UMEM Educational Pearls - Cardiology

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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In order to minimize interruptions in compressions due to pulse checks, continuous end tidal CO₂ (ETCO₂) monitoring during compressions is recommended. Before spontaneous circulation returns, the ETCO₂ is likely to be on the order of < 10 mmg Hg. At the moment spontaneous circulation returns, the ETCO₂ is expected to abruptly increase to at least 35-40 mm Hg. Be wary, though, that the administration of sodium bicarbonate may transiently increase the ETCO₂ even in the absence of return of spontaneous circulation (ROSC).

Use of ETCO₂ in this manner allows one to assess the patient for ROSC without ever having to stop compressions for pulse checks.
 

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In the second half of pregancy, we've traditionally learned that the gravid uterus compresses the inferior vena cava and therefore decreases cardiac output when patient is in a supine position. Therefore, we've learned that patients in the second half of pregnancy the patient should be placed in a left lateral tilt position.

However, it is difficult to perform good quality chest compressions when the patient is in a titled position.

Therefore, the optimal position for chest compressions on the patient in cardiac arrest in the second half of pregnancy is to have the patient in a supine position; and have another rescuer manually deflect the uterus to the patient's left side. This provides optimal compressions + optimal venous return.

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We mentioned atropine's elimination from the cardiac arrest (asystole, PEA) protocols last week. Atropine (0.5 mg) is still indicated in unstable bradycardias that appear to be vagally-mediated, such as sinus bradycardia and Mobitz I bradycardia.

Beware, however, that atropine is not recommended in patients with transplanted hearts. These hearts lack vagal innervation, and in fact there's one small study suggesting that atropine may be associated with paradoxical slowing of the heart rate and worsening AV block. Go straight to pacing with these patients.

 

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The new 2010 AHA Guidelines no longer recommend the use of atropine in caring for patients with cardiac arrest. While it may be useful in vagally-mediated bradycardias, the evidence does NOT support the use of atropine in patients with asystole or PEA; therefore, it has been removed from the cardiac arrest algorithm.

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