UMEM Educational Pearls - Cardiology

Today's cardiology pearl provided by EMS guru Dr. Ben Lawner. Consider this one if you are caring for a patient with what appears to be shock-resistant VFib.

An intervention that has its roots in the electrophysiology lab has now gained traction on the front lines of resuscitation: double sequential defibrillation. Prospective studies are currently underway to examine the feasibility of this technique. New Orleans (LA) EMS boasts several anectodal accounts of survival, with neurologically intact recovery, from refractory ventricular fibrillation. The next time you can’t stop the fibbing, consider this:

·       Apply TWO sets of defibrillator pads to the patient; one in traditional sternum/apex configuration and the other in anterior/posterior configuration

·       If ventricular fibrillation persists despite several shocks, coordinate the simultaneous firing of BOTH defibrillators

Some caveats:
This treatment is based upon EP lab data; each MONOPHASIC defibrillator was set at 360J. EMS services in New Orleans and Wake County (NC) have used two biphasic defibrillators, each set a 200J. There is not sufficient data to make any widespread recommendation, but the idea of double sequential defibrillation may be another tool in a limited ACLS bag of tricks for patients who simply cannot come out of V-fib. New Orleans EMS has initiated the double-defib protocol after four shocks, and Wake County’s protocol recommends initiation after five. Wake's protocol also recommends firing the defirbillators "as synchronously as possible."

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"Women experience higher mortality rates and more adverse outcomes after acute MI than men, despite less obstructive CAD and plaque burden."(1)

How can this be explained? It turns out that women have more frequent coronary remodeling of vessels. "Remodeling" refers to the concept that as plaques grow, they tend grow into the vessel wall causing outward bulging of the wall, rather than growing into the vessel lumen. That means that standard coronary angiography and even stress testing often miss significant lesions because they only evaluate lumen obstruction....which is not directly reflective of plaque size/burden.

The net effect of the above is that women are more likely to have false negative stress tests and angiograms that appear to show non-significant occlusions. Until we have reliable tests that evaluate true plaque burden rather than just vessel occlusion, we can't completely rely on stress testing and angiography to rule out the the presence of significant plaques.

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Elevated BNP levels are found in conditions besides acutely decompensated CHF. These conditions can include:
Older age
Renal failure
Severe sepsis
PE
Chronic CHF

These conditions will often produce BNP elevations in an intermediate range, but if the elevation is markedly positive, the acutely decompensated CHF is much more likely.

[adapted from ACEP speaker Matthew Strehlow, MD]

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ST depression in the right precordial leads can be anteroseptal ischemia, but it can also be a posterior STEMI. What are the clues to posterior STEMI?

• tall R waves in these leads is highly suggestive of posterior STEMI
• upright T-waves in these leads is also suggestive of posterior STEMI

Posterior leads (a couple of leads placed in the left mid-back area below the tip of the scapula) can help confirm posterior STEMI if there's STE in those leads. If there's no STE, call it just ischemia!

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Hostile behavior appears to be a predictor of ischemic heart disease and myocardial infarction. Prior studies have demonstrated this association, and now one more study has supported this. In short, researchers from Nova Scotia demonstrated that observed hostility was a predictor of ischemic heart disease and myocardial infarction (2-fold), independent of age, sex, Framingham Risk Score, and other psychosocial risk factors.

The key takeaway point of this fun, but validated concept, is that in addition to exercising and eating right, we all just need to relax a bit more. And the next time you have to deal with an angry consultant, just tell him to chill out or he'll die!

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A patient presents to the ED in pulmonary edema, hypotensive, and has JVD. There's a new systolic murmur. The patient had an acute MI 7-10 days ago and had appropriate treatment and uncomplicated course, then discharge. What's the diagnosis and what do you do?

Step 1: Sign out immediately.

Step 2: If it's not time to sign out (just kidding about step 1), listen carefully to the murmur. If it's heard best at the lower sternal border, it's probably a ruptured papillary muscle with acute MR. If it's a "machinery" type murmur heard throughout the precordium loudly, it's probably an acute VSD.

Step 3: VSD patient is likely to die, but with either one, you've got to move quickly. IMMEDIATELY call cardiology AND cardiac surgery. The patient is in need of a balloon pump and OR.
All you can do is buy time until the patient goes upstairs....pressors for BP, IV NTG as tolerated for preload reduction, and be judicious with diuretics. Vasodilators might help unload the heart also. This patient may end up on 2-3 drips, and make sure ALL meds are titrateable. And just keep your fingers crossed!

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SVT is rarely, if ever, the presenting rhythm associated with an acute MI. As a result, physicians should not feel compelled to send troponin levels and perform rule-outs purely based on an SVT presentation. Instead, the decision to rule out a patient presenting with SVT should be based on whether there is a constellation of other concerning symptoms, exclusive of the SVT (e.g. if the patient presented with chest pressure radiating down the arm and diaphoresis, in addition to the SVT).

Two recent studies confirmed that routine troponin testing in patients with SVT is extremely low-yield, and instead often produces false-positive troponin results that lead to unnecessary admissions and workups. In other words, mild troponin elevations may occur in SVT but they do not correlate with true ACS.

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Approximately 7-10% of cases of ACS are not related to atherosclerotic coronary disease. Some other causes of ACS include the following:
trauma
vasculitis
congenital abnormalities
emboli (e.g. bacterial)
thoracic aortic dissection
infectious diseases
DIC, TTP

These conditions can produce ST-segment changes that resemble those of true STEMI or non-STEMI, and therefore some of these patients are diagnosed retrospectively after a negative catheterization.

 

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If you're like me, you've been a bit confused about what exactly defines "coma" in the current recommendations for post-arrest hypothermia in "comatose" patients with return of spontaneous circulation. Fortunately, a recent NEJM article has helped clarify this by suggesting that hypothermia should be induced in these post-arrest patients with either:

1. GCS < 8
2. "patients who do not obey any verbal command at any time after restoration of spontaneous circulation and before initiation of cooling."

Naturally, if the patient was comatose before the arrest, don't bother.

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Clues to RV infarction:

1. This almost always occurs in the presence of a concurrent inferior MI.
2. Clinical findings may include the triad of hypotension, JVD, and clear lungs.
3. ECG clues: in the presence of inferior lead ischemia or injury pattern, look for:
     a. Combination of ST depression in lead V2 + ST elevation in lead V1; OR
     b. Combination of ST depression in lead V2 + isoelectric ST segments in leads V1 and V3; OR
     c. ST elevation in lead III markedly greater than the ST elevation in lead II; OR
     d. ST elevation in right-sided leads (requires you to obtain right-sided leads)

Why is this diagnosis important?
1. It suggests a larger infarction and worse prognosis, so BE AGGRESSIVE in management.
2. Be very cautious with preload-reducing medications (e.g. nitrates) in the acute management of these patients, as they may induce significant reductions in blood pressure and extension of the infarction. Be aggressive with IVF, while maintaining close attention to the lung sounds.

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With recent national shortages of norepinephrine, our typical go-to drug in sepsis, it's become important for us all to familiarize ourselves with alternative pressors in this setting. Phenylephrine is a commonly chosen alternative.

Phenylephrine is a potent alpha-agonist associated with peripheral vasoconstriction. It has no beta effects so it is not associated with tachydysrhythmias. On the other hand, it is associated with reflex bradycardia which can be treated or prevented with atropine (although there are no specific recommendations to routinely administer atropine prophylactically). Phenylephrine may take 10 minutes to demonstrate an effect, and its duration is approximately 15 minutes. It should be used cautiously in patients with underlying cardiac disease because of the vasoconstrictive effect, and it should be avoided in patients with narrow-angle closure glaucoma.

Extravasation can cause tissue necrosis and should be treated with phentolamine.

There has been some controversy regarding the actual clinical benefit of non-invasive ventilation (NIV) for patients with cardiogenic pulmonary edema in recent years. However a recent Cochrane review has confirmed the benefit of NIV for these patients. Early (ED) use of NIV is associated with a decrease in both intubation rates and mortality. The NNT to prevent one intubation is 8, and the NNT to prevent one hospital mortality is 13. To put this in perspective, the NNT for NIV to prevent death in patients with cardiogenic pulmonary edema is lower than the NNT for thrombolytics to prevent death in acute MI.

One key point to remember is that it MUST be used early! If you wait until your patient is decompensating, it is often too late. Start the NIV as soon as possible in these patients.

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DDx for JVD + hypotension + clear lungs:
     RV infarction
     massive PE
     tension PTX (clear lung)
     pericardial tamponade

Assuming your physical exam diagnoses tension PTX, you only need two simple tests to make the diagnosis amongst the other possibilities:
    1.  EKG: RV infarction will almost always show a concurrent inferior MI;
    2.  bedside U/S: tamponade patients have effusion, PE patients have RV distension

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Paroxysmal supraventricular tachycardia (PSVT) is a common tachydysrhythmia encountered in ED practice. PSVT in itself has not been found to be an isolated manifestation of myocardial infarction or unstable angina (i.e. "isolated" = in the absence of other concerning symptoms, such as anginal-type pain, etc.).  Nevertheless, some physicians will routinely test cardiac troponin levels to evaluate for ACS in these patients. We should all remember, though, that tachydysrhythmias including PSVT are a potential cause of elevated troponin levels in the absence of coronary disease, and these elevations do NOT correlate with adverse outcomes unless other concerning symptoms/signs are present as well.

A recent study¹ corroborated this point: 11 out of 38 patients with PSVT had a positive troponin level. Only 2 of the 11 ruled in for ACS, and all of the patients were well at 30 days. Both patients presented with hypotension (SBP in the 70s) and also had other concerning symptoms, such as chest pain (both), dizziness (both), and dyspnea (one).

The takeaway point is simple: if you routinely send troponin levels on your patients for PSVT in the absence of other concerning symptoms/signs, you'll find yourself chasing a lot of false-positive levels.

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Patients with Non-STE-ACS should not be given any NSAIDs aside from aspirin...that includes COX-2 agents. These medications in patients with acute or recent NSTE-ACS have been associated with an increased risk of hypertension, reinfarction, heart failure, myocardial rupture, and death.

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Proton pump inhibitors should be avoided in patients being treated with clopidogrel. PPIs appear to attenuate the effect of clopidogrel, and there's even some suggestion that the addition of PPIs to the medication regimen of patients taking clopidogrel may be associated with an increased risk of rehospitalization or death.

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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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