UMEM Educational Pearls - By Amal Mattu

Rib fractures are associated with significant morbidity and mortality in the elderly, and the risk increases dramatically with each successive rib fractured. An elderly patient with 3 rib fractures has a mortality of 20% and risk of pneumonia is 31%. As a general rule, you should really think twice about discharging home any elderly patients with rib fractures.

[credit to Dr. Joe Martinez for bringing forth this information]

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Elderly patients are prone to hypovolemia for the following two major reasons:
1. They have a decreased thirst response.
2. They have decreased renal vasopressin response to hypovolemia.

The result is that elderly patients have an impaired ability to compensate for a decreased cardiac output, which causes them to develop shock earlier and more easily with stressor.

Takeaway point: Always assume that most elderly patients are hypovolemic, and when they are stressed, give them fluids early!
 

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Adverse drug effects are a major issue in geriatrics.
Elderly patients take, on average, 5 prescription medications + 2 over-the-counter medications.
Adverse drug effects account for approximately 5% of all hospital admissions.
Nearly 20% of patients brought to the ED for psychiatric complaints have symptoms that are primarily caused by medication effects.

Be very wary whenever prescribing ANY new medications for even a short time to elderly patients.

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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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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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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.

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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.

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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.
 

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