UMEM Educational Pearls - Cardiology

17-18% of cases of syncope are attributable to dysrhythmias.
The best predictors of dysrhythmias in these patients are:
1. abnormal ECG (odds ratio 8.1)
2. history of CHF (odds ratio  5.3)
3. age > 65 (odds ratio 5.4)

[reference: Sarasin FP, et al. A risk score to predict arrhythmias in patients with unexplained syncope. Acad Emerg Med 2003.]

 HIV positive patients are at increased risk of premature atherosclerosis for at least a few reasons:
1. HIV disease causes increased activation of platelets.
2. HIV produces arterial endothelial dysfunction [which promotes thrombosis formation].
3. Protease inhibitors produce dyslipidemias and insulin resistance.

HIV-associated CAD is also unusual in that the vessel involvement is frequently diffuse and circumferential along the whole artery.

HIV positive patients are known to have their first MI at an earlier age than non-HIV controls, and the effect is not related to CD4 count (not related to severity of disease).

The takeaway point here is to always strongly consider ACS in the differential diagnosis of patients with HIV that are presenting with cardiopulmonary complaints, even in relatively younger patients.

Amal

[reference: Khunnawat C, Mukerji S, Havlichek D, et al. Cardiovascular Manifestations in Human Immunodeficiency Virus-Infected Patients. Am J Cardiol 2008;102:635-642.]

 Troponin levels are often elevated in patients with sepsis. This doesn't necessarily mean that the patient has suffered an acute Mi or ACS, but rather it seems to correlate with myocardial dysfunction that is caused by sepsis. Much like with true MI, troponin elevations predict a greater risk of in-hospital mortality in these patients.

Patients with HIV are at increased risk for several cardiovascular complications of the disease. The most common cardiac manifestation in HIV disease is reported to be pericardial effusion. 

The presence of a pericardial effusion in HIV is a poor prognostic sign, an independent predictor of mortality (62% mortality at 6 mos is reported, compared to 7% in those without effusion).

The pericardial effusion is often associated with TB in endemic areas, but can also be associated with other organisms including Staph, Strep, Chlamydia, and some viruses. HIV itself can cause an effusion as part of a generalized serous effusive process.

Takeaway: In late-stage HIV patients with any cardiopulmonary complaints, it would be prudent to make bedside ED ECHO part of your usual initial evaluation.

[reference: Khunnawat C, Mukerji S, Havlichek D, et al. Cardiovascular manifestations in human immunodeficiency virus-infected patients. Am J Cardiol 2008;102:635-642. Authors are from Michigan State Univ.]

The longitudinal subcostal view on bedside ultrasound can be very helpful at addressing a patient's fluid status. 
Take a look at the diameter of the IVC 2 cm proximal to the hepatic vein on this view and ask the patient to quickly sniff. If the patient has normal fluid status, the diameter of the IVC will collapse approximately 50%.

If you notice that the IVC completely collapses during the sniff, the finding is highly accurate at predicting hypovolemia and a low CVP.

If, on the other hand, the IVC doesn't appear to collapse much at all, the finding is highly accurate at predicting a high CVP and elevated right atrial pressure. This may occur in the presence of fluid overload from decompensated CHF, cardiac tamponade, and conditions associated with RV failure (e.g. massive pulmonary embolism).

The apical 4-chamber view of the heart on bedside ultrasound gives an excellent comparative view of the sizes of the right ventricle (RV) and left ventricle (LV). The RV is normally ~ 0.5-0.6 the size of the LV. When the RV appears too large, certainly if the RV > LV in size, it indicates RV dilatation.

RV dilatation can be chronic (e.g. COPD or sleep apnea with pulmonary hypertension, etc.) or acute (e.g. PE, RV MI). How can you tell whether the condition is chronic or acute? Just take a look at the RV free wall. If the RV free wall measures < 5 mm, it's a pretty good indication that you are dealing with an acute condition. Think PE or RV MI!

[thanks to Dr. Jim Hwang from Brigham and Women's Hospital for providing this pearl]

"The most common EKG abnormalities are non-specific ST-T wave changes, followed by RBBB. A normal EKG does not exclude the possibility of cardiac injury, although some investigators report a negative predictive value of up to 80-90%."

[El-Chami MF, Nicholson W, Helmy T. Blunt cardiac trauma. J Emerg Med 2008;35:127-133.]

Hemorrhagic and ischemic strokes are well-known to produce ECG changes that resemble cardiac ischemia. Large T-wave inversions are the most classic findings, but ST changes, prolonged QT interval, tachydysrhythmias, bradydysrhythmias, and AV blocks have also been described.

The exact cause of these changes is uncertain. One theory is that the strokes can produce catecholamine surges which cause the changes; another theory is that intracranial events produce a vagal response that causes ECG changes. Regardless of the reason, one should always keep stroke in the differential diagnosis for patients with ischemic-appearing ECG changes, especially when the patient has an altered mental status or neurologic deficit.

There are many causes of rightward axis on electrocardiography: RVH, COPD, acute (e.g. PE) or chronic (e.g. COPD, cor pulmonale) pulmonary hyptertension, sodium channel blocking drug toxicity (e.g. TCAs), ventricular tachycardia, hyperkalemia, dextrocardia, left posterior fascicular block, prior lateral MI, and of course misplaced leads.

In emergency medicine, however, the causes of acute/NEW rightward axis constitutes a smaller list. Perhaps the two most important causes of acute/new rightward axis in emergency medicine that should be remembered are PE and sodium channel blocker toxicity. In both of these conditions, the rightward axis may be the only obvious finding on the ECG.

The takeaway point is this: when you see new righward axis (compared to an old ECG) and you see nothing else "jumping out" at you, consider PE and consider sodium channel blocker toxicity.

 The most common misdiagnosis in cases of missed acute MI is reflux esophagitis. Various studies have demonstrated the following factors that lead to this misdiagnosis:
1. 20% of patients with acute MI describe their pain using the words "indigestion" or "burning."
2. Almost 50% of patients with acute MI report an increase in belching during their ischemic symptoms.
3. 15% of patients get some relief of their ischemic pain with antacids and 7% of patients get complete relief of their ischemic pain with antacids.
4. 8% of patients report that their ischemic pain began while eating.

Before you ever write "Reflux esophagitis" or "GERD" on the chart of a patient you are about to send home, think twice about the possibility of acute cardiac ischemia.
 

The pericardium is electrically silent, and so true acute pericarditis should not be associated with ECG changes. STE actually implies concurrent involvement of the myocardium; i.e. myopericarditis. The greater the degree of myocardium involved, the more ECG changes will develop, including STE, AV blocks, and dysrhythmias. Additionally, myocardial involvement is implied by elevated troponin levels, the magnitude of which is related to the amount of myocardial involvement.

[Imazio M, Trinchero R. Myopericarditis: etiology, management, and prognosis. Int J Cardiol 2008;127:17-26.]

Both acute pericarditis and myopericarditis are intensely inflammatory. As a result, CRP testing is extremely sensitive for these conditions and is excellent for evaluating their presence or absence.

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Low QRS voltage on the ECG has various definitions; here's my simple definition for low voltage...either one of the following:
     If the added QRS amplitudes (whole R wave + S wave) in leads I + II + III total < 15 mm, OR
     If the added QRS amplitudes (whole R wave + S wave) in leads V1 + V2 + V3 total < 30 mm.

The potential causes of  low QRS voltage includes pericardial effusions, pleural effusions, obesity, COPD, infiltrative cardiac diseases (e.g. sarcoid, amyloid), end-stage cardiomyopathies, severe hypothyroidism.

If the patient has NEW low voltage compared to an old ECG, the only real possibilities are pericardial effusion, pleural effusion, and severe hypothyroidism (e.g. myxedema).

Patients with cancer that present with pleuritic chest pain often have pulmonary emboli, but don't forget about pericarditis. Lung and breast cancer, especially, are known to metastasize to the pericardium and produce pericarditis or pericardial effusions. Anticoagulation for presumed PE in patients with pericardial mets. can produce hemorrhagic tamponade, a disastrous iatrogenic complication, so think twice before starting empiric anticoagulation on patients...make sure your patient doesn't have pericarditis or an pericardial effusion.

The ECG in patients with cancer-related pericarditis or pericardial effusion does not always demonstrate the classic ST elevation wtih PR depression (which is most commonly seen in viral pericarditis). Patients with pericardial effusions often demonstrate low voltage and tachycardia. Electrical alternans, though "classic," only appears in 1/3 of patients with pericardial effusions.

Just a reminder...an initially normal or non-specific ECG can certainly occur in patients that are actively having chest pain from acute MI. A 2001 study published in JAMA nicely pointed this out:

7.9% of patients having an acute MI had an initial normal ECG.
35.1% of patients having an acute MI had non-specific abnormalities on ECG.
57% of patients having an acute MI had diagnostic changes on ECG.

The greater the abnormality on the ECG, the worse the prognosis, but note that even when the ECG was normal, the in-hospital mortality in acute MI patients was 5.7%.

Although serial ECGs won't detect 100% of acute MIs, the diagnostic yield does certainly increase, and so whenever a patient has a concerning presentation, especially in the presence of on-going pain, make sure to get repeat ECGs!

[ref: Welch RD, et al, JAMA 2001]

Chronic kidney disease is a risk factor for accelerated atherogenesis. It is also a poor prognostic factor for patients with ACS or after MI. Elevated serum creatinine has been found to be an independent predictor of death after ACS and also a predictor of recurrent cardiovascular events. Cardiovascular death is 10-30 times higher in dialysis patients with ACS than in the general population.

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Just a few quick pearls about cocaine-chest pain and myocardial infarction:
 

• 0.7%-6% of patients presenting to the ED with chest pain during or immediately after using cocaine will rule in for an MI based on cardiac biomarkers. The 6% figure is the most commonly-quoted number.
• The risk of MI rises as much as 24-fold during the first hour after cocaine use. Although the risk decreases significantly after that, cocaine-related vasoconstriction can still cause acute MI hours or as many as 4 days later.
• Chest pain is not reliably present in patients with cocaine-associated MI, with one study reporting that only 44% of patients with cocaine-associated MI had chest pain (Hollander and Hoffman, J Emerg Med 1992). Dyspnea and diaphoresis are other common symptoms that should prompt concern for acute MI if chest pain is not present.

[McCord J, et al. Management of cocaine-associated chest pain and myocardial infarction. Circulation 2008;117:897-1907.]

It is well-accepted that good, rapid compressions are one of the best interventions we can employ in managing patients with cardiac arrest. It is imperative that we minimize interruptions. Unfortunately, delivering shocks to a patient is a frequent cause of interruptions in compressions. It now appears that we may not need to discontinue compressions during shocks.

A recent study indicates that if shocks are delivered using the common self-adhesive pregelled pad electrodes and the person performing compressions is wearing gloves, the rescuers do not sense a shock at all. Compressions, therefore, do NOT have to stop during the cardioversion or defibrillation.

Whether this statement is true regarding handheld manual defibrillators also is uncertain.


Lloyd MS, Heeke B, Walter PF. Hands-on defibrillation: An analysis of electrical current flow through rescuers in direct contact with patients during biphasic external defibrillation. Circulation 2008;117:2510-2514.

Kerber RE. "I'm clear, you're clear, everybody's clear:" a tradition no longer necessary for defibrillation? Circulation 2008;117:2435-2436.

According to the most recent (2007 Updated) ACC/AHA Guidelines for management of STEMI, the ECG is one of the most important tools to assess for successful reperfusion after thrombolytics. The treating physician should assess the ECG at 90 minutes after administration of lytics. Failure of the ST elevation to decrease by at least 50% in magnitude in the lead with the greatest initial amount of ST elevation is an indication of failed thrombolysis...regardless of whether or not the patient has persistent symptoms. In fact, the Guidelines specifically state that signs and symptoms are considered unreliable indicators of successful reperfusion.

Patients with ECG evidence of failed thrombolysis at 90 minutes should be referred for emergent PCI ("rescue PCI").

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.