UMEM Educational Pearls

Adenosine is everyone's favorite drug for SVTs, and it is often even used as a diagnostic maneuver in some tachydysrhythmias of uncertain origin. BUT there are some definite cautions of which we must all be wary:

1. Adenosine CAN convert some types of ventricular tachycardia to sinus rhythm. This "adenosine sensitive VT" is very well reported in the cardiology literature. Don't use adenosine as a diagnostic method of distinguishing VT from SVT (with aberrant conduction).

2. Atrial fibrillation with WPW can sometimes mimic SVT if one doesn't look closely and notice the irregularity. If you misdiagnose these patients as having SVT and give adenosine, you will likely induce VFib. Not good, Mav, not good!

3. Adenosine causes some histamine release (thus the flushing and hot sensation that patients report). That's bad for patients that have reactive airway disease (RAD). Adenosine should be avoided in patients with severe RAD by history (asthma, COPD) or if patients have active wheezing.

4. Concurrent use of adenosine in patients on digoxin or patients that have received digoxin or verapamil has been reported to cause VFib in rare cases.

5. The effects of adenosine appear to be potentiated by dipyridamole and carbamazepine. Lower the dose of adenosine in patients that take these medications.

6. The effects of adenosine are antagonized by methylxanthines such as caffeine or theophylline. You will probably need higher doses of adenosine in these patients.

7. There are rare cases of adenosine inducing atrial fibrillation. I'm not sure what to say about this, except don't be surprised if your patients goes from SVT into atrial fibrillation. Rare, fortunately.

8. And finally...always remember to push adenosine very quickly and follow immediately with saline BOLUS flush (don't just open up the IVF...you must PUSH 10-20cc of NS); and warn your patient that for ~10 seconds they are going to feel like they are about to die while the adenosine takes effect. If you don't warn them, they will never trust you or the drug again.

9. And finally finally...always have your code cart ready to go when you are using potent cardiac drugs such as adenosine. Don't let yourself be unprepared for a side effect.

Bad luck only happens when you are unprepared!

AM

 

Patients with catastrophic cardiovascular conditions often manifest with JVD + hypotension. The DDx for this combination is therefore critical to know:

1. large LV MI
2. right ventricular MI
3. cardiac tamponade
4. tension PTX
5. massive PE
6. acute mitral regurgitation
7. acute aortic regurgitation

You can make a diagnosis clinically among these 7 entities by:

1. Listening to the lungs
2. Listening for murmurs
3. Getting an ECG.

Of course if you have bedside U/S, it becomes even easier. ECG is almost always diagnostic with either the large LV MI or RV MI. Wet lungs found in large LV MI, acute MR, and acute AR. Murmur found in MR (systolic) and AR (diastolic).

Traditional teaching for patients with hypotension in the setting of MI and heart failure (i.e. not just RV MI) is to give dobutamine as a first-line agent when the SBP is 80-100, and to use dopamine when the SBP is 70-80s [note that this recommendation is NOT based on good evidence, but primarily on consensus opinion]. The problem with using these medications, especially at higher doses (e.g >10-15 mcg/kg/min) is that they result in excessive alpha-1 adrenergic stimulation that can produce end-organ ischemia.

However, there is some evidence that rather than using high dosages of dobutamine or dopamine, "the deliberate combination of dopamine and dobutamine at a dose of 7.5 mcg/kg/min each was shown to improve hemodynamics and limit important side effects compared with [high dosages of] either agent [alone]."

[Overgaard CB, Dzavik V. Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease. Circulation 2008;118:1047-1056.]

Non-invasive ventilation and standard mechanical ventilation can have very deleterious hemodynamic effects on patients with cardiac tamponade because of the drop in preload that results from positive pressure ventilation. The threshold for intubation in these patients should probably be raised. If you are ever caring for a patient with cardiac tamponade that definitely needs to be intubated and ventilated, be prepared for a significant drop in blood pressure and the potential need for pericardiocentesis. Once the patient is intubated, do everything possible to avoid high ventilatory pressures. [Ho AM, Graham CA, Ng CSH, et al. Timing of tracheal intubation in traumatic cardiac tamponade: a word of caution. Resuscitation 2009;80:272-274.]

Initially normal ECGs may be found in 8% of patients with an acute MI, and 35% of patients with acute MI may have an initially non-specific ECG. The sensitivity of electrocardiography increases with serial ECG testing, but never reaches 100% in terms of sensitivity or reliability. The bottom line is that although ECGs are very good for ruling IN acute MI, they are not so great at ruling OUT acute MI. The HPI is the most important tool. ["Prognostic Value of a Normal or Nonspecific Initial ECG in AMI," JAMA 2001]

Although intubation, oxygenation, and ventilation have been downplayed in recent years in the early management of patients with cardiac arrest, late-term pregnant patients DO require early airway support. Paients in the later stages of pregnancy have increased oxygen consumption and therefore have much lower oxygen reserves than non-pregnant patients. As a result, they tend to have central circulation desaturation much sooner. Additionally, they are at higher risk for aspiration because of delayed gastric emptying and lower esophageal sphincter relaxation. "This need for rapid intubation is a key difference between the pregnant women in cardiac arrest and nonpregnant patients." [reference: Atta E, Gardner M. Cardiopulmonary resuscitation in pregnancy. Obstet Gynecol Clin N Am 2007;34:585-597.]

Torsades de pointes and polymorphic ventricular tachycardia are two terms that are often used interchangeably. However, they are not the same!

Torsades is a type of PVT that is characterized by an undulating appearance of the QRS complexes which give the rhythm the appearance of QRS complexes twisting around a central axis. The defining feature of torsades, however, is the presence of a prolonged QTc on the ECG before or after the run of torsades.

Although either rhythm is usually amenable to cardioversion/defibrillation, post-cardioversion treatment is very different between the two. Torsades should be treated with magnesium, whereas PVT can be treated with lidocaine, amio, or procainamide. Beware that treatment of torsades with any of these sodium channel blockers can actually prolong the QTc further and induce intractable torsades.

Elevated troponin levels can have been found to be prognostic of complications, morbidity, and mortality (in-hospital, short-term, and long-term) in many non-ACS conditions, such as sepsis, myocarditis, stroke (including subarachnoid hemorrhage), CHF, and pulmonary embolism.

The elderly are less likely than younger patients to manifest significant (i.e. > 1mm) ST segment elevation on ECG when they have an acute MI. ST depresson and subtle or non-specific changes are more common and should be treated very aggressively. Despite this apparently more benign appearance in the ECGs of elderly patients, they account for 80% of all deaths from acute MI.

The use of a glycoprotein 2b/3a receptor antagonist (often inaccurately referred to as a "G2b3a inhibitor") is considered a Class I intervention for patients with unstable angina/non-STE-MI that are going for percutaneous coronary intervention, according to the ACC/AHA 2007 Guidelines.

The exact timing of the initiation of the G2b3aRA is the subject of some debate, but it is certainly worth discussing with your cardiologist consultant/receiving physician whether they want one of these medications initiated in the ED before taking the patient to the cath. lab, and if so which one of these meds they prefer.

Show References

Most clinicians maintain ventilation with 100% oxygen for cardiac arrest patients with return of spontaneous circulation (ROSC). However, there is increasing literature demonstrating that "hyperoxia in the early stages of reperfusion harms postischemic neurons by causing excessive oxidative stress," and this may result in worse neurological outcomes. It is recommended to avoid unnecessary arterial hyperoxia and simply focus on maintaining oxygen saturations in the 94-96% range during the initial post-cardiac arrest period. [Reference: Neumar RW, Nolan J. Post-cardiac arrest syndrome and management. In The Textbook of Emergency Cardiovascular Care and CPR. Lippincott Williams & Wilkins, Philadelphia 2009.]

Diastolic dysfunction is recognized as a much more common cause of CHF and cardiogenic pulmonary edema than traditionally recognized. Diastolic dysfunction is associated with impaired relaxation, which results in a decrease in LV filling, which results in pulmonary congestion. Common causes of diastolic dysfunction are cardiac ischemia, LVH, and infiltrative diseases.

An increasing amount of attention in the literature is now being paid to ways of optimizing care of patients that are post-cardiac arrest. Simple things to focus on for us in the ED are the following:
1. induction of therapeutic hypothermia
2. aggressively manage hypotension and cardiac ischemia
3. treat hyperglycemia aggressively
4. avoid hyperventilation, though maintain adequate oxygenation

 

Exchange resins (sodium polystyrene sulfonate, Kayexalate) are useful for elimination of potassium from the body in the setting of hyperkalemia, though they work slowly. When given orally, the onset of action is at least 2 hours and peak effect may take > 6 hours. SPS normally produces constipation so it is almost always given with sorbitol. Patients that cannot tolerate oral SPS can receive the therapy as a retention enema, though the magnitude of effect is lower. There is controversy regarding exactly how much SPS will decrease the potassium level, so it seems best to recheck levels to be certain that it's achieving the desired results. Don't rely on this as the sole therapy in moderate to severe cases of hyperkalemia. There are rare case reports of patients receiving SPS + sorbitol that developed intestinal necrosis. The reports seem to indicate that is is a bit more common in post-operative patients and perhaps renal transplant patients. I'm not certain of the mechanism or if there's another way of predicting which patients are at high risk. [Weisberg LS. Management of severe hyperkalemia. Crit Care Med 2008;36:3246-3251.]

Beta adrenoreceptor agonists administered by nebulization (e.g. albuterol nebulizers) are thought to be rapidly effective for lowering serum potassium levels in hyperkalemic patients. The mechanism is via a transient shift of the potassium intracellularly. It makes sense. But don't count on it. At least not much. The truth is that the beta-agonist nebs work much slower than you might think. Though they are quickly effective for bronchospasm, the potassium-shifting effect takes at least 30 minutes, and there's not much peak effect for perhaps as many as 60 minutes. Also, the "peak effect" is only approximately a 1.0 mmol/L reduction...and that's with a 20 mg dose. That's 8-times the normal dose than a typical albuterol neb (one of those albuterol "bullets" has 2.5 mg in 3 cc of solution, so a 20 mg dose would be 24 cc of the albuterol solution). The bottom line is that albuterol nebs are not really effective treatment, even transient, for patients with severe hyperkalemia. If you want do something while people are trying to gain IV access on a "tough stick," then it's certainly better than nothing. Ask the nurses or respiratory techs to start continuous nebs...but the IV calcium and insulin are still the key early temporizing measures to focus on until you've got elimination measures underway (kaexylate, hemodialysis, etc.). [Weisberg LS. Management of severe hyperkalemia. Crit Care Med 2008;36:3246-3251.]

Sodium bicarbonate A recent review of the literature revealed to me something which I never knew about treatment of hyperkalemia: sodium bicarbonate doesn't work the way we thought. In fact, there's no good evidence indicating that it actually produces a substantial shift of plasma K concentration. Our original teaching was based on prolonged (4-6 hour) infusions of bicarbonate, but short-term infusions do not seem to work. Insulin, on the other hand, is effective and works within 20 minutes. [Weisberg LS. Management of severe hyperkalemia. Crit Care Med 2008;36:3246-3251.]

Have you seen any elderly patients with altered mental status (AMS) lately? How quickly did you get an ECG on those patients? Elderly patients often present with mental status changes when they develop cardiac ischemia or acute MI, and this is especially common in the oldest of the elder group. Up to one-quarter of patients > 85 yo with myocardial infarction will present to the ED with delirium or confusion. Get the ECG early on these patients...remember, time is muscle! The delay can be deadly.

Death from ruptured aortic aneurysms and thoracic aortic dissection has a few key features that often help in distinguishing these entities from other causes of rapid decompensation and sudden death:
1. These aortic disasters have a tendency to present with hypotension but without necessarily any specific complaints of pain (in contrast to common teaching).
2. These aortic disasters tend usually to produce PEA as the initial arrest rhythm.
3. These aortic disasters are often diagnosable on bedside ultrasound (AAA seen when scanning the abdomen; dissections frequently produce pericardial tamponade as they dissect backwards into the pericardial sack).

ALWAYS take a look at a patient's aorta and pericardium with the ultrasound when that patient presents in extremis or in cardiac arrest. The results can help make some critical diagnostic and therapeutic decisions.

[recent article related to this topic: Pierce LC, Courtney DM. Clinical characteristics of aortic aneurysm and dissection as a cause of sudden death in outpatients. Am J Emerg Med 2008;26:1042-1046.]

Low QRS voltage (LV) on the ECG is generally defined as the presence of QRS amplitudes which are < 0.5 mV (5 mm) in all of the limb leads and < 1.0 mV (10 mm) in all of the precordial leads. This is a fairly tight definition and for practical purposes, the definition is sometimes expanded to include patients with the sum of QRS amplitudes in leads I, III, and III adding up to < 15 mm; OR the sum of the QRS amplitudes in leads V1, V2, and V3 adding up to < 30 mm. Causes of LV can be divided into two major groups: (1) deficiency of the heart's generated potentials, or "cardiac causes," and (2) attenuating influences outside the heart, or "extracardiac causes." Cardiac causes include: cardiomyopathies (which can sometimes be caused by multiple prior MIs), infiltrative cardiac diseases (e.g. amyloid), severe hypothermia, and inflammatory diseases of the heart due to chemicals or infections (incl. myocarditis). Extracardiac causes include: large pericardial or pleural effusions, obesity, COPD (esp. if a barrel chest is present), pneumothorax and other forms of barotrauma (esp. left-sided).

The classic risk factors for coronary artery disease (e.g. hypertension, diabetes, smoking, etc.) are helpful at predicting the long-term risk of CAD, but they have limited utility at predicting whether a patient with acute symptoms is having an acute coronary syndrome or not. In one recent study of > 800 patients with suspected cardiac chest pain, 12% of patients with NO cardiac risk factors ruled-in for acute MI.

Never rule out ACS in a patient purely based on the absence of traditional cardiac risk factors!

[Body R, McDowell G, Carley S, et al. Do risk factors for chronic coronary heart disease help diagnose acute myocardial infarction in the Emergency Department? Resuscitation 2008;79:41-45.]