Cardiology Pearls

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Cardiology Pearls
2010-12-05 08:57:10
Cardiology Pearls

Cardiology Pearls
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  1. In non-ST-elevation acute coronary syndrome, the thrombus that occurs following plaque rupture is usually only partially occlusive. How, then, does ischemia and infarction occur?
    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).
  2. What differentiates nonsustained ventricular tachycardia as opposed to sustained VT?
    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
  3. What do the EKG findings of Wellens syndrome indicate?
    It indicates critical stenosis high in the LAD coronary artery (JEM, In Press, 5/26/10).
  4. What does the literature say about early cardioversion for patients in atrial fibrillation?
    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 will be!
  5. What portion of patients older than 85 years and with non-ST-elevation myocardial infarction have chest pain as their main complaint?
    Only 40%, as compared with 77% of non-STEMI patients younger than 65 years (Annals of EM, In Press, Online 7/12/10).
  6. What is the significance of ST elevation in aVR in a patient with narrow complex tachycardia?
    ST elevation in lead aVR in such a patient is strongly suggestive of WPW-related narrow complex tachycardia (AJEM, Vol. 24:864).
  7. EKG distinction between Ventricular Aneurysm and STEMI:
    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.
  8. Classic electrocardiographic findings for hypokalemia:
    • -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
  9. You diagnose a patient with an acute inferior ST elevation MI in the ED. You note greater ST elevation in lead III than lead II. Of what is this indicative?
    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).
  10. ST segment elevation: MI vs. mimics
    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)
  11. Typical ECG findings associated with hypercalcemia:
    -Short QT (e.g. QTc < 400 msec)

    -ST-segment depression
  12. Typical ECG findings associated with hypocalcemia:
    • 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
  13. Some confusion exists regarding proper distinction and treatment between the different tachydysrhythmias associated with WPW. Here's the scoop:
    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
  14. Why does acute use of cocaine cause increase the risk of acute MI?
    Acute use of cocaine increases risk of acute MI due to:

    • -Tachydysrhythmias
    • -Vasospasm
    • -Increased platelet aggregation.
  15. There is a ???-fold increased risk of MI in the first hour after use of cocaine. Fill in the blank.
    24-fold increased risk
  16. What percent of patients presenting with cocaine-chest pain rule in for acute MI?
    6% of patients presenting with cocaine-chest pain rule in for acute MI.
  17. In the presence of WPW, what does the delta wave indicate on an EKG?
    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).
  18. While cocaine-associated MI occurs most often soon after cocaine use, some studies report MI days after. How is this explained?
    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).
  19. What is the classic 4-stage evolution through which the ECG progresses with acute pericarditis?
    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).
  20. What percentage of syncope cases are attributable to arrythmias?
    17-18% of cases of syncope are attributable to arrhythmias
  21. The greatest predictors of arrhythmias as the cause of syncope are:
    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
  22. Acute coronary ischemic syndromes can be seen in the setting of endocarditis. What is the mechanism by which this happens?
    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).
  23. What is the critical factor determining whether the clinical presentation of acute coronary ischemia is silent or results in UA, NSTEMI, or STEMI?
    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).
  24. Right ventricular infarcts are seen in 10% to 50% of inferior infarcts –what is typically the culprit lesion?
    Occlusion of the proximal right coronary artery is typically the culprit lesion (Mayo Clin Proc, 8/10, pg. e52).
  25. The diagnosis of posterior STEMI is made by looking for:
    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)
  26. How common are posterior MI's
    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.
  27. Big tip on how to diagnose a posterior MI:
    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.
  28. According to current American College of Cardiology recommendations what energy level should be used initially when using a biphasic waveform device for cardioversion of atrial fibrillation?
    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).
  29. In the setting of an acute ST elevation inferior myocardial infarction, what is the significance of the EKG finding of a greater ST elevation in lead III than lead II?
    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)
  30. The diagnosis of posterior STEMI is made by looking for:
    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)
  31. Why is it important to distinguish between anterior ischemia and posterior MI?
    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.
  32. How do you make the diagnosis of posterior MI?
    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.
  33. What is first line treatment for ventricular arrhythmias that occur immediately following cocaine use?
    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).
  34. What portion of patients with presumed recent-onset atrial fibrillation spontaneously convert to normal sinus rhythm within 2–3 days?
    Approximately 2/3 of such patients spontaneously convert to NSR wtihin 2-3 days

    (JEM, Articles in press, Online 7/16/10).
  35. The sensitivity of ECG for acute coronary ischemia is affected by the anatomic location of the culprit vessel. It is particularly less likely to be diagnostic in patients with lesion in what location?
    • The sensitivity of ECG is less likely to be diagnostic in patients with left circumflex lesions
    • (Mayo Clin Proc, 3/10, pg. 284).
  36. Distinguishing BER from STEMI:
    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.
  37. The diagnosis of hypertrophic cardiomyopathy must be considered when evaluating a teenage athlete in the ED for a syncopal event. What is the most specific ECG finding in young patients with HCM?
    • 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).
  38. Microvascular obstruction with diminished myocardial perfusion occurs in a large proportion of patients after primary PCI, and is associated with increased infarct size and increased mortality. What is the cause of this micrvascular obstruction?
    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).
  39. Dosing of Magnesium for Torsades de Pointes:
    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.
  40. A patient presents with a third-degree AV block with a new wide-QRS complex. Why should you not rely on atropine to help stablize this patient?
    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).
  41. Why is the differentiation between monomorphic and polymorphic ventricular tachycardia important in terms of the underlying etiology of the arrhythmia?
    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).
  42. What is the role of angiographically noncritical coronary lesions (<50% stenosis in the diameter of the vessel) in the development of acute coronary syndromes? Are they simply a marker for eventual development over time to a complete occlusion?
    • 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).
  43. The standard dose of adenosine for the treatment of PSVT is 6 mg as a rapid IV push. Under what circumstances should the initial dose be reduced to 3 mg?
    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).
  44. Urgent PCI for patients with STEMI restores normal coronary flow in >90% of subjects. How effective is fibrinolysis for restoring coronary flow?
    Optimal fibrinolysis restores normal coronary flow in 50% to 60% of subjects

    (Circulation. 2010;122:S787-S817).
  45. In some patients with WPW, intravenous verapamil can increase the ventricular response to atrial fibrillation and has resulted in ventricular fibrillation. By what 2 mechanisms does this occur?
    (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).
  46. Abnormalities of the ECG, elevated cardiac markers, and abnormal left ventricular dysfunction (collectively called)
    • Cardiac stun appears to result from excessive catecholamine release in response to intracranial hemorrhage
    • (NEJM, Vol. 355:928-39).
  47. Hyperacute T waves are early changes that may be seen on the EKG in an acute MI. How soon after coronary occlusion can hyperacute T waves appear?
    Hyperacute T waves are noted as early as 30 min after the onset of coronary occlusion

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