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.
The diagnosis of posterior STEMI is made by looking for:
1. ST segment depression, typically in leads V1-V3
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)
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.
The first ECG below shows ST depression in the anteroseptal leads, suspicious for posterior STEMI. The ECG was then repeated, second ECG, with leads V3-V6 placed wrapping around to the left mid-back area. The ST elevation in these leads confirmed the presence of a posterior STEMI and justified immediate reperfusion therapy.
17-18% of cases of syncope are attributable to arrhythmias
The greatest predictors of arrhythmias as the cause of syncope are:
a. Abnormal ECG (odds ratio 8.1)
b. History of CHF (odds ratio 5.3)
c. Age older than 65 (odds ratio 5.4)
[Sarasin, et al. Academic Emergency Medicine 2003]
Acute use of cocaine increases risk of acute MI due to tachydysrhythmias, vasospasm, and increased platelet aggregation. There is a 24-fold increased risk of MI in the first hour after use of cocaine. 6% of patients presenting with cocaine-chest pain rule in for acute MI.
[Weber, Acad Emerg Med 2000]
Some confusion exists regarding proper distinction and treatment between the different tachydysrhythmias associated with WPW. Here's the scoop:
1. orthodromic SVT: narrow regular tachycardia, looks just like a routine SVT, treat just like any other SVT (AV nodal blockers work fine)
2. antidromic SVT: wide regular tachycardia, looks just like VTach, treat like VTach (amiodarone, procainamide, shock; lidocaine won't work, though won't harm either)
3. 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
typical ECG findings associated with hypercalcemia: short QT (e.g. QTc < 400 msec), ST-segment depression
typical ECG findings associated with hypocalcemia: prolonged QT
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
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!
The ECG distinction between ventricular aneurysm vs. true STEMI is a tough one. Aside from reviewing the patient's history, here are a few pearls that may help.
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.
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
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)
Pericardial tamponade is a physiological diagnosis, not an ECG diagnosis. At best, the ECG can suggest the presence of large pericardial effusions--look for the combination of low voltage, tachycardia, and electrical alternans.
Be aware, however, that electrical alternans is only present in < 1/3 of patients with large pericardial effusions. Although it is "classic" and always seems to show up on board exams, in the textbooks, and in lectures, electrical alternans in not a consistent finding in patients with large effusions or tamponade.
The most likely considerations for a regular, narrow complex tachycardia are sinus tachycardia (ST), atrial flutter with 2:1 conduction, and supraventricular tachycardia (SVT, a generic terms that encompasses a few remaining rhythms originating above the ventricle). Atrial flutter is diagnosed when one sees atrial beats at a rate of 250-350/minute.
The distinction between ST and SVT can be difficult at very rapid rates. Here are a few clues that may help in this distinction:
1. Generally the maximal sinus rate that a patient produces will be 220-age. That means that a 20 year old can possibly have a ST up to 200 beats/min, but a 70 year old can only have a ST has fast as 150 beats/min. Rates that exceed that simple formula are extremely unlikely to be ST.
2. If the rate varies with respiration, with positional changes, with relaxation, or with fluid administration, these all favor ST.
3. If the rate reduces slowly, it favors ST. SVT, on the other hand, tends to "break" suddenly.
4. SVT generally will either have no P-waves visible or there may be P-waves just after the QRS complexes. These are referred to as retrograde Ps.
5. History, history, history. Is there a reason for tachycardia, for example a history consistent with dehydration or anxiety? That favors ST. If the patient reports palpitations or other symptoms that were of abrupt onset, that favors SVT.
6. Valsalva maneuvers may gently slow down ST but will either not affect SVT or will abruptly break the SVT....SVT shouldn't gently slow down.
Slight revisions have been made in what is considered to be normal QRS duration.
In children < 4yo, a normal QRS duration is < 90ms.
In children 4-16yo, a normal QRS duration is < 100ms.
Above the age of 16, a normal QRS duration is < 110m.
Consider these numbers when evaluating patients for aberrant conduction (e.g. toxicologic reasons as well) and when defining conduction blocks.
Reference:
Surawicz B, Childers R, Deal BJ, et al. AHA/ACCF/HRS Recommendations for the standardized interpretation of the electrocardiogram, Part III: Intraventricular conduction disturbances. A scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. J Am Coll Cardiol 2009;53(11):976-981.
Three common herbal supplements are reported to be associated with clinically significant hypokalemia: aloe vera, gossypol (used as a male contraceptive), and licorice.
Another popular herbal supplement is reported to be associated with clinically significant hyperkalemia: oleander.
Always ask your cardiac patients (especially those on digoxin) if they are taking any of these herbal supplements!
[Tachjian A, Maria V, Jahangir A. Use of herbal products and potential interactions in patients with cardiovascular diseases. J Am Coll Cardiol 2010;55:515-525.]
Patients with pericarditis are generally treated with high-dose aspirin (e.g. 2-4 gms/day) or other NSAIDs in high dose. However, when myocarditis is also present (e.g. elevated TN levels), lower dosages of aspirin (e.g. 500 mg TID) or other NSAIDS should be used. The higher dosages of anti-inflammatory medications in the setting of myocarditis are thought to exacerbate the myocarditic process and increase mortality (animal studies).
Imazio M, Spodick DH, Brucato A, et al. Controversial Issues in the management of pericardial diseases. Circulation 2010;121:916-928.
Though most causes of acute pericarditis in patients from developed countries are viral or idiopathic, the etiology of pericarditis in patients visiting from developing countries is usually TB, and the TB accounts for > 90% of cases of pericarditis in patients with HIV infection. This group of patients, therefore, should almost always be admitted for a full workup of the cause and for appropriate treatment.
Three groups of patients are at especially high risk of bleeding from excessive anticoagulation with renally-excreted medications: women, the elderly, and patients with chronic renal insufficiency. For all of these patients, ALWAYS dose their renally-cleared medications based on creatinine clearance, NOT just the creatinine.
Which medications in ACS does this apply to?--enoxaparin and G2B3A inhibitors are the most prominent here to consider.
The literature not only demonstrates increased bleeding complications but also increased MORTALITY if you don't dose based on creatinine clearance!
Although supplemental oxygen has long been considered standard care for patients with ACS, the evidence supporting this concept is largely based on animal studies in which acute MI was artificially induced. Should these studies be extrapolated to humans? Maybe not....
Further review of the animal and human literature actually indicates that the routine use of supplemental oxygen and induction of hyperoxia can actually induce adverse hemodynamic consequences such as increased coronary artery tone and reduction in coronary artery blood flow; reductions in cardiac output and increased systemic vascular resistance; and potentially increased infarction size. It certainly seems prudent to treat hypoxia, but if the patient is not hypoxic, skip the supplemental oxygen!
Wijesinghe M, et al. Routine use of oxygen in the treatment of myocardial infarction: systematic review. Heart 2009;95:198-202.
AND
Farquhar H, et al. Systematic review of studies of the effect of hyperoxia on coronary blood flow. Am Heart J 2009;158:371-377.
A recent study of nearly 800 patients with chest pain evaluated symptoms and signs that are most predictive of ruling in for ACS. The following characteristics made acute MI more likely (likelihood ratios in parentheses): observed diaphoresis (5.18), central location of chest pain (3.29), associated vomiting (3.50), radiation of the pain to bilateral arms (2.69), and radiation of pain to the right arm (2.23).
As we've said before, if your patient sweats, it ought to make YOU sweat!
[BodyR, et al. Resuscitation 2010;81:281-286.]
Major and minor clinical prognostic predictors for pericarditis have been described as follows:
Major: fever > 38 degrees C, subacute onset, large effusion, tamponade, lack of response to aspirin or NSAIDs after at least 1 week of therapy
Minor: myopericarditis, immunodepression, trauma, oral anticoagulant therapy
Patients with any of these criteria [major or minor] should strongly be considered for admission. In the absence of these factors, studies show that patients managed as outpatients do well.
[Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of pericardial diseases. Circulation 2010;121:916-928.]
Many cardiac patients take warfarin...no surprise.
Many patients use herbal supplements...no surprise.
Many herbal supplements can produce increased bleeding risk with warfarin, and some produce decreased effects of warfarin...that may be a bit of a surprise. Here's a few that are worth knowing:
Herbals that increase the bleeding risk of warfarin: alfalfa, angelica (dong quai), bilberry, fenugreek, garlic, ginger, and ginkgo
Herbals that decrease the effect of warfarin: ginseng, green tea
In addition to asking your patients about their prescription medications, specifically ask your patients if they take herbal supplements, over-the-counter products, or green tea (since many patients don't consider green tea to be either an herbal supplement)...especially if the patient takes warfarin. You just might diagnose or prevent a disastrous bleeding complication.
[Tachjian A, Maria V, Jahangir A. Use of herbal products and potential interactions in patients with cardiovascular diseases. J Am Coll Cardiol 2010;55:515-525.]
