The new 2010 AHA guidelines have provided greater focus on airway issues in patients suffering from cardiac arrest. Amongst the important areas of new emphasis are: (1) Cricoid pressure is no longer routinely recommended during intubation, and in fact it has been given a Class III rating ("harmful"); and (2) there is now a very strong push to use quantitative end-tidal CO2 monitoring (rather than just qualitative confirmation) of the airway after endotracheal intubation.
In honor of Halloween and candy....
Hyperglycemia (> 140 mg/dl) at the time of admission is an independent risk factor for adverse outcomes and mortality both during the hospital stay and long-term in patients with acute MI. Hyperglycemia is associated with adverse platelet function, thrombolysis, and coagulation. Tight glucose control is recommended to begin as soon as possible after admission in patients with acute MI in order to optimize outcomes.
Magnesium is considered a mainstay of treatment of prolonged QT syndrome leading to torsade de pointe, including those cases caused by drugs. 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 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.
ECG early repolarization (or sometimes referred to as "benign early repolarization" or BER) is a common finding on ECGs, especially in young patients. It is a common "confounding" pattern when trying to identify STEMI. Here are some pearls that help in distinguishing BER vs. true STEMI. Remember at the outset, though, nothing in medicine is 100%....and that getting old ECGs or getting serial ECGs can be incredibly helpful.
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 traditional teaching has always been to use supplemental high-flow oxygen routinely for patients with acute MI. I recall specifically being taught in residency by EM, IM, and cardiology attendings that every acute MI patient should receive a minimum of 6 liters of supplemental oxygen via nasal canula, if not 100% oxygen, regardless of the initial pulse oximetry.
Mounting evidence, however, is demonstrating that the use of supplemental oxygen in patients that are "normoxic" (i.e. the production of "hyperoxia") is detrimental. Studies are demonstrating that there is no improvement in mortality or prevention of dysrhythmias; and in fact a trend towards increased mortality when patients are hyperoxic. This detrimental effect is likely the result of coronary vasoconstriction which occurs through several different mechanisms, all induced by hyperoxia. Oxygen, it turns out, is a vasoactive substance.
The takeaway point is very simple: if an AMI patient is not hypoxic, don't go overboard with the supplemental oxygen!
[Moradkhan R, Sinoway LI. Revisiting the role of oxygen therapy in cardiac patients. J Am Coll Cardiol 2010;56:1013-1016.]
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.
