UMEM Educational Pearls - Cardiology

Post-cardiac arrest care of patients is a hot topic in the resuscitation literature and is gaining increasing attention. We've discussed induced hypothermia; another important intervention is to apply the concepts of goal-directed therapy for these patients. The goal is to optimize MAP (> 65 mm Hg) and provide IVF and pressors when needed. Look for more literature on this in the coming year. Also, for more on this topic, be sure to listen to the June EM Cast, in which Dr. Evie Marcolini will be discussing post-cardiac arrest care of patients.

There are multiple causes of electrocardiographic ST-segment elevation which are well-known to mimic STEMI and often are a cause of misdiagnosis of STEMI.  These are:

• Benign early repolarization
• Pericarditis
• Left ventricular aneurysm
• Brugada syndrome
• Left ventricular hypertrophy
• Left bundle branch block
• Paced rhythms
• Hyperkalemia

Whenever there is doubt regarding whether you are dealing with a STEMI or a mimic, look for reciprocal ST-depression. Most of these will not produce ST-depression (LVH, LBBB, Pacers, and hyperkalemia WILL). The other key intervention is to perform serial ECGs and look for evolving changes, which strongly points to the presence of a true STEMI.

Cardiocerebral resuscitation is a new approach to CPR which has demonstrated improvements in survival and neurological recovery. The main focus is early defibrillation and good compressions with an early dose of EPI, but with a strong de-emphasis on early intubation or bagging. Most patients with sudden cardiac arrest don't need early oxygenation anyway, and the previous emphasis on ventilations only serves to take time and effort away from the important chest compressions. Intubation is deferred for 6-8 minutes after the cardiac arrest in favor of simple passive oxygenation with a non-rebreather.

The bottom line is that when facing a patient in cardiac arrest, the traditional mantra in emergency medicine of "A-B-C" needs to now be changed to emphasize the "C" coming first, second, and third.

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The distinction between pericarditis and acute MI on ECG can often be difficult. Here are a few things that can help rule in acute MI:
1. If the ST-segment elevation is convex upwards in any leads (e.g. appearing like a tombstone) or flat/horizontal across the top, it very strongly favors AMI. Pericarditis should always demonstrate STE that is concave upwards.
2. If ST-segment depression is present in any lead other than aVR or V1, it strongly favors AMI.
3. If PR-depression is present in multiple leads (not just a 2-3 leads, but in MANY) and PR-elevation > 1-2 mm is present in aVR, it favors pericarditis...but only if rules #1 and #2 above are not present.

Be careful about the HPI and description of chest pain...AMI pain is often described as sharp, and in up to 15% it may be described as sharp, pleuritic, or positional in nature, making you think about pericarditis.

 

 

Dark chocolate is being touted more and more as being beneficial to vascular health. It contains polyphenols which has been found to exert anti-oxidant effects and improve endothelial and platelet function. The benefit appears to occur anywhere from 2-8 hours after ingestion of dark chocolate. Unfortunately, the same has not been found true for white chocolate or milk chocolate.

The only caveat is that most of the studies seem to originate in Switzerland and are funded by the Mars Company and Nestle...but who care?? Go ahead and have some dark chocolate every day!

[Dark Chocolate Improves Endothelial and Platelet Function (Hermann F, Heart 2006); Cocoa and Cardiovascular Health (Corti R, Circulation 2009)]
 

Pregnancy is a risk factor for AMI, increasing the risk 3-4-fold. The risk is accentuated with age, especially in women > 40 yo in whom the risk is 30-fold higher. Overall, heart disease is the biggest [non-obstetric-related] killer of pregnant women in the developed world, surpassing even thromboembolic disease. [Roos-Hesselink, et al. Pregnancy in high risk cardiac conditions. Heart 2009;95:680-686.]

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.]