UMEM Educational Pearls - Cardiology

Prasugrel is a new thienopyridine alternative to clopidogrel and is now listed as an option in the 2011 ACC/AHA Non-STEMI ACS Guidelines. Studies comparing it versus clopidogrel show a slight benefit in terms of adverse cardiac events, but at the expense of a slight increase in bleeding complications. Though the guidelines state no preference between prasugrel vs. clopidogral for NSTEMI ACS patients, prasugrel is finding a role in patients who appear to have a genetic resistance to the effects of clopidogrel (unlikely you'll know this in the ED, but you'll start seeing more patients started on this medication in the outpatient setting).

Prasugrel is contraindicated in patients with a history of TIA or stroke and it should not be given before cath is performed (in contrast, some protocols push for clopidogrel as early as possible, even before cath).

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Therapeutic hypothermia in post-cardiac arrest patients with return of spontaneous circulation + coma (GCS < 8) is now well-accepted, and the current recommendations are for continued sedation of these patients. Consider avoiding the use of midazolam for sedation in these patients. Midazolam is metabolized more slowly in hypothermic patients, resulting in accumulation and the potential for longer ventilation and ICU time.

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It is now well-accepted that induction of hypothermia should be initiated in victims of cardiac arrest who regain spontaneous circulation and remain unresponsive. Studies are now being performed and published that suggest that the earlier that hypothermia is induced, the better the neurological outcome. With this in mind, some experts are now recommending that cool IVF be the initial resuscitation fluid that these patients receive when resuscitation is initiated. It appears that aggressive use of cool IVF right from the initiation of attempted resuscitation results in improvements in survival to hospital admission and discharge.

The bottom line here is that when caring for victims of primary cardiac arrest, we should be certain to cool the patients fast and early!

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Beck's triad is well known to many physicians, but here's some simple things you may not have known.

Beck actually described two triads, one for acute and one for chronic tamponade.
The triad for chronic tamponade consists of increased CVP (JVD), ascites, and a small quiet heart (muffled heart sounds).
The triad for acute tamponade consists of JVD hypotension, and muffled heart sounds.

Almost 90% of patients have at least 1 of the signs, but only one-third have all 3. Furthermore, it appears that the simultaneous occurrence of all 3 signs is a very late manifestation of tamponade, usually preceding cardiac arrest.
 

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Cocaine-associated MI occurs fairly early after acute cocaine use. 50% of MIs occur in patients prior to their arrival in the ED, and 24% of the total will occur within the first hour of cocaine use. If a patient has not ruled in by 12 hours post-arrival in the ED, it is extremely unlikely that the patient will rule in or suffer ACS-related complications from the cocaine....thus the concept behind using rapid rule out protocols in these patients.

The most important thing we as physicians can do for these patients is to strongly emphasize discontinuation of cocaine use and refer to rehab whenever possible. If the patient discontinues using cocaine, the prognosis for absence of subsequent cardiac events is excellent.

[thanks to Dr. Ellen Lemkin for her contribution to this pearl}

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Traditional teaching for many years has been that new or presumed new LBBB in patients with anginal type of symptoms should be treated as a STEMI, i.e. with immediate PCI or lytics. However, that teaching is based on poor evidence. Newer, increasing evidence is suggesting that new/presumed new LBBB in patients with anginal symptoms is actually not associated with acute MI any more often than when a patient has an old LBBB with those symptoms.

Probably the best management in patients with anginal type of symptoms and a new/presumed new LBBB is to contact the cardiologist on call and ask them for their preference in terms of treatment. Those patients are not necessarily definite AMIs.

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Dabigatran is a new oral anticoagulant (direct thrombin inhibitor) which is being marketed as the new drug to replace warfarin in many cardiac patients. You'll hear much more about it in the coming year, but for now you should know the main advantage and disadvantage:
1. advantage: no need to check levels, e.g. INRs
2. disadvantage: no reversal agent; if a patient is actively bleeding, all you can do is to hold further doses and provide supportive therapy, e.g. tranfusions; hemodialysis is another option, but not ideal to place new dialysis catheters emergently in patients that are coagulopathic!

This second point, the disadvantage of having no reversal agent, is potentially a big issue, especially in older patients at risk for falls. Stay tuned for more information...

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Severe hemolysis/hemolytic anemia in a patient with a prosthetic cardiac valve suggests a paravalvular leak. In this condition, a portion of the valve becomes dislodged from the valve annulus. It can occur immediately after surgery or delayed if from endocarditis. Paravalvular leaks are more common with mechanic valves. Patients may also present with sudden pulmonary edema.

The treatment will focus on management of the pulmonary edema and prompt surgical repair.

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Aortocaval compression occurs often when gestational age is > 20 weeks. This compression significantly compromises the chances of maternal survival in cardiac arrest. Because it is often difficult to know the exact gestational age, it is commonly recommended that emergency C-section in maternal cardiac arrest be performed when the fundus extends above the level of the umbilicus.

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The long QT syndrome and causes of acquired long QT interval are well-known to most emergency physicians, but a short QT can be problematic as well. Short QT-syndrome is an inherited ion-channel disease that predisposes to ventricular dysrhythmias and sudden death. The QTc in these patients is generally < 340 msec. This condition is more common in children, and it should be considered in the differential diagnosis and evaluated on ECG in children presenting with syncope.

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[Here's a nice simple pearl from Jeff Tabas, MD (Prof of EM at UCSF).]

3 causes of bradycardia to consider when the rhythm is not clearly sinus bradycardia:
1. Junctional bradycardia
2. Hyperkalemia
3. Digoxin toxicity

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Is there a difference in the workup, etiologies, or prognosis between patients with syncope vs. near-syncope? Traditional teaching indicates that there is no difference, but that doesn't necessarily reflect common practice. Physicians sometimes are a bit less concerned about patients with near-syncope vs. patients with true, full-blown syncope; and many syncope studies exclude patients with near-syncope.

Grossman and colleagues recently published a useful reminder that patients with syncope and near-syncope have a similar 30-day rate of adverse outcome. However, they have a lower admission rate, reflecting the lower level of concern physicians have in their evaluation. Be wary of those patients with near-syncope. Don't be reassured just because they didn't hit the floor...yet!


 

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For those that listen to EmedHome's EM Cast, you may have already heard this but I thought it's worth sharing with everyone else:

Many of us learned in our training that you should never give calcium to a hyperkalemic patient that is on digoxin or has digoxin toxicity. However, there's a paucity of data to support this contention. Here's one more article suggesting that calcium in the presence of digoxin or dig-toxicity may, in fact, be okay.

Levine and colleagues retrospectively evaluated 161 patients with digoxin toxicity, of whom 23 patients received calcium for hyperkalemia. None of the patients developed significant dysrhythmias in the first hour after calcium, and there was no increase in mortality rate.

Though not definitive, this is further support for treating hyperkalemia with calcium even in the presence of digoxin toxicity.

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Well, there may finally be a replacement for patients with atrial fibrillation who take warfarin (Coumadin).

In late 2010, the FDA approved the drug Dabigatran (Pradaxa) for use in patients with atrial fibrillation.

Dabigatran is an oral direct thrombin inhibitor that has been approved for stroke prevention in patients with A Fib. The drug does not need monitoring like warfarin, and has been deemed to be safer than warfarin.

Be on the lookout for Dabigatran...

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Bretylium was touted for many years as the drug of choice for patients with ventricular dysrhythmias in the setting of hypothermia...in fact it still is recommended by some. Bretylium was actually touted to be effective based on animal studies in which the dogs were PRE-treated with bretylium and then hypothermia was induced. It was found that dogs that were pretreated had fewer episodes of ventricular fibrillation than dogs that were not pretreated. On the other hand, if bretylium was used as a treatment for VFib rather than a prophylactic, it was ineffective. The bottom line....don't bother with bretylium.

Up to 30-40% of patients with infective endocarditis have neurological symptoms as a result of embolization. This is a good reminder of the frequency of embolization, and also that infective endocarditis should always be part of the differential when you are evaluating a patient with fever + neurological abnormalities.

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Therapeutic hypothermia is generally accepted as a useful intervention that should be employed in patients that are resuscitated after cardiac arrest. Many protocols for cooling are relatively complicated, involving endovascular catheters, cooling blankets, cooling helmets, or other devices that are expensive and not widely available. The cooling process can actually be fairly simple, however, with ice and cool IV fluids. The most recent study that demonstrated this used nothing more than application of ice to the groin, neck, and axillae; and administration of 4^o C IVF infused at 30cc/kg at 100ml/min via two peripheral catheters. Sedation or paralysis + intubation was used as per the norm.

Patients receiving this simple intervention were able to achieve goal temperature of 32^o-34^o C within 3-4 hours, and hypothermia was maintained for a full 24 hours before rewarming.

The study shows that expensive equipment and complicated protocols are not necessary for therapeutic hypothermia.

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Induced hypothermia is associated with a decline in serum potassium levels. The cold myocardium is already mildly predisposed to arrhythmias, and the combination of hypokalemia + hypothermia appears to increase the risk of polymorphic ventricular tachycardia. Two simple measures should be taken during post-arrest therapeutic hypothermia:
1. Correct hypokalemia before and during cooling.
2. Monitor the patient's potassium level and QT interval during cooling, and correct as needed.

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Isoproterenol is a non-selective beta-1 and beta-2 agonist. The beta-1 effect produces an increase in heart rate, and the beta-2 effect produces mild vasodilation. Two times to consider its use are the following:
1. For overdriving pacing in cases of intermittent torsades de pointes when magnesium is ineffective.
2. For intractable bradycardia, this is another option besides dopamine or epinephrine. Because of the vasodilation, isoproterenol might be preferred to these other drugs when the bradycardia is accompanied by severe hypertension or when vasoconstrictors are not desired.

The drug is not commonly used anymore but is effective in treating persistent bradycardia or for overdrive pacing in patients with intermittent torsades de pointes when magnesium is ineffective. Be wary, though, that the beta-2 effect produces vasodilation so there may be a mild reduction in blood pressure when the drug is used.

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The September 5 2006 issue of Circulation contained a guideline, based on collaboration between the American Heart Assn, the American College of Cardiology, and the European Society of Cardiology, indicating that procainamide was preferable to amiodarone for the treatment of stable monomorphic ventricular tachycardia.

The 2010 AHA Guidelines have now also listed procainamide as the preferred drug for stable monomorphic ventricular tachycardia, giving it a Class IIa ("probably helpful") rating vs. amiodarone which has a Class IIb ("possibly helpful") rating. [thanks to Dr. Mike Abraham for pointing this out]

Procainamide is also the safest drug for use in tachydysrhythmias when an accessory pathway (e.g. Wolff-Parkinson-White syndrome) is present.

The caveat is that neither procainamide nor amiodarone should be used in the presence of a prolonged QTc.

Acute care physicians should (re-)familiarize themselves with the use of procainamide, and emergency departments should maintain quick access to this drug to stay up-to-date with current national and international guidelines.

 

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