should be more prominent than the STE in the inferior leads.
• 5. BER should usually not have STE > 5 mm. However, I've seen some occasional exceptions when the patient has large voltage QRS complexes.

• The most specific ECG finding in young patients with HCM is the appearance of Q waves in leads II, III, aVF, V5, and V6 in the early teenage years
• (Am J EM, Vol. 25, pg. 688).

Microvascular obstruction is related to the embolization of plaque or thrombotic material downstream in the infarct-related artery. Embolization can occur spontaneously or by means of mechanical fragmentation during PCI

(NEJM, Vol. 358, pg. 557).

The dose is 2 g IV followed by an infusion (similar to treatment of eclampsia/preeclampsia). The bolus should be given slowly if the patient is relatively stable, but can be pushed over 1 minute in a patient with ongoing torsade that is not responding to electricity.

The exact mechanism of action is unknown, though it is thought to stabilize the myocardium. Interestingly, magnesium infusions will not necessarily change the heart rate or QT interval on ECG.

The block in this patient is likely to be in non-AV nodal tissue (such as in the bundle of His or more distal conduction system) and is not likely to be responsive to reversal of cholinergic effects by atropine

(Circulation, 2010;122:S729).

Patients with monomorphic VT typically have structural heart disease, whereas patients with polymorphic VT characteristically have electrolyte abnormalities, a drug effect, ischemia, or a genetic cardiac channelopathy

(Mayo Clin Proc,Vol 83,p. 1392).

• Angiographically, noncritical coronary lesions may be associated with abrupt progression to severe or total occlusion and may eventually account for as many as two-thirds of cases of ACS
• (Mayo Clin Proc, Vol. 84, pg. 917).

The initial dose should be reduced to 3 mg in patients taking dipyridamole or carbamazepine, those with transplanted hearts, or if given by central venous access

(Circulation. 2010;S729).

Optimal fibrinolysis restores normal coronary flow in 50% to 60% of subjects

(Circulation. 2010;122:S787-S817).

(1) Increased sympathetic discharge after verapamil-induced hypotension enhances accessory conduction

(2) Verapamil slows AV nodal conduction, allowing penetration of the accessory pathway by normally conducted beats

(Am J EM,Vol. 25, pg. 459).

• Cardiac stun appears to result from excessive catecholamine release in response to intracranial hemorrhage
• (NEJM, Vol. 355:928-39).

Hyperacute T waves are noted as early as 30 min after the onset of coronary occlusion

(JEM, In Press, Online 11/18/09).