UMEM Educational Pearls - Cardiology

Brugada syndrome, believed to be responsible for up to 4-5% of all episodes of cardiac arrest, has now been associated with atrial fibrillation as well (atrial fibrillation is the most common atrial dysrhythmia associated with Brugada syndrome). Patients with atrial fibrillation that have a full or incomplete right bundle branch block with ST segment elevation in leads V1-V2 should be referred to an electrophysiologist for evaluation of Brugada syndrome. The best treatment for these patients is still placement of an ICD.
 

The three factors that are most predictive of an arrhythmia as the cause of a syncopal episode are, in order:
1. abnormal ECG
2. history of CHF
3. age > 65

Overall, approximately 15-20% of cases of syncope are determined to be caused by an arrhythmia.

Infections occur in up to 8-9% of ICD sites. Early infections usually occur within the first 2 months of placement and are associated with typical findings...redness, tenderness, systemic symptoms, etc. Late infections, however, are often associated with nothing more than JUST pain.

Lack of diagnosis of ICD site infections is associated with a mortality > 50%.

When infected, the entire ICD (including wires) must be replaced.

The most commor organisms associated with ICD infections are Staph and Strep. Treat them all with vancomycin.

Patients with ICDs presenting to the ED reporting that their ICD fired once do not need mandatory ICD interrogation, admission or an extensive ED workup purely based on the single shock. A workup should be initiated purely based on any other associated symptoms...chest pain, dyspnea, etc. If the patient was doing well and had no other symptoms prior to the shock, the patient should simply have close follow up with cardiology.

Patients presenting after multiple shocks, on the other hand, do need a workup and emergent ICD interrogation (most of these cases also are later deemed inappropriate shocks).

ICD shocks are often associated with ST segment elevation and even positive troponin levels that can simulate acute MI. So how do you know if the patient experienced an acute MI with VF that triggered the ICD shock? Or if there simply was an aberrant ICD shock that triggered STE with positive troponins?

STE that is due purely to the ICD shock generally resolves after only 15-20 minutes. Persistent STE beyond that time should be assumed to be true ischemia.

Troponin elevations that are due purely to an ICD shock are usually mild and normalize within 24 hours. Huge troponin elevations and those that last beyond 24 hours should be assumed to be caused by true infarction.

NOTE THE CORRECTION TO THIS PEARL BELOW:

If a patient with an implantable cardioverter defibrillator needs to receive a paralytic for rapid sequence intubation, succinylcholine alone is not the best choice. The muscle fasciculations sometimes produced by succ can cause enough electrocardiographic artifact that inappropriate discharges of the ICD can occur.

Therefore, giving defasciculating doses of a paralytic before administering succ is recommended. Alternatively, use a nondepolarizing paralytic. Give 'em the rock!
Yet another reason to go with rocuronium.

AM

Dr. Ron Walls and colleagues emailed me about the pearl above, which was adapted from an article in AJEM [McMullan J, Valento M, Attari M, Venkat A. Care of the pacemaker/implantable cardioverter defibrillator patient in the ED. Am J Emerg Med 2007;25:812-822.]

The authors of the AJEM article reference another article for the statement [Stone KR, McPherson CA. Assessment and management of patients with pacemakers and implantable cardioverter defibrillators. Crit Care med 2004;32(4)Suppl:S155-S165.]. The CCM article actually states that SCH-induced fasciculations may cause artifact which may cause problems with some pacemakers, not ICDs. So it appears that there is no reported problem in using SCH in patients with ICDs. Sorry for the confusion.

Pulsus paradoxus (exaggerated decrease in BP during inspiration) > 10 mm Hg is a physical exam finding that is often considered diagnostic of cardiac tamponade. The sensitivity of the finding, based on pooled studies, is actually only 82% and specificities are reported as low as 70%. In other words, the presence of the PP does not guarantee the presence of tamponade, and (more importantly) the absence of PP does not rule it out.

Conditions that can mask the presence of PP include hypotension, pericardial adhesions, aortic regurgitation, atrial septal defects, and RVH.

Conditions that can produce a PP in the absence of tamponade include severe COPD, CHF, mitral stenosis, massive PE, severe hypovolemic shock, obesity, and tense ascites.

The bottom line...when you are considering the diagnosis of tamponade, get the bedside ECHO. Don't hang your hat (and the patient's life!) on a pulsus paradoxus.

Here's a nice, simple pearl for cardiogenic shock:
"A normal ECG virtually rules out shock due to myocardial infarction."

Essentially, even though MI may be associated with a normal ECG in approximately 5-8% of cases, if a patient has cardiogenic shock due to MI, the ECG will ALWAYS be abnormal.

Gowda RM, Fox JT, Khan IA. Cardiogenic shock: basics and  clinical considerations. Int J Cardiol 2008;123:221-228.

Amal

Cardiogenic shock associated with LV outflow obstruction is managed best without the use of vasoconstrictive agents and vasopressors. Ideally, patients should be treated with IVF and beta blockade. Alpha agonists (e.g. ISO) can also be added.

Typical vasopressors may actually worsen LV outflow obstruction in these patients.

Post-MI cardiogenic shock, while traditionally thought to carry a mortality > 80%, actually has perhaps half that mortality when patients are treated aggressively with prompt invasive therapy (PCI, possibly CABG). Fibrinolytics have traditionally been discouraged, but authors now indicate that they should be given if all of the following three conditions are present:

1. PCI will take greater than 90 minutes,
2. Less than 3 hours have elapsed since onset of STEMI
3. No contraindications to lytics are present.

Sent on behalf of Dr. Amal Mattu

Show References

Right ventricular (RV) dysfunction in the setting of acute MI accounts for only 5% of cases of cardiogenic shock but carries nearly the same mortality as LV shock. Shock due to RV dysfunction is usually treated by aggressive volume loading with IVF. However...

In some cases of RV dysfunction, RV end-diastolic pressure can be very high, resulting in shiftng of the invterventricular septum into the LV cavity, which in turn decreases LV filling and cardiac output. Aggressive fluid resuscitation in these patients may actually further worsen RV pressures, leading to further reductions in cardiac output. These patients should instead be treated early with vasopressors.

How do you tell if your patient needs aggressive fluid resuscitation or early vasopressors? Bedside ultrasound can be the answer...if you find marked distension of the RV, go with early vasopressors. If the RV appears normal in size (smaller than LV), go with the IVF.

And of course early revascularization is critical as well.

(adapted from: Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation 2008;117:686-697.)

Just a reminder, after a recent case of a patient that had a large AMI the day after a negative dobutamine stress test...

Neither stress testing nor coronary angiography are definitive for ruling out unstable/vulnerable plaques. If the HPI for your patient is very concerning, don't obviate your concern just because of a recent negative stress test or angiography. These tests are good at identifying large occlusions, but they tell us nothing about recent rupture or about composition of the plaques, and we now know that it is the composition that determines plaque instability. Size doesn't always matter...

Adenosine should never be used in the setting of a wide complex regular tachycardia as a diagnostic maneuver. Adenosine will convert some types of VT, and this may mislead the health care provider into thinking that the WCT is an SVT. The electrophysiology literature is rife with reports of "adenosine-sensitive VT," and these patients are often young and without prior history of CAD...the very patients that we'd most be inclinded to assume have SVT.

The bottom line is that one should always assume that a regular WCT (without obvious evidence of sinus tachycardia) is VT, and treat the tachydysrhythmia as such.

The 5 most important factors at predicting the presence of ACS in a patient presenting with chest pain (in order of importance):
1. nature of anginal symptoms (i.e. the HPI)
2. prior history of CAD
3. male gender
4. older age
5. increasing number of traditional risk factors

Notice this means that the MOST important factor is the HPI...the OLDCAAAR. If the patient has a concerning HPI, NEVER drop your concerns just because the patient is young or has minimal other risk factors.

The ACC/AHA just recently published a "Focused Update" of their guidelines for management of ST-elevation MI. Amongst the changes:

Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI who receive thrombolytics.

Clopidogrel 300-600 mg orally should be added to aspirin in patients that are going for PCI for STEMI. This is listed as a Class I intervention, although the level of evidence is rated "C." In other words, it is judged to be definitely helpful though based on not-so-robust evidence (you figure that one out!).

Glycoprotein receptor antagonists can also be added (Class IIa, level of evidence B).

[I personally believe there is better evidence for the GP2B3A inhibitors than for clopidogrel, but there is a general push for more and more guideline writers to support clopidogrel. The number of writers for these ACC/AHA guidelines who have affiliations with the drug companies, including the ones that manufacture clopidogrel (Plavix), is tremendous; the list of disclosures is listed at the back of the document. Nevertheless, people tend to want to follow guidelines, and the boards will test you on this stuff so it is worth knowing.]

[Also for the record, if I have a STEMI, here's what I want: 162 mg ASA (not 325 mg), unfractionated heparin (not enoxaparin), abciximab/ReoPro (not eptifibitide/Integrilin) in the cath lab (not in the ER), and quick PCI; if I can't get the PCI within 60 minutes (not 90, but 60 minutes!), give me either tenectaplase or retaplase (not tPA) + 162 mg ASA + UFH; if I have a lot of pain that is not responding to NTG, give me dilaudid or fentanyl (not morphine)...and some Bailey's on ice; add oral BBs, ACEIs, and a statin at the 24 hour mark, NOT any earlier (early BBs only if I have Bailey's-resistant hypertension). Thanks.]

Amal

 

Recent literature (Collins, et al, Ann Emerg Med, Jan 2008; and Cotter, et al, Am Heart J, Jan 2008) confirms something that we've been talking about for YEARS....more than 50% of patients presenting with acute cardiogenic pulmonary edema are not fluid overloaded, but rather have fluid mis-distributed into the lungs. Management should focus on fluid re-distribution rather than diuresis. Use of diuretics in these patients is associated with worsening renal function, which is a significant predictor of in-hospital mortality.

The best patients to use diuretics on are patients with slow progression of dyspnea, lower extremity edema, and weight gain over days-weeks. In the absence of a history of this slow progression, don't go crazy with the diuretics!

Aspirin is the only NSAID that should be used in the acute treatment and also the in-hospital management of patients with STEMI or NSTEMI/unstable angina, even if the patient is chronically managed on other NSAIDs. The use of any of the non-ASA NSAIDS, both nonselective as well as COX-2 selective agents, in these patients is associated with increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture. Their use should be discontinued immediately at the time of admission.

Transient ST-segment depression during rapid atrial fibrillation is of uncertain clinical significance (much as is true for ST segment depression in SVTs). A recent study indicates that ST-segment depression in rapid AFib is not consistently associated with positive stress testing or occlusions on cardiac catheterization.

On the other hand, if the ST-segment depression persists after the rate is controlled, then there should be greater concern.

[Androoulakis A. J Am Coll Cardiol 2007;50:1909-1911.]

In the setting of an ACS, the minimum dose of ASA that should be given is 162 mg. Chewing provides antiplatelet effects slightly faster than simply swallowing, though the difference is probably not clinically significant. Enteric coated aspirin, however, clearly takes longer to work and should therefore be avoided in patients with ACS.

A dose of 325 mg does not appear to provide any further benefit beyond the 162 mg dose, though there might be a slightly higher bleeding rate. Despite that the 2005 PCI guidelines recommend a dose of 325 mg as the initial dose for patients with ACS if they are not chronically taking ASA. Otherwise, 162 mg is sufficient.